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Mo tries Metta

Colleen M.Brophy Editors

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tmm

Lumley Series Editor

Springer
Specialist
Surgery
Series

Other titles in this series include:

Upper Gastrointestinal Surgery, edited by Fielding & Hallissey, 2005
Neurosurgery: Principles and Practice, edited by Moore & Newell, 2004
Transplantation Surgery, Edited by Hakim & Danovitch, 2001

Alun H. Davies and Colleen M. Brophy (Eds)

Vascular Surgery

With 46 Illustrations

^Spri

ringer

Alun H. Davies, MA, DM, FRCS Colleen M. Brophy, MD, FACS

Department of Vascular Surgery Chief of Vascular Surgery

Reader and Honorary Consultant in Surgery Carl T. Hayden VAMC

Imperial College London Research Professor Bioengineering

Charing Cross Hospital Arizona State University

London, UK Clinical Professor of Surgery

University of Arizona

Phoenix, AZ

USA

A catalogue record for this book is available from the British Libuary

Library of Congress Control Number: 2005923614

ISBN-10: 1-85233-288-3 Printed on acid-free paper.

ISBN-13: 978-1-85233-288-4

Apart from any fair dealing for the purposes of research or private study, or criticism, or review, as permitted
under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or trans-
mitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of
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Inquiries concerning reproduction outside those terms should be sent to the publishers.
The use of registered names, trademarks, etc, in this publication does not imply, even in the absence of a specific
statement, that such names are exempt from the relevant laws and regulations and therefore free for general use.
Product liability: The publisher can give no guarantee for information about drug dosage and application
thereof contained in this book. In every individual case the respective user must check its accuracy by con-
sulting other pharmaceutical literature.

Printed in the United States of America. (BS/MVY)

987654321

Springer Science+Business Media
springeronline.com

Preface

This book provides coverage of a broad range of topics in the field of vascular surgery to
residents, registrars in training, and to recent graduates of training programs. The book
is meant to be a practical rendition of the basic knowledge and clinical management
required for optimal care of vascular surgical patients. Each chapter contains input from
specialists in vascular surgery from the United States and Great Britain. There are up-
to-date perspectives on common clinical conditions and emerging techniques encoun-
tered by vascular surgeons from both an American and British perspective. The chapters
are organized under broad topics including medical management, noninvasive and inva-
sive diagnostic approaches, perioperative care, indications and approaches for vascular
procedures, and a discussion of newer endovascular techniques. The information con-
tained in this text is not meant to be exhaustive, but rather a practical overview that will
be useful in directing the management of patients with vascular diseases. The informa-
tion in this text is also meant to be useful for certification examinations and recent grad-
uates of vascular surgical training programs can utilize this text as an update of the most
important vascular topics.

Alun H. Davies
Colleen M. Brophy

Contents

Preface v

Contributors ix

1. The Epidemiology and Etiology of Atherosclerosis

Paul B. Kreienberg, R. Clement Darling III, and F.G.R. Fowkes 1

2. Clinical Evaluation of Patients with Vascular Disease

William G. Tennant 9

3. Noninvasive Vascular Examination

Colleen M. Brophy 19

4. Radiological Investigations

Steven M. Thomas, Kong T. Tan, and Mark F. Fillinger 25

5. Bleeding and Clotting Disorders

Vivienne J. Halpern and Frank C.T Smith 39

6. Medical Management of Peripheral Arterial Disease

Jill J.F. Belch and Andrew H. Muir 53

7. Anesthesia for Vascular Surgery

Jamal J. Hoballah and Farid Moulla 65

8. Nonatherosclerotic Vascular Disease

Jonathan R.B. Hutt and Alun H. Davies 73

9. Lower Limb Ischemia

Rajabrata Sarkar and Alun H. Davies 91

vii

CONTENTS

10. Chronic Venous Insufficiency, Varicose Veins, Lymphedema,
and Arteriovenous Fistulas

Andrew W. Bradbury and Peter J. Pappas 105

1 1 . Vascular Trauma

Kathleen J. Ozsvath, R. Clement Darling III, Laila Tabatabai,

Sacha Hamdani, Alun H. Davies, and Meryl Davis 125

12. Complications in Vascular Surgery
Jeremy S. Crane, Nicholas J.W. Cheshire, and

Gilbert R. Upchurch, Jr. 133

13. Vascular Access

David C. Mitchell and C. Keith Ozaki 141

14. Outcome Measures in Vascular Surgery

Christopher J. Kwolek and Alun H. Davies 149

15. Carotid Artery Disease

A. Ross Naylor, Peter H. Lin, and Elliot L. Chaikof 155

16. Arch Vessel, Vertebrobasilar, and Upper Extremity

Eva M. Rzucidlo and A. Ross Naylor 181

17. Aneurysmal Disease

Philip Davey and Michael G. Wyatt 191

18. Renovascular Hypertension and Ischemic Nephropathy

Sherry D. Scovell 221

19. Visceral Ischemic Syndromes

George Geroulakos, Peter A. Robless, and William L. Smead 231

20. Endovascular Approaches and Techniques

Steven M. Thomas, Kong T Tan, and Mark F. Fillinger 237

Index 253

Contributors

Jill J.F. Belch, MB ChB, MD, FRCP
Peripheral Vascular Diseases Research Unit,
Department of Medicine, Ninewells Hospital
and Medical School, Dundee, UK

Andrew W. Bradbury, BSc, MB ChB, MD, FRCS
University Department of Vascular Surgery,
Research Institute, Birmingham Heartlands
Hospital, Birmingham, UK

Colleen M. Brophy, MD, FACS

Chief of Vascular Surgery, Carl T. Hayden

VAMC, Research Professor Bioengineering

Arizona State University, Clinical Professor of

Surgery, University of Arizona, Phoenix, AZ,

USA

Elliot L. Chaikof, MD, PhD, FACS
Division of Vascular Surgery, Brown
Whitehead Department of Surgery, Emory
University School of Medicine, Atlanta, GA,
USA

Nicholas J.W. Cheshire, MB ChB, MD, FRCS
Regional Vascular Unit, St Mary's Hospital,
London, UK

Jeremy S. Crane, MB ChB, MRCS
Regional Vascular Unit, St Mary's Hospital,
London, UK

R. Clement Darling III, MD

Institute for Vascular Health and Disease,

Albany Medical Center, Albany, NY, USA

Philip Davey, MB ChB
Newcastle upon Tyne, UK

Alun H. Davies, MA, DM, FRCS
Department of Vascular Surgery, Reader and
Honorary Consultant in Surgery, Imperial
College, Charing Cross Hospital, London, UK
London

Meryl Davis

Charing Cross Hospital, London, UK

Mark F. Fillinger, MD, FACS
Department of Vascular Surgery, Dartmouth
Medical School, Dartmouth-Hitchcock
Medical Center, Lebanon, NH, USA

F.G.R. Fowkes, MB ChB, PhD, FRCPE, FFPHM
Wolfson Unit for Prevention of Peripheral
Vascular Diseases, Public Health Sciences, The
University of Edinburgh, Edinburgh, UK

George Geroulakos, MD, FRCS, DIC, PhD
Vascular Unit, Ealing Hospital, London, UK

Vivienne J. Halpern, MD, FACS
Department of Surgery, Division of Vascular
Surgery, Long Island Jewish Medical Center,
New Hyde Park, NY, USA

Sacha Hamdani

Institute for Vascular Health and Disease,

Albany Medical Center, Albany, NY, USA

Jamal J. Hoballah.MD

Department of Surgery, Division of Vascular
Surgery, University of Iowa Hospitals and
Clinics, Iowa City, IA, USA

CONTRIBUTORS

Jonathan R.B. Hutt, BA, MBBS
Department of Accident and Emergency,
Imperial College, Charing Cross Hospital,
London, UK

Paul B. Kreienberg, MD

Institute for Vascular Health and Disease,

Albany Medical Center, Albany, NY, USA

Christopher J. Kwolek, MD, FACS

Division of Vascular Surgery, Massachusetts

General Hospital, Boston, MA, USA

Peter H. Lin, MD, FACS
Division of Vascular Surgery and
Endovascular Therapy, Michael E. DeBakey
Department of Surgery, Baylor College of
Medicine, Houston, TX, USA

David C. Mitchell, MA, MS, FRCS
Department of Surgery, Southmead Hospital,
North Bristol NHS Trust, Bristol, UK

Farid Moulla, MD, MBA

Department of Anaesthetics, Charing Cross

Hospital, London, UK

Andrew H. Muir, MB ChB
Peripheral Vascular Diseases Research Unit,
Department of Medicine, Ninewells Hospital
and Medical School, Dundee, UK

A. Ross Naylor, MB ChB, MD, FRCS
Department of Vascular Surgery, Leicester
Royal Infirmary, Leicester, UK

C. Keith Ozaki, MD, FACS
Division of Vascular Surgery and
Endovascular Therapy, University of Florida
College of Medicine, Gainesville, FL, USA

Kathleen J. Ozsvath, MD

Institute for Vascular Health and Disease,

Albany Medical Center, Albany, NY, USA

Peter J. Pappas, MD

Department of Surgery, Section of Vascular
Surgery, University of Medicine and Dentistry
of New Jersey - New Jersey Medical School,
Newark, NJ, USA

Peter A. Robless, MB ChB, FRCS, MD, FEBVS
Department of Cardiac, Thoracic and Vascular
Surgery, National University Hospital,
Singapore, Republic of Singapore

Eva M. Rzucidlo, MD

Department of Vascular Surgery, Dartmouth-
Hitchcock Medical Center, Lebanon, NH,
USA

Rajabrata Sarkar, MD, PhD

Division of Vascular Surgery, University of

California, San Francisco, CA, USA

Sherry D. Scovell, MD

Division of Vascular Surgery, Beth Israel

Deaconess Medical Center, Boston, MA, USA

William L. Smead, MD

Division of General Vascular Surgery, Ohio

State University, Columbus, OH, USA

Frank C.T. Smith, BSc, MD, FRCS

University Department of Surgery, University

of Bristol, Bristol Royal Infirmary, Bristol, UK

Laila Tabatabai

Institute for Vascular Health and Disease,

Albany Medical Center, Albany, NY, USA

Kong T. Tan, MB ChB, BAO, FRCSI, FRCR
Sheffield Vascular Institute, Vascular Office,
Northern General Hospital, Sheffield, UK

William G. Tennant, BSc, MB ChB, MD, FRCS
Department of Vascular Surgery, Queens
Medical Centre, Nottingham, UK

Steven M. Thomas, MRCP, FRCR, MSc
Sheffield Vascular Institute, Vascular Office,
Northern General Hospital, Sheffield, UK

Gilbert R. Upchurch, Jr., MD
Surgery Department, Vascular Surgery
Section, University of Michigan Health
System, Ann Arbor, MI, USA

Michael G. Wyatt, MB BS, MSc, MD, FRCS
Department of Vascular Surgery, Freeman
Hospital, Newcastle upon Tyne, UK

The Epidemiology and Etiology
of Atherosclerosis

Paul B. Kreienberg, R. Clement Darling III,
and F.G.R. Fowkes

The underlying disorder in the vast majority of
cases of cardiovascular disease is atherosclero-
sis, for which low-density lipoprotein (LDL)
cholesterol is recognized as a major risk factor.
Evidence from epidemiological and clinical
studies continues to improve our understanding
of the pathogenesis of atherosclerosis. Athero-
sclerosis contributes to myocardial infarction,
stroke, and peripheral vascular disease. Despite
major advances in the development of diagnos-
tic methods and effective treatments, cardiovas-
cular disease remains the leading cause of
mortality in the Western world.

Vascular surgeons treat patients who have
already developed end-stage cardiovascular
disease. These surgeons have a unique opportu-
nity to intervene not only in the arterial pathol-
ogy itself, but also in the main factors that
contribute to the development of atherosclero-
sis. Atherosclerosis is a systemic disorder and all
aspects of the disease must be addressed in
treating these patients.

Epidemiology

Cardiovascular disease is responsible for
approximately 30% of all mortality worldwide,
amounting to approximately 15 million deaths
(Sueta et al., 1999). Furthermore, cardiovascular
disease is the principal cause of mortality in all
developed countries, responsible for 50% of all
deaths, and is also emerging as a prominent
public health problem in developing countries,

representing approximately 16% of all deaths. In
the United States cardiovascular disease is the
most common cause of mortality in both men
and women and accounts for almost 500,000
deaths/year. Additionally, 58,800,000 Americans
have one or more types of cardiovascular
disease according to current estimates (Table
1.1).

Coronary artery disease (CAD) has been rec-
ognized as the leading cause of death since the
late 1940s. Hypertension, hypercholesterolemia,
cigarette smoking, and diabetes mellitus were
identified as key contributors to atherosclerosis
and the development of cardiovascular risk.
These risk factors are also related to cere-
brovascular and peripheral vascular disease
(Table 1.2).

The data support aggressive treatment of ath-
erosclerosis in populations at risk. In patients
with peripheral arterial disease (PAD), there
is a high prevalence of myocardial infarction,
stroke, and increased mortality. Lack of patient
and physician awareness of peripheral vascular
disease is associated with low atherosclerosis
risk factor treatment intensity (Sueta et al.,
1999). In this study of patients with known
cardiovascular disease, only 35% had smoking
behavior treated, 73% had lipid abnormal-
ities treated, and 71% were on antiplatelet
therapy. Recognition and treatment in patients
with symptomatic or asymptomatic [ante-
brachial index (ABI) <0.9] PAD were
significantly lower than the rates for patients
with CAD.

VASCULAR SURGERY

Table 1.1. Cardiovascular Disease in the United States:
58.8 million Americans have one or more types of
cardiovascular disease

Type

Number (in millions)

Hypertension

Coronary artery disease

Stroke

4.4

Congestive heart failure

4.6

Peripheral arterial disease

8.4

Table 1 .2. Selected risk factors for atherosclerosis

Age
Diabetes

I Smoking
Hyperlipidemia
Hypertension
Hyperhomocystinemia
Hyperfibrinogenemia

Risk Factors

Smoking

Nearly 440,000 Americans die each year of
smoking-related illness, at a cost of about $50
billion annually. In general, smoking is associ-
ated with a threefold increase in the risk for
peripheral atherosclerosis (Hiatt et al., 1995).
Two large follow-up studies of patients with
intermittent claudication demonstrate the
benefits of smoking cessation (Jonason and
Bergstrom, 1987; Smith et al, 1996). In these
studies, 11% to 27% of the patients complied
with the advice to stop smoking. Within 3 years
of stopping, there was no reduction in limb-
threatening complications of the vascular
disease. However, after 7 years, rest pain had
developed in 16% of persistent smokers, but in
none of those who had stopped smoking. After
10 years, 53% of persistent smokers suffered a
myocardial infarction compared to only 11% of
stopped smokers; 54% of persistent smokers
died compared to 18% of stopped smokers. In a
comprehensive review of the literature, absti-
nence from smoking was found to be associated
consistently with better outcomes following
revascularization, lower amputation rates, and
improved survival (Hirsch et al., 1997).
However, smoking cessation had probably only

a minimal effect in improving walking distance
in claudicants.

Hyperlipidemia

An estimated 50% of American adults have total
blood cholesterol levels of 200mg/dL and
higher, and about 20% of American adults
have levels of 240mg/dL or higher. Levels of
240mg/dL or higher are considered high risk
and levels from 200 to 239mg/dL are considered
borderline high risk. Evidence linking lipids to
atherosclerosis has grown, suggesting that low-
ering serum cholesterol, whether through diet
and lifestyle modification alone or in combina-
tion with cholesterol-lowering pharmacother-
apy, decreases the incidence of vascular events.
For example a 1 mg/dL increase in high-density
lipoprotein (HDL) cholesterol concentration is
associated with a 2% to 3% decrease in CAD and
a 4% to 5% decrease in cardiovascular mortal-
ity. Data from the Multiple Risk Factor Inter-
vention Trial (MRFIT) demonstrate a strong,
graded, positive correlation between serum
cholesterol and cardiovascular mortality rate
(Neaton and Wentworth, 1992). Elevations in
lipoprotein (a) [Lp(a)] constitute a more
recently recognized independent risk factor
for cardiovascular disease. Elevations of LP(a)
greater than 30 mg/dL increase the risk of CAD
approximately twofold (Beckman et al., 2002).

Diabetes

Diabetes mellitus magnifies the risk of cardio-
vascular morbidity and mortality. Diabetics
have a two- to fourfold increase in the risk
of CAD. Diabetics, particularly those with
non-insulin-dependent diabetes mellitus
(NIDDM) are at high risk of vascular disease
because of high levels of triglycerides, LDL, and
very low-density lipoprotein (VLDL) particles.
Patients with NIDDM tend to produce small,
dense LDL particles that are more vulnerable to
oxidation. Other mechanisms for the adverse
effects of diabetes that promote vascular disease
include glycation of arterial wall proteins,
enhancement of LDL oxidation, microvascular
disease of the vasa vasorum, change in cellular
function, promotion of thrombogenesis, and the
development of renal disease and hypertension
(Beckman et al, 2002).

THE EPIDEMIOLOGY AND ETIOLOGY OF ATHEROSCLEROSIS

Hypertension

Hypertension is a well-recognized risk factor
for atherosclerotic disease, particularly stroke
and to a lesser extent ischemic heart disease and
peripheral vascular disease. There are several
possible mechanisms for the underlying poten-
tiation of atherogenesis by hypertension,
including direct mechanical disruptive effects,
actions on vasoactive hormones, and changes in
the response characteristics of the arterial wall.
It is thought that, although hypertension may
potentiate or enhance atherogenesis, hyperten-
sion alone is probably not sufficient for athero-
genesis (Valentine et al., 1996).

Homocysteine

Alterations in homocysteine metabolism are an
independent risk factor for the development of
vascular disease. Elevations of plasma homo-
cysteine levels are associated with increased
risks of all forms of atherosclerotic vascular
disease. Homocysteine can react with LDL cho-
lesterol to form oxidized LDL, which is found
in early atherosclerotic lesions. Through this
mechanism homocysteine can promote
endothelial dysfunction, lipid peroxidation, and
oxidation of LDL cholesterol.

Atherogenesis and Lipid Metabolism

Central to the discussion of atherogenesis is the
metabolism of the peripheral blood lipopro-
teins. These are a complex macromolecule of
lipid and protein in which the nonpolar lipid
core is surrounded by a polar monolayer of
phospholipids and heads of free cholesterol
and apolipoproteins. This structure allows for
the transport of the relatively insoluble lipids
through the liquid plasma. The lipoproteins
differ in their proportions of lipid content and
proteins found on their surface. Lipid disorders
alter the composition and structure of the
lipoprotein. For example, as mentioned earlier,
patients with high triglycerides produce LDL
with a higher protein-to-lipid ratio, yielding a
small dense LDL.

Cholesterol

The body uses cholesterol for numerous func-
tions including cell membrane biogenesis,

steroid synthesis, and formation of bile acids.
The human body can produce all the cholesterol
it needs. The liver is the primary producer of
endogenous cholesterol. Cholesterol is derived
from the in vivo form acetate by a mechanism
characterized by a rate-limiting step in which 3-
hydroxy-3-methylglutaryl coenzyme A (HMG
CoA) is converted into melavalonic acid by
HMG CoA reductase. Statin-type drugs inhibits
this step. This action decreases endogenous
cholesterol production.

Lipoproteins

The major lipoproteins are chylomicrons,
VLDL, intermediate-density lipoprotein (IDL),
LDL, and HDL.

Chylomicrons are larger triglyceride carrying
particles formed after ingestion of a meal. They
result from the processing of ingested fat by
intestinal mucosal cells. They are transported to
the thoracic duct via the intestinal lymphatics to
eventually end up in the peripheral circulation.
At peripheral sites the chylomicrons are acted
upon by lipoprotein lipase bound to capillary
endothelium. Chylomicrons have the lowest
density of any of the lipoproteins.

Very low-density lipoproteins are not as large
as chylomicrons and are slightly more dense.
They carry triglycerides and other fats synthe-
sized in the liver. The IDLs are formed when
some of the triglyceride is removed from VLDL.
Under normal circumstances it is removed so
rapidly from plasma that its concentration is
quite low.

Low-density lipoprotein is normally pro-
duced from the catabolism of VLDL. It is the
major carrier of cholesterol in the plasma.
It is cleared by both receptor-mediated and
non-receptor-mediated processes from the
plasma. Low-density lipoprotein may be modi-
fied through acetylation, oxidation, or both.
These modified forms are particularly impor-
tant in the development of atherogenesis.
First, these molecules are cytotoxic and may
damage the vascular endothelium, initiating
atherosclerosis. They may also aggregate in the
intima of the vessel wall and are chemotactic
for inflammatory cells such as monocytes.
These modified LDL particles have a decreased
affinity for the normal LDL receptor and thus
require clearance through other scavenger
pathways.

VASCULAR SURGERY

Lipoprotein (a)

Lipoprotein (a) [Lp(a)] is a particle comparable
in size to LDL. It is assembled from LDL and a
large glycoprotein called apolipoprotein (a). It
has a decreased affinity for the LDL receptor
compared with LDL itself. Evidence links ele-
vated levels of Lp(a) with increased risk of vas-
cular disease. Lipoprotein (a) may also be taken
up by scavenger pathways and thus accumulates
in foam cells in the early atherosclerotic lesion.

Small-Density LDL

Alterations of LDL metabolism may create
species of LDL particles with higher protein-
lipid concentrations. Increased levels of these
types of particles (termed small, dense LDL) are
associated with increased risk of atherosclerotic
disease and with elevated triglycerides (TGs)
and low levels of HDL cholesterol. The mecha-
nism linking these particles and hypertriglyc-
eridemia relates to the production of
chylomicrons and VLDL that are particularly
rich in TGs. Catabolism of these TG-saturated
VLDL particles produce LDL particles that have
higher than normal TG content. These TG-rich
LDLs are susceptible to further lipolysis by
hepatic lipase, producing a decrease in size and
increase in the density of the particle. Small,
dense LDLs are believed to be more susceptible
to oxidative modification and hence are thought
to be highly atherogenic. Metabolic disorders
such as diabetes and insulin resistance syn-
drome often produce this lipid particle.

High-Density Lipoprotein

High-density lipoprotein is the lipoprotein
responsible for the transport of cholesterol from
cells to other lipoprotein or catabolic sites.
High-density lipoprotein may be formed de
novo in the liver and intestines, and intravascu-
larly from the redundant surface material of
chylomicrons and VLDL. Newly formed HDL
consists of free cholesterol phospholipids and
apoproteins. Free cholesterol from cells and
perhaps from other lipoproteins reacts in the
plasma with a complex containing the enzyme
lecithin-cholesterol acetyltransferase (LCAT),
apoprotein A-l, and an HDL-associated apopro-
tein D. This complex attaches to, and the cho-
lesterol is esterified by, LCAT. As nonpolar

esterified cholesterol migrates to the interior of
the particle, a sphere with an outer coating of
free cholesterol and an inner core of esterified
cholesterol and small amounts of triglyceride is
formed.

In epidemiological studies elevated HDL
levels are associated with a reduced risk of ath-
erosclerotic vascular disease. It is thought that
HDL mediates this benefit through reverse cho-
lesterol transport, which does not involve a
direct route from peripheral tissues to the liver
but rather depends on repeated transfer of cho-
lesterol esters among lipoproteins before excre-
tion through the liver.

Lipid Metabolism

Chylomicrons are formed in the intestine from
ingested fat and taken by the intestinal lym-
phatics to peripheral blood and then to adipose
and other tissues. There, most of the triglyceride
is acted upon by the enzyme lipoprotein lipase,
transported across the cell membrane as fatty
acid and monoglyceride, resynthesized into
triglyceride, and stored. When necessary, intra-
cellular triglyceride can undergo lipolysis. The
released fatty acid is then transported out of the
cell and bound to albumin to be transported in
the plasma. After lipolysis a remnant of the chy-
lomicron is transported to the liver and catabo-
lized as a portion of the particle apolipoprotein
A [Apo(A)] free cholesterol, and phospholipid is
transferred to HDL formed in the liver; HDL
may also pick up free cholesterol from cells. The
cholesterol from other cells is esterified under
the influence of LCAT. This ester is then avail-
able for storage or transport.

Very low-density lipoprotein is synthesized in
the liver from fatty acids obtained from the pro-
cessing of chylomicrons or from endogenously
produced triglyceride. These particles are
smaller and more dense than chylomicrons. The
apolipoproteins associated with VLDL are Apos
B-100, C-l, C-II, C-III, and E.

Very low-density lipoprotein exchanges
triglycerides for cholesterol esters from HDL.
Like chylomicrons, lipoprotein lipase catalyzes
the hydrolysis of triglyceride in VLDL to fatty
acids that are used by muscle or stored as fat
in adipose tissue. This hydrolysis step reduces
VLDL to IDL. Intermediate-density lipoprotein
can be taken up by the LDL receptor or be
reduced to LDL by hepatic lipase. Intermediate-

THE EPIDEMIOLOGY AND ETIOLOGY OF ATHEROSCLEROSIS

density lipoprotein clearance is mediated by
Apo E, which has a higher affinity for the LDL
receptor than Apo BB. Low-density lipoprotein
contains only the apolipoprotein B-100. Two
thirds of the LDL is cleared through the LDL
receptor, 60% to 70% of which is located in the
liver. Peripheral cells can also take up LDL for
membrane biogenesis and steroid synthesis.

Low-density lipoprotein is removed from
plasma by binding to these specific receptors
located in many tissues, including the liver. After
binding, LDL is internalized and metabolized to
free cholesterol and other products. Cholesterol
is stored in cells as the ester. Saturation of LDL
receptors inhibits intracellular cholesterol syn-
thesis by inhibiting HMG CoA reductase. This
negative feedback system operates so that intra-
cellular cholesterol synthesis varies inversely
with the availability of intracellular LDL.

Theories of Atherogenesis

Numerous theories exist regarding the patho-
genesis of atherosclerosis (Table 1.3). One uni-
fying hypothesis linking the various theories is
the "response to injury" model that in a broad
context embraces many aspects of the theories
(Ross, 1999).

The Atheroma

Whatever the initiating process, the first lesion
of arteriosclerosis occurs with the entry of LDL
through the intima and into the arterial wall.
The lipids of human plasma are similar to what
can be found in these early lesions. These early
lesions, termed fatty streaks, are minimally
raised yellow lesions found in the aorta of
infants and children. The lipid deposits in these
lesions are found within macrophages and
smooth muscle cells. Foam cells, which are
macrophages containing lipid particles, are

Table 1.3. Pathogenesis of atherogenesis

Response to injury
Monoclonal hypothesis
Lipid hypothesis
Inflammatory
Lesion regression
Unstable plaque

Figure 1.1. Atherosclerotic plaque. The appearance of
complex atherosclerotic plaque removed during a carotid
endarterectomy.

characteristic of these earlylesions.lt is believed
that these lesions represent the precursor to
more advanced atherosclerotic lesions. As these
lesions grow they then intrude into the arterial
lumen.

Fibrous plaques are composed of large
numbers of smooth muscle cells and connective
tissue forming a cap over an inner core con-
taining mainly lipid cholesterol esters believed
to be from disrupted foam cells. The fibrous cap
may provide structural support or may function
as a barrier to sequester thrombogenic debris in
the underlying plaque from the arterial lumen.
These plaques can show evidence of uneven and
episodic growth. Intermittent ulceration and
healing may occur, and there is evidence that
thrombi formed on lesions are incorporated
into them and resurfaced with a fibro cellular
cap and an intact endothelial layer. Whether all
fibrous plaques are characteristic of advanced
atherosclerosis evolving from the fatty streak
is uncertain. However, fibrous plaques often
appear chronologically after fatty streaks in the
same anatomical locations and characterize
clinically apparent atherosclerosis.

Complicated plaques comprise the end stage
of atherosclerosis and cause clinical symptoms
(Fig. 1.1). These are fibrous plaques that have
become calcified, ulcerated, or necrotic. The
consensus, at least for coronary ischemic events,
is that they are thrombotic in origin, resulting
from the rupture of the complicated atheroscle-
rotic lesions. In most patients myocardial
infarction occurs as a result of erosion or

VASCULAR SURGERY

uneven thinning and rupture of the fibrous cap,
often at the shoulders of the lesion where
macrophages enter and accumulate. Degrada-
tion of the fibrous cap may occur by release of
metalloproteinases, collagenases, and elastases
by these cells.

Response to Injury

The response-to-injury hypothesis initially
proposed that endothelial denudation was the
first step in atherosclerosis. More recent data
suggest that endothelial dysfunction rather
denudation is the primary problem. According
to this model, atherogenesis is a response to
injury of the vascular endothelium. At its
mildest, atherosclerosis may represent a repara-
tive process that leads to thrombus formation
and smooth muscle cell proliferation at the site
of endothelial injury. The production of the
endothelial injury may be from hypertension,
cytotoxic molecules, or blood flow changes. Ath-
erosclerosis develops at sites exposed to unusual
shear stress, such as in the abdominal aortic
bifurcation. Hypercholesterolemia, hyperhomo-
cystinemia, and smoking may all contribute to
endothelial injury.

Lipid Hypothesis

Cholesterol accumulation in atherosclerotic
lesions was initially considered an incidental
accompaniment of the degenerative changes in
the arterial wall. Forty years ago the normal
range of blood cholesterol encompassed every-
one within two standard deviations from the
mean. Cardiologists and cardiovascular sur-
geons concluded that serum cholesterol must be
unimportant because most myocardial infarc-
tions occurred in patients well below this arbi-
trary normal level. The notion that the mean
cholesterol level in the average American was
high enough to cause serious clinical illness
seemed improbable, and thus the lipid hypoth-
esis had few advocates.

However, the most important study to
demonstrate that blood cholesterol is a risk
factor for CAD is the Framingham study. The
results of this study demonstrated the risk for
developing clinically evident CAD was a contin-
uous curvilinear function of blood cholesterol
level. Larger trials would follow substantiating
the link between cholesterol level and clinical

risk, so that eventually experts agreed on the
causal link between blood cholesterol levels and
CAD risk.

As mentioned previously, the endothelial
injury hypothesis postulated the loss of
endothelial cell integrity; however, in areas of
atheroma often the endothelium remains intact.
These results suggested that monocytes pene-
trate the intact endothelium, settle in the intima,
and then take up cholesterol particles to become
foam cells. The lesion is initiated by elevated
blood cholesterol characterized by lipid accu-
mulation in foam cells.

This process is accelerated in vivo under con-
ditions in which the circulating LDL is modified
to oxidized LDL. Many biological properties of
oxidized LDL make it more atherogenic than
native LDL including cytotoxicity. These facts
are supported by data that demonstrate benefits
of antioxidants in preventing oxidation of LDL
on lesion progression.

Inflammatory Theory

This theory stems from the observations that
atherosclerosis represents a different stage in
chronic inflammatory process in the artery.
Unchecked, this process may eventually result in
the advanced complicated lesion.

The different forms of injury increase the
adhesiveness of the endothelium to leukocytes
and platelets. It also induces the endothelium
to have procoagulant activities and to form
vasoactive cytokines and growth factors. The
response then triggers the migration and prolif-
eration of smooth muscle cells that form the
fibrous lesion. Macrophages and T lymphocytes
regulate the majority of the inflammatory com-
ponent of this process.

Macrophages have the ability to produce
cytokines (such as tumor necrosis factor-oc,
interleukin-1, and transforming growth factor-
P), proteolytic enzymes, and growth factors
such as platelet-derived growth factor and
insulin-like growth factor. In addition, they
express class II histocompatibility antigens
that allow them to present antigens to T
lymphocytes.

Plaque Regression

Plaque regression refers to a discernible
decrease in intimal plaque. Apparent regression

THE EPIDEMIOLOGY AND ETIOLOGY OF ATHEROSCLEROSIS

of atherosclerosis has been documented by
serial contrast arteriography in both coronary
and peripheral vascular beds. Although plaque
regression is usually thought of as a decrease in
plaque bulk, it may proceed by other means.
This lessening of luminal intrusion on sequen-
tial angiography coincides experimentally with
decreased plaque size and lipid content.
However, as intimal plaques enlarge, a closely
associated enlargement of the affected artery
segment tends to limit the stenosing effect of the
enlarging intimal plaque (Glagov et al., 1987).
In the human left main coronary artery such
enlargement keeps pace with increases in
intimal plaque and is effective in preventing
lumen stenosis until plaque area occupies on
the average approximately 40% of the cross-
sectional area. Continued plaque enlargement
or complication apparently exceeds the ability
of the artery to enlarge and stenosis may then
develop. Thus the development of critical lumen
stenosis, the maintenance of normal cross-
sectional area, and the development of an
increase in luminal diameter are dependent on
the respective rates of plaque growth and arte-
rial enlargement.

Unstable Plaque

Plaque rupture is the major cause of acute
coronary syndromes (Table 1.4). Often, however,
plaque rupture may be asymptomatic but con-
tributes to the rapid growth of lesions as throm-
bus fibroses.

A number of characteristics distinguish
stable plaque from the unstable plaque that
might produce acute symptoms. The common
underlying feature of the unstable plaque is
thinning of the fibrous cap, which is composed
mainly of vascular smooth muscle cells and
matrix. In plaques that have ruptured, the
fibrous cap at the shoulders of lesion where the
cap meets the normal segment of the arterial
wall is where this thinning occurs. Another
typical feature of the unstable plaque is a large

Table 1.4. Characteristics of the unstable plaque

Thinning of fibrous cap
Lipid core

Intraplaque thrombosis
Macrophage infiltration

necrotic core filled with lipid and cellular debris
with intraplaque and intraluminal thrombosis.
The final feature is that of intense macrophage
infiltration. Proteases and elastases released
form inflammatory cells may contribute to the
thinning of the fibrous cap seen in these lesions.
Additionally, they contribute to the thrombotic
nature of the unstable plaque through the elab-
oration of tissue factor.

Prevention

Hypotheses of pathogenesis and etiology of
atherosclerosis have been tested through the
manipulation of risk factors associated with this
disease process. Among the various strategies
tried, only those strategies that promote a
decrease in LDL or an increase in HDL have
been associated with favorable changes in the
plaque itself.

Additionally, large epidemiological studies
have demonstrated that lower cholesterol levels
are associated with a lower overall risk of mor-
bidity and mortality due to CAD (Martin et al.,
1986). Numerous clinical trials support these
epidemiological data, and show that cholesterol
lowering therapies lead to a significant reduc-
tion in morbidity and mortality associated with
CAD. Additionally, these benefits extend to a
population presenting with peripheral arterial
disease as well. The benefits of statin therapy to
decrease risk is seen as early as the first year of
treatment and extend not only to prevention
of cardiovascular disease but also to the quality
of life. In this era of evidence-based medicine, it
would be difficult not to treat patients identified
at risk with statin therapy based on these data.
Recommended treatment guidelines are given
in Table 1.5.

However, one must understand that the treat-
ment to prevent or stabilize atherosclerotic
plaques extends not just to those patients with
demonstrable severely stenotic lesions. In fact,
it seems to be that most myocardial infarctions
occur at sites that did not have prior angio-
graphically recognized severe lesions. These
facts are supported by the finding that thallium
studies in stable CAD show that the site of
stress-induced myocardial ischemia is fre-
quently not the site of myocardial infarction. To
extend this concept, it would seem reasonable to
start statin therapy in patients at risk before the

VASCULAR SURGERY

Table 1 .5. Risk factors that modify low-density lipoprotein

Cigarette smoking

Hypertension (>140/90) or on antihypertensive

I medication
Low HDL cholesterol (<40mg/dL)
Family history of premature coronary artery disease in
male first-degree relative or female <65 years of
age
Age (men >45 or women >55 years of age)

Risk categories that modify LDL cholesterol goals
Risk category LDL goal

Coronary artery disease <100mg/dL

Multiple (2+) risk factors <130mg/dL

0-1 risk factors <160mg/dL

development of these unstable plaques or to
stabilize the ones already present.

Controversy

The importance of treating patients to lower the
cholesterol levels and to lessen the risk of devel-
oping atherosclerosis is well accepted. However,
the question remains whether there is a thresh-
old below which cholesterol reduction may
translate into clinical benefit.

On average drug therapy with simvastatin
loweres LDL cholesterol levels by 35% and
reduces heart risk by 34% (Pedersen et al.,
1998). The goal of this study was to reduce total
cholesterol below 200. However, many patients
achieved reductions greater than this and were
associated with continuing but progressively
smaller reductions in heart attack risk. This
subgroup analysis estimated a 1% reduction in
LDL, reducing the risk of major coronary events
by 1.7%. However, at what point this benefit can

be extrapolated to remains to be determined.
Another active debate is whether the treatment
for acute myocardial infarction in high-risk
patients should be lipid-lowering therapy rather
than revascularization (Forrester and Shah,
1997).

Additional therapeutic approaches that are
receiving attention include antioxidant treat-
ment such as vitamin E. In a situation where
oxidation of LDL is a major target in atheroge-
nesis, antioxidant therapy obviously might play
a role. To what extent it may be of benefit is still
under investigation.

Fundamental to the treatment of atheroscle-
rosis is recognizing it as a systemic disease with
the potential to affect a variety of end organs.
Therefore, when patients are identified it
appears advantageous to screen, counsel, and
treat patients as soon as possible.

References

Beckman JA, Creager MA, Libby P. (2002) JAMA 287:

2570-81.
Forrester JS, Shah PK. (1997) Circulation 96:1360-2.
Glagov S, Weisenberg E, Zarins CK, Stankunavicius R,

Kolettis GJ. (1987) N Engl J Med 316:1371-5.
Hiatt WR, Hoag S, Hamman RE (1995) Circulation 91:

1472-9.
Hirsch AT, Treat-Jacobson D, Lando HA, Hatsukami DK.

(1997) Vase Med 2:243-51.
Jonason T.Bergstrom R. (1987) Acta Med Scand 221:253-60.
Martin MJ, Hulley SB, Browner WS, Kuller LH, Wentworth

D. (1986) Lancet 2:933-6.
Neaton JD, Wentworth D. (1992) Arch Intern Med 152:56-64.
Pedersen TR, Olsson AG, Faergeman O, et al. (1998) Circu-
lation 97:1453-60.
Ross R. (1999) N Engl J Med 340:115-26.
Smith I, Franks PJ, Greenhalgh RM, Poulter NR, Powell JT.

(1996) Eur J Vase Endovasc Surg 11:402-8.
Sueta CA, Chowdhury M, Boccuzzi SJ, et al. (1999) Am J

Cardiol 83:1303-7.
Valentine RJ, Kaplan HS, Green R, Jacobsen DW, Myers SI,

Clagett GP. ( 1996) J Vase Surg 23:53-61, discussion 61-3.

Clinical Evaluation of Patients with
Vascular Disease

William G. Tennant

The primary goal of the clinical evaluation of
patients with vascular disease is to decide which
tests will help the surgeon treat the patients'
problem while at the same time minimizing
patient discomfort. Investigation of patients
with vascular disease differs from that of other
surgical patients and depends mainly on the
underlying disease process. For instance,
patients with lower extremity occlusive vascular
disease suffer not only from their index problem
(claudication, ischemic rest pain, gangrenous
ulcers) but also from some of the conditions that
have predisposed them to vascular disease in the
first place (diabetes, hypercholesterolemia, etc.).
In addition, they are likely to require a number
of medications for these predisposing condi-
tions, some of which require consideration in
diagnosing and treating vascular disease. It is
also important to keep in mind that the presence
of occlusive vascular disease in the lower limbs
indicates the likely involvement of other vessels
(coronary, carotid, cerebral, renal, mesenteric,
etc.). Because the underlying pathology is very
different, the clinical evaluation of patients with
aneurysmal disease is strikingly different. These
patients are healthier overall and their clinical
evaluation is less intense.

Patients' Characteristics

Vascular surgery patients suffer many of the
fears and anxieties of other surgical patients.
Added to this are fears of gangrene, amputa-

tion, and aneurysm rupture. Many elderly
patients suffer other severe illness or disability.
They may, as a result, have limited aims and
aspirations when seeking investigation and
treatment. In contrast, younger patients' family
life or career may be threatened by their disease,
and very high expectations of investigation and
treatment have to be realistically modified. It is
these human characteristics that deserve our
consideration when deciding on an investigative
pathway. Although it is important to gain all the
information required to execute an effective
treatment plan, it is equally important to do this
in as noninvasive and humane a way as possi-
ble. Fortunately, the technology is on our side in
this regard, and the days of highly invasive
investigations are probably numbered.

The History

The value of a good clinical history is increas-
ingly overlooked as techno-diagnosis advances.
One should remember that the history is usually
the first interaction that takes place between the
doctor and patient. It is at this time that the
therapeutic relationship is forged. With skill and
practice it is possible to elicit not only symp-
toms but also their significance to the patients,
the patients' expectations and fears, and their
attitudes toward treatment. It is possible to
avoid unnecessary diagnostic tests and limit
the investigative mill that the patient is put
through.

VASCULAR SURGERY

There are some general points in the clinical
history that warrant mention:

1. Lifestyle. Risk factors that can lead to
the progress of vascular disease such as
smoking, diabetes, hypertension, and
hyperlipidemia are ascertained in the
history. Additionally, an adequate exercise
history should be elicited. One question
that elucidates the rate-limiting organ
system is how far patients can walk, and
what stops them (leg pain, shortness of
breath, chest pain, etc.). It is also important
to know if the patient is taking hormonal
medications such as oral contraceptives
or hormone replacement therapy. These
medications can predispose to venous
and occasionally arterial thrombosis. It is
during the history taking that a physician
can begin to address many of these risk
factors. By recruiting antismoking clinics
or eliciting the help of diabetes and cardiac
specialist physicians, a surgeon can
improve a patient's overall health both pre-
and postoperatively.

2. Family history. It is especially important to
question the patient about the prevalence
of early cardiovascular disease or throm-
bosis (i.e., stroke, occlusive limb disease, or
cardiac disease) that manifests before age
50. Aneurysm disease has a clear familial
association, and an incidence approaching
20% in first-degree relatives.

3. Atherosclerosis. Atherosclerosis is a sys-
temic disorder, so inclusion of a discussion
of stroke/transient ischemic attacks and
coronary artery disease/myocardial infarc-
tion/angina is important.

Although the points covered above may elicit
factors predisposing the patient to vascular
occlusive or aneurysm disease, they are non-
specific and nondiagnostic. Because the symp-
toms of occlusive vascular, aneurysmal, and
venous disease differ, they will be dealt with sep-
arately below. It should be remembered,
however, that they may occur in combination.

Chronic Limb Ischemia

The principal symptom of chronic limb
ischemia (CLI) is that of claudication (claudi-
care, to limp). This is effort-related muscular

pain relieved by rest. In the lower limb, patients
in the initial stages of disease complain of calf,
thigh, or buttock pain brought on by walking,
which is relieved after a few minutes of rest.
This is commonly a condition that follows a
variable course with periods of remission and
relapse, often according to changes in lifestyle,
medications, or the progress of a comorbid con-
dition such as diabetes mellitus. With worsen-
ing ischemia, the patient begins to feel pain
at night usually in the distal forefoot, toes,
and instep (rest pain). As the patient becomes
horizontal in bed (removing the effect of gravity
on blood flow), and the blood pressure drops
with the onset of sleep, perfusion of the lower
limbs worsens. Patients often wake up in the
middle of the night with pain that they can
relieve only by getting out of bed and, paradox-
ically, walking around the bedroom. Some
patients with rest pain learn to sleep with the
affected leg hanging over the side of the bed to
regain the assistance of gravity (Fig. 2.1). When
patients sleep with ischemic limbs dependent,
there is a gradual onset of edema and worsen-
ing tissue perfusion, which create a vicious
circle of pathologies.

Acute Critical Limb Ischemia

Acute critical limb ischemia (ACLI) can be
defined as sudden onset of severe limb
ischaemia of less than 24 hours' duration. The
principal causes are arterial embolism and
thrombosis. A history should be taken to
include the common sources of emboli (Table
2.1). A history suggestive of claudication in
the affected limb makes thrombosis in situ of
a chronic arterial stenosis more likely than
embolus.

The symptoms of ACLI include paresthesia,
pain in the limb at rest, numbness, coldness, and
paralysis. Symptoms are likely to be more severe
in cases of embolus than in cases of thrombosis
because thrombosis usually occurs at the site of
a chronic stenosis, completely occluding the
vessel. Where a stenosis has existed, it is likely
that a collateral circulation has developed that
will continue to function even when the main
vessel is occluded. In cases where an embolus
has suddenly occluded a previously normal
limb artery, there are no collaterals to support
adequate perfusion.

CLINICAL EVALUATION OF PATIENTS WITH VASCULAR DISEASE

Figure 2.1. Rest pain. This elderly woman is adopting a classic
posture, which gives gravity assistance to blood flow while she
is recumbent.

Upper Limb Vascular
Occlusive Disease

Chronic occlusive vascular disease in the arm is
considerably less common than that in the leg.

Table 2.1. Common sources of emboli

Cardiac arrhythmias (commonly atrial fibrillation)
Cardiac mural thrombus from recent myocardial

infarction
Diseased heart valves

Atheroma of aortic arch or more distal aorta
Areas of chronic arterial damage (cervical rib, thoracic

outlet syndrome)
Aortic aneurysm (rare)
Broken catheter tips

Bullets and other materials introduced violently
Air

Amniotic fluid
Fat (long bone fractures)

Perhaps because of its rarity, the diagnosis is
often made late and by exclusion. Arm claudi-
cation presents with effort-induced heaviness
or tiredness that is relieved by rest. The patient
may also complain of relative pallor and an
impression of coldness of the affected limb,
exacerbated by cold exposure.

Subclavian occlusive disease may also cause
cerebrovascular symptoms because of the
anatomical relationship between the vertebral
arteries that arise off of the subclavian arteries.
This is best exemplified by the subclavian steal
syndrome. Tight stenosis or occlusion of the
subclavian artery proximal to the origin of the
vertebral artery leads to effort-induced reversal
of flow in the vertebral artery that contributes
to the arterial supply of the arm (Fig. 2.2). When
the arm is exercised, increased (reversed) flow
from the vertebral artery to the subclavian can
lead to marked but transient symptoms of
brainstem ischemia in addition to arm claudi-
cation. Although most patients with this condi-
tion have no symptoms of cerebrovascular steal
at rest, symptoms can occur during exercise,
including dizziness, ataxia, diplopia, and bilat-
eral blurred vision.

Acute upper limb vascular disease is usually
due to embolism. Trauma is a less common

Severe stenosis
or occlusion
of proximal
subclavian artery

Figure 2.2. Subclavian stenosis can lead to reversal of flow in
the vertebral artery and vertebrobasilar symptoms.

VASCULAR SURGERY

cause. The symptoms are the same as for acute
lower limb disease: pain or numbness, paralysis,
and pallor. A history of recent myocardial
infarction or of known atrial fibrillation should
be taken. Traumatic causes can range from a
"simple" supracondylar humeral fracture to the
massive bone and soft tissue disruption caused
by motorcycle accidents. It is also important to
find out how the symptoms have developed over
time. For instance, many elderly patients with
brachial emboli give a history of severe pain ini-
tially followed by gradual resolution over the
succeeding hours. These patients then present
to the vascular surgeon with viable limbs and
minor symptoms. Other patients may complain
of worsening symptoms, and the need for
urgent intervention becomes obvious. Where an
artery has been damaged by trauma, there may
be a clear history of resolution of symptoms
and restoration of pulses after, for instance, the
reduction of a fracture.

Aortic Aneurysm

Whether the aneurysm affects the thoracic or
abdominal aorta, there are usually very few
symptoms. Chronic symptoms that do occur are
usually due to pressure effects on the surround-
ing structures. Even in quite small abdominal
aneurysms, erosion of adjacent vertebral bodies
can occur, leading to back pain. One of the com-
monest symptoms of large thoracic aneurysms
is dysphagia from direct pressure on the esoph-
agus. Patients who notice abnormal abdominal
pulsation (frequently while bathing, or in bed)
often present with amusing self-diagnoses that
belie the serious nature of the condition. This
has been called "slipped-heart syndrome."

In the special case of inflammatory abdomi-
nal aortic aneurysm (vide infra), fibrosis can
extend laterally in the retroperitoneum to
include the ureters, which can result in ureteral
stenosis. The presentation of such aneurysms
is often via the urologist, the patient having
presented with symptoms due to obstructive
uropathy and hydronephrosis or even renal
failure.

The acute presentation of abdominal aortic
aneurysm is usually as a differential diagnosis
of acute abdominal pain. Symptoms are not
always due to rupture, and the aneurysm may
be intact but acutely symptomatic. Symptoms in
an intact aneurysm, though the etiology is

unknown, are principally severe abdominal and
back pain of sudden onset. The pain may radiate
into the groin, flanks, or genitalia and can
closely mimic renal colic. When the aneurysm is
ruptured, there is also collapse and hypov-
olemia. The distinction between acutely symp-
tomatic intact aneurysms and ruptured
aneurysms is impossible to make on history
alone.

Superficial Venous Disease

Patients frequently complain about the
unsightly nature of varicose veins, and imbue
them with many symptoms. These include
aching, itching, and swelling. Symptoms,
however, correlate poorly with the apparent
severity of the disease. When superficial venous
disease is extensive and severe, symptoms are
common and include those above with the addi-
tion of ulceration.

Deep Venous Disease

Symptoms are usually of swelling, heaviness,
and occasionally severe discomfort. The symp-
toms are usually worse after prolonged stand-
ing. There may be a history of deep venous
thrombosis or previous abdominal or pelvic
surgery with venous damage. Symptoms result
from venous hypertension in the limb affected,
and this is the final common pathway of both
occlusion and incompetence of the deep veins.
There may be a history of ulceration even if
none is present at the time of examination.

Clinical Examination

Inspection

The general signs of a predisposition to occlu-
sive vascular disease include deposits of fat in
the thin skin around the eyes (xanthelasma),
and in the corneas themselves (arcus senilis).
Patients may have white hair; the fingertips may
be tinted yellow with tar from cigarettes, and
patients may smell strongly of cigarette smoke.
Some of these patients assert that they have
stopped smoking. Patients may be short of
breath at rest or on minimal exertion because of
coexistent cardiac or respiratory disease.

CLINICAL EVALUATION OF PATIENTS WITH VASCULAR DISEASE

The specific effects of occlusive vascular
disease may produce clinical signs apparent
on general examination, such as limb swelling
ulceration or gangrene. There may be signs of a
previous stroke or of severe loss of weight.

Aneurysms may appear as a localized
swelling if present in the periphery, for instance,
traumatic aneurysms of the femoral, popliteal,
or radial artery (Fig. 2.3). There are often very
few signs of abdominal aortic aneurysms on
general examination, unless the patient is very
slim and the abdominal wall may be "draped"
across the aneurysm with the patient supine and
relaxed. The pressure caused by an aneurysm on
adjacent structures may rarely cause related
clinical signs (Fig. 2.4).

Palpation: Examination
of the Pulses

Lower Limbs

Pulses are normally palpable in the femoral tri-
angle at the midinguinal point, in the popliteal
fossa, posterior to the medial malleolus, and on
the dorsum of the foot between the first and
second metatarsals. In the normal subject, the
popliteal pulse is felt by compressing the artery
against the tibial plateau anteriorly. This is best
done with the patient's leg flexed at the knee.
It is particularly important to distinguish aor-
toiliac disease from infrainguinal disease. In
aortoiliac disease the femoral pulses are dimin-
ished, whereas in infrainguinal disease the
femoral pulses are normal.

Figure 2.3. This aneurysm of the superficial femoral artery was
caused by previous trauma. It presented as a pulsatile swelling
of the mid thigh.

Figure 2.4. Swelling due to venous congestion from a popliteal
aneurysm. A popliteal aneurysm caused the swelling of this
patient's left leg by pressure on the adjacent popliteal vein.
There are also multiple small skin infarcts caused by emboliza-
tion from the aneurysm.

Upper Limbs

The subclavian pulse is present in the supra-
clavicular fossa and the axillary artery in the
infraclavicular fossa. Thereafter, the brachial
artery is usually palpable in the cubital fossa
deep to the bicipital aponeurosis. The ulnar
pulse is palpable just medial to the tendon of the
flexor carpi ulnaris and the radial lateral to the
tendon of the flexor carpi radialis on the radial
styloid process. A pulse is usually also palpable
in the "anatomical snuff box" between the
tendons of the extensor pollicis longus and
brevis, where it overlies the scaphoid bone.

Neck

The carotid pulse can be felt medial to the
muscle belly of sternomastoid. Occasionally

VASCULAR SURGERY

there may be marked tortuosity of the carotid
artery in the neck, giving the impression of an
aneurysm.

Abdomen

It is usually difficult to feel the normal abdom-
inal aorta without causing the patient discom-
fort. The aorta is best palpated between the
xiphoid and umbilicus. Below the umbilicus,
the aorta bifurcates. When aneurysmally dilated
the pulse is easier to feel, and may in fact be a
presenting symptom.

Auscultation

In each case, palpation of the pulses should
be followed by auscultation in the same sites.
Where there is a stenosis either at or immedi-
ately proximal to the point of examination, a
bruit will be heard in time with the cardiac
systole. This is particularly relevant in carotid
stenosis. Carotid bruits are not very sensitive
or specific for carotid stenosis and require
confirmation by carotid ultrasound (Magyar
et al., 2002). However, a carotid bruit is often
indicative of systemic atherosclerosis. Rarely,
the bruit of a stenosed renal artery can be heard
during auscultation of the abdomen.

Differential Diagnosis of Leg Ulcers

Many vascular patients present with ulcera-
tions. There are three major types of leg ulcers:
venous, ischemic, and neuropathic (Table 2.2).
Ischemic ulcers tend to be very distal in the vas-
cular tree and painful. Venous stasis ulcers tend
to occur in the region of the medial malleolus
and have associated brownish discoloration of
the skin (lipatodermatosclerosis) and edema.
Neuropathic ulcers tend to occur in diabetic
patients under pressure points. Patients with
diabetes present particular challenges in terms

Table 2.2. Differential diagnosis ol

leg ulcers

Type of

Location

Pain

Associated

ulcer

findings

Ischemic

Distal foot

Yes

No pulses

Venous stasis

Medial

Maybe

Stasis

malleolus

dermatitis

Neurotropic

Pressure

Diabetes

points

Figure 2.5. Pallor on elevation. The patient's leg is elevated,and
the foot displays profound pallor.

of diagnosis and management (Sumpio et al.,
2003).

Other Clinical Tests

Capillary Refill

With the patient supine and the great toes
together, both toes are gripped by the examiner
using one hand and compressed. On release, the
toes should change symmetrically from white to
pink in less than 5 seconds. Asymmetry suggests
arterial disease on the slowest side.

Buerger's Test

This is a test for severe chronic arterial occlu-
sive disease. With the patient supine the straight
legs are raised as far as possible. In arterial
disease, there is extreme pallor of the feet in this
position (Fig. 2.5). The legs are then placed on
the examination bench and the patient is told to
sit with the legs dependent over the side of the
bench. Where there is severe chronic arterial
disease, the feet become suffused with a deep
ruddy red color, commonly described as "sunset
foot." This is caused by ischemic maximal dila-
tion of the arteriolar bed of the skin, allowing
the skin to fill with partially oxygenated blood
(Fig. 2.6).

Trendelenburg Test

In cases where incompetence of the saphe-
nofemoral junction is suspected as a major

CLINICAL EVALUATION OF PATIENTS WITH VASCULAR DISEASE

Figure 2.6. Dependent rubor. The leg has been placed depend-
ent over the side of the bed, and is extremely hyperemic.

cause of superficial varicose veins, the patient is
asked to lie supine and raise the affected limb to
about 45 degrees. Venous blood is "milked"
proximally by firm stroking of the leg to empty
all of the superficial veins. A tourniquet is
applied as proximally as possible to occlude the
superficial venous system. The patient is then
asked first to sit up and swing the legs over the
side of the examination couch, and then to
stand. Where saphenofemoral incompetence is
the major cause of superficial varicosities, the
varicosities will remain collapsed. It is usual for
the superficial veins to fill slowly, but rapid
filling of the varicosities with the tourniquet in
place indicates significant perforator disease
distal to the tourniquet. It is possible to localize
incompetent perforating veins by repeating the
test with the tourniquet just above the knee. In
this case calf varicosities will remain collapsed
if the guilty perforating vein is between the
saphenofemoral junction and the tourniquet. If
the incompetent perforating vein is below the
knee, the below knee varices will fill rapidly.
Although the Trendelenburg method is some-
what insensitive in localizing incompetent per-
forating veins, it can provide useful clinical
information. For more accurate localization of
incompetent thigh perforators, and for all those
in the calf, it is best to use duplex examination.

Fixed Wave Doppler Examination

A number of small and portable battery-
operated machines are available, operating at

frequencies between 5 and 10 MHz depending
on the depth of penetration required (Fig. 2.7).
In each case the signal from the insonation of
the examined artery is converted into an audible
sound from a built-in speaker. Normally the
signal has a "triphasic" sound. Although it is
possible to use the Doppler simply to locate an
artery, the most common use is to measure the
blood pressure at the periphery of a limb. For
this, the Doppler machine is used in the same
way as a stethoscope when measuring the blood
pressure using Korotkoff sounds. A blood pres-
sure cuff is placed around the limb proximal to
the artery to be examined. The artery is then
insonated and the cuff inflated above the sys-
tolic pressure. As the cuff is deflated, the signal
returns, and the pressure at which this happens
is noted. When the pressure in all the required
arteries has been measured, the pressure in the
brachial artery is measured using the same tech-
nique. The ratio between the ankle pressure
and the brachial pressure is known as the
ankle-brachial index (ABI). The ABI in normal
patients without arterial occlusive disease is
greater than 1.

Handheld Doppler examination is also useful
in the diagnosis of superficial venous disease

Figure 2.7. An example of the type of handheld Doppler device
suitable for use in the clinic.

VASCULAR SURGERY

to confirm the incompetence of the saphe-
nofemoral or saphenopopliteal junctions, and to
localize incompetent perforating veins. At each
of the saphenous junctions, there is physiologi-
cal retrograde flow into the superficial system of
under 1 second' duration, which is audible using
a handheld Doppler machine. If the reflux is of
longer duration, it is indicative of pathological
incompetence of the junction. With an experi-
enced operator, it is possible to localize incom-
petent perforating veins.

Clinical Examination
of Specific Conditions

Chronic Lower Limb Ischemia

In mild disease the legs may appear normal to
inspection, but capillary return is delayed and
the feet may be cool to touch. Distal pulses are
be either weak and difficult to feel or absent.
With increasing severity, the legs may be hair-
less below the knee, and the toes cyanotic. As
ischemia progresses, more proximal pulses may
disappear and ulcers may appear on or between
the toes. Buerger's test becomes positive. Even-
tually more proximal painful ulcers over the
lower leg, and digital gangrene signals very
severe occlusive disease.

Acute Lower Limb Ischemia

Where there is thrombosis of a collateralized
chronic stenosis, the signs of acute ischemia
may be less severe than in cases of embolus
(vide supra). In these less severe cases, the acute
onset of the symptoms maybe the most obvious
clue. The limb may appear normal to inspection
but have reduced capillary return, pale rapidly
on elevation, and have slightly altered sensation
on formal testing. There may be some weakness,
principally of the anterior muscle groups of the
lower leg. With increasing ischemia, the signs
of pallor and weakness increase, and there may
be complete paralysis of the foot and toe
dorsiflexor muscle groups. In these cases, the
foot usually lies at rest in equinovarus due to
paralysis of the peroneal muscles. In severe
acute ischemia, such as that caused by
embolism, the skin becomes mottled with blue
blotches on a background of sallow white. If the

blotches blanche on finger pressure (unfixed
mottling), it may still be possible to save the leg
if immediate action is taken to revascularize it.
Where the mottling is fixed, that is, it fails to
blanche on pressure, it is too late to save the
limb. Muscle ischemia and impending necrosis
in these severe cases cause the muscles to swell
and become tender. This is often best seen in the
anterior muscle compartment where the ten-
derness is often exquisite and the compartment
is almost stone hard to palpation. Examination
of the pulses allows approximate localization of
the level of disease. The presence of normal
pulses on the opposite extremity supports the
diagnosis of acute embolic disease.

Mesenteric Ischemia

In chronic cases there are often few signs on
examination of the abdomen, but signs of
weight loss and systemic vascular disease
are present. Where the disease is acute, the
abdomen can feel curiously doughy in the early
stage and is diffusely tender. Bowel sounds may
still be present. As time passes and transmural
infarction supervenes, peritoneal signs develop.

Upper Limb Ischemia

Chronic arterial occlusive disease seldom affects
the upper limb except as part of rare conditions
affecting the aortic arch and subclavian ar-
teries. Upper limb ischemia is usually due to
embolism. The commonest embolic source in
these cases is the myocardium in atrial fibrilla-
tion or following myocardial infarction. Other
sources include proximal stenoses in the aortic
arch and subclavian arteries (Fig. 2.8). The clin-
ical signs of acute upper limb ischemia are the
same as in the lower limb: sensory alteration,
paresthesia, weakness, and muscle tenderness. It
is uncommon for the ischemia to be so severe as
to lead to irreversible change because of the rich
collateral supply in the arm. In intravenous drug
abusers, intraarterial injection of illicit medica-
tions "cut" with insoluble excipients may lead to
extensive acute occlusion of small distal vessels
(Fig. 2.9). Patients often present following delib-
erate or accidental intraarterial injection, with
a short history of almost overwhelming pain
together with exquisite muscle tenderness and
forearm muscles stone hard to touch. The skin

CLINICAL EVALUATION OF PATIENTS WITH VASCULAR DISEASE

Figure 2.8. Gangrene from an arterial embolus. The distal
aspect of the digit is gangrenous secondary to an embolus
arising from a subclavian stenosis.

of the forearm and hand is fixed and mottled
and the hand clawed.

Chronic Venous Disease

Inspection with the patient standing is one of
the most important aspects of the examination
of chronic venous disease. The dilated veins of
superficial disease are frequently obvious. Other
signs of importance include swelling, hemo-
siderosis of the skin of the malleolar area,
lipodermatosclerosis, atrophie blanche, and
ulceration (Fig. 2.10). Deep venous disease may
be less obvious and present simply with chronic
swelling of the limb. In later stages, all of the
above signs may be present.

Figure 2.9. Gangrene from drug injection. Injection into
the radial artery led to gangrene to the thumb and thenar
eminence.

Figure 2.10. Chronic venous insufficiency. The limbs demon-
strate the brownish discoloration associated with lipatoder-
matosclerosis. Varicosities are also present.

VASCULAR SURGERY

Conclusion

Clinical evaluation of the patient with vascular
disease is of the utmost importance. Many clues
about a patient's temperament, the disease, and
expectations of treatment can be obtained from
a thorough interview. Assessing a patient's risk
factors for vascular disease not only helps the
physician better understand the patient's chief
complaint but also directs the preoperative
workup of the patient. Despite the recent
advances in vascular radiology, nothing replaces
an excellent physical examination, which can

shed light on the clinical extent of a patient's
disease process. Finally, when radiological
studies may take valuable time, there are several
bedside tests that can be performed rapidly,
allowing a vascular surgeon to make immediate
treatment decisions.

References

Magyar MT, Nam EM, Csiba L, Ritter MA, Ringelstein EB,

Droste DW. (2002) Neurol Res 24:705-8.
Sumpio BE, Lee T, Blume PA. (2003) Clin Podiatr Med Surg

20:689-708.

Noninvasive Vascular Examination

Colleen M. Brophy

The noninvasive vascular laboratory assists
with the diagnosis of peripheral arterial disease.
In general, two basic approaches are used: (1)
indirect measures that characterize the func-
tional severity of the disease, such as segmental
pressures, Doppler waveform analyses, plethys-
mography, and skin perfusion pressures; and (2)
direct measures that characterize the anatomy
of the disease using color duplex imaging. These
studies are used to accurately diagnose the loca-
tion and extent of peripheral arterial disease,
assist with the planning of therapeutic options
for the disease, and follow the outcomes of
peripheral vascular interventions.

Indirect Evaluation of
Arterial Disease

Ankle-Brachial Index

In patients without palpable pedal pulses, the
next step in the clinical evaluation is to perform
a Doppler analysis. This is usually performed in
the clinic or at the bedside using a handheld
Doppler device. The probe is placed at an angle
(Fig. 3.1) over the dorsalis pedis and posterior
tibial arteries to determine if a signal can be
obtained. The complete absence of Doppler
signals suggests significant peripheral arterial
disease. Approximately 10% of the normal pop-
ulation does not have a dorsalis pedis artery;
hence, the absence of a dorsalis pedis signal
alone is not a significant finding. It is important

to place the probe directly over the artery but at
a 45- to 60-degree angle to obtain the best
signal. Doppler signals can be used to assess the
severity of the disease. A blood pressure cuff
is inflated just above the ankle and a Doppler
signal is listened for while the cuff is deflated.
The highest pressure in which a signal is heard
(dorsalis pedis compared to posterior tibial) is
the ankle index. A similar approach with a blood
pressure cuff on the upper arm and a Doppler
probe on the brachial artery is used to deter-
mine the brachial index. The ratio of the
ankle to the brachial index represents the
ankle-brachial index (ABI). The ABI is usually
1 or greater. An ABI of 0.5 to 0.8 is consistent
with claudication, and less than 0.4 is consistent
with critical limb ischemia. Diabetic patients
often develop medial calcinosis. Simply stated,
the medial wall of the vessels become calcified
("bone-like") and cannot be compressed by a
blood pressure cuff. Thus, the ABI in a diabetic
patient may be falsely elevated, and other
studies are needed to accurately assess the
peripheral vascular status. In general, however,
the ABI is a useful screening test for peripheral
vascular disease.

Segmental Limb Pressures

Segmental limb pressures assist with determin-
ing the location of disease by measuring the
pressure in the upper thigh, lower thigh, below
the knee, just above the ankle, and at the trans-
metatarsal level (Figs. 3.2 and 3.3). Again using

VASCULAR SURGERY

Figure 3.1. Doppler signals are best obtained by holding the
Doppler probe at an angle over the artery that is being
insonated.

a Doppler, an arterial signal is found at the dor-
salis pedis or posterior tibial artery, the cuff
is inflated until no signal is heard, and then
deflated until the signal resumes. The systolic
pressure is recorded for each cuff at each loca-
tion. A gradient (decrease) in pressure greater
than 20 mm Hg between adjacent levels suggests
arterial occlusive disease in the vessel between
the two cuffs (Fig. 3.3). An arterial pressure in
the thigh that is less than that in the arm sug-
gests aortoiliac occlusive disease. A drop in
pressure between the upper thigh and lower
thigh cuffs suggests superficial femoral artery

disease. It is important to make a distinction
between aortoiliac and infrainguinal disease
because the overall approach is somewhat
different.

An additional useful measurement, particu-
larly in diabetic patients, is to measure the
digital pressures. The digital arteries are less
likely to be affected by medial calcification and
hence provide useful information when the ABI
is falsely elevated. Digital pressures are meas-
ured by placing a pneumatic cuff around the
digit and measuring a plethysmographic arte-
rial waveform using a photoelectrode on the
end of the digit. In general, a normal toe pres-
sure is 80% to 90% of the brachial pressure
(normal toe-brachial index is 0.8 to 0.9). A toe
pressure less than 38 mm Hg has been correlated
with impaired forefoot wound healing (Vitti
et al, 1994).

In patients with symptoms consistent with
claudication but relatively normal indices, exer-
cise testing should be performed. A standard
exercise test involves measuring the ABI at rest
followed by walking on a treadmill at 2 miles/
hour at a 10% to 15% incline for 5 minutes.
The ABI is recorded 1 minute after exercise.
Normally, after exercise, there is a slight in-
crease or no difference in the ABI. If the ABI
decreases after exercise, this is consistent with
claudication.

Pulse Volume Recording

Pulse volume recordings (PVRs) are a plethys-
mographic measure of limb perfusion.

Figure 3.2. Segmental limb pressures are
measured by placing the cuffs along the
extremity.

NONINVASIVE VASCULAR EXAMINATION

SEGMENTAL PRESSURE
AND PVR STUDY

Brachial
RIGHT LEFT

134 |

1.25 y i7i

1.23
0.81

RIGHT

0.74

101
110

[dp

0.80

ABI: 0.80

ABI

0.63G,

Plethysmography is essentially a measurement
of volume. In general, the same cuffs are used to
obtain segmental limb pressures and PVRs. The
cuff is inflated and the volume shift that occurs
with the cardiac cycle in that limb segment is
recorded as a waveform. The PVRs do not
provide quantitative data but can be analyzed in
a qualitative manner. In normal patients there is
a brisk upstroke, rapid decline, and dicrotic
notch in the waveform. In the presence of
peripheral arterial disease, the waveform
becomes broader with a decreased amplitude. A
PVR tracing that is flat at the forefoot (trans-
metatarsal) level is consistent with significant
peripheral vascular diseases and suggests that
revascularization will be required for any fore-
foot lesion to heal.

Doppler Waveform Analysis

Similar to PVRs, the Doppler waveform can be
analyzed to determine if there is disease. Instead
of an audio signal, a digital signal is converted
to a tracing. Normally the waveform is triphasic
(Fig. 3.4). With moderate disease the reverse
flow component is lost and the waveform is
monophasic. With severe disease, the waveform
is blunted and/or absent.

Skin Perfusion Pressure

The skin perfusion pressure (SPP) is an addi-
tional noninvasive vascular evaluation that is
useful to determine which foot ulcers will heal
with local wound care or minor amputation and
which will require revascularization or major
amputation. An SPP of less than 30mmHg can
predict failure of forefoot wound healing with

Figure 3.3. Segmental limb pressures show a low high-thigh
pressure, indicating iliac disease, and a drop-off between the
high-thigh and low-thigh pressures, indicating superficial
femoral artery disease on the left side. On the right side there is
a drop-off between the pressures in the low thigh and popliteal,
indicating distal superficial femoral artery/popliteal artery
disease. ABI, ankle-brachial index; Dorsaus Pedis (DP), Posterior
Tibial (PT), prothrombin time; PVR, pulse volume recording.

Figure 3.4. Normal triphasic Doppler waveform.

VASCULAR SURGERY

Table 3.1 . Noninvasive measurements consistent with

Daired wound healing

Ankle-brachial index (ABI)

<0.3-0.4

Toe pressure

<35-40mmHg

Skin perfusion pressure

<30mmHg

Pulse volume recording (PVR)

Flat forefoot tracing

an accuracy of 80% (Castronuovo et al., 1997).
Skin perfusion pressure has largely replaced
transcutaneous oximetry.

What Wounds Will Heal?

The aggregate measurements that are consistent
with impaired wound healing are listed in
Table 3.1. However, it is ultimately the clinical
response to wound care that is the most impor-
tant factor. If debridement and wound care leads
to consistently unhealthy appearing wounds,
angiography and revascularization should be
considered. If good wound care leads to healthy
granulation tissue, further evaluation is likely
unnecessary.

Direct Evaluation of
Arterial Disease

Color duplex imaging or "duplex" imaging
incorporates real-time B-mode imaging and
pulsed Doppler spectral analysis (Fig. 3.5). B-
mode imaging directly views the blood vessel
and provides anatomical detail of the vessel.
This modality can analyze plaque characteris-
tics, identify thrombus and the intimal flaps,
and measure vessel diameter (to detect
aneurysms and pseudoaneurysms).

B-mode imaging is also used to localize areas
of stenosis so that Doppler velocities can be
determined. Velocity analyses are an indirect
measure of the degree of stenosis. For carotid
artery analyses, the degree of stenosis is esti-
mated based on the peak systolic velocity (PSV),
end-diastolic velocity (EDV), and the ratio of
the PSV at the stenosis to the velocity in the
common carotid artery (V r ). In general a V r
greater than 4 is indicative of clinically
significant stenosis (Table 3.2).

Infrainguinal graft surveillance can be per-
formed with duplex imaging. Because most

Figure 3.5. Color duplex image of a high-grade carotid
stenosis with a peak systolic velocity of 319 and end-diastolic
velocity of 123.

abnormalities occur in the first 2 years after
implantation, graft surveillance is most impor-
tant in this time frame. A PSV greater than 150
to 200 cm/second is considered abnormal. In
addition, the ratio of the velocity at the stenosis
to the normal proximal velocity is used to
determine the degree of stenosis (V r ). In addi-
tion, high EDVs (>100 cm/second) are also sug-
gestive of high-grade stenoses. Although the
high-velocity criteria (PSV, EDV, V r ) are the
most accurate to assess the risk of graft throm-
bosis, low-velocity criteria are also helpful. The
graft flow velocity (GFV) should normally
exceed 45 cm/second. The velocities are used to
stratify the risk of thrombosis (Table 3.3) (Mills,
2001). Prophylactic graft revision should
be considered in grafts with a high risk of
thrombosis.

Duplex examination is also useful for the
diagnosis of popliteal artery aneurysm. This
condition should be suspected if a widened
popliteal pulse is palpated. An arterial diameter

Table 3.2. Doppler velocity criteria for carotid stenosis

Stenosis (%)

PSV

EDV (cm/sec)

Normal

<123

<140

<4.0

1-15

<123

<140

<4.0

16-49

<123

<140

<4.0

50-79

>123

<140

<4.0

80-99

>123

>140

>4.0

EDV, end-diastolic velocity; PSV, peak systolic velocity; V r , velocity
ratio.

NONINVASIVE VASCULAR EXAMINATION

Table 3.3. Risk stratification for graft thrombosis

Category

PSV

EDV

GFV

(cm/sec)

Highest risk

>300

>3.5

>100

<45

High risk

>300

>3.5

<100

>45

Intermediate

180-300

>2.0

<100

>45

risk

Low risk

<180

<2.0

<100

>45

EDV,end-diastolicvelocity;GFV,graft flow velocity; PSV, peak systolic
velocity; V„ velocity ratio.

Conclusion

Noninvasive vascular laboratory tests comple-
ment the clinical evaluation in determining
the appropriate therapeutic approaches to
patients with peripheral vascular disease. The
specific laboratory tests should be tailored to
the individual patient's diagnoses. The labora-
tory provides noninvasive information on both
functional and anatomical aspects of vascular
disease.

greater than 10 mm is considered abnormal.
Bilateral aneurysms are seen in about 50% of
cases, and proximal aneurysms occur in approx-
imately 30% to 50% of patients. Consequently, it
is imperative that aneurysms at other locations
be excluded, with abdominal aortic aneurysms
and femoral aneurysms the most common.

References

Castronuovo JJ Jr, Adera HM, Smiell JM, Price RM. (1997)

J Vase Surg 26:629-37.
Mills JL Sr. (2001) Semin Vase Surg 14:169-76.
Vitti MJ, Robinson DV, Hauer-Jensen M, et al. (1994) Ann

Vase Surg 8:99-106.

Radiological Investigations

Steven M. Thomas, Kong T. Tan, and Mark F. Fillinger

This chapter offers an overview of the available
imaging techniques used in vascular radiological
practice for the investigation of vascular diseases
and how they can be used for a range of common
vascular conditions. This discussion emphasizes
the move away from invasive techniques and
toward noninvasive techniques for the diagnosis
of vascular diseases. We then describe the range
of endovascular techniques currently required
for the investigation and treatment of vascular
disease. The most important contemporary
approaches andtherapies are described,showing
the important role these techniques now play in
the management of a range of vascular disease
processes. This discussion demonstrates how the
area of endovascular intervention remains at the
forefront of developments in minimally invasive
techniques to treat vascular disease. Approaches
for specific manifestations of peripheral vascular
disease are not discussed, but the Trans Atlantic
Inter-Society Consensus (TASC) document is
recommended as an overview of endovascular
intervention in the management of specific as-
pects of peripheral arterial disease (Dormandy
andRutherford,2000).

Controversies

The following controversies currently exist in
the field of vascular radiology:

• Conventional diagnostic catheter angiog-
raphy is likely to be made obsolete by non-
invasive vascular imaging.

• When considering endovascular treatment
of carotid artery stenosis, the current lim-
itations of noninvasive testing mean that
catheter arch angiography is required to
assess the arch vessels and the whole of the
carotid artery.

• Computed tomography (CT) pulmonary
angiography has resulted in little need
for conventional pulmonary angiography
in the diagnosis of pulmonary embolic
disease.

■ Arterial closure devices enhance patient
throughput, and this may offset the
increase in cost from their use. However,
they can produce serious complications.

• There is little evidence that primary stent-
ing is superior to primary angioplasty
alone in the treatment of arterial occlusive
disease in the peripheral circulation.

• Following endovascular aneurysm repair
(EVAR) for abdominal aortic aneurysms
(AAAs), long-term costs of stent-graft
surveillance, and secondary treatment, may
outweigh the short-term benefits of EVAR.

Radiological Investigations
and Endovascular Approaches

The first vascular imaging technique was
described at the end of the 19th century shortly
after the discovery of the x-ray. This technique,
described by Haschek and Lindenthal, involved

VASCULAR SURGERY

the injection of a chalk-based contrast agent
into the vein of an amputated hand. In vivo
vascular imaging was first described in the
1920s using agents such as lipiodol, strontium
bromide, sodium iodide, and Selectan. The
contrast agents were usually introduced by a
catheter, following exposure of the vessel used
for catheterization, or by percutaneous needle
puncture to directly inject contrast into the
vessel. Translumbar aortography used this type
of technique as early as the 1930s. However, it
was developments from the mid-20th century
that brought angiography and subsequently
vascular intervention to the forefront in vascu-
lar diagnosis and treatment. The first of these
was the introduction of the Seldinger technique
in the 1950s that allowed safe percutaneous
access to vascular structures. There then fol-
lowed significant improvements in the range of
available catheters to aid in gaining access to the
different vascular beds, and rapid film changers
allowed high-quality images to be obtained of
all the major vascular beds. As a result, vascular
imaging became a major branch of diagnostic
medicine. However, arteriography remained
an uncomfortable, if not painful, experience
because of the use of conventional ionic contrast
agents. The introduction of digital subtraction
angiography (DSA) and nonionic contrast
agents in the last two decades of the 20th
century made arteriography much more accept-
able to patients and their doctors. Digital sub-
traction angiography allowed smaller amounts
of contrast to be used, and the newer contrast
agents rarely produced intense heat or pain. The
combination produced fewer systemic side
effects as well.

At the same time, attention was directed
toward less invasive therapeutic interventions,
such as Dotter's technique of sequential dilation
for atherosclerotic occlusive lesions. The devel-
opment of the balloon angioplasty catheter, first
described by Gruntzig and Hopff in 1974, her-
alded an era in which a range of manifestations
of arterial occlusive disease became amenable
to treatment using percutaneous vascular inter-
ventional techniques. There followed develop-
ments of a range of techniques for treating
arterial occlusive disease such as arterial stents,
atherectomy catheters, lasers, and thrombolysis.
From these, implantable devices such as inferior
vena cava (IVC) filters and stent grafts for
aneurysmal disease were developed. All these

devices broadened the range of conditions
amenable to treatment using interventional
vascular radiological techniques.

Improvements in the design of catheters and
other devices have resulted in smaller caliber
catheters and introduction sheaths. These along
with the introduction of closure devices to seal
the access site puncture allowed the develop-
ment of day case ("same day") arterial proce-
dures for both diagnosis and intervention.
Despite these improvements, developments in
other noninvasive imaging modalities meant
that for arterial imaging and diagnosis, the use
of what remains an invasive technique is
required less frequently. Whereas arteriography
was once a first-line investigation, noninvasive
techniques such as ultrasound, radionuclide
imaging, CT, and magnetic resonance imaging
(MRI) now have a much wider role to play in
both general diagnostic radiology and in the
radiological investigation of vascular disease.
Not only are these techniques safer, they also
have the potential for a greater diagnostic yield
because of the additional information that can
often be obtained using these techniques. As a
result of improvements in these noninvasive
vascular imaging techniques, it is possible that
the need for conventional diagnostic catheter
angiography will become obsolete. However, at
present, despite the reduced requirement for
angiography for general diagnostic work, there
remains a role for angiography in the investiga-
tion of vascular disease, either as a first-line
investigation or following other imaging inves-
tigations. Also angiography remains paramount
as part of all percutaneous endovascular inter-
ventional techniques.

Imaging Modalities

The imaging techniques available for the inves-
tigation of vascular diseases are best divided
into invasive (i.e., catheter angiography) and
noninvasive techniques. The following is a brief
description of the commonly used modalities.

Catheter Angiography

Catheter angiography is an x-ray investigation
in which a contrast agent is injected into the vas-
cular system via a catheter, and sequential x-ray
exposures are performed. The x-ray receiver can

RADIOLOGICAL INVESTIGATIONS

be plain x-ray film (older machines), but are
now almost universally digital systems, using an
image intensifier or a flat panel detector. Older
machines using cut plain x-ray films were cum-
bersome and difficult to operate. In addition,
the postprocessing facilities were very limited.
In contrast, digital systems are easy to operate,
require lower contrast dosage, produce better
contrast resolution, have real-time display,
and have facilities for image manipulations,
such as pixel shifting and digital subtraction
angiography.

Contrast Agents

The primary aim of the contrast agent is to allow
imaging of vessel anatomy and morphology.
During fluoroscopy, x-ray contrast agents act
by changing the attenuation between tissues.
Iodinated agents and gadolinium have a higher
density than surrounding tissue, whereas
carbon dioxide has a lower density.

Iodinated Contrast Agents

The most widely used contrast agents for
catheter angiography are the water-soluble
iodine-based agents. They can be divided into
ionic and the newer nonionic agents. Nonionic
agents have the advantage of considerably
reducing the risk of adverse reactions to con-
trast, but are more expensive. In the United
Kingdom the low-osmolar nonionic agents are
used almost exclusively for intravascular proce-
dures. These agents are denser than blood, and
the commonly used strength for diagnostic and
interventional work is 300 mg of iodine per
milliliter of contrast. For hand injections, this
strength of contrast is usually diluted 50 : 50
with saline. Patients with a previous history of
adverse reactions to these contrast media, a
strong history of allergic disease, or a hyper-
sensitivity to iodine are at risk of developing a
severe allergic reaction to these contrast agents.
Other investigative modalities that do not
require iodinated contrast media such as MRI
or ultrasound should be considered, or alterna-
tive non-iodine-based contrast such as carbon
dioxide (C0 2 ) or gadolinium, as described
below. The other major problem with iodinated
contrast is nephrotoxicity. Overall, contrast-
induced nephropathy occurs in approximately
5% of all procedures requiring iodinated con-

trast media. For the majority, the effect is
temporary. However, in high-risk patients the
incidence of contrast-induced nephropathy is
around 20% to 30%, and in a significant number
of cases the effect is permanent and nonre-
versible. High-risk groups are those patients
with preexisting renal impairment, diabetes
mellitus, dehydration, on nephrotoxic drugs,
and a history of multiple myeloma. These
patients should be well hydrated prior to the
procedure, if necessary by the administration of
intravenous saline, and their renal function
should be checked 48 hours postprocedure.
Recently, some studies involving a small
number of patients suggest that acetylcysteine
and calcium channel blockers may reduce the
incidence of contrast-induced nephropathy
(Kay et al., 2003). There is also evidence that at-
risk patients, particularly those with diabetes
mellitus, have a lower incidence of contrast-
induced nephropathy following the use of
recently introduced iso-osmolar contrast agents
(Aspelin et al., 2003). There is also a risk of
potentially fatal lactic acidosis if a patient
taking metformin develops acute renal impair-
ment following the administration of iodinated
contrast. Ideally metformin should be discon-
tinued at the time of, or prior to, the procedure
and withheld for 48 hours subsequent to the
procedure and reinstituted only after renal
function has been reevaluated and found to be
normal.

Other Agents

Mainly because of the risk of nephrotoxicity
with iodine-based agents, C0 2 has recently
been advocated as avascular contrast media for
patients with renal impairment. It can also be
used when there are contraindications to iodi-
nated contrast such as a history of iodine or
contrast allergy. Minor alterations in techniques
and software are required for C0 2 angiography.
Although dedicated C0 2 pump injectors are
available, these are expensive to purchase.
Cheaper alternative techniques, not requiring a
dedicated pump injector, have been described
and used with complete safety if appropriate
measures are utilized (Snow and Rice, 1999).
Stacking software is required to overcome frag-
mentation of the C0 2 gas column by the flowing
blood (Fig. 4.1). For adequate imaging of the
tibial and distal arteries, elevation of the feet by

VASCULAR SURGERY

Figure 4.1. Carbon dioxide angiography showing the application of stacking software to remove the beading effect seen in panels
AandB.

10 to 20 degrees may be necessary. Unlike
iodine-based agents, C0 2 can be administered in
large quantity, even in patients with pulmonary
disease, without any adverse effect. The C0 2 gas
displaces the blood and appears radiolucent in
relation to surround tissue (negative contrast
agent). Unfortunately, due to its low density, C0 2
angiography has a lower contrast resolution
compared to iodine-based agents and hence
produces a poorer image quality, particularly
in the small peripheral vessels. Furthermore,
C0 2 gas can cause the vapor lock phenom-
enon, a condition in which the gas is collected
over the most anterior aspect of an artery,
in particular the aorta, causing poor visualiza-
tion of the mesenteric arteries and producing
temporary abdominal pain, thought to be sec-
ondary to bowel ischemia. Finally, C0 2 angiog-
raphy is contraindicated for "above-diaphragm"
angiography, because of the risk of cerebral
embolization.

Gadolinium chelate, an MRI contrast agent,
can also be used as an intravascular contrast
media. However, it is a poor radiographic con-
trast agent, and it should not be used in patients
with renal impairment, as there is evidence that
at the doses required for conventional angiog-

raphy (as opposed to MRI) it is potentially more
nephrotoxic than iodinated contrast (Thomsen
et al., 2002). It can be useful in patients with
other contraindications to iodinated agents, uti-
lized as a problem solver to answer specific
questions that cannot adequately be defined by
C0 2 angiography. Because of dose limitations
(maximum 0.3mmol/kg), careful planning is
required prior to its use.

Even with the introduction of smaller
catheters and safer contrast agent, the role of
contrast catheter angiography as the primary
investigation tool of vascular diseases is dimin-
ishing due to its many drawbacks (Table 4.1). In
the future, it will be employed mainly as part of
an interventional procedure or in special diag-
nostic situations.

Computed Tomography

Until relatively recently, the images obtained
from CT examinations were of suboptimal
quality for the assessment of most vascular dis-
eases except aneurysmal conditions. This was
due to the long examination time (minutes) and
thick slice width (5 to 10 mm); hence, images
were subjected to movement artifacts and were

RADIOLOGICAL INVESTIGATIONS

Table 4.1. Complications of angiography

Contrast medium-related complications
Minor adverse reactions: common, but rarely life

threatening (e.g., urticaria, nausea)
Major adverse reactions: rare, but serious

(idiosyncratic anaphylactoid reactions)
Local vascular changes (e.g., effects on red

cells/coagulation)
Systemic vascular changes (e.g., increases in blood

volume)
Individual organ toxicity (e.g., renal)
Access site complications
Hemorrhage

Intramural or perivascular injection of contrast
Vascular thrombosis (following dissection or local

trauma)
Peripheral embolization
Vascular stenosis or occlusion
Pseudoaneurysm formation
Arteriovenous fistula
Local infection
Nerve damage

Damage to other local structures
Catheter and general complications
Air embolism

Catheter thrombus embolization
Dissection or perforation of vessels
Organ ischemia or infarction secondary to spasm,

dissection, or embolization
Fracture and loss of guidewire or catheter fragments
Catheter knot formation
Mistaken injection of toxic material (e.g., skin

cleansing agent)
Vasovagal reactions
Adverse reaction to local anesthetic or other drugs

of low spatial resolution. These shortcomings
prohibited the high-quality reconstruction
often necessary for vascular studies. However,
the introduction of spiral/helical CT shortened
the examination time dramatically to less than
30 seconds and allowed the use of thin collima-
tion (i.e., slice thickness). This short acquisition
time meant the examination could be per-
formed in a single breath-hold, reducing the
motion artifact that was frequently encountered
with older scanners. Thin collimation in turn
improved spatial resolution, further enhancing
image quality. These factors were further
improved with the introduction of multislice/
detector spiral CT. In comparison to the first-
generation spiral CT scanners that have a single
bank of x-ray detector, multidetector scanners

have multiple banks of detectors (up to 64),
allowing several slices to be acquired with
each revolution of the scanner. The volumetric
data obtained from recent scanners can be
processed and displayed as multiplanar refor-
mats (MPRs), maximum intensity projections
(MIPs), or surface shaded displayed (SSD) (Fig.
4.2). Details about these reconstructions are
beyond the scope of this chapter, but it is prob-
ably fair to say that MPR is most frequently used
clinically.

With the new generation of multidetector
scanners, the best spatial resolution of the
images obtained is around 0.5 mm, which is ade-
quate for assessing most vascular systems.
However, as with contrast angiography, the
main limitation of CT examinations is the
requirement of large volumes (100 to 150mL) of
potentially nephrotoxic iodine-based contrast
agent even with the new generation machines.
Alternative contrast agents such as gadolinium
can be used for CT, but produce less contrast
and are more expensive.

Currently, the main roles of CT in relation to
vascular diseases are (1) diagnosis of aortic

Figure 4.2. Surface shaded reconstruction showing the rela-
tionship of an infrarenal abdominal aortic aneurysm to the bony
landmarks.

VASCULAR SURGERY

aneurysms, (2) assessment for open or en-
dovascular treatment of aortic aneurysm, (3)
endovascular stent graft surveillance, and (4)
vascular trauma. Although CT provides accurate
imaging of visceral and peripheral arteries,
magnetic resonance angiography (MRA), which
has none of the disadvantages of CT (i.e.,
nephrotoxic contrast agent and ionizing radia-
tion), is more widely accepted by clinicians.
Because magnetic resonance provides poor
visualization of calcified arteries, a combination
of MRA and noncontrast CT is often required in
these cases.

Magnetic Resonance Angiography

Prior to the advent of gadolinium-enhanced
three-dimensional (3D) MRA by Prince and
coworkers, MRA played a small role in the inves-
tigations of vascular diseases, mainly because
the images obtained were of poor quality due to
movement and turbulence-induced artifacts
(Prince et al., 1993). The use of gadolinium
chelate as a contrast agent shortens the exami-
nation time significantly, allowing the examina-
tion to be performed in a single breath-hold,
reducing movement artifacts. In addition,
gadolinium-enhanced MRA is not susceptible to
the flow artifacts that plague noncontrast MRA.
The data range in 3D MRA is acquired as a
continuous volume, and this allows 3D recon-
struction of the images, producing images com-
parable to catheter angiography. The resolution
limit of current MR scanners is approximately 1
mm, which is adequate for the imaging of most
arteries, including the pedal vessels. Visualiza-
tion of smaller vessels is software dependent,
however, and MR images of distal vessels are
limited by contrast issues, as the gadolinium
dilutes as it travels distally and enhances the
veins soon after the distal arteries. Despite these
issues, MRA of the infrainguinal vessels can be
performed with adequate quality for planning
distal bypasses in centers with very high quality
MRI.

The main advantage of MRA, in relation to
CT, is the use of gadolinium as a contrast agent,
which is safe and does not cause renal impair-
ment, except in rare cases. The current limita-
tions of MRA are high cost, lack of availability,
patient claustrophobia, narrow range of field
of view (for example, it is unable to image the
entire aorta in one continuous acquisition), and

poor display of intraluminal thrombus and
calcification of the arterial wall. The latter two
limitations are important to consider in
endovascular procedures, such as aneurysm
stent grafting. In addition, MRA has the ten-
dency to over-grade the degree of stenosis.
Hence, in most units, confirmatory catheter
angiography is routinely performed prior to
intervention in cases where the MRA has shown
significant stenotic disease.

Currently, the main roles of MR are for the
investigations of aortoiliac disease, visceral
arteries, and extent of arteriovenous malforma-
tions. In addition, as it involves no ionizing
radiation, MR is the most appropriate imaging
modality for young patients requiring long-
term follow-up, such as those with aortic dis-
section, aortic root replacement surgery, or
aortic coarctation. Although MR is not widely
used at the moment as the primary imaging
modality for vascular disease, with further
advances in software and hardware designs
expected in the future, it will become an ideal
imaging tool.

Radiation Safety

X-rays are an ionizing radiation, interacting
with water molecules, producing radicals that
cause cellular damage and death. The effect can
be immediate, for example, skin necrosis, or late,
such as genetic mutation or cancer formation. It
is important to bear in mind that radiation
exposure is cumulative and permanent; hence,
it is prudent that the exposure to x-rays be
minimized. There are several simple methods
to reduce the exposure to both patients and
operators:

1. Radiation exposure is proportional to
fluoroscopy time, and hence the most
effective way to reduce exposure is to
reduce the fluoroscopy time. Use pulse
mode rather than continuous mode when
possible and plan cases in advance to
obtain only the necessary views.

2. Increase the distance from the source.
Exposure decreases with the square of the
distance from the source (inverse square
law).

3. Use lower magnification and careful
collimation.

RADIOLOGICAL INVESTIGATIONS

4. Use posterior-anterior imaging, that is, the
x-ray source is from the posterior of a
supine patient.

5. Position the image intensifier as close as
possible to the patient to reduce scatter.

6. Use protective barriers such as table aprons,
lead glass shields, as well as the usual lead
apron, thyroid shield, andglasses.

The use of dosimeter badges by all persons
working with ionizing radiation is mandatory.
In the United Kingdom, the badge must be posi-
tioned at waist level under the lead apron. Addi-
tional badges can be worn (such as on the
fingers or forehead) for specific exposed areas.
In the United States, badges are required either
outside the apron at the neck level, beneath the
lead apron, as in the U.K., or in both locations
(with finger badge an option). In the U.K. and
U.S., no individual working in the controlled
area should receive doses in excess of (1)
20mSv/year to the body, (2) 150mSv/year to the
lens, and (3) 500mSv/year to hands or forearm.
Finally, although the use of dosimeters is man-
dated, it is the responsibility of the operator to
wear and use them correctly.

Investigations of
Vascular Diseases

This section is divided into system-based cate-
gories. Common conditions and appropriate
investigations for each system are discussed.

Peripheral Vascular Disease
(Lower Limb)

This is the most common of all vascular condi-
tions, accounting for the majority of the work
load in any vascular unit. Clinically, this condi-
tion is best divided into two subcategories: (1)
patients with symptoms of claudication without
any tissue loss or rest pain; and (2) patients
with rest pain or tissue loss, suggesting limb-
threatening ischemia. In those patients with
symptoms that are severe enough to warrant
intervention, further investigation is justified.
However, most claudicants do not require inter-
vention and are treated conservatively, and thus
further imaging is not necessary. In most cases,

duplex examination is adequate as a first-line
investigation for the demonstration of the exter-
nal iliac arteries, femoral arteries, and even as
distally as the tibial trifurcation. Conventional
catheter angiography, MRA, or CT angiography
can be performed if the examination is of
suboptimal quality or if the assessment of
distal arteries is required, for example in cases
where distal bypass surgery is considered. This
depends on staff expertise and equipment avail-
ability in individual centers. In some centers
distal bypass decisions can be based on duplex
arterial mapping, MRA or even CT angiography
(CTA), but currently most units still depend
on catheter angiography. In patients with sus-
pected aorto iliac disease, duplex examination is
more difficult due to anatomical constraints. In
this situation, MRA or CTA is generally pre-
ferred. If these two options are not available, an
angiogram can be performed via a catheter that
is positioned in the distal abdominal aorta. If
brachial or radial artery access is used, access
should be obtained from the left arm to mini-
mize the risk of embolic complications to the
cerebral circulation.

Catheter angiography is useful to diagnose
vasculitic conditions such as thromboangiitis
obliterans (Buerger disease). This condition
classically affects small and medium-size arter-
ies and veins of the lower limbs in young
smokers with a typical angiographic appear-
ance. In patients with blue digit syndrome,
catheter angiography may show the source of
emboli, typically atherosclerotic plaques in the
aorta or iliac arteries. However, CT or other
noninvasive modalities are preferred for the
initial evaluation in blue digit syndrome,
because the catheter-based modalities carry the
risk of further athero emboli.

Finally, although conventional catheter
angiography plays an ever-diminishing role as
the primary diagnostic tool in the investigation
of peripheral vascular disease (PVD), it still has
a few advantages in comparison to noninvasive
techniques. Direct pressure measurement can
be performed in equivocal stenosis (>10mmHg
systolic gradient is considered significant), with
the use of enhanced gradients in cases of possi-
ble "subcritical" stenosis [by the use of distal
vasodilators such as glyceryl trinitrate (nitro-
glycerin in the U.S.) or papaverine], as well as
allowing intervention to be performed in the
same sitting.

VASCULAR SURGERY

Upper Limb Vascular Diseases

Upper limb vascular diseases are far less fre-
quently encountered than those of the lower
limb. These can usually be attributed to subcla-
vian steal syndrome, embolic disease, or blue
digit syndrome (distal embolization), and rarely
due to diffuse atherosclerotic disease commonly
seen in the lower limbs. Duplex ultrasonogra-
phy is useful as a preliminary test. Although it is
anatomically not possible to visualize the first
part of the subclavian artery directly, waveform
analysis of flow in the distal segments may
reveal changes (such as damped signal or spec-
tral broadening) that are suggestive of proximal
occlusion or stenosis. In addition, duplex exam-
ination may detect flow reversal in the vertebral
artery, which suggests a steal phenomenon and
is a good indication of significant ipsilateral
proximal subclavian artery stenosis or occlu-
sion. Magnetic resonance angiography is widely
accepted for the visualization of arch vessels, but
aortic pulsation artifact may obscure anatomi-
cal detail at the origins of the great vessels. Com-
puted tomography angiography is useful but
subjected to beam-hardening artifacts from the
thoracic cage and contrast in the venous system,
both of which are in close proximity to the
arteries of interest. Ultimately, catheter angiog-
raphy is still the definitive test for the investiga-
tions of patients with upper limb ischemia. It is
pertinent that a flush aortic arch angiogram is
performed in two planes (left and right anterior
oblique), as origin disease is frequently missed
if only one projection is obtained.

A rare cause of upper limb ischemia is
Takayasu arteritis (pulseless disease), a condi-
tion most commonly seen in young female
Asians. It is a granulomatous disease involving
major arteries, in particular the aortic branches
and pulmonary arteries. Clinically, the patient is
systemically unwell with symptoms and signs of
limb ischemia or renovascular hypertension.
Radiological features suggestive of the condi-
tion are enhancing thickened arterial wall on
CT, segmental stenotic or occlusive disease of
major arteries, and aneurysm formations.

Carotid Arteries

Duplex ultrasonography examination is the pre-
liminary test for patients with suspected carotid
artery stenosis in whom intervention is consid-

ered appropriate (see Chapter 3). The procedure
is relatively easy to perform with good accuracy
in experienced hands. In addition, it provides
morphological assessment of the plaque. Hence,
in many vascular centers, duplex examination
is the sole radiological investigation prior to
carotid endarterectomy However, when endo-
vascular treatment is an option, it is important
that the entire carotid artery is assessed for
synchronous stenotic disease, tortuosity, and
a favorable angle of origin of the vessel to be
treated (Fig. 4.3). These factors determine if
endovascular treatment is feasible. Unfortu-
nately, duplex examination cannot answer all
these questions, and in our unit we presently
rely on conventional arch aortography for full
assessment (selective catheterization should not
be required). However, it is likely that as
improvements in MRA and CTA continue to be
made, the full characterization of carotid steno-
sis, the arch vessels, and cerebral circulations
will be of sufficient quality to eliminate the
requirements for catheter angiography to deter-
mine whether a patient is a good candidate for
endovascular intervention.

Carotid body tumor is a rare condition that
classically presents as a painless pulsatile mass
below the angle of the jaw, and is laterally
mobile but fixed vertically. Approximately 10%
of cases are bilateral. The typical ultrasonic
feature is an oval mass splaying the carotid
internal and external carotid arteries. This mass
enhances avidly on CT or MR examinations.

Pulmonary Arteries

There are few medical conditions that require
the imaging of the pulmonary vasculature. Most
frequently this is required for suspected acute
pulmonary embolic (PE) disease or as part of
the investigation of pulmonary hypertension, to
exclude chronic thromboembolism. In the
majority of cases with suspected acute PE, the
initial investigations should consist of a chest
radiograph and a radionuclide ventilation-
perfusion (V/Q) scan or a CTA. Unfortunately,
up to 50% of V/Q scans are of no diagnostic
value, and in these circumstances supplemen-
tary investigations are required. Previously,
catheter angiography was the imaging modality
of choice, but with the advent of spiral CT the
role of catheter angiography is limited to situa-
tions such as massive PE, where immediate

RADIOLOGICAL INVESTIGATIONS

Figure 4.3. Tortuous common and
internal carotid arteries (arrow), a
contraindication to carotid artery
stenting.

intervention may be required. Although CTA is
undoubtedly accurate for the diagnosis of mod-
erate to large emboli, it is limited by its inabil-
ity to reliably diagnose subsegmental embolism,
particularly with the older single-slice spiral
scanners. However, the clinical significance of
subsegmental PE is uncertain and may have
only minimal impact in the long-term outcome.
The results of ongoing outcome studies where
patients are managed on the basis of multide-
tector/slice helical CT findings are eagerly
awaited.

Magnetic resonance angiography has not
been thoroughly evaluated as a tool for the diag-
nosis of PE,but a recent study showed that it has
reasonable accuracy in comparison to catheter
angiography (Haage et al., 2003). However MRA,
as with CTA, is limited by the poor visualization
of subsegmental arteries, and resolution tends
to be approximately half that of CT in most
institutions. Magnetic resonance angiography is
unlikely to be widely used for the diagnosis of
PE until further data are available (Haage et al.,
2003).

In certain situations, the catheter pulmonary
angiogram remains the investigation of choice.
Patients with acute massive PE and cardiorespi-
ratory instability should proceed directly to
catheter angiogram, where treatment such as
thrombectomy or thrombolysis can be adminis-

tered immediately following the confirmation of
the diagnosis. Furthermore, it is possible to
insert an IVC filter at the same time to prevent
further embolism, if this remains a risk.
Pulmonary angiography is also indicated in
patients in whom noninvasive diagnostic tests
remain inconclusive and a reasonable suspicion
for PE exists. In this situation, pulmonary
angiography is aimed at excluding PE, thus
allowing withdrawal of anticoagulant therapy
with its inherent bleeding risk. In patients in
whom the consequence of bleeding is unfor-
giving, for instance following recent neuro-
surgery, pulmonary angiography can provide a
definitive diagnosis. The disadvantages of pul-
monary angiography are that it is invasive and
uses nephrotoxic contrast agents. Nevertheless,
the safety of this technique has improved dra-
matically over the past 10 years. Current esti-
mates of mortality and morbidity are around
0.03% and 0.47%, respectively, in experienced
hands.

Pulmonary arteriovenous malformation
(AVM) is a rare condition in which there is an
abnormal large vascular communication
between the pulmonary artery and vein. This
allows shunting of blood from the pulmonary
circulation to the systemic circulation and
hence the risk of complications such as cere-
brovascular accident and cerebral abscess. The

VASCULAR SURGERY

Figure 4.4. Coil embolization of pulmonary arteriovenous malformation (AVM). A: Pulmonary angiogram shows an AVM in the
periphery of left lobe (arrow). B: Selective angiogram demonstrates the characteristic early draining vein. C: Angiographic appear-
ance after successful embolization.

AVM can be solitary (40% of cases) or multiple,
often associated with hereditary hemorrhagic
telangiectasia (Rendu-Osler-Weber syndrome).
Diagnosis can be reliably confirmed by CT or
MR examinations, showing a vascular mass with
a large feeding artery and draining vein (Fig.
4.4). Catheter angiogram is indicated only as a
part of the current treatment of choice, i.e.,
embolotherapy

Mesenteric Arteries

The main indications for the investigation of
mesenteric arteries are gastrointestinal (GI)
bleeding, intestinal angina, and mesenteric
artery aneurysms or pseudoaneurysms. For GI
bleeding, endoscopy is the first-line investiga-
tion. If the bleeding site or cause is not identified
(up to 40% of endoscopic examinations), the
patient should have a radionuclide test if the
hemorrhage is not life threatening, or urgent
selective catheter angiography if the patient is
hemodynamically unstable and actively bleed-
ing. Radionuclide investigations are more
sensitive than catheter angiography for the
investigation of GI bleeding (isotope remains in
the vascular system far longer than contrast
agent), but less accurate in identifying the exact
anatomical site or the nature of the disease.

Technetium 99m ( 99m Tc) sulfur colloid or 99m Tc-
labeled erythrocytes are used to localize mild-
to-moderate intermittent bleeding, particularly
in the lower GI tract, and 99m Tc pertechnetate is
used to detect Meckel's diverticulum. Selective
catheter angiography may reveal the exact site
of hemorrhage but this is highly dependent on
the timing of the procedure. Many investiga-
tions turn out to be false negatives (reported
accuracy of 40% to 90%), as the patients are not
actively bleeding at the time of investigation.
Nonetheless, the tests may still show areas of
abnormal vascularity such as angio dysplasia. In
addition, endovascular treatment such as
embolization or vasopressin infusion may be
initiated, and, it is hoped, avoid the high mor-
bidity and mortality (up to 30%) of emergency
surgery. The treatment may permanently stop
the bleeding or allow a window of opportunity
to stabilize the patient prior to definitive surgi-
cal resection if deemed necessary.

Although atheromatous disease of the mesen-
teric arteries is common, mesenteric angina is a
rare entity. This is because there are numerous
large collaterals between the mesenteric arter-
ies, and hence the symptoms of mesenteric
angina only manifest if there is severe stenosis
or occlusion in two of the three mesenteric
arteries (celiac, superior mesenteric, and infe-

RADIOLOGICAL INVESTIGATIONS

rior mesenteric arteries). The first-line investi-
gation should be duplex ultrasonography, as it
has excellent diagnostic value in many institu-
tions. The origins of celiac and superior mesen-
teric artery are relatively straightforward to
assess. However, the inferior mesenteric artery
is frequently not seen due to overlying bowel
gas. Because of this, many radiologists prefer
MRA as the primary investigational modality
for this condition. The 3D acquisition allows
accurate assessment of the ostial disease with
sensitivity and specificity comparable to that of
catheter angiography. Computed tomography
angiography is also being used as an adjunctive
diagnostic modality in some institutions, pri-
marily to aid in evaluation of calcific aortic
plaque that is not seen well on MRA, but may
have a substantial impact on the approach to
surgical intervention. Currently, catheter angio-
graphy is usually reserved for cases in which
other imaging modalities are equivocal, or when
endovascular intervention is considered.

Mesenteric artery aneurysm is an uncommon
condition, and is best assessed with cross-
sectional studies such as CT. This allows the
identification of the vessel of origin, the size of
the aneurysm, and the mass effect on the sur-
rounding structure. Catheter angiography can
then be performed as part of the embolization
treatment or for evaluation of potential
aneurysms in the mesenteric arcades.

Renal Arteries

The main indications for imaging of the renal
arteries are (1) diagnosis of renal artery steno-
sis, most commonly atherosclerotic or fibro-
muscular dysplasia (FMD); and (2) evaluation
of potential live renal donors. Although conven-
tional catheter angiography is still considered
the gold standard, it involves the use of nephro-
toxic contrast agent in a group of patients with
a high incidence of preexisting renal impair-
ment, and hence is employed only in cases
where other tests are unavailable or inconclu-
sive. In many institutions MRA is currently the
investigation of choice in patients with sus-
pected renovascular disease, primarily due to
the lack of nephrotoxicity with gadolinium-
chelate. It has high sensitivity and specificity for
the assessment of ostial disease, but is unproven
for distal stenosis such as in FMD. In our unit,

patients with suspected FMD have MRA as the
first-line investigation, followed by catheter
angiography if the MRA is of suboptimal
quality or there is strong clinical suspicion of
FMD. Although CTA is accurate for assessing
renal artery stenosis, it is subjected to a similar
drawback as catheter angiography, that is,
requiring iodinated contrast media and ionizing
radiation. Duplex examination is the initial
imaging modality of choice in many institutions
due to its low cost and relatively high accuracy
for renal artery stenosis, but it is more prone to
missing duplicate renal arteries, and it is highly
operator- and patient-dependent, with up to a
15% technical failure rate.

With the current shortage of cadaver renal
donors, living-related renal transplant surgery
has become a common procedure. Previously,
the donors had to undergo catheter angiogra-
phy, ultrasonography, and intravenous urogra-
phy as part of the assessment. Currently, MR is
the imaging method of choice as it provides the
most comprehensive and accurate assessment of
the donor in one sitting. It allows anatomical
and morphological evaluation of the renal
parenchyma, veins, arteries, and ureters with
confidence. In addition, it may show other
intraabdominal pathologies such as adrenal or
pelvic masses. Computed tomography angiog-
raphy with 3D reconstruction can also be used
in patients who are known to have normal renal
function, as is true for most potential renal
donors.

Aortic Aneurysms and Dissections

The conventional treatment for patients with
aneurysmal disease of the aorta is surgical.
Patients with abdominal aortic aneurysms
(AAAs) or thoracic aortic aneurysms of greater
than 5.5 or 6.5 cm in diameter, respectively,
are generally best treated, depending on the
patient's fitness for surgery, because of the
increasing risk of rupture above these sizes. In
most cases, CT examination alone is adequate
to provide all the information needed prior to
open surgical repair. Computed tomography
shows the relation of visceral arteries to the
aneurysm sac, the size and extent of the
aneurysm, and other conditions that may pre-
clude surgical repair, such as horseshoe kidney.
In the early 1990s endovascular aneurysm
repair (EVAR) revived the role of catheter

VASCULAR SURGERY

angiography for the assessment of aortic
aneurysms. Catheter angiography began to
diminish again, however, as spiral CT with 3D
reconstruction and specialized software in the
mid-1990s allowed high-quality reconstructions
not previously possible. Accurate preoperative
imaging is crucial to ensure proper selection of
patients, stent-graft types, and potential intra-
operative adjuncts such as coil embolization,
iliac angioplasty, renal stenting, femoral
endarterectomy, and iliac conduits. To eliminate
the need for catheter angiography preopera-
tively, work focused on 3D reconstruction of CT
and MR data, with specialized software for
detailed measurements and even endograft
simulations preoperatively Currently, CT or MR
with 3D reconstruction and computer-aided
measurement, planning, and simulation is the
standard for imaging prior to EVAR, with meas-
urement accuracy and outcomes equal or supe-
rior to catheter angiography and without the
morbidity or expense (Broeders et al., 1997;
Fillinger, 1999, 2000). The main disadvantages of
MR are the difficulty in visualizing thrombus
and calcification, important points to be con-
sidered, as thrombus in the neck of the
aneurysm may preclude endovascular repair.
Nevertheless, future advances in MR technolo-
gies are expected to resolve these problems.

Although the technical success of stent-graft
implantation is well established, only modest
data are available for midterm results, and data
on long-term efficacy and safety are not yet
established. The goals of postprocedure imaging
are to (1) confirm appropriate stent-graft place-
ment, (2) assess the effectiveness of aneurysm
exclusion, (3) follow the aneurysm sac size, and
(4) detect device failure and/or migration.
Because late complications have been observed,
lifelong follow-up is felt to be essential at the
present time. The current imaging strategy
should include plain radiographs of the stent
graft in four projections (anterior-posterior,
lateral, and two obliques) and CT angiography
at 1, 6, and 12 months postoperative, and then
annually. More or less frequent imaging may
be recommended depending on the imaging
results (e.g., endoleak or migration), type of
stent graft, and manufacturer recommenda-
tions. Plain radiographs are an excellent and
inexpensive means to assess the metallic stent-
graft frame for structural failure, angulation,
and kinking. Plain radiographs have typically

been recommended for establishing migration,
but this is best performed on CT. Triple-phase
CT examinations (nonenhanced, arterial phase,
and delayed "venous" phase) allow serial meas-
urements of aneurysm sac diameters, monitor-
ing of the integrity and position of the device,
and detection of an endoleak (reperfusion of
the aneurysm sac) (Fillinger, 1999). Three-
dimensional reconstruction with volume
measurements is the most sensitive method
for detecting aneurysm sac size changes, but
requires expertise in image segmentation or
outsourcing to a commercial entity. It may allow
earlier detection of problems that require inter-
vention after EVAR or earlier reassurance to the
patient and less frequent surveillance in suc-
cessful repairs (Fillinger, 1999; Kay et al., 2003).
Duplex ultrasound is a useful adjunct for the
detection of endoleak, without the risk of con-
trast nephrotoxicity and ionizing radiation.
However, it may not show the source of
endoleak and is unable to assess stent-graft
integrity accurately. Three-phase contrast-
enhanced MRA serves as an attractive alterna-
tive to CTA in patients with renal impairment
and relative contraindications to iodinated con-
trast media. There is evidence that it is superior
to CT in depicting small type 2 (collateral)
endoleaks. Unfortunately, it is not suitable for
stainless steel devices, which cause severe image
degradation secondary to metal artifacts. Cur-
rently, the role of catheter angiography is to
characterize endoleaks (inflow and outflow
channels) detected by the noninvasive tests or to
further evaluate sacs that appear to have
enlarged without an endoleak.

Aortic dissection is a condition in which a
spontaneous tear of the tunica intima allows cir-
culating blood to gain access to the tunica
media, splitting it longitudinally. The objective
of imaging is not only to diagnose the condition
but also to localize the site of entry, assess the
extent of dissection, and identify associated
complications. The potential complications that
may occur are occlusion of major aortic
branches such as coronary and visceral arteries;
aortic valve insufficiency; rupture into the peri-
cardial sac, mediastinum, or pleural cavity;
and aneurysm formation in the long-term. At
present, the imaging modality of choice for
acute dissection is CT angiography. It has excel-
lent sensitivity and specificity in comparison to
catheter angiography, which is considered the

RADIOLOGICAL INVESTIGATIONS

standard of reference. However, it is vital that
the examination be performed in the arterial
phase of contrast enhancement, as failure to do
so may lead to misinterpretation of a dissection
as an aneurysm. Transesophageal ultrasonic
examination is a useful adjunct, showing the
presence or absence of aortic valve incompe-
tence and pericardial effusion, and confirming
the presence of the intimal flap. Magnetic reso-
nance is as accurate as CT, if not more so, in
diagnosing acute dissection. However, it is
rarely employed because of the lack of immedi-
ate availability, the delay from bedside to
scanner, the long examination time, the limited
access to the patient, and the restricted moni-
toring of vital signs, which is especially prob-
lematic in these often hemodynamically
unstable patients.

Vascular Trauma

Vascular injuries can occur in a number of ways,
such as motor vehicle accidents, knife or
gunshot wounds, or iatrogenically In most
cases, the history and clinical features provide
the diagnosis. Hemodynamically unstable
patients usually proceed immediately to the
operating room for control of the hemorrhage.
If the patient is stable enough, imaging can be
used to confirm hemorrhage or injury, localize
the site, and assess the severity. In addition,
treatment options can be planned from the
information acquired, and in some cases
catheter-based therapeutic intervention can be
performed. Direct vascular injuries in a stable
patient are often best investigated initially by
CT examination. One major advantage of con-
trast-enhanced CT over ultrasound is the ability
to identify the exact site of bleeding and poten-
tially help plan the approach for surgical or
endovascular intervention.

Aortic injury occurs most often following a
rapid deceleration injury, and the vast majority
of cases are due to motor vehicle accidents.
Complete rupture accounts for 85% of cases,
and most patients do not survive. The remain-
ing 15% have incomplete rupture (contained
rupture) and they require immediate treatment,
as half of them will progress to complete
rupture within 24 hours. The most common site
of injury (90%) is at the aortic isthmus, just
distal to the left subclavian artery. The prelimi-

nary investigation is a chest radiograph. It may
show features suggestive of transection, such as
a widened mediastinum, apical cap, and dis-
placement of the trachea, left main bronchus, or
nasogastric tube. A normal chest x-ray does not
exclude transection, but will diagnose condi-
tions such as pneumothorax or hydrothorax.
Arterial phase contrast-enhanced spiral CT with
fine collimation is the most widely used modal-
ity for the imaging of aortic transection. Fea-
tures of aortic injury are the presence of an
abrupt change in aortic contour, false aneurysm,
intimal flap, or extravasation of contrast. Medi-
astinal hematoma is a frequent finding in trau-
matic chest injury, but in the majority of cases,
the source of hematoma is the azygos or hemi-
azygos veins and paraspinal and intercostals
vessels rather than aortic injuries. Although
catheter angiography is still considered the
standard of reference for investigation of aortic
transection, it is employed only when the CT
examination is equivocal or as part of the
endovascular treatment. When performing
catheter angiography, it is vital that at least two
projections of the arch and descending aorta be
obtained prior to pronouncing the investigation
normal. In addition, an awareness of ductus
diverticulum is required. This is the vestigial
remnant of the ductus arteriosus and is present
in approximately 10% of the population. This
anatomical variant appears as a small bulge on
the medial wall of the aorta, just inferior to the
origin of the left subclavian artery, and is fre-
quently misinterpreted as a false aneurysm.

Conclusion

We have presented an overview of available
imaging techniques in use in vascular radiolog-
ical practice, emphasizing the move away from
invasive techniques and toward noninvasive
techniques for diagnosis of vascular diseases.
The most important contemporary approaches
and therapies have also been described,
showing the important role these techniques
now play in the management of a range of vas-
cular disease processes.

References

Aspelin P, Aubry P, Fransson SG, Strasser R, Willenbrock R,
Berg KJ. (2003) N Engl J Med 348:491-9.

VASCULAR SURGERY

Broeders IA, Blankensteijn JD, Olree M, Mali W, Eikelboom

BC. (1997) J Endovasc Surg 4:252-61.
Dormandy JA, Rutherford RB. (2000) J Vase Surg 31:S1-

S296.
Fillinger ME (1999) Surg Clin North Am 79:451-75.
Fillinger ME (2000) Semin Vase Surg 13:247-63.
Haage P, Piroth W, Krombach G, et al. (2003) Am J Respir

Crit Care Med 167:729-34.

Kay J, Chow WH, Chan TM, et al. (2003) JAMA 289:553-8.
Prince MR, Yucel EK, Kaufman JA, Harrison DC, Geller SC.

(1993) J Magn Reson Imaging 3:877-81.
Snow TM, Rice HA. (1999) Clin Radiol 54:842-4.
Thomsen HS, Almen T, Morcos SK. (2002) Eur Radiol 12:

2600-5.

Bleeding and Clotting Disorders

Vivienne J. Halpern and Frank C.T. Smith

Bleeding and clotting disorders have major
implications for the effective management of
vascular patients. Such disorders can influence
disease progression, perioperative complica-
tions, graft patency, limb salvage, and wound
healing. Most of these disorders are relatively
rare, and diagnosis requires an index of clinical
suspicion combined with a need to obtain a
relevant medical history and appropriate
specialized investigations. Correct and timely
treatment may help prevent some of the com-
plications associated with these disorders. This
chapter reviews the presentation, diagnosis,
and management of some of the more common
disorders. Medications frequently associated
with abnormal bleeding or clotting are also
discussed.

History, Physical and
Laboratory Evaluation

Recognition of a patient with a bleeding or
clotting disorder involves taking an adequate
history. A screening questionnaire, such as that
provided in Table 5.1 is useful and may help to
direct further investigation. Obtaining a history
of mucosal bleeding involving epistaxis, gum
bleeding, or menorrhagia may be more consis-
tent with platelet disorders (thrombocytopenia,
von Willebrand disease, etc.) than, for instance,
bleeding into a joint or muscle, which occurs
more commonly with hemophilia. Patients with

a history of myeloproliferative, myelodysplastic,
and lymphoproliferative disorders may also
have increased bleeding through several mech-
anisms, which may not appear in routine pre-
operative testing. Renal failure predisposes to
bleeding tendencies based on platelet dysfunc-
tion, whereas, for instance, recent splenectomy
may induce thrombocythemia predisposing to
abnormal clotting. An abnormal history of clot-
ting, such as multiple episodes of deep venous
thrombosis (DVT), may warrant screening for
thrombophilia.

Medications can influence both bleeding
and clotting. Commonly used drugs such as
aspirin and other nonsteroidal antiinflamma-
tory drugs (NSAIDs) affect platelet function, as
do Aggrenox and Plavix. Herbal remedies and
various vitamin combinations may also increase
bleeding risks (Table 5.2). Furthermore, malnu-
trition and vitamin deficiencies, such as vitamin
C deficiency, may contribute to abnormal bleed-
ing tendencies. Estrogen or estrogen-like med-
ications including phytoestrogens predispose
to thrombotic episodes. PC-SPES is an herbal
preparation with several components used for
treatment of prostate carcinoma. It contains
phytoestrogens, which may induce thrombosis.
However, it also contains Baikal skull cap
(Scutellaria baicalensis georgi), which is a
coumarin (a naturally occurring group of
substances, structurally similar to warfarin).
These examples illustrate the importance of
querying the use of herbal medications as well
as more conventional pharmacotherapies when

VASCULAR SURGERY

Table 5.1 . Screening survey for abnormal bleeding or clotting

Do you suffer from a bleeding disorder?

Do you have bleeding from the gums or from the nose?

Have you ever coughed up or vomited blood?

Do you notice easy or spontaneous bruising or does it take you a long time to stop bleeding when cut?

Do you have excessive bleeding with menstrual cycles?

Have you had any blood in the urine or with stools?

Have you had any bleeding into muscles or joints?

Have you had a tooth extraction or any other procedure after which bleeding has taken a long time to stop?

Have you needed to receive any blood products, plasma, or vitamin K to help stop bleeding?

Do you have any problems with your liver or kidneys?

Has anyone in your family had any of the above problems?

Have you or anyone in your family had a history of clots in the blood vessels, either artery or veins?

Do you take oral contraceptives?

Do you take aspirin or any medications for pain or arthritis?

Do you take any steroid medications?

Do you take any herbal medications or vitamins?

Do you take Coumadin or other blood thinners?

Do you take any medications to prevent stroke or heart attacks?

Do you have any blood diseases?

Table 5.2. Common medications, herbs, and vitamins associated with increased bleeding

Medication

Mechanism of action

When to stop preoperatively

Medications that may increase bleeding

Aspirin

Inhibits platelet aggregation via

5-7 days before major surgery

thromboxane B 2

3-4 days before minor surgery

Persantine

Inhibits phosphodiesterase to increase
cyclic AMP

Omit dose before surgery

Aggrenox

Combined Persantine and aspirin: increased
effects of aspirin

As aspirin

Plavix

Irreversible binding to platelet inhibits ADP
binding to platelet

Stop 7-10 days before surgery

NSAIDs

Various mechanisms

24 hours prior to surgery

Herbs/vitamins that may

increase bleeding

Feverfew

Used for migraines, ? inhibits platelet
aggregation via thromboxane B 2 ,may be
irreversible

Stop at least 1 week before surgery

Garlic

Inhibits platelet function by inhibiting
thromboxane synthesis; may be
irreversible

Stop at least 7-10 days before surgery

Gingko

Inhibition of platelet activating factor

Stop at least 36 hours prior to surgery

Ginseng

Inhibits platelet aggregation; prolongs PT
and PTT; may be irreversible

Minimum of 24 hours prior to surgery

Vitamin E

May decrease platelet adhesiveness; may

Unclear; should stop around

effect vascular endothelium

5 days before surgery

Willow bark

Salicylate precursors

Stop 7-10 days before surgery, similar to aspirin

Oil of wintergreen

Affects platelet function

Meadowsweet flower

ADP, adenosine diphosphate; AMP, adenosine monophosphate; NSAID, nonsteroidal antiinflammatory drug; PT, prothrombin time; PTT, partial
thromboplastin time.

BLEEDING AND CLOTTING DISORDERS

assessing the patient with a bleeding or clotting
disorder.

Investigations

Standard preoperative investigations for most
vascular surgery patients include prothrombin
time (PT), international normalized ratio (INR),
activated partial thromboplastin time (aPTT),
platelet count, and activated clotting time
(ACT). A platelet count of 50,000/uL should
ensure adequate hemostasis, whereas a count of
10,000/|J,L or less may result in spontaneous
bleeding. The aPTT evaluates the intrinsic and
contact activation pathways of coagulation
with the exception of factors VII and XIII. This
investigation is used to monitor the effects of
treatment with heparin. The extrinsic pathway
(factors II, V, VII, and X, and fibrinogen) is
evaluated with the PT and INR. These tests
are employed to check the effectiveness of oral
anticoagulation with warfarin. Additional tests
should be directed by the history and clinical
picture.

The prevalence of inherited bleeding and
clotting disorders is relatively rare. Patients with
a recurrent, familial, or juvenile history of DVT;
arterial thrombosis at a young age or without
evidence of atherosclerosis; or thrombosis in an
unusual location, such as mesenteric or cerebral
veins, should be assessed for a hypercoagulable
state. Recurrent graft failure whether in a bypass
or an arteriovenous fistula, when not explained
by the presence of an anatomical lesion, may
also imply a prothrombotic state. Components
of a thrombophilia screen include those listed in
Table 5.3 (Donaldson et al, 1990).

Patients with a history of abnormal bleeding,
but not requiring medication, should undergo
routine preoperative investigations as above.
Excessive or prolonged bleeding during surgical
procedures where routine preoperative testing
of PT, aPTT, and platelet counts was normal may
represent a platelet functional abnormality, a
dysfibrinogenemia, factor XIII deficiency, vas-
cular endothelial disorders, other mild factor
deficiencies (if >25% of factor present), or oc-
antiplasmin deficiency. Surreptitious use of
medication might also be considered. Where
abnormal preoperative investigations are
encountered, there is a rationale for further
tests. A protocol is suggested in Table 5.4.

Table 5.3. Thrombophilia screen

Protein C levels
Protein S levels
Antithrombin III
Factor V Leiden
Activated protein C
Lupus anticoagulant
Anticardiolipin antibody
Antiphospholipid antibody
Homocysteine levels
Prothrombin 20210A mutation
Factor VIII and XI levels

Bleeding Disorders

Bleeding disorders may be secondary to abnor-
malities of plasma clotting factors, blood
vessels, or platelets. Some hemostatic defects
involve more than one of these systems.

Table 5.4. Protocol for further investigation of abnormal
preoperative blood tests

Repeat abnormal PT/INR,aPTT with 50:50 mix with

normal plasma (mixing study)
If then normal, undertake the following investigations:
Normal PT/INR, increased aPTT:

Test for factor deficiency: usually isolated XI, IX, VIII
Increased PT/INR, normal aPTT:

Test for factor deficiency: isolated VII or can be
multiple

Test for liver abnormalities

Look for vitamin K deficiency (malnourished patient,
patient on prolonged antibiotics)
Increased PT/INR and aPTT:

Test for factor deficiency: isolated X, V, prothrombin,
fibrinogen, or can be multiple
If abnormal mixing study, undertake the following

investigations:
Normal PT/INR, increased aPTT:

Test for inhibitor activity, especially for XI, IX, VIII

Test for nonspecific inhibitors, e.g., antiphospholipid
antibodies
Increased PT/INR, normal aPTT:

Test for factor VII inhibitor

Test for nonspecific inhibitors (rarely cause isolated
increase in PT/INR)
Increased PT/INR and aPTT

Test for inhibitors of X,V, prothrombin, fibrinogen

Test for nonspecific inhibitors

aPTT, activated partial thromboplastin time; INR, international nor-
malized ratio; PT, prothrombin time.

VASCULAR SURGERY

In normal hemostasis, the blood vessel con-
stricts in response to injury to reduce bleeding.
Circulating platelets adhere to sub endothelial
collagen that is exposed by injury, promoted by
release of tissue factor (TF) from the damaged
vessel wall. Platelets bind von Willebrand factor
(vWF) at the glycoprotein lb receptor, stabiliz-
ing adhesion. Fibrinogen binds to platelet gly-
coprotein Ilb/IIIa receptors forming bridges
between adjacent platelets and causing aggre-
gation. Activated platelets also release potent
aggregating agents to recruit more platelets.

Coagulation is initiated through the extrinsic
pathway. Exposed endothelium releases TF,
which complexes with and activates factor VII.
Factor Vila then activates both the common
pathway and the intrinsic pathway. The intrin-
sic pathway requires factor VIII and factor IX to
proceed to the common pathway. Von Wille-
brand factor also forms a noncovalent bond
with factor VIII and is essential for its survival
in the circulation. Von Willebrand factor also
potentiates factor VIII activity in clot formation
and protects it from proteolysis. In the final step
of the coagulation pathway, thrombin cleaves

fibrinogen to generate fibrin monomers, which
then polymerize and link to one another to form
a chemically stable clot. Thrombin also feeds
back to activate cofactors VIII and V, thereby
amplifying the coagulation mechanism.
Together platelet aggregates and fibrin form the
clot that achieves hemostasis. The coagulation
cascade is illustrated in Figure 5.1. Any disrup-
tion of these pathways may lead to increased
bleeding.

Features in the history and physical examina-
tion that may help to differentiate among factor
deficiencies, platelet disorders, and endothe-
lial (blood vessel) dysfunction are listed in
Table 5.5.

Inherited Disorders
of Coagulation

Factor Deficiencies

Hemophilia A and B represent 80% of inherited
bleeding diatheses. These are both sex-linked
recessive deficiencies affecting mostly males.

Intrinsic
Pathway

XII

XI I, i

▼ *•

Villa

Vila

Common

Pathway

T *'

I In

-► Va

Prolbrombin (II)

Thrombin (I la)

Extrinsic

Pathway

Tissue Factor

Fibrinogen

Fibrin

■ VII

Figure 5.1. The coagulation cascade.
Under physiological conditions, tissue
factor is not exposed to blood. However,
after injury, tissue factor is exposed to
blood and activates the extrinsic pathway
by acting in concert with activated VII and
phospholipids to convert factor IX to IXa
and factor X to Xa. The "intrinsic pathway"
includes activation of factor XII to Xlla,
which activates factor XI to Xla, IX to IXa,
and X to Xa. Factor Xa is the active cat-
alytic ingredient of the prothrombinase
complex, which includes factor Va and
phospholipase and converts prothrombin
to thrombin. Thrombin is a protease that
cleaves fibrinogen to fibrin. The result-
ing fibrin monomers polymerize, forming
a clot.

BLEEDING AND CLOTTING DISORDERS

Table 5.5. The relationship of factor disorders, platelet and blood vessel (endothelial) dysfunction to aspects of clinical
presentation

Clinical picture

Factor disorder

Platelet dysfunction

Endothelial
dysfunction

Onset of bleeding

Delayed

Immediate

Duration of bleeding

Prolonged

Short

Variable

Precipitant of bleeding

Often spontaneous

Trauma

Variable

Site

Joints, muscle, viscera

Skin, mucous membranes, Gl tract

Skin, Gl tract

Family history

Usually present (unless factor
inhibitor)

Absent

Usually absent

Drug-related

Rarely

Often

Sometimes

Sex predominance

Usually male

Often female

Usually
female

Response to focal pressure

No response

Sometimes responds

Responds

Platelet count

Normal

Normal, low, or high

Normal

Prothrombin time

Abnormal in cases of factor II,
VII, IX, and X deficiency
(and inhibitors)

Normal

Partial Thromboplastin

Abnormal with factor VIII

Normal

time

or IX deficiency (and

inhibitors)

Gl, gastrointestinal.

They are caused by factor VIII (classic hemo-
philia) and factor IX (Christmas disease)
deficiencies, respectively. Hemophilia A is four
to six times more common than hemophilia
B. Together they have a prevalence of about
20/100,000 in the United States and 9/100,000 to
15/100,000 in Great Britain.

The risk for bleeding depends on the degree
of factor deficiency. At levels less than 1% to
2% of normal (severe disease), spontaneous
bleeding is likely to occur and the aPTT is pro-
longed. Patients may present with spontane-
ous soft tissue or intramuscular hemorrhage,
hemarthroses, hematuria, and spontaneous
retroperitoneal bleeding. Patients with mild
(>5%) and moderate (1% to 5%) disease usually
have bleeding only with injury or surgery.
Patients may have increased bleeding with levels
above 25%, but these deficiencies are hard to
detect as the aPTT will be normal.

Treatment for hemophilia A involves infusion
of recombinant factor VIII concentrates of
which several are commercially available, the
amount depending on the deficiency present.
This includes a loading dose and then a main-
tenance dose for the appropriate period
depending on the location of the bleed if spon-
taneous or perioperative. For milder hemophilia
or cases of mild hemorrhage, or if factor VIII

concentrates are not available, cryoprecipitate
or fresh frozen plasma (FFP) may be used.

The treatment for hemophilia B is similar,
using specific factor IX concentrates or factor IX
complex transfusion. The factor IX complex
contains one unit of factor IX per milligram of
protein with varying amounts of other vitamin
K-dependent proteins. The concentrates are
preferred treatment. Again, loading dose and
maintenance doses are administered according
to the given situation.

Another factor deficiency (vWF), which can
present like hemophilia, occurs in von Wille-
brand disease (vWD). Overall, this is the most
common bleeding disorder with an incidence of
up to 1% in some populations. There are three
subtypes of VWD, the most severe and uncom-
mon being type 3. In this form, vWF in plasma
and platelets is markedly reduced or absent,
thereby reducing factor VIII activity to 1% to
10% of normal. Patients can present with spon-
taneous or severe bleeding. Inheritance is auto-
somal recessive. Type 1 is the most common
type, representing around 70% of cases. vWF is
reduced to the range of 20% to 50% with a con-
comitant reduction of factor VIII activity. The
structure of vWF is generally normal in this
type, and inheritance is autosomal dominant.
Patients usually present with mild to moderate

VASCULAR SURGERY

bleeding diatheses, and the levels of vWF do not
necessarily correlate with clinical symptoms.
This may be because some patients with type 1
VWD have reduced levels of both plasma and
platelet vWF, whereas some just have reduced
plasma levels.

Type 2 VWD is divided into further subtypes
2A, 2B, 2M, and 2N based on the site of the
genetic mutation. Type 2A is the most common
and accounts for around 10% of all vWF
deficiency cases. Inheritance is autosomal dom-
inant. The largest multimers of vWF are absent,
and this leads to a lack of platelet binding. Activ-
ity of factor VIII, however, can be near normal
in this subgroup. Clinical presentations in this
group are therefore variable. In type 2B, patients
lack multimers in the plasma but have near-
normal levels in platelets. However, these
patients are usually thrombocytopenic, which
can be made worse with exercise, stress, preg-
nancy, or advanced age. Levels of factor VIII are
low to normal. Presentation is again variable
and inheritance is autosomal dominant. Type
2M is very rare and has abnormal multimers as
its cause of abnormal coagulation. This has not
been well defined in terms of inheritance. Type
2N is inherited as an autosomal-recessive con-
dition and sometimes mimics mild hemophilia.
These patients have normal vWF multimers and
normal vWF activity but reduced factor VIII
activity due to poor binding between vWF and
factor VIII. This variant should be considered
in the differential diagnosis of factor VIII
deficiency, especially if the patient is female
and other aspects of the pedigree support
autosomal-recessive inheritance rather than
sex-linked. Von Willebrand disease may be
treated with desmopressin acetate [deamino-
8-D-arginine vasopressin (DDAVP)], which
probably increases vWF, tissue plasminogen
activator (tPA), and factor VIII secretion from
stored sources. Some of the subtypes may also
require factor replacement. More recent treat-
ments include recombinant factor VIII/vWF
concentrates, which reduce risks of transmis-
sion of infection.

Other factor deficiencies are quite rare. Factor
V deficiency is inherited as an autosomal-
recessive trait. It has a wide range of clinical
manifestations but seems to have less bleed-
ing associated with it than hemophilia A. Severe
factor V deficiency (levels <1% of normal) pres-

ents with abnormal bruising, soft tissue hemor-
rhage, and epistaxis. Bleeding from the umbili-
cal stump at the time of birth is common.
Women commonly have abnormally heavy
menstrual bleeding and postpartum bleeding.
Most cases present in adulthood. Fresh frozen
plasma is the mainstay of treatment.

Factor VII deficiency is inherited as an auto-
somal-recessive disorder and affects males and
females equally with an incidence of about 1 in
500,000. Clinical manifestations can be similar
to those of hemophilia with severe deficiencies
(<1% level) as the factor Va/tissue factor com-
plex is the key initiator of coagulation in vivo.
However, about half of patients are asymp-
tomatic, and levels of factor V do not correlate
well with clinical manifestations. Interestingly,
diminished or defective function of tissue
factor has not been documented as a cause of
decreased factor VII activity. The most common
presentations include easy bruising, soft tissue
hemorrhage, and menorrhagia in women.
Patients with levels less than 1% of normal may
present like hemophiliacs with pathology
including intracranial bleeds and hemarthroses.
Current treatment in the United States is with
FFP, although factor VII concentrates and
recombinant factor VII are available in Europe.

Factor X deficiency is transmitted as an auto-
somal-recessive trait and has an estimated inci-
dence of 1 in 500,000. Usually those with greater
than 15% of normal levels do not have severe
bleeding, although bleeding with major surgery
or trauma may occur. However, with more
severe deficiencies, severe bleeding episodes
similar to those seen in hemophilia may occur,
including hemarthroses, retroperitoneal
hematomas, hematuria, pseudotumors, and
menorrhagia. Another cause of factor X
deficiency is amyloidosis. In this situation,
transfusion of factor X is not helpful because of
its absorption by the extracellular amyloid.
Improvement does not occur unless the amyloi-
dosis resolves, although splenectomy may help
by debulking splenic amyloid. Treatment for
standard factor X deficiency is with FFP or pro-
thrombin complex concentrates. Pure factor X
concentrates are not available for commercial
use yet. Concentrations of 10% to 15% give
adequate hemostasis. Overtransfusion can lead
to thromboembolic events and disseminated
intravascular coagulation (DIC).

BLEEDING AND CLOTTING DISORDERS

Factor XI deficiency occurs mostly in
Ashkenazi Jews with a gene frequency in this
population of 4.3%. Bleeding usually occurs
with levels <20% of normal and usually only
after major trauma or surgery. Rarely, there is
spontaneous bleeding as seen with hemophilia,
although soft tissue hemorrhage, epistaxis, and
bleeding after dental extraction and with major
surgical procedures may occur. Menorrhagia
may occur in females. Bleeding risk is signifi-
cantly increased in patients taking aspirin.
Treatment when necessary is with FFP and with
cryoprecipitate-poor plasma. Factor XI concen-
trates are available.

Fibrinogen Abnormalities

The dysfibrinogenemia are mostly inheritable
abnormalities of fibrinogen structure and func-
tion. Clinically, many patients are asymptomatic
but some present with either bleeding or a
thromboembolic event or both. There are mul-
tiple different abnormalities too diverse to dis-
cuss in detail in this chapter because they have
variable inheritance, affect different portions of
the molecule, and have different manifestations.
Suffice it to say they should be considered in
patients with a history of bleeding and abnor-
mal coagulation testing. Inheritable afibrino-
genemias and hypofibrinogenemias also exist.
Patients present with bleeding episodes in the
afibrinogenemias and with hypofibrinogene-
mias with levels above 50mg/dL. Afibrinogene-
mias are inherited as an autosomal-recessive
trait but hypofibrinogenemias are less pre-
dictable. Bleeding complications when they
occur can be severe, with a high incidence of
bleeding in the neonatal period. This may result
in death in about one third of patients with
severe hypo- and afibrinogenemias.

Platelet Disorders

Bernard-Soulier syndrome (glycoprotein Ib-IX
deficiency) is a disorder of platelet adhesion and
is a relatively rare cause of bleeding. It is char-
acterized by a prolonged bleeding time, large
platelets, and thrombocytopenia due to an
inability to adhere to vWF in the subendothelial
matrix. It presents in infancy or childhood with
epistaxis, ecchymosis, and bleeding gums. Treat-
ment is with platelet transfusion. Hormonal

control may be helpful with menorrhagia, and
DDAVP may be useful for prophylaxis prior to
procedures.

Deficiencies of platelet collagen receptors
also exist but do not cause significant bleeding,
although they may prolong bleeding time.

Disorders of platelet aggregation include a
deficiency of Ilb/IIIa, known as Glanzmann's
thrombasthenia, characterized by a prolonged
bleeding time and abnormal clot retraction. It is
inherited as an autosomal-recessive trait in
clusters of disease. It presents with mucocuta-
neous bleeding in the neonatal period or in
infancy and occasionally as bleeding following
circumcision. Epistaxis and purpura are the
most common presentation. Severe bleeding
with menses may be encountered. If it is unrec-
ognized, significant bleeding with surgery or
trauma will occur if the patient is not transfused
with normal platelets. Platelet counts and
smears are normal, but bleeding times are very
prolonged. Platelet aggregation is absent in
normal testing except with epinephrine, where
it is weak. Platelet secretion is normal with
strong agonists like thrombin but is absent with
weak stimulators like epinephrine and adeno-
sine diphosphate (ADP). Clot retraction is
either absent or reduced. Treatment is under-
taken with platelet transfusion if bleeding is
present. Leukocyte-depleted platelets may
reduce risks with future transfusions. Hormonal
therapy is useful with menorrhagia. Regular
dental care is important to reduce the risk of
gingival bleeding but Amicar (e-aminocaproic
acid) may be valuable in helping to control
bleeding after dental extractions.

Disorders of platelet secretion are related to
deficiencies in one or more of the four types
of platelet granules or to abnormalities in the
secretory mechanism. Platelets have four types
of granules:

1. Dense or 8 granules containing ADP,
adenosine triphosphate (ATP), calcium,
serotonin, and pyrophosphates

2. a-granules containing a variety of pro-
teins, some of which are obtained from
the plasma and others synthesized by
megakaryocytes; these include fibrinogen,
vWF, albumin, factor V, immunoglobulin
G (IgG), fibronectin, and proteinase
inhibitors from the plasma and platelet

VASCULAR SURGERY

factor-4, (3-thromboglobulin, platelet-
derived growth factor, and throm-
bospondin from megakaryocytes

3. Lysosomes containing acid hydrolase

4. Microperoxisomes containing peroxidase
activity

Secretory dysfunction usually results in mild
to moderate bleeding manifested by easy bruis-
ing, menorrhagia, and excessive postoperative
or peripartum bleeding. Testing reveals a pro-
longed bleeding time, a decreased second wave
of aggregation with ADP and epinephrine
stimulation, and decreased aggregation with
collagen. Secretory dysfunction should be dif-
ferentiated from acquired disorders with acetyl-
salicylic acid (ASA) use, uremia, and multiple
myeloma, and from VWD.

Gray platelet syndrome is an a-granule
deficiency. Platelets occur without these gran-
ules but with vacuoles and small a-granule pre-
cursors containing material that stain positive
for vWF and fibrinogen. Additionally, the vac-
uoles and these precursors contain P-selectin
and Gllb-IIIa. These factors indicate the pres-
ence of a-granules, but the normal proteins they
contain cannot be packaged. Other granules
are present in normal quantity. Patients have
a history of mild to moderate mucocutaneous
bleeding. They have prolonged bleeding times
with moderate thrombocytopenia (60,000 to
100,000), reticular fibrosis of the bone marrow,
and large platelets that appear gray on Wright-
stained blood smears-hence the name. Platelet
aggregation studies are variable. Treatment
requires transfusion of normal platelets and at
least one patient responded to DDAVP. The
Quebec platelet disorder is extremely rare and
again involves a-granules that appear grossly
normal but are deficient in many of the proteins
normally seen including factor V, fibrinogen,
vWF, and fibronectin. Patients present similarly
to the gray platelet syndrome and are treated the
same way.

Dense granule deficiency or 8-storage pool
disease is a heterogeneous group of disorders,
which can be divided into deficiency states asso-
ciated with albinism and those in otherwise
normal patients. With albinism, the disease is
related to a qualitative deficiency in these gran-
ules. In nonalbinos, the number of granules
is near normal. In some of these nonalbino
patients it is associated with a variable

deficiency of a-granules. The content of lysoso-
mal hydrolase is normal, but thrombin-induced
acid hydrolase secretion is impaired, which can
only be corrected with ADP. Patients present
with mild to moderate bleeding. Platelet counts
are usually normal, but bleeding times are
prolonged. The quantity of thromboxane B 2 ,
a metabolite of thromboxane A^ is reduced.
Secondary aggregation induced by ADP and
epinephrine is reduced. Collagen-induced
aggregation is abnormal at low concentrations
of collagen but is normal with high concentra-
tions. Therapy requires transfusions of normal
platelets if there is massive bleeding. Otherwise,
DDAVP is the initial treatment and cryoprecip-
itate can also be used. In one study, pred-
nisolone seemed to reduce bleeding in patients
with inherited platelet disorders but not in
patients with thrombasthenia or ASA use.

Platelet function in patients with inherited
disorders of platelet secretion resembles that of
patients receiving platelet function inhibitors
like ASA. These disorders are a heterogeneous
collection of abnormalities of secretion-
response adhesion. In families where these dis-
orders have been noted, the pattern appears to
be autosomal dominant. A prolonged bleeding
time and marked impairment of aggregation
and secretion in response to ADP, epinephrine,
and low concentrations of collagen occur.
Stronger agonists like high levels of collagen,
however, may induce a near-normal or normal
response. Treatment is the same as that for
patients with platelet storage disorders.

Vascular Defects

Inheritable conditions that lead to defects in the
vascular bed include Marfan's syndrome and
Osier- Weber-Rendu disease. These may increase
bleeding through mechanisms that are not
entirely clear.

Acquired Disorders
of Coagulation

This group of disorders includes factor
inhibitors as well as acquired diseases that affect
platelet and endothelial function. Factor
inhibitory proteins can be classified as neutral-
izing, nonneutralizing, or altering. They are

BLEEDING AND CLOTTING DISORDERS

usually autoantibodies. The most common
factor inhibitor is factor VIII, often referred
to as acquired hemophilia, but inhibitors have
been found to thrombin and prothrombin,
fibrinogen, thrombin and prothrombin, fibrino-
gen, vWF, and factors V, VII, IX, X, and XI as
well (Fig. 5.1). These are seen in response
to inflammatory diseases such as rheumatoid
arthritis and other autoimmune diseases like
systemic lupus erythematosus (SLE) and
Sjogren's syndrome and even inflammatory
bowel syndrome. They also appear during preg-
nancy and the puerperium, as well as with
various tumors. They may be associated with a
variety of medications including aminoglyco-
sides, penicillins, valorous acid, etc. They are
also seen with cirrhosis and major surgery.

Interestingly, factors V and X and thrombin
inhibitors have been seen following the use of
topical thrombin and fibrin glue, usually after
multiple exposures. Not only can this lead to
perioperative bleeding, but also inhibitors of
factor X can interfere with monitoring of low-
molecular-weight heparin (LMWH) anticoagu-
lation with the antifactor Xa assay.

Factor inhibitors may lead to increased bleed-
ing and, rarely, spontaneous bleeding. Most
conditions are initially detected as a prolonga-
tion of one or more of the coagulation screen-
ing tests — PT/INR/aPTT — or thrombin time.
To differentiate between the different types of
inhibitors, a clotting study should be done on a
1 : 1 mixture of the patient's plasma with normal
plasma. A lack of correction of clotting time
indicates a neutralizing antibody. Vigilance in
testing is essential because at body temperature
some studies initially correct and then return to
a prolonged state after an hour. This is particu-
larly true of factor V and VIII inhibitors.

If the mixing study corrects, this suggests the
presence of a nonneutralizing antibody that
may facilitate clearance of the clotting factor
from circulation. The antibody should be
isolated to differentiate its presence from a
deficiency of the factor.

Treatment of bleeding includes infusion of
factors to levels that overwhelm the antibodies
and return the coagulation profile to normal.
Long-term treatment includes immunosup-
pression with steroids or other agents and
plasmapheresis with immuno absorption with
Ig-Therasorb. The latter can be used in con-
junction with transfusion.

Hypercoagulable States

Like bleeding disorders, these states can be
categorized as inherited or acquired (Table 5.6).
Hyperhomocystinemia, however, can be either
inherited or acquired. Indications for throm-
bophilia screening have already been outlined
and the components of such a screen are
referred to in Table 5.3. For most of the hyper-
coagulable states, treatment involves the use of
LMWH or unfractionated heparin with conver-
sion to oral warfarin. Often, if the patient has
already had a thrombotic episode, anticoagula-
tion is undertaken for life.

Table 5.6. Differential diagnosis for hypercoagulable states

Inherited (primary)
Protein C and S deficiencies
Antithrombin III deficiency
Factor V Leiden mutation leading to activated

protein C resistance
Prothrombin 20210A gene mutation
Heparin cofactor II deficiency and other heparin

binding proteins
Cystathionine synthase deficiency

(hyperhomocystinemia)
Dysfibrinogenemia
Dys- and hypoplasminogenemia

Acquired (secondary)
Cancer
Pregnancy
Oral contraceptives and other hormone replacement

therapy (HRT)
Myeloproliferative disorders
Hyperlipidemia
Diabetes mellitus
Vasculitis
Antiphospholipid syndrome (lupus anticoagulant,

anticardiolipin antibodies)
Postoperative states/trauma
Immobilization
Nephrotic syndrome
Congestive heart failure
Increased levels of factor VII and fibrinogen
Obesity

Heparin thrombocytopenia
Anticancer drugs (bleomycin, vinca alkaloids,

mitomycin, etc.)
Paroxysmal nocturnal hemoglobinuria
Age

Undetermined
Elevated factor XI levels and \

I levels

VASCULAR SURGERY

Inherited

Inherited hypercoagulable states account for 5%
to 15% of patients with venous thromboem-
bolism (VTE). The most common appear to be
the factor V Leiden mutation followed by the
prothrombin G20210A mutation of the pro-
thrombin gene among the white population, but
these are rare in Asians and Africans. Table 5.7
shows the overall incidence of the various inher-
ited hypercoagulable states. These are estimates
from several studies and vary with ethnic back-
ground and location.

Factor V Leiden, also known as activated pro-
tein C resistance (APCR), results from a point
mutation in the factor V gene, leading to a loss
of protein C cleavage sites (Ouriel et al., 1996).
The consequence of this is impaired activation
of protein C. The most common presentations
are VTE and fetal loss. It usually does not result
in arterial thrombosis unless other risk factors
are also present, for example smoking.
Homozygotes have an 80-fold increased risk of
DVT, and heterozygotes have much less. Many
patients with factor V Leiden remain asympto-
matic, and about 60% of those who present with
thrombosis have another risk factor such as use
of oral contraceptives (OCs) or hormone
replacement therapy (HRT). The overall risk of
VTE is 3% to 7%.

The prothrombin 202 10A gene mutation
appears in 2.3% of healthy control patients. The
incidence is twice as high in southern Euro-
peans compared to northern Europeans and is
rare in Asians and Africans. The mutation
increases prothrombin levels and activity. The
relative risk of clotting is two to three times that
of normal individuals.

Table 5.7. Incidence of inherited disorders

Disorder

Incidence

Factor V Leiden (activated protein

25%

C resistance)

Sticky platelet syndrome

14%

Protein C deficiency

10%

Protein S deficiency

10%

Prothrombin G20210A

5-10%

Increased homocysteine

5-10%

Dysfibrinogenemia

1.5%

Antithrombin III

<1% (1/250-500)

Dys- or hypoplasminogenemia

1-3%

Protein C and S deficiencies have relatively
the same incidence. They both result from
numerous different mutations. A heterozygote
pattern is much more frequent as homozygotes
present soon after birth with purpura fulminans
or massive venous thrombosis. Protein C has
type I and type II deficiencies. Type I deficien-
cies are those mutations causing a decrease in
levels and in activity; most of these are missense
mutations. Type II deficiencies are those in
which levels are normal but activity is affected;
most of these are point mutations. Patients with
protein C deficiency tend to present with VTE
and fetal loss and rarely with arterial thrombo-
sis. Protein S deficiency is harder to define.
Many studies have shown the coexistence of
protein S deficiency with APCR in as high as
40% of the patient population studied. This
makes it hard to determine which is more
important. However, there are more numerous
reports of arterial thrombosis with protein S
deficiency, including stokes, compared to
protein C deficiency. Many conditions may
result in lowered levels of these proteins, partic-
ularly protein S (for instance in liver disease,
nephrotic syndrome, pregnancy, sepsis, etc.)
and some medications like HRT may have the
same effect. Therefore, measurement of levels of
protein S may need to be repeated to ensure
accuracy as well as to allow checking for specific
genetic defects. Overall, as many as 50% of
heterozygotes for protein C and S deficiencies
develop VTE up to the age of 50 years.

Antithrombin III (AT III) deficiency occurs as
an autosomal-dominant disorder and in 1/5000
healthy blood donors. It may also have type I
and type II deficiencies. The type I deficiencies
are caused by both gene segment mutations as
well as point mutations, whereas the type II
deficiencies are caused mostly by point muta-
tions. Most patients are heterozygotes,
as homozygous deficiency is probably incom-
patible with life unless it is a type II deficiency
of the heparin-binding site. All types are at
increased risk of VTE, with as many as 80% of
heterozygotes by age 50 having an episode of
VTE. Like protein C and S, AT III deficiency can
be acquired in association with the medical con-
ditions described above.

Hyperhomocystinemia and homocystinuria
have both been described as associated with
VTE and arterial thrombotic events (Nehler
et al., 1997). Homocysteine is an intermediate of

BLEEDING AND CLOTTING DISORDERS

methionine metabolism. Elevated levels arise
from both genetic defects affecting the transsul-
furation or remethylation pathways as well as
with folate, B 6 and B 12 deficiency, renal failure,
hypothyroidism, increased age, and smoking.
Homozygotes for cystathionine P-synthase
deficiency and methylene-tetrahydrofolate re-
ductase may have severe vascular disease and
appear even in childhood. As many as 60% have
thromboembolic events before age 40 and 50%
by age 29. Heterozygotes have a high incidence
of premature arterial occlusive disease, which
may represent as much as 1/70 of the normal
population. However, the most common cause is
dietary folate and B 6 and B 12 deficiencies, which
account for around two thirds of the cases
of hyperhomocystinemia. Measuring fasting
homocysteine plasma levels establishes the
diagnosis. The mechanism of thrombosis is
thought to involve several mechanisms includ-
ing induction of endothelial cell tissue factor
activity, inhibition of thrombomodulin,
decreased AT III activity, decreased protein C
activation, increased factor V activity, and
increased affinity of lipoprotein (a) and fibrin.
Dietary supplements with B 6 , B 12 , and folate help
lower the homocysteine levels, but unfortu-
nately this may not reduce the risk of thrombo-
sis and therefore anticoagulation may also be
indicated.

The dysfibrinogenemias can cause thrombo-
sis as well as bleeding in around 20% of patients.
The conversion of fibrinogen to fibrin consists
of three main steps: release of fibrinopeptides A
and B from the alpha and beta chains to form
fibrin monomers, followed by polymerization of
these monomers to a visible fibrin gel, which is
then stabilized by activated factor XIII. Fibrin
may then be broken down via fibrinolysis path-
ways. Inherited dysfibrinogenemias result from
mutations that alter one or more of these steps.
They are usually autosomal dominant. One may
be suspicious if there is a prolongation of the
PT and PTT. Thrombosis can occur secondary
to either an abnormal fibrinogen with reduced
binding to thrombin and increased thrombin
levels, or decreased fibrinolysis. It is relatively
rare for this to be the sole cause of VTE (around
0.8% of VTE) and is frequently associated with
precipitating risk factors such as HRT, pro-
longed bed rest, etc. Treatment remains anti-
coagulation, but it is preferable initially to use
LMWH, as unfractionated heparin activity can

be difficult to monitor with a baseline elevated
aPTT. Acquired dysfibrinogenemia is seen with
liver disease, multiple myeloma, Waldenstrom's
macroglobulinemia, and autoimmune diseases;
the end result of all of these conditions is altered
polymerization or delayed fibrinopeptide
release.

Dys- or hypoplasminogenemias occur even
more rarely. These are usually autosomal dom-
inant. Patients usually present in their late teens,
most commonly with VTE. Routine tests are
normal. There are also rare congenital deficien-
cies of tPA and congenital increases of plas-
minogen activator inhibitor (PAI). These
disorders are more commonly acquired with
diabetes, inflammatory bowel disease, and coro-
nary atherosclerosis.

Factor XII is involved with plasmin genera-
tion. There is an autosomal-dominant genetic
deficiency, which is quite rare but results in both
VTE and arterial thrombosis. About 8% of
deficient patients have thrombotic episodes. An
elevated PTT is present, but it corrects with the
addition of normal plasma. Treatment is with
LMWH and then warfarin. Standard unfrac-
tionated heparin again is difficult to monitor
with baseline elevated PTT.

Heparin factor II and other heparin-binding
molecules are found to have deficiencies; how-
ever, the association with thrombotic events is
weak. The same is true for thrombomodulin
defects.

The sticky platelet syndrome is a rare
autosomal-dominant disorder that results in
platelets that aggregate more readily with epi-
nephrine or ADP. Venous and arterial thrombo-
sis occur, and retinal vascular thrombosis
appears to be associated with this entity. Treat-
ment is initially with low-dose aspirin. If aggre-
gation does not normalize, then this dose can be
increased to 325 mg daily. Clopidogrel (Plavix)
provides an alternative potential therapy.
Another platelet defect is the Wein-Penzing
deficit. This is a deficiency of the lipoxygenase
metabolic pathway resulting in an increase in
the cyclooxygenase pathway and therefore ele-
vated thromboxane levels. Platelets are thus in a
state of increased activation.

Other abnormalities that may be genetically
based include elevated factor XI and factor XIII
levels. Both these groups seem to have increased
risk of VTE, and the level of increased risk
appears to be proportional to the increase in the

VASCULAR SURGERY

levels of these factors. Hormone replacement
therapy and pregnancy are also implicated in
raised levels of these factors. Patients on HRT or
OC and with elevated factor VIII levels have a
10-fold increased risk of VTE compared to those
without these risk factors.

Acquired

The most common cause in this group of con-
ditions is the antiphospholipid antibody (APA)
syndrome (Fligelstone et al., 1995). These anti-
bodies bind to plasma proteins that have a high
affinity for phospholipid surfaces. The most
common of these proteins are the lupus antico-
agulant (LA), anticardiolipin (ACL) antibodies,
and anti-(3 2 -glycoprotein-l antibodies (B 2 G).
These are usually acquired. Lupus anticoagulant
can be suspected if there is an elevated PTT, and
ACL and B 2 G are detected only by immunoas-
says. These conditions can be primary, that is,
not associated with other autoimmune condi-
tions. They can present with VTE or arterial
thrombosis as well as fetal demise. Antiphos-
pholipid antibodies may be associated with
infections, cancer, and even certain drugs and
hemodialysis, but these are usually IgM as
opposed to IgG antibodies and are present in
low levels. They do not seem to be associated
with thrombotic events.

The overall incidence is 1% to 5% of the
normal population. The incidence increases
with age and coexisting chronic disease. The
incidence in patients with SLE is 12% to 30% for
ACL and 15% to 34% for LA. The risk of throm-
bosis in patients found to have these autoanti-
bodies is unclear but seems to be increased in
those with a history of previous thrombosis,
with LA and with increased IgG ACL — each of
which increases the risk of thrombosis fivefold.
The persistent presence of APA also increases
the risk of thrombosis. These patients have a
high proportion of pregnancy losses as well as
an increased incidence of premature births.
These patients are best treated with ASA plus
heparin to achieve live births.

Interestingly, not all arterial episodes of
ischemia or infarction are due to primary
thrombosis. Up to 63% of patients with APA
syndrome have coexisting valve abnormalities
on echocardiography and 4% have vegetations
of the mitral or aortic valve. These patients may
also be thrombocytopenic (as many as 40-50%)

and may have hemolytic anemia (14-23%) and
livedo reticularis (11-22%). Renal involvement
may occur, and when it does it usually results in
hypertension.

Catastrophic APA syndrome is acute, and
multiple simultaneous vascular thrombotic
events can occur throughout the body. Small
vessels of multiple organs are often affected. The
syndrome may result in death. In 78% of these
patients the kidneys are involved, followed by
the lungs in 66%, the central nervous system in
56%, the heart in 50%, and the skin in 50%. Dis-
seminated intravascular coagulation is a com-
ponent of this event in 25% of patients. The
mortality rate is 50%, usually due to multisys-
tem organ failure. The optimal treatment is
not well defined but includes, in various com-
binations of anticoagulation, steroids and either
plasmapheresis or intravenous immune globu-
lin. The condition can be precipitated by
surgery, infection, withdrawal of anticoagula-
tion therapy, and drugs, including oral
contraceptives.

Heparin-induced thrombocytopenia (HIT)
also warrants some discussion. The entity was
first described by Towne in 1979 as the white
clot syndrome and occurs in 1% to 30% of
patients on heparin. Heparin-induced thrombo-
cytopenia is diagnosed by one or more HIT-
associated clinical events, such as thrombosis of
a graft, and the presence of heparin antibodies.
Various tests (Table 5.8) are now available to
help in making the diagnosis (Warkentin and
Greinacher, 2004). The problem is that the onset
of HIT is often delayed or seen after multiple
exposures to heparin, where the first few expo-
sures resulted in minimal or no decrease in
platelets. Additionally, the delayed onset may
be seen only after the offending heparin has
been removed. The initial exposure can be
as inconsequential as heparin lock flushes to
maintain the patency of intravenous lines or
standard subcutaneous heparin prophylaxis.
Treatment includes stopping the heparin.
Coumadin alone is not a good treatment due to
the hypercoagulable period before anticoagula-
tion is achieved, leading to potential skin necro-
sis. Additional therapy is switching to hirudin
(Refludan), argatroban (Novastartan), or dana-
parnol (Orgaran). Additionally, some of the
Gllb-IIIa inhibitors have been successfully
employed in this situation. Newer agents are
under investigation including a recently Food

BLEEDING AND CLOTTING DISORDERS

Table 5.8. Testing for heparin-induced thrombocytopenia

Ig, immunoglobulin; PF4, platelet factor 4.

Sensitivity

(%)

Specificity

(%)

Positive
predictive

(%)

value

Negative
predictive value

PF4 + heparin coated plate: anti IgG, IgA,

and IgM
Serotonin release
Platelet aggregation

88
91

100
77

100
89

and Drug Administration (FDA)-approved oral
anti-factor Xa agent.

Most malignancies can be associated with a
higher incidence of thromboembolic events, in
particular, adenocarcinoma and myeloprolifer-
ative disorders.

Conclusion

Bleeding and clotting disorders are encountered
sufficiently frequently in vascular surgical prac-
tice to encourage an awareness of the range of
disorders and of the different available thera-
peutic modalities. A high index of suspicion, a
comprehensive medical history, and judicious
employment of investigations help guide the
experienced clinician to a correct diagnosis. The
bleeding disorders are varied, and each requires
specific management. The majority of throm-
bophilic tendencies may simply be treated with

appropriate anticoagulation with the exception
of catastrophic amyotrophic lateral sclerosis
(ALS). The cumulative risks of different inher-
ited and acquired thrombophilic factors have
appreciable significance. Individual personal-
ized risk profiles for thrombotic events may
have a role to play for patients in the future. An
awareness of the broad extent of these condi-
tions helps vascular surgeons provide optimal
management for their patients.

References

Donaldson MC, Weinberg DS, Belkin M, Whittemore AD,

Mannick JA. (1990) J Vase Surg 11:825-31.
Fligelstone LJ, Cachia PG, Ralis H, et al. (1995) Eur J Vase

Endovasc Surg 9:277-83.
Nehler MR, Taylor LM Jr, Porter JM. (1997) Cardiovasc Surg

5:559-67.
Ouriel K, Green RM, DeWeese JA, Cimino C. (1996) J Vase

Surg 23:46-51, discussion 51-2.
Warkentin TE, Greinacher A. (2004) Chest 126:3 11S-337S.

Medical Management of Peripheral
Arterial Disease

Jill J.R Belch and Andrew H. Muir

Atherosclerosis

Peripheral arterial disease (PAD) is a marker
for multisystem vascular disease. Workers in
this field recognized this over 150 years ago,
noting the similarity between claudication
symptoms and angina. Since then, published
work has supported this view, but the com-
monality of the link between PAD and coronary
artery disease (CAD) has only now been fully
recognized. Myocardial infarction (MI) and
stroke are the biggest risks to life and health
for the PAD patient rather than amputation
or critical limb ischemia (CLI). The natural
history of intermittent claudication (IC), the
usual symptom of lower limb atherosclerosis, is
often benign. Most patients improve or their
disease remains stable. Less than 5% of patients
require amputation. In contrast, however, the
death rate in these patients is three to four
times higher than in patients of similar age
without IC (Fig. 6.1). This mortality occurs due
to atherosclerosis at other sites within the body.
Only one quarter of the mortality of these pa-
tients is from nonvascular events. One half die
from CAD, 15% as a result of stroke, and 10%
from vascular pathology within the abdomen
such as ruptured aortic aneurysm. The associa-
tion between PAD and generalized vascular
mortality is so strong that even in asymptomatic
PAD [detected by a decrease in the ante-
brachial index (ABI)] the patient's relative risk
of a cardiac or cerebrovascular event is very
much higher.

Thus we now recognize that atherosclerosis is
a systemic disorder affecting the entire vascular
tree. Extracranial carotid disease can lead to
stroke, CAD to myocardial ischemia/infarction,
renovascular disease to hypertension, and aor-
toiliac and infrainguinal arterial disease to IC or
limb-threatening ischemia. The mainstay of the
medical management of vascular disease is to
understand that it is a systemic disorder and
must be managed as such. Thus the medical
management of PAD is a complex area that
includes strategies for vascular risk reduction,
lifestyle advice, and direct pharmacotherapy
for the vascular disease. Its implementation
requires a multidisciplinary team, which in-
cludes not only vascular physicians, vascular
surgeons, and interventional radiologists but
also many of the professions allied to medicine
and, importantly, our primary care colleagues.
Areas of focus for such a vascular team are out-
lined in Table 6.1.

Vascular Risk Factor
Modification in Peripheral
Arterial Disease

The medical management of vascular disease
must focus on modification of the following
specific risk factors that promote the progres-
sion of the disease: (1) platelet aggregation, (2)
smoking, (3) obesity, (4) diabetes, (5) dyslipi-

VASCULAR SURGERY

100

-1
<

COLO
RECTAL)

BREAST

PROSTATE

PAD

LUNG

Figure 6.1 . Mortality of peripheral arterial disease (PAD). The 5-
year mortality of PAD is relatively equivalent to numerous
cancers (prostate, breast, colorectal, and lung).

demia, (6) hypertension, (7) sedentary lifestyle,
and (8) type A personality or stress.

The literature suggests that cigarette smok-
ing, hypertension, dyslipidemia, and diabetes
mellitus are important factors in the develop-
ment of PAD, and these will be addressed in turn
(Table 6.2). A key risk factor for PAD is platelet
aggregation along with other hemorheological
factors such as increased plasma fibrinogen and
decreased fibrinolysis. Currently an area of
interest that is being explored is that of the con-
tribution of inflammation to PAD. The high
white blood count (WBC) contributes vascular
risk to the patient with PAD (Belch et al, 1999)
as does increased oxidative stress. Of the above,
however, platelet activation and release in the
patient with PAD has been well documented
and has led to the evidence-based use of
antiplatelet agents in PAD.

Platelet Aggregation

Platelet aggregation is increased in patients with
PAD, and the role of such aggregates in arterial
thrombosis has been well documented. Platelet
release products also contribute to the underly-
ing pathology. (3-Thromboglobulin is one such
product that, once released from platelets, con-
tributes to neutrophil activation. Platelet factor
4 neutralizes heparin, and platelet-derived
growth factor stimulates proliferation of vas-
cular smooth muscle cells. Some of the release

products are vasoactive, and these include
thromboxane A 2 and serotonin, both potent
vasoconstrictors.

Antiplatelet Agents

Current interest in antiplatelet agents relates to
their use as prophylactic treatments against
arterial events in other beds and atherosclerosis
disease progression.

Aspirin in Peripheral Arterial Disease

Aspirin is the most commonly used antiplatelet
agent, reflecting the fact that it is currently
the cheapest agent available and one of the
best studied agents in clinical trials. Its action
includes the irreversible inhibition of the cyclo-

Table 6.1 . Medical strategies for the management of
peripheral arterial disease

Address vascular risk

Antiplatelet therapy

Cigarette smoking

Dyslipidemia

Hypertension

Diabetes

Obesity

Thrombophilia
Specific therapy for intermittent claudication

Exercise

?Drug therapy
Vasculitides as a cause of symptoms

Connective tissue disease

Raynaud's phenomenon

Vasculitis

Antiphospholipid syndrome
Embolism as a cause of symptoms

Detect and treat arrhythmia and/or cardiac
thrombus

Exclude aortic aneurism
Chronic limb symptoms

Control edema

Control infection

Improve cardiac output
Acute critical limb ischemia (CLI)

Thrombolysis

Anticoagulation
Deep vein thrombosis (DVT)

Prophylaxis

Treatment

MEDICAL MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE

Table 6.2. Risk factors for intermittent claudication
Risk

Other cardiovascular events, e.g., Ml, stroke

• Antiplatelet agent

Aspirin, clopidogrel, dipyridamole

Smoking

• Cessation program

Counseling

Nicotine replacement, e.g., patch, gum, spray

Dyslipidemia

• Lipid-lowering therapy

Diet + drug

Target: LDL cholesterol <3.0 mmol/L

HDL >20%

Triglycerides <1. 8 mmol/L

Hypertension

• Antihypertensive therapy

Select: ACE inhibitor

Calcium channel blockade

Diuretic

Avoid beta-blockade (unless vasodilatory)

Target BP <140/85 (in diabetes <140/80)

(Note: 25% will have renal artery stenosis; watch renal function)

Diabetes

• Check for hyperglycemia

Fasting glucose > 7.8 mmol/L

If borderline glucose (random or fasting), glucose tolerance test with

fasting and 2-hour sample

2-hour sample: <7.8 mmol/L normal

>7.8-1 1.0 impaired

>1 1.1 diabetic

Obesity

• Check for obesity

Body mass index >30

Low-fat, high-fiber diet, healthy eating

Calorie control

Thrombophilia

• Consider referral for thrombophilia screen (inherited or acquired)

Suspect if:

Young (<50 years of age)

Connective tissue disease, e.g., SLE

Additional history of unexplained venous thrombosis

Previous failed vascular reconstruction

Strong family history of thrombosis

SLE, systemic lupus erythematosus.

oxygenase enzyme. Platelet aggregation is there-
fore decreased.

Primary Prevention of Peripheral
Arterial Disease

As yet there is no published evidence to suggest
that aspirin prevents the primary development
of PAD in a normal population. Such a study
would require a huge population base. One
method of decreasing the numbers required
to be studied would be to increase the risk of
the population enrolled in the trial. Two such

studies are currently under way. In both these
studies aspirin is being evaluated in subjects
with decreased ABIs but who are currently
asymptomatic in terms of PAD. One of the
studies is a population-based study and the
other is a study of patients with diabetes melli-
tus. This latter study, Prevention of Progression
of Arterial Disease in Diabetes (POPADAD) has
recruited 1250 patients with decreased ABI, and
aspirin versus placebo is one of the arms of this
study, which has a composite end point of vas-
cular events and mortality. This is a Scotland-
wide study and results should be available soon.

VASCULAR SURGERY

Primary Prevention of Vascular Surgery

Aspirin has been evaluated in the primary pre-
vention of requirement for peripheral vascular
surgery in the U.S. Physicians' Health Study. In
the aspirin group the risk of undergoing surgery
for PAD was decreased by 46% (p = .03). Aspirin
did not, however, affect the likelihood of devel-
oping claudication de novo during the trial
period.

Aspirin in the Prevention of Coronary and
Cerebrovascular Events in Peripheral
Arterial Disease

The Antiplatelet Trialists Collaboration, now
called the Antithrombotic Trialists Collabora-
tion, has provided the most convincing data
supporting the use of aspirin in PAD. In a meta-
analysis of 174 randomized trials of various
antiplatelet agents (mainly aspirin), a decrease
in nonfatal MI, nonfatal stroke, and vascular
death in patients treated by antiplatelet therapy
was detected. Subgroup analysis of high-risk
patients was carried out. This included patients
with PAD, and the percentage of risk reduction
versus placebo were as follows: 46% for non-
fatal stroke, 32% for the risk of vascular disease,
MI, or stroke, and for nonfatal MI, and 20% for
death from vascular causes. The most frequently
used dosages of aspirin were between 75 and
325 mg per day. Subsequent work has confirmed
that there is no evidence that the higher doses
are more effective than the lower ones (i.e.,
>75mg per day), although bleeding risk is dose
dependent.

Clopidogrel

Clopidogrel irreversibly blocks the binding of
adenosine diphosphate (ADP) and thus its
activation of platelets. The Clopidogrel versus
Aspirin in Patients at Risk of Ischemic Events
(CAPRIE) study evaluated the risk of vascular
death, MI, and stroke in patients with vascular
disease receiving either clopidogrel or aspirin.
Clopidogrel reduced the event rate by 5.32% per
annum versus 5.83% with aspirin (p = .043).
These figures reflect a relative rate reduction of
8.7% in favor of clopidogrel. No major differ-
ences in safety issues between the two drugs
was detected. An ad hoc subgroup analysis in

patients with PAD suggested greater benefit to
these patients from clopidogrel than in other
patient populations. An event rate of 3.1 per
annum compared to 4.86 per annum in the
aspirin group gave a relative risk reduction of
23.8% [95% confidence interval (CI) 8.9-36.2] in
favor of clopidogrel (p = .0028). A reasonable
strategy, therefore, in the 30% of all patients who
developed gastrointestinal (GI) side effects from
aspirin is to combine the aspirin initially with
the gastric protectant, and if this fails, change to
clopidogrel. This drug provides an improve-
ment to our therapeutic resources in terms of
tolerated antiplatelet drugs.

Dipyridamole

Dipyridamole is an antiplatelet agent that is
thought to work through a number of mecha-
nisms including increasing the effect of prosta-
cyclin (PGI 2 ), and inhibiting the cellular uptake
of adenosine and platelet phosphodiesterase,
thus enhancing further the effects of PGI 2 . The
use of dipyridamole itself or in combination
with aspirin has produced much controversy.
Three decades ago there was excitement about
the potential benefits of combining aspirin and
dipyridamole, but by the 1980s aspirin alone
became the favorite choice. Evidence that the
combination treatment is effective has been
forthcoming in one of the large stroke studies
(Diener et al., 1996), and certainly the combina-
tion has been found to be more effective in the
prevention of peripheral graft failure in one
study. It is our current practice to use both
aspirin and dipyridamole in patients with
stroke or transient ischemic attack (TIA) but to
use aspirin or clopidogrel alone in patients with
PAD. In stable PAD we usually reserve dipyri-
damole for the aspirin-intolerant patient, al-
though clopidogrel is now our first choice for
this indication.

Conclusion

There is convincing evidence that antiplatelet
agents such as aspirin and clopidogrel are effec-
tive in preventing cardiac and stroke events in
patients with PAD. It is therefore recommended
that an antiplatelet drug should be prescribed
for these patients unless there is a clear con-
traindication to such therapy.

MEDICAL MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE

Smoking

Both the risk of PAD and its progression is
significantly increased by the smoking of
tobacco. Patients who smoke have a significantly
increased risk of atherosclerosis and of another
tobacco-related peripheral vascular disease,
thromboangiitis obliterans (Buerger's disease).
Of all the risk factors discussed here, the use of
tobacco contributes most to the development of
PAD. A number of studies have linked tobacco
smoking and the development of IC. In the
Framingham study smokers were twice as likely
to develop IC. The progression to critical limb
ischemia is more likely in smokers, as is ampu-
tation. The effect of cigarette smoking on vas-
cular graft patency is well recognized. In one
study the 5-year cumulative patency rate for
grafts was between 80% and 90% for nonsmok-
ers, with the corresponding patency rates being
between 30% and 45% for those who smoked
more than five cigarettes a day.

Smoking cessation slows the progression
of peripheral arterial disease to critical limb
ischemia and lowers the risk of MI and death.
The nicotine present in tobacco products is
highly addictive; hence, smoking cessation is
a very difficult process for patients, and the
recidivism rate is high. The key feature in the
approach to smoking cessation is for the physi-
cian to positively encourage the patient to stop
smoking. Without a clear message from the
physician that smoking is an underlying cause
of atherosclerosis and promotes the progression
of atherosclerosis, patients will continue to
smoke. Thus, the first step is to clearly tell
patients that it is medically indicated that they
stop smoking.

Although the majority of smokers would like
to quit, 90% are physically addicted to nicotine
and at least 75% have tried to stop smoking
more than once. Three quarters of those who
do stop restart within 3 months, and it is clear
that the issue of nicotine dependence must be
addressed. During the early stages of quitting,
smokers experience both behavioral and physi-
cal withdrawal symptoms. It is crucial to explain
to the patient that the chemical withdrawal
symptoms are short lived as they can exert
strong pressure on the smoker's will to stop.
This also underlines the fact that we must
provide support to these patients. After re-
ceiving only medical advice, only 5% of

PAD patients stop smoking. Improved cessation
rates, however, can be achieved through increas-
ing support through counseling or the provision
of judicious nicotine replacement therapy.
There are numerous smoking cessation pro-
grams and pharmacological aids available for
patients. Smoking cessation aids such as nico-
tine patches and nicotine gum work best in the
setting of a specific smoking cessation program.
Nicotine chewing gum was the first type of nico-
tine replacement therapy (NRT) to become
widely available, with subsequent development
of transdermal patches, intranasal sprays, and
inhalers. These latter forms of therapy may
attenuate some problems with the gum such as
transfer of dependency. A meta-analysis of 53
trials of NRT (42 gum, nine patch, one spray, and
one inhaler) (Silagy et al., 1994) showed that
NRT increased the odds ratio for abstinence:
1.61 for gum, 2.07 for patch, 2.92 for nasal spray,
and 3.05 for inhaled nicotine. Nicotine replace-
ment therapy can be an effective aid to smok-
ing cessation. However, it is contraindicated in
acute MI, unstable angina, and in patients with
cardiac arrhythmias. Thus, it is important to
work with patients to engage them in a specific
program.

Finally, because the recidivism rate is high, it
is important to be encouraging at follow-up
visits once a patient has stopped smoking.
Physician encouragement throughout the
process of smoking cessation and remaining
tobacco free is essential.

Conclusion

Smoking causes PAD. Its cessation is difficult
without support. Nicotine replacement and
other aids to cessation should be made available
to PAD patients.

Obesity

Obesity has reached epidemic proportions in
developed countries. Obesity contributes to
numerous medical problems including athero-
sclerosis. It is important to recognize if patients
are overweight and to obtain the appropri-
ate dietary consultation to assist patients with
weight loss. Most weight-loss programs are
not successful unless they include lifestyle
modification and a specific exercise program.

VASCULAR SURGERY

Conclusion

Obesity contributes to the development of type
2 diabetes, hypertension, and dyslipidemia, all
known to be associated with PAD. Appropriate
weight-reduction programs should be recom-
mended. It should be noted that smoking cessa-
tion promotes weight gain, and that in a patient
with PAD smoking cessation is the most impor-
tant element in risk reduction. A level of weight
gain therefore should be tolerated, at least in the
short term.

Diabetes Mellitus

Peripheral arterial disease and diabetes mellitus
frequently occur together. Probably half of all
patients with diabetes mellitus have evidence of
PAD 10 to 15 years after diabetes onset. Fur-
thermore, glucose intolerance correlates with
angiographic disease extent. Diabetic patients
account for one third of below-knee amputa-
tions and 50% of amputations when distal
amputations are included. The pathology of the
diabetic limb is multifactorial, including contri-
butions from both micro- and macrovascular
disease. Asymptomatic PAD occurs in 20% of all
diabetic patients with no other evidence of
vascular disease (POPADAD screening of 8000
patients). Thus the occurrence of overt diabetes
and PAD is well documented. We are less expert
at detecting early diabetes in our patients with
PAD, however. Distal disease on angiography or
increased ABI (due to vessel stiffening) can lead
to the retrospective diagnosis of diabetes melli-
tus, but this still underestimates the figure. Of
100 consecutive patients presenting at our vas-
cular surgery clinic, 40% had abnormal glucose
tolerance tests. The majority of these patients
had normal random or fasting sugars and were
diagnosed only on the basis of this glucose tol-
erance test. Currently we do not give a glucose
tolerance test to all PAD patients but do use this
form of diagnosis for patients who have raised
ABI in the presence of symptomatic IC, in those
in whom the distal distribution of the PAD
would arouse a suspicion of diabetes, and in
those with a "diabetic" lipid profile where both
cholesterol and fasting triglyceride levels are
elevated and high-density lipoprotein (HDL)
levels are low. Detection of asymptomatic dia-
betes mellitus in the PAD patient is a major part
of the medical management of these patients. It

is consistently underdiagnosed in PAD and this
can have serious consequences.

Diabetes contributes to atherosclerosis, and
studies have indicated that tight glucose control
limits the progression of end-organ damage due
to diabetes, including atherosclerosis. Physi-
cians involved in the care of diabetic patients
with atherosclerosis must work closely, as a
team, with other caregivers involved in the man-
agement of diabetes to ensure tight glucose
control.

Conclusion

It should be remembered that all risk factors
are synergistic in terms of vascular disease, not
merely additive, and the failure to diagnose
underlying diabetes in a PAD patient who
smokes will have serious consequences for that
patient.

Dyslipidemia

Abnormal lipid profiles are well recognized in
patients with atherosclerosis. The relationship
between cholesterol level and CAD risk is con-
tinuous, with no obvious "safe" cut-off point.
Patients with PAD are likely to be identical. A
number of studies investigated cholesterol in
PAD and found it to be a significant, though
weak, risk factor for claudication, and above the
age of 55 years to correlate with ABI. Reduced
HDL is associated with increased PAD severity, 6
with strong inverse relationships between HDL
cholesterol and PAD that persist after adjust-
ment for other risk factors. Furthermore, ele-
vated serum triglyceride levels have been
reported in both cross section and longitudinal
studies. It has been suggested that the link
between increased triglyceride level in patients
with PAD and the development of the disease
might be explained by the increase in low-
density lipoprotein (LDL) providing the
enhanced vascular risk.

Despite the links between abnormal lipid
profiles and PAD, there have been no clinical
studies with the PAD patient as primary end
point. The situation has now been overtaken by
the Heart Protection Study (2002) and various
guidelines with recommendations for lipid-
lowering therapy if there is a >3% chance of a
vascular event per annum. Such a risk clearly
occurs in patients with PAD.

MEDICAL MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE

All of the major trials in the field of lipid
lowering that have been reported over the
past decade have showed variously a decrease
in CAD mortality, major coronary events,
and the need for coronary revascularization.
Together the data suggest that four out of nine
deaths occurring in a group of subjects with
cholesterol >5.5mmol/L will be prevented by
treatment.

More recently, the Heart Protection Study
(HPS) demonstrated for the first time a benefit
from statin therapy for prevention of vascular
events in patients with PAD (HPS Collaborative
Group, 2002). This largest-ever trial of choles-
terol-lowering therapy enrolled more than
20,000 high-risk patients, of whom 2700 had
symptomatic PAD but no prior CAD. Treatment
with simvastatin 40mg/day reduced major vas-
cular events (coronary events, stroke, and revas-
cularization) by 20% in patients with PAD, a
similar reduction to that observed in the study
overall. Moreover, the benefits observed in the
HPS were not influenced by baseline levels of
blood lipids. The findings of the HPS, therefore,
strongly suggest that statin therapy should be
considered on the basis of high risk rather than
high cholesterol, a category into which patients
with PAD undoubtedly fall.

Conclusion

Elevated cholesterol and triglycerides contri-
bute to the development and progression of
atherosclerosis. Thus, it is important to obtain a
lipid profile on any patient with atherosclerosis.
Management of dyslipidemia initially involves
dietary change followed by specific medical
management if necessary. The goal of lipid-
lowering therapy is to achieve a serum LDL
cholesterol concentration less than lOOmg/dL
or 3mmol/L and a serum triglyceride less than
150mg/dL.

The first choice for pharmacological therapy
is a statin.

Hypertension

Although it has been suggested that raised sys-
tolic and raised diastolic blood pressure (BP)
are linked to PAD development, results from
prospective studies are less convincing. Target
levels of blood pressure have been clearly
defined in a number of guidelines, For example

the Scottish Intercollegiate Guidelines Network
(SIGN) guideline on the management of hyper-
tension and the British Hypertension Society
guidelines have given clear guidance in terms of
acceptable BP levels. Therapy should be started
in all PAD patients with sustained systolic BP
elevations recorded above 140mmHg or dias-
tolic BP above 90mmHg. The optimum target
blood pressure is a systolic BP of <135mmHg
and a diastolic of <85mmHg. A more stringent
target is required for those patients with
diabetes and this is important, as many PAD
patients have diabetes nielli tus where a target
of <130/80mmHg is recommended. Three
long-term double-blind studies (Materson et al.,
1993) have compared all the major classes of
antihypertensive drug therapy and overall
showed no consistent or important differences
in terms of efficacy of BP control, side effects
from the drugs, or quality of life. It has been
suggested that hypertensive patients whose BP
is controlled by thiazides or beta-blockers may
continue to experience the excess risk of coro-
nary death. These two drug classes change
glucose intolerance and lipid profiles in a dose-
dependent fashion, and it may be that the lower
doses of thiazides currently employed do not
show this effect. Although (3-adrenergic antago-
nist drugs have been previously reported to
enhance PAD symptoms through their vasocon-
strictor effects, more recently it has been sug-
gested that this is not so. It is of interest that the
new vasodilating beta-blockers do not even
have this theoretical contraindication and might
be used safely in patients with PAD. The use
of angiotensin-converting enzyme inhibitors
in patients with PAD may confer protection
against future atherosclerotic events. However
care must be taken in the presence of renal
artery stenosis, another common finding in
patients with PAD.

Care must be taken when treating hyperten-
sion in the patient with CLI, as limb perfusion
might only be maintained through the elevated
BP. Too profound or rapid a decrease in BP may
worsen the symptoms, and care must be taken
with CLI in the same way as with patients with
severe carotid disease.

Conclusion

Hypertension has been implicated in the
etiology of PAD and contributes to its vascular

VASCULAR SURGERY

comorbidity. Blood pressure should be con-
trolled to levels consistent with local guidelines.
Polypharmacy is likely to be required. Caution
is advised when high BP is diagnosed in a
patient with CLI, as too rapid a decrease in pres-
sure may worsen the limb ischemia.

Sedentary Lifestyle/
Exercise Therapy

Intermittent claudication is a symptom of lower
limb peripheral arterial disease. It arises when
the blood flow is insufficient to meet the meta-
bolic demands of the leg muscles in ambulating
patients. Intermittent claudication is a "lever-
aged" disability, as pain increases with walking,
patients walk shorter distances, muscle strength
erodes, and walking distances continue to
decrease. This leads to other negative conse-
quences such as weight gain, hypertension, and
diabetes. Overall, patients with claudication
have a 60% lower functional capacity than
age-matched individuals without the disease
(Eldridge and Hossack, 1987).

Intermittent claudication is a symptom of
systemic atherosclerosis. At least 60% of pa-
tients with claudication have significant disease
of the cerebral or cardiac circulation. Mortality
rates for patients with claudication are very
high, with 30% to 50% of patients dying from
cardiovascular causes within 5 years of the
initial diagnosis. A meta-analysis of 21 studies
on the effects of exercise on patients with clau-
dication suggested that the average improve-
ment in walking distance was 122% (Gardner
and Poehlman, 1995) and the benefits have
been shown to be as high as 180% (Fig. 6.2).
The programs with the greatest benefit were
those in which patients exercised for 30 minutes
at least three times a week for 6 months. How-
ever, supervised exercise programs are not
currently covered by most medical insurance
policies.

There are numerous salutary effects of
exercise that contribute to the reduction of
cardiovascular events. Exercise is associated
with beneficial changes in body fat percentage,
lipoprotein profile, carbohydrate tolerance and
insulin sensitivity, neurohormonal release, and
blood pressure. There is substantial evidence
that regular aerobic exercise can even alter

t/3

1 — 1

w
u

PL,

1 — 1

W200

i h 150

|l 10 °

is son

u <
**

Figure 6.2. Walking distance.The improvement in walking dis-
tance is much greater for a graded exercise program compared
to the best medical management (cilostazol), percutaneous
transluminal angioplasty (PTA),or placebo.

vessel structure. The progression of coronary
lesions can be inhibited in those patients who
modify risk factors and engage in regular exer-
cise. Numerous studies have demonstrated a
significant correlation between exercise and
an increase in vessel diameter. Exercise may
also induce changes in the lumen diameter in
patients after coronary angioplasty. Patients
randomized to a 12-week intervention program
consisting of daily exercise after balloon
angioplasty of the coronary vasculature had
a significantly lower rate of re-stenosis than
patients in the control group. However, the
major benefit of exercise is likely due to the
training response.

Thrombophilia

Patients under the age of 50 with manifestations
of vascular disease have an increased risk of a
defined hypercoagulable disorder. Thus, some
believe that these patients should be screened
for hypercoagulable disorders. In contrast, most
hematology societies indicate that screening for
thrombophilia in arterial disease does not yet
have an evidence base.

There are two general categories used to
describe the hypercoagulable or prothrombotic
state: hereditary and acquired. The former is
often referred to as inherited thrombophilia
disease. Acquired thrombophilia is a term re-
served for well-defined syndromes such as the
antiphospholipid syndrome (APS). This was

MEDICAL MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE

previously termed the lupus anticoagulant.
However, the name was changed for two very
good reasons. First, the anticoagulant referred
to in this latter term reflects the behavior of
the blood in the test tube, and in fact a pro-
thrombotic effect is observed in vivo. Second,
although it can be associated with the connec-
tive tissue disease systemic lupus erythemato-
sus, this is by no means necessary and we
are increasingly recognizing APS occurring in
isolation.

Although the inherited thrombophilic disor-
ders are historically linked to venous thrombo-
sis, there is some evidence suggesting that they
may contribute to arterial thrombosis and in
particular in patients with PAD. It has been
recorded that inherited thrombophilias link to
failure of vascular grafting following surgery. In
a prospective study hypercoagulability occurs
in between 10% and 25% of patients, increasing
to about 50% in the presence of clinical markers
for thrombophilia. Preoperative identification
of such patients is important, as the short-
and medium-term failure rates of the graft are
reported to be approximately 50% in such
patients. Furthermore, such patients are at
increased risk of deep vein thrombosis during
the operative procedure (see Chapter 5 for the
evaluation of these patients).

to 40% of patients presenting with premature
PAD have been found to have heterozygous
homocystinemia. Pyridoxine supplementation
reduces the thrombotic events in homozygous
patients. However, it is not known whether this
or other vitamins such as folate affect the course
of the premature atherosclerosis in the het-
erozygous sufferers.

Vascular Risk Factor
Management in Patients with
Peripheral Arterial Disease

The presentation of a patient with PAD to a
provider of medical care presents an ideal
opportunity for the critical assessment of vas-
cular risk factors. Intervention at this time both
decreases the risk of coronary and cerebral
events and is likely to limit progression of the
arterial disease in the periphery, although the
latter is theoretical rather than evidence-based
as yet. Thus the modification of vascular risk is
of crucial importance in the patient with PAD
and is likely to become an even more important
area in the future for clinicians involved with
the care of these patients.

Conclusion

As the inherited hypercoagulable states such as
protein C, protein S, antithrombin II deficien-
cies, and factor V Leiden occur only infrequently
in this patient group, it is not possible to make
a formal recommendation for screening of PAD
patients. Probably a selective approach is war-
ranted, reserving screening to those patients
with bypass failure, a history of thrombotic
events, or atherosclerosis at an early age.

Homocystinemia

The clinical features of homocystinemia include
the development of premature atherosclerosis,
along with manifestations of arterial and
venous thrombosis. Disease severity leads to
early diagnosis in homozygous patients, but
patients with heterozygous disease present
merely with premature atherosclerosis; 20%

Drug Treatment of
Intermittent Claudication

It is a poor reflection on us, as clinicians
involved in the care of the PAD patient, that
angina of the legs is addressed far less aggres-
sively than symptoms of claudication in the
heart! Part of the problem reflects the concern
about the effectiveness of the drug treatment for
the symptoms of intermittent claudication and
the consequent unease over the use of financial
resources to purchase these compounds. Guide-
lines have been developed for prescribing. There
are four oral drug therapies that have a license
for use as a treatment for IC in the United
Kingdom and two in the United States:
Naftidrofuryl (Praxilene, not available in the
U.S.), oxpentifylline (Trental), cilostazol
(Pletal), and inositol nicotinate (Hexopal).
These drugs have been evaluated in clinical

VASCULAR SURGERY

trials in terms of their effectiveness for alleviat-
ing the symptoms of leg pain associated with
walking (IC).

Naftidrofuryl

Naftidrofuryl is thought to mediate its benefits
through vasoactivity (vasodilatation) and via a
local anesthetic action. Studies have docu-
mented increased tissue oxygenation, increased
ADP levels, and reduced lactic acid. The recom-
mended maximum dose is 200 mg three times a
day.

A number of double-blind, placebo-
controlled studies in this area tend to show a
significant placebo response in walking dis-
tance approximately 25% improvement in
walking distance with placebo. With Naftidro-
furyl a further 30% improvement can be
expected. These estimates are supported by two
meta-analyses.

Pentoxifylline/Oxpentifylline

This is a rheological agent that has been
approved for the treatment of intermittent
claudication. Only two of the double-blind,
placebo-controlled studies of oxpentifylline that
measured walking distance using treadmills
showed any statistical improvement in such
walking distance by patients on oxpentify-
line. Furthermore, one of these was a retrospec-
tive subanalysis of short-distance claudicants,
patients who could only walk short distances
before claudication ocurred already included in
another study. A meta-analysis of ten random-
ized, double-blind, controlled studies concluded
that the limited amount and quality of data for
this drug precluded an overall reliable estimate
of its efficacy. We recommend, in the absence of
any consistent clinical trial evidence, that oxpen-
tifylline should not be prescribed for use in this
indication.

Cilostazol

Cilostazol has recently been approved for the
treatment of intermittent claudication. It is a
phosphodiesterase inhibitor that has been
shown in randomized placebo-controlled trials
to improve walking distance by approximately

50%. However, the improvement remains
modest compared to exercise programs (180%
to 200% improvement). Cilostazol is contraindi-
cated in patients with a history of congestive
heart failure.

Inositol Nicotinate (Hexopal)

Inositol nicotinate is licensed for use in the
United Kingdom for patients with intermittent
claudication. However, the evidence base for this
compound is weak. Of the four double-blind,
randomized, placebo-controlled trials, three
were primary care based and used subjective
or questionable objective criteria for assessment
of IC without treadmill use. None showed clear
evidence of improvement in symptoms with
drug use. We suggest, therefore, that the drug
may not be of value for patients with IC.

Conclusion

Some patients with IC merit drug treatment
due to the severity of their symptoms. It is rea-
sonable to consider Naftidrofuryl or cilostazol
for the symptomatic relief of moderate disease.
The patients, however, should be reviewed 6 to
12 months after drug commencement to assess
its efficacy and the need for continuation.
Neither oxpentifylline nor inositol nicotinate
can be recommended for the treatment of
symptomatic IC.

Summary

Peripheral arterial disease is a marker of sys-
temic atherosclerosis. Patients with PAD are at
high risk for MI and stroke. Thus, an integrative
approach to risk factor modification and the
prevention of the sequelae of atherosclerosis
is the mainstay of therapy. Patients must be
advised to "stop smoking and keep walking." In
addition, however, antiplatelet therapy (e.g.,
aspirin) is indicated in all patients with periph-
eral arterial disease in whom there is no
contraindication. Hypertension must be appro-
priately treated and diabetes mellitus detected
and managed optimally. The medical manage-
ment of the symptoms of intermittent claudica-
tion should also be addressed if these are
significantly impairing the patient's lifestyle.

MEDICAL MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE

The key feature, however, in managing these
patients is to assess their overall vascular risk
and treat accordingly.

References

Belch JJ, Sohngen M, Robb R, Voleske R Sohngen W. (1999)
Int Angiol 18:140-4.

Diener HC, Cunha L, Forbes C, Sivenius J, Smets P,
Lowenthal A. (1996) J Neurol Sci 143:1-13.

Eldridge JE, Hossack KF. (1987) Cardiology 74:236-40.

Gardner AW, Poehlman ET. (1995) JAMA 274:975-80.

Materson BJ, Reda DJ, Cushman WC, et al. (1993) N Engl J
Med 328:914-21.

Silagy C, Mant D, Fowler G, Lodge M. (1994) Lancet 343:
139-42.

Anesthesia for Vascular Surgery

Jamal J. Hoballah and Farid Moulla

Surgery of the peripheral vascular system
requires technical precision and perioperative
vigilance. The outcome of vascular procedures
depends on various factors. These factors
include patient selection, the procedure per-
formed, the surgeon's skills, and the periopera-
tive care. The importance of the perioperative
care cannot be underestimated. Patients pre-
senting with a vascular pathology often have
comorbidities. The incidence of coronary artery
disease (CAD) in patients with carotid disease
is estimated at 50%.

Patients with operative lower extremity
peripheral vascular disease (PVD) have an
even higher incidence of CAD. Hypertension,
diabetes, and renal insufficiency are all more
frequent in patients with PVD compared to
the general population. Following aortic
surgery, carotid endarterectomy, and lower
extremity revascularization procedures, the
most common major complication is a cardiac
event. Anesthesia is a risk factor contributing
to the perioperative morbidity and mortality
of the vascular patient. The preoperative
preparation and the intraoperative manage-
ment can predict and influence the postopera-
tive course. This chapter provides an overview
of the various anesthetic techniques that can
be used in patients presenting for vascular
procedures.

Anesthesia Risks

Depending on the complexity of the vascular
pathology, a vascular procedure can be per-
formed under local, regional, or general anes-
thesia, or a combination of these techniques.
Minimally invasive approaches to vascular
reconstructions are continuing to be developed,
allowing for more localized anesthesia. Often it
is assumed that performing a procedure under
local or regional anesthesia results in lower
mortality and morbidity and allows earlier
recovery. Certain trends are apparent in the
literature, although not without controversy,
comparing these anesthetic techniques and can
be outlined as follows:

• While laboratory and monitoring tech-
niques are improving, historically many
perioperative cardiac events are "silent"
(Steen et al., 1978; Von Knorring and
Lepantalo et al., 1986).

• There does not appear to be a discernible
difference between regional and general
anesthesia with regard to cardiac risk or
mortality within the field of vascular sur-
gery. There is a large amount of recent con-
troversy, practice variability, and research
related to this point (Bode et al., 1996;

VASCULAR SURGERY

Christopherson et al, 1993; Rigg et al.,2002;
Rivers et al, 1991; Rodgers et al.,2000).

• Regional and general anesthesia offer dif-
ferent advantages and disadvantages, but
both are safe and appropriate for carotid
endarterectomy (Rockman et al., 1996).

• Combinations of anesthetic techniques
may offer advantages over single-mode
therapy.

• There is a trend toward less need for
(immediate postoperative) reoperation for
thrombosis when regional anesthesia is
employed in lower extremity revascular-
izations (Christopherson et al., 1993).

• Minimally invasive techniques warrant
equally minimally insulting anesthetic
techniques, contributing to improved out-
comes over standard surgical intervention.

Because of the relative equity of major anes-
thetic risk between regional and general anes-
thesia, the site and probable duration of the
procedure itself are often the main determi-
nants of anesthetic technique. Lower extremity
revascularizations typically last from 2 to 6
hours with significant variability. A single
administration of spinal anesthesia offers no
ability to redose if the initial infiltration wears
off. Epidural anesthesia can be continuously
infused both for long procedures and for post-
operative pain management. However, it does
little to treat the musculoskeletal complaints of
an awake patient prostrate for several hours.
Conversely, general anesthesia does not allow
for patient interaction and requires prophylac-
tic measures to avoid the complications of
pressure and immobility. It also has the dis-
advantage of requiring mechanical ventilation
with its potential respiratory complications and
possible hemodynamic stresses with induction
or extubation. In most cases, regional and
general anesthesias are both acceptable alterna-
tives for the common vascular surgeries. Some
issues to remember when deciding on anes-
thetic techniques are as follows:

• Open abdominal vascular surgery such as
for an abdominal aortic aneurysm (AAA)
is theoretically possible with a celiac axis
block or regional anesthesia, but in prac-
tice, warrants general anesthesia.

• Epidural anesthesia for supplementation
of general anesthesia, as well as for post-
operative pain management in major

abdominal surgery, is becoming the stan-
dard of care as it gains a wealth of sup-
porting literature.

• The need for postoperative full anticoagu-
lation with (or the use of even prophylactic
subcutaneous doses of) low-molecular-
weight heparin usually precludes epidural
catheter use for fear of developing an
epidural hematoma upon the removal of
the catheter.

• Both prophylactic and therapeutic un-
fractionated heparin therapy have to be
interrupted to allow for normalization of
coagulation prior to removing the epidural
catheter to avoid a potentially devastating
complication.

• Upper extremity vascular procedures can
be approached with general, regional,
local, or epidural anesthesia. Axillofemoral
bypass is a relative contraindication to
regional anesthesia as is harvesting of arm
veins, although on occasions the vein may
be harvested using infiltration of local
anesthetics.

• The most common vascular surgery,
carotid endarterectomy, has been studied
extensively, with ongoing debate regarding
the effectiveness of intraoperative moni-
toring techniques and regional versus
general anesthesia.

The following sections review the various
anesthetic techniques available for commonly
performed vascular procedures.

Anesthesia for Endovascular
Interventions

Endovascular procedures vary in complexity
and include diagnostic angiograms, balloon
angioplasty and stenting, endovascular aortic
aneurysm treatment with endografts, and vari-
cose vein treatment by radiofrequency or laser
ablation. There is a paucity of studies on the
anesthetic requirements of vascular patients
treated by endovascular techniques. In general,
percutaneous angiography, balloon angioplasty,
and stenting are typically performed under
local anesthesia. Infiltration of the skin with 1%
lidocaine or bupivacaine can provide ample
control of pain at the puncture site. It is prefer-
able to premedicate the patient prior to the pro-

ANESTHESIA FOR VASCULAR SURGERY

cedure and to augment sedation at the onset
of the intervention. Premedication with 25 to
50 mg of diphenhydramine and 5mg of
diazepam given orally 1 hour prior to the pro-
cedure relieves many patients of the anxiety and
anticipation of the intervention. Once the
patient is on the catheterization table, sedation
with 1 to 2 mg of lorazepam in addition to 50 [ig
of fentanyl provides further sedation and excel-
lent pain control. The skin at the puncture site
is infiltrated with the chosen local anesthetic
and the potential track of the puncture needle
is also infiltrated. If during the arterial puncture
the patient complains of pain, additional local
anesthetic can be infiltrated in the area directly
through the Seldinger needle prior to arterial
puncture.

Endovascular Aortic
Aneurysm Repair

With respect to aortic aneurysm endovascular
treatment, most of the procedures were origi-
nally done under general anesthesia. As the
comfort level of the surgeons with the proce-
dure increased, epidural and local anesthesia
started to be used and were noted to be a rea-
sonable alternative to general anesthesia. The
idea of being able to treat an abdominal aortic
aneurysm under local anesthesia is very excit-
ing and appealing. The question of need for
general anesthesia to treat AAA with endovas-
cular technology has been examined (Henretta
et al., 1999). In 47 patients treated with local
anesthesia and intravenous sedation without
intubation, only one required conversion
to general anesthesia. The conversion was
needed to repair an injury to the external iliac
artery. In the remaining 46, there were lower
rates of cardiac complications (zero) and
shorter hospital stay when compared to those
reported with the open technique. Although
this study did not compare the results of
endovascular AAA treatment under general
anesthesia versus local or epidural anesthesia, it
clearly proved the feasibility and efficacy of
local anesthesia with sedation as an anesthetic
technique for endovascular AAA treatment. At
the University of Iowa, epidural anesthesia is
our preferred technique for endovascular AAA
treatment. However, patients' wishes and prefer-
ences often play a decisive role in the selection
of the anesthetic technique used. The require-

ments for anesthesia are likely to change as
rapidly as the endovascular techniques and
devices employed.

Lower Extremity Vein Therapy

Radiofrequency or laser ablation of the greater
saphenous vein (GSV) is gaining popularity as
an alternative, less invasive method for GSV
stripping in the treatment of varicose veins.
This transforms varicose vein treatment into an
office practice and limits the anesthesia needs to
infiltration of local anesthetics. The skin is typ-
ically infiltrated at the site of insertion of the
sheath through which the laser or radioablation
catheter is introduced. Because of the heat
generated with the venous ablation, additional
anesthesia is needed along the course of the
GSV. Tumescent anesthesia is used for this
purpose. Tumescent anesthesia is prepared by
the following concentration:

500 cc of normal saline in IV bag
16 cc of 8.4% sodium bicarbonate solution
50 cc of 1% lidocaine with epinephrine
1:100,000

It is infiltrated along the course of the GSV using
a long spinal needle. In addition to providing
anesthesia to the infiltrated area, tumescent
anesthesia provides a protective layer between
the vein and the dermis to avoid thermal skin
injury during the laser or radiofrequency abla-
tion. This tumescent anesthesia is also used
during stab avulsion of branch varicosities. In
addition to providing pain control, it is useful in
minimizing subcutaneous bleeding from the
ends of the avulsed veins.

Anesthesia for Open
Aortic Surgery

Physiological and Mechanical
Considerations

Open aortic procedures are typically performed
under general anesthesia. The anesthesia issues
in open aortic surgery depend on the level of
aortic clamping and the extent of the surgical
incision. These issues include the need for
cardiopulmonary arrest, spinal cord protection,
renal protection, and management of the hemo-
dynamic changes associated with clamping and

VASCULAR SURGERY

unclamping of the aorta. Other issues include
the need for single-lung ventilation, intraopera-
tive hemodynamic monitoring, and the use of
combined epidural and general anesthesia.
Although aortic valve, ascending aortic, and
arch vessel surgery often require cardiopul-
monary bypass, debate still exists regarding
descending thoracic and suprarenal aortic
surgery. For descending thoracic and suprarenal
aortic surgery, the approaches include the clamp
and sew technique versus the use of an adjunc-
tive atriofemoral bypass, aortofemoral bypass,
or temporary axillofemoral bypass.

In patients requiring a thoracoabdominal
incision, the placement of a double-lumen or
balloon excluder endotracheal tube is essential
to deflate the left lung when needed and main-
tain the patient on single-lung ventilation. Such
a maneuver facilitates better exposure to the
thoracic aorta. With respect to spinal cord pro-
tection, maintaining distal and pelvic perfu-
sion, reimplantation of intercostals vessels,
and control of spinal fluid pressure have been
described as essential to minimizing spinal cord
ischemia during thoracoabdominal aortic
surgery. Although debatable, a spinal catheter is
usually inserted prior to induction of general
anesthesia, and the spinal pressure is monitored
intraoperative ly and for 2 to 3 days after the pro-
cedure. Spinal fluid is drained to keep the spinal
pressure below 10 mm Hg or 14 cm H 2 0. Rever-
sal of spinal cord ischemia has been observed in
situations where neurological symptoms have
developed in the postoperative period in associ-
ation with elevated spinal fluid pressure. Debate
still exists with respect to hemodynamic goals
and monitoring, visceral organ protection, and
control of cardiac responses to clamp stresses.

Aortic cross-clamping leads to an increase in
cardiac afterload. This acute increase in after-
load is both measurable and manipulable,
directly and indirectly. Uncontrolled hyperten-
sion, although tolerated by the healthy heart,
can lead to systolic or diastolic dysfunction and
cardiac decompensation. Blood pressure is
often viewed as dependent on circulating blood
volume, cardiac preload and afterload, and
cardiac function. All of these factors are
influenced by, and essentially precluded by, the
ability of the heart to withstand the stress of any
acute physiologic change. The effects of aortic
cross-clamping are initially mechanical due to
abrupt change of afterload. The rough percent-

age of cardiac output blocked by clamping at
various levels is as follows: infrarenal, 10% to
15%; suprarenal, 15% to 25%; and supraceliac,
55%. The precise percentage varies with certain
disease states, such as aortic occlusive disease
and collateralization. Typically, the surgeon
works in concert with the anesthesiologist to
decrease the afterload (lower the blood pres-
sure) prior to applying a clamp on the aorta.
In thoracoabdominal procedures where an
aortofemoral or axillofemoral bypass is being
used, the increase in afterload with cross-
clamping is less pronounced. The use of the car-
diopulmonary pump in these procedures
facilitates easier manipulation and removal of
circulating blood volume to treat hypertension.
The importance of continuous communication
between the surgeon and the anesthesia team
cannot be overemphasized. Cross-clamping or
unclamping of the aorta should not be per-
formed before the anesthesia team has made all
the necessary interventions needed to address
the hemodynamic changes expected with the
aortic clamp application or removal.

Pharmacological Considerations

Although mechanical intervention related to
circulating blood volumes are undertaken rou-
tinely, so too is pharmacological control of the
vascular system. Nitroprusside and nitrogly-
cerine titrations are often employed to decrease
afterload and preload, respectively. The advan-
tages of nitroprusside include its effectiveness
in peripheral arteriolodilatation and treatabil-
ity Furthermore, the vasodilatation of the vas-
cular beds causes decreased oxygen extraction
ratio and decreased cardiac work. Nitroprusside
effects cardiac preload to a lesser extent, but it
can possibly decrease the perfusion pressure
to infra-clamp tissues provided by collateral
arterial supply due to arteriolar dilatation. A
common side effect is pulmonary vasoconstric-
tion, arteriovenous shunting, and resultant
desaturation of blood. Furthermore, prolonged
use of nitroprusside can result in systemic
cyanide toxicity. Nitroglycerine decreases
cardiac preload and is titratable. It vasodilates
coronary circulation and indirectly decreases
cardiac work. It does not effect infra-clamp
organ perfusion and has less systemic toxicity,
seen as methemoglobinemia; however, it is not

ANESTHESIA FOR VASCULAR SURGERY

as potent as nitroprusside. Other factors for
visceral protection include the use of mannitol
12.5 g intravenously a few minutes prior to
suprarenal cross-clamping in an attempt to
decrease renal reperfusion injury.

Anesthesia in
Carotid Surgery

General anesthesia is the traditional anesthetic
technique for carotid endarterectomy (CEA). In
1962 Spencer and Eiseman described a local
anesthetic technique for CEA. A "cervical block"
is regional anesthesia consisting of infiltration
of the paravertebral nerve roots at C2-C4 with
one or a mix of local agents. General anesthesia
and regional anesthesia are equally acceptable
approaches to anesthesia for a patient undergo-
ing a carotid endarterectomy and depend on the
experience of the operative team.

Pros and Cons of Regional
Anesthesia and General Anesthesia
for Carotid Endarterectomy

The advantage of general anesthesia goes
beyond keeping the patient motionless. The
brain's metabolic demand is usually reduced
with general anesthesia, and thus acts as a
protective mechanism against ischemia. The
disadvantages of general anesthesia in carotid
surgery include the need to routinely place a
shunt or the use of EEG or stump pressure mon-
itoring to selectively shunt. The decision to
shunt is sometimes determined preoperatively
in cases of contralateral occlusion, history of
ipsilateral stroke, or known lack of collateral
circulation (from cerebral angiogram). In these
cases, many surgeons would routinely shunt
during general anesthesia.

The advantages of regional anesthesia are
more often seen in a different patient popula-
tion than with that of general anesthesia.
Published selective shunt rates in regional
anesthesia are in the range of 15%, which is a
lower rate of shunting than techniques that
involve monitoring. Regional anesthesia has
been shown to invoke less postoperative hyper-
tension and hypotension and reduced posto-
perative intensive care unit and hospital stay.

"Cerebral protection" in CEA refers to pro-
tection of the brain from ischemia induced by
blood flow changes at the time of CEA. Cerebral
protection can be obtained from a shunt, or
monitoring for its need. The placement of a
shunt from the common carotid artery to the
internal carotid artery is the standard way
to maintain intracerebral blood flow during
CEA. The disadvantages of shunting include
potential injury to the proximal and distal ends
of the shunted vessel (intimal flaps), increased
blood loss, the rare potential for embolism
through the shunt, and the technical aspects of
performing the endarterectomy around the
shunt device. It is for these reasons that selective
shunting is advocated by some. Monitoring for
significant cerebral effects of carotid cross-
clamping has been shown to decrease the need
for shunting, and thus allows for use of a selec-
tive shunt only if brain tissue is thought to
be compromised. Electroencephalography, tran-
scranial Doppler, and ipsilateral stump pres-
sure measurement are techniques most often
employed.

Cerebral perfusion pressure (CPP) is equal to
the mean arterial pressure (MAP) minus the
intracranial pressure (ICP). Thus, an additional
approach to cerebral protection is to maintain
an elevated MAP during CEA. One approach is
to maintain the patient's blood pressure at the
same level or within 20 mm Hg higher than
the patient's baseline blood pressure. Again,
this requires a coordinated effort between the
surgeon and anesthesiologist.

Regional Anesthesia Techniques
for Carotid Endarterectomy

The dermatomal distribution of the neck inner-
vation is in cervical nerves 2 through 4. Regional
block anesthesia is targeted at these nerves in a
paravertebral location. The cervical plexus is
comprised of the anterior divisions of cervical
nerves 1 through 4. The plexus sits anterior to
the median scalene and levator scapulae, and
behind the sternocleidomastoid muscles. The
cervical plexus divides into superficial and deep
branches. It is the deep branches that innervate
the deep structures of the neck including the
muscles via an internal and an external series of
nerves. The internal series consists of the fol-
lowing nerves: communicating branches, mus-

VASCULAR SURGERY

cular branches, communicantes cervicales, and
phrenic. The external series includes the com-
municating and the muscular nerves. The
superficial branches of the cervical plexus
become the following sensory nerves: smaller
occipital, great auricular, cutaneous cervical,
and supraclaviculars. A deep cervical plexus
block is a paravertebral block targeted to C2
through C4. Due to its proximal location, an
effective block involves the superficial and deep
branches. A superficial cervical block has the
advantage of not involving any nerves that
innervate muscle including the phrenic, and
the disadvantage of not involving the deeper
sensory nerves that the deep branches of the
plexus innervate.

Deep Cervical Plexus Block: Selected
Division Blockade Technique

After placing the patient in a neutral supine
position, and appropriately prepping the skin
for aseptic technique, a 4- or 5-cm 22-gauge
needle with a short bevel is used to instill local
anesthetic. An example of local anesthetic that
could be used is a half-and-half mix of 1%
lidocaine and 0.5% bupivacaine. A total of about
3 or 4cc of local anesthetic should be used at
each level. To find the proper position for needle
placement at all levels, an imaginary line can be
drawn between the tip of the mastoid process
and Chassaignac's tubercle of C6, which is pal-
pable at the level of, and posterior to, the cricoid
cartilage. The C2 injection is performed about
1 to 1.5cm below the mastoid process on this
line, just posterior to the sternocleidomastoid.
Moving about 1.5 cm caudad from the C2 site
along the same line can place injections at C3
and C4. A horizontal line from the ramus of the
mandible posterior can be a guide to the level of
the C4 injection site as well. A slight caudal
angle of the needle can prevent the needle from
tracking to the intervertebral space, and thus
avoiding peridural or spinal anesthesia. If the
transverse process is hit with the tip of the
needle, paresthesias result. This indicates that
the needle tip is in the proper vicinity and the
injection can be performed.

The complications of this approach to deep
cervical block include intravertebral artery
injection causing convulsions, unconsciousness,
or temporary blindness. The nerve block can

also spread to prevertebral (superficial) fascia
and the cervical sympathetic chain, causing
Horner's syndrome or hoarseness secondary to
recurrent laryngeal nerve involvement.

Deep Cervical Plexus Block:
Interscalene Technique

This technique utilizes the proximity of the cer-
vical plexus branches' proximity to each other
to administer a single dose of anesthetic. Using
the same needle as the selective approach but a
larger syringe to inject 10 yo 12 cc of an equiva-
lent anesthetic, a single bolus of local is injected
in an "interscalene" location as follows: Palpate
the interscalene groove separating the anterior
and middle scalenes at a level of the cricoid again
using Chassaignac's tubercle of C6. At this loca-
tion, enter using a caudal and slightly posterior
angle. A C5-6 dermatomal paresthesia is elicited,
and 10 to 40 cc of local is injected while hold-
ing caudal pressure. A 40-cc injection without
caudal pressure also involves the brachial plexus.
Regardless of the amount or pressure used, the
ipsilateral phrenic nerve is blocked by this proce-
dure, an effect that is usually well tolerated.

The complications of this approach of deep
cervical blockage include phrenic nerve involve-
ment and the same complications as for the
selective technique; however, there is a lower
chance of inadvertently puncturing the verte-
bral artery.

Superficial Cervical Plexus Block

Using a 22-gauge, 4-cm needle, local is injected
just posterior to the midpoint of the posterior
border of the sternocleidomastoid muscle. The
injection should be angled to attempt infiltra-
tion of the posterior and medial aspects of the
muscle. As it only affects the cutaneous nerves,
the complications of this approach are minimal.

Anesthesia for Vascular
Surgery of the Lower
Extremity

Transfemoral thromboembolectomy, focal vein
bypass revisions, and even femorofemoral
bypasses can be effectively performed under

ANESTHESIA FOR VASCULAR SURGERY

local anesthesia. In most other procedures
where long skin incisions, long segments of vein
harvesting, deep exposures, and tunneling are
required, the options include regional or general
anesthesia. Regional anesthesia appears to avoid
the hypercoagulability noted with general anes-
thesia and appears to provide an early patency
advantage with infrainguinal bypass procedures
(Christopherson et al., 1993). However, in pro-
longed procedures, the patient may become
restless and uncomfortable due to prolonged
immobility.

Conditions that suggests avoiding regional
anesthesia include tremor at rest, inability to
follow commands (the level of cooperation of
the patient), peripheral neuropathy limiting the
sensation of pain of the distal lower extremities,
and a history of lower back surgery or pain. In
the presence of severe heart failure or diastolic
dysfunction, general and regional anesthesia
have been shown to be similar in overall
outcome. In these high-risk patients, local anes-
thesia with monitored anesthesia care is the best
option if the surgical procedure is appropriate
for such anesthesia.

In the presence of significant pulmonary
disease [forced expiratory volume in 1 second
(FEV]) <1.0], the risk of prolonged intubation
or pulmonary infection after endotracheal intu-
bation would indicate regional anesthesia.
However, some patients with significant pul-
monary disease are unable to maintain a supine
position for prolonged periods.

Significant coagulopathy precludes spinal
and epidural anesthesia due to the risk of
epidural hematoma and subsequent paralysis.
Furthermore, an infection either in the region of
placement of a regional anesthetic or causing
systemic sepsis usually precludes regional anes-
thesia due to the risk of seeding the paraspinal
space.

During procedures involving the foot such
as toe or forefoot amputations, an ankle
block can be an ideal regional anesthesia. The
technique for ankle block involves infiltrating
the ankle circumferentially with a local anes-
thetic just at the level of the medial malleolus.
Further infiltration of the posterior tibial nerve
is usually needed to achieve adequate anesthe-
sia. The neuropathy associated with diabetes
can lead to a nearly anesthetic foot, and pro-
cedures can be performed with minimal
anesthesia.

Anesthesia for Vascular
Surgery of the Upper
Extremity

In general, most vascular procedures in the
upper extremity can be managed by local or
regional anesthesia. In spite of the lack of evi-
dence of the benefit of regional anesthesia
versus general anesthesia in randomized studies
in terms of morbidity and mortality, there is
enough proven or anecdotal benefit in terms of
pain relief, cost-efficiency, and time to dis-
charge. These benefits of regional anesthesia are
particularly valued in outpatient surgery and
should therefore encourage its use.

Regional Anesthesia Techniques
for the Upper Extremity

The brachial plexus supplies all of the motor,
and most of the sensory, innervation to the
upper extremity. It is important to remember
that the medial aspect of the upper arm to near
the elbow is enervated by the medial cutaneous
and intercostobrachial nerves and not the
brachial plexus. Similarly, the skin on the shoul-
der is supplied by the "caudal" branches of the
cervical plexus supply. The common regional
anesthesia techniques of the upper extremity
are categorized based on location of surgical
dissection.

Axillary Artery /Vein Dissection

Axillary artery and vein exposure including
axillofemoral bypass proximal dissection can be
performed under local anesthesia, or with an
intrascalene approach to block the brachial and
cervical plexus. Applying inferior pressure on
the interscalene groove can guide the infiltra-
tion of local anesthesia superiorly along the
scalene muscles to effect a predominantly cer-
vical plexus block. Using less pressure inferiorly
can result in a predominantly brachial plexus
block.

Brachial Artery /Vein

This is the "gray zone" of brachial plexus blocks,
as the skin overlying the brachial vessels is often

VASCULAR SURGERY

at least partially innervated by the medial cuta-
neous and intercostobrachial nerves. However, if
local anesthesia is used in combination with the
brachial plexus block, adequate and safe anes-
thesia can result.

Radial, Ulnar,and Antecubital
Regional Anesthesia

The region from the elbow to the wrist is ideal
for a brachial plexus block. The techniques
include an intrascalene approach, as mentioned
above, and a subclavian approach. The intrasca-
lene approach, as mentioned in the discussion
of cervical plexus block, above, often involves
the ipsilateral phrenic nerve and possibly some
cranial nerves. The subclavian approach has less
phrenic nerve involvement (50%) and requires
smaller volumes of anesthetic, but can lead to
pneumothorax.

Distal Ulnar and Radial Artery,and
Hand Surgery

Local anesthesia is the best option in the com-
pliant patient. Axillary blockade is another
option for distal arm/hand surgery and is rela-
tively easy and safe. However, axillary blockade
effects only the forearm, requires arm abduc-
tion, and can lead to hematoma.

Conclusion

Numerous approaches to vascular anesthesia
are available. The approach must be tailored to
the patient and the procedure. It is important

that the operative team, surgeons and anes-
thetists, work in concert throughout any vascu-
lar procedure.

References

Bode Jr RH, Lewis KP, Zarich SW, et al. (1996) Cardiac
outcome after peripheral vascular surgery: comparison
of general and regional anesthesia. Anesthesiology
84:3-13.

Christopherson R, Beattie C, Frank SM, et al. (1993) Periop-
erative morbidity in patients randomized to epidural or
general anesthesia for lower extremity vascular surgery.
Anesthesiology 79:422-34.

Henretta JP, Hodgson KJ, Mattos MA, et al. (1999) Feasibil-
ity of endovascular repair of abdominal aortic
aneurysms with local anesthesia with intravenous
sedation. J Vase Surg.

Rigg JRA, Jamrozik K, Myles PS, et al. (2002) Epidural anaes-
thesia and analgesia and outcome of major surgery: a
randomized trial. Lancet 359:1276-82.

Rivers SP, Scher LA, Sheehan E, Veith FJ. (1991) Epidural
versus general anesthesia for infrainguinal arterial
reconstruction. J Vase Surg 14:765-70.

Rockman CB, Riles TS, Gold M, Lamparello PJ, Giangola G,
Adelman MA. (1996) A comparison of regional and
general anesthesia in patients undergoing carotid
endarterectomy. J Vase Surg 24:946-56.

Rodgers A, Walker N, Schug S, et al. (2000) Reduction of
postoperative mortality and morbidity with epidural or
spinal anaesthesia: results from overview of random-
ized trials. BMJ 321:1493-7.

Steen PA, Tinker JH, Tarhan S. (1978) Myocardial reinfarc-
tion after anesthesia and surgery. JAMA 239:2566.

Von Knorring J, Lepantalo M. (1986) Reduction of periop-
erative cardiac complications by electrocardiographic
monitoring during treadmill exercise testing before
peripheral vascular surgery. Surgery 99:610.

Nonatherosclerotic Vascular Disease

Jonathan R.B. Hutt and Alun H. Davies

Vasospastic Disorders

Raynaud's Phenomenon

In 1862 Maurice Raynaud first described the
problem of an asphyxia and symmetrical gan-
grene of the extremities. Raynaud's phenome-
non is now defined as episodic vasospasm of
arterioles in the extremities. It is classified as
either an idiopathic form, known as primary
Raynaud's or Raynaud's disease, or as secondary
Raynaud's or Raynaud's syndrome, where it
occurs in the presence of an underlying cause
(Table 8.1).

Raynaud's has an incidence of up to 5%. It is
found worldwide, but due to the common pre-
cipitant factor of cold extremities, it appears to
have a higher incidence in countries with a low
ambient temperature. It affects women far more
than men at a ratio of 9: l.In the case of primary
Raynaud's, there is evidence of a genetic predis-
position, as 25% of sufferers have a first-degree
relative who is affected.

The underlying pathophysiology of Ray-
naud's presents a complicated picture. The
overall effect is due to vasospasm of small mus-
cular arteries and arterioles. Many factors and
mechanisms have been implicated in this
process, and it is occasionally unclear whether
they are causal as part of the primary pathology
or consequential as a result of it. That there are
many causes of secondary Raynaud's is testa-
ment to the fact that there may be subtly differ-

ent underlying mechanisms with a similar final
end point. In a similar vein, although some
factors may not be primary instigators of the
problem, their activation and subsequent action
may contribute to the severity of the pathology
and thus provide therapeutic targets in certain
situations. The increasing number of implicated
mechanisms may also indicate the future poten-
tial for further delineation of the spectrum of
disorders associated with Raynaud's into more
distinct pathological mechanisms.

Broadly speaking, the etiological factors that
have so far been implicated in the development
of Raynaud's can be divided into local factors
present at the immediate neurovascular level,
and more general humoral factors (Fig. 8.1).

The Local Microvascular Unit

Neurogenic Mechanisms

Vasoconstriction of the cutaneous vessels when
induced by cold is regulated by a 2 receptors.
This mechanism is open to derangement in the
pathology of Raynaud's. It has been shown that
sufferers have a reduced basal blood flow, which
would obviously be further decreased in the
setting of sympathetic-induced vasoconstric-
tion. Notably, it also appears that baseline
cutaneous blood flow is decreased in healthy
women compared with men, which may provide
an insight into the condition's preference for
the female sex. Although there is no increase
in background catecholamine circulation
detected in affected patients, dermal arteriolar

VASCULAR SURGERY

Table 8.1 . Secondary causes of Raynaud's phenomenon

Mechanical

Frostbite

Vibration

Rheumatological disease
Scleroderma

I Systemic lupus erythematosus
Dermatomyositis
Polymyositis
Rheumatoid arthritis
Sjogren's syndrome
Takayasu's arteritis
Giant cell arteritis

Arterial disease

Brachiocephalic atherosclerosis
Buerger's disease
Thoracic outlet syndrome

Vasospastic disorders
Migraine
Prinzmetal's angina

Endocrine disorders
Carcinoid syndrome
Hypothyroidism

Blood dyscrasias
Cryoglobulinemia
Paraproteinemia
Polycythemia

Infective causes
Parvovirus B19
Helicobacter pylori

Drugs
Vinblastine
Bleomycin
Methysergide
Ergot alkaloids
Beta blockers

samples from Raynaud's patients show an exag-
gerated response to a 2 -stimulating agents. The
use of sympathectomy as a therapy and the
documented benefits from the a 2 -blocking
agent Prazosin also support a place for
abnormal sympathetic activity in Raynaud's
pathophysiology.

Another neurological factor is calcitonin
gene-related peptide, a powerful vasodilator
found in cutaneous nerve endings. Response
to this mediator is unaffected in diseased
tissue, but immunocytochemistry demonstrates
a decrease in calcitonin gene-related peptide
levels in the local digital neurons of people with
primary and secondary Raynaud's. Intravenous
infusion of calcitonin gene-related peptide has
also been shown to increase blood flow in the
hands and may also help digital ulceration in
more severe cases.

Endothelial Mechanisms

At the level of the endothelium, there are a
number of mechanisms which may have been
implicated in the pathophysiology of Raynaud's.
Endothelin-1 is a vasoconstrictor derived from
vascular endothelial cells. Increased levels of
this mediator have been described in patients
presenting with Raynaud's. Similarly, nitric
oxide, an endogenous vasodilator, appears to be
present at reduced levels. It appears, however,
that these findings may be more consequential
than causal. Reports on patients with primary
Raynaud's have not shown increased levels of
endothelin-1, and it is accepted that endothelial
damage is more a feature of secondary disease.
Moreover, endothelin-1 levels correlate with
severity of disease and are also shown to
decrease in patients with systemic sclerosis as
digital ulcers undergo healing. Administration
of L-arginine, a precursor of nitric oxide
synthesis, has no benefit, and samples from

' HUMORAL

FACTORS

^r^

Cellu

br ^

r '

1 Mod- Cellular

Erythrocytes
Neutrophils

Platelets

v. >

Hormones

Figure 8.1. Etiological mechanisms in
Raynaud's phenomenon. Both local and
humoral factors have been implicated.
CGPR, calcitonin gene-related peptide.

NONATHEROSCLEROTIC VASCULAR DISEASE

nonaffected arterioles from patients with sys-
temic sclerosis show normal endothelium-
mediated vasodilatory responses. This suggests
that this mechanism is unlikely to be a primary
causative one.

Erythrocytes

Abnormalities of erythrocyte aggregation and
deformability have been described in Raynaud's
patients.

Humoral Factors

Cellular

Platelets

The potential for platelets to act as a significant
pathological factor is high. Activated platelets
have the ability to aggregate and cause mechan-
ical blockage, or release mediators that are both
prothrombotic and stimulate vasoconstriction.
Similar to the effects seen on endothelial cells,
increased expression of a 2 receptors on platelets
in Raynaud's patients may provide a lower
threshold for activation in the presence of sym-
pathetic stimulation. Platelets from Raynaud's
patients also appear to be hypersensitive to 5-
hydroxytryptamine (5-HT) (serotonin) stimu-
lation. An increase in activation of platelets is
seen in Raynaud's, with augmented release of
the mediators thromboxane A 2 and serotonin.
Similar to endothelin-1, thromboxane A 2 is
related to disease severity, primarily in second-
ary disease. Administration of antagonists to
this substance, however, does not appear to
have a marked effect on disease expression or
progression.

The potential for platelets to be primary
etiological agents is also called into question
with the interesting observation that sufferers
of Glanzmann's thrombasthenia, who display
a complete lack of platelet aggregation, may still
suffer attacks of Raynaud's syndrome.

Neutrophils

Although they are unlikely to be causative
factors, circulating neutrophils may certainly
have a propensity for causing damage. Trapping
and activation in the setting of occluded
vessels followed by ischemia and reperfusion
lead to an escalation of the reactive response in
the local vicinity of the arterioles. However, in
primary Raynaud's, endothelial damage is not
really a feature. In light of this fact, this mecha-
nism may simply represent an augmenting
effect.

Hormonal

Estrogen

Certainly the large predilection for the female
sex that Raynaud's displays is cause enough to
consider an underlying hormonal basis. Differ-
ent phases of the menstrual cycle are associated
with varying responses of digital blood flow to
cold stimuli, which certainly suggests that
female sex hormones may have an etiological
role.

Clinical Factors

Raynaud's is characterized classically by the
following symptoms:

• Initial pallor due to vasoconstriction

• Cyanosis due to sluggish blood flow

• Redness due to hyperemia

This gives the classical picture of white, blue,
and then red discoloration described by suf-
ferers. This picture usually occurs in the pres-
ence of cold or emotional stress. It may be
accompanied by numbness and burning pain,
which may be severe as the blood flow returns.
The most common site to be affected is the
fingers, with the toes involved to a lesser extent.
More rarely, other extremities such as the nose,
ears, tongue, or nipple may be affected. The
attacks range from mild, with an asymptomatic
picture when seen by the clinician, to more
severe effects with necrosis and gangrene of
peripheral tissues. In extreme cases, this may
progress from superficial to deep structures and
require amputation.

In the setting of the presentation of
Raynaud's as a primary complaint rather than
on the background of known disease, investiga-
tion into underlying causes is required. Up to
5% of patients presenting with primary
Raynaud's ultimately develop a connective
tissue disorder. It does appear that there are
notable differences in the demographics and
presentation between primary and secondary
disease, as outlined in Table 8.2.

VASCULAR SURGERY

Table 8.2. Clinical differences between primary and
secondary Raynaud's

Feature

Primary

Secondary

Age at onset

<30

>30

Digital gangrene

Rare, superficial

Common

Nail fold capillaries

Normal

Large and
tortuous

Auto antibodies

Negative or low

Frequent

titer

History and examination should be directed
at the exclusion of secondary causes of
Raynaud's phenomenon. History should include
questioning on symptoms of connective tissue
diseases as well as details of drugs and exposure
to toxic agents. A history of vibrating tool use,
trauma, or positional triggering consistent with
thoracic outlet syndrome is also helpful.
Routine examination should not omit careful
examination of the peripheral pulses and
blood pressure (BP) in both arms, along with
neck examination for the presence of a cervical
rib.

A further test that can be performed at the
consultation is capillaroscopy of the nail fold,
where capillary loops lie horizontal to the
surface (Box 8.1). Other techniques for the
measurement of peripheral blood flow such as
analysis of digital systolic pressure during
cooling or red blood cell velocity in nail fold
capillaries have yet to find their way into clini-
cal practice.

A chest radiograph shows a cervical rib if
it is present, and may also show changes con-
sistent with connective tissue disease. Blood
testing for autoantibodies or prothrombotic
states can provide good indicators for the pres-

Box 8.1. Capillaroscopy

The nail-fold capillaries can be visualized
through immersion oil placed on the finger.
Although best seen with a microscope, they
can also be viewed using an ophthalmoscope
set at a diopter of 10-40. In the presence of
connective tissue disease, the nail-fold
vessels are tortuous and dilated.

ence of underlying disease. Further tests such as
Doppler imaging or angiography of vessels as
well as further blood tests, should be instigated
on the basis of previous indications. A potential
pathway for diagnosis in Raynaud's is shown in
Figure 8.2.

As an idiopathic cause, primary Raynaud's
should be considered a diagnosis of exclusion,
to coincide with the following criteria:

• Symmetrical vasospastic attacks

• Absence of necrosis or gangrene

• History and physical findings not indica-
tive of secondary cause

• Normal capillaroscopy of nail bed

• Normal erythrocyte sedimentation rate
(ESR) and negative serology for
autoantibodies

A follow-up period of 2 years is likely to be
sufficient to pick up any underlying pathology
of what initially appears to be Raynaud's
disease. The most likely culprits by far that may
reveal themselves are the connective tissue
diseases.

Treatment

Acute Ischemia

In the setting of acute tissue-threatening
ischemia, instigation of vasodilatation is the key
treatment. Intravenous prostaglandin analogues
such as iloprost are effective. In the absence of
the availability of such therapy, a short-acting
calcium channel blocker such as nifedipine
can be given, along with aspirin as antiplatelet
therapy. A digital or wrist block with local anes-
thesia without adrenaline may be beneficial
both for pain relief and for the underlying
pathology, as it effectively provides a localized
chemical sympathectomy.

In persistent cases, a prolonged infusion of
IV heparin may be required, and in intract-
able cases, surgical intervention with localized
digital sympathectomy is indicated.

In the absence of tissue-threatening compli-
cations, disease therapy is best approached in a
stepwise manner. Increasing levels of inter-
vention can then be introduced if the disease
proves refractory to a particular level of therapy.
A potential pathway for the treatment of
Raynaud's disease is shown in Figure 8.3.

NONATHEROSCLEROTIC VASCULAR DISEASE

Figure 8.2. Algorithm for the
diagnosis of Raynaud's
phenomenon.

History suggestive of
Raynaud's phenomenon

Exclusion of causative or exacerbating factors

• Drugs, Toxins

• Environmental agents. Occupation

• Trauma

ROUTINE TESTS

Examination
Capillaroscopy

Blood tests: FBC, U+Es, Autoantibodies
Chest radiograph

In the presence of:

• Abnormal capillaroscopy or CXR

• Autoantibodies

In the presence of:

• Asymmetrical disease

• Abnormal vascular examination

Rheumatic disease likely

May require

• Doppler studies/angiography

If all tests normal

Low suspicion of 2 Raynaud's

• No digitat lesions/gangrene

High suspicion of 2 Raynaud's

• Severe symptoms

• Evidence of tissue damage/gangrene

> These patients can be considered to have primary Raynaud's
1 Infrequent follow-up for two years may be necessary to rule
out developing CTD

Further tests

• Thyroid function

• Cryoglobulins

• Serum protein electrophoresis

Nonpharmacological Therapy

Initial treatment is based on the avoidance of
precipitants, such as cold and emotional stress.
Prevention of exposure to cold is best based on
a total body approach, rather than just localized
to fingers and toes, and may include specifically
designed clothing such as heated gloves. The
cessation of contributing factors is also involved
at this step. This includes lifestyle modifications
regarding smoking and caffeine intake, plus
other vasoconstricting substances such as
cocaine and amphetamines. Any medical thera-
pies that may be contributing to the disease
should be stopped or modified to other, less

harmful agents. Use of vibration-proof impact
tools or in certain cases a change of job may
prevent the progression of secondary Raynaud's
associated with hand-arm vibration syndrome.

Pharmacological Therapy

There are a multitude of putative pharmacolog-
ical therapies for Raynaud's, some of which have
a more solid evidence base than others:

Ca + channel blockers: These have been the
mainstay of treatment for some time. The
best agents are those based on dihydropy-
ridines, due to their decreased action on

VASCULAR SURGERY

Figure 8.3. Algorithm for the
treatment of Raynaud's disease.

Sympathectomy
Proximal sympathectomy
Digital artery sympathectomy

cardiac muscle and relative selectivity
for vascular smooth muscle. Classically,
nifedipine is the drug of choice, but newer
dihydropyridines such as amlodipine and
felodipine are also effective. These are
usually started at a low dose with gradual
escalation as required.

Angiotensin II receptor antagonists: Trials
with losartan show a good efficacy com-
pared with nifedipine in reduction of
quantity and severity of attacks (Dziadzio
et al., 1999).

Serotonin modulation: The serotonin antago-
nist Ketanserin has been used in treatment,
particularly in the setting of scleroderma,
although its evidence base may be ques-
tionable. There is also some evidence that
selective serotonin reuptake inhibitors
(SSRIs) such as fluoxetine may have a
beneficial effect.

Nitroglycerines: The use of topical nitrates
may aid in symptomatic relief and in the
reduction of the number of attacks,
although side effects may limit their
usefulness.

Prostaglandins: There is good evidence that
an intravenous infusion of iloprost, a syn-
thetic prostacyclin analogue, is efficacious
in Raynaud's, certainly in severe disease.
The key to its widespread use in less acute
settings lies in the production of an effec-
tive oral preparation. However, attempts to
date to produce a similar effect to that seen
with intravenous administration have
proved equivocal and have been troubled
by a high incidence of side effects.

Future possibilities: Further medical treat-
ments are likely to continue to appear, in
the light of the large quantity of mooted
causative factors. Initial trials with calci-

NONATHEROSCLEROTIC VASCULAR DISEASE

tonin gene-related peptide certainly indi-
cate potential for development. Further
delineation of the genomics behind
primary Raynaud's may show the road to
more interventional possibilities in the
setting of gene therapy.

Surgical Therapy

Due to its invasive nature as well as its inherent
complications, surgery for Raynaud's is usually
reserved for cases that are refractory to medical
therapy. The main surgical option is sympa-
thectomy, which may be performed as a proxi-
mal procedure, or as a microsurgical localized
operation:

Upper limb: This involves destruction of the
second and third thoracic ganglia and their
interconnections, which maybe performed
through a number of surgical approaches.
Results are disappointing in terms of
relapse rate, although it may still have a
role in severe cases.

Lower Limb: This involves destruction of
the second, third and sometimes fourth
lumbar sympathetic ganglia plus intercon-
nections. It appears to be a more effective
therapy than the similar procedure in the
upper limb.

Another option, this one microsurgical, is
digital artery sympathectomy, a more effective
procedure than proximal sympathectomy.
Although effective, its place probably lies in
treatment of tissue-threatening disease or in
cases refractory to medical therapy.

Other Vasospastic Disorders

Erythromelalgia

This is a rare condition characterized by vasodi-
lation associated with erythema and increased
temperature of the extremities along with a
burning pain. Similarly to Raynaud's phenome-
non, it may occur in an idiopathic form or
secondary to other disease. Associated pathol-
ogy includes hypertension, myeloproliferative
disorders, diabetes, rheumatic disease such as
rheumatoid arthritis or systemic lupus erythe-
matosus (SLE), gout, spinal cord disease, and
multiple sclerosis.

The clinical picture varies in severity. Therapy
with aspirin and vasoconstrictive agents can be
helpful, and treatment of the underlying disease
may aid symptoms in secondary disease.

Acrocyanosis

This presents as a symmetric cyanosis of the
hands or less commonly of the feet, which is
both persistent and painless. Affected body
parts show decreased temperature and blue dis-
coloration, and they may be swollen and sweaty.
Examination of peripheral pulses is normal.
Generally, it is not a harbinger of underlying or
threatening pathology, and supportive treat-
ment with reassurance and advice about
avoiding the cold is usually sufficient.

Vasculitis

Vasculitis is broadly defined as inflammation of
the vessel wall. It covers a wide range of clinical
and pathological entities, which have both
confusing similarities and yet important dis-
tinctions, most notably in their treatment and
prognosis.

Classification of these diseases is compli-
cated, as there is considerable overlap both in
clinical presentation and histological appear-
ance. The most common approach used is to
classify them by consideration of the size of
the vessels that the disease affects (Table 8.3).
Vasculitis that affects the smaller arteries can be
further classified according to whether or not
antineutrophil cytoplasmic antibodies (ANCAs)
are found. Such a distinction is possible at a his-
tological level, as only those associated with
ANCAs affect the small arteries, with the others
affecting arterioles, venules, and capillaries.

The underlying pathophysiology of many of
the noninfective vasculitides appears to have an
immunological basis. This is clear not only from
the temporal associations of some of the con-
ditions with certain viral infection, but also
from the fact that the majority are treated with
various combinations of immunosuppressants.

Their clinical presentation arises from the
consequences of vessel wall inflammation.
These include thrombosis and subsequent
ischemia or infarction, aneurysm formation,
and hemorrhage. The extremely broad range of
clinical phenomena and affected target vessels

VASCULAR SURGERY

Table 8.3. Classification of the vasculitides

Large-vessel vasculitis
Giant cell arteritis
Takayasu's arteritis

Medium-vessel vasculitis
Kawasaki's disease
Polyarteritis nodosa

Small-vessel vasculitis
ANCA associated
Wegener's granulomatosis
Churg-Strauss syndrome
Microscopic polyangiitis

Not ANCA associated
Henoch-Schbnlein purpura
Cryoglobulinemic vasculitis
Cutaneous leukocytoclastic angiitis

ANCA,antineutrophil cytoplasmic antibody.

means that the vasculitides present to a myriad
of clinicians: dermatologists, rheumatologists,
and gastrointestinal(GI) and vascular surgeons.

Large-Vessel Vasculitis

Giant Cell Arteritis

This is a granulomatous inflammatory disease
of the aorta and its branches. It has a tendency
to affect the extracranial branches of the carotid
artery, hence its other name of temporal arteri-
tis. It was first described by Sir Jonathan
Hutchinson in 1890, who noticed it in a retired
hospital porter who was unable to wear his hat
due to tender and inflamed temporal arteries. It
is a disease that is predominantly seen in Euro-
peans over 50 years old, and has a slightly higher
incidence in women, with a male to female ratio
of 1 :2. Incidence can be up to 25/100,000 in the
older age groups. Although the actual cause
remains a mystery, it has a strong association
with polymyalgia rheumatica, which is present
in up to 50% of cases. Both these conditions
share genetic risk factors and geographical
populations.

At a microscopic level, there is intimal thick-
ening and edema. A chronic inflammatory
picture is seen with giant cell and granuloma
formation.

The usual clinical presentation is with severe
unilateral occipital or temporal headaches.
There is scalp tenderness, which classically
becomes evident on brushing or combing hair.

Features of vascular insufficiency may also be
present, such as jaw claudication, or, more
rarely, tongue or limb claudication. These symp-
toms may be accompanied by systemic symp-
toms of fever, malaise, fatigue, and a sore throat.

The most feared complication is involve-
ment of the ophthalmic artery. This leads to
ischemia of the optic nerve and sudden painless
visual loss, which can be temporary or may be
permanent.

On examination, there may be swelling and
tenderness of affected superficial arteries, which
will be pulseless. The most notable finding on
simple blood tests is a significantly raised ESR
and C-reactive protein (CRP).

The key to diagnosis of this condition is
obtaining histology from an arterial biopsy,
which is usually taken from the temporal arter-
ies. Due to the nature of the disease, which
occurs as skip lesions, it is important to take a
multiple sections, each of an amount of at least
3 to 5 cm.

The most effective treatment is corticos-
teroids, and if a diagnosis of giant cell arteritis
(GCA) is suspected, immediate initiation of
steroid therapy is required to prevent the onset
of blindness. A prompt biopsy should then be
organized, preferably within 7 days of starting
the steroid course. This reduces the possibility
of a negative biopsy in an affected patient,
avoiding the clinical conundrum that follows
of a patient on long-term steroids without a
definitive diagnosis.

In 75% of patients, the disease settles within
a period of 3 years, but in others it proves refrac-
tory to treatment. As in all diseases treated with
long-term steroids, the side effects of the treat-
ment itself can lead to difficulties. Currently,
however, it appears that no steroid-sparing
agent has emerged as a suitable alternative or
adjunct.

Takayasu's Arteritis

In 1908 Mikito Takayasu, a Japanese ophthal-
mologist, described the association of retinal
arteriovenous anastomoses and absent upper
extremity pulses. Takayasu's arteritis is a rare
granulomatous arteritis of the aorta and its
major branches. It has a predilection for
females, and tends to affect people in their
second and third decades, although it has been
reported in patients as young as 6 months and

NONATHEROSCLEROTIC VASCULAR DISEASE

in adults at every age. Although it is encoun-
tered worldwide, it is especially prevalent in
people of Asian descent.

Pathologically, Takayasu's arteritis somewhat
resembles giant cell arteritis, displaying severe
necrotizing inflammation that leads to marked
intimal thickening. This causes eventual nar-
rowing and occlusion of the lumen. It can also
weaken the vessel wall, providing a predisposi-
tion to aneurysm formation.

Clinically, patients suffer from systemic
symptoms such as fever, malaise, weight loss,
arthralgia or myalgia, and night sweats. More
specific symptoms are related to the affected
arterial system and related end-organ ischemia,
(Table 8.4). Clinical presentation can vary from
incidental discovery in the asymptomatic pa-
tient to a catastrophic event.

Physical examination may reveal bruits or
decreased pulses (Takayasu's is also known as
pulseless arteritis). Blood pressure may be ele-
vated, and also asymmetrical due to subclavian
stenosis. There may be valvular regurgitation
and arterial tenderness. This latter sign may be
especially noticeable over the carotids.

Investigation is primarily by arteriography.
Neither the level of symptoms nor other indica-
tors of disease such as the ESR provide a clear
indication of disease extent or severity. As a rule,
these indicators are thus not a good guide to
management.

Treatment

Some patients demonstrate a self-limiting
disease that requires minimal intervention,
whereas others require more intensive therapy.

Medical

In the first instance, treatment is with glucocor-
ticoids. If the disease proves refractory to
steroid therapy, or if the patient is unable to be
weaned off their long-term use, further treat-
ment with cytotoxic agents is indicated.
Adjunct therapy with methotrexate is effective
in increasing progression to remission as well a
having steroid-sparing effects. Cyclophos-
phamide has similar properties, but due to its
significant toxicity is probably best used as a
third-line treatment in those who are intolerant
of or nonresponsive to methotrexate.

Surgical

There is a place for open vascular surgery and
endovascular options in the cure of fixed vascu-
lar lesions producing significant ischemia. Indi-
cations include cerebral hypoperfusion,
hypertension due to renovascular disease, and
aneurysms or valvular insufficiency. Clinically
significant improvement of symptoms is usually
possible with surgery, although restenosis is
common.

Table 8.4. Site-dependent presentation of Takayasu's arteritis Prognosis

Clinical presentation

and severity depend on:

Site

Degree of stenosis

Availability of collateral blood supply

Subclavian:

Arm claudication, Raynaud's

Carotids:

Visual changes, syncopeJIAs/

stroke

Vertebrals:

Visual changes, dizziness

Aortic arch:

Aortic insufficiency, CHF

Aorta

(includes main enteric branches):

Abdominal pain, nausea,

vomiting

Renal arteries:

Hypertension/renal failure

Iliac arteries:

Leg claudication

Pulmonary arteries:

Atypical chest pain, dyspnea

Coronary arteries:

Chest pain/Ml

CHF, chronic heart failure; Ml, myocardial infarction; TIA, transient
ischemic attack.

Takayasu's is a chronic disease with a 45%
relapse rate, although 23% of patients never
reach a state of remission. Following diagnosis,
survival rates are greater than 80%. However,
the disease still carries a significant morbidity.

Cogan's Syndrome

This rare disorder of young adults of either sex
warrants a mention at this point primarily due
to the vessel it affects. It is an inflammatory
process that leads to interstitial keratitis and
may lead to permanent hearing damage or
effects on the vestibulo auditory system,
although these effects appear unrelated to the
vasculitic phenomena. From a vascular point
of view, patients may suffer aortitis or other
large-vessel inflammation. The primary source

VASCULAR SURGERY

of morbidity is cardiovascular involvement and
auditory problems.

Treatment is with prednisolone, and is indi-
cated for severe ocular or auditory disease and
vasculitis. Prompt treatment at the first sign of
hearing damage improves the prognosis for
overall hearing loss and return of function.

Medium-Vessel Vasculitis

Kawasaki's Disease

Kawasaki's disease was first identified in 1967 by
Tomisahu Kawasaki, a Japanese pediatrician,
and is also called mucocutaneous lymph node
syndrome. Although it is seen in adults, this is
primarily a disease of childhood, and the major
cause of acquired heart disease in children
in the United States and Japan. Despite the
original demographical description, it is a
disease that is found worldwide. In the United
Kingdom the incidence is less than 5/100,000 in
children less than 5 years old; 80% of sufferers
are in this age bracket, and males are affected
with slightly greater frequency than females at
a ratio of 2 : 1.

Clinical Factors

The condition begins with an acute febrile
illness. This is followed by a polymorphic rash
that may affect any part of the body, congestion
of the conjunctivae, dryness and erythema of
the oral mucosa, cervical lymphadenopathy, and
erythematous edema of the palms and soles.
These features are the criteria for the diagnosis
of Kawasaki disease (Table 8.5). Other clinical
features are outlined in Table 8.6.

The major cause of morbidity and mortality
in the disease arises from the cardiovascular
complications, including pancarditis, but more
specifically the vasculitic changes in the coro-
nary arteries may lead to the formation of

Table 8.5. Diagnostic criteria for Kawasaki's disease

Fever plus:
Rash

Conjunctival injection
Oral mucosal changes
Brawny induration of extremities
Cervical lymphadenopathy

Table 8.6. Other clinical features of Kawasaki's disease
System Feature

Cardiovascular Pancarditis

Gastrointestinal Diarrhea

Genitourinary Albuminuria

Neurological Aseptic meningitis

Joints Arthralgia

Blood Leukocytosis, thrombocytosis, raised
C-reactive protein

aneurysms. These occur 1 to 4 weeks after the
onset of fever, and are seen in up to 25% of
untreated cases. Thus, monitoring of the disease
is usually structured with an electrocardiogram
(ECG) performed in the first week of illness,
with an echocardiogram both initially at diag-
nosis and repeated 2 to 4 weeks later.

Treatment is twofold. High-dose IV
immunoglobulin is given as a single infusion.
This prevents the formation of coronary
aneurysms but also decreases fever and
inflammation in the myocardium. Patients are
also given aspirin as an antithrombotic
measure. In certain cases, long-term follow-up
and anticoagulation maybe required.

Polyarteritis Nodosa

Polyarteritis nodosa (PAN) was the name even-
tually given to the disease process in the first
definitive report of a patient with necrotizing
arteritis, which was written in 1866. For some
time, before it was clear that there were fur-
ther underlying pathological mechanisms, all
patients presenting with necrotizing arteritis
were given a diagnosis of PAN. In truth, it is an
uncommon disorder. Unlike other vasculitic
disorders, PAN is most frequently observed in
middle-aged men. It often leads to severe sys-
temic complications affecting many of the organ
systems. The underlying pathology of PAN is
one of florid acute inflammatory changes seen
in a pattern of fibrinoid necrosis. This is similar
to what is seen in models of immune complex
vasculitis, and there is some evidence that
certain viruses have associations with the devel-
opment of PAN. These include the hepatitis B
and C viruses and HIV. Clinically, the patient
may present with a number of complaints, due
to the widespread nature of the disease (Table
8.7).

NONATHEROSCLEROTIC VASCULAR DISEASE

Table 8.7. Clinical manifestations of polyarteritis nodosa

System

Manifestation

Cardiovascular

Coronary arteritis may lead to Ml or
HF

Respiratory

Asthmatic symptoms + hemoptysis,
(rare)

Gastrointestinal

Hemorrhage and mucosal ulceration
Presentation may mimic the acute
abdomen

Genitourinary

Hematuria

Neurological

Mononeuritis multiplex
(involvement of vasa nervorum)

Joints

Subcutaneous nodules,*

hemorrhage, and gangrene
Livedo reticularis, (seen if chronic)

Blood

Leukocytosis, thrombocytosis, raised
CRP

* These occur due to the involvement of subcutaneous arteries and,
although uncommon, they are part of the reason why the disease
was originally named.

CRP, C-reactive protein; HF, heart failure; Ml, myocardial infarction;
TIA, transient ischemic attack.

Blood tests in PAN reveal anemia, leukocyto-
sis, and a raised ESR; ANCA is rarely positive
in classic PAN. Diagnosis is primarily by
two methods. Histologically, biopsied lesions
show a classical pattern of necrotizing arteritis,
whereas angiography reveals microaneurysms,
which may be found in hepatic, intestinal, or
renal vessels.

Treatment of the condition is primarily with
immunosuppressants. Therapy is initially with
corticosteroids, but further agents such as
azathioprine or cyclophosphamide maybe indi-
cated in life-threatening disease.

In cases where the vasculitis occurs in a
picture of viral infection, control of the
inflammation with immunosuppression may be
necessary before effective antiviral therapy can
be considered. However, combination antiviral
therapy may prevent the problems of conven-
tional treatment, which may enhance viral repli-
cation, increasing the chance of progression to
chronic infection. In viral-associated vasculitis,
plasma exchanges may also be considered, as
they are effective in reducing the amount of
circulating immune complexes.

The prognosis, perhaps unsurprisingly, is
worse in those patients who suffer multisystem

involvement. Five-year survival with treatment
is 80%, and it is a disease that relapses only
infrequently.

Small-Vessel Vasculitis

Estimates of incidence of the small-vessel vas-
culitides vary, most likely due to variations in
the diagnosis. They share similar nonspecific
systemic features such as fever, malaise, weight
loss, arthralgia, and myalgia. Investigation of
these patients should include screening for anti-
neutrophil cytoplasmic antibodies (Box 8.2).

Broadly speaking, the vasculitides of the
small vessels can be divided into those in which
the ANCAs are positive or negative (Table 8.8).

Wegener's Granulomatosis

In Wegener's (named for Friedrich Wegener,
a German pathologist, 1907-1990), the small
arteries are predominantly affected above all
others. It may occur at any age, and appears to
show no predilection for either sex (Hoffman
et al, 1992).

Pathologically, it has a pattern of necrotizing
granulomatous vasculitis and is typically char-
acterized by lesions that involve three main

Box 8.2. Antineutrophil
cytoplasmic antibodies

Antineutrophil cytoplasmic antibodies
(ANCA)

There are two primary types of ANCA,
differentiated on the basis of their pattern
of immunofluorescence on ethanol-fixed
neutrophils.

cANCA

Antibodies directed against serine pro-
tease proteinase 3 (PR3).

These give a cytoplasmic pattern.

pANCA

Antibodies directed against the enzyme
myeloperoxidase (MPO).

These give a perinuclear pattern.

The ANCA typing can be combined with
antigen-specific testing for PR3 and MPO to
increase specificity.

VASCULAR SURGERY

Table 8.8. Distribution of ANCA among the small vessel
vasculitides

ANCA, antineutrophil cytoplasmic antibody.

organ systems: the upper respiratory tract, the
lungs, and the kidneys. Greater than 90% of
patients seek help for symptoms related to the
respiratory tract.

Patients suffer initially from severe rhinor-
rhea. This is followed by nasal and sinus
inflammation, which eventually leads to carti-
laginous ischemia, the sequelae of which are
perforation of the nasal septum and saddlenose
deformity of the nasal bridge. Tracheal
inflammation and sclerosis lead to stridor and
potentially dangerous airway stenosis. This par-
ticular complication is more common in chil-
dren who are affected. Disease activity in the
lower respiratory tract leads to cough, hemopt-
ysis, and pleuritic pain. Renal tract disease man-
ifests as glomerulonephritis. This is present in
only 20% of patients at the time of diagnosis,
but appears overall in 80% eventually.

A chest radiograph may show nodular
masses, which can be multiple. There may also
be ground-glass infiltration and cavitation. Over
time, the lesions show a migratory pattern, dis-
appearing in one area only for new lesions to
appear in others.

The typical histology of Wegener's is best
seen in the kidney. A renal biopsy demonstrates
necrotizing microvascular glomerulonephritis.
However, diagnosis is often by nonrenal biopsy,
which demonstrates the granulomatous necro-
tizing inflammation with neutrophil aggrega-
tion and vasculitis. The site of biopsy is
important. An upper airway biopsy, although
easy to perform, demonstrates diagnostic
changes in only 20% of cases. A more invasive
biopsy of the lung parenchyma shows the diag-
nosis in 90%.

Before treatment became available, patients
suffering from Wegener's granulomatosis would
have a mean survival time of only 5 months

before succumbing to pulmonary or renal
failure. Even with treatment, relapse is seen in
around 50% of cases. The presence of lung or
kidney involvement at diagnosis is a poor
prognostic indicator. Wegener's also has an
especially mutilating form, known as midline
granuloma, which carries a particularly poor
outlook.

Therapy is with a combination of glucocorti-
coids and other immunosuppressants. Treat-
ment with prednisolone alone is ineffective,
and the decision on which further agent to use
is based on a number of factors. In active
Wegener's where the disease is life threatening,
treatment with prednisolone is combined with
cyclophosphamide. This leads to a 90%
improvement rate, achieving complete remis-
sion in around 75% and giving a survival rate
of 80%. The main drawback with this regimen
is the significant toxicity associated with
cyclophosphamide use. To avoid it, a progressive
approach may be needed, using cyclophos-
phamide until the disease is in remission, then
changing to another agent such as methotrexate
or azathioprine, which can then be tapered out.
In active disease that is not life threatening,
combination treatment with prednisolone and
methotrexate is equally as good at maintain-
ing remission compared with a cyclophos-
phamide, and a similar regimen may also be
used in those patients who are intolerant of
cyclophosphamide.

Churg-Strauss Syndrome

Churg-Strauss syndrome, named for Jakob
Churg, a Polish-American pathologist (1910-
1966) and Lotte Strauss, an American pathol-
ogist (1913-1985), has an incidence of about
3 per million. The typical patient is usually
male and in the fifth decade of life. Classically
the syndrome is a triad of rhinitis and asthma,
eosinophilia, and systemic vasculitis. Because
of its makeup, there are a number of theories
about the underlying pathophysiology. It may
be a progression of an allergic phenomenon,
or a primary vasculitis that has an asthmatic
component due to the involvement of
eosinophils.

Pathologically, the picture is one of
eosinophilic infiltration, which typically affects
the lung, peripheral nerves, and the skin. Histo-
logically, a necrotizing vasculitis of the small

NONATHEROSCLEROTIC VASCULAR DISEASE

arteries is seen along with extravascular,
allergic granulomas.

Although initially presenting as above, the
syndrome has a progressive nature, which is
eventually vasculitic and involves the lungs,
nerves, heart, and the GI and renal tracts. A
complete blood count shows a high eosinophil
count.

Treatment is primarily with corticosteroids
alone, although in life-threatening cases
cyclophosphamide can be added. Due to its
association, it may be difficult to taper pred-
nisolone treatment when the vasculitic parts of
the disease are in remission, as this may lead to
asthmatic exacerbations.

Microscopic Polyangiitis

Another vasculitis that primarily affects the
small vessels, microscopic polyangiitis has only
recently been distinguished from PAN, and for
this reason there is a relative dearth of data
about the disease. Pathological distinction from
PAN is accepted to be on the basis that micro-
scopic polyangiitis leads to vasculitis in vessels
smaller than arteries, whereas PAN can be diag-
nosed if these vessels are not involved. Histo-
logically, it represents a necrotizing vasculitis,
with few immune deposits and no granuloma
formation.

Clinically, microscopic polyangiitis mainly
affects the kidney, presenting with glomeru-
lonephritis and hemoptysis. It may also be asso-
ciated with mononeuritis multiplex and fever.
Diagnosis is usually based on clinical features,
testing for ANCAs, and renal biopsy. It can be
severe, and survival rates at 5 years may be as
low as 74%. In disease that is potentially life
threatening, treatment is with prednisolone and
cyclophosphamide.

Non-Antineutrophil Cytoplasmic
Antibody-Associated Small-Vessel
Vasculitis

Henoch-Schonlein Purpura

This is the most common systemic vasculitis in
children. It is named for Edouard Henoch, a
German pediatrician (1820-1910), and Johann
Schonlein, a German physician (1793-1864).
The peak incidence is at 5 years. Pathologically,

it is characterized by the deposition in vascular
structures of immunoglobulin A (IgA)-contain-
ing immune complexes. It has a preference for
venules, capillaries, and arterioles. The common
clinical presentation is usually with arthralgia,
colicky abdominal pain, and a purpuric rash;
50% of sufferers have hematuria or proteinuria.
However, this compromises renal function in
only 15%.

It is important to distinguish Henoch-
Schonlein as a distinct pathological entity from
other small-vessel vasculitides. It has an excel-
lent prognosis, and supportive care is usually
sufficient for most patients, in contrast to the
life-threatening disease that can be caused by
the other inflammatory disorders. End-stage
renal failure occurs in less than 5% of patients.

Cutaneous Leukocytoclastic Angiitis

This is the most common cutaneous vasculitic
lesion. It is an acute purpuric skin lesion, under-
lying which is an inflammation of the dermal
postcapillary venules. Although primarily
affecting the skin, it may also be associated with
an arthralgia or glomerulonephritis. Etiologi-
cally, there is some indication that viral agents
such as hepatitis C virus may play a part. It
can also result from drug therapy with certain
agents such as sulfonamides or penicillin.

Most patients suffer a single episode, with
resolution occurring over a few months. About
10% suffer recurrent disease at varying inter-
vals. Symptomatic relief from cutaneous irrita-
tion and associated arthralgia and myalgia is
possible with antihistamines and nonsteroidal
antiinflammatory drugs. Treatment of severe
cutaneous disease is with corticosteroids.

Cryoglobulinemic Vasculitis

Cryoglobulins are cold-precipitable immuno-
globulins that maybe monoclonal or polyclonal.
They are encountered in myriad disease pic-
tures including lymphoid and plasma cell neo-
plasms and chronic infective and inflammatory
processes. Essential mixed cryoglobulinemia
describes the presence of cryoglobulins in the
absence of any precipitating underlying pathol-
ogy. Although this has been described his-
torically, it appears that most of these cases
are related to infection with hepatitis C virus
(HCV).

VASCULAR SURGERY

Vasculitis occurring in association with cryo-
globulins affects people at about 50 years of age.
A clinical picture of palpable purpuric lesions,
arthritis, weakness, neuropathy, and glomeru-
lonephritis is seen. The latter complication has
an association with a poor prognosis, if not
always a progression to end-stage renal failure.
A useful diagnostic test is to look at complement
levels. A distinctive picture of low levels of C4
with normal or slightly low C3 is seen. Renal
biopsy shows an endothelial membranoprolifer-
ative glomerulonephritis with intraglomerular
deposits.

Mild disease can be approached symptomati-
cally Antiviral therapy that produces a sus-
tained response appears to be the most effective
way of treating HCV-associated cryoglobuline-
mic vasculitis. In severe disease, the use of
immunosuppressants has been advocated,
although as expected, these agents may lead to
an increase in HCV viremia.

Miscellaneous Disorders

Buerger's Disease

This eponymous disease, named for Leo
Buerger, an Austrian-born American physician
and urologist (1879-1943), is also known by the
more descriptive term thromboangiitis obliter-
ans. It is an occlusive disease of the small and
medium-size arteries of the extremities, which
it affects in a segmental fashion. It primarily
affects young people, with a median age of 34
years. Initial descriptions by Buerger noted a
strong predilection of the disease for men,
affecting 2 of 500 cases that he reported. More
recent studies report a male to female ratio of
up to 5:1. The disease also has a somewhat
unusual geographical distribution. It has a low
incidence in people of European descent, but is
high in India, Japan, Korea, and the Middle East,
especially among Jews of Ashkenazi descent. In
fact, in this latter micropopulation, Buerger's
disease accounts for up to 80% of cases of
peripheral vascular disease.

The primary causative factor associated with
Buerger's disease is tobacco usage. Although
this usually manifests as smoking, it has also
been observed in patients who chew tobacco.
Tobacco use holds the key not only to causation
but also to persistence, progression, and recur-

rence. This much is clear from observations of
the patient base, although interestingly the
actual underlying mechanism has proved
elusive. The indications appear to be that of an
immune-mediated pathology, and a high preva-
lence has been associated with certain tobacco
types in India and Bangladesh. Histologically,
the disease manifests as an intense endarteritis
with cellular infiltration, giant cell foci, and the
presence of cell rich thrombi, which may show
recanalization. Other immunological markers
have also been demonstrated within the intima
of the vessels. The internal elastic lamina and
overall vascular wall architecture are well
preserved.

Clinically, there is a picture of ischemia of the
distal extremities with rest pain, ulceration, and
gangrene (Ohta and Shionoya, 1988). Both
upper limb and lower limb disease is seen in
40% of cases. In 10% there is only upper limb
involvement, and in 50% only the lower limb is
affected. Claudication is a rare symptom due to
the distal nature of the diseases, and if present
occurs most notably on the instep.

Diagnosis is based both on typical clinical
features as well as the exclusion of other causes,
as outlined in Table 8.9.

The investigations are thus directed initially
at ruling out other conditions. The next step is
to image the affected vessels. Arteriograms of
the upper limb often show occluded radial and
ulnar arteries that have become tortuous where
they have recanalized. There may also be
"pruning" of the digital arteries. In the lower
limb, the vessels are often normal down to the
popliteal trifurcation. Distal to this, segmental
occlusive disease is seen. This frequently
affects the tibial branches more than the
popliteal. None of these changes, however, is
pathognomonic.

Although the treatment of infected lesions
with antibiotics and debridement where neces-
sary is similar to that of other ischemic disease,
the mainstay of therapy in Buerger's disease is
the cessation of smoking. Recurrence is almost
always associated with resumption of tobacco
usage, and new ischemic lesions are rare
without reexposure. Conversely, persistent
abstinence from tobacco results in quiescence of
the disease process. As the lesions in Buerger's
disease appear to have healing potential, this
intervention can have a significant clinical
effect.

NONATHEROSCLEROTIC VASCULAR DISEASE

Table 8.9. Features of Buerger's disease

1. Distal extremity ischaemic symptoms

2. Exclusion of other causes

Proximal embolic source
Localised lesion (popliteal entrapment, cystic
disease
° Vasculitis
Drugs — ergot
Hypercoagulable states
Trauma

3. Onset at <45yrs

4. Tobacco usage

5. Supporting features

Migratory superficial phlebitis
Raynaud's phenomenon
Upper limb involvement

Distal extremity ischemic symptoms
Exclusion of other causes

Proximal embolic source

Localized lesion (popliteal entrapment, cystic
disease)

Vasculitis

Drugs: ergot

Hypercoagulable states

Trauma

Onset at <45 years of age
Tobacco usage
Supporting features

Migratory superficial phlebitis

Raynaud's phenomenon

Upper limb involvement

Other options are used in refractory progres-
sive disease. Sympathectomy has been advo-
cated, and surgical bypass may occasionally be
attempted. This latter treatment, however, has
a poor rate of success. The results are affected
not only due to the segmental, distal nature of
the disease, but also because the associated
phlebitis makes the veins poor conduits.

A number of new treatments are being eval-
uated, including implantation of spinal cord
stimulators and intramuscular injections of
vascular endothelial growth factor. The use of
iloprost has also been advocated, although a
significant clinical effect seems to be absent.

The final surgical option is amputation. It
should be noted that healing of surgical ampu-
tation is much improved when patients are free
from tobacco usage.

Compared with other necrotizing arteritides,
Buerger's disease has a worse prognosis with

regard to limb loss. Some form of amputation,
ranging from digital to major lower limb
removal, is required in up to 20% of patients.
The extreme importance of smoking is again
evident here. In one study, 94% of patients who
quit smoking remained amputation free,
whereas 43% of those who continued eventually
required at least one amputation. Interestingly,
and perhaps due to the distal nature of the
vasculature affected, the long-term survival of
patients with Buerger's disease is affected only
very slightly, with life expectancies approaching
that of the normal population.

Fibromuscular Dysplasia

This is a noninflammatory, nonatherosclerotic
vascular disease affecting arteries of small and
medium size. It appears in a variety of histol-
ogical manifestations depending on the arterial
wall layer that is most significantly involved
(Table 8.10). Although different types show a
slight variation epidemiologically, the common-
est form has a predilection for females in their
second to fourth decades. Disease has been
noted in patients as young as 2 months old.

The etiology of fibromuscular dysplasia
(FMD) is still unclear, but it appears to be mul-
tifactorial. Suggested factors include localized
ischemia due to poor perfusion from the vasa
vasorum, sequelae of mechanical damage, and
there is evidence for a familial link. There are
also many documented associations, both with
diseases such as pheochromocytoma, neurofi-
bromatosis, Ehlers-Danlos, Alport's, Rubella
syndrome, and heterozygous OCj-antitrypsin
deficiency as well as other factors such as
ergotamine and methysergide.

Symptomatic disease from FMD may result
from vessel stenosis, dissection, embolization,
thrombosis, or rupture of associated ane-
urysms. Disease and thus symptoms have been
recorded across the whole spectrum of the

Table 8.10. Histological classification of fibromuscular
dysplasia

Classification

Intimal fibroplasia
Medial fibroplasias
Medial hyperplasia
Perimedial fibroplasia

Frequency (%)

1-2
80-90
10-15

VASCULAR SURGERY

vascular bed, and it is likely that there will be
subclinical disease present in other areas in
most patients. The most common manifesta-
tions are hypertension from renovascular
disease and stroke from carotid disease. In
terms of the kidney, a significant proportion of
renovascular disease arises on a background of
FMD, the primary result of which is hyperten-
sion. However, as renovascular disease is a
relatively uncommon cause of hypertension in
itself, FMD is not a major contributing factor to
adult hypertension. When it affects the cere-
brovascular system, it is predominantly seen in
the internal carotid artery, and frequently is
seen bilaterally. Vertebral artery involvement
also occurs, although rarely in isolation from
carotid disease. There is also a reported
association between cerebrovascular FMD and
intracranial "berry" aneurysms of an order of
around 7%. The symptoms of cerebrovascular
disease depend on the location and severity of
the lesions.

Where visceral vessels are affected, symptoms
are usually due to ischemia. Infarction is rare
due to the collateral arterial supply. In the
peripheral vascular tree, lesions at all levels have
been identified. The commonest sites are the
subclavian artery in the upper limb and the
external iliac artery in the lower limb.

Investigations are directed at ruling out other
causes of disease, but ultimately are based on
imaging of the affected arterial system. As a
noninflammatory process, FMD is not associ-
ated with any of the acute-phase changes seen
in the vasculitides, which can be detected by
simple blood tests.

Imaging can be either by noninvasive
methods such as duplex scanning or magnetic
resonance angiography (MRA), or by angio-
graphy. The angiographic appearance of the
most common histological type of FMD is of a
string of beads. If duplex scanning is used to
image the carotid system, it is important to
image as distally as possible in order not to miss
FMD, which in contrast to atherosclerotic
lesions is not commonly seen around the
carotid bifurcation.

Therapeutic intervention in FMD should be
considered on an individual basis and depend
on the individual as well as the location and
severity of the disease. In renovascular disease,
initial medical therapy for hypertension is
usually indicated. It should be remembered

that as with other reno -occlusive disease
angiotensin-converting enzyme (ACE) inhi-
bitors should be avoided. If pharmacological
treatment fails, there are a number of options.
Percutaneous transluminal angioplasty (PTA) is
an effective intervention, and although it is
associated with up to a one in five re-stenosis
rate, the rate of reappearance of hypertension is
lower. Given the success in actually curing
hypertension, PTA should probably be consid-
ered earlier in younger patients to avoid unnec-
essarily long courses of medical therapy along
with progressive deterioration of renal func-
tion. There are also a number of surgical
options, which carry a higher morbidity and
mortality. However, if considered in the appro-
priate setting both in terms of patient suitabil-
ity and available expertise, they can be very
effective.

Management of cerebrovascular FMD
depends on the presence or absence of symp-
toms to a certain extent. However, there is not a
great deal of information on the progression of
the disease with which to make this judgment.
In the asymptomatic setting, medical therapy is
appropriate. In the presence of symptoms, intra-
operative or percutaneous dilatation of lesions
can be considered.

Where the visceral vessels are affected, surgi-
cal treatment may be indicated when medical
therapy fails. Treatment of peripheral disease
can broadly be considered as medical therapy,
dilation therapy, either percutaneously or by
open technique, and surgical bypass or
reconstruction.

Cystic Adventitial Disease

This is a rare, nonatherosclerotic cause of limb
claudication. Since being first reported in 1947,
there have been less than 350 documented cases.
It affects people mostly in the fourth and fifth
decades, with a male to female ratio of 5: 1.

Pathologically, it is defined by synovial-
like cysts in the adventitial layer of the arterial
wall. These contain a mucinous gel that
contains various proportions of mucoproteins,
mucopolysaccharides, hyaluronic acid, and
hydroxyproline. Although the exact underlying
etiology is unclear, a number of mechanisms
have been proposed. It has been suggested
that the fluid may come from the reactivation
of mesenchymal cells trapped in developing

NONATHEROSCLEROTIC VASCULAR DISEASE

vessels during embryological vessels. Another,
more widely supported hypothesis is that the
cysts develop from a herniation of adjacent
synovium. This latter theory is backed up by
imaging results and by the late age of onset of
disease.

From the reported cases, cystic adventitial
disease has a predilection for the popliteal
artery above all others, but has also been
described in the external iliac, axillary, and
distal brachial, radial, and ulnar arteries. In the
acute setting the picture is of sudden onset and
progressive claudication. Physical examination
may reveal a mass. Indeed, some of the cases are
discovered in patients referred for investiga-
tions of a soft tissue mass, before the emergence
of significant vascular symptoms.

The mainstay of investigation is imaging.
Although the main accepted method is angiog-
raphy, good diagnostic results can also be
obtained from less invasive techniques. Duplex
ultrasonography can reveal the cystic disease
itself, which appears as anechoic or hypoechoic
masses in the external wall. It also has the
advantage of providing information as to the
degree of vascular impairment. Magnetic reso-
nance imaging also produces characteristic

images, demonstrating multiple intramural
cystic masses oriented along the long axis of the
vessel.

There are numerous therapeutic options.
Spontaneous resolution of symptoms with
conservative management has been docu-
mented. The cysts can also be drained percuta-
neously under computed tomography or
ultrasound guidance. Surgical intervention con-
sists of either excision of the cysts and diseased
wall with preservation of the artery or use of an
interposition graft. Both of these techniques
have good initial results, although long-term
follow-up data are lacking.

Given the paucity of cases on which to base
interventional judgment, the decision is pro-
bably best made by considering the clinical
urgency and available expertise.

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Hoffman GS, Kerr GS, Leavitt RY, et al. (1992) Ann Intern

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Ohta T, Shionoya S. (1988) Br J Surg 75:259-62.

Lower Limb Ischemia

Rajabrata Sarkar and Alun H. Davies

Lower limb ischemia is an increasingly preva-
lent disorder that has a wide range of clinical
presentations and variable consequences for
the patient. Although atherosclerosis is by far
the most common cause of lower extremity
ischemia, a variety of other conditions can cause
either acute or chronic lower extremity
ischemia. Three major factors are contributing
to an increase in both the prevalence and inci-
dence of lower extremity ischemia. The first
is the general aging of the population in devel-
oped countries, with its attendant increase in
the prevalence of atherosclerosis, peripheral
aneurysms, and other vascular lesions associ-
ated with advanced age. The second factor is the
alarming increase in the incidence of diabetes,
particularly among adolescents and younger
adults. As diabetes accelerates the progression of
atherosclerosis and lower extremity ischemia,
we can anticipate further increases in the
number of patients presenting at a younger age
with lower extremity ischemia. The third factor
is the increasing numbers of patients who have
undergone prior peripheral arterial bypass
surgery and are potentially at risk for either
graft occlusion or progression of disease. At
many major medical centers the majority of
patients presenting with acute limb ischemia
are those with thrombosis of a prior lower
extremity arterial reconstruction. This chapter
reviews the causes, clinical presentations, diag-
nostic approach, treatment options, and out-
comes of chronic and acute lower extremity
ischemia.

Etiology and Presentation

Peripheral arterial occlusive disease due to ath-
erosclerosis is the most common cause of lower
extremity ischemia in developed countries, with
3% to 6% of the population over the age of 65
suffering from symptomatic disease. The clini-
cal presentation of long-standing ischemia can
be variable, with symptoms ranging from inter-
mittent claudication to rest pain, arterial ulcers,
and frank gangrene. The classic progression of
symptoms in atherosclerotic lower extremity
ischemia is (1) decreased pulses without any
symptoms, (2) intermittent claudication, (3) rest
pain, and (4) arterial ulceration or gangrene
(Fig. 9.1). Patients with limited ambulation due
to other causes (e.g., stroke, musculoskeletal dis-
orders) or diabetic neuropathy may present ini-
tially with evidence of advanced ischemia such
as arterial ulceration or frank gangrene. Limb
ischemia should always be considered in the
evaluation of the older patient who presents
with a nonhealing ulcer of the lower extremities,
or with an extensive or persistent skin or soft
tissue infection of the foot.

Other causes of limb ischemia include
embolic or thrombotic sequelae of aortic or
peripheral aneurysms, embolization from the
heart or proximal arterial sources, and arterial
dissection (usually aortic). More unusual causes
include popliteal entrapment syndrome, ad-
ventitial cystic disease, and Buerger's disease
(thromboarteritis obliterans). Some of these eti-
ologies such as embolization or thrombosis of

VASCULAR SURGERY

Loss of pulses

Claudication

Rest pain

Gangrene/Ulceration

Figure 9.1 . Chronic limb ischemia, progression of disease. Atherosclerosis leads to arterial occlusion, resulting in loss of pulses fol-
lowed by claudication. In patients with mild peripheral arterial disease, the best treatment option is risk factor modification and exer-
cise. In more severe cases there is rest pain, which usually occurs at night followed by gangrene (photo insert) or ulceration. Rest pain
and gangrene/ulceration are considered limb threatening ischemia and the surgical options are amputation or revascularization.
Aggressive attempts at revascularization are usually undertaken in ambulatory patients.

an aneurysm present as acute limb ischemia,
which is characterized by the 5 P's: pulseless-
ness, paralysis, paresthesia, poikilothermia
(coolness), and pallor.

Chronic Ischemia

Patient History

Patients are often referred for vascular evalua-
tion if they have reproducible pain in the lower
extremities with walking. Although many disor-
ders can cause these symptoms, several basic
questions can be asked to ascertain a vascular
etiology. Patients with vascular claudication
always have pain when they walk a relatively
constant distance on level ground; they do not
have variable days when they can walk for con-
siderably greater distances without pain. Often
patients know exactly how far or for how long
they can walk before the symptoms occur. This
is in contrast to patients with neurogenic clau-
dication or musculoskeletal causes of lower
extremity pain, where the symptoms occasion-
ally occur at rest or at with highly variable
walking distances. Stopping results in resolution
of vascular claudication within a few minutes,

and this resolution occurs if the patient simply
stops and stands in place. Patients with neuro-
genic claudication usually have to sit down to
relieve their pain. Neurogenic claudication and
musculoskeletal pain are often induced by
standing in one place for prolonged periods
(waiting in line at the bank or washing dishes).
This is not the case with vascular claudication,
where lower extremity muscular oxygen
demands are not as greatly increased by
standing as they are by prolonged walking.
Neurogenic claudication is relieved by leaning
forward, so patients with this disorder often
note that they can lean forward onto a grocery
cart or lawn mower and go substantially further
than they can walk unaided. Similarly, the
patient with neurogenic claudication often can
walk further on an incline, whereas vascular
claudication is marked worsened if the patient
is on an incline. Patients with musculoskeletal
disorders often have pain that is present at rest,
or worsened by standing or sitting in certain
positions. The pain in neurogenic claudication
often is described as originating in the thigh
and then extending down the leg, which is quite
different from the focal posterior calf pain
usually noted in vascular claudication. Together,
these aspects of the history of the patient's

LOWER LIMB ISCHEMIA

symptoms help differentiate vascular from neu-
rogenic claudication.

More pronounced ischemia results in pain at
rest, which also has specific features that distin-
guish it from the many other causes of lower
extremity pain. Ischemic rest pain occurs when
the blood flow to the foot is decreased to the
point where ischemia of the sensory nerves
occurs, hence the burning causalgia-like quality
of the pain. Cardiac output decreases with sleep,
and most patients describe symptoms that are
initially present only at night. As the ischemia
becomes advanced, the pain is present con-
stantly. The more distal aspects of the lower
limb are the most ischemic, and rest pain is
most commonly described as occurring across
the metatarsal heads of the affected foot.
Ischemic pain awakens the patient from sleep
and is relieved by dangling the affected limb
over the edge of the bed, which patients quickly
learn will allow uninterrupted sleep. Alterna-
tively patients awakened by the pain find that
rubbing the foot or walking to stimulate circu-
lation relieves the pain. Dangling (or standing)
causes the perfusion pressure of the foot to be
augmented by the hydraulic pressure due to the
gravity component of the height of the calf.
This is approximately 40 cm of water pressure
(length of the calf), which equals a 29mmHg
augmentation of foot perfusion pressure.
This increase is enough to overcome the critical
closing pressure (CCP) of the precapillary
sphincter in the vascular bed and restore flow to
the ischemic regions of the foot. With progres-
sion of disease and more pronounced ischemia,
this maneuver no longer provides relief as the
net pressure falls below the CCP and capillary
perfusion ceases. Several other disorders cause
lower extremity pain at night and can be
confused with ischemic rest pain. Diabetic leg
cramps are quite common and occur at night,
but the site of pain is variable and the pain often
migrates up or down the leg. Musculoskeletal
pain rarely occurs in the midfoot at night, and
is usually localized to the joint in question
(commonly the ankle or knee). Musculoskeletal
causes of foot pain are usually exacerbated by
walking or standing and relieved by rest, in con-
trast to ischemic pain. Infections in the foot,
particularly osteomyelitis, can cause constant
pain at rest but are often easily recognized due
to other signs and symptoms.

History-taking in the patient with lower
extremity ischemia should also focus on
symptoms of atherosclerosis in other vascular
beds, particularly the cerebral and coronary
circulation. Patients with symptomatic lower
extremity ischemia have a 20% to 60% in-
cidence of significant coronary artery disease,
and the coexistence of cerebrovascular and
lower extremity arterial occlusive disease is also
well established. Symptoms of angina, conges-
tive heart failure, and transient ischemic attacks
or strokes should be diligently investigated as
many patients may ascribe these symptoms to a
nonvascular cause and may not volunteer this
important information. The history should also
include any prior events, such as blue or painful
toes, which may be suggestive of an embolic
cause of the ischemia.

Physical Examination

The physical examination should be complete
and focused on the detection of occlusive and
aneurysmal disease throughout the peripheral
circulation. The presence (or absence) of carotid
bruits, cardiac arrhythmias, peripheral pulses,
and bruits should be documented, and any prior
scars consistent with arterial bypass surgery
or vein harvest should be noted. This is of par-
ticular importance when planning reoperative
infrainguinal bypass surgery, which may involve
harvesting autogenous vein from multiple
sites and limbs. The stigmata of chronic occlu-
sive or embolic disease should be diligently
sought, including muscle atrophy, loss of sec-
ondary skin structures such as hair and nails,
dependent rubor, splinter hemorrhages, and
embolic skin lesions or dusky toes. Nonpalpable
pulses should be interrogated with a handheld
Doppler, and a bedside ankle — brachial index
(ABI) determined with an inflatable blood pres-
sure cuff placed above the site of the Doppler
signal and then at the wrist. Peripheral and
aortic aneurysms may be difficult to detect on
physical examination, particularly in the obese
patient. A wide or easily palpable popliteal pulse
is suspicious for a popliteal aneurysm, and eval-
uation with ultrasound or computed tomogra-
phy (CT) scanning is indicated to determine the
true diameter of the vessel.

More advanced limb ischemia may be asso-
ciated with arterial ulcers or frank gangrene.

VASCULAR SURGERY

Arterial ulcers are distinguished from venous
ulcers by their location on the more distal
aspects of the foot, and their exquisite sensitiv-
ity to touch. They appear as small, dry, punched-
out lesions in the skin, and have often been
present for long periods of time without evi-
dence of granulation tissue or scar contracture
at the edges. Larger ulceration located at the
ankle, particularly if moist or weeping, is more
characteristic of venous disease, although
patients with combined arterial and venous
insufficiency may present with long-standing
ankle ulceration that fails to heal despite
aggressive treatment of venous insufficiency.
All patients with presumed venous ulceration
should undergo examination of peripheral
pulses, and if not present, prompt evaluation for
arterial ischemia and consideration for revascu-
larization. Even moderate degrees of arterial
insufficiency in conjunction with venous
insufficiency may result in failure of a primarily
venous ulcer to heal. Similarly, mo derate arterial
occlusive disease (ABI 0.4 to 0.5), which ordi-
narily does not cause tissue loss, may cause a
surgical incision in the lower extremity not to
heal in a timely fashion. This is most commonly
seen after harvest of the lower aspect of the
greater saphenous vein for coronary artery
bypass surgery, but can occur after orthopedic
or podiatric surgery in the lower limb.

Gangrene of a toe may be produced by
advanced ischemia alone, or can be secondary
to infection, particularly in diabetic patients. If
associated with infection, the infectious process
often extends further into the forefoot than the
extent of cutaneous changes. Less frequently a
patient presents with isolated toe gangrene or
pregangrenous changes (blue toe) without evi-
dence of either infection or advanced ischemia
of the limb. This scenario, particularly if present
in more than one toe, and especially if found in
nonadjacent toes, is suspicious for embolic
disease, or so-called blue-toe syndrome. If the
involved toes are on both feet, then an embolic
source proximal to the aortic bifurcation is the
cause. All patients with evidence of chronic
peripheral embolization should undergo
echocardiography and complete angiography of
the thoracic and abdominal aorta, ileofemoral
system, and proximal aspect of the involved
limbs. Embolic sources can include proximal
aneurysms, which may not be readily detectable
by angiography, and ultrasound examination of

the aorta and femoral and popliteal arteries
should be performed.

Diagnostic Studies

The history and physical examination generally
facilitate classification of the degree of arterial
insufficiency. Diagnostic studies are indicated
when the diagnosis is in question, or in prepa-
ration for intervention. Noninvasive vascular
testing is also useful in establishing the degree
of ischemia when there are other confounding
factors present, such as venous disease, diabetic
foot ulcers, or active infection. Usually the ABI
facilitates accurate determination of the degree
of limb ischemia; however, several conditions
exist in which the ABI and segmental pressures
may be falsely elevated. These include diabetes,
chronic renal failure, and advanced age (over 80
years), which can cause calcification of the
medial layer of the arterial wall, which in turn
causes incompressibility and subsequent false
elevation of any cuff-based determination of
peripheral perfusion pressure. An ABI of greater
than 0.9 is associated with a readily palpable
pulse, and the absence of a pulse with such an
ABI value is evidence of incompressibility. In
these cases several alternatives can be used to
establish the diagnosis of arterial ischemia. A
toe cuff can be used to determine a toe —
brachial index (TBI), as the medial calcification
rarely extends into the vessels of the foot. The
waveform tracings from the pulse volume
recorder are not altered by vessel calcification,
and examination of the contour of these wave-
forms at the various arterial levels can suggest
the site of the occlusive lesions. Flattened wave-
forms at the ankle or more distal level or a TBI
less than 0.6 is an indication of arterial insuffi-
ciency. More sophisticated diagnostic measures
such as transcutaneous oxygen measurement
are sometimes useful to determine perfusion
in the foot of patients with confounding
factors such as lymphedema or severe venous
insufficiency.

Exercise testing plays an important role in the
subset of patients with symptoms of early occlu-
sive disease despite relatively normal perfusion
at rest. Increasing lower extremity blood flow by
treadmill testing can accentuate the gradient
across a moderate stenosis and demonstrate a
drop in distal perfusion pressures after exercise
that is not present at rest. This is based on

LOWER LIMB ISCHEMIA

Poiseuille's law where the pressure drop across
a stenosis is directly proportional to the volume
flow across the lesion. Patients with a normal
ABI at rest and a decreased ABI after exercise
testing are uncommon and almost always
have aortoiliac occlusive disease. Many patients
cannot complete exercise testing on a treadmill
because of angina or pulmonary dysfunction;
however, a normal ABI after exercise testing
excludes arterial insufficiency as a cause of
lower extremity pain with walking.

Imaging studies of the aorta and lower
extremity arteries are not necessary to deter-
mine the presence or extent of arterial
insufficiency and are thus reserved for planning
interventions to revascularize the lower extrem-
ity. The most widely used study is contrast
angiography, although duplex scanning and
magnetic resonance angiography are less inva-
sive modalities that can provide images that can
obviate the need for conventional angiography.
These are utilized in patients with documented
adverse reactions to contrast agents, or with
renal insufficiency that increases their risk of
contrast-induced nephropathy. In most patients,
contrast angiography provides the most de-
tailed information to direct catheter-based or
surgical limb revascularization. Other imaging
modalities that play a lesser role in the evalua-
tion of limb ischemia include CT scans and
ultrasound studies to determine the presence
of aortic and peripheral aneurysms (especially
as sources of emboli), echocardiography to
evaluate potential cardiac embolic sources, and
duplex evaluation of veins preoperatively for
use as bypass conduits.

Treatment

Mild to moderate limb ischemia that does
not warrant invasive revascularization can be
followed with serial examinations. An ABI
determination is obtained at the initial visit to
establish a baseline, as this measure may
improve with exercise or deteriorate with pro-
gression of disease. The emphasis in treatment
of these patients is on risk factor modification
to prevent progression of disease and con-
currently increase longevity, and a walking
program to encourage exercise and increase
exercise tolerance. The most common causes of
death in patients with symptoms of lower
extremity arterial insufficiency are ischemic

cardiac disease and cerebrovascular disease,
which are both responsive to reduction of the
same causative risk factors as lower extremity
ischemia. An important risk factor reduction is
cessation of tobacco use, and management of
dyslipidemia, diabetes, and hypertension also
plays a role. A critical factor is reassurance to
patients and their family that disease progres-
sion to critical limb ischemia and possible
amputation, which is many patients' greatest
fear, is unlikely, particularly with cessation of
further tobacco use. The 10-year risk of limb
loss with claudication is less than 10%, and
often simply alleviating this fear is the most
valuable aspect of evaluation and treatment of
mild to moderate limb ischemia.

A wide range of pharmacological agents
and alternative therapies have been utilized to
treat the symptoms of mild to moderate limb
ischemia. Unfortunately, controlled clinical
trials coupled with careful evaluation of long-
term improvement have demonstrated a consis-
tent lack of benefit for the vast majority of
agents tested. This includes vasodilator drugs,
pentoxifylline, antiplatelet and antithrombotic
drugs, chelation therapy, and a variety of herbal
medications such as gingko. The agents that
have been shown to be of some value in con-
trolled clinical trials include cilostazol, a phos-
phodiesterase inhibitor that cannot be used in
patients with cardiac dysfunction, the Tibetan
herbal supplement Padma Basic, and high doses
of L-arginine, the amino acid precursor of
the endogenous vasodilator nitric oxide. The
benefit in walking distance with these agents,
although statistically significant in clinical
trials, is often minimal in terms of functional
improvement for the patient. For example in a
randomized multicenter trial, the mean walking
distances after 4 weeks of either cilostazol or
placebo were 306 versus 267 m (Money et al.,
1998). It is unclear whether these minimal
increases represent a meaningful improvement
over a graduated exercise program alone.
Studies of graded exercise programs have
demonstrated that motivated patients can
double their walking distance; however, this
requires walking to near-maximal pain levels
for 30 minutes on a regular basis for at least 6
months (Gardner and Poehlman, 1995).

Many patients with moderate chronic limb
ischemia have symptoms that they consider dis-
abling, and seek revascularization to increase

VASCULAR SURGERY

their ability to exercise or perform job-related
tasks. The role of revascularization, whether
catheter-based or surgical, in patients with
claudication remains controversial. Factors that
should be considered include ongoing cigarette
use, the patient's commitment to exercise and
physical activity, and the anatomical level of
occlusive disease that requires correction. Aor-
toiliac occlusive disease, as judged by physical
examination and noninvasive studies, can be
treated well by angioplasty and stenting with
minimal risk to the patient. More extensive
disease, particularly involving either the
infrarenal aorta or the external iliac arteries, is
better treated with aortobifemoral bypass graft-
ing. The long-term results of aortobifemoral
bypass grafting are excellent, with patencies
exceeding 90% at 5 years. Although aortoiliac
endarterectomy was the first procedure devel-
oped for the treatment of occlusive disease of
these vessels, it has largely been replaced by
bypass grafting. Extensive unilateral disease,
particularly occlusion of the external iliac
artery, can often be treated with femoral-
femoral bypass grafting. This is a procedure of
substantially smaller magnitude than an aorto-
bifemoral bypass, and is often the procedure of
choice in patients with coexisting cardiac and
pulmonary disease. Femoral-femoral bypass
requires normal flow in the contralateral ile-
ofemoral system, and mild to moderate disease
of the contralateral artery can be treated with
angioplasty and stenting to obtain sufficient
inflow to support the femoral-femoral bypass
graft. Although some centers have advocated
axillofemoral bypass grafts for mild to
moderate limb ischemia and claudication, our
policy is to reserve this form of extensive extra-
anatomical bypass for poor-risk patients with
limb-threatening ischemia or when revascular-
ization is required after removal of infected
aortic grafts.

Occlusive disease of the distal superficial
femoral artery, another common site in mild
to moderate limb ischemia, generally requires
bypass with either prosthetic or autologous
grafts (Table 9.1). Femoral-popliteal bypass
grafting is often performed with excellent
results in patients with disabling claudication.
A randomized prospective trial of prosthetic
versus greater saphenous vein bypass grafts
in the femoral to above-knee popliteal artery
did not demonstrate a difference in long-term

Table 9.1 . Conduits for revascularization

Axillofemoral, aortofemoral,

Dacron or ePTFE

femoral-femoral

Femoral: above the knee

Autologous vein,

Dacron, or PTFE

Femoral: below the knee

Autologous vein

PTFE, polytetrafluoroethylene; ePTFE, expanded PTFE.

patency (Veith et al., 1986). A randomized mul-
ticenter trial demonstrated an improved graft
patency and decreased risk of subsequent
amputation with heparin-bonded Dacron grafts
in comparison to polytetrafluoroethylene
(PTFE) grafts (Devine et al., 2001), and repre-
sents the first major advance in synthetic vas-
cular grafts that has been shown to improve
clinical results relative to standard materials.
Self-expanding and balloon-expandable stents
in conjunction with balloon angioplasty are
being applied to stenoses and occlusions of the
distal superficial femoral artery with improving
results, and are extending the ability to provide
percutaneous revascularization of moderate
lower limb ischemia.

Occlusive disease of the popliteal artery or
more distal vessels, although uncommon in the
nondiabetic patient with claudication, requires
bypass with autogenous vein to the distal
popliteal artery or tibial vessels. These proce-
dures are generally reserved for more severe
ischemia where salvage of the extremity is in
question. If there is calf claudication with exten-
sive occlusive disease of the proximal aspects of
the tibial arteries, a femoral-tibial bypass to a
distal vessel may result in excellent perfusion of
the foot with minimal relief of claudication.
This is due to the lack of retrograde perfusion
to the geniculate arteries that supply the major
muscles of the upper calf.

More advanced ischemia of the lower limb
generally requires a more aggressive approach
to revascularization if long-term viability of the
limb is to be preserved. The need for revascu-
larization needs to be combined with a complete
evaluation of the medical and functional status
of the patient. Patients with critical limb
ischemia, which presents with rest pain, arterial
ulcers, or frank gangrene, commonly have mul-
tilevel occlusive disease, which usually requires

LOWER LIMB ISCHEMIA

major surgical revascularization to achieve
long-term limb salvage. They also have corre-
spondingly more advanced atherosclerosis in
their coronary and cerebrovascular circulation,
and their perioperative morbidity and mortal-
ity is higher than for patients with claudication.
The incidence of renal insufficiency or chronic
failure as well as diabetes is higher in patients
who present with signs of critical limb ischemia,
and these medical factors have been noted in
several multivariate analyses to be independent
predictors of poor outcomes and higher mor-
tality after arterial reconstruction.

Revascularization in patients with critical
limb ischemia often requires correction of
both aortoiliac and infrainguinal (femoral-
popliteal-tibial) occlusive disease. In patients
who present with advanced tissue loss or gan-
grene and multilevel occlusive disease, restora-
tion of in-line arterial flow to the foot is
required to heal the large tissue defects. A com-
bination of percutaneous treatment of the aor-
toiliac disease (if anatomically suitable) with
femoral-popliteal or femoral-tibial bypass can
be used to rapidly restore foot perfusion in
these cases. If the presenting ischemic symp-
toms are rest pain or small arterial ulcers, then
correction of one level of occlusive disease
(usually the aortoiliac) with angioplasty/stent-
ing or surgical bypass relieves the symptoms.

The conduit of choice for femoral-tibial
bypass, or femoral-popliteal bypass with poor
runoff is the greater saphenous vein (Table 9.1).
Prospective studies comparing reversed versus
in situ saphenous vein grafts have not demon-
strated a difference in patency or limb salvage
rates between the two techniques (Harris et al.,
1987). In many patients with critical limb
ischemia, the ipsilateral greater saphenous vein
is not available for use as a conduit due to prior
harvest or vein stripping. If the contralateral
greater saphenous vein is not available, then
secondary sources of autogenous vein such as
the lesser saphenous vein or arm veins should
be preoperatively mapped by duplex scanning
and utilized. The use of spliced segments of
autologous vein was recently compared to PTFE
grafts with vein cuffs in a randomized prospec-
tive trial of patients without an available greater
saphenous vein (Kreienberg et al., 2002).
Patency was greater in the spliced arm vein
group (87% vs. 59% at 2 years) with similar rates
of limb salvage (94% and 85%). Alternative

choices for conduit include cryopreserved
cadaver saphenous vein, umbilical vein grafts,
conventional prosthetic grafts (PTFE and
Dacron), and heparin-bonded Dacron. These
have variable patency rates, all of which are infe-
rior to saphenous vein or spliced autologous
veins when utilized for femoral-tibial bypass.

A useful technique in patients with limited
amounts of available vein is to originate the
graft from a more distal site than the common
femoral artery, thus requiring shorter segment
of vein conduit. Long-term patency is not com-
promised by originating the graft from the deep
femoral artery, the superficial femoral artery, or
the popliteal artery provided that there is not
significant occlusive disease above the inflow
site (Wengerter et al., 1992). Autogenous vein
grafts should be studied postoperatively along
their entire length periodically with duplex
ultrasound to identify potential areas of mid-
graft stenosis, which should be corrected with
either balloon angioplasty or surgical repair
before graft thrombosis occurs.

Many patients with critical limb ischemia
are bedridden or do not ambulate because of
neurological or musculoskeletal problems. In
these patients, primary amputation is a safer
and more expeditious means of dealing with
foot gangrene than surgery for revasculariza-
tion. The level of amputation, which is always
of great patient concern even when ambula-
tion is not an issue, is determined by the ambu-
lation potential of the patient and the degree
of perfusion required to heal the amputation.
Although there are numerous guidelines and
means of measuring skin perfusion to deter-
mine the appropriate level of amputation,
clinical judgment remains the final factor.
Enthusiasm for various quantitative means of
measuring limb and skin blood flow has been
tempered by prospective studies of these
various techniques, which have failed to identify
one quantitative test that preoperatively esti-
mates probability of healing with sufficient
positive and negative predictive value. Transcu-
taneous oxygen testing (TcP0 2 ) is the most
readily available of these sophisticated blood
flow measurements, which include radiolabeled
xenon washout, laser Doppler velocimetry, and
photoplethysmography perfusion studies. A
TcP0 2 of greater than 40mmHg at the level of
proposed amputation is predictive of healing,
and a TcP0 2 of less than 20mmHg is indicative

VASCULAR SURGERY

of a high likelihood of failure to heal. Unfortu-
nately, many patients with lower extremity
ischemia fall into the range of 20 to 40mmHg,
where clinical judgment must be used to decide
on the level of amputation.

We recommend attempting a below-knee
amputation in any ambulatory patient with rea-
sonable rehabilitation potential in whom there
is detectable popliteal artery Doppler signal.
This approach is based on the known benefits
with preservation of the knee joint for ambula-
tion, and will predictably result in a small
number of failures that require revision as a cost
of salvaging as many below-knee amputations
as possible. In the nonambulatory patient with
advanced ischemia, a primary above-knee
operation is performed if perfusion at the level
of the popliteal artery is poor or nondetectable.
Although there is some benefit to preservation
of the knee joint even in the nonambulatory
patient for aid in transferring from bed, major
amputations in this population carry at least a
10% to 15% mortality per procedure and it is
recommended to perform a single definitive
above-knee procedure if there is questionable
perfusion in a nonambulatory patient.

Outcomes

There has been a steady improvement in limb
salvage rates due to refinements in both percu-
taneous and surgical revascularization for
chronic limb ischemia. In particular, the wide-
spread application of femoral-tibial bypass
has led to revascularization of limbs that until
recently would have been deemed inoperable.
Awareness of limb ischemia as a cause of non-
healing ulcers and patient and practitioner edu-
cation are responsible for earlier evaluation and
referral of patients for revascularization. The
success of aortoiliac angioplasty and stenting
has led to relief of claudication in patients
without the morbidity and length of hospital stay
previously associated with aorto femoral bypass.
Despite the advances in percutaneous and
surgical revascularization, a large number of
patients with critical limb ischemia will eventu-
ally undergo an amputation (>50,000 cases per
year in the United States). Many patients are
not candidates for standard revascularization
techniques because of anatomical or medical
factors. The discovery that endogenous peptides
can induce growth of new blood vessels (angio-

genesis) has spurred interest in applying angio-
genic therapy to patients with limb ischemia.
Preliminary results with growth factors such
as fibroblast growth factor are encouraging
(Lederman et al., 2002), and further studies are
needed to define the optimal growth factor,
route of delivery, and duration of therapy. Sim-
ilarly, the finding that circulating bone
marrow — derived stem cells contribute to the
angiogenesis and spontaneous revasculariza-
tion seen in experimental hindlimb ischemia
has led to trials of stem cell therapy for the treat-
ment of chronic limb ischemia in humans, with
promising preliminary results (Tateishi-Yuyama
et al., 2002). These areas of investigation should
lead to therapies for critical limb ischemia that
will complement surgical revascularization and
extend our ability to provide limb salvage.

Acute Ischemia

Patient History

The most important determination in the eval-
uation of acute limb ischemia is whether the
ischemia is due to an arterial embolus or throm-
bosis of a chronically diseased artery. Two
aspects of the patient's history contribute to this
decision. The first is the onset of symptoms.
Embolic occlusion of a normal arterial bed
results in sudden onset of symptoms, and the
patient can often recollect the exact moment of
onset of the ischemia. In contrast, thrombotic
occlusion of a diseased native artery occurs
more gradually, with symptoms often worsen-
ing over several days. The second important
aspect of the history is the presence or absence
of chronic peripheral arterial occlusive disease,
which is more frequently associated with
thrombosis rather than embolism. Thus the
presence of previous symptoms such as claudi-
cation or rest pain, or a history of prior
interventions for peripheral arterial occlusive
disease, strongly suggests that the acute
ischemia is secondary to thrombosis of a dis-
eased vessel or bypass graft. Many of these
patients have an antecedent history of acute
dehydration from gastrointestinal causes or
poor perfusion, from acute cardiac dysfunction.
Conversely a lack of prior claudication coupled
with the presence of risk factors for arterial
embolization (atrial fibrillation, a recent

LOWER LIMB ISCHEMIA

myocardial infarction, dilated cardiomyopathy,
or prior embolic event) is more consistent with
either arterial embolization or another unusual
nonatherosclerotic cause of acute ischemia such
as dissection or thrombosis of a peripheral
aneurysm. Unfortunately, this maxim cannot
always be relied on, as up to 25% of patients
with embolism as a cause of acute limb ischemia
have long-standing signs and symptoms of
prior peripheral arterial occlusive disease.

Physical Examination

Acute limb ischemia is characterized by the five
P's: pulselessness, paralysis, paresthesia, pain,
and pallor. The level of arterial occlusion is gen-
erally one anatomical level higher that the clin-
ical manifestation of the ischemia. Thus patients
with an embolus lodged in the proximal superfi-
cial femoral artery present with an ischemic
calf. The severity of the ischemia can be deter-
mined from the physical findings, with pain and
pallor occurring early and paresthesia and
paralysis being later findings. Paresthesia is due
to direct ischemia of the sensory nerves within
the extremity and is often reversed with prompt
revascularization. Paralysis can be due to either
ischemia of the motor neurons or muscle death.
Muscle death can be determined on examina-
tion by rigidity of the ischemic muscle to pal-
pation (rigor) and corresponding difficulty
moving the joints with passive motion. If skele-
tal muscle death has occurred, there is little to
no chance for meaningful limb salvage.

A major problem with diagnosis of acute
limb ischemia remains the failure to consider
ischemia as a cause of acute symptoms in the
limb, leading to delays in treatment that can lead
to limb loss. These delays are usually seen in
patients without known prior peripheral vascu-
lar disease, such as those with undiagnosed
popliteal aneurysms, aortic dissection, or
(most commonly) arterial embolism. The most
common misdiagnosis is a primary neurologi-
cal problem, such as spinal cord impairment or
stroke, to which the paresthesia and paralysis of
ischemia is attributed.

Diagnostic Studies

The history and physical examination in acute
limb ischemia are focused on the critical issue

of whether the occlusion is due to embolism
or thrombosis of a diseased artery, as this dis-
tinction leads to either immediate surgical
embolectomy or preoperative angiography to
delineate the cause of ischemia. The arteries of
the lower extremity have tremendous capacity
for collateral flow, and thus thrombosis of a
native artery occurs only when atherosclerotic
lesions are very advanced. Such advanced ath-
erosclerosis is usually symmetrical, and the con-
tralateral limb does not have a normal pulse
exam. The presence of normal pulses in the
contralateral limb is highly suggestive of an
embolism as a cause of acute ischemia, and
warrants operative embolectomy without the
delay associated with preoperative angiography.
Unfortunately, the converse is not always true,
as signs and symptoms of prior peripheral
arterial occlusive disease do not guarantee
that the acute ischemia is due to thrombosis
rather than embolism. Thus the presence of
significant peripheral arterial occlusive disease
(defined by both prior symptoms or physical
findings in the contralateral limb) in patients
with acute limb ischemia is an indication for
angiography. Angiography definitively identi-
fies the cause of the acute ischemia and delin-
eates the proximal and distal arterial anatomy
should a bypass be required either immediately
or subsequently to relieve ischemia. Nonem-
bolic causes of acute ischemia include
thrombosis of a chronically diseased vessel,
thrombosis of a previous bypass graft, throm-
bosis of a peripheral aneurysm (particularly a
popliteal aneurysm), and proximal arterial dis-
section (usually aortic). The treatment of these
conditions is quite varied, and immediate surgi-
cal exploration without angiography is often
unsuccessful in restoring flow. In many cases,
angiography is not only diagnostic but is thera-
peutic in terms of initiating thrombolytic
therapy for occlusion of bypass grafts or throm-
bosed popliteal artery aneurysms. Aside from
assessment of limb perfusion by Doppler exam-
ination, immediate angiography is the only
diagnostic study utilized in the evaluation of
acute limb ischemia.

Treatment

For any form of acute limb ischemia, systemic
anticoagulation with intravenous unfraction-
ated heparin is immediately instituted while

100

VASCULAR SURGERY

preparations are made for surgery or angiogra-
phy. Patients with known sensitivity to heparin
or a documented history of heparin-induced
thrombocytopenia can be treated with direct
thrombin inhibitors. Anticoagulation alone
usually does not relieve the ischemia, but it
helps prevent further propagation of the throm-
bus and preserve flow in collateral vessels
around the occlusive thrombus. The specific
treatment of acute limb ischemia rests on pre-
operative establishment of the cause of the acute
ischemia. In a patient with a prior history of
peripheral bypass surgery, the most common
cause of acute limb ischemia is thrombotic
occlusion of the bypass graft. In these patients,
as well as patients with preexisting chronic
peripheral vascular occlusive disease, preopera-
tive angiography is usually obtained to deter-
mine the location of the occlusion and the
inflow and outflow sites for bypass grafting. Pre-
operative angiography is not utilized in those
cases of advanced acute ischemia where the
location of the problem is clinically obvious,
such as a patient with a prior aortobifemoral
bypass graft, an absent femoral pulse, and a pro-
foundly ischemic limb. The delay associated
with obtaining preoperative angiography is also
avoided in patients with suspected arterial
embolism, which is treated with emergent
catheter embolectomy.

Restoration of a functional and viable intact
limb is extremely rare when skeletal muscle
death has already occurred. If physical exami-
nation suggests that limb paralysis is due to
death of the skeletal muscle, then the status of
the muscle is determined by operative explo-
ration. The high likelihood of amputation is dis-
cussed with the patient and family members
prior to surgery, and primary amputation is per-
formed if there is no bleeding from the muscle
and no muscle contraction with direct electrical
stimulation. Aortoiliac revascularization maybe
subsequently required to obtain adequate blood
flow to allow healing of the definitive amputa-
tion site.

Treatment of lower limb ischemia secondary
to aortic dissection can be either directed at cor-
recting the dissection or an extra-anatomical
bypass to relieve the limb ischemia. Correction
of the underlying dissection may require
surgical repair of the thoracoabdominal aorta,
although these procedures are formidable
undertakings in patients who are often critically

ill with concurrent renal, mesenteric, or spinal
cord ischemia. Mortality rates approaching 40%
have been reported from major centers in
patients with coexisting cardiac and renal
disease. Advances in catheter-directed therapy
for acute dissection are allowing rapid restora-
tion of perfusion to the involved branches of the
aorta without the physiological stress of opera-
tive repair of the thoracoabdominal aorta
(Slonim et al., 1996). These procedures include
endovascular stenting of dissections within the
thoracic aorta and catheter-based percutaneous
fenestration to restore perfusion to both false
and true aortic lumina.

For limb ischemia secondary to suspected
femoral, iliac, or aortic bifurcation emboli,
embolectomy is performed via the common
femoral artery. For bilateral limb ischemia
where the embolus is lodged in the aortic bifur-
cation, bilateral transfemoral embolectomy is
performed. Catheter embolectomy should be
performed both proximally and distally from
the common femoral artery. This is usually per-
formed through a transverse arteriotomy in the
common femoral artery placed opposite the
orifice of the deep femoral artery to facilitate
passage of the catheter into both the superficial
and deep femoral arteries. The first priority
should be establishment of adequate inflow to
the common femoral artery. This is usually
accomplished easily with catheter embolectomy,
but occasionally the arterial flow from the exter-
nal iliac artery may be unsatisfactory even after
removal of all possible thrombus. This is usually
due to preexisting chronic occlusive disease
of the iliac arteries, but can also be caused
by dissection of a diseased vessel during the
embolectomy. There are two options to manage
inadequate inflow after transfemoral em-
bolectomy. The traditional solution is surgical
bypass, usually with a femoral-femoral or
axillofemoral graft. More recently, intraopera-
tive angioplasty and stenting of the iliac system
can be used to treat occlusive disease or dissec-
tion of the ipsilateral iliac arteries. This can be
performed via either an ipsilateral retrograde
approach or the contralateral femoral artery.
The use of angioplasty and stenting in this
setting can often restore adequate inflow more
rapidly than constructing an extra-anatomical
bypass, and is the procedure of choice if
the appropriate expertise and equipment are
available.

101

LOWER LIMB ISCHEMIA

Caution must be taken when restoring blood
flow to the severely ischemic limb, as the stag-
nant and ischemic venous blood contains toxic
metabolites from the limb. Sudden return
into the systemic circulation can be associated
with serious complications including acido-
sis, cardiac arrhythmias, or arrest and renal
damage. Release of the venous return from the
ischemic limb to the body is done in close
cooperation with the anesthesiologists, and
administration of antiarrhythmic agents,
sodium bicarbonate, and mannitol may be
required. In patients with prolonged ischemia,
particularly those with preexisting cardiac dys-
function, consideration is given to draining the
initial venous return from the limb to prevent
flow of these toxic metabolites back to the cir-
culation of a compromised patient. The com-
mon femoral vein is encircled at the level of the
inguinal ligament with a Rummel tourniquet
and the first 300 to 600 mL of venous blood is
exsanguinated via a transverse venotomy at the
time that arterial inflow to the limb is restored.
Appropriate replacement with banked blood is
essential to maintain adequate cardiac output
and oxygen delivery, and should be done con-
currently with the venous drainage.

Most emboli of cardiac origin lodge in the
common femoral or proximal superficial fe-
moral artery. Smaller emboli may lodge in the
popliteal artery, and embolic occlusion of indi-
vidual tibial arteries from a cardiac source is
unusual. Once adequate inflow to the common
femoral artery is established as described above,
the embolectomy catheter is directed distally
down the superficial femoral artery to retrieve
distal thromboemboli. Restoration of back-
bleeding from the superficial femoral artery is
followed by embolectomy of the profunda
femoris artery, which is rarely the site of
embolization. Propagation of a secondary
thrombus, however, does occur in the proximal
aspect of this vessel, although more distal seg-
ments remain patent due to collateral circula-
tion via the numerous branches. Transfemoral
embolectomy of the distal circulation may
sometimes not result in restoration of a satis-
factory Doppler signal at the level of the ankle.
There may be subsequent propagation of
thrombus distally into tibial vessels, or frag-
ments of more proximal emboli may become
dislodged into the distal circulation during
catheter embolectomy. In this case on-table

angiography is performed to determine the
location and amount of residual thrombus. If
thrombus is found in the proximal aspects of the
individual tibial arteries and blood flow to the
remains poor, then more distal embolectomy is
performed to restore blood flow to the foot. This
is usually performed via the infrageniculate
popliteal artery, which is exposed via a medial
incision down distally to the tibioperoneal
trunk in order to allow the passage of the
embolectomy catheter into each of the tibial
vessels. If the infrageniculate popliteal artery is
small or diseased, a longitudinal arteriotomy is
closed after embolectomy with a small vein
patch; otherwise a transverse arteriotomy can
be primarily closed with interrupted sutures.

Irrigation of the distal circulation with
heparinized saline containing papaverine helps
relieve spasm of the tibial vessels induced by
passage of the embolectomy catheter. Intra-
operative instillation of thrombolytic therapy,
usually urokinase or streptokinase, has been
described as a means of treating residual
thrombus that cannot be retrieved by catheter
embolectomy. Dramatic increases in patency of
the distal circulation have been noted after
intraoperative thrombolytic therapy, and this
technique is particularly useful when there
appears to be insufficient runoff to maintain
patency of either a distal bypass graft or the
native proximal popliteal artery.

Arterial bypass plays an important role in the
management of acute limb ischemia, particu-
larly in patients with ischemia secondary to
thrombosed popliteal artery aneurysms, arte-
rial dissection of the ileofemoral arteries, or
thrombosis of a chronically diseased aortoiliac
segment. Bypass operations for acute occlusion
of the aortoiliac segment include aortofemoral
bypass, femoral-femoral bypass, and axillo-
femoral bypass. The latter two are less extensive
procedures that are particularly useful in the
emergent management of acute aortoiliac
thrombosis secondary to acute medical illness
such as cardiogenic shock. The femoral-femoral
bypass is performed for acute unilateral
ischemia if embolectomy fails to restore ade-
quate inflow or if the acute ischemia is due to
any nonembolic cause. A clinically normal con-
tralateral femoral pulse is a prerequisite for a
femoral-femoral bypass graft, and a decreased
contralateral pulse would favor the placement of
an axillofemoral bypass or aortofemoral bypass

102

VASCULAR SURGERY

in the patient whose medical condition will
tolerate it. Emergent axillofemoral bypass and
aortofemoral bypass are also used to treat bilat-
eral acute limb ischemia. Axillofemoral bypass
is applied in the unstable or critically ill patient
in whom the more extensive incisions, pro-
longed time to revascularization, and greater
fluid shifts associated with aortofemoral bypass
may be detrimental. Emergent aortofemoral
bypass for acute ischemia has the advantage of
providing definitive revascularization from the
most reliable source of inflow, namely the
nondiseased juxtarenal aorta. The disadvantage
of urgent or emergent aortofemoral bypass is
the substantial magnitude and duration of an
aortic procedure in a potentially ill or medically
unstable patient with insufficient time for pre-
operative optimization of associated medical
conditions.

Infrainguinal bypass procedures are also
commonly used in the management of acute
limb ischemia. Thrombosis of a popliteal artery
aneurysm or a diseased popliteal artery is a
typical indication, as are symptomatic acute
thrombosis of the superficial femoral artery
and dissections extending more distal to the
common femoral artery. Acute thrombosis of a
popliteal artery aneurysm or diseased popliteal
artery can be successfully treated with popliteal
or tibial bypass only if a patent target vessel
below the popliteal artery is identified on pre-
operative angiography. Although some authors
have advocated bypass to isolated or "blind"
segments of the popliteal or tibial arteries, we
prefer to utilize target vessels that flow across
the ankle joint to supply the pedal arch, or in the
case of the peroneal artery, collateralize via the
anterior or posterior branch at the malleolus to
provide flow to either the anterior tibial or pos-
terior tibial artery that subsequently supplies
the foot. Failure to visualize any target vessel
in the calf below the level of acute thrombosis
is an indication for intraarterial thrombolytic
therapy to improve the outflow and provide a
suitable target for a subsequent bypass graft.
Neurological changes secondary to acute
ischemia are traditionally considered con-
traindications for thrombolytic therapy due to
the time required for effective thrombolysis.
However, the results with thrombolytic therapy
for moderate to severe acute ischemia (particu-
larly thrombosed popliteal aneurysms) are
substantially better than the dismal outcomes

Table 9.2. Controversies in the management of limb ischemia

Primary amputation versus complex bypass for limb

salvage in patients with critical limb ischemia and

renal failure and diabetes
Thrombolytic therapy versus surgical thrombectomy

for aortofemoral graft occlusion.
Thrombolytic therapy versus surgical therapy for

primary aortoiliac thrombosis.

of attempted bypass surgery to a distal vessel
not angiographically visualized below the level
of acute thrombosis. Accordingly, we utilize
thrombolytic therapy even in the presence of
early neuromuscular changes if there are no
vessels visualized initially that are suitable
targets for bypass grafting (Table 9.2). Although
thrombolytic therapy is usually associated with
improvement in the acute ischemia, serial exam-
ination of these patients for worsening ischemia
is critical to determine if thrombolytic therapy
should be terminated and surgical bypass
performed.

The conduit of choice for infrainguinal
bypass to treat acute limb ischemia is the
greater saphenous vein, either from the involved
limb or if necessary from the contralateral leg.
There is usually insufficient time for preopera-
tive vein mapping in such patients, and the suit-
ability of the saphenous vein is defined by
operative exploration if there are no signs of
prior harvest. If there is no available saphenous
vein, which is often the case in patients with
acute ischemia secondary to thrombosis of a
prior saphenous vein graft, then a prosthetic
(usually PTFE) graft with a vein patch or cuff or
a cryopreserved cadaver vein can be used. Both
of these options are associated with substan-
tially worse long-term patency than autologous
saphenous vein, particularly when used for
bypass to the below-knee popliteal artery or
tibial arteries.

After revascularization for acute limb
ischemia, consideration is given to immediate
fasciotomy if the ischemia was severe and of
greater than 4 to 6 hours' duration. Immediate
prophylactic fasciotomy avoids problems with
identifying compartment syndrome subse-
quently in patients who are receiving pain med-
ication or sedation and already have pain in the
limb from the surgical incisions (particularly if
the popliteal artery was exposed below the

103

LOWER LIMB ISCHEMIA

knee). The need for fasciotomy is less common
in patients with preexisting arterial insuffi-
ciency, as they possess preformed arterial col-
lateral pathways that decrease the degree of
acute ischemia induced by the superimposed
thrombosis or embolus. Nonetheless, either
immediate fasciotomy or careful observation for
development of elevated compartment pres-
sures is mandatory following any prolonged
period of ischemia of the lower extremity. This
is particularly true in patients with thrombosis
of an aortobifemoral bypass limb with poor
outflow, as profound ischemia is produced when
the inflow graft occludes.

The early signs and symptoms of compart-
ment syndrome are the 3 P's: pink, painful,
and pulses (present). Before the capillary leak
induced by the ischemia-reperfusion causes
intracompartment pressures to eventually ex-
ceed mean arterial pressure, there is a palpable
pulse in the involved limb. The skin appears
pink as the dermal plexus of arterioles main-
tains perfusion despite ischemia of the underly-
ing muscle. The pain induced by compartment
syndrome in the conscious patient is initially
present only with motion of the muscles in the
affected compartment. Thus passive stretching
of the first toe is one of the most sensitive tests
for compartment syndrome of the anterior
compartment of the lower leg. As the ischemia
becomes advanced, pain is present at rest
and becomes excruciating. Immediate four-
compartment fasciotomy is performed via
double incisions if there is any clinical suspi-
cion or signs of compartment syndrome after
revascularization.

In the intubated or otherwise unresponsive
patient where the diagnosis is unclear, meas-
urement of intracompartment pressures with
either a Stryker device or an intravenous infu-
sion pump [with pressure sensing capability,
i.e., an intravenous accurate control (IVAC)
machine] enables the diagnosis of compartment
syndrome to be made in the absence of the
characteristic signs and symptoms. Pressures
greater than 12 to 15mmHg are treated with
fasciotomy. Fasciotomy of the lower limb is
usually performed through two incisions,
although a single incision fasciotomy with
fibulectomy can enable decompression of all
four fascial compartments. The skin incisions
can often be closed at the time of fasciotomy,
and this allows more rapid healing than the

weeks associated with healing open wounds by
secondary intention. If there is a question of
whether the edema will compromise skin
closure, we place interrupted nylon horizontal
mattress sutures in the skin and leave them
untied at the time of fasciotomy. Once the
edema subsides (usually 1 to 3 days), delayed
primary closure is accomplished by tightening
and tying these sutures at the bedside under
intravenous sedation. The muscle ischemia in
compartment syndrome results in myoglobine-
mia and myoglobinuria, and precautionary
measures to protect the kidneys from precipita-
tion of myoglobin within the renal tubules are
instituted in all patients with compartment
syndrome. Alkalinization of the urine is
accomplished by administration of intravenous
sodium bicarbonate, and close monitoring of
serum electrolytes as well as serum myoglobin
and creatine kinase (CK) levels is continued
until the syndrome subsides. In patients with
documented myoglobinurea, we routinely
monitor urine pH to confirm alkalinization of
the urine.

Outcomes

The probability of limb salvage in acute lower
limb ischemia is dependent on two factors. The
first and more important is the duration and
degree of ischemia prior to revascularization. In
patients with prior peripheral vascular surgery,
diagnosis and treatment are usually not
delayed, as both the patient and physician are
focused on ischemia as a cause of the symptoms
in the limb. As discussed above, patients with
arterial embolism or aortic dissection can be
misdiagnosed as having a primary nonvascular
cause of their limb symptoms. The associated
delay in treating the ischemia can often con-
tribute to ultimate limb loss. The second factor
in determining the outcome in acute limb
ischemia is the success of revascularization,
which is related to the level of disease responsi-
ble for the acute ischemia. More proximal occlu-
sive disease, particularly aortoiliac disease or
occlusion, is readily treated with embolectomy
or bypass and generally associated with good
outcomes. Acute limb ischemia due to failure of
a prior infrainguinal bypass graft placed for
prior critical limb ischemia, particularly if there
have been multiple prior bypass procedures
in the involved limb, is associated with worse

104

VASCULAR SURGERY

outcomes as the quality of the distal target
vessel and available bypass conduit progres-
sively decreases.

Long-term outcomes after arterial embolism
are determined by the underlying medical con-
dition of the patient, particularly the cardiac
status. Despite long-term anticoagulation, up to
20% of patients with arterial embolism suffer
another embolic event. Ischemic neuropathy of
either the sensory or motor nerves can persist
after revascularization for acute limb ischemia,
and can be a source of frustration to both the
patient and physician. Newer nonnarcotic
modalities for chronic pain and dysesthesia are
emerging, including electrical nerve stimula-
tion, use of tricyclic drugs, and other options to
treat chronic neuropathy.

Patients who present with acute ischemia sec-
ondary to thrombosis of a popliteal aneurysm
have a high rate (40% to 50%) of limb loss
despite modern advances in thrombolytic
therapy and peripheral bypass surgery. These
results reinforce the need to aggressively diag-
nose and treat popliteal aneurysms prior to
thrombosis, and the finding that 15% of patients

with aortic aneurysms have evidence of an
aneurysm in the lower limb when prospectively
screened (Diwan et al., 2000) provides a basis for
such a strategy.

References

Devine C, Hons B, McCollum C. (2001) J Vase Surg 33:

533-9.
Diwan A, Sarkar R, Stanley JC, Zelenock GB, Wakefield TW.

(2000) J Vase Surg 31:863-9.
Gardner AW, Poehlman ET. (1995) JAMA 274:975-80.
Harris PL, How TV, Jones DR. (1987) Br J Surg 74:252-5.
Kreienberg PB, Darling RC 3rd, Chang BB, et al. (2002) J Vase

Surg 35:299-306.
Lederman RJ, Mendelsohn FO, Anderson RD, et al. (2002)

Lancet 359:2053-8.
Money SR, Herd JA, Isaacsohn JL, et al. (1998) J Vase Surg

27:267-74; discussion 274-5.
Slonim SM, Nyman U, Semba CP, Miller DC, Mitchell RS,

Dake MD. (1996) J Vase Surg 23:241-51; discussion

251-3.
Tateishi-Yuyama E, Matsubara H, Murohara T, et al. (2002)

Lancet 360:427-35.
Veith FJ, Gupta SK, Ascer E, et al. (1986) J Vase Surg 3:104-14.
Wengerter KR, Yang PM, Veith FJ, Gupta SK, Panetta TF.

(1992) J Vase Surg 15:143-9; discussion 150-1.

Chronic Venous Insufficiency,
Varicose Veins, Lymphedema, and
Arteriovenous Fistulas

Andrew W. Bradbury and Peter J. Pappas

Chronic Venous Insufficiency

Chronic venous insufficiency (CVI) may be
denned as symptom or signs of ambulatory
venous hypertension. In developed countries,
CVI affects up to half of the adult population.
Furthermore, the treatment of CVI consumes
up to 2% of total health spending and is a major
cause of lost economic productivity. These
startling data, coupled with the ineffectiveness
of current treatment modalities in many of the
most severely affected patients, underscore the
need for more research.

Classification

Chronic venous insufficiency has proved
difficult to classify for the purposes of scientific
reporting. This has obfuscated attempts to
directly compare the findings of different epi-
demiological, pathophysiological, and clinical
studies. The clinical, etiological, anatomical, and
pathophysiological (CEAP) classification, pro-
posed in 1994 by the American Venous Forum,
is now the most widely accepted system
(Table 10.1).

Epidemiology

In industrialized countries the lifetime risks of
developing varicose veins (VVs), skin changes
(corona phlebectatica, lipodermatosclerosis,
varicose eczema, atrophie blanche), and chronic

venous ulceration (CVU) are 30% to 50%, 5% to
10%, and 1% to 2%, respectively. The bulk of
advanced disease affects the elderly, with up to
5% of women over the age of 65 years having a
history of CVU. However, up to 50% of affected
patients, especially men, develop their ulcer
before their 50th birthday. Women often relate
the development of VVs to pregnancy and child-
birth. The increase in female sex hormones and
blood volume during the first trimester may be
responsible. However, there is little evidence of
an association with (multi)parity, and men and
women appear to be affected almost equally by
CVI. The excess of women observed in clinical
practice is mainly due to their longevity and the
reluctance of men to seek medical attention.
There is no clear evidence that low socioeco-
nomic class predisposes to CVI, although CVU
healing and recurrence rates may be worse.
Clinical experience suggests that occupations
involving prolonged standing are associated
with an increased prevalence and severity of
CVI, poor ulcer healing, and increased recur-
rence rates. Data on the relationships between
physical activity and CVI are conflicting, but it
seems reasonable to assume that an individual
with a well-developed calf muscle pump is less
likely to develop CVI. Although a consistent
relationship between weight and height is
lacking, VVs appear to be commoner in tall men
and CVU in obese women. Similarly, there is
growing evidence of a hereditary predisposition
to CVI. For example, patients whose parents
both have VVs have a 90% chance of developing

105

106

VASCULAR SURGERY

Table 10.1. Clinical, etiological, anatomic, and
pathophysiological (CEAP) classification

Clinical 1

Class

No visible or palpable signs of venous

disease

Class 1

Telangiectasia 2 or reticular veins 3

Class 2

Varicose veins 4

Class 3

Edema

Class 4

Skin changes (lipodermatosclerosis,

atrophie blanche, eczema)

Class 5

Healed ulceration

Class 6

Active ulceration

Etiological

Congenital (may be present at birth or

recognized later)

Primary (with undetermined cause)

Secondary (with known cause):

postthrombotic, posttraumatic,

other

Anatomical

A S

Superficial veins (numbered 1 to 5) 5

A D

Deep veins (numbered 6 to 16) 6

A P

Perforating veins (numbered 17 and

18)

Pathophysiological

Reflux

Obstruction

Pr,o

Both

1 Supplemented with (A) for asymptomatic or (5) for symptomatic,
e.g,C M .

2 Intradermal venules up to 1 mm in diameter.

3 Subdermal, nonpalpable venules up to 4mm.

4 Palpable subdermal veins usually larger than 4 mm.

5 Telangiectasia/reticular veins (1); greater (long) saphenous vein
above (2) below (3) knee; lesser (short) saphenous vein (4); non-
saphenous (5).

6 Inferior vena cava (6); common (7), internal (8), external (9) iliac;
pelvic (10); common (11), deep (12), superficial (13) femoral;
popliteal (14); crural (15); muscular (16).

VVs, and CVU patients have a higher prevalence
of inherited thrombophilia (TP). The influence
of race and ethnicity is unclear, as there are few
reliable data from nonwhite populations.

Normal Venous Function

Venous blood from the lower limbs returns to
the right heart against gravity through the deep
and superficial venous systems. The deep veins
follow the named arteries and are often paired.
The superficial system comprises the long

saphenous vein (LSV) and short saphenous
vein (SSV) and their tributaries. As there are
numerous communications between the long
and short saphenous systems, and between the
superficial and deep systems through junctional
and nonjunctional perforators, these three ele-
ments are highly interdependent, both anatom-
ically and functionally, in health and in disease.
Most of the blood draining into the superficial
veins from skin and subcutaneous tissues
immediately enters the deep venous system via
perforators in the foot, calf, and thigh. In healthy
subjects, less that 10% of the total venous return
from the lower limb passes through the LSV and
SSV to the saphenofemoral junction (SFJ) and
saphenopopliteal junction (SPJ), respectively.
Blood is forced back up the leg during leg
muscle systole, and prevented from flowing
back down the leg under the influence of gravity
during diastole, through the actions of the
muscle pumps and closure of venous valves,
respectively. The act of walking sequentially
compresses venous sinuses in the sole of the
foot, the calf (soleus, gastrocnemius), and to a
lesser extent the thigh and buttock. During
relaxation these sinuses fill from the deep and
superficial venous systems and valves close in
the superficial and axial veins to prevent reverse
flow (reflux). In both the superficial and deep
systems, the density of valves is greatest in the
calf and gradually diminishes in the thigh. The
iliac veins and inferior vena cava are frequently
devoid of valves.

When standing completely motionless, with
all the leg muscles relaxed, the venous valve
leaflets come to lie in a neutral midposition. As
a result, the venous pressure in the dorsal foot
veins comes to represent the hydrostatic pres-
sure exerted by the unbroken column of venous
blood stretching up from the foot to the right
atrium (approximately 90 to lOOmmHg in a
person of average height). Contraction of the leg
muscles immediately leads to the compression
of deep veins and sinuses and to the movement
of venous blood cranially Retrograde blood
flow is terminated by valve closure, and perfo-
rators that allow unidirectional flow from the
superficial to the deep venous system only.
Conventionally, this has also been ascribed to
the closure of valves within the perforators.
However, several studies have shown that many
perforators are devoid of valves. Instead,
outward flow through perforators may be

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

limited by external compression from contract-
ing muscle and a pinch-cock mechanism involv-
ing the deep fascia. The importance of these
mechanisms is that the very high pressures
(up to 200mmHg) generated within the calf
muscle pump are used exclusively to propel
blood back up the leg against gravity, and are
not transmitted to the superficial or distal deep
systems. When the muscle pump relaxes, the
previously expelled venous blood tends to flow
caudally under gravity but is prevented from
doing so by valve closure. This has the effect of
dividing a single long (and heavy) column of
blood into a series of shorter columns lying
between closed valves. The pressure within each
of these segments is low and the ambulatory
venous pressure (AVP) in the dorsal foot veins
falls typically to <25mmHg. During muscle
pump diastole, blood in the superficial system
flows in to the deep system along a pressure
gradient.

Pathophysiology

There are three basic mechanisms that lead to
raised AVP and the symptoms and signs of CVT:
(1) muscle pump dysfunction, (2) valvular
reflux, and (3) venous obstruction.

Aging, general debility, and a wide range
of musculoskeletal or neurological lower limb
pathologies can impair calf muscle pump func-
tion. The "fixed" ankle secondary to arthritis or
trauma is a common example. Muscle bulk and
tone are also important factors in the mainte-
nance of perforator competence (see above).
Failure of perforator competence leads to calf
pump inefficiency (akin to mitral regurgita-
tion), as well as the transmission of high pres-
sures directly to the skin of the gaiter area.

Reflux is present in more than 90% of patients
with CVI; 5% to 10% have isolated deep, 30% to
50% isolated superficial, and 50% to 60% com-
bined. In general, superficial reflux has a better
prognosis than deep reflux (especially when the
latter is postphlebitic), and proximal reflux has
a better prognosis than distal reflux. Valvular
reflux can arise in two ways that are not mutu-
ally exclusive in any one patient:

Primary valvular incompetence (PVI): A loss
of elastin and collagen in the vein wall
around the valve commissures leads to
dilatation, separation of the valve leaflets,

and reflux. As the vein dilates, the tension
in the wall increases according to the law of
Laplace, which leads to further dilatation.
The end result is an incompetent, elongated
and tortuous varicose vein. Primary valvu-
lar incompetence may also affect the deep
venous system.
Postthrombotic syndrome (PTS): Approxi-
mately 25% of CVU patients have a clear
history of deep venous thrombosis (DVT),
and many more have probably suffered a
subclinical or undiagnosed thrombosis.
Deep venous thrombosis leads to endothe-
lial hypoxia, valvular destruction, and
mural inflammation. Even though most
DVTs recanalize, the end result is a thick-
ened, valveless tube that permits gross
reflux and poses an anatomical (narrow-
ing, fibrous webs) and functional (lack
of compliance) obstruction to venous
outflow. Obstruction leads to the formation
of collateral pathways. For example, blood
may be forced out of the calf via perfora-
tors into the superficial venous system and
thence up the leg with the formation of
secondary VVs. Removal of such VVs
increases AVP. Most patients with severe
and intractable CVU have PTS.

Clinical Assessment

History

Inquiry should be made as to the duration of the
present ulcer as well as the duration of ulcer
disease, the number of episodes, and any pre-
cipitating factors (Table 10.2). Previous treat-
ment history and contact allergies are recorded.
Peripheral artery disease (20%), diabetes melli-
tus (5%), and rheumatoid arthritis (8%) often
coexist. Malignancy must not be overlooked.
Many patients with lower limb symptoms, and
who coincidentally have VVs, have other pathol-
ogy to explain their symptoms. Orthopedic,
neurological, and arterial causes of leg symp-
toms must be excluded. Particular attention
must be paid to a history of "white leg" of preg-
nancy, prolonged immobilization, phlebitis, and
major lower limb fracture, any of which may
suggest previous the PTS. A family history of
venous disease, particularly early-onset, recur-
rent, or unusual thrombotic events, should be
sought (Cornu-Thenard, 1994).

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VASCULAR SURGERY

Table 10.2. Distinguishing

features of arterial and venous ulcers

Clinical features

Arterial ulcer

Venous ulcer

Gender

Men > women

Women > men

Age

Usually presents >60 years

Typically develops at 40-60 years but patient may
not present for medical attention until much
older; multiple recurrences are the norm

Risk factors

Smoking, diabetes, hyperlipidemia and
hypertension

Previous DVT, thrombophilia, varicose veins

Past medical

history

Most have a clear history peripheral,

More than 20% have clear history of DVT, many

coronary, and cerebrovascular disease

more have a history suggestive of occult DVT,
e.g., leg swelling after childbirth, hip/knee
replacement or long bone fracture

Symptoms

Severe pain is present unless there is

About a third have pain but it is not usually

(diabetic) neuropathy, pain may be

severe and may be relieved on elevation

relieved by dependency

Site

Normal and abnormal (diabetics)

Medial (70%), lateral (20%) or both malleoli and

pressure areas (malleoli, heel,

gaiter area

metatarsal heads, fifth metatarsal

base)

Edge

Regular, punched-out, indolent

Irregular, with neoepithelium (whiter than mature
skin)

Base

Deep, green (sloughy) or black (necrotic)

Pink and granulating but may be covered in

with no granulation tissue, may

yellow-green slough

comprise major tendon, bone and joint

Surrounding

skin

Features of SLI

LDS, varicose eczema, atrophie blanche

Veins

Empty, guttering on elevation

Full, usually varicose

Swelling

Usually absent

Often present

Symptoms

Localized discomfort in the leg: Usually at the
site of the visible VV, particularly after pro-
longed standing. Prominent varices may
be tender, particularly in menstruating
women.

Pain: Severe pain is unusual and suggests
infection or arterial insufficiency.

Swelling: A feeling of swelling is common.

Venous claudication: This is unusual and due
to extensive postthrombotic iliofemoral
venous occlusion. There is bursting pain in
the calf on walking, which is relieved only
by elevating the leg. In addition, patients
often complain of heaviness in the calf with
ambulation.

Itching: This is common and may lead to
scratching, infection, and ulceration.

Physical Examination

Varicose veins: Note the distribution of
varices and any surgical scars.

Corona phlebectatica (ankle/malleolar flare):
One of the earliest skin manifestations of
CVI comprises dilated intra/subdermal
veins at or just below the medial malleolus.
Overlying skin is thin and fragile leading
to a blue-bleb appearance. Trauma
frequently leads to hemorrhage and
ulceration.

Lipodermatosclerosis: The skin is brown
(red or purple) and indurated due to
hemosiderin and plasma protein deposi-
tion, leading to dermal fibrosis.

Atrophie blanche: Thin and pale skin due to
the thrombotic obliteration of papillary
capillaries; often at the site of previous
ulceration.

Varicose eczema: Scaly dry (or weeping)
skin that is often intensely pruritic and
can demonstrate blanching erythema
(mimicking cellulitis).

Edema: A common presentation in patients
with CEAP class 3 or greater CVI. Chronic
venous insufficiency may coexist with
other diseases that cause edema, such as

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

congestive heart failure, and must be
considered when evaluating CVI patients
(Table 10.3).

Hemorrhage: Can be alarming, even life
threatening, may be spontaneous or follow
trauma. Direct pressure and elevation
always arrest venous hemorrhage. As
recurrent bleeding is almost inevitable,
the patient should be hospitalized for
definitive treatment.

Ulceration: Most CVUs can be easily differen-
tiated from other forms of ulceration.

Arterial circulation: If pedal pulses are impal-
pable, measure the ankle-brachial index
(ABI). An ABI of <0.8 mandates referral to
a vascular surgeon. The ABI is unreliable in
diabetic patients.

Investigations

Virtually all patients with CVI require further
investigation, and duplex ultrasound (DU) has
largely replaced all other modalities in routine
clinical practice. It allows Doppler velocity
information to be color coded and superim-
posed in real time upon a gray scale (B-mode)
image. It determines the location and severity of

Table 10.3. Etiological classification of lymphedema

Primary
lymphedema

Secondary
lymphedema

Congenita (onset <2 years old):

sporadic
Congenita (onset <2 years old):

familial (Milroy's disease)
Praecox (onset 2-35 years):

sporadic
Praecox (onset 2-35 years):

familial (Meige's disease)
Tarda (onset after 35 years of age)

Bacterial infection
Parasitic infection (filariasis)
Fungal infection (tinea pedis)
Exposure to foreign-body

material (silica particles)
Primary lymphatic malignancy
Metastatic spread to lymph nodes
Radiotherapy to lymph nodes
Surgical excision of lymph nodes
Trauma (particularly degloving

injuries)
Superficial thrombophlebitis
Deep venous thrombosis

reflux, the location of the SPJ and nonfunctional
perforators, and whether the deep veins are
patent. Plethysmography involves the assess-
ment of venous function through the measure-
ment of limb volume and nowadays is primarily
a research tool. Photo (PPG) and air (APG)
plethysmography are probably the most
popular techniques. Ambulatory venous pres-
sure is measured by cannulating and transduc-
ing a dorsal foot vein; it remains the research
reference standard. Ascending venography
determines the presence of residual thrombus,
the extent of recanalization,and the distribution
of collaterals. Contrast medium is injected into
a dorsal foot vein and directed into the deep
veins by the placement of an ankle tourniquet.
The iliac system and the vena cava may not be
visualized, in which case a separate injection
can be made in the common femoral vein (CFV)
(cavography). Descending venography involves
injecting contrast medium into the CFV with
the subject positioned at 60 degrees with the
head up in order to assess reflux. Venography is
largely reserved for patients being considered
for deep venous reconstruction because it is
superior to DU in determining the presence and
extent of the PTS. Ovarian vein reflux and pelvic
varices can be visualized by placing a catheter
into the ovarian or internal iliac veins via the
CFV approach. As well as this imaging being
diagnostic, it also enables the ovarian vein to be
embolized in women suffering from pelvic
congestion syndrome. Ulcers that fail to heal,
tend to bleed, or have unusual features should
be biopsied at base and margin under local
anesthesia.

Nonsurgical Management

The mainstay of treatment is compression with
or without superficial venous surgery in the
great majority of patients who have CVI due to
reflux. A small minority of patients who have
deep venous obstruction may benefit from
surgical or endovascular reconstruction. There
is considerable controversy over the role of
sclerotherapy.

Dressings

No particular dressing or topical agent has
been shown unequivocally to significantly

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VASCULAR SURGERY

hasten CVU healing. However, they do have
different physical properties, and the surgeon
needs to have a basic grasp of the underlying
science (and art) of wound care. Enzymatic
agents (e.g., streptokinase-streptodornase)
undoubtedly digest the constituents of slough.
However, they are relatively ineffective against
deep necrosis or hard eschar. There is evidence
that they speed up healing, and may damage the
wound environment. Hydrocolloid dressings
come in many forms, and are generally imper-
meable to gases, water vapor, and bacteria. They
produce a moist, acidic, low-oxygen tension
wound environment that has been shown exper-
imentally to enhance wound healing. Patients
like these dressings because they are easy to use,
and patients can bathe with the dressing in situ.
The dressings absorb exudate (reducing the fre-
quency of dressing changes, smell, risks of
cross-infection, and costs) and may provide
superior pain relief. However, in randomized
controlled trials where both treatment arms
have received equal and adequate compression,
hydrocolloid dressings have not be shown to
improve overall healing compared to any other
dressing. Bead dressings (such as cadexomer
iodine and dextranomer) comprise hydrophilic,
polysaccharide materials that absorb large
amounts of fluid and slough. The former also
releases iodine in to the wound. Although they
may speed up desloughing, they have not been
shown to enhance healing. Paste bandages com-
prise a plain weave cotton fabric impregnated
with zinc oxide paste, either alone or with
calamine, calamine and clioquinol, coal tar, or
ichthammol. These additives are designed to
soothe venous eczema but are actually a
common cause of contract allergy, and patch
testing is recommended. Paste bandages do not
retain moisture, and for this reason, and to
apply compression, additional layers of bandag-
ing are required. The Unna boot is a paste
bandage containing glycerin that hardens into
semirigid dressing. In trials where equal
amounts of compression are applied, no form of
paste bandage has been shown to improve
healing over other forms of dressing. Their
principal benefit is provision of inelastic com-
pression. Alginate dressings absorb exudate and
create a moist wound environment but have not
been proved to speed healing. Biological dress-
ings comprising cultured human epithelium or
fibroblasts may act as a source of growth factors

and act as a scaffold for the patient's own epithe-
lial cells. But they are extremely expensive and
as yet unproven.

Topical Agents

Dermatitis is common and maybe endogenous
(varicose or venous stasis dermatitis) or
exogenous due to topically applied substances
(contact dermatitis). Dermatitis is extremely
morbid, associated with nonhealing, and maybe
irritant or allergic due to cell-mediated, delayed
hypersensitivity. Early patch testing is manda-
tory. The use of bland paraffin preparations
greatly reduces the risks of dermatitis. In
patients with marked exudate, zinc oxide paste
can be used to protect the surrounding skin.
Acute dermatitis must be treated with removal
of the offending allergen and topical steroid
therapy. Topical antibiotics should be avoided.

Physical Therapy

Prolonged bed rest with leg elevation will heal
virtually all CVUs. However, it is logistically
impossible, and associated with decubitus com-
plications, and as it does not address the under-
lying hemodynamic abnormality, recurrence is
virtually inevitable. Exercise therapy aimed at
improving calf muscle pump function maybe of
benefit and trials are under way.

Compression Therapy

Compression undoubtedly retards the develop-
ment and progression of CVI. However, it is still
more of an art than a science, and the quality of
scientific reporting remains low. Elastic band-
aging (the four-layer bandage) is favored in the
United Kingdom, whereas in mainland Europe
and North America inelastic bandaging (the
Unna boot) is preferred. The four-layer bandage
comprises orthopedic wool (to protect the bony
prominences and to absorb any exudates); crepe
bandage (to compress and shape the wool, and
to provide a firm base for the compression
bandages), elastic bandage (e.g., Elset™, Seton,
applied at 50% stretch) and a self-adhesive elas-
ticated bandage (e.g., Coban™, 3M to add to
compression and fix the bandaging in place).
This bandage typically exerts 40mmHg at the
ankle and 20mmHg just below the knee. Once
the ulcer is healed, the patient should be pre-

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

scribed stocking. There is no evidence that
extending compression above the knee confers
benefit. Compliance is a major problem.

Sclerotherapy

The role of sclerotherapy is controversial, with
practitioner's views based largely on profes-
sional background and country of origin rather
than on clinical comparative studies. Some scle-
rotherapists believe they can treat all VVs, but
most accept the superiority of surgery in the
presence of main stem, SFJ, or SPJ incompe-
tence. However, the advent of foam sclerosants
may revolutionize the management of such
disease. The aim is to place a small volume of
sclerosant in the lumen of a vein empty of
blood, and then appose the walls of that vein
with appropriate compression. The vein then
fibroses closed without the formation of clot.
Some practitioners use magnifying loupes for
smaller veins, and there is increasing interest in
injecting larger veins under ultrasound guid-
ance (echosclerotherapy). The vein must be kept
empty of blood both during and after the injec-
tion to prevent thrombophlebitis. Adequate
compression is difficult in the perineum, upper
thigh, and popliteal fossa, especially in the
obese. Patients should be mobilized immedi-
ately afterward. In the U.K., most surgeons use
detergents that act by directly damaging the
endothelium. In mainland Europe and North
America, hypertonic saline is also popular. Err
on the side of caution with regard to volume and
concentration until the patient's response can
be assessed. The complications of injection
sclerotherapy include anaphylaxis (<0.1%),
allergic reactions (uncommon), ulceration
(extr avascular injection), arterial injection (rare
and serious), pigmentation (extravasation),
superficial thrombophlebitis (inadequate com-
pression), and DVT (inadequate mobilization).

Surgical Management

There is growing evidence that saphenous
surgery improves the quality of life in patients
with VVs, and augments the healing and
reduces the recurrence of CVU better than com-
pression alone (Dwerryhouse et al., 1999). For
optimal results, it is necessary to define the
extent and severity of venous disease, usually by
means of DU, prior to surgery. Surgery for CVU

is different from that for uncomplicated VVs in
a number of important ways. The patients are
older and often have multisystem, medical
comorbidity; the risks, especially DVT, are
higher. Patients may require inpatient optimiza-
tion of cardiorespiratory function, treatment of
dermatitis, edema reduction, and desloughing
of the ulcer. The effect of deep venous reflux on
the efficacy of superficial venous surgery is con-
troversial and incompletely defined. Deep reflux
due to PVI may reverse once superficial reflux
has been eradicated. However, most agree that
patients with extensive PTS gain less benefit
from surgery. Secondary VVs that are acting as
collaterals must not be removed. Although post-
operative compression therapy has been shown
to reduce VVs and CVU recurrence, compliance
is poor.

Varicose Vein Surgery

Long Saphenous Surgery

Safe and effective surgery depends on observing
a few sound principles. In a patient of normal
build the SFJ lies directly beneath the groin
crease; in the obese it lies above. An incision
made below the crease is likely to be too low.
Resist the temptation to operate through an
excessively small incision. Do not divide any
vein until the SFJ has been unequivocally iden-
tified. Unless all tributaries are taken beyond
secondary branch points, a network remains of
superficial veins connecting the veins of the
thigh with those of the perineum, the lower
abdominal wall, and the iliac region. These
cross-groin connections are a frequent cause of
recurrence. Ligate the LSV deep to all tributar-
ies flush with the CFV using nonabsorbable
transfixion suture to reduce neovascularization
through the stump. Directly ligate, and if large,
consider stripping, any high anterolateral or
posteromedial or thigh branches to reduce
hematoma formation and recurrence. There is
evidence to show that stripping the LSV to a
hand's breadth below the knee significantly
reduces recurrence by disconnecting the thigh
perforators and saphenous tributaries and by
removing the conduit that will allow neovascu-
larization in the groin to reconnect with the
remaining superficial venous system of the
thigh and calf. Confining stripping to just below
the knee, and to a downward direction, reduces

112

VASCULAR SURGERY

saphenous nerve injury. The theoretical advan-
tages of invagination stripping in terms of
reducing blood loss, hematoma, nerve injury,
and scars have not been confirmed in trials.

Short Saphenous Surgery

Saphenopopliteal junction ligation can prove to
be a challenging procedure, especially when
performed for recurrent disease. Always mark
the junction preoperatively with DU (some
surgeon still prefer venography). The SSV can
be found by following the Giacomini vein, which
is a superficially placed tributary of the SSV that
runs up the thigh to join the LSV. This may be
large and confused with the SSV, especially if the
SPJ is absent; the importance of this will be
apparent on the preoperative DU. Be aware that
traction on the SSV can tent up and damage the
mobile and thin-walled popliteal vein. Palpation
of the artery gives an indication of the depth of
dissection. Beware the common peroneal nerve
under medial edge of biceps femoris, which is
at risk from overzealous lateral retraction as
well as from a careless stitch when closing the
popliteal fascia. The SSV is often closely associ-
ated with sural nerve injury and is also at risk,
particular if stripping is undertaken. There are
still a number of controversial issues regarding
the SSV. Is it always necessary to ligate the SSV
flush with the popliteal vein? Experience sug-
gests that this counsel of perfection is hard to
achieve in a significant proportion of patients
without risk of collateral damage. This raises the
question of what should be done with the gas-
trocnemius and other, often large and refluxing,
muscular veins? Should the SSV be stripped or
is it permissible just to remove a segment
through the popliteal fossa wound? It seems
likely, although there is no proof, that SSV strip-
ping, for the same reasons as for the LSV, would
reduce recurrence. However, there is concern
about sural nerve injury.

Perforator Ligation

Although the advent of DU-guided subfascial
endoscopic perforator surgery (SEPS) has
rekindled interest in perforator ligation, there is
no evidence that it alters the natural history of
venous disease. Clearly, the only way to resolve
this issue once and for all is to perform a

randomized controlled trial of compression vs.
compression and saphenous surgery vs. com-
pression, saphenous surgery, and SEPS.

Surgery for Recurrent Veins

Recurrent LSV VVs arise because of inadequate
dissection of, or neovascularization at, the SFJ in
the presence of a nonstripped or incompletely
stripped LSV. Standard teaching is to approach
the SFJ through nonoperated tissues (usually
from a lateral approach that first exposes the
common femoral artery) so that the CFV can be
skeletonized of branches using nonabsorbable
sutures for 1 to 2 cm above and below the junc-
tion. The top of the LSV is dissected from the
mass of scar tissue so that it can be stripped.
However, this can be a difficult and potentially
morbid operation. When the preoperative DU
indicates neovascularization as opposed to an
intact SFJ, the LSV can be located at the knee, a
stripper passed up toward the groin, and the
vein stripped without a formal redissection.

Complications

Fortunately, major complications following VV
surgery are relatively rare. However, up to 20%
of patients may suffer some form of minor mor-
bidity, such as hematoma, lymphatic leak, pain,
saphenous neuritis, and venous thrombosis. In
the U.K., VV surgery is the commonest cause of
litigation against general and vascular surgeons.
This not a field for the unsupervised, inexperi-
enced surgeon and it behooves surgeons who
undertake VV surgery to carefully audit their
management, techniques, and outcomes.

Deep Venous Reconstruction

These procedures have not gained widespread
acceptance largely because there is little data to
support their efficacy. Several different tech-
niques have been described for suturing the
edges of "floppy" valve cusps to the vein wall,
rendering the valve competent. Autologous
valve transplantation interposes a segment of
axillary or brachial vein, containing a competent
valve, into an incompetent deep vein, usually the
popliteal. Procedures using synthetic, mixed,
and animal valves are still experimental. An
incompetent superficial femoral vein can be
transected and anastomosed end to end or end

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

to side to a profunda femoris or long saphenous
vein that has a competent valve (vein transposi-
tion). An obstructed femoral segment may be
bypassed by anastomosing a transected, compe-
tent LSV to the side of the popliteal vein. Again,
satisfactory long-term patency rates have been
reported in small series.

Conclusions

Although the most difficult cases of leg ulcera-
tion are multifactorial in origin, CVI is the
single most common underlying pathology. As
such, there is hope that the prevalence of CVU
may decline in the future as a result of improved
thromboembolic prophylaxis and treatment.
For the moment, however, CVU is a common
and disabling condition that is often resistant to
conservative therapy, prone to recurrence, and
very expensive to manage. There needs to be a
low threshold for referral to a vascular surgeon,
preferably through a one-stop assessment clinic
where a thorough venous and arterial duplex-
based assessment can be performed. This will
enable patients who might benefit from surgical
intervention to be identified and treated early. It
will also enable ongoing outpatient treatment to
be based on an in-depth understanding of the
pathophysiological mechanisms responsible in
each patient. Great progress in the management
of CVU has been made over the last decade
because of an increased understanding of the
pathophysiology and the availability of data
from clinical trials that have provided a
scientifically robust platform on which to base
treatment algorithms. Despite all this, further
research is required into the epidemiology and
natural history of CVU, models of care, primary
prevention, and pathogenesis.

Lymphedema

The Lymphatic System

The lymphatic system performs the following
functions:

1. It removes water, electrolytes, low-
molecular-weight moieties (polypeptides,
cytokines, growth factors), and macromol-
ecules (fibrinogen, albumen, globulins,
coagulation and fibrinolytic factors) from

the interstitial fluid (ISF) and returns them
to the circulation.

2. It permits the circulation of lymphocytes
and other immune cells.

3. It returns intestinal lymph (chyle), which
transports cholesterol, long chain fatty
acids, triglycerides, and the fat-soluble
vitamins (A, D, E, and K), directly to the
circulation, bypassing the liver.

Lymph from the lower limbs and abdomen
drains via the cisterna chyli and thoracic duct
into the left internal jugular vein at its
confluence with the left subclavian vein. Lymph
from the head and right arm drains via the right
lymphatic duct into the right internal jugular
vein. Lymphatics accompany veins everywhere
except in the cortical bony skeleton and central
nervous system, although the brain and retina
possess cerebrospinal fluid and aqueous humor,
respectively. The lymphatic system comprises
lymphatic channels, lymphoid organs (lymph
nodes, spleen, Peyer's patches, thymus, tonsils),
and circulating elements (lymphocytes and
other mononuclear immune cells).

Lymphatics originate within the ISF space
from specialized endothelialized capillaries
(initial lymphatics) or nonendothelialized
channels such as the spaces of Disse in the liver.
Initial lymphatics are unlike arteriovenous cap-
illaries in that they are blind-ended, are much
larger (50 |J.m) and allow the entry of molecules
up to 1000 kd in size. This is because the
basement membrane of these lymphatics is
fenestrated, tenuous, or lacking intra- and
intercellular endothelial pores. Lymphatic capil-
laries are anchored to interstitial matrix by
filaments. In the resting state they are collapsed,
but when ISF volume and pressure increases,
they are held open by these filaments to facili-
tate increased drainage. Initial lymphatics drain
into terminal (collecting) lymphatics that
possess bicuspid valves and endothelial cells
rich in the contractile protein actin. Larger col-
lecting lymphatics are surrounded by smooth
muscle. Valves partition the lymphatics into seg-
ments (lymphangions) that contract sequen-
tially in order to propel lymph into the lymph
trunks. Terminal lymphatics lead to lymph
trunks comprising endothelium, basement
membrane, and a media of smooth muscle
cells that are innervated with sympathetic,

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VASCULAR SURGERY

parasympathetic, and sensory nerve endings.
About 10% of lymph arising from a limb is
transported in deep lymphatic trunks that
accompany the main neurovascular bundles.
The majority of lymphatic flow, however, is con-
ducted against the venous flow from deep to
superficial in epifascial lymph trunks. Super-
ficial trunks form lymph bundles of various
sizes, are located within strips of adipose tissue,
and tend to follow the course of the major
superficial veins.

The distribution of fluid and protein between
the vascular and ISF spaces depends on hydro-
static and oncotic pressures (Starling's forces),
together with the relative impermeability of the
blood capillary membrane to molecules over
70 kd. In healthy subjects there is net capillary
filtration, which is removed by the lymphatic
system. Small particles enter the initial lym-
phatics directly; larger particles are phagocy-
tosed by macrophages and transported through
the lymphatic system intracellularly Lymph
flows against a small pressure gradient due to
transient increases in interstitial pressure sec-
ondary to muscular contraction and external
compression, the sequential contraction and
relaxation of lymphangions, and the prevention
of reflux due to valves. Lymphangions respond
to increased lymph flow in much the same way
as the heart responds to increased venous
return in that they increase their contractility
and stroke volume. Transport in the main lymph
ducts also depends on intrathoracic (respira-
tion) and central venous (cardiac cycle) pres-
sures. In the healthy limb, lymph flow is largely
due to intrinsic lymphatic contractility aug-
mented by exercise, limb movement, and exter-
nal compression. However, in lymphedema,
where the lymphatics are constantly distended
with lymph, these external forces assume a
much more important functional role.

Definition and Pathophysiology

Lymphedema maybe defined as abnormal limb
swelling due to the accumulation of increased
amounts of high-protein ISF secondary to
defective lymphatic drainage in the presence of
(near) normal net capillary filtration (Szuba and
Rockson, 1997). In order for edema to be clini-
cally detectable, the ISF volume has to double.
About 8L of lymph is produced and, following
resorption in lymph nodes, about 4L enters the

venous circulation. In one sense, all edema is
lymphedema in that it results from an inability
of the lymphatic system to clear the ISF com-
partment. However, in most types of edema this
is because the capillary filtration rate is patho-
logically high and overwhelms a normal lym-
phatic system, resulting in the accumulation of
low-protein edema fluid. By contrast, in true
lymphedema, capillary filtration is normal and
the edema fluid is relatively high in protein.
Both mechanisms frequently coexist, as in
patients with CVI.

Lymphedema can result from lymphatic
aplasia, hypoplasia, dysmotility (reduced con-
tractility with or without valvular insuffi-
ciency), obliteration by inflammatory, infective
or neoplastic processes, or surgical extirpation
(Table 10.4). Whatever the primary abnormality,
the resultant physical or functional obstruction
leads to lymphatic hypertension and distention
with further secondary impairment of contrac-
tility and valvular competence. Lymphostasis
and lymphotension lead to the accumulation in
the ISF of fluid, proteins, growth factors and
other active peptide moieties, glycosaminogly-
cans, and particulate matter, including bacteria.
As a consequence, there is increased collagen
production by fibroblasts, an accumulation
of inflammatory cells (predominantly macro-
phages and lymphocytes), and activation of ker-
atinocytes. The end result is protein-rich edema
fluid, increased deposition of ground substance,
subdermal fibrosis, and dermal thickening and
proliferation. Lymphedema, unlike all other
types of edema, is confined to the epifascial
space. Although muscle compartments may
be hypertrophied due to the increased work
involved in limb movement, they are character-
istically free of edema.

Two main types of lymphedema are
recognized:

• Primary, in which the cause is unknown
(or at least uncertain and unproved) but
often presumed to be due to congenital
lymphatic dysplasia

• Secondary, in which there is a clear under-
lying cause such as inflammation, malig-
nancy, or surgery

Primary lymphedema is usually further subdi-
vided on the basis of the presence of a family
history, age of onset, and lymphangiographic
findings (see below).

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

Table 10.4. Differential diagnosis of the swollen limb
Nonvascular or lymphatic General disease states

Local disease processes

Venous

Arterial

Retroperitoneal fibrosis

Gigantism

Drugs

Trauma
Obesity

Deep venous thrombosis
Postthrombotic syndrome

Varicose veins

Klippel-Trenaunay
syndrome and other
malformations

External venous
compression
Ischemia- reperfusion

Arteriovenous

malformation
Aneurysm

Cardiac failure from any cause; liver failure; hypoproteinemia due
to nephrotic syndrome, malabsorption, protein losing
enteropathy; hyperthyroidism (myxedema); allergic disorders
including angioedema and idiopathic cyclic edema; prolonged
immobility and lower lib dependency

Ruptured Baker's cyst; myositis ossificans; bony or soft tissue
tumors; arthritis; hemarthrosis; calf muscle hematoma;
Achilles tendon rupture

May lead to arterial, venous and lymphatic abnormalities

Rare; all tissues are uniformly enlarged

Corticosteroids; estrogens; progestogens; monoamine oxidase
inhibitors; phenylbutazone; methyldopa; hydralazine;
nifedipine

Painful swelling due to reflex sympathetic dystrophy

Lipodystrophy, lipoidosis

There may be an obvious predisposing factor such as recent
surgery; the classical signs of pain and redness may be absent

Swelling, usually of the whole leg, due to iliofemoral venous
obstruction; venous skin changes, secondary varicose veins on
the leg and collateral veins on the lower abdominal wall;
venous claudication may be present

Simple primary varicose veins are rarely the cause of significant
leg swelling

Rare; present at birth or develops in early childhood; comprises
an abnormal lateral venous complex, capillary nevus, bony
abnormalities, hypo(a)plasia of deep veins, and limb
lengthening; lymphatic abnormalities often coexist

Pelvic or abdominal tumor including the gravid uterus;
retroperitoneal fibrosis

Following lower limb revascularization for chronic and
particularly chronic ischemia

May be associated with local or generalized swelling

Popliteal; femoral; false aneurysm following (iatrogenic) trauma

Epidemiology

Lymphedema is estimated to affect around 2%
of the population and causes significant physi-
cal symptoms and complications, as well as
emotional and psychological distress, which can
lead to difficulties with relationships, school,
and work. Many sufferers choose not to seek
medical advice because of embarrassment and
a belief that nothing can be done. Patients
who do come forward, especially those with
non-cancer-related lymphedema, often find
they have limited access to appropriate expert-
ise and treatment. Lymphedema is often mis-
diagnosed and mistreated by doctors, who
frequently have a poor understanding of the
condition, believing it to be primarily a cos-

metic problem. However, early diagnosis and
treatment are important because relatively
simple measures can prevent the development
of disabling late disease, which is often very
difficult to treat.

Clinical Assessment

In most cases the diagnosis of primary or sec-
ondary lymphedema can be made, and the con-
dition differentiated from other causes of a
swollen limb, on the basis of history and exam-
ination without recourse to complex investiga-
tion. Unlike other types of edema, lymphedema
characteristically involves the foot. The contour
of the ankle is lost through infilling of the sub-
malleolar depressions; a "buffalo hump" forms

116

VASCULAR SURGERY

on the dorsum of the foot, the toes appear
square due to confinement of footwear, and
the skin on the dorsum of the toes cannot
be pinched due to subcutaneous fibrosis
(Stemmer's sign). Lymphedema usually spreads
proximally to knee level and less commonly
affects the whole leg. In the early stages, lym-
phedema "pits," and the patient reports that the
swelling is down in the morning. This repre-
sents a reversible component to the swelling,
which can be controlled. Failure to do so allows
fibrosis, dermal thickening, and hyperkeratosis
to occur. In general, primary lymphedema
progresses more slowly than secondary lym-
phedema. Chronic eczema, fungal infection of
the skin (dermatophytosis) and nails (ony-
chomycosis), Assuring, verrucae, and papillae
(warts) are frequently seen in advanced disease.
Ulceration is unusual except in the presence of
chronic venous insufficiency.

Lymphangiomas are dilated dermal lymphat-
ics that blister onto the skin surface. The fluid is
usually clear but may be blood stained, and in
the long term they thrombose and fibrose,
forming hard nodules, raising concerns about
malignancy. If they are <5 cm across, they
are termed lymphangioma circumscriptum; if
more widespread, lymphangioma diffusum. If
they form a reticulate pattern of ridges, they are
termed lymphedema ab igne. Lymphangiomas
frequently weep (lymphorrhea, chylorrhea),
causing skin maceration and act as a portal
for infection. Protein-losing diarrhea, chylous
ascites, chylothorax, chyluria, and discharge
from lymphangiomas suggest lymphangiectasia
(megalymphatics) and chylous reflux.

Ulceration, nonhealing bruises, and raised
purple-red nodules should lead to suspicion of
malignancy. Lymphangiosarcoma was origi-
nally described in postmastectomy edema
(Stewart-Treves syndrome) and affects about
0.5% of patients at a mean onset of 10 years.
However, lymphangiosarcoma can develop in
any long-standing lymphedema but usually
takes longer to manifest (20 years). It presents
as single or multiple bluish/red skin and subcu-
taneous nodules that spread to form satellite
lesions that may then become confluent. The
diagnosis is usually made late, and confirmed
by skin biopsy. Amputation offers the best
chance of survival, but even then most patients
live less than 3 years. It has been suggested
that lymphedema leads to an impairment

of immune surveillance and so predisposes
to other malignancies, although the causal
association is not as definite as it is for
lymphangiosarcoma.

Primary Lymphedema

It has been proposed that all cases of primary
lymphedema are due to an inherited abnormal-
ity of the lymphatic system, sometimes termed
congenital lymphatic dysplasia. However, it is
possible that many sporadic cases of primary
lymphedema occur in the presence of a (near)
normal lymphatic system and are actually
examples of secondary lymphedema for which
the triggering events have gone unrecognized.
These might include seemingly trivial (but
repeated) bacterial or fungal infections, insect
bites, barefoot walking (silica), DVT, or episodes
of superficial thrombophlebitis. In animal
models, simple excision of lymph nodes or
trunks leads to acute lymphedema that resolves
within a few weeks, presumably due to collater-
alization. In animals, the human condition can
only be mimicked by inducing extensive lym-
phatic obliteration and fibrosis. Even then, there
may be considerable delay between the injury
and the onset of edema. Primary lymphedema
is much commoner in the legs than the arms.
This may be due to gravity and a bipedal
posture, the fact that the lymphatic system of
the leg is less well developed, or the increased
susceptibility of the leg to trauma or infection.
Furthermore, loss of the venoarteriolar reflex
(VAR), which protects lower limb capillaries
from excessive hydrostatic forces in the erect
posture, with age and disease (CVI, diabetes)
may be important.

Primary lymphedema is often classified on
the basis of apparent genetic susceptibility, age
of onset, or lymphangiographic findings (Table
10.5). None of these is ideal, and the various
classification systems in existence can appear
confusing and conflicting as various terms and
eponyms are used loosely and interchangeably.
This problem has hampered research and
efforts to gain a better understanding of under-
lying mechanisms, the effectiveness of therapy,
and prognosis. Primary lymphedema, where
there appears to be a genetic susceptibility or
element to the disease, may be further divided
into those cases that are familial (hereditary),
where typically the only abnormality is lym-

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

Table 10.5. Lymphangiography classification of primary lymphedema

Congenital hyperplasia

Distal obliteration

Proximal obliteration

(10%)

(80%)

(10%)

Age of onset

Congenital

Puberty (praecox)

Any age

Sex distribution

Male > female

Female > male

Male = female

Extent

Whole leg

Ankle, calf

Whole leg, thigh only

Laterality

Uni = bilateral

Often bilateral

Usually unilateral

Family history

Often positive

Progression

Progressive

Slow

Rapid

Response to compression

Variable

Good

Poor

therapy

Comments

Lymphatics are increased

Absent or reduced distal

There is obstruction at the

in number, although

superficial lymphatics;

level of the aortoiliacor

functionally defective;

also termed aplasia or

inguinal nodes; if associated

there is usually an

hypoplasia

with distal dilatation, the

increased number of

patient may benefit from

lymph nodes; may have

lymphatic bypass

chylous ascites,

operation; other patients

chylothorax,and

have distal obliteration as

protein-losing

well

enteropathy

phedema and there is a family history, and those
cases that are syndromic, where the lym-
phedema is only one of several congenital
abnormalities and is either inherited or spo-
radic. Syndromic lymphedema maybe sporadic
and chromosomal [Turner's (XO karyotype),
Klinefelter's (XXY), Down (trisomy 21) syn-
drome], or clearly inherited and related to an
identified or presumed single gene defect
[lymphedema-distichiasis (autosomal domi-
nant)], or of uncertain genetic etiology (yellow-
nail and Klippel-Trenaunay- Weber syndromes).
Familial (hereditary) lymphedema can be
difficult to distinguish from nonfamilial lym-
phedema because a reliable family history may
be unobtainable, the nature of the genetic pre-
disposition is unknown, and the genetic
susceptibility may translate into clinical disease
only in the presence of certain environmental
factors. Although the distinction may not
directly affect treatment, the patients are often
concerned lest they be passing on the disease
to their children. Two main forms of familial
(hereditary) lymphedema are recognized:
Noone-Milroy (type I) and Letessier-Meige
(type II). It is likely that both eponymous dis-
eases overlap and represent more than a single
disease entity and genetic abnormality. Milroy's
disease is estimated to be present in 1 in 6000
live births and is probably inherited in an

autosomal-dominant manner with incomplete
(about 50%) penetrance. In some families, the
condition maybe related to abnormalities in the
gene coding for a vascular endothelial growth
factor (VEGF) on chromosome 5. The disease is
characterized by brawny lymphedema of both
legs (and sometimes the genitalia, arms, and
face) that develops from birth or before puberty.
The disease has been associated with a wide
range of lymphatic abnormalities on lymphan-
giography. Meige's disease is similar to Milroy's
disease except the lymphedema generally devel-
ops between puberty and middle age (50 years).
It usually affects one or both legs but may
involve the arms. Some, but not all, cases appear
to be inherited in an autosomal-dominant
manner. Lymphangiography generally shows
aplasia or hypoplasia.

Lymphedema congenita (onset at or within 2
years of birth) is commoner in males, more
likely to be bilateral and to involve the whole leg.
Lymphedema praecox (onset from 2 to 35 years)
is three times commoner in females, has a peak
incidence shortly after menarche, is three times
more likely to be unilateral than bilateral, and
usually only extends to the knee. Lymphedema
tarda develops, by definition, after the age of 35
years and is often associated with obesity, with
lymph nodes being replaced by fibrofatty tissue.
The cause is unknown. Lymphedema develop-

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VASCULAR SURGERY

ing for the first time after 50 years should
prompt a thorough search for underlying
(pelvic, genitalia) malignancy. It is worth noting
that, in such patients, lymphedema often com-
mences proximally in the thigh rather than
distally

Secondary Lymphedema

This is the most common form of lymphedema.
There are several well-recognized causes, in-
cluding infection, inflammation, neoplasia, and
trauma.

Filariasis is the commonest cause of lym-
phedema worldwide, affecting up to 100 million
individuals. It is particularly prevalent in Africa,
India, and South America, where 5% to 10%
of the population may be affected. The vivipa-
rous nematode Wucheria bancrofti, whose only
host is humans, is responsible for 90% of cases
and is spread by the mosquito. The disease is
associated with poor sanitation. The parasite
enters lymphatics from the blood and lodges
in lymph nodes, where it causes fibrosis and
obstruction, due partly to direct physical
damage and partly to the immune response of
the host. Proximal lymphatics become grossly
dilated with adult parasites. The degree of
edema is often massive, in which case it is
termed elephantiasis. Immature parasites
(microfilariae) enter the blood at night and can
be identified on a blood smear, a centrifuged
specimen of urine, or in lymph itself. A com-
plement fixation test is also available and
is positive in present or past infection.
Eosinophilia is usually present. Diethylcarba-
mazine destroys the parasites but does not
reverse the lymphatic changes, although there
may be some regression over time. Once the
infection has been cleared, treatment is as for
primary lymphedema. Public health measures
to reduce mosquito breeding, protective cloth-
ing, and mosquito netting may be usefully
employed to combat the condition.

Endemic elephantiasis (podoconiosis) is
common in the tropics and affects more than
500,000 people in Africa. The barefoot cultiva-
tion of soil composed of alkaline volcanic rocks
leads to destruction of the peripheral lymphat-
ics by particles of silica, which can be seen in
macrophages in draining lymph nodes. Plantar
edema develops in childhood and rapidly
spreads proximally. The condition is prevented,

and its progression slowed, by the wearing of
shoes.

Lymphangitis and lymphadenitis can cause
lymphatic destruction that predisposes to
lymphedema complicated by further acute
inflammatory episodes (AIEs). Interestingly, in
such patients lymphangiography has revealed
abnormalities in the contralateral, unaffected
limb, suggesting an underlying, possibly inher-
ited, susceptibility. Lymphatic and lymph node
destruction by tuberculosis is also a well-
recognized cause of lymphedema, especially in
developing countries.

Treatment (surgery, radiotherapy) for breast
carcinoma is probably the commonest cause of
lymphedema in developed countries but is
decreasing in incidence as surgery becomes
more conservative. Lymphoma may present
with lymphedema, as may malignancy of the
pelvic organs and external genitalia. Kaposi's
sarcoma developing in the course of human
immunodeficiency virus (HlV)-related illness
may cause lymphatic obstruction and is a
growing cause of lymphedema in certain parts
of the world.

It is not unusual for patients to develop
chromic localized or generalized swelling fol-
lowing trauma. The etiology is often multifacto-
rial and includes disuse, venous thrombosis,
and lymphatic injury or destruction. Degloving
injuries and burns are particularly likely to
disrupt dermal lymphatics. Tenosynovitis can
also be associated with localized subcutaneous
lymphedema, which can be a cause of trouble-
some persistent swelling following ankle and
wrist sprains and repetitive strain injury.

It is important to appreciate the relationship
between lymphedema and CVI. As both condi-
tions are relatively common and often coexist in
the same patient, it can be difficult to unravel
which components of the patient's symptom
complex are due to each pathology. There is no
doubt that superficial venous thrombophlebitis
(SVT) and DVT can both lead to lymphatic
destruction and secondary lymphedema, espe-
cially if recurrent. Lymphedema is an important
contributor to the swelling of the postphlebitic
syndrome. It has also been suggested that lym-
phedema can predispose to DVT and possibly
SVT through immobility and AIEs. Certainly,
tests of venous function (duplex ultrasonogra-
phy, plethysmography) are frequently abnormal
in patients with lymphedema.

119

CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

It is not uncommon to see patients (usually
women) with lymphedema in whom a duplex
ultrasound scan has revealed superficial reflux
(such reflux is present subclinically in up to a
third of the adult population). Although isolated
superficial venous reflux rarely, if ever, leads
to limb swelling, such patients are frequently
misdiagnosed as having venous rather than
lymphedema, and mistakenly subjected to VV
surgery. Not only does such surgery invariably
fail to relieve the swelling, it usually makes it
worse as saphenofemoral and saphenopopliteal
ligation, together with saphenous stripping,
compromise still further the drainage through
the subcutaneous lymph bundles (which follow
the major superficial veins) and draining
inguinal and popliteal lymph nodes.

Rheumatoid and psoriatic arthritis (chronic
inflammation and lymph node fibrosis), contact
dermatitis, snake and insect bites, and retroperi-
toneal fibrosis are all rare but well-documented
causes of lymphedema. Pretibial myxedema is
due to the obliteration of initial lymphatics by
mucin. Factitious lymphedema is caused by
application of a tourniquet (a "rut" and sharp
cut-off is seen on examination) or "hysterical"
disuse in patients with psychological problems.
Generalized or localized immobility due to any
cause leads to chronic limb swelling that can
be misdiagnosed as lymphedema. Examples
include the elderly person who spends all day
(and sometimes all night) sitting in a chair
(armchair legs), the hemiplegic stroke patient,
and the young patient with multiple sclerosis.

Lipedema presents almost exclusively in
women and comprises bilateral, usually sym-
metrical, enlargement of the legs and, some-
times, the lower half of the body due to the
abnormal deposition of fat. It may or may not
be associated with generalized obesity. There
are a number of features that help to differ-
entiate the condition from lymphedema, but
lipedema may coexist with other causes of limb
swelling. It has been proposed that lipedema
results from, or at least is associated with, fatty
obliteration of lymphatics and lymph nodes.

Investigation

It is usually possible to diagnose and manage
lymphedema purely on the basis of the history
and examination, especially when the swelling is
mild and there are no apparent complicating

features. In patients with severe, atypical, and
multifactorial swelling, investigations may help
confirm the diagnosis, inform management, and
provide prognostic information. A full blood
count, urea and electrolytes, creatinine, liver
function tests, chest radiograph, and blood
smear for microfilariae may be indicated. Direct
lymphangiography involves the injection of
contrast medium into a peripheral lymphatic
vessel and subsequent radiographic visualiza-
tion of the vessels and no des. It remains the gold
standard for showing structural abnormalities
of larger lymphatics and nodes. However, it can
be technically difficult, is unpleasant for the
patient, may cause further lymphatic injury,
and has largely become obsolete as a routine
method of investigation. Indirect lymphangiog-
raphy involves the intradermal injection of
water-soluble nonionic contrast into a web
space, from where it is taken up by lymphatics
and then followed radiographically It shows
distal lymphatic but not normally proximal
lymphatics and nodes. Isotope lympho-
scintigraphy has largely replaced lymphangiog-
raphy as the primary diagnostic technique
in cases of clinical uncertainty. Radioactive
technetium-labeled protein or colloid particles
are injected into an interdigital web space and
specifically taken up by lymphatics, and serial
radiographs are taken with a gamma camera.
The technique provides a qualitative measure of
lymphatic function rather than quantitative
function or anatomical detail. A single axial
computed tomography (CT) slice through the
mid-calf has been proposed as a useful diag-
nostic test for lymphedema (coarse, nonen-
hancing, reticular honeycomb pattern in an
enlarged subcutaneous compartment), venous
edema (increase volume of the muscular com-
partment), and lipedema (increased subcuta-
neous fat). Computed tomography can also be
used to exclude pelvic or abdominal mass
lesions. Magnetic resonance imaging (MRI) can
provide clear images of lymphatic channels and
lymph nodes, and can be useful in the assess-
ment of patients with lymphatic hyperplasia. It
can also distinguish venous and lymphatic
causes of a swollen limb. In cases where
malignancy is suspected, samples of lymph
nodes may be obtained by fine-needle aspira-
tion, needle core biopsy, or surgical excision.
Skin biopsy will confirm the diagnosis of
lymphangiosarcoma.

120

VASCULAR SURGERY

Management

Ideally, a multiprofessional team comprising
physical therapists, nurses, orthotists, physi-
cians (dermatologists, oncologists, palliative
care specialists), surgeons, and social services
should deliver the care. Although surgery itself
has a very small role, surgeons (especially breast
and vascular) are frequently asked to oversee
the management of these patients. Early
diagnosis and institution of management are
essential because at that stage relatively simple
measures can be highly effective and will
prevent the development of disabling late-stage
disease, which is extremely difficult to treat.
There is often a latent period of several years
between the precipitating event and the onset of
lymphedema. The identification, education, and
treatment of such at-risk patients can slow
down, even prevent, the onset of disease. In
patients with established lymphedema, the
three goals of treatment are to relieve of pain,
reduce swelling, and prevent the development of
complications.

On initial presentation 50% of patients with
lymphedema complain of significant pain. The
pain is usually multifactorial, and its severity
and underlying cause(s) vary depending on the
etiology of the lymphedema. For example,
following treatment for breast cancer, pain
may arise from the swelling itself, radiation and
surgery induced, nerve (brachial plexus and
intercostobrachial nerve), bone (secondary
deposits, radiation necrosis) and joint disease
(arthritis, bursitis, capsulitis), and recurrent
disease. The detailed treatment of such patients
is beyond the scope of this chapter but involves
the considered use of nonopioid and opioid
analgesics, corticosteroids, tricyclic antidepres-
sants, muscle relaxants, antiepileptics, nerve
blocks, physiotherapy, adjuvant anticancer ther-
apies (chemo-, radio-, hormonal therapy), as
well as measures to reduce swelling if possible.
In patients with non-cancer-related lym-
phedema, the best way to reduce pain is to
control swelling and prevent the development of
complications.

Physical therapy for lymphedema comprising
bed rest, elevation, bandaging, compression
garments, massage, and exercises was first
described at the end of the 19th century, and
through the 20th century various eponymous
schools developed. Although there is little doubt

that physical therapy can be highly effective
in reducing swelling, its general acceptance
and practice has been hampered by a lack of
proper research and confusing terminology.
The current preferred term is decongestive lym-
phedema therapy (DLT) and comprises two
phases. The first is a short intensive period of
therapist-led care, and the second is a mainte-
nance phase where the patient uses a self-care
regimen with occasional professional interven-
tion. The intensive phase comprises skin care,
manual lymphatic drainage (MLD), multilayer
lymphedema bandaging (MLLB), and exercises.
The length of intensive treatment depends on
the disease severity, the degree of patient com-
pliance, and the willingness and ability of
the patient to take more responsibility for the
maintenance phase. However, weeks rather
than months should be the goal.

The patient must be carefully educated in the
principles and practice of skin care. The patient
should inspect the affected skin daily, with
special attention paid to skin folds where mac-
eration may occur. The limb should be washed
daily, the use of bath oil (e.g., balneum) is rec-
ommended as a moisturizer, and the limb must
be carefully dried afterward. A hair drier, on low
heat, is more effective and hygienic, and less
traumatic, than a towel. If the skin is in good
condition, daily application of a bland emollient
is recommended to keep the skin hydrated. If
the skin is dry and flaky, then a bland ointment
[e.g., 50/50 white soft paraffin/liquid paraffin
(WSP/LP)] should be used twice daily, and if
there is marked hyperkeratosis, then a kera-
tolytic agent such as 5% salicylic acid can be
added. Many commercially available soaps,
creams, and lotions contain sensitizers, and, as
patients with lymphedema are highly suscepti-
ble to contact dermatitis (eczema), are best
avoided. Apart from causing intense discomfort,
eczema acts as an entry point for infection.
Management comprises avoidance of the aller-
gen (patch testing maybe required) and topical
corticosteroids. Fungal infections are common,
difficult to eradicate, and predispose to AIEs.
Chronic application of antifungal creams leads
to maceration, and it is better to use powders
in shoes and socks. Ointment containing 3%
benzoic acid helps prevent athlete's foot and can
be used safely over long periods. Painting at-risk
areas with an antiseptic agent such as eosin may
be helpful. Lymphorrhea is uncommon but

121

CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

extremely troublesome. Management comprises
emollients, elevation, compression, and some-
times cautery under anesthesia.

Apart from lymphangiosarcoma, AIEs are
probably the most serious complications of
lymphedema and frequently lead to emergency
hospital admission. About 25% of primary and
5% of secondary lymphedema patients are
affected. The AIEs start rapidly, often without
warning or precipitating event, with tingling,
pain, and redness of the limb. Patients feel viral,
and severe attacks can lead to the rapid onset of
fever, rigors, headache, vomiting, and delirium.
Patients who have suffered previous attacks can
usually predict the onset, and many learn to
carry antibiotics with them and self-medicate at
the first hint of trouble. This may stave off a
full-blown attack and prevent the further lym-
phatic injury that each AIE causes. It is rarely
possible to isolate a responsible bacterium, but
the majority are presumed to be streptococcal
or staphylococcal in origin. The diagnosis is
usually obvious but dermatitis, throm-
bophlebitis, and DVT are in the differential.
Benzyl (intravenous) or phenoxymethyl (oral)
penicillin, and flucloxacillin (or clindamycin in
severe attacks), are the antibiotics of choice and
should be given for 2 weeks. Rest reduces lym-
phatic drainage and the spread of infection,
elevation reduces the edema, and heparin pro-
phylaxis reduces the risk of DVT. Co-amoxiclav
can be taken by patients who self-medicate. The
use of long-term prophylactic antibiotics is not
evidence-based but is probably reasonable in
patients who suffer frequent attacks. However,
the benefits of scrupulous compliance with
physical therapy and skin care cannot be under-
estimated.

Several different techniques of MLD have
been described and the details are beyond the
scope of this chapter. However, they all aim to
evacuate fluid and protein from the ISF space
and stimulate lymphangion contraction. Thera-
pists should perform MLD daily; they should
also train the patient or caregiver to perform a
simpler, modified form of massage termed
simple lymphatic drainage (SLD). In the inten-
sive phase, SLD supplements MLD, and once the
maintenance phase is entered, SLD will carry on
as daily massage.

Elastic bandages provide compression, pro-
duce a sustained high resting pressure, and
compress more as limb swelling reduces.

However, the sub-bandage pressure does not
alter greatly in response to changes in limb cir-
cumference consequent upon muscular activity
and posture. By contrast short-stretch bandages
exert support through the production of a semi-
rigid casing, where the resting pressure is low
but changes quite markedly in response to
movement and posture.

It is generally believed that nonelastic MLLB
is preferable (and arguably safer) in patients
with severe swelling during the intensive phase
of DLT, whereas compression (hosiery, sleeves)
is preferable in milder cases and during the
maintenance phase. Whether the aim is to
provide support or compression, the pressure
exerted must be graduated (100% ankle/foot,
70% knee, 50% mid-thigh, 40% groin), and the
adequacy of the arterial circulation must be
assessed. As it is rarely possible to feel pulses in
the lymphodematous limb, noninvasive assess-
ment of ABI using a handheld Doppler ultra-
sound device is usually necessary. The details of
MLLB are beyond the scope of this chapter;
however, it is highly skilled and in order to be
effective and safe, it needs to be applied by a
specially trained therapist. It is also extremely
labor intensive, needing to be changed daily.
Compression garments form the mainstay of
management in most clinics. The control of
lymphedema requires higher pressures (30 to 40
mmHg in the arm, 40 to 60mmHg in the leg)
than are typically used to treat CVI. The patient
should put the stocking on first thing in
the morning before rising. It can be difficult
to persuade patients to comply. Donning
lymphedema-grade stockings is difficult, and
many patients find them intolerably uncomfort-
able, especially in warm climates. Furthermore,
although intellectually they understand the
benefits, emotionally they may find wearing
them presents a greater body image problem
than the swelling itself.

Enthusiasm for pneumatic compression
devices has waxed and waned. Unless the device
being used allows the sequential inflation of
multiple chambers up to 50 mm Hg, it will prob-
ably be ineffective for lymphedema. Patient
benefit is maximized and complications mini-
mized if these devices are used under the direc-
tion of a physical therapist as part of an overall
package of care.

Lymph formation is directly proportional to
arterial inflow, and 40% of lymph is formed

122

VASCULAR SURGERY

within skeletal muscle. Vigorous exercise, espe-
cially if it is anaerobic and isometric, tends to
exacerbate lymphedema, and patients should
be advised to avoid prolonged static activities,
for example, carrying heavy shopping bags or
prolonged standing. By contrast, slow rhythmic
isotonic movements (e.g., swimming) and mas-
sage increase venous and lymphatic return
through the production of movement between
skin and underlying tissues (essential to the
filling of initial lymphatics) and augmentation
of the muscle pumps. Exercise also helps to
maintain joint mobility. Patients who are unable
to move their limbs benefit from passive exer-
cises. When at rest, the lymphedematous limb
should be positioned with the foot/hand above
the level of the heart. A pillow under the mat-
tress or blocks under the bottom of the bed
encourage the swelling to go down overnight.

There are considerable, and scientifically
inexplicable, differences in the use of specific
drugs for venous disease and lymphedema
between different countries. The benzpyrenes
are a group of several thousand naturally occur-
ring substances, of which the flavonoids have
received the most attention. Enthusiasts argue
that a number of clinical trials have shown
benefit from these compounds, which are
purported to reduce capillary permeability,
improve microcirculatory perfusion, stimulate
interstitial macrophage proteolysis, reduce ery-
throcyte and platelet aggregation, scavenge free
radicals, and a exert an antiinflammatory effect.
Detractors argue that the trials are small and
poorly controlled, with short follow-up and soft
end points, and that any benefits observed can
be explained by a placebo effect. Diuretics are of
no value in pure lymphedema. Their chronic use
is associated with side effects including elec-
trolyte disturbance and should be avoided.

Surgery

Surgery benefits only a small minority of
patients with lymphedema. Operations fall into
two categories: bypass procedures and reduc-
tion procedures. The rare patient with proximal
ilioinguinal lymphatic obstruction and normal
distal lymphatic channels might benefit, at least
in theory, from lymphatic bypass. A number of
methods have been described including the
omental pedicle, the skin bridge (Gillies), anas-
tomosing lymph nodes to veins (Neibulowitz),

the ileal mucosal patch (Kinmonth), and, more
recently, direct lymphovenous anastomosis.
The procedures are technically demanding, not
without morbidity, and there is no controlled
evidence to suggest that these procedures
produce an outcome superior to the best
medical management alone. Limb reduction
procedures are indicated when a limb is so
swollen that it interferes with mobility and
livelihood. These operations are not cosmetic in
the sense that they do not create a normally
shaped leg and are usually associated with
significant scarring. Four operations have been
described:

1. Sistrunk: A wedge of skin and subcuta-
neous tissue is excised and the wound
closed primarily. This is most commonly
employed to reduce the girth of the thigh.

2. Homan: Skin flaps are elevated; subcuta-
neous tissue is excised from beneath the
flaps, which are then trimmed to size to
accommodate the reduced girth of the
limb and closed primarily. This is the most
satisfactory operation for the calf. The
main complication is skin flap necrosis.
There must be at least 6 months between
operations on the medial and lateral sides
of the limb, and the flaps must not pass
the midline. This procedure has also been
used on the upper limb but is contraindi-
cated in the presence of venous obstruc-
tion or active malignancy.

3. Thompson: One denuded skin flap is
sutured to the deep fascia and buried
beneath the second skin flap (the so-called
buried dermal flap). This procedure has
become less popular as pilonidal sinus for-
mation is common, the cosmetic result is
no better than that obtained with the
Homan's procedure, and there is no evi-
dence that the buried flap establishes any
new lymphatic connections within the
deep tissues.

4. Charles: This operation was initially
designed for filariasis and involved exci-
sion of all the skin and subcutaneous
tissues down to the deep fascia with cover-
age using split skin grafts. This leaves a
very unsatisfactory cosmetic result, and
graft failure is not uncommon. However, it
does enable the surgeon to reduce greatly
the girth of a massively swollen limb.

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CHRONIC VENOUS INSUFFICIENCY, VARICOSE VEINS, LYMPHEDEMA, AND ARTERIOVENOUS FISTULAS

Arteriovenous Fistulas

Classification

Arteriovenous fistulas (AVFS) are broadly
classified into congenital and acquired.
Acquired fistulas may be traumatic, iatrogenic,
or associated with malignancy, aneurysmal
disease, and infection. These are not considered
further. Congenital AVFs are further classified
as hemangiomas or malformations. The former
are characterized by endothelial hyperplasia,
are not present at birth, and grow in early child-
hood, but in 90% of cases involute by the age
of 5 to 10 years. The latter exhibit normal
endothelial cell kinetics, are always preset at
birth, grow and continue to grow with the child,
and may enlarge dramatically at puberty or in
pregnancy. Whenever vascular lesions appear
and grow rapidly, it is important to exclude
malignancy. Malformations may be high flow
(predominantly cardiac and great vessel anom-
alies) or low flow (arterial, venous, lymphatic, or
mixed). The processes leading to the develop-
ment of the mature vascular tree are largely
unknown, but presumably congenital fistulas
represent a localized disorder of vessel forma-
tion. Occasionally they may be familial, and
some abnormalities have been mapped to
certain chromosomal loci.

Symptoms and Signs

The clinical presentations are protean and
depend on the nature of the lesion, anatomical
site, size, and flow.

Malformations

Although malformations are present at birth,
they do not usually become symptomatic, and
even go unnoticed, until later at life. They typi-
cally present at puberty or during pregnancy or
following trauma to the part. There is usually
an obvious swelling and discoloration, and
there maybe limb enlargement. Adults typically
present with a lump, VVs, (ischemic) ulceration,
bleeding, or an inequality in limb length. That
which is visible is often the "tip of the iceberg,"
and the deep component may cause pain, pres-
sure on local strictures, organ dysfunction, and
internal bleeding. On examination there is dis-

coloration and a lump. If arterial, it is typically
firm, pulsates, and is associated with a thrill and
a murmur and sometimes pulsatile draining
veins. If primarily venous, it is soft and com-
pressible, and reduces in size and enlarges upon
elevation and dependency, respectively.

Hemangiomas

Hemangiomas present at or within a few weeks
of birth. They are said to be present in 10%
of Caucasian children on their first birthday, to
be three times commoner in girls, to be multi-
ple in 20%, and to affect the head and neck
(60%), trunk (25%), and extremities (10%). If
superficial, they are bright (strawberry nevus),
and if deep dark (cavernous hemangioma), red.
They are firm and rubbery and cannot be
emptied of blood on compression or elevation.
After an initial phase of rapid growth, they
begin to involute at about 6 to 12 months of
age when the red color turns to purple,
gray/while flecks appear, the lesion becomes
softer, and the overlying skin wrinkles. Resolu-
tion is typically completed in 50% at 5 years,
70% at 7 years, and 90% or more by 10 years.
Apart from cosmetic concerns there may be
ulceration and bleeding. On the face they may
block vision, and depending on where they are
sited may cause mass effects. Large heman-
giomas involving internal organs may cause
heart failure and anemia.

Diagnosis and Investigation

The diagnosis can usually be made on clinical
examination. Handheld Doppler helps to con-
firm if there is an arterial component, and DU
provides more detailed anatomical and func-
tional information. In particular, DU permits
detailed assessment of the venous system in
patients with Klippel-Trenaunay syndrome
where the deep venous system maybe hypoplas-
tic or even absent, having been replaced by an
abnormal laterally placed venous malformation.
Duplex ultrasound has largely replaced venog-
raphy. Phleboliths may be seen on plain x-rays
and are only usually seen in venous lesions.
Magnetic resonance imaging, rather than CT, is
now regarded as the definitive investigation for
assessing the extent of AVF. Angiography is
performed only where there is an intention to
treat radiologically

124

VASCULAR SURGERY

Management

Management is complex, multidisciplinary (vas-
cular, plastic, maxillofacial, and orthopedic sur-
geons, interventional radiologist, cardiologist),
difficult, and highly tailored to the individual
patient. Many patients (and parents) simply
require reassurance, and in general it pays to be
as conservative as possible. Only 10% of heman-
giomas fail to resolve spontaneously and many
malformations remain asymptomatic. Pallia-
tion, not cure, is the principal aim, and it is
important to ensure that the treatment is not
worse than the disease. Venous lesions may
be treated with compression bandaging and
hosiery. A small minority of patients are suit-
able for excisional surgery. Complete excision is
rarely possible, and usually the aim is to remove
the most symptomatic part. Such surgery can be
difficult and bloody, and recurrence is common.
For these reasons, most patients are treated
radiologically either by transcatheter emboliza-

tion (arterial lesions) or by direct injection
(venous lesions), usually under general anesthe-
sia. This is a highly skilled and specialized
branch of interventional radiology, and great
care must be taken to avoid collateral damage.
Extremities are particularly vulnerable. Surgical
skeletonization of the arterial inflow to the
lesion is now avoided, as recurrence is inevitable
and such intervention prevents radiological
intervention. Strong indications for interven-
tion are hemorrhage, distal ischemia due to
steal, and ulceration due to ischemia or venous
hypertension.

References

Cornu-Thenard A, Boivin P, Baud JM, De Vincenzi I,
Carpentier PH. (1994) J Dermatol Surg Oncol
20:318-26.

Dwerryhouse S, Davies B, Harradine K, Earnshaw JJ. (1999)
J Vase Surg 29:589-92.

Szuba A, Rockson SG. (1997) Vase Med 2:321-6.

Vascular Trauma

Kathleen J. Ozsvath, R. Clement Darling III,
Laila Tabatabai, Sacha Hamdani, Alun H. Davies,
and Meryl Davis

Trauma is the leading cause of death in patients
under the age of 44 in the United States. North
American trauma centers have an incidence of
penetrating trauma of 35% as compared with
5% to 8% in Europe, the difference being ex-
plained by the higher rate of weapon-related
crimes in North America. The treatment of trau-
matic vascular injuries today is based on prin-
ciples gained during the military conflicts of the
20th century; previously treatment of vascular
injuries was limited to the staunching of bleed-
ing by cautery, compression, and ligature. The
concept of repair was documented in anecdotal
reports only. William Hunter in 1759 recounts
the first successful vascular repair on a brachial
artery using a farrier's stitch.

Reports of vein grafting were available in
the early 20th century; however, these tech-
niques were not suitable for the injuries en-
countered during World War I, in which the
amputation rate was noted to be 72.5%. In 1946
DeBakey and Simeone published a review of
World War II experiences with vascular surgery.
They concluded that ligation was "of stern
necessity," required to control hemorrhage;
attempts at vascular repair were superior to
ligation and led to an amputation rate of
49%.

The application of vessel reconstruction in
the Korean War, despite the mean lag time of
over 6 hours between injury and repair, reduced
the lower limb amputation rate to 13% (Hughes,
1959); a comparable figure was achieved during
the Vietnam War. The Vietnam Vascular Regis-

try was established during the Vietnam War;
surgeons were able to document and analyze the
long-term management and outcome of vascu-
lar trauma (Rich and Hughes, 1969). The
significantly improved long-term results of vas-
cular repair were attributed to faster evacuation
of casualties within 3 hours of injury, thereby
allowing surgeons to treat injuries that had pre-
viously been otherwise fatal. Operations were
performed by experienced surgeons using auto-
logous vein grafts.

The rise of civilian trauma in the United
States has resulted in surgeons becoming more
adept and experienced at dealing with vascu-
lar injuries (Mattox et al., 1989). Penetrating
injuries have been the number one cause of
vascular trauma in both urban and rural com-
munities, whereas blunt trauma has accounted
for approximately 50% of vascular injuries,
most commonly secondary to road traffic
accidents.

Regardless of the etiology of the vessel injury,
the essential principles of treatment are emer-
gency resuscitation at the scene, triage and
rapid transport to an appropriate hospital, vig-
orous resuscitation, diagnosis, and definitive
surgery. Ideally, vascular injuries should be
treated by surgeons with expertise in vascular
reconstruction and trauma, in an environment
with the necessary ancillary support services to
allow the best results.

This chapter reviews the workup and treat-
ment of traumatic vascular injuries involving
the head and neck, chest, abdomen, and extrem-

125

126

VASCULAR SURGERY

ities, and discusses the approach to iatrogenic
injuries and the endovascular treatment of vas-
cular injuries.

Mechanisms of Injury

Vascular injuries can be divided into penetrat-
ing and blunt. Penetrating injuries include stab-
bing and gunshot wounds. Stab wounds are
usually clean with minimal soft tissue injury;
however, in the neck and upper limb concurrent
nerve damage must also be suspected.

Gunshot wounds are classified according to
the bullet velocity. Low velocity bullets have
a velocity of less than 250 m/s, whereas 750 to
900 m/s represents the speed of high-velocity
bullets. Low-velocity bullets injure the tissue
through which they pass, whereas high-velocity
bullets create a cavitational effect, thereby caus-
ing a suctional effect contaminating the entire
wound. If a high-velocity bullet strikes bone,
there is extensive comminution with a large exit
wound. Shotgun injuries particularly to a limb
can cause vascular damage at several levels.
Bombs, mines, and rocket-propelled grenades
produce complex injuries that frequently result
in amputation.

Blunt vascular trauma is often caused by
deceleration in road traffic accidents and is fre-
quently associated with other injuries. Femoral
shaft fractures and fracture dislocations of the
knee carry a 10% to 40% incidence of vascular
injury. It is important to realize that although
the artery can remain intact, intimal damage
with concomitant thrombosis risk can occur.
Blunt trauma to the upper limb is often asso-
ciated with avulsion injuries to the brachial
plexus. Extensive crush injuries to the limbs are
associated with a poor prognosis due to soft
tissue damage and reperfusion injury.

Iatrogenic injuries are increasing in inci-
dence as a consequence of invasive procedures.
Cardiological and radiological catheterization
cause between 60% and 76% of all iatrogenic
injuries. Orthopedic procedures including joint
replacements may cause vascular injury, com-
monly to the external iliac, common femoral, or
popliteal arteries. In such cases where iatrogenic
arterial injury is suspected, expeditious referral
to a vascular surgeon must be made.

Diagnosis

The clinical manifestations of vascular injury
are divided into hard and soft signs (Table 11.1).
The management of penetrating limb trauma in
the presence of one hard sign is exploration in
the operating room. In blunt trauma, closed
head injuries, spinal damage, and cervical and
brachial plexus injuries may complicate the
clinical findings; a careful neurological exami-
nation is mandatory.

Clinical examination in blunt and complex
penetrating trauma may be unreliable, and
trauma centers advise early angiography. The
role of duplex ultrasound in vascular trauma is
less clear; currently it has a major role in the
diagnosis of occult vascular injuries and in
postoperative assessment. Doppler arterial pres-
sure index (API) is a useful tool. It is the systolic
arterial pressure in the injured extremity
divided by the arterial pressure in a noninjured
arm. A result of <0.90 has been found to have a
sensitivity of 95% and specificity of 97% for
major arterial injury (Johansen et al., 1991).

Once the diagnosis of major vascular injury
has been made, the majority of patients require
exploration and repair. The principles of emer-
gency vascular repair are to control bleeding
and prevent limb ischemia. Hemorrhage is
usually apparent, but ischemia maybe insidious
and must be sought. Time is paramount; it is
generally accepted that more than 6 to 8 hours
of warm ischemia time makes limb survival
unlikely. If there is significant concurrent nerve
damage, then limb reconstruction may not be
appropriate and amputation should be per-
formed. The input of multidisciplinary teams is
vital to ensure optimal treatment.

Table 11.1. The clinical manifestations of vascular injury are
divided into hard and soft signs

Hard signs

Soft signs

No pulse

Hematoma (small)

Thrill or bruit

History of bleeding at scene

Active bleeding

Hypotension

Hematoma (large/

Nerve damage

expanding)

Distal ischemia

127

VASCULAR TRAUMA

Vascular Injuries in the Neck

Wounds of major vessels are often lethal, and
frequently these patients have multiple injuries.
This is particularly true in penetrating in-
juries of the brachiocephalic vessels, where air-
way compromise, hemorrhage, and neurological
damage secondary to impaired brain blood flow
may occur, along with associated injuries to the
pharynx, esophagus, and brachial plexus.

In the neck penetrating trauma is more
common than blunt trauma, although vascular
injuries caused by blunt trauma can be more
difficult to diagnose and treat. Blunt injuries
include steering wheel injuries, deceleration
forces, and crushing blows.

Injuries to the carotid artery occur in 6% of
penetrating injuries to the neck and make up
22% of all vascular neck injuries, whereas 3% to
5% of carotid injuries are secondary to blunt
trauma (Demetriades et al., 1996). The mortal-
ity rate of patients with penetrating neck vas-
cular trauma is 5% to 20%. Patients presenting
with obvious signs of penetrating vascular
injury (expanding hematoma, pulsatile bleed-
ing) should be rapidly explored operatively

Treatment of vascular injuries in the neck is
based on dividing the neck into three zones:
zone I is 1cm above the manubrium including
the thoracic outlet, zone II extends from the
upper limit of zone I to the angle of the man-
dible, and zone III lies between the angle of the
mandible and the base of the skull (Fig. 11.1).

Zone I injuries are best explored through a
median sternotomy, which can then be extended
superiorly along the anterior border of the ster-
nocleidomastoid muscle as needed. Penetrating
trauma to vessels in zone II can be approached
directly for definitive repair. Zone III injuries
can be difficult to access and sometimes require
subluxation of the mandible or mandibular
osteotomy. Patients with zone III asymptomatic,
angiographically documented injuries are now
being managed with endovascular stenting or
embolization (Feliciano, 2001).

Arterial defects are repaired with primary
repair, transposition, patch, or bypass. Patients
found to have an acutely occluded carotid artery
are anticoagulated in an effort to prevent clot
propagation. Neurologically impaired patients
with carotid injuries are aggressively treated
surgically. Patients with small intimal defects

Figure 11.1. Treatment of vascular injuries in the neck is based
on dividing the neck into three zones: zone I is 1 cm above the
manubrium to include the thoracic outlet, zone II extends from
the upper limit of zone I to the angle of the mandible, and zone
III lies between the angle of the mandible and the base of the
skull.

and dissections of the carotid artery who are
otherwise stable may be followed with physical
examination and follow-up duplex ultrasound,
because these lesions may resolve without inter-
vention. Venous injuries may be dealt with by
ligation. In the unusual circumstance of both
internal jugular veins having been damaged it is
imperative that one vein be reconstructed.
Patients with blunt carotid artery injuries can
be difficult to diagnose due to either other
distracting injuries or altered mental status.
Carotid artery blunt injuries are associated with
a high mortality and poor neurological out-
comes in most patients.

Mechanisms of blunt carotid artery in-
juries include hyperextension, direct injury,
basilar skull fractures, and intraoral injuries.
Patients may present with carotid artery dissec-
tions, thrombosis, pseudoaneurysms, carotid-
cavernous sinus fistulas, or arterial disruption.
Carotid artery dissections and thrombosis are
treated with anticoagulation. Cogbill et al.
(1994) reported that two thirds of patients with
carotid dissections eventually have normal
studies on follow-up, whereas one third pro-
gress. Pseudoaneurysms may be treated surgi-

128

VASCULAR SURGERY

cally or radiologically depending on their size.
Carotid-cavernous sinus fistulas are generally
treated by endovascular techniques. Complete
disruption of the carotid artery is associated
with a high mortality.

Injury to the vertebral arteries is rare. The
anatomical location of the injury determines the
best operative approach when intervention is
required. Proximal vertebral artery exposure is
performed by a transverse supraclavicular inci-
sion or an anterior cervical incision. The cervi-
cal vertebral artery is best approached through
an incision along the anterior border of the ster-
nocleidomastoid muscle, and can be extended
to the posterior auricular area. Once the verte-
bral artery takes its course from the C2 foramen
and enters the skull, the exposure becomes very
difficult. Ligation or occlusion of the vertebral
artery is usually the treatment of choice. Per-
cutaneous techniques have been successfully
employed in managing arteriovenous fistulas,
pseudoaneurysms, and occlusions (Halbach
et al, 1993).

Thoracic Vascular Injuries

Thoracic vascular trauma constitutes approxi-
mately 10% of vascular trauma (Bongard et al.,
1990). Although penetrating trauma remains
the most common etiology of thoracic vascular
injuries, deceleration injuries and crush injuries
can result in major thoracic vascular trauma.
Injuries to the vessels in the thoracic cavity
can lead to rapid blood loss and hemodynamic
collapse; many patients die before reaching
the hospital. It is often more appropriate to
bypass the nearest hospital and transfer the
patient to a unit able to manage cardiothoracic
problems.

These patients may require immediate treat-
ment for tension pneumothorax or cardiac tam-
ponade. Thoracotomy may be required as an
emergency procedure and is usually carried out
via a left anterolateral thoracotomy incision
(which can be extended across the sternum) or
a posterolateral thoracotomy. Access to carotid
arteries and innominate artery can be obtained
through a median sternotomy. Middle and distal
subclavian artery injuries can be controlled
with infra- and supraclavicular approaches.

Clinical findings suggesting thoracic injury
include external evidence of severe chest

bruising, reduced or absent lower limb pulses,
raised jugular venous pressure, and unex-
plained hypotension. The chest radiograph may
show a widened mediastinum, fracture of the
first or second rib, hemothorax, and thoracic
spine injury.

In stable patients the investigations of choice
are chest radiographs (suggesting great vessel
or aortic injury), spiral computed tomography
(CT) with contrast, angiography, and trans-
esophageal echocardiography.

The most common intrathoracic injury
caused by deceleration involves disruption of
the descending thoracic aorta at the isthmus.
Sudden death is common, and it is estimated
that 90% die before reaching the hospital; of
those who reach the hospital, 25% die within
24 hours.

Commonly the site of aortic disruption is
distal to the left subclavian artery. Access is
gained via a left posterior thoracotomy with
cardiopulmonary bypass. The incidence of
paraplegia is approximately 8%. Recent endolu-
minal treatment has been described and shown
to be successful with a lower mortality rate.

The subclavian arteries are relatively well
protected from blunt trauma. Patients may
present with absent distal pulses, and injury
should be suspected in patients with a first rib
fracture or traction injury to the brachial
plexus. In stable patients, careful clinical assess-
ment of the brachial plexus and magnetic reso-
nance imaging (MRI) should be performed
prior to surgical exploration.

Direct repair of the vessel, patch, and pros-
thetic or autologous interposition grafts are
possible choices in repairing aortic and great
vessel injuries. Some centers are now opting to
use endovascular techniques (Ohki et al., 1997).
At present this method of treatment should be
pursued only in institutions with adequate sur-
gical and radiological expertise.

Abdominal Vascular Injuries

One third of patients with vascular trauma pre-
sent with abdominal vascular injuries. These
patients are more commonly victims of pene-
trating injuries, with mortality rates averaging
50%. Deceleration and compression injuries are
common blunt injuries and may cause damage
to the renal or superior mesenteric arteries and

129

VASCULAR TRAUMA

portal vein tributaries. Vessels can be injured
by transection or partial transection, or have
intimal defects causing thrombosis. Major vas-
cular injury in the abdomen is often associated
with injuries to other intraabdominal organs. Of
those patients who reach the hospital, the mor-
tality postsurgery remains high (50% to 70%
for aortic injury and 30% to 53% for vena caval
injury).

Resuscitation is based on Advanced Trauma
Life Support (ATLS) guidelines, with unstable
patients being transferred promptly to the oper-
ating room (Fig. 11.2). Intrathoracic injuries are
associated in up to 25% of patients with gunshot
wounds of the abdomen.

The assessment of stable patients with intra-
abdominal pathology has been extensively dis-
cussed; ultrasound and CT are the modalities of
choice. Angiography in the stable patient with
blunt injuries may be useful in documenting
unusual injuries.

In unstable patients with significant hemor-
rhage, laparotomy should be performed and the
abdomen packed, and systematic evaluation
of the abdomen undertaken. Large defects in
the gastrointestinal tract should be temporarily
controlled with soft bowel clamps to reduce
contamination. If hemorrhage is not controlled,
it maybe necessary to cross-clamp the proximal
supraceliac aorta via the lesser sac; alternatively
(via the left thorax) the descending thoracic
aorta may be cross-clamped. The goal is to
obtain proximal and distal control of the hem-
orrhaging vessels so that repair or ligation can
quickly be undertaken. Hypothermia and coag-
ulopathy is a serious risk; therefore, expeditious
control is important. Aortic injuries can be
repaired with a transverse primary repair, a

patch with autologous or prosthetic material, or
interposition grafting with prosthetic material.
The use of antibiotic-soaked grafts may over-
come concerns regarding the use of prosthetic
material in the presence of penetrating injuries.

The decision to explore a retroperitoneal
hematoma depends on the mechanism of injury
and stability of the patient. For a retroperitoneal
hematoma caused by blunt trauma, a conser-
vative approach is advised especially when it
is associated with pelvic fractures. This can
be addressed by external fixation of the pelvis,
angiography, and coil embolization. In contrast
an expanding or pulsatile retroperitoneal
hematoma requires immediate exploration.

Retrohepatic caval injuries are difficult to
control and carry a high mortality. Mobilization
of the liver with division of the right triangular
ligament and right thoracotomy with dissection
of the diaphragm may be required. Bleeding
from the porta hepatis can be controlled by
compression of the hepatic artery and portal
vein (Pringle's maneuver).

The mortality rate for patients with
significant superior mesenteric artery (SMA)
injury can be high (58% mortality rate). Injuries
to the proximal SMA are technically challenging
due to the proximity of the pancreas and the
presence of multiple short branches. Control of
the suprameso colic vessels can be obtained by
medial visceral rotation via the left paracolic
gutter. Injuries to the celiac artery and branches
may present with an expanding hematoma dis-
placing the stomach and pancreas forward.
Celiac axis vessels may be ligated if there is
a patent SMA. Retropancreatic SMA control
may have to be obtained by transection of the
pancreas.

Haemodynamically
Unstable

Figure 11.2. Algorithm for the
management of a patient with
abdominal trauma.

Theatre

Resuscitation as per
ATLS guidelines

Haemodynamically
Stable

Ultrasound

Angiography

130

VASCULAR SURGERY

Injury or transection of the SMA may require
either autologous or prosthetic bypass. Bowel
viability may be difficult to assess intraopera-
tively; therefore, second-look laparotomy in
these patients is advisable.

Inframesocolic vessel injuries can be ap-
proached by mobilizing the small intestines and
transverse colon superiorly. The inferior mesen-
teric artery can be ligated in most patients, as
collaterals exist that provide adequate blood to
the intestine.

Access to the inferior vena cava, right renal
vein, suprarenal aorta, and porta may be gained
by an extended mobilization of the duodenum,
head of pancreas, and right colon (Kocher
maneuver). The infrarenal aorta is exposed by
retracting the small bowel to the right and incis-
ing the retroperitoneum from the root of the
mesocolon to the pelvis. Simple stab wounds to
the aorta may be closed primarily; more exten-
sive injuries may require a prosthetic patch or
bypass graft. In the presence of significant con-
tamination, an axillobifemoral bypass may be
preferred after ligation of the aorta. Iliac vessel
injuries can be approached via the retroperi-
toneum; such injuries carry a high mortality
(10% to 40%) and morbidity including limb
loss.

Renal artery injury may occur after rapid
deceleration, resulting in acute renal artery
thrombosis or laceration. The diagnosis of
thrombosis is often made late, and if explored
12 hours after the injury, renal salvage is often
limited. In patients with a functioning kidney
on the opposite side, a "watch and wait" policy
can be adopted.

The control of venous hemorrhage can be
difficult. Simple injuries to the inferior vena
cava can be repaired primarily with intermittent
digital pressure. In severe hemorrhage, ligation
of the infrarenal vena cava may be necessary; in
contrast, injury to the suprarenal vena cava
requires reconstruction.

Extremity Vascular Injuries

Experience both with trauma patients and with
noninvasive techniques are paramount in the
management of extremity vascular trauma. A
low threshold for angiography should be main-
tained to diagnose ischemia.

In those patients requiring surgical inter-
vention, vessels are repaired by primary repair,
interposition grafting, or bypass with vein
(from the uninjured limb) or prosthetic mate-
rial; 31% of patients with arterial trauma have
concomitant venous injuries. Repair of venous
injuries has been found to improve the outcome
of patients with combined arterial and venous
injuries (Martin et al., 1994; Pappas et al.,
1997).

Grossly contaminated wounds and massive
soft tissue and bone injuries require a multi-
disciplinary team approach to management.
Orthopedic injuries should be reduced with
external fixators, and arterial and venous shunts
can be used to minimize the ischemia time. Soft
tissue coverage either by extraanatomical by-
pass or muscle flaps maybe necessary to protect
vascular repairs.

Debridement of devitalized tissue is impor-
tant for postoperative wound care. Fasciotomies
are also of great importance in those patients
with extremity injuries who have suffered
delayed repair, extensive tissue injury, swelling,
elevated compartment pressures, and prolonged
hypotension. The development of compartment
syndrome can lead to myoglobinuria, renal
failure, and skeletal muscle necrosis.

Controversies arise in the presence of exten-
sive tissue damage, vascular injuries, and con-
comitant nerve injuries. Unfortunate patients
may be facing the future with a viable limb that
is nonfunctioning and painful after multiple
operations. These patients may be best served
with a primary amputation. This is a difficult
decision to make, and therefore should be made
only after extensive discussion with the patient
and family, and after the expertise of the com-
bined team has been sought.

Injuries of the subclavian and axillary vessels
rarely cause upper extremity ischemia due to
the rich collateral network at the shoulder.
Penetrating and blunt injuries can both lead
to brachial plexus injuries. Brachial artery
injuries below the level of the profunda brachii
may not present with ischemia due to the col-
lateral supply around the elbow. Isolated injury
to the ulnar or radial arteries may be treated
with ligation in the presence of a complete pal-
mar arch.

Injuries to the femoral vessels occur in 70%
of all arterial injuries, with penetrating trauma

131

VASCULAR TRAUMA

being the most common etiology. In 20% to 35%
of cases in which the popliteal artery is injured,
the popliteal vein and tibial nerve are also
involved. Blunt injuries to the knees leading
to posterior dislocation can result in popliteal
artery injury in 30% to 40% of patients. Single
tibial vessel injury can generally be dealt with by
ligation; however, if more than one vessel is
involved, repair is advocated.

Iatrogenic Vascular Injuries

With an increasing use of percutaneous tech-
niques, there is also a higher risk of iatrogenic
vascular injuries. In a survey of 10,500 cases
following femoral artery puncture, the in-
cidence of complications was 0.44% (Dorfman
and Cronan, 1991). For cardiac catheterization
the incidence was 0.55%, whereas peripheral
angiography resulted in a complication rate of
0.17%.

The most important risk is bleeding, which
may be controlled with direct pressure after a
catheter has been removed. Occasionally, surgi-
cal repair is undertaken to repair the punctured
vessel; direct repair is adequate in most
instances. Retroperitoneal bleeding is generally
self- limiting; however, when the patient has
been taking anticoagulants blood or pharmaco-
logical products maybe required to correct clot-
ting abnormalities.

Pseudo aneurysms can also complicate punc-
tures in 0.5% to 5.5% of diagnostic femoral
punctures. Most of these pseudoaneurysms
thrombose spontaneously. Many false aneur-
ysms respond well to ultrasound-guided com-
pression, which has now been superseded by
compression with concomitant injection of
procoagulant products. Surgical intervention
must be undertaken acutely in the presence of
a femoral neuropathy, hemodynamic instabil-
ity, overlying skin necrosis, and extremity
ischemia.

Arteriovenous fistulas usually present late
and complicate up to 2% of cardiac catheteriza-
tions. Although most of these fistulas throm-
bose, a small percentage can lead to congestive
heart failure or limb ischemia requiring either
radiological or surgical intervention.

Vascular injury secondary to intraarterial
injection of drugs can lead to extensive soft

tissue infection, mycotic aneurysm formation,
and gangrene.

Endovascular Treatments

With the emergence and development of endo-
vascular techniques, arterial trauma is being
treated at some centers with coil embolization,
intravascular stent grafts, and covered stent
grafts. The use of endovascular techniques has
minimized the need for extensive operative dis-
sections and anesthesia; this is especially impor-
tant in injuries involving vessels difficult to
assess. Endovascular techniques are best uti-
lized in institutions equipped and ready to
handle trauma in this fashion.

Conclusion

Improvements in patient transport to a level-
one trauma center combined with prehospital
care have allowed patients to present earlier for
treatment. The multidisciplinary team approach
to the management of these patients has led to
better outcomes.

In vascular reconstructive surgery autologous
bypasses should be used wherever possible
(vein being harvested from the uninjured limb).
In the event of this not being possible, the newer
antibiotic-soaked prosthetic grafts is advocated.

Interventional radiology with deployment of
endoluminal stents will continue to develop its
role in vascular trauma. It is important that vas-
cular surgeons remain involved in all aspects of
vascular trauma to facilitate improvements.

References

Bongard F, Dubrow T, Klein S. (1990) Ann Vase Surg 4:415-8.
Cogbill TH, Moore EE, Meissner M, et al. (1994) J Trauma

37:473-9.
Demetriades D, Asensio JA.Velmahos G,ThalE. (1996) Surg

Clin North Am 76:661-83.
Dorfman GS, Cronan JJ. (1991) Radiology 178:629-30.
Feliciano DV. (2001) World J Surg 25:1028-35.
Halbach VV, Higashida RT, Dowd CF, et al. (1993) J Neuro-

surg 79:183-91.
Hughes CW. (1959) Milit Med 124:30-46.
Johansen K, Lynch K, Paun M, Copass M. (1991) J Trauma

31:515-9; discussion 519-22.

132

VASCULAR SURGERY

Martin LC, McKenney MG, Sosa JL, et al. (1994) J Trauma

37:591-8; discussion 598-9.
Mattox KL, Feliciano DV, Burch J, et al. (1989) Ann Surg

209:698-705; discussion 706-7.
Ohki T, Veith FJ, Marin ML, Cynamon J, Sanchez LA. ( 1997)

Semin Vase Surg 10:272-85.

Pappas PJ, Haser PB, Teehan EP, et al. (1997) J Vase Surg

25:398-404.
Rich NM, Hughes CW. (1969) Surgery 65:218-26.

Complications in Vascular Surgery

Jeremy S. Crane, Nicholas J.W. Cheshire, and
Gilbert R. Upchurch, Jr.

Complications in vascular surgery are often life
threatening. However, with treatment options
for vascular disease ever widening, patient
selection for operative procedures is governed
not only by evidence-based treatment options
but also by immediate and long-term compli-
cations. The major impact complications of
vascular surgery, in particular long-term com-
plications, have on patient quality of life, inpa-
tient hospital costs, psychological problems,
and health care resources cannot be stressed
enough.

A useful working definition of a vascular
surgical complication is a procedure-related
adverse event that harms a patient (Table 12.1).
Many of the same complications that are ubiq-
uitous in general surgery are pertinent to vas-
cular surgery.

Cardiac and Pulmonary
Complications

The most important cause of mortality and
morbidity after major peripheral vascular sur-
gery is perioperative cardiac complications.
Atherosclerosis is a systemic arterial vascular
disorder typically involving multiple vascular
territories in the same patient. Accordingly,
coronary artery disease is the most frequently
associated vascular territory affected in patients
with peripheral arterial disease. Consequently,
cardiac manifestations of atherosclerosis in the

perioperative and postoperative occur, leading
to myocardial ischemia. Naturally, the type of
surgery is related to cardiac risk; procedures
associated with blood pressure and cardiac
rhythm changes with significant blood loss are
at high risk (e.g., aortic aneurysm repair),
whereas carotid endarterectomy carries moder-
ate cardiac risk.

Patients at high risk of a coronary event may
be considered for preoperative stress testing
or may be directly referred for coronary angio-
graphy with possible coronary bypass or
angioplasty prior to vascular surgery. Cardiac
complications influence the outcome of vascu-
lar surgery to such an extent that the existence
of cardiac disease may lead the vascular surgeon
to pursue an alternative surgical technique,
such as extraanatomical bypass to treat aortic
disease, or to cancel vascular surgical interven-
tion altogether.

The magnitude of the effect of coronary
disease following vascular surgery is such that
even 2 years following vascular surgery, 19%
of patients experience a late cardiac event
(Krupski, 1993).

In addition, many elderly vascular surgery
patients have a degree of underlying pulmonary
disease. Therefore, postoperative respiratory
complications are exceedingly common after
major vascular surgery. Predisposing patient
risk factors that may give rise to respiratory
problems include advancing age, cigarette smok-
ing, and the presence of chronic obstructive
pulmonary disease. Predisposing procedure-

133

134

VASCULAR SURGERY

Table 12.1. Classification of complications by outcome

Minor complications
No therapy, no consequence
Nominal therapy, no consequence; includes overnight
admission for observation only

Major complications

I Requires therapy, minor hospitalization (<48 hours)
Requires major therapy, unplanned increase in level of
care, prolonged hospitalization (>48 hours)
Permanent adverse sequelae
Death

specific risk factors include emergency proce-
dures, lengthy general anesthesia, thoracic or
upper abdominal incisions, massive blood
transfusions, and a postoperative period of pro-
longed immobility. Similar to cardiac disease,
screening for pulmonary dysfunction preope-
ratively can reduce postoperative respiratory
morbidity. A thorough history to ascertain
whether the patient suffers from dyspnea on
exertion or has significant sputum produc-
tion, coupled with a plain chest radiograph,
identifies most respiratory disease. Pulmonary
function tests and arterial blood gas samples
further aid diagnosis.

Preoperative therapy involving chest physio-
therapy, smoking restriction, antibiotics, and
bronchodilators can greatly reduce postopera-
tive pulmonary complications. The severity of
postoperative pulmonary complications can
range from benign minor atelectasis, which is
usually self-limiting, to a fulminant acute respi-
ratory failure that carries a very high mortality.
Accordingly, recognition and management of
postoperative cardiac and pulmonary complica-
tions are essential for the vascular surgeon.

Complications of Arterial
Reconstruction

Vascular surgical complications arising specifi-
cally from peripheral arterial reconstruction
are becoming more prevalent. This is due to
increasing numbers of operations being under-
taken, with up to 50,000 patients being admitted
annually to hospitals in the United Kingdom for
treatment of lower limb ischemia. Due to the
growing aging population coupled with the
ever-expanding role of vascular surgery, sur-
geons will be faced with increasing numbers of
complications following lower extremity revas-
cularization. As these complications may be life
or limb threatening, treating these complica-
tions is one of the most significant challenges
facing the contemporary vascular surgeon.

Specific complications associated with peri-
pheral arterial reconstructions usually occur
within predictable time frames, and can be
classified as immediate, early, intermediate, or
late (Table 12.2). For the purpose of this chapter,
immediate complications refer to those events
occurring intraoperatively or within the first
24 hours after surgery, early complications
occur less than 30 days after surgery, inter-
mediate occur within the first year, and late
occur after the first postoperative year. Compli-
cations occurring immediately perioperatively
and within the first 30 days after surgery are
most often due to technical error or poor
patient selection. Technical errors include inad-
equate anastomotic suturing technique, kinking
of the graft, and the injudicious choice of a
poor-quality, small-diameter graft. Poor quali-
ties of either inflow or distal run-off are pre-
dictors of poor graft longevity. Complications
ensuing from these errors are usually anasto-
motic hemorrhage or a partially or completely

Table 12.2. Time frame for

complications of peripheral vascular

grafts

Immediate

Early

Intermediate

Late

Anastomotic bleeding
Graft thrombosis
Embolic sequelae

Myointimal hyperplasia
Graft thrombosis

Accelerated atherosclerosis
Myointimal hyperplasia
Vein graft stenosis
Graft infection

Graft infection
Atherosclerosis
Myointimal hyperplasia
Graft aneurysm formation
Vein graft stenosis

135

COMPLICATIONS IN VASCULAR SURGERY

thrombosed graft with possible distal embolic
sequelae.

The wide range of vascular grafts now avail-
able has revolutionized vascular surgery. How-
ever, before a graft is declared competent and
durable, long-term follow-up is needed, as graft
failure may only become apparent several years
after implantation. There are three types of vas-
cular graft: autologous (venous and arterial),
prosthetic [e.g., Dacron, polytetrafluoroethyl-
ene (PTFE)] and biological prosthetic (e.g.,
modified human umbilical vein graft). Once
functioning in the arterial circuit, each type of
graft has its inherent drawbacks, leading to
specific complications. These complications can
be categorized into two groups. Direct compli-
cations involve those where the graft itself fails
(e.g., thrombosis), whereas indirect complica-
tions are those that relate to a graft that still
functions (e.g., graft infection, suture line false
aneurysm).

Autologous Grafts

Autologous vein is the conduit of choice for
lower limb arterial reconstruction, as this has
been repeatedly demonstrated in large retro-
spective studies (Bergamini, 1991).

Due to its anatomical constancy, the long (or
greater) saphenous vein (GSV) is generally con-
sidered to be the vein of choice. However, when
the GSV has been affected by thrombophlebitis,
been removed for previous bypass surgery, or
has become dilated and varicosed, the short (or
lesser) saphenous vein or upper extremity vein
(basilic or cephalic) are often used and have
acceptable long-term patency rates. Regard-
less of the conduit, there remains a significant
failure rate in autologous vein graft, which is
associated with considerable morbidity and
mortality.

The most common cause of autologous vein
graft failure in the intermediate and long term
is the development of myointimal hyperplastic
lesions that lead to vein graft stenosis, subse-
quent graft occlusion, and ultimately graft
failure. Myointimal hyperplasia (MIH) is the
morphological lesion that underlies vein graft
stenosis. It can be described as an abnormal
accumulation of cells and extracellular matrix
in the intima of the vessel wall. The mechanical

injury caused by a bypass procedure or angio-
plasty of the peripheral arteries can initiate and
maintain the process of MIH. The clinical rele-
vance of MIH is pertinent, as the development
of MIH at the outflow anastomosis of a vein
bypass placed in the arterial system is respon-
sible for most complications leading to revi-
sion surgery. Proliferating smooth muscle cells
migrate to the injury-provoked denuded endo-
thelial layer area and forms a hyperplastic
lesion, which is associated with vein graft steno-
sis and obstruction of the vascular lumen. The
pathogenesis of MIH remains under investiga-
tion. However, it has been established that both
mechanical and chemical factors may induce
this process. Arterial injury is believed to stim-
ulate the production of growth factors, such as
platelet-derived growth factor (PDGF), which
have been shown to stimulate the proliferation
of arterial smooth muscle cells and the forma-
tion of the hyperplastic lesion in the vascular
system. A variety of cells, including endothe-
lial cells, macrophages, platelets, and smooth
muscle cells, have been shown to secrete growth
factors and cytokines. Blocking the effects of
growth factors such as PDGF or fibroblast
growth factor (FGF), by the administration of
antibodies against these growth factors, may
limit the development of the hyperplastic lesion
(Neville and Sidawy, 1998). The role of hemody-
namic changes in the vein graft, including
altered vessel wall shear stress and increased
particle residence time, has also been shown to
play an important part in MIH growth. Inves-
tigations aimed at modifying blood flow dy-
namics within vein grafts to diminish MIH
development are currently under way.

It has been theoretically proposed that
leaving a vein graft in situ, instead of using the
reversed vein graft technique, may lead to fewer
subsequent complications. Due to the natural
tapering of the vein, an in situ vein graft has a
better diameter match between the vein and the
native artery at the proximal and distal ends of
the vein graft. This makes the construction of
both the proximal and distal anastomosis easier
to perform and therefore reduces the probabil-
ity of technical errors. A more suitable diameter
match leads to more favorable blood flow fea-
tures with decreased incidence of graft throm-
bosis, anastomotic aneurysm, and development
of MIH. Also as the blood supply to the vein

136

VASCULAR SURGERY

graft through the vasa vasorum is still partially
intact, the vein graft remains less hypoxic.
Conversely, as the need to use a valvulotome
to obliterate the valves is essential, damage to
the vessel wall may ensue, possibly leading
to increased risk of early graft thrombosis.
However, biological studies of the integrity of
the vein wall in in situ and reversed vein grafts
have failed to show significant differences. It is
important to note that several studies have
found no significant difference in complication
rates resulting from either technique.

Prosthetic Grafts

Once incorporated into the circulation, the
luminal surface of a prosthetic graft becomes
lined with fibrinogen, followed by fibrin and
red and white blood cells. This layer is known
as a pseudointima. Whereas prosthetic grafts
perform well in a high-flow environment (e.g.,
in aortic reconstruction), their performance in
the infrageniculate position is poor compared
with that of autologous vein. The main problem
leading to poor long-term graft patency is the
increased thrombogenicity of prosthetic distal
bypass grafts. Some have advocated the case for
primary amputation being first-line treatment
when autologous vein is unavailable for a distal
bypass.

Originally, Dacron grafts were used as the
material of choice for distal bypass. However,
due to very poor patency rates, PTFE took over
as the prosthetic conduit of choice. As well as the
complications resulting from increased throm-
bogenicity of prosthetic grafts, graft infection
has dire consequences, described later in this
chapter.

Lower Limb Graft Occlusion

As the majority of vascular grafts in the lower
limb are performed for critical limb ischemia,
graft occlusion often reverts the limb back to
its original critical state or worse. Moreover,
ischemia may be compounded due to a reduc-
tion in collateral flow caused by division of
vessels during surgery, by physiological reduc-
tion of collateral flow as a result of a successful
graft, or by thrombosis extending distally into
the run-off vessels.

Diagnosis

The diagnosis of an occluded infrainguinal graft
is made clinically, but can be confirmed by
duplex ultrasound. Presentation ranges from
a sudden onset of a reduction in pain-free
walking distance to acute limb ischemia. From
the history, the time of onset of occlusion can be
ascertained, and the time frame between ori-
ginal surgery and occlusion can aid in the
etiology (Table 12.2).

Management

If a thrombosed graft presents within hours or
days of the occlusion, the limb is usually viable
and the aim is to restore graft patency. In the
absence of contraindications, thrombolysis is
indicated. Hemorrhage at the site of catheter
thrombolysis insertion occurs in 10% to 30% of
cases and is the most common complication.
The most catastrophic complication of throm-
bolysis is intracranial hemorrhage that is often
fatal, in particular in elderly patients with a
history of stroke. Bleeding into other organs is
also commonly recognized. Due to the high
complication rate during thrombolysis, if an
occluded lesion does not render the patient crit-
ically ischemic, it can be argued that thrombol-
ysis is not justified.

If after successful thrombolysis an underlying
lesion is identified, the patient should be
heparinized and the lesion corrected. Jump
grafting or patch angioplasty is an appropriate
procedure. When a myointimal hyperplastic
lesion postthrombolysis is found, transluminal
balloon angioplasty, patch angioplasty, or inter-
position grafting can be used, as well as jump
grafting. Autologous vein is preferable for sec-
ondary reconstructions.

An emergency revascularization is the man-
agement of a graft occlusion associated with a
threatened limb. Loss of neurological function
coupled with a tender and tense calf is an indi-
cation for urgent surgery. The procedure differs
depending on the type of graft. The aim of treat-
ment of a thrombosed vein graft threatening the
limb is restoration of graft flow with correction
of any underlying abnormality. The distal anas-
tomosis should be opened and the graft and
distal vessels cleared of thrombus. On-table
angiography should be performed once flow has
been restored. Then any abnormality can surgi-

137

COMPLICATIONS IN VASCULAR SURGERY

cally be corrected as previously described. With
a prosthetic graft, the aim of an emergency
procedure is restoration of the original graft
function with or without correction of an
underlying cause. The long-term patency of
salvaged occluded autologous or prosthetic
infrainguinal grafts is disappointing, and com-
plete replacement with a new vein graft, reserv-
ing graft revision for those patients' with no
better bypass options, has been advocated. Fol-
lowing an emergency procedure for lower extre-
mity graft thrombosis, particularly if there has
been significant preoperative ischemia, the sur-
geon should have an extremely low threshold
for performing a fasciotomy to prevent muscle
necrosis.

Complications of
Aortic Reconstruction

Reconstruction of the aorta for atherosclerotic
aneurysmal or occlusive disease brings about a
different spectrum of complication when com-
pared with lower-extremity revascularization.
The aortic graft used is either Dacron or PTFE,
as there is no autologous conduit large enough
to replace the aorta. Due to the high flow
through a large-caliber vessel, prosthetic grafts
replacing native aorta perform well and have
well-documented excellent long-term results.
The two most common local complications after
aortic reconstruction are occlusion and graft
infection (see Infected Prosthetic Graft, below).
When an aortic graft or the limb of an aorto-
bifemoral graft occludes, the limb is usually
viable. Occlusion of a single limb of an aortic
graft is most often caused by anastomotic stric-
ture at the femoral anastomosis. If the onset of
the occlusion is in the early phase (within 30
days) postsurgery and the graft can be throm-
bolyzed successfully, subsequent patch angio-
plasty or distal jump grafting is usually
successful. Thrombolysis of retroperitoneal
knitted Dacron grafts must be performed with
caution because of the risk of extravasation of
blood into the retroperitoneum. Thrombectomy
using ring strippers or adherent clot catheters is
more successful than using ordinary thrombec-
tomy balloon catheters. It is more common that
the time of graft failure is not known and is
likely to be of several weeks' duration. In these

circumstances, open graft thrombectomy or
thrombolysis is not possible, and so common
practice involves revascularizing the affected
limb with a femoral artery-to-femoral artery
crossover graft taken from the contralateral
limb. Other extraanatomical reconstructions are
also feasible in this situation.

When the body and limbs of an aortic graft
are thrombosed, proximal disease advancing
into the graft from the proximal aorta is usually
the cause. This complication can be avoided by
placing the initial graft on the aorta near the
level of the renal arteries. However, once a diag-
nosis of total aortic graft occlusion is made,
most surgeons would undertake an axillob-
ifemoral graft as an option; redo aortic grafting
is major corrective surgery carrying great risk
to the patient. Occasionally, a failed aortic graft
will not produce new or acute symptoms
because of the development of collateral vessels
in a relatively mobile patient or because immo-
bility masks claudication symptoms. If this were
the case, it may be that the patient will present
many months after the graft has failed, with
either nonhealing ulcers or rest pain. In either
case, and to thwart the onset of critical ischemia,
a complete graft replacement is the only option,
as at this stage the graft is usually unsalvageable.

Infected Prosthetic Graft

One of the most challenging complications in
vascular surgery is a graft infection. Infection
radically changes patient outcomes and is both
life and limb threatening. Quantifying incidence
of graft infection is not easy, as many reports are
anecdotal and this is compounded by the long
and variable time period between original sur-
gery and evidence of graft infection. The
incidence of graft infection, however, is influ-
enced by anatomical site of graft, indications for
original intervention, underlying disease, and
the patients' host defense. The literature quotes
figures that range between 0.7% and 7% for
graft infection after aortic surgery. Prosthetic
graft infection is more common after emer-
gency procedures (e.g., ruptured abdominal
aortic aneurysm), or when the graft is anasto-
mosed to the femoral artery in the groin or sited
superficially (e.g., axillofemoral bypass). When
and how a graft becomes infected is often
difficult to ascertain, and there are multiple risk

138

VASCULAR SURGERY

Table 12.3. Risk factors for graft infection

Local factors

Prosthetic graft

Groin invasion

Emergency or lengthy surgery

Leg ulceration or gangrene

Postoperative wound infection

Systemic factors
Diabetes mellitus
Malnutrition or obesity
Chronic renal failure
Malignancy
Steroid therapy

factors for graft infection (Table 12.3). However,
there are three modes whereby the graft may
become contaminated: (1) the infection maybe
seeded onto the graft at the time of surgery
(perioperative contamination), (2) subsequent
bacteremia may seed the graft, and (3) direct
spread from a nearby source (e.g., skin or duo-
denum) may occur.

Presentation

Any symptoms and signs of sepsis in a patient
with a vascular graft should alert the clinician
to the possibility of a graft infection. With a sub-
cutaneous graft, localized erythema and cellu-
litis or a discharging sinus may be clinically
visible over the length of the graft, or prosthetic
material maybe visualized eroding through the
skin. With a deep infected graft (e.g., an aortic
graft), the patient may present with vague
symptoms and have pyrexia of unknown origin.
An infected aortic prosthesis may form an aor-
toduodenal fistula and present with upper gas-
trointestinal bleeding that may be mistaken for
peptic ulceration. Less commonly, lower gas-
trointestinal hemorrhage may be seen from
aortoenteric fistulas into distal bowel sites.
Alternatively, signs of septic emboli to the
extremities may present as a purpuric rash.
Other more rare sequelae of a graft infection
included metastatic mycotic aneurysm forma-
tion, anastomotic pseudoaneurysm formation,
or anastomotic hemorrhage. With all these
potential sequelae, the clinician must have a
high index of suspicion in the presence of a
prosthetic graft.

Making a definitive diagnosis of graft infec-
tion can be difficult. The presence of a perigraft

collection should be determined whenever pos-
sible. Determining which organisms are in-
fecting a graft is also imperative to help guide
antibiotic choice following graft removal. Once
these two factors have been elucidated, the like-
lihood of infection must be balanced against the
general condition of the patient, the extent of
the revision surgery required, and the necessity
for immediate intervention.

Investigations

Having bacteriological cultures done on swabs
taken from a discharging sinus may identify
the organism involved. Blood cultures may
also be positive, particularly if blood is drawn
from the femoral artery, downstream to a pos-
sible graft infection. The organisms most com-
monly isolated from blood or from wounds
are gram-positive bacteria, Staphylococcus and
Streptococcus species. A particularly worrying
phenomenon is the continued rise in the num-
ber of reports of methicillin-resistant Staphylo-
coccus aureus (MRSA) isolated from infected
grafts. This organism and gram-negative infec-
tions are associated with severe systemic sepsis,
and experience in our unit and elsewhere has
shown these organisms to carry a less favorable
outcome in terms of limb salvage and mortality
than infection with less virulent organisms.
Early graft infection is usually associated with
virulent organisms such as S. aureus, Strep-
tococcus faecalis, Escherichia coli, Klebsiella,
Pseudomonas aeruginosa, and Proteus or mixed
pathogens. Late graft infections are usually
caused by less virulent bacteria (e.g., Staphylo-
coccus epidermidis, which is a common skin
commensal). Interestingly, this organism has
been cultured from grafts that have been
removed for purposes other than infection,
which may signify that only a small proportion
of such contaminated drafts develop graft-
threatening infection. The type of antibiotic
therapy differs between centers, but it is prudent
to discuss an appropriate antibiotic regimen
with a microbiologist.

There are a few imaging techniques to eluci-
date the presence and extent of a graft infection.
Computed tomography (CT) scanning can help
in demonstrating fluid collections around a sus-
pected infected graft. The presence of gas within
a perigraft collection is pathognomonic of an
infection; however, around an aortic graft, gas

139

COMPLICATIONS IN VASCULAR SURGERY

may represent resolving thrombus. Computed
tomography scanning may also not be able to
differentiate free gas that is around a graft and
gas within the bowel that is adhered closely to
the graft. Computed tomography-guided aspi-
ration of perigraft fluid may be undertaken to
aid in diagnosis; however, this carries the risk of
introducing infective seedlings into a poten-
tially sterile field.

A radioisotope-labeled white blood cell scan
enables localization of occult sites of infection,
as labeled granulocytes concentrate around an
infected focus. Magnetic resonance angiogra-
phy of the aorta is believed to be complemen-
tary to a tagged white cell scan and may increase
the likelihood of appropriately diagnosing a
graft infection. Angiography, even though
unable to pinpoint sites of infection, is neces-
sary for preoperative planning for revision
surgery. It demonstrates the nature of distal
run-off and the state of arteries that may be
used in an extraanatomical bypass. Occasionally
it may aid diagnosis in an aortoenteric or aor-
tocaval fistula. Gastrointestinal endoscopy to
rule out aortoduodenal fistula must be the first-
line investigation in a patient presenting with
hematemesis or melena.

Management

Graft conservation involves local debridement
of infected tissues surrounding a superficial
graft, followed by a primary wound closure and
local irrigation with gentamicin antibiotic solu-
tion via suitably placed drainage catheters or
impregnated collagen sponge or beads. Another
method of graft preservation involves covering
the debrided area and graft with a vascularized
omental or muscle flap. This form of manage-
ment is strongly proposed for localized groin
wound infection in the presence of a patent
graft and is said to be associated with a low mor-
tality, high limb salvage rate and an acceptable
incidence of recurrent infection. The decision to
excise an infected graft should be undertaken
carefully, and whenever possible the patient's
condition needs to be optimized prior to the
operation. The best-case scenario is when ade-
quate collateralization has taken place and no
further revascularization procedure is required
once the graft is removed. More commonly,
though, graft removal results in a return to the
preoperative state, often rendering one or both

legs ischemic, and at the time of removal of
the infected graft further revascularization is
required.

Complications Related to
Disorders of Coagulation

The acute thrombosis of an arterial procedure
in the perioperative period is usually seen
before the patient exits the operating room and
may occur up to 12 hours following surgery.
Dealing with unexplained thrombosis intra-
operatively or in the immediate postoperative
period is one of the greatest uncertainties faced
by the vascular surgeon.

Hypercoagulability as grounds for an unex-
plained vascular thrombosis poses a challeng-
ing clinical problem. Graft failure in the
perioperative period is presumed to result from
technical errors in the construction of the
anastomosis, problems with the choice of
and quality of vascular conduit, or unsuitable
patient selection. Only once these other factors
as a cause of failure have been excluded can the
diagnosis of abnormal coagulability be formu-
lated. When it becomes apparent there is abnor-
mal coagulation (i.e., heparin is not preventing
clotting in the operating field or when there is
an immediate thrombosis of a vascular repair),
the diagnosis can be confirmed only by the
analysis of a blood clotting profile. It therefore
stands to reason that detection of clotting dis-
orders prior to surgery is most often associated
with a favorable surgical outcome. It is with
experience that a surgeon develops an intuition
as to which reconstructions are likely to succeed
and has some ideas as to the types of complica-
tions that may occur. Likewise, with experience
a surgeon develops a feel for the character-
istic presentations of atherosclerotic occlusive
disease. When abnormal or unexplained throm-
bosis is diagnosed (e.g., a thrombosed supra-
renal aorta or upper extremity thrombosis in a
patient who is not diabetic and has little evi-
dence of atherosclerotic occlusive disease else-
where), the surgeon should investigate clotting
disorders as a possible cause. Unusual angio-
graphic findings, particularly young patients
who present with an occlusion in one limb with
pristine vasculature in the contralateral limb,
should prompt an investigation into the coagu-

140

VASCULAR SURGERY

lation system. The role of screening for poten-
tial thrombophilia states in vascular surgical
patients has been studied. Approximately 10%
of all patients scheduled for a variety of vascu-
lar surgical procedures had test results indicat-
ing a potential hypercoagulable state. The three
most common clotting disorders are heparin-
induced platelet aggregation, lupus anticoagu-
lants, and protein C deficiency. The incidence of
infrainguinal graft occlusion within 30 days was
27% among patients who were in the hyperco-
agulable group compared with 1.6% in patients
who were not in this group. At present, an estab-
lished screening program does not exist to
exclude the wide variety of coagulation disor-
ders present in vascular surgical patients. We
depend on taking a careful history and clinical
examination to identify those patients who may
be at a risk of abnormal clotting due to an inher-
ent thrombophilic status. At this time this is
probably the more cost-effective and efficient
means to establish a hypercoagulable diagnosis
prior to operation.

Complications of
Interventional Vascular
Radiological Procedures

As more minimally invasive interventional radi-
ological procedures are being used as first-line
treatment for occlusive and aneurysmal vascu-
lar disease, the incidence of complications is
rising accordingly. These complications can be
divided into three categories: (1) puncture-site
related, (2) catheter related, and (3) systemic
complications.

About 0.5% of femoral punctures and 1.7%
of axillary punctures have been reported to
require treatment for a complication. Hema-
tomas at the puncture site are not usually con-
sidered a complication and rarely need surgical
treatment. Large hematomas (e.g., retroperi-
toneal, pelvic, and anterior abdominal wall

hematomas) that require surgical intervention
occur more often in patients with coagu-
lopathies and in patients who are obese. The risk
of puncture-site pseudoaneurysm has been
shown to increase with increasing catheter size
and when a low puncture site is used. Preven-
tion of puncture-site hematomas and pseudoa-
neurysms can be achieved by using the
smallest-caliber catheter possible to perform
the necessary intervention. Accordingly, there
are fewer puncture-site complications with
angioplasty procedures when compared with
stenting, as the catheter needed to place a stent
is of a larger caliber.

Catheter-related complications include the
formation of arterial dissections, subintimal
injections, and embolization from the catheter.
Fortunately, as the dissections produced are ret-
rograde and are pushed closed by the direction
of blood flow, most of these complications are
asymptomatic. However, some acute dissections
become extensive chronic dissections or cause
acute occlusion. Catheter thromboembolism
occurs in less than 0.5% of cases.

There are myriad systemic complications
associated with angiographic procedures. Exam-
ples include vasovagal syncope, cardiac arrest
and arrhythmias, myocardial infarction, and
nausea and vomiting. Contrast reactions can be
reduced by adequate hydration and by using low
osmolar contrast in high-risk patients. Rarely
radiation injury in the form of a skin burn o ccurs
when the procedure is lengthy and the patient is
exposed to over 2 Gy.

References

Bergamini TM, Towne JB, Bandyk DF, Seabrook GR and

Schmitt DD. (1991) J Vase Surg 13:137-47; discussion

148-9.
Hannon RJ, Wolfe JH, Mansfield AO. (1996) Br J Surg 83:

654-8.
Krupski WC, Layug EL, Reilly LM, Rapp JH, Mangano DT.

(1993) J Vase Surg 18:609-15; discussion 615-7.
Neville RF.SidawyAN. (1998) Semin Vase Surg 11:142-8.

Vascular Access

David C. Mitchell and C. Keith Ozaki

Vascular access is required to assist in the man-
agement of patients requiring frequent venous
or arterial cannulation. Its principal role is to
provide circulatory access for hemodialysis, al-
though such techniques are also used to pro-
vide chemotherapy, intravenous nutrition, and
access for plasma exchange.

The two techniques used are either implant-
able synthetic lines, which may have one or
more lumina, or a surgically created fistula
between the arterial and venous circulation.
This latter approach may involve joining artery
and vein together, the so-called autogenous
arteriovenous (AV) access [arteriovenous fistula
(AVF)], or the insertion of a synthetic bridge
graft between artery and vein (nonautogenous
AV access).

Principles of Vascular Access

The guiding principles of access surgery are to
use AVF in preference to synthetic grafts, which
are preferred to in-dwelling central venous
catheters. Access should be sited as far distally
in the chosen limb as possible. The principle is
to conserve veins to permit proximal revision if
the initial procedure fails. An exception is very
old patients, who often have poor distal vessels.
Some young patients may have strong wishes to
avoid visible forearm scars. The nondominant
limb should be used wherever possible.

In patients who may require vascular access,
venepuncture, or the insertion of intravenous

cannulae in the main named veins of the upper
limb, should be avoided. If central venous
catheters are required, they should be sited in
the jugular and not the subclavian veins to avoid
central venous stenosis in the draining veins of
the upper limb.

Standards

The United States has led the way in this area
with the publication of specific guidelines
[National Kidney Foundation-Disease Out-
comes Quality Initiative (NKF-DOQI) (www.
kidney.org/professionals/doqi/guidelines)].
These guidelines were a response to the rapid
growth in patient numbers and costs associated
with treatment for renal failure. A multidiscipli-
nary group of nephrologists, nurses, vascular
and transplant surgeons, and interventional
radiologists reviewed the world literature. The
resulting document was approved by all the rep-
resented national societies prior to adoption.

The principal recommendations are that the
majority of patients starting dialysis should do so
using a native vessel AVF at the wrist. Grafts
require six times as many interventions as AVF to
achieve the same patency, and their use is dis-
couraged. Central catheters have inferior patency
and are discouraged for "permanent" access.
Their principal role should be for emergency or
temporary access. Since the distribution of these
standards, placement rates for simple fistulas has
increased 35% in the United States.

141

142

VASCULAR SURGERY

The Europeans have not produced a similar
document, although it is hoped that a National
Service Framework for renal disease manage-
ment in the United Kingdom will set standards
for vascular access within the National Health
Service.

Observational studies have helped to define
standards. The Dialysis Outcomes and Practice
Patterns Study (DOPPS) was a prospective
global study of practice in seven countries
involving 309 facilities and over 9500 patients.
It showed that there are significant differences
between varying health cultures in the devel-
oped world. The AVF rates varied from 0% to
87% in the United States, and 39% to 100%
in Europe. Graft usage in new hemodialysis
patients ranged from 2 to 24%. Central venous
lines were particularly common in the United
Kingdom and the United States but rare in Japan
and Italy.

These differences are not dictated solely by
differences between patients, but principally by
clinician preference. This study has clarified
what is being done at present to provide access.
By demonstrating widely differing practice,
it informs the debate over ideal practice and
can guide future trials to answer questions
about treatment where widely differing views
are held.

Interpretation of the literature is further com-
plicated by differences in reporting of the re-
sults of access surgery. A recent study from the
United States should help to standardize report-
ing in the future (Sidawy et al., 2002).

Types of Access

The principal modes of vascular access are
autogenous AVF, synthetic AV bridge grafts
(nonautogenous AV access), and in-dwelling
synthetic central venous catheters. Considera-
tion of patient demographics, anatomical suit-
ability, and other factors are important in the
preoperative planning for access (Table 13.1).

Arteriovenous Fistula

Most clinicians agree that the most durable
form of vascular access is the AVF. The prefer-
ential site is between the cephalic vein and
the radial artery at the anatomical snuffbox, or
the wrist, in the nondominant upper limb, the

Table 13.1. Preoperative planning for autogenous or
nonautogenous arteriovenous fistula (AVF) placement

Consider patient age, projected life span, time to

initiation of dialysis, dominant hand
Elicit history of previous access attempts/subclavian

vein cannulations; consider contrast venography to

rule out central venous pathologies
Check Allen's test, upper extremity blood pressures,

arterial pulse exam — > if abnormal then segmental

arm pressures, plethysmography — > if abnormal

then consider ultrasound or angiography
Venous exam with tourniquet — > if no clear conduit

then duplex; protect that vein from

puncture/trauma
Ensure patient is optimized for operation (e.g., address

cardiac, metabolic, volume status, nutritional,

infectious issues)
Consider risks of steal in elderly and diabetic patients

undergoing proximal access construction

Brescia-Cimino fistula (Brescia et al., 1966). The
end of the vein is joined to the side of the radial
artery, usually under local anesthesia.

The success of this procedure is dependent on
the quality of the vein and artery and the tech-
nical skill of the surgeon. Where good vessels
are not clinically evident, duplex ultrasonogra-
phy or venography may help to identify the
best sites for access formation. The suggested
sequence for AVF placement is listed in Table
13.2).

Widely varying success rates are quoted, but
about 60% of wrist AVFs mature and become
useful for dialysis. The AVFs are robust once
established, but may take many (typically 6 to
12) weeks to mature. Many factors may affect

Table 13.2. Suggested sequence for AVF placement

1. Autogenous AVF in hand/forearm (nondominant
before dominant)

2. Upper arm autogenous AVF (usually cephalic before
basilic)

3. Forearm nonautogenous AVF

4. Upper arm nonautogenous AVF

5. Upper arm or thigh autogenous (using transposed
or translocated saphenous/superficial femoral vein)
AVF

6. Thigh nonautogenous AVF

7. Central configurations such as axillary artery to
contralateral axillary vein, subclavian artery to
subclavian vein

143

VASCULAR ACCESS

maturation, such as the size of artery and vein,
change in flow, and the presence or absence of
arterial disease (e.g., diabetes). In patients in
whom the fistula is failing to become prominent
within a few weeks, duplex ultrasound scanning
can examine flow rates and identify problems.
Surgeons willing to undertake revision may
produce higher success rates. The principal
reasons for failure are damaged or inadequate
veins and (more rarely) inadequate arteries. In
such cases, alternative forearm veins may be
used. The basilic vein on the ulnar side of the
forearm is often large and may not have been
traumatized by venesection. This can be mobi-
lized and swung across the forearm to the radial
artery, or anastomosed to the adjacent ulnar
artery if large enough, although the failure rates
for this procedure are higher.

Any vein can be damaged by repeat venesec-
tion or placement of in-dwelling catheters. Such
veins develop areas of fibrosis that cannot dilate
when subjected to arterial flows. For this reason,
in those in whom the need for access can be anti-
cipated, every effort should be made to avoid
needling the cephalic vein, the antecubital veins,
or the subclavian vein.

The radial artery at the wrist is often insuffi-
cient in the elderly and particularly those with
diabetes. The artery usually shows evidence of
arteriosclerosis with calcification. The artery is
unable to increase its flow rate in response to
fistula formation. The result is failure of the vein
to enlarge, or thrombosis. In this situation, it
may be better to place the fistula more proxi-
mally in the limb, typically at the elbow. Pre-
operative evaluation can assist in identifying
suitable patients for distal AVFs (Malovrh,
2002).

The standard procedure at the elbow is an
end of cephalic vein to side of brachial artery
fistula. This can usually be fashioned through
a transverse antecubital incision or two lon-
gitudinal incisions under local anesthesia. The
depth of the basilic vein within the arm com-
plicates its use as a direct fistula. This vein,
however, may be easily mobilized through a lon-
gitudinal incision in the medial arm. The basilic
vein is then divided distally, tunneled subcuta-
neously, and anastomosed to the brachial artery
in the distal arm. The procedure can be per-
formed using minimally invasive techniques.
Such transposed fistulas may give good service
over many years. This technique may also be

applied to the lower limb in patients with good
arterial circulation, by transposing the long
saphenous vein subcutaneously in the thigh and
anastomosing it to the distal superficial femoral
artery.

Synthetic Access Grafts
(Nonautogenous
Arteriovenous Access)

Where veins are inadequate, or dialysis is
needed urgently (within 2 weeks), AVF may be
inappropriate. In such circumstances, access can
be rapidly established using synthetic bridge
grafts between suitable arteries and veins. The
most common material for this is polytetra-
fluoroethylene (PTFE), which may be cannu-
lated within a week if required. Dacron is not
widely used for access as it is difficult to needle,
but newer composite grafts that are reported
to bleed less after cannulation are available.
The role of these grafts has yet to be clearly
established.

As veins are often deficient, grafts tend to
be placed more proximally in the limb than
AVFs. They may be placed in either straight
or curved/looped configurations. No data exist
demonstrating that one configuration is signi-
ficantly better than any other. Grafts should be
appropriately sized with the arterial anastomo-
sis not bigger than 6 mm to avoid excessive flows
and either vascular steal or high output cardiac
failure.

Although easier to establish, PTFE grafts are
known to have higher thrombotic and septic
complication rates, and to need more frequent
revision than native AVFs. For this reason, it is
advised that AVFs are preferred. This has never
been formally tested in a prospective random-
ized trial. In the elderly patient with limited
life expectancy, a rapidly established graft may
provide superior access with sufficient durabil-
ity, compared to several unsuccessful attempts
to establish an AVF.

Central Venous Catheters

A well-organized renal failure service should
anticipate the need for access in patients ap-
proaching end-stage disease, and appropriate
access surgery should be planned in advance.

144

VASCULAR SURGERY

This counsel of perfection is not always realized
as patients may present acutely after a long
period of stability.

Those requiring emergency access (e.g., im-
mediate need for dialysis) need the insertion
of a dual-lumen central venous catheter. These
should be left in place for as short a time as pos-
sible. Definitive access surgery should follow as
a matter of urgency.

Central catheters become infected easily, and
often have to be removed or re-sited. In addi-
tion, they stimulate fibrosis in the veins and can
cause stenosis. For this reason, subclavian lines
are to be avoided, as the loss of the subclavian
vein prejudices further access in the ipsilateral
upper limb. Lines should be placed via the
jugular route if at all possible. If access is needed
only for a few days, then in the absence of suit-
able jugular veins the femoral veins may be
used.

Patients needing more permanent catheters
(longer than 3 weeks) should have tunneled
catheters inserted. Placement considerations
are the same as for temporary lines. Tunneled
catheters should be cuffed, as the cuffs reduce
the risk of infection from the site of skin
entry.

Failure to Mature

Failure to mature is the most common problem
seen in AVFs. Fistulas demonstrate significant
increase in flow within 48 hours and enlarge
thereafter. Most successful AVFs are capable
of being needled in about 6 to 8 weeks after
formation, although longer may be required.
Detecting those that will fail to mature may be
difficult. Ideally, AVFs should be placed well
in advance of the time that they are likely to
be required. This permits time for assessment
and revision if the fistula is not developing
satisfactorily. An alternative approach if time
is pressing is to scan the fistula with ultra-
sound soon after formation. Flow rates greater
than 500 mL/min signify that the fistula is likely
to develop successfully. Scanning can also be
used for the early detection of technical
deficiencies, stenoses, and other problems. In
constructions that are failing to mature, some
groups advocate early liberal use of fistulograms
to aid in diagnosis and therapeutic planning.
Others rely primarily on the diagnostic vascular
laboratory, and reserve fistulography for cases
in which duplex scanning is equivocal or
unavailable.

Complications of
Vascular Access

Arteriovenous Fistula

Once the AVF is established, AVF revision
rates are low at about 15% or less per annum.
Fistulas are robust and withstand multiple
cannulations well.

Technical Failure

The most immediate complication of AV access
is that the fistula occludes shortly after forma-
tion. This maybe due to obvious problems such
as inadequate vessels or to technical imperfec-
tions in the procedure. In the former, re-siting
the fistula is the best course of action. In the
latter situation, revision, often under local
anesthesia, may salvage a functioning AVF. This
is rarely an emergency and can be managed
during the next available elective operating
session.

Vascular Stenosis

Vein stenosis and aneurysmal dilatation are
both seen following development of AVFs. The
former may compromise both the quality of
dialysis and the longevity of the fistula. Some
centers advocate routine fistula scanning, but
this has not yet been shown to be an effective
way of monitoring fistulas for complications.
Where obvious stenoses exist, or dialysis is
inadequate despite an apparently satisfactory
fistula, then ultrasound may reveal a stenosis.
Stenoses greater than 50% or AVFs with flows
below 500 mL/min are more likely to fail and
may need revision. Stenoses within 1 to 2 cm of
the anastomosis are most easily dealt with by
surgical revision. This can be undertaken under
local anesthesia with an occlusive tourniquet.
The fistula is ligated and divided and reanasto-
mosed to an adjacent portion of artery. More
remote stenoses may often be dealt with by
angioplasty. If this fails, then short skip grafts of
vein may bypass a stenosis and permit continu-
ous use of the fistula without the need for tem-
porary lines.

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VASCULAR ACCESS

Vascular Steal and High-Output
Cardiac Failure

Proximal fistulas tend to have higher flow rates
and may divert blood from the hand. The risk
of vascular steal should be borne in mind in
proximal fistula. It is uncommonly seen (about
1% to 8%), but the neurological effects are irre-
versible if the steal is not quickly corrected
(Tordoir et al., 2004). Any suspicion of hand
ischemia demands immediate attention, begin-
ning with bedside examination. Temporary
finger occlusion of the AVF can assist in deter-
mining whether there is an inflow problem, or
whether the arterial flow distal to the arterial
anastomosis has been interrupted. If hand arte-
rial perfusion returns to baseline with AVF com-
pression, then inflow is inadequate to maintain
flow to the hand and through the AVF. If the
extremity remains ischemic, then there may be
a problem with the arterial anastomosis that
occludes outflow, or thromboembolic complica-
tions. Segmental arm and finger pressures, fol-
lowed by repeated exam while the access is
occluded, confirm the diagnosis. If inflow is
inadequate, then improvement of distal pres-
sures and symptoms should occur while the AVF
or graft is compressed.

If steal physiology is demonstrated, then
appropriate urgent imaging to screen for occult
inflow arterial occlusive disease may be under-
taken, and lesions addressed. Fistula revision is
often required. If preservation of the fistula is
not essential, taking it down and creating a
new one is probably the procedure of choice.
The alternatives are banding to reduce flow, or
bypass from the artery at least 6 cm above the
anastomosis to an artery distally and then liga-
tion of the artery immediately beyond the anas-
tomosis. This last procedure is known as the
distal revascularization-interval ligation (DRIL)
procedure. It is gaining in popularity as it takes
flow to the distal arterial tree from above the
fistula and prevents steal due to reversed flow in
the artery distal to the anastomosis.

Banding is a complex procedure, necessitat-
ing intraoperative flow measurement. Flows
may fluctuate during the procedure, but ideally
the banding should produce a flow between 800
mL and 1.5 L per minute. Success rates for this
procedure are low, and it is not recommended if
an alternative is available. Postoperative throm-
bosis is common and maybe due to overvigor-

ous banding. If this happens, the fistula is
usually lost.

High fistula flows can also cause high-output
cardiac failure, which is seen more commonly in
proximal AVFs. In these cases, fistula revision to
reduce flows is required. The choices include
sacrificing the fistula and siting new access, or
attempting a flow reduction procedure.

Infection

Infection is rare, but if associated with bac-
teremia, abscess, or aneurysm formation, revi-
sion is usually required. The clinical features
are of an area of inflammation in relation to
the fistula, sometimes with rapid enlargement.
Fever and rigors, particularly on dialysis, may
be seen, but are not a universal feature. Sudden
rapid bleeding can occur at infected needling
sites. Immediate pressure and placement of a
skin suture will achieve acute control, but
should be followed by a definitive revision in
most cases.

Thrombosis

Thrombosis is uncommon, but when it occurs
it can often be retrieved by acute intervention,
with salvage of the fistula and avoidance of tem-
porary central lines. Overdialysis is an uncom-
mon cause of fistula thrombosis, but should be
suspected if no stenosis can be found. Imaging
of the whole fistula and ipsilateral central veins
should always follow surgical or radiological
declotting. Dilatation of fistula or central vein
stenosis may be required to restore normal
function. When the stenosis is in close proxim-
ity to the anastomosis, then surgical revision to
an adjacent proximal arterial segment is often
the best procedure.

The complications associated with trans-
posed fistulas are the same as those seen with
other native AVFs. They tend to have high flows,
so cardiac failure and steal are more common in
these fistulas.

Arteriovenous Access
Grafts (Nonautogenous
Arteriovenous Access)

Arteriovenous grafts can usually be established
easily, with a high technical success rate. How-

146

VASCULAR SURGERY

ever, complications are common, and the fre-
quent need for intervention should prompt the
surgeon and dialysis team to undertake regular
surveillance.

Thrombosis

Thrombosis is usually the consequence of
intimal hyperplasia at the venous end of the
graft. This can be recognized by regular intra-
dialysis monitoring of flow or pressure. It has
been shown that monitoring of flow or pressure
can detect developing graft stenosis. Timely
intervention can prolong graft survival. One
approach is to use balloon angioplasty where
possible, keeping surgical revision to a
minimum. Where thrombosis occurs, prompt
declotting undertaken by either an endovascu-
lar or open approach can retrieve graft function.
It is important to identify and correct the cause
of the thrombosis or further thrombosis is
likely. There is no clear evidence whether open
or endovascular approaches are superior in this
situation, and each approach has its proponents.
As grafts require relatively frequent interven-
tions, many advocate using minimally invasive
techniques first and reserving open surgery
for those in whom the vascular interventionist
fails.

Infection

Like any foreign material, infection is an
ever-present hazard, especially as needles are
frequently introduced into the graft. Septic
episodes in dialysis patients are most likely to
originate from the graft. Great care must be
taken to use aseptic techniques when cannulat-
ing grafts, as once organisms are seeded into
a graft the only way to get rid of them is to
replace the graft. Eradication of nasal car-
riage of Staphylococcus aureus by use of topical
mupirocin has been shown to reduce the rate of
graft sepsis.

Grafts are often placed in European prac-
tice as a dialysis access of last resort, and there
may be limited alternative sites if an infected
graft is removed. Clearly if there is inflamma-
tion along the length of the graft, then removal
is the only option. Where localized sepsis exists,
or a small area of the graft is exposed, local

excision with skip grafting through uninvolved
tissue may keep the graft functioning. The site
of infection should be left open to drain freely,
and the patient treated with parenteral anti-
biotics until the inflammation has completely
subsided.

Vascular Steal

This is most commonly seen in arm grafts in
older or diabetic patients. Rates vary from
between 1% to 19%. The approach is the same
as steal in an autogenous AVF, with nonautoge-
nous graft ligation or DRIL being the potential
management approaches.

Aneurysm Formation

With repeated cannulation over small areas of
a graft, there is a tendency for "aneurysm" for-
mation (actually a pseudoaneurysm). This is a
result of longitudinal splitting of the graft. It
is not a problem if there is good skin coverage,
but if enlarging rapidly or if inflamed, then
early revision should be undertaken to prevent
rupture and bleeding. The technique is similar
to that used for infection, with the exception
that excision of the aneurysmal portion of the
graft is not always necessary in the absence of
infection.

Central Venous Catheters

Infection

Infection is the main problem from central
venous (CV) catheters, and rigorous aseptic
technique is required to manage dialysis. Newer,
totally implantable catheters that are accessed
through the skin may reduce the risk of sepsis.
The teaching of correct hand and skin prepara-
tion prior to needling remains an important
part of the management of patients with CV
catheters.

Once infected, lines need to be changed.
Ideally, the old line should be removed and the
patient treated until he or she is well before
inserting a new line. This is not always possible.
Rotating the line to a new site is to be preferred
in such situations, but if the situation is desper-
ate, removing the old line and reinserting in the

147

VASCULAR ACCESS

same location while treating with antibiotics
may be successful.

Fibrinous Encasement and Clotting

The tips of catheters become covered with a
"biofilm" of fibrin that may contain bacteria.
Even if sterile, this film can build up until a large
tube of fibrin encases the catheter tip. This can
interfere with blood flow and obstruct dialysis.
If the line is not infected, removal and replace-
ment may still be necessary to reestablish dial-
ysis. Passing guidewires down the catheter is
not usually successful, but snaring the catheter
tip radiologically and stripping the fibrin cuff
can clear the offending plug. This technique can
significantly prolong the life of central lines.

Thrombosis is a common problem, especially
if the line is not used frequently. Lines should
be flushed with the correct volume of heparin
(1000 U/mL) after each use to remove blood
from the lumen and prevent thrombosis. Extra
care must be paid to this in children, as it is easy
to give excessive volumes of heparin and induce
systemic anticoagulation and bleeding.

The Avoidance of
Complications:
Access Surveillance

Concerns about the frequent need for access
revision have stimulated inquiry into tech-
niques for the early detection of access com-
plications before symptoms develop. Most
techniques concentrate on intradialytic moni-
toring of flow, pressure, dialysis efficacy, or a
combination of these. The advantage of intradi-
alytic monitoring is that it minimizes the need
for extra hospital resources for these ill patients.
Each technique has its proponents, and the tech-
niques mentioned are not mutually exclusive.

The DOQI guidelines state, "Access flow
measured by ultrasound dilution, conductance
dilution, thermal dilution, Doppler or other
technique should be performed monthly. The
assessment of flow should be performed during
the first 1.5 hours of the treatment to eliminate
error caused by decreases in cardiac output
related to ultrafiltration. The mean value of

three separate determinations performed at
a single treatment should be considered the
access flow. If access flow is less than 600 mL/
min, the patient should be referred for fistulo-
gram. Access flow less than lOOOmL/min that
has decreased by more than 25% over 4 months
should be referred for fistulogram."

This is a counsel of perfection and some
centers would advocate duplex ultrasound prior
to fistulography Where there is evidence of a
stenosis of >50%, there is a significant sub-
sequent thrombosis rate. Such fistula should
undergo endovascular or surgical revision as
appropriate. Juxta-anastomotic stenoses are
often best dealt with by surgery, with endovas-
cular dilatation being reserved for those in the
body of the access.

Desperate Access

Dialysis is becoming more successful in pro-
longing the lives of patients in renal failure.
Unfortunately, this improvement in survival is
not being matched by increases in transplanta-
tion. As a result, many more people are depend-
ent on long-term dialysis. As successive access
procedures fail, the establishment of secure vas-
cular access becomes increasingly difficult.

Surgeons and interventionists have become
ingenious at inserting grafts or lines into
various veins, sometimes accidentally. Grafts
can be placed in necklace fashion between one
axilla and the contralateral one. Arteries can
be divided and interposition grafts inserted.
The superficial femoral vein has been utilized
as a hemodialysis access conduit. Lines may
be inserted directly into the inferior vena cava
(IVC) through the back. Such procedures should
be reserved for those in whom no alternative
can be found after an extensive search using
ultrasound, venography, and magnetic reso-
nance angiography if necessary. It should be
made clear to patients undergoing these proce-
dures that the risks involved in establishing such
access are high, and the consequence of failure
may be fatal.

Although successful arterial access can be
obtained for numerous patients with reason-
able durability, numerous controversies remain
(Table 13.3). These controversies will be
resolved with further clinical trials.

148

VASCULAR SURGERY

Table 13.3. Contemporary controversies

Role of endovascular vs. open management of the

failing and failed autogenous AVF and

nonautogenous AVF
Construction of upper arm autogenous AVF prior to

utilization of forearm nonautogenous AVF
Role of invasive imaging (routine arteriograms and

venograms) prior to vascular access constructions
Adjuvant therapies to improve vascular access patency

(anticoagulants, antiplatelet therapies, etc.)
Unknown value of new nonautogenous AVF conduits

(modified Dacron,homografts,etc.)
Role of duplex surveillance in identifying the failing

graft

References

Brescia MJ, Cimino JE, Appell K, Hurwich BJ, Scribner BH.

(1966) J Am Soc Nephrol 10:193-9.
Malovrh M. (2002) Am J Kidney Dis 39:1218-25.
Sidawy AN, Gray R, Besarab A, et al. (2002) J Vase Surg

35:603-10.
Tordoir JH.Dammers R, van der Sande FM. (2004) Eur J Vase

Endovasc Surg 27:1-5.

Outcome Measures in Vascular Surgery

Christopher J. Kwolek and Alun H. Davies

Background

Initial efforts within the health care reform
movement in the United States largely focused
on reducing cost. This became the preeminent
issue as health care expenditures continued to
increase on an annual basis, reaching 14% of
gross domestic product in 1994. Although some
of these expenses can be attributed to improve-
ments in diagnostic and therapeutic regimens,
particularly in those areas highly influenced
by new technologies, concern has also been
expressed about the quality of the product being
provided to patients.

The publication of the Institute of Medicine's
(IOM) Committee on Quality of Care report,"To
Err Is Human: Building a Safer Health System,"
shifted the focus of attention from cost alone
to medical errors within the U.S. health care
system and the costs associated with these
errors. This has led to an erosion of patient trust
in the medical care system. It has been estimated
that medical errors are responsible for between
44,000 and 98,000 deaths annually, becoming
the eighth leading cause of death in the U.S.,
ahead of other causes such as breast cancer
and motor vehicle accidents. Over 7000 of these
deaths were attributed to medication errors
alone, with the total cost to society of these
errors estimated to be $11637.6 billion a year.
Much of the initial research describing the
problem of medical errors was performed in the
1990s and supported by the Agency for Health-
care Research and Quality (AHRQ).

The IOM report also led to the establishment
of the Quality Interagency Coordination Task
Force (QuIC), which was charged with coordi-
nating the quality improvement activities in U.S.
federal health care programs. These groups
have been responsible for the establishment of
standardized guidelines and protocols based on
clinical trials, which may decrease variability in
the patient care processes while improving care
and reducing costs. The vast majority of the
errors identified in these studies were systems
related and not attributable to negligence or
misconduct. In fact, up to 75% of the medical
errors and 54% of the surgical errors were found
to be preventable.

The U.S. Veterans Administration (VA) hospi-
tal system had already begun to look at these
quality and outcomes issues through the estab-
lishment of the National VA Surgical Quality
Improvement Program (NSQIP), which has been
responsible for assessing specific surgical out-
comes throughout the U.S. VA hospital system,
while using risk adjusted data to assess surgical
morbidity and mortality and providing specific
institutional feedback (Khuri et al., 1998). In
fact, this program was so successful that in the
late 1990s it was expanded to include three large
academic medical centers at the University
of Kentucky, the University of Michigan, and
Emory University in Atlanta. Currently this
program is being expanded to include multiple
academic medical institutions across the U.S.

In addition, large companies, which are pur-
chasers of health care for their employees, have

149

150

VASCULAR SURGERY

Table 14.1. Current recommendations of the Leap Frog Group

Computerized physician order entry: mandated use to

minimize medication errors
Intensive care unit (ICU) physician staffing: use of

critical care certified physicians to provide exclusive

care of ICU patients
Evidence-based hospital referral: preferential referral of

patients undergoing five high-risk surgical

procedures to "high volume centers"

Procedure

Coronary artery bypass grafting
Percutaneous coronary angioplasty
Carotid endarterectomy
Abdominal aortic aneurysm repair
Esophagectomy

Annual volume
requirement

500/year

400/year

100/year

30/year

6/year

begun to take an interest in improving the
quality and potentially decreasing the cost of
health care as demonstrated by the activities of
the Leap Frog Group (www.leapfroggroup.org).
The stated purpose of this group of Fortune 500
companies is to mobilize employer purchasing
power to trigger breakthroughs in the safety
and overall value of health care to American
consumers. Using the results of these and other
studies aimed at evaluating medical outcomes,
the Leap Frog Group has already identified three
areas to decrease errors and improve the quality
in U.S. -based health care systems. Health care
providers who adopt these recommendations
will be rewarded with preferential use and
other incentives by this group of health care
purchasers. The current recommendations are
listed in Table 14.1. It is estimated that imple-
mentation of this program would save 60,000
lives with a monetary savings of $3.8 billion a
year.

Although these recommendations are sup-
ported by reviews of outcome studies in the
current medical literature, certain limitations
do exist. For example, volume-based outcome
studies demonstrate that on average, high-
volume centers have better patient outcomes for
certain high-risk procedures such as repair of
abdominal aortic aneurysm (AAA) or carotid
endarterectomy (CEA). However, some high-
volume centers may have average or poor out-
comes, whereas some smaller centers with low
volumes may have excellent outcomes. It maybe
more important to measure the clinical process

for a health care system to identify the reasons
and processes that allow one facility to have
excellent outcomes so that these can be utilized
by other facilities to achieve the same excellent
results. This concept was used by the Northern
New England Cardiovascular Disease Study
Group to improve the outcomes of patients
undergoing coronary artery bypass grafting in
northern New England (O'Connor et al., 1996).

Outcomes Measures

It has become important that we evaluate the
relative value of different treatment regimens to
include individual and societal costs and poten-
tial risks and benefits. Individual patient per-
spectives on quality have also become an
important part of the evaluation process.

There are several reasons for physicians to
participate in this process. Ideally, our partici-
pation should lead to an overall improvement in
the quality of care that we deliver. In addition,
participation in these programs will soon be
necessary to qualify for reimbursement from
many insurers and purchasers of health care
such as the U.S. government and the Leap Frog
Group. Finally, as physicians we have a societal
responsibility to maximize the good and mini-
mize adverse outcomes in health care, while
best utilizing the limited resources that exist.
If physicians choose not to participate in this
process, then others will make these difficult
decisions for us.

These changes have led to the development
of "extended outcome assessment" rather than
just the traditional physician-oriented out-
comes measures that we are used to. The con-
cept of a value compass has been proposed
to describe the interplay between traditional
medical outcomes, patient satisfaction, func-
tional assessment, and cost/utility outcomes
(McDaniel et al, 2000).

Clinical Status

The most traditional group of medical out-
comes measures utilized by vascular surgeons
usually describes clinical status. These measures
are physician oriented and include measure-
ments of morbidity and mortality, graft patency,
limb salvage, complications, and laboratory
testing such as the ankle-brachial index (ABI)

151

OUTCOME MEASURES IN VASCULAR SURGERY

and duplex ultrasound results. Many of these
outcomes are important measures of technical
success and are easily evaluable by statistical
methods such as life table analysis. However,
even the long-term results within this category
such as patient survival after aneurysm repair,
stroke-free survival after carotid endarterec-
tomy, or amputation-free survival after lower
extremity bypass grafting do not necessarily
correlate with patients' overall well-being, day-
to-day functioning, or their perceived quality of
life. Physicians are also comfortable with these
outcomes since the Society for Vascular Surgery
(SVS) and the International Society for Cardio-
vascular Surgery (ISCVS) have published guide-
lines for measuring these types of outcomes for
commonly performed arterial and venous vas-
cular procedures.

Patient Satisfaction

Patient-oriented outcomes tend to be less fre-
quently measured and not as well defined. None
of these outcomes are included in the SVS-
ISCVS reporting standards. Patient satisfaction
with the health care process is one area being
more closely evaluated. Although customer sat-
isfaction surveys have long been used in the
world of business, they are now being applied
to the area of health care. Two areas being fre-
quently evaluated include patient satisfaction
with the physician-patient relationship and sat-
isfaction with the health care delivery process.
This may include such issues as timeliness and
access to care, provider and staff communica-
tion, the physical environment where care is
delivered, and courtesy and respect shown to
the patient. Managed care plans in the U.S. are
now required to assess themselves using stan-
dardized patient satisfaction surveys such as the
Health Plan Employer Data and Information Set
(HEDIS), which was developed by the National
Committee for Quality Assurance (NCQA).
Many employers and purchasers of health care
are now utilizing this information when decid-
ing on which health care providers to include in
their panel of providers.

Functional Status

Functional status is another of the patient-
oriented outcomes that is being more com-
monly described in the vascular literature. These

health assessment instruments are designed to
quantify how illnesses and treatments affect
different aspects of patient functioning in every-
day life. This will allow physicians to evaluate
not only the presence or absence of a leg or the
patency of a graft, but how patients are func-
tioning after a specific intervention. These meas-
ures are also helpful when evaluating patients'
expectations before and after specific interven-
tions. A list of commonly used measures of func-
tional status is included in Table 14.2. There
are two types of assessment tools. The specific
instrument focuses on a specific disease or client
group, and changes in this are more likely to
detect subtle changes in quality of life, whereas
generic tools give a broader summary of health-
related quality of life, hence enabling compar-
isons with patients suffering from other disease
processes (Table 14.3).

The most widely used generic functional
health assessment instrument in the United
States is the Medical Outcomes Short Form 36
(SF-36). This survey evaluates patient function
in physical and social roles, limitations due to
health or emotional problems, patient percep-
tions of general health, mental health, bodily
pain, and vitality. In addition, a question con-
cerning change in health status compared to 1
year previously is included in the survey. This
survey combines aspects of a Quality of Well-
Being Scale and a Functional Status Question-
naire. The reason that this survey has become so
useful is that large numbers of patients have
been evaluated using this instrument, thus
allowing researchers to compare results to the
general population or a patient subgroup with
specific characteristics. These results may be

Table 14.2. Examples of measures of functional status

General status: quality of life

SF-36

Euro-QOL

Nottingham Health Profile

Functional Status Questionnaire

Quality of Well-Being Scale

Sickness Impact Profile
Disease/symptom specific: quality of life

Walking Impairment Questionnaire: for patients
with lower extremity arterial occlusive disease

Charing Cross Claudication Questionnaire

Charing Cross Venous Ulcer Questionnaire

VascQuol

152

VASCULAR SURGERY

Table 14.3. Advantages and disadvantages of quality of life instruments

Instrument

Generic

Specific

Advantages

Single instrument

Detects different aspects of health

Enables comparison between different conditions

Can be used in cost analysis

Focus on primary are of interest

More relevant to clinicians and clinical condition

May be more responsive

Disadvantages

May not focus adequately on main problem
May lack responsiveness

Does not take account of values attributed to levels
of quality of life

Not comprehensive

May miss side effects

Cannot compare across conditions

helpful in predicting long-term functional out-
comes in patients. Thus patients scoring above
a certain level in the area of bodily pain may
have a decreased chance of successfully return-
ing to work, and patients with decreased overall
scores in the areas of physical and social func-
tion and health may have an increased 5-year
mortality. However, the abbreviated form of the
SF-36, the SF-12, is growing in popularity.

In addition to general evaluations of func-
tional status, disease-specific instruments have
also been developed. One of the most widely
used surveys for the evaluation of patients with
lower extremity arterial occlusive disease is
the Walking Impairment Questionnaire (WIQ);
however, there are newer and more specific
questionnaires becoming available (Chong et
al., 2002). Because peripheral vascular disease
has a detrimental effect on quality of life even
in patients without the most severe forms of
limb-threatening ischemia, these instruments
may be very useful in evaluating the benefit to
patients undergoing treatment for claudication.
These surveys may be even more important for
evaluating patients undergoing prophylactic
interventions for the management of asympto-
matic disease.

Some authors have recommended that a com-
bination of two different surveys such as the
SF-36 and the EuroQol be used to evaluate the
quality of life outcomes in patients with and
without ischemic complications who are under-
going infrainguinal bypass grafting (Tangelder
et al., 1999). Tangelder et al. found that the com-
bination of the SF-36 and the EuroQol provided
useful information concerning the patients'
quality of life after lower extremity bypass graft-
ing. Interestingly, patients' functional outcomes
were similar for those with asymptomatic
graft occlusions and patent grafts, although the

lowest outcomes were found in patients who
underwent amputation after failed attempts
at secondary revascularization. These results
confirm clinical findings that are often well
known in clinical practice but that are not shown
by primary or secondary patency rates or limb
salvage.

Additional concerns have been expressed
about the potential for patient bias with self-
reporting of health status. However, patient
reports of functional health status appear to
have good face value validity. Thus patients who
suffer from severe strokes report worse func-
tioning in the areas of physical and general
health than patients with mild strokes. Similarly,
patients with venous ulcers report impaired
social interaction, domestic activity, and emo-
tional status with improved functioning after
healing of their venous ulcers (Smith et al.,
2000). Also, the benefits of varicose vein surgery
can be justified in terms of improvements in
quality of life scores.

Cost/Utility

Cost outcomes are another important area of
recent interest. Increasing pressures are being
exerted by the government and insurers to
optimize the quality of the health care while
minimizing expenditures. True costs to the indi-
vidual and society must be calculated both for
the acute illness and over the long term.

Practice guidelines can often be established
based on the results from existing controlled
clinical trials. These guidelines can then be used
on a regional or national basis to evaluate physi-
cians and health care organizations. Using the
same processes of continuous quality improve-
ment (CQI) found in major industrial manufac-

153

OUTCOME MEASURES IN VASCULAR SURGERY

turing plants, these guidelines should reduce
variation in the processes of care, thus improv-
ing quality while decreasing cost. These guide-
lines are designed to evaluate processes, with
the ultimate philosophy of continuously impro-
ving the process to ensure the best possible
outcome.

This process is in contradistinction to the
more traditional concept of quality analysis
(QA), where minimum standards or thresholds
are set to ensure a good outcome and only out-
liers are evaluated rigorously. The pitfall of this
approach is that it encourages organizations to
be just "good enough" and meet the minimum
standards set rather than aim for being the best
possible. In addition, it singles out only those
groups or individuals doing a poor job rather
than rewarding groups that are doing a good job
and trying to reproduce those results in other
areas.

The value that patients and society place
on certain outcomes and levels of functioning
can also play a role in evaluating the cost-
effectiveness of certain procedures. The cost-
effectiveness of a certain intervention can be
expressed as the net benefit to a population by
using statistical probabilities of certain out-
comes occurring along with specific costs asso-
ciated with various outcomes as documented
from the medical literature. One example of
this is the use of the Markov decision model to
evaluate the cost-effectiveness of performing
carotid endarterectomy in asymptomatic pa-
tients with >60% stenosis (Cronenwett et al.,
1997). The measurement units in this study are
in quality-adjusted life years (QALYs) defined as
the fraction of a year in perfect health that the
patient believes to be equivalent in value to a
year in the health state in question.

In this study, Cronenwett et al. demonstrated
that from a societal standpoint, carotid endar-
terectomy appeared to be cost-effective for the
young asymptomatic patient with standard
risk factors in the hands of a surgeon with a
2.3% 30-day perioperative stroke and death rate.
However, the procedure was not found to be
cost-effective for patients older than 79 years of
age, those with a high perioperative stroke risk,
or those with a particularly low stroke risk with
medical management. In this study it is impor-
tant to note that cost-effectiveness is compared
to cost/QALY for other medical interventions,
and that a cost of over $100,000/additional

QALY was defined as not cost-effective. Inter-
estingly, one could extend the evaluation even
further to include the individual's risk aversion
and risk taking behavior when defining the
cost-effectiveness for that person. This is es-
sentially what occurs every time we obtain
informed consent from a person who is about to
undergo a high-risk procedure.

Conclusion

The reasons for physicians to utilize extended
outcomes assessment include the following:
(1) to achieve a better understanding of the
effectiveness of our interventions; (2) to pro-
vide health care consumers, both patients and
insurers, with information that will allow them
to make better informed decisions; and (3) to
develop public health standards that will allow
us provide the most cost-effective care
(McDaniel et al, 2000).

In addition, the Accreditation Council for
Graduate Medical Education (ACGME) in the
United States has mandated that all residency
training programs evaluate as part of their core
competency requirements six areas, all of which
involve some component involving outcomes
measures: (1) practice-based learning, (2)
systems-based practice, (3) medical knowledge,
(4) patient care, (5) interpersonal and com-
munication skills, and (6) professionalism
(www.acgme.org/outcomes).

Finally, the incorporation of outcomes meas-
ures are now being studied by the task force on
competence of the American Board of Medical
Specialties to be used in the process of recer-
tification. In fact, recommendations have already
been published stating that outcomes measures
should be included as part of the requirement
for recertification in vascular surgery by the
American Board of Surgery (Hertzer, 2001).

References

Chong PF, Garratt AM, Golledge J, Greenhalgh RM, Davies
AH. (2002) J Vase Surg 36:764-71; discussion 863-4.

Cronenwett JL, Birkmeyer JD, Nackman GB, et al. (1997)
J Vase Surg 25:298-309; discussion 310-1.

Hertzer NR. (2001) J Vase Surg 34:371-3.

Khuri SF, Daley J, Henderson W, et al. (1998) Ann Surg
228:491-507.

154

VASCULAR SURGERY

McDaniel MD, Nehler MR, Santilli SM, et al. (2000) J Vase

Surg 32:1239-50.
O'Connor GT, Plume SK, Olmstead EM, et al. (1996) JAMA

275:841-6.

Smith JJ, Guest MG, Greenhalgh RM, Davies AH. (2000)

J Vase Surg 31:642-9.
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J Vase Surg 29:913-9.

Carotid Artery Disease

A. Ross Naylor, Peter H. Lin, and Elliot L. Chaikof

Epidemiology

Stroke

A stroke is defined as a focal (occasionally
global) loss of cerebral function lasting for more
than 24 hours, and which after investigation is
found to have a vascular cause. Stroke is respon-
sible for 4.5 million deaths worldwide, with the
majority occurring in nonindustrialized coun-
tries. In the United States, stroke is the third
most common cause of death, with approxi-
mately 160,000 Americans dying from the
disease each year. Stroke management con-
sumes $45 billion annually, including indirect
costs and is responsible for more than one
million hospital discharges per annum.

The demographics are remarkably similar in
the United Kingdom, where stroke is also the
third leading cause of death (12% of deaths
overall) and 58,000 Britons die each year. Five
percent of the National Health Service budget is
used in stroke care (excluding indirect costs),
and stroke patients occupy 20% of acute hospi-
tal beds and 25% of rehabilitation beds.

The incidence of stroke is 2 in 1000 per
annum, but significantly increases with con-
current risk factors of age, sex, and ethnic
background. Overall, the 20-year risk for a 45-
year-old man is 3%, but this increases to 25% for
a 40-year risk (Bonita, 1992). The annual inci-
dence of stroke doubles for each decade over the

age of 55 years. For those aged to 44 years, the
annual incidence of stroke is 0.09 in 1000,
increasing to 2.9 in 1000 for those aged 55 to 64
and 14.3 in 1000 in those aged 75 to 84. The
largest incidence is observed in populations
aged >85 years, where the incidence is almost
20 in 1000. In both the United States and the
United Kingdom, the incidence of stroke is twice
as high in blacks as in white. This ethnic dif-
ference is thought to be due to the increased
incidence in blacks of risk factors such as hyper-
tension, diabetes, smoking, obesity, and sickle
cell disease.

Transient Ischemic Attack

A transient ischemic attack (TIA) has the same
definition as stroke but it lasts for less than
24 hours. The 24-hour threshold is somewhat
arbitrary, as up to 28% of TIA patients have an
infarct on computed tomography (CT) scan, of
which 36% are bilateral. In the U.S., the preva-
lence of TIA in men aged 65 to 69 years is 2.7%,
increasing to 3.6% for men aged 75 to 79 years.
The respective prevalence figures for women are
1.6% and 4.1%. In the U.K., the overall incidence
of TIA is 0.4 in 1000, but this varies with age.
The incidence is 0.25 in 1000 for those aged 45
to 54 years, increasing to 1.61 in 1000 in the 65-
to 74-year age group and 2.57 in 1000 in those
aged 75 to 84 years.

155

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VASCULAR SURGERY

Etiology of Ischemic Stroke

Approximately 80% of strokes are ischemic and
20% hemorrhagic. This section deals primarily
with the etiology of ischemic carotid territory
stroke.

Thromboembolism

Approximately 50% of all ischemic carotid ter-
ritory strokes follow a carotid thrombosis or
embolism from a carotid stenosis (Fig. 15.1)
into territories supplied by either the middle
cerebral artery (MCA) or the anterior cerebral
artery (ACA). The sequelae of carotid thrombo-
sis depend on a number of factors, including the
status of the circle of Willis (potential for col-
lateralization),the chronicity of the thrombosis,

Figure 15.1. Selective intraarterial digital subtraction angio-
gram of left carotid bifurcation showing diffuse disease of the
upper third of the common carotid artery,a stenosis at the origin
of the external carotid artery, and a complex severe stenosis at
the origin of the internal carotid artery with deep ulceration.

and the extent of the thrombosis. Once the
internal carotid artery (ICA) has thrombosed,
the column of thrombus usually propagates
distally to the ophthalmic artery. However, the
thrombus may occasionally extend beyond the
ophthalmic artery and propagate into the circle
of Willis.

A very small proportion of strokes (<4%) are
secondary to isolated cerebral hypoperfusion.
Patients susceptible to this type of stroke include
those with critical ICA stenoses, poor collateral-
ization via the circle of Willis, and a secondary
trigger such as hypotension following an acute
cardiac event.

Rarely, carotid thromboembolism may cause
posterior (vertebrobasilar) territory strokes.
This arises because, embryologically, the ICA
provides the blood supply to the developing
posterior cerebral hemispheres and brainstem
via the posterior communicating and posterior
cerebral arteries. In a very small proportion of
the population, this anatomical arrangement
persists into adult life.

Intracranial Small-Vessel Disease

Occlusion of the penetrating end arteries
(lenticulostriate, thalamoperforate) in the
deep structures of the brain causes discrete
wedge-shaped infarctions of brain tissue. These
ischemic lesions, termed lacunar infarcts, are
responsible for up to 25% of ischemic carotid
territory strokes. Conditions predisposing
toward lacunar infarction include hypertension
and diabetes. There is still considerable debate
as to whether embolization from a carotid
stenosis can cause lacunar infarction.

Cardiac Embolism

Cardiac embolism accounts for 15% of ische-
mic carotid territory strokes. The emboli con-
sist of fibrin, cholesterol, calcified debris, and
atheroma depending on the underlying pathol-
ogy. Sources include valvular heart disease,
prosthetic valves, atrial myxoma, ventricular
aneurysm thrombus, cardiomyopathy, and in-
fective endocarditis. However, the commonest
causes are atrial fibrillation and embolization
of mural thrombus overlying a dyskinetic seg-
ment of myocardium following a myocardial
infarction (MI).

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CAROTID ARTERY DISEASE

Hematological Causes

A variety of pathologies predisposing toward a
hypercoagulable state are responsible for about
5% of ischemic strokes. These include poly-
cythemia, sickle cell disease, leukemia, throm-
bocythemia, malignancies, functional protein S
deficiency, lupus anticoagulant (antiphospho-
lipid antibody syndrome), antithrombin III
deficiency, and the paraproteinemias.

Miscellaneous Causes

Miscellaneous causes account for the remain-
ing 5% of ischemic carotid territory strokes.
These include migraine, oral contraceptive use,
trauma, dissection, giant cell arteritis, Takayasu
arteritis, systemic lupus erythematosus (SLE),
polyarteritis nodosa, amyloid angiopathy, co-
caine abuse, fibromuscular dysplasia, and radi-
ation arteritis.

Pathology of Carotid
Artery Disease

Atherosclerosis

Atherosclerosis is the commonest pathology
affecting the carotid artery. The typical plaque
encountered at carotid endarterectomy (Fig.
15.2) is the culmination of a sequence of patho-
physiological processes starting with endothe-
lial dysfunction/damage. The tendency for
atherosclerotic plaque to form at the carotid
bifurcation is related to a number of factors,
including geometry, velocity profile, and shear
stress.

It was originally proposed that local turbu-
lence predisposed to high wall shear stress and
endothelial injury. This hypothesis, however,
was refuted by Zarins et al. (1983), who showed
that plaque formation was increased within
areas of low flow velocity and low shear stress
and decreased in areas of high flow velocity and
elevated shear stress. Postmortem specimens
showed that atherosclerosis was particularly
pronounced along the outer (lateral) aspect of
the proximal ICA and carotid bulb. This zone
corresponds to areas of low velocity and low
shear stress. The medial or inner aspect of the
carotid bulb (associated with high blood flow

Figure 15.2. Atheromatous plaque excised at carotid endar-
terectomy. Note the deep area of ulceration in the plaque
surface.

velocity and high shear stress in the flow model)
were relatively free of plaque formation.

The smooth muscle cell has an important
role in the initial stages of plaque develop-
ment. Smooth muscle cells migrate through
the intima, proliferate within the media, and
promote accumulation of cholesterol and other
lipid molecules within the evolving lesion.
Thereafter, the macrophage becomes a source of
growth factor production that stimulates further
smooth muscle cell proliferation and extracellu-
lar matrix production. Smooth muscle cells and
macrophages initiate a secondary inflammatory
cell reaction and are capable of ingesting lipid
and of being transformed into vacuolated foam
cells that are characteristic of atherosclerotic
lesions.

Besides these cellular components, the major-
ity of carotid plaques have a necrotic core con-
sisting of loose cellular debris and cholesterol
crystals. The necrotic core is separated from the
carotid lumen by a fibrous cap, which is com-
posed of a rim of variable thickness comprising
cellular components and extracellular matrix.
The structural integrity of the fibrous cap is
crucial to the final stage of plaque disruption
and its clinical and pathological sequelae. It is
now generally accepted that acute changes
within the plaque, notably Assuring/splitting
of the fibrous cap (Fig. 15.2), with exposure of
the deeper lipid contents predisposes toward
thrombosis with or without secondary emboli-
zation. It is not known what actually pre-
disposes toward acute plaque disruption, but
recent studies suggest that excess matrix metal-
loproteinase activity or cytokine expression

158

VASCULAR SURGERY

within the plaque may be associated with this
process (Loftus et al., 2002).

Another feature characteristic of advanced
atherosclerotic plaques is intraplaque hemor-
rhage that can occur in the absence of a dis-
rupted fibrous cap. Symptomatic carotid disease
is associated with increased neovascularization
within the atherosclerotic plaque and fibrous
cap. These vessels are larger and more irregular
and may contribute to plaque instability and the
onset of thromboembolic sequelae.

Fibromuscular Dysplasia

Fibromuscular dysplasia (FMD) is the com-
monest nonatherosclerotic disease to affect
the ICA. Approximately one quarter of patients
with carotid FMD have associated intracranial
aneurysms, and up to two thirds of these
patients will have bilateral carotid fibromuscu-
lar dysplasia.

Fibromuscular dysplasia can be divided into
three pathological subtypes. Medial fibroplasia
is the most common (>85% of cases) and is
usually found in long segment arteries with few
side branches. It is characterized by stenoses
alternating with intervening fusiform dilata-
tions that resemble a string of beads, particu-
larly in the upper ICA. Pathologically, smooth
muscle cells in the outer media are replaced
by compact fibrous connective tissue, whereas
the inner media contains excess collagen and
ground substance in disorganized smooth
muscle cells. Because of its prevalence in
females, a possible role for estrogen and prog-
esterone has been postulated. Others have sug-
gested that the absence of vasa vasorum in long
nonbranching arteries such as the ICA or renal
arteries may predispose to mural ischemia
that leads to the development of fibromuscular
dysplasia.

Intimal fibroplasia accounts for less than 10%
of cases of FMD and affects men and women
equally. It typically appears as a focal narrowing
in older patients and long segmental stenoses in
younger patients. The lesion is confined to the
intimal layer while the medial and adventitial
structures are always normal. Its pathophysiol-
ogy is due to irregularly aligned sub endothelial
mesenchymal cells within a loose matrix of con-
nective tissue. Perimedial dysplasia is char-
acterized by accumulation of elastic tissue
between the media and the adventitia. This

subtype predominantly affects the ICA and
renal arteries and may be associated with
secondary aneurysm formation.

Coils and Kinks of the Extracranial
Carotid Arteries

Redundancy of the extracranial carotid artery
is thought to be due to abnormalities in devel-
opment. Occasionally, the ICA may undergo
a complete 360-degree rotation. The ICA is
derived embryologically from the third aortic
arch and the dorsal aortic root. In its early
stages, a normally occurring redundancy is
straightened as the heart and great vessels
descend into the mediastinum. Incomplete
descent of the heart and great vessels may result
in the development of complex coils and kinks.
These are bilateral in approximately 50% of
affected patients.

Elongation of the ICA, which can also result
in kinking of the ICA, is usually due to degen-
erative changes associated with increasing age
and atherosclerosis. The loss of elasticity of the
arterial wall due to the aging process (coupled
with hemodynamic shear stresses) predisposes
toward kinks of the elongated carotid artery
between the proximal and distal fixed points of
the skull base and thoracic inlet.

Carotid Artery Aneurysms

As with aneurysms anywhere else in the body,
carotid aneurysms may be either true or false.
In the past,most true aneurysms (Fig. 15.3) have
traditionally been classified as part of the
atherosclerotic process, but emerging evidence
suggests that aneurysmal disease may be yet
another manifestation of abnormalities of
matrix metalloproteinase enzyme expression
and production, unless associated with other
distinct pathologies, for example, arteritis (giant
cell, Takayasu) or FMD. False aneurysms may
arise as a consequence of iatrogenic injury, blunt
trauma, spontaneous dissection, or infection
(e.g., prosthetic patch infection after carotid
endarterectomy).

Carotid Dissection

Acute carotid dissection can complicate athero-
sclerosis, FMD, cystic medial necrosis, or blunt

159

CAROTID ARTERY DISEASE

Figure 15.3. Intraarterial digital subtraction angiogram of the
aortic arch and great vessels. There is a large aneurysm just
beyond the left carotid bifurcation.

trauma, or be associated with a collagen vascular
disorder such as Ehlers-Danlos syndrome type
IV or Marfan syndrome. Angiographic studies
suggest that the most likely mechanism is an
intimal tear followed by an acute intimal dissec-
tion, which produces luminal occlusion due to
secondary thrombosis within the false lumen.
This appears as a flame-shaped occlusion 2 to 3
cm beyond the bifurcation (Fig. 15.4). Autopsy
studies typically reveal a sharply demarcated
transition between the normal carotid artery
and the dissected carotid segment. The ICA is
commonly affected, with the dissection plane
typically occurring in the outer medial layer.
The classical triad of clinical signs/symptoms
following carotid dissection include (1) pain in
the face and neck (20%), (2) a partial Horner
syndrome (50%), and (3) retinal or cerebral
ischemia (50% to 90%). About one in ten will
suffer cranial nerve palsy.

Takayasu's Arteritis

Takayasu's arteritis (TA) is a nonspecific arteri-
tis affecting the thoracic and abdominal aorta
and their major branches. Although this dis-
ease is uncommon in Western countries, it is

more prevalent in Asia and usually affects young
females. Its pathogenesis relates to an inflam-
matory process involving all three layers of the
arterial wall with proliferation of connective
tissue and degeneration of the elastic fibers.
Granulomatous lesions may also develop, and
the condition may also be associated with fusi-
form or saccular aneurysms.

Takayasu's arteritis is classified according
to its mode of involvement. Type I involves
branches of the aortic arch; type Ha involves the
ascending aorta, aortic arch, and branches; type
lib involves the vessels involved in Ha plus the
descending aorta; type III involves the descend-
ing thoracic aorta and abdominal aorta (with
or without renal arteries); type IV involves the
abdominal aorta (with or without renal arter-
ies) and type V involves a combination of type
lib and IV

Figure 15.4. Selective intraarterial digital subtraction angio-
gram in a patient with acute carotid dissection. The internal
carotid artery is almost completely occluded 2 to 3cm beyond
the origin of the internal carotid artery.There is virtually no flow
visible up the true lumen.

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VASCULAR SURGERY

Giant Cell Arteritis

Giant cell arteritis predominantly affects elderly
women. Although it commonly involves the
temporal arteries, it can involve other major
vessels including the carotid artery and upper
extremity vasculature. There is usually ten-
derness over the inflamed artery. Laboratory
evaluation generally reveals elevation of C-
reactive protein and the erythrocyte sedimenta-
tion rate. Biopsy of an affected artery shows
characteristic giant cell granulomata with abun-
dant T lymphocytes. However, a negative biopsy
does not exclude the diagnosis. Management
of giant cell arteritis usually includes the use of
high-dose corticosteroids as well as other forms
of immunosuppression including cyclophos-
phamide or azathioprine. Steroids can usually
be tailed off after 1 year of treatment.

Radiation Arteritis

The principal effects of radiation on arteries
include immediate arterial spasm and endo-
thelial denudation, intimal disruption, sub-
intimal edema, and degeneration of collagen and
smooth muscle. These acute changes predispose
toward an increase in vessel wall permeability to
circulating lipids, which produce a plaque char-
acterized by fibrosis, fatty infiltration, and elastic
tissue destruction. Hyperlipidemia and hyper-
cholesterolemia appear to predispose patients
who have received radiation therapy to develop
accelerated atherosclerotic lesions. The sensitiv-
ity of elastic tissue to radiation may account for
the mechanism of structural weakening and
eventual rupture in elastic arteries.

As a result of the increased use of external
radiation to treat neck malignancies, a rise in
radiation-induced atherosclerotic disease in
association with symptomatic carotid stenosis
has been noted. Radiation-induced carotid
lesions can present either in a segmental or
diffuse manner. The affected carotid segments
typically lie within the field of radiation treat-
ment. One or both common carotid arteries may
be involved, whereas the carotid bifurcation is
often spared. The severity of carotid injury is
related to radiation dose. Smaller doses cause
less cellular damage, whereas larger doses may
even lead to arterial wall necrosis.

Carotid Body Tumor

Carotid body tumors (CBTs) originate from the
chemoreceptor cells located at the carotid bifur-
cation. Because cells of the carotid body typi-
cally detect change in the P0 2 , PC0 2 , and pH,
CBTs have been reported to be more prevalent
in individuals who live at high altitudes, which
suggests that chronic hypoxia may be an etio-
logical factor. A CBT typically presents as a
palpable, painless mass over the carotid bifur-
cation region in the neck. Cranial nerve palsy
may occur in up to 25% of patients, particularly
involving the vagus and hypoglossal nerves.
The differential diagnosis includes cervical
lymphadenopathy, carotid artery aneurysm,
branchial cleft cyst, laryngeal carcinoma, and
metastatic tumor.

The treatment of choice of CBT is surgical
excision. Because these tumors are highly vas-
cularized, preoperative tumor embolization has
been advocated by some surgeons to minimize
operative blood loss when dealing with tumors
>3cm in diameter, but there is no consensus on
this strategy. An important surgical principle in
CBT resection is to maintain the plane of dis-
section within the subadventitial space, which
enables complete tumor excision without inter-
rupting carotid artery integrity.

Carotid Trauma

Blunt trauma to the neck can cause carotid
artery injury either by forceful compression
or extension of the artery. Common scenar-
ios include motor vehicle or motorcycle
accidents, pedestrian injuries, hanging, or
strangulation.

Patients with carotid trauma may present
with focal physical findings such as neck hema-
toma, pulsatile cervical mass, carotid bruit, or
localized bleeding. More generalized physical
findings include loss of consciousness and lat-
eralizing neurological deficits. Arteriography
remains the diagnostic test of choice for carotid
trauma, since it has the highest sensitivity
and specificity compared to all other imaging
modalities. Treatment of all blunt carotid artery
injuries usually involves anticoagulation. Anti-
platelet therapy should be considered if sys-
temic anticoagulation is contraindicated.

161

CAROTID ARTERY DISEASE

Clinical Presentation
of Carotid Disease

Syndromes

Transient Ischemic Attack

A transient ischemic attack is a focal loss of neu-
rological function (lasting <24 hours) that has a
vascular cause upon investigation. It is conven-
tional to describe a TIA as being carotid or ver-
tebrobasilar (see below).

Nonhemispheric Symptoms

These are a group of nonfocal symptoms that,
on their own, are not indicative of true carotid
or vertebrobasilar events. Classical nonhemi-
spheric symptoms include isolated dizziness,
isolated vertigo, isolated syncope (drop attacks,
blackouts), isolated double vision (diplopia),
and presyncope (faintness). In the absence of
any corroborative carotid or vertebrobasilar
symptoms, they cannot be ascribed to extracra-
nial carotid or vertebral disease alone.

Completed Stroke

A completed stroke is a focal (occasionally
global) loss of neurological function, lasting
for more than 24 hours, that is found to have a
vascular cause upon investigation. The term
completed refers to the fact that the severity of
the neurological deficit has now reached its
maximum.

Stroke in Evolution

A stroke in evolution is a progressive worsening
of the neurological deficit, either linearly over a
24-hour period or interspersed with transient
periods of stabilization and/or partial clinical
improvement.

Crescendo Transient Ischemic Attacks

This condition has never been properly defined.
Traditionally, it refers to a syndrome compris-
ing repeated TIAs within a short period of
time with complete neurological recovery in
between. At a minimum, the term should prob-
ably be reserved for those with daily events.

Hemodynamic Transient Ischemic Attacks

These attacks are focal cerebral events (hemi-
sensory or retinal) that are aggravated by exer-
cise or hemodynamic stress and typically occur
after short bursts of physical activity, post-
prandially or after getting out of a hot bath. It
is implied that they are due to severe extra-
cranial disease and poor intracranial collateral
recruitment.

Clinical Features

Ocular Symptoms

Ocular symptoms associated with extracranial
carotid and vertebrobasilar disease include
amaurosis fugax (transient monocular blind-
ness), Hollenhorst plaques, retinal/optic nerve
ischemia, the ocular ischemia syndrome, and
visual field deficits secondary to cortical infarc-
tion and ischemia of the optic tracts.

The blood supply to the retina originates
from two sources. The short posterior ciliary
arteries supply the outer two layers, together
with the optic disk and optic nerve. The central
retinal artery supplies the inner layers of the
retina. Amaurosis fugax is a temporary loss of
vision in one eye (likened to a shutter coming
down), but which can also refer to graying of the
vision. The blindness usually lasts for a few
minutes and then resolves. Most (>90%) are
due to embolic occlusion of the main artery or
its upper/lower divisions. It remains unclear,
however, why some patients always have
repeated episodes of amaurosis and never
hemispheric signs.

Monocular blindness progressing over a 20-
minute period suggests a migrainous etiology.
Hemodynamic amaurosis is rare but can be pre-
cipitated by heavy exercise or arising from a hot
bath. In this situation, where there is a severe
carotid stenosis and poor collateralization, the
visual loss tends to start at the periphery and
move toward the center. Occasionally, a patient
recalls no visual symptoms, but the optician
notes a yellowish plaque within the retinal
vessels (the Hollenhorst plaque). This is fre-
quently derived from cholesterol embolization
from the carotid bifurcation and it warrants
further investigation (Fig. 15.5).

162

VASCULAR SURGERY

Figure 15.5. Funduscopic examination. Note the two choles-
terol emboli within the retinal vessels.

Monocular visual loss due to central retinal
artery occlusion, persisting for more than 24
hours is analogous to cerebral infarction, with
the occlusive process usually occurring in the
intraneural part of the central retinal artery. In
addition to an embolic etiology, it is also impor-
tant to consider microatheroma, and arteritis in
occasional patients with other atypical symp-
toms. Bilateral visual loss (cortical blindness)
is due to infarction of the visual cortex in the
occipital lobe and therefore is never a carotid
territory event.

The optic nerve head can be rendered
ischemic by thromboembolic phenomena,
although it is rarely due to extracranial carotid
artery disease. Optic nerve ischemia is usually
due to intrinsic disease of the short posterior
ciliary arteries and can present as an acute loss
of either central or peripheral vision in one
eye. If the upper or lower visual fields are lost,
this suggests occlusion of the upper and lower
branch divisions of the ciliary artery.

The ocular-ischemia syndrome is a relatively
rare condition where there is global under-
perfusion of the eye, deteriorating monocular
vision, and excessive proliferation of the con-
junctival vessels. It is indicative of extremely
poor eye collateralization.

Homonymous hemianopia can occur as a
consequence of ischemia at varying points in

the optic tracts. Occipital lesions cause a con-
gruous homonymous hemianopia (visual field
defects exactly overlap in each eye). Homony-
mous hemianopia involving the lower visual
fields is usually due to a parietal infarction and
follows ischemia of the upper fibers of the visual
pathway that traverse the parietal lobe. Con-
versely, temporal lobe infarcts can extend to
involve the lower fibers of the visual pathways
and so cause a hemianopia involving the upper
fields. Of practical importance is the observa-
tion that homonymous hemianopia secondary
to occipital lesions tends to cause a very per-
ceptible visual void to the patient. In contrast,
the patient with homonymous hemianopia due
to parietal or temporal lobe lesions is often
unaware of the deficit and may bump into
objects.

Motor/Sensory Symptoms

A number of cerebral pathologies can cause
motor or sensory symptoms that may mimic
the focal symptoms observed in TIA or stroke.
These primarily include intracranial hemor-
rhage, tumor, migrainous phenomena, and
arteritis. Overall, the pattern of onset in con-
junction with the distribution and nature of
the symptoms enables the clinician to be more
discriminating in developing a differential
diagnosis.

Ischemic events tend to have an abrupt onset,
with the severity of the insult being apparent
from the outset. By contrast, motor/sensory
signs associated with migraine often progress
from one part of the body to the next over a
15- to 20-minute period of time. Ischemic
TIAs rarely include positive phenomena. For
example, the hemisensory/motor signs with
ischemic TIAs are not usually associated with
seizure or paresthesia but represent loss or
diminution of neurological function. Migrain-
ous or postictal events frequently include
seizures, clonic contractions, and enhanced
sensory phenomena.

Motor/sensory deficits can be unilateral or
bilateral, with the upper and lower limbs being
variably affected depending on the site of the
cerebral lesion. For example, occlusion of the
anterior cerebral artery causes a hemiparesis,
with the leg being more severely affected than
the arm. The combination of a motor and

163

CAROTID ARTERY DISEASE

sensory deficit in the same body territory is sug-
gestive of a cortical thromboembolic event as
opposed to lacunar lesions secondary to small-
vessel disease of the penetrating arterioles.
However, a small proportion of the latter may
present with a sensorimotor stroke secondary to
small-vessel occlusion within the posterior limb
of the internal capsule. Pure sensory and pure
motor strokes and those strokes where the
weakness affects one limb only or does not
involve the face are more typically seen with
lacunar as opposed to cortical infarction.

Higher Cortical Dysfunction

A number of clinical phenomena, including
speech and language disturbances, can be
caused by thromboembolic phenomena within
the anterior and posterior circulations. There
are a large number of examples of higher corti-
cal dysfunction (dysphasia, apraxia, visuospa-
tial neglect, alexia) that are beyond the scope of
this review. However, the most important clini-
cal example for the dominant hemisphere is
expressive dysphasia/aphasia, with visuospatial
neglect being an example of nondominant
hemisphere injury.

Dysphasia is a language disorder as opposed
to dysarthria, which is a locomotor speech
problem. Differentiation between the two is im-
portant, as dysarthria is a vertebrobasilar symp-
tom whereas dysphasia is of carotid origin.
In expressive dysphasia, patients know what
they wish to say but either cannot find the
word or produce seemingly meaningless verbal
output. Dysarthria can be defined as a simple
inability to "get your tongue" around the word.
Visuospatial neglect is the result of injury to
the nondominant parietal lobe. Here patients
may exhibit inattention to one side of their
body.

Carotid or Vertebrobasilar Territory?

Typical carotid territory symptoms (anterior
and middle cerebral arteries) include hemi-
sensory/motor symptoms, amaurosis fugax,
and evidence of higher cortical dysfunction.
Homonymous hemianopia alone is not a fea-
ture of injury to the carotid territory. Classical
vertebrobasilar symptoms comprise bilateral

motor/sensory symptoms, bilateral visual loss,
homonymous hemianopia, dysarthria, nystag-
mus, ataxia and gait problems, dysphagia and
dizziness, and vertigo, provided they accom-
pany other vertebrobasilar features.

Discrimination between carotid and verte-
brobasilar symptoms is usually straightfor-
ward but can be difficult. For example, 10%
of patients with vertebrobasilar stroke have
hemisensory/motor signs. This is because of
anatomical variations in the vascular boundary
zones between the carotid and vertebrobasilar
system. Similarly, a small number of patients
with thromboembolic carotid artery disease
present with vertebrobasilar symptoms because
the posterior cerebral artery is embryologically
derived from the carotid artery as opposed to
the vertebrobasilar system. If there is any ques-
tion regarding interpretation of the clinical
picture, advice from a neurologist or stroke
physician should be sought.

Clinical Features of
Nonatherosclerotic Disease

One of the characteristic features of the non-
atherosclerotic pathologies listed earlier is the
potential for thrombosis/stenosis and aneurysm
formation. Accordingly, each condition can
cause ischemic stroke/TIA, but most are rela-
tively rare. The onset of stroke/TIA in a patient
exhibiting other atypical features should raise
the possibility of a nonatheromatous pathology.
Sudden onset of temporal headache or neck
pain associated with a neurological or visual
deficit is suggestive of carotid dissection. The
initial neurological symptoms are thought to
be due to acute expansion of the dissection
resulting in compression of cranial nerves IX,
X, XI, or XII, followed by cerebral ischemia.
Horner syndrome can also occur, which is
believed to be due to disruption of periadventi-
tial sympathetic fibers adjacent to the carotid
artery. Systemic illness, malaise, weight loss,
and myalgia suggest an underlying arteritis
(Takayasu, giant cell, SLE, polyarteritis). Jaw
claudication is an important presentation in
giant cell arteritis. Takayasu arteritis patients
also present with symptoms attributable to
involved vascular beds (renovascular hyperten-
sion, TIA/stroke, MI).

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VASCULAR SURGERY

Prognosis of Ischemic Stroke

Mortality and Persisting Disability

Stroke is the commonest cause of persisting
neurological disability in the Western world
and accounts for 4.5 million deaths per annum
worldwide. The overall mortality rate for stroke
is about 26% at 30 days and 38% at 1 year, but
varies according to subtype (see below).

At 6 months, 15% to 25% of stroke survivors
are still dysphasic/aphasic, 7% to 11% remain
incontinent of urine or feces, up to 33% require
help with dressing/feeding or toileting, 15%
are unable to walk independently indoors, and
17% are classified as moderately or severely
disabled.

Outcome Based on Presentation

The Oxfordshire Community Stroke Project
(OCSP) was the first community-based study to
develop a bedside classification that could reli-
ably predict outcome, vascular pathology, and
CT scan/autopsy findings following ischemic
stroke (Bamford et al., 1990). Patients who were
classified as total anterior circulation infarction
(TACI) presented with the triad of (1) hemi-
sensory/motor deficit affecting the face, arm,
and leg; (2) homonymous hemianopia; and
(3) higher cortical dysfunction (e.g., dysphasia,
visuospatial neglect). These patients had the
largest infarction volumes on CT scan or
autopsy, occlusion of either the extracranial ICA
or intracranial MCA mainstem, and a 30-day
mortality rate of 37%. Only 7% were alive and
independent at 1 year. Patients with TACI are
rarely ever candidates for carotid surgery.

Patients presenting with one or two compo-
nents of the TACI triad were classified as partial
anterior circulation infarction (PACI). These
patients had focal, cortical infarcts on CT scan
and rarely had evidence of major vessel occlu-
sion. The majority followed embolization of
MCA branches from a carotid plaque. The 30-
day mortality following PACI was 13%, and 71%
were alive and independent at 1 year. Patients
with a nondisabling PACI stroke were exposed
to a 5% risk of recurrent stroke within 30 days
of the initial event and a 17% risk of stroke
within 1 year. Patients with PACI constitute
the majority of patients being considered for
carotid endarterectomy

Patients classified as lacunar infarction
(LACI) presented with symptoms and signs
associated with disease of the deep perforating
arteries (pure motor stroke, pure sensory
stroke, sensorimotor stroke, and ataxic hemi-
paresis). Patients with LACI never have evidence
of higher cortical dysfunction and major vessel
occlusion was not a feature.

Patients classified as posterior circulation
infarction (PoCI) presented with vertebrobasi-
lar symptoms and had infarcts localized to the
posterior circulation territory. The 30-day mor-
tality rate was 7%, and 80% were independent at
30 days.

Investigation of
Ischemic Stroke

All patients should undergo simple baseline
investigations (full blood count, urea/elec-
trolytes, glucose, lipids, chest x-ray, electro-
cardiogram). This not only enables diagnosis of
unexpected coexistent pathologies (sickle cell
disease, thrombocytosis, etc.), but also enables
important risk factors to be corrected (hyper-
tension, diabetes, ischemic heart disease, etc.).
There is no need for more complex investiga-
tions to be performed routinely (autoantibod-
ies, echocardiograms, thrombophilia screens).
These should only be undertaken if the history
or initial investigations suggest it is appropriate.

Duplex Ultrasound

Noninvasive diagnostic testing should be per-
formed in the preliminary evaluation of all pa-
tients suspected of having suffered a stroke or
TIA. Color duplex is now the most accessible
screening technique for diagnosing carotid
stenosis. One of the great advantages of duplex
is that the machine can be brought down into a
single visit outpatient clinic. Duplex combines
B-mode imaging and pulsed wave Doppler sam-
pling of velocity spectra to assess the potential
hemodynamic significance of the carotid lesion.
Indications for carotid duplex scanning typi-
cally fall into three categories: symptoms, signs,
and risk factors. Symptoms include those that
define a classic TIA. The primary sign is the
presence of a carotid bruit, whereas risk factors
include diabetes mellitus, hypertension, ciga-

165

CAROTID ARTERY DISEASE

rette smoking, hypercholesterolemia, peripheral
vascular disease, and coronary artery disease. As
the number of risk factors increases, the likeli-
hood of an associated carotid lesion rises.

The accuracy of a carotid duplex scan is
largely dependent on the technician who per-
forms the study, as well as the type of scanner
that is used. Ultrasound criteria vary among
units, and each vascular laboratory should vali-
date the technical skills of the ultrasonographer
before duplex imaging is used as the sole diag-
nostic study.

An increasing number of units now perform
carotid surgery on the basis of duplex ultra-
sound alone. However, corroborative magnetic
resonance angiography (MRA) or diagnostic
angiography may be required in patients with
(1) gross calcification causing severe acoustic
shadowing, (2) inability to image proximal or
distal limits of plaque, (3) damped inflow wave-
form suggestive of proximal common carotid
disease, and (4) a high-resistance ICA waveform
suggestive of distal severe disease. Some units
may still wish to undertake corroborative
studies in patients with a duplex diagnosis of
ICA occlusion.

Magnetic Resonance Angiography

The principal advantages of MRA are that no
radiation is involved, it can be combined with
functional brain imaging, and the surgeon is
provided with a hardcopy for easy interpre-
tation. Disadvantages include problems with
interpretation of images and, more importantly,
rapid access to imaging in TIA clinics.

The principle underlying MRA is that the
patient is positioned within a magnetic field.
This causes protons in the body's water mole-
cules in the area of interest to become aligned
with their axis to the magnetic field. Radio wave
pulses are then applied to the region of interest
that excite the protons and cause them to rotate.
As the protons return to their original align-
ment they emit energy that is picked up by
external detectors. There are two principal
methods for imaging blood vessels: time of
flight (TOF) and phase contrast.

In the TOF method, stationary tissue is dark
because the repeated radio wave pulsations sat-
urate their signal. In contrast, flowing blood
emerging from the chest has not been subject to
the radio waves and is represented by a white

signal against the black background. Two-
dimensional (2D) TOF involves the sequential
acquisition of tomographic slices of data that
are then reconstructed by a computer algorithm
to create the axial angiogram. Three-dimen-
sional (3D) TOF acquires multiple slices of data
at the same time. Each has its advantages and
disadvantages. Two-dimensional TOF is better
at discriminating abnormalities within fields of
slow flowing blood. Therefore, it is useful in dif-
ferentiating subtotal occlusion from complete
occlusion. It is, however, limited by its inability
to reliably interpret kinks and loops, and the
creation of flow voids tends to lead to overin-
terpretation of stenosis degree. The latter is not
a problem with 3D TOF. As with duplex, advo-
cates of MRA must validate their own findings
with either angiography or resected plaque
specimens.

Contrast Angiography

Few centers now perform routine contrast
angiography on all patients prior to surgery.
This is partly due to the inevitable delay, but
mainly because of the potential for angio-
graphic-related strokes. This risk is between 1%
and 2%. Interestingly, 50% of the operative risk
in the Asymptomatic Carotid Atherosclerosis
Study was attributable to the angiographic
stroke risk. The risk of angiographic stroke is
reduced by (1) employing arch injections where
possible, (2) using small volumes of nonionic
contrast material, (3) using small bore catheters,
(4) using experienced practitioners, and (5)
being sure the patients are well hydrated.

Intraarterial digital subtraction arteriogra-
phy (DSA) is still indicated in patients in
whom there is discordance between duplex and
MRA or problems with interpretation of these
modalities.

Functional Imaging

This is another contentious issue. Some centers
advocate routine CT or magnetic resonance
imaging (MRI) on all stroke/TIA patients on the
basis that unexpected pathology (neoplasms,
vascular malformations, subarachnoid or sub-
dural hematomas) must be considered in the
overall differential diagnosis. Others argue that
the yield is <2%, it incurs an unnecessary delay,

166

VASCULAR SURGERY

it does not alter management decisions, and it
incurs undue cost.

In an ideal world, all patients should undergo
functional imaging (preferably MRI) combined
with MRA. However, all clinicians would agree
that patients presenting with a stroke require
imaging within 2 weeks of onset (so as to iden-
tify patients with intracranial hemorrhage), as
should patients reporting atypical symptoms
(seizure, progressive neurological symptoms,
headaches, cranial nerve signs). Centers that
continue to advocate routine CT/MRI must
ensure that implementation of such a policy
does not lead to unacceptable delays in planning
management strategies.

Management of Occlusive
Carotid Artery Disease

Best Medical Therapy

There is more to investigating and treating
patients with stroke or TIA than simply identi-
fying those who might benefit from carotid
endarterectomy More importantly, the imple-
mentation of the best medical therapy should
not be delegated to the most junior member of
the team. Although some risk factors (age, sex,
gender, family history) are nonmodifiable, there
is an increasing body of systematic evidence to
guide the clinician with regard to implementing
optimal medical therapy in patients with cere-
bral vascular disease.

Antiplatelet Therapy

Aspirin irreversibly blocks cyclooxygenase-
mediated breakdown of arachidonic acid,
thereby inhibiting the formation of thrombox-
ane A 2 (platelet aggregator and vasoconstric-
tor). Meta-analyses have shown no evidence that
aspirin has any beneficial role in the primary
prevention of stroke. However, in patients with
a history of vascular disease, the Antiplatelet
Trialists' Collaboration showed that aspirin con-
ferred a 22% relative risk reduction (RRR) in all
vascular events (nonfatal stroke, nonfatal MI,
vascular death). A more recent meta-analysis
has shown that aspirin confers a 15% reduction
in stroke alone in patients presenting with
symptomatic cerebral vascular disease.

There has been much debate about the
optimal aspirin dose. A balance must be struck,
as there is a 1.0% annual risk of adverse events
associated with aspirin therapy, with the risk
increasing as the aspirin dose increases. In
Europe, there is a trend toward using low-dose
aspirin (50 to 150mg daily), whereas larger
doses have previously been recommended in
North America (300 to 1200 mg). Meta-analyses
have shown that aspirin doses of <100mg daily
confer a 13% RRR in subsequent vascular events
in patients with a presenting history of stroke or
TIA, falling to 9% for medium doses (300 mg
daily) and 14% for daily doses in excess of 900
mg. The North American Symptomatic Carotid
Endarterectomy Trial (NASCET) originally
observed that the incidence of perioperative
stroke was significantly higher in patients
receiving lower-dose aspirin. However, a sub-
sequent randomized trial in more than 2500
patients undergoing carotid endarterectomy
indicated that the 30-day risk of stroke, MI, or
death was significantly lower in patients taking
81 mg or 325mg aspirin as compared with 650
to 1300mg.

Dipyridamole inhibits platelet aggregation by
partially blocking the adenosine diphosphate
(ADP) receptor on the platelet and by elevat-
ing levels of cyclic adenosine monophosphate
(cAMP) and cyclic guanosine monophosphate
(cGMP). Dipyridamole on its own does not
significantly reduce the risk of secondary
stroke, but a number of studies have suggested
that combination therapy with aspirin is more
effective. This has been confirmed in a recent
meta-analysis that showed that aspirin and
dipyridamole conferred a 23% RRR in stroke.
However, the benefit was slightly offset by the
fact that about a quarter of patients experienced
adverse side effects, necessitating dipyridamole
withdrawal.

Ticlopidine and clopidogrel have similar
modes of action. Both inhibit platelet activation
through inhibition of ADP binding to its platelet
receptor, thereby blocking the GpIIb-IIIa re-
ceptor complex that is the principal receptor
for platelet fibrinogen binding. Although some
studies showed a beneficial reduction in the
risk of stroke, an overview by the Antiplatelet
Trialists' Collaboration suggested that ticlopi-
dine conferred no extra benefit over aspirin
alone in terms of reducing the risk of all vascu-
lar events. However, ticlopidine was associated

167

CAROTID ARTERY DISEASE

with a 20% incidence of adverse complications
including neutropenia in 2% and a tendency
to increased cholesterol levels. Overall, 6% of
patients had to stop the drug.

Clopidogrel is the newest antiplatelet agent
and has a greater antiplatelet effect than ticlopi-
dine. Although the CAPRIE study observed a
significant reduction in the incidence of vascu-
lar events in favor of clopidogrel (75 mg daily), as
compared with aspirin (325 mg daily), it should
be borne in mind that the relative risk reduc-
tion was 8.7%, the absolute risk reduction only
0.5%, and subgroup analyses failed to show a
significant reduction in stroke risk relative to all
vascular events (CAPRIE Steering Committee,
1996). In the U.K., a course of clopidogrel is 30
times more expensive than aspirin.

In summary, aspirin remains the antiplatelet
agent of choice. The dose should be between 75
and 300 mg daily, and therapy should continue
throughout the perioperative period in patients
undergoing carotid endarterectomy Medically
treated patients who suffer repeated throm-
boembolic events while on aspirin should either
have dipyridamole (200 mg) added to the
aspirin regime or convert to clopidogrel (75 mg
daily). Clopidogrel is preferable to dipyridamole
alone in patients who are aspirin intolerant.
Surgeons, however, should be aware that clop-
idogrel trebles the bleeding time whereas a
combination of aspirin and full-dose clopido-
grel increases the bleeding time by a factor of
five as compared with aspirin alone.

Treatment of Hypertension

A systematic review of randomized trials com-
prising 48,000 hypertensive patients found that
a sustained reduction of 5mmHg in diastolic
blood pressure over a 3-year period was asso-
ciated with a 38% reduction in the risk of
late stroke (Collins and MacMahon, 1994). How-
ever, relatively few of these patients had a prior
history of stroke or TIA. More recently, the
Antithrombotic Trialists' Collaboration per-
formed a review of the randomized trial data
from 150,000 patients with cerebral or coronary
events, and found that for every 5 mm Hg reduc-
tion in the diastolic blood pressure, there was a
15% relative reduction in the risk of stroke.
Interestingly, there was no evidence of a lower
diastolic threshold below which the risk of
stroke did not fall.

There remains some controversy over the
threshold for therapeutic intervention in
patients with hypertension. In the U.S., the
recommendation is to maintain blood pressure
less than 140/90 mm Hg, whereas in the U.K.
the advice is for control to also reflect the age of
the patient. The exception might be the diabetic
patient with hypertension who warrants more
careful control of blood pressure (see below).
The one other golden rule is that patients
undergoing carotid endarterectomy should not
undergo surgery with uncontrolled hyperten-
sion, as this is associated with a twofold excess
risk of perioperative stroke.

Smoking

For obvious reasons, there have never been
any randomized trials comparing stroke risk
in patients who continue to smoke! A meta-
analysis of epidemiological and cohort studies
indicates that the relative risk of stroke is
doubled in smokers as opposed to nonsmokers.
The excess risk of stroke declines with time after
smoking cessation and is equivalent to that of
nonsmokers after about 5 years.

Diabetes

Diabetes is associated with a twofold excess
risk of stroke, and, intuitively, one would have
thought that careful glycemic control would be
associated with a significant reduction in stroke
risk. However, one of the few randomized trials
to address this issue showed that the risk of late
stroke appeared to be unchanged in patients
randomized to aggressive glycemic control. The
available evidence suggests that it is the hyper-
tensive type 2 diabetic who is most at risk of late
stroke. The U.K. Prospective Diabetes Study
Group randomized hypertensive, type 2 diabetic
patients to strict antihypertensive therapy
(mean blood pressure 144/82 mm Hg) or less
stringent control (mean blood pressure 154/
87mmHg). During follow-up, the former strat-
egy was associated with a 44% reduction in late
stroke.

Treatment of Atrial Fibrillation

About 20% of all strokes are secondary to non-
valvular atrial fibrillation (NVAF). Approxi-

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VASCULAR SURGERY

mately 5% of the population aged >65 years
have NVAF, incurring a 3% to 5% annual risk of
stroke. Treatment with warfarin reduces the risk
of stroke by 68% but decisions regarding the
role of anticoagulation must take into account
the potential hemorrhagic risks. The annual
risk of significant bleeding in anticoagulated
patients is 1.3%, including a 0.3% incidence of
intracranial hemorrhage. Patients at increased
risk of significant hemorrhage include those
with the following findings: a previous history
of bleeding, age >75 years, an international nor-
malized ratio (INR) >3.0, fluctuating INRs, and
uncontrolled hypertension.

Although each case must be considered
individually, it is generally recommended that
patients considered high risk for embolic
stroke be warfarinized with a target INR of
<3.0. High-risk patients (6% annual stroke risk)
include (1) those of any age with a past history
of TIA or stroke, rheumatic heart disease,
ischemic heart disease, and evidence of im-
paired left ventricular function on echocardio-
graphy; and (2) patients aged >75 years with
hypertension and/or diabetes. Low-risk patients
(1% annual stroke risk), including patients
aged <65 years with no risk factors, should be
treated with aspirin. The medium-risk group
(2% annual stroke risk) are more difficult to
categorize. It comprises (1) those aged <65 years
with a history of diabetes, hypertension, periph-
eral vascular disease, and ischemic heart dis-
ease who should be warfarinized; and (2) those
aged 65 to 75 with no risk factors in whom it
might be reasonable to treat with aspirin.
Aspirin therapy should be considered in all
patients with NVAF who are unable to take
warfarin.

Treatment of Hyperlipidemia

In a meta-analysis of the available epidemiolog-
ical studies (450,000 patients), no association
was observed between cholesterol level and
overall stroke rate. However, meaningful inter-
pretation of these data was confounded by the
fact that although a higher cholesterol level was
associated with an increased risk of ischemic
stroke, this was offset by an increased risk of
hemorrhagic stroke in patients with lower
cholesterol levels. A subsequent systematic re-
view of randomized trials indicated that statin

therapy was associated with a 25% reduction in
the risk of late stroke, but only in those patients
with coexistent symptomatic ischemic heart
disease. The principal problem regarding plan-
ning lipid lowering therapy based on evidence
is that most of the randomized trials have been
undertaken in patients with coronary heart
disease. Few have specifically examined the role
of statin therapy in patients with TIA or stroke,
although several should be reporting in the next
year or so.

In the U.K., there is conflicting advice regard-
ing statin therapy. The National Service Frame-
work for Coronary Heart Disease recommends
statin therapy (cholesterol to be reduced to
<5mmol/L) in all patients with coronary heart
disease or other occlusive disease (including
those with TIA or stroke irrespective of cardiac
status). In contrast, the National Clinical Guide-
lines for Stroke recommends therapeutic
intervention only in patients with symptomatic
cerebrovascular disease and coronary heart
disease. This conflicting advice will almost cer-
tainly be revised following the recent publica-
tion of the British Heart Protection Study. This
trial randomized 20,000 patients with vasc-
ular disease (including stroke/TIA) to placebo
or simvastatin (40 mg daily). Overall, statin
therapy conferred a 12% reduction in all mor-
tality, a 17% reduction in vascular mortality, a
24% reduction in all coronary events, and a 27%
reduction in stroke. Of most importance was the
observation that there did not appear to be any
lower cholesterol limit below which benefit was
not observed.

In the U.S., statin therapy is advised in all
patients with TIA/stroke and coronary heart
disease. In patients with no coronary heart dis-
ease and fewer than two vascular risk factors
(selected from men aged >45 years, women aged
>55 years, family history of heart disease,
smoking, hypertension, diabetes, high-density
lipoprotein (HDL) cholesterol <35mg/dL), the
advice is to try dietary modification for 6
months and to introduce statin therapy only if
the low-density lipoprotein (LDL) cholesterol
is >190mg/dL with a target of <160mg/dL. The
TIA/stroke patients with no history of coronary
heart disease (but having more than two risk
factors) should undergo dietary modification
for 6 months followed by statin therapy if the
LDL cholesterol is >160mg/dL with a target of
reducing it to <130mg/dL.

169

CAROTID ARTERY DISEASE

Surgery for Occlusive disease

Carotid endarterectomy (CEA) is one of the few
surgical procedures to have been subjected to
evidence-based scrutiny with large, multicenter
randomized trials. An overview of the principal
results from the European Carotid Surgery Trial
(ECST), the NASCET, and the Asymptomatic
Carotid Atherosclerosis Study (ACAS) is pre-
sented below. One other carotid surgical pro-
cedure (extracranial-intracranial bypass) has
been intermittently advocated for recurrent
TIAs/stroke in the presence of a chronically
occluded ICA. This procedure was popularized
during the 1980s, but a randomized trial there-
after showed no level I evidence of benefit. The
methodology of this study has been challenged
but few surgeons currently advocate this form of
surgery.

Overview of ECST and NASCET

In ECST and NASCET almost 6000 patients
in over 200 centers around the world were
randomized, comparing "best medical therapy"
against "best medical therapy" and CEA. All
patients had to have reported ipsilateral carotid
territory symptoms within the preceding 6
months; all were seen by a neurologist prior
to randomization and all underwent CT scan-

ning and contrast angiography. Follow-up was
coordinated by the neurologists and stroke
physicians.

The basic results are summarized in Table
15.1. Both trials showed that CEA conferred
significant benefit in symptomatic patients with
a 70% to 99% stenosis. The ECST found no evi-
dence of benefit in patients with lesser degrees
of disease. The NASCET observed a small but
significant benefit in patients with 50% to 69%
stenoses. The reason for these apparent discrep-
ancies lies in the method for calculating degree
of stenosis. The ECST compared the residual
luminal diameter against the diameter of the
carotid artery at the level of the stenosis (usually
the carotid bulb). The NASCET compared the
residual luminal diameter against the diameter
of the ICA at least 1 cm above the stenosis.
As a consequence, the ECST tends to systemati-
cally overestimate stenoses (as compared with
the NASCET method), particularly in those
with mild/moderate disease. In reality, a 50%
NASCET stenosis is approximately equivalent to
a 65% ECST, whereas a 70% NASCET stenosis
equates to an 82% ECST.

The ECST and NASCET have identified
predictive factors that are associated with a
significantly higher risk of late stroke in
medically treated patients. These include male
sex, 90% to 94% stenosis, surface irregularity/
ulceration, coexistent syphon or intracranial

Table 1 5.1 . Long-term risk of ipsilateral stroke (including perioperative stroke or death)

Trial stenosis

Surgical risk

Medical risk

ARR

RRR

NNT

Strokes prevented

(%)

per 1000 CE As

ECST

<30%

9.8 at 5 y

3.9at5y

-5.9

n/a

30-49%

10.2 at 5y

8.2 at 5 y

-2.0

n/a

50-69%

15.0 at 5y

12.1 at 5y

-2.9

n/a

70-99%

10.5 at 5y

19.0 at 5y

+8.5

83at5y

NASCET

30-49%

14.9 at 5y

18.7 at 5y

+3.8

38at5y

50-69%

15.7 at 3y

22.2 at 3y

+6.5

67at3y

70-99%

8.9 at 3 y

28.3 at 3y

+19.4

200 at 3 y

ACAS

60-99%

5.1 at 5y

11.0 at5y

+5.9

59at5y

ACST

60-99%

6.4 at 5 y

11.8 at5y

+5.4

53at5y

ARR, absolute risk reduction; RRR, relative risk reduction; NNT, number of CEAs to prevent one ipsilateral stroke at specified time interval; n/a =
not applicable;/, years.

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VASCULAR SURGERY

disease, no recruitment of intracranial collat-
erals, hemispheric symptoms, cerebral events
within 2 months, multiple cerebral events, con-
tralateral occlusion, multiple concurrent risk
factors, and age >75 years. In contrast, a lower
relative risk of stroke is observed in patients
with lesser degrees of disease [70% to 79%
stenosis (ECST), 50% to 69% (NASCET)], near
occlusion with a string sign, smooth stenoses,
female sex, retinal symptoms, and those pre-
senting with lacunar stroke.

A pooled analysis of data from the ECST,
NASCET, and the Veterans Affairs (VA) trial
has recently been performed (Rothwell et al.,
2003). All the angiograms were standardized to
the NASCET method, and the overall database
contained >6000 randomized patients. Table
15.2 summarizes the 30-day death/ any stroke
rates following endarterectomy for each of the
principal trials. Overall, 7.1% of patients [95%
confidence interval (CI) 6.3-8.1] in the three
trials either died or suffered a stroke within 30
days of surgery. This is an important observa-
tion, as the track record for all participating
surgeons was vetted before they were allowed to
randomize patients.

Figure 15.6 illustrates how the benefit of CEA
increases with time and with increasing degrees
of stenosis. By contrast, CEA was harmful in
patients with <50% stenoses. It conferred a
small but significant benefit in symptomatic
patients with 50% to 69% stenoses, with the
maximal benefit being observed in patients
with 70% to 99% stenoses. Note, however, that
patients with near-occlusion did not derive any

systematic benefit from CEA. Near-occlusion
was defined angiographically as severe stenosis
with evidence of reduced flow in the distal ICA
(delayed arrival of contrast in the distal ICA or
recruitment of collateral flow toward the symp-
tomatic hemisphere, or both) and evidence of
narrowing of the poststenotic ICA (lumen
diameter similar to, or less than, that of the
ipsilateral external carotid artery and less than
that of the contralateral ICA). Accordingly,
there is increasing evidence that patients with
subocclusion and distal vessel collapse should
be treated conservatively.

Overview of ACAS and ACST

A number of randomized studies have evalu-
ated the role of CEA in patients with severe
asymptomatic carotid artery disease (MACE,
CASANOVA, VA study), but ACAS and ACST are
generally accepted to be the best (ACST, Lancet
2004). The ACAS randomized 1600 patients with
asymptomatic 60% to 99% stenoses. Table 15.1
summarizes the principal findings. Although
there was a 53% RRR in late stroke, this only
equated to a 5.9% actual risk reduction at 5
years. Clinicians in North America and main-
land Europe have embraced the findings of
ACAS more liberally than their U.K. or Scandi-
navian colleagues. In the latter countries, con-
cerns remain that the ACAS showed no benefit
in women, there was no reduction in disabling
stroke, and (unlike ECST and NASCET) no rela-
tionship between increasing stenosis and stroke

Table 15.2. Analysis of pooled data from the ECST, NASCET, and the Veterans Affairs trial: 30-day risk of death and/or stroke after
carotid endarterectomy

Trial

<50%

50-69%

>70%

Near occlusion

ECST

73/1044
7.0% (5.4-8.6)

37/371

10.0% (6.9-13.1)

17/249

6.8% (4.0-10.8)

3/78

3.8% (0.8-10.8)

NASCET

43/663

6.5% (4.7-8.6)

30/421
7.1% (4.8-10)

14/261

5.4% (3.0-8.8)

5/70

7.1% (2.4-15)

VA309

2/20

10.0% (1.2-3.2)

5/71

7.0% (2.3-15.7)

Combined

116/1707
6.8% (5.6-8.0)

69/812

8.5% (6.6-10.5)

36/581

6.2% (4.4-8.5)

8/148

5.4% (2.4-10.4)

Note: The data shown are the observed percents.The 95% confidence interval is shown in parentheses.

Source: Adapted from Rothwell et al. (2003). Here the individual data from each trial were reanalyzed and combined after having standardized

all the angiograms to the NASCET method of stenosis measurement.

171

CAROTID ARTERY DISEASE

45 1

40
35
30
25
20
15
10

-5

] ARRat3
] ARRat5

ARR at 8

<30% 30-49% 50-59% 60-69% 70-79% 80-89% 90-99% near occ
degree of stenosis

Figure 15.6. Pooled results from European Carotid Surgery Trial (ECST),the North American Symptomatic Carotid Endarterectomy
Trial (NASCET), and Veterans Affairs (VA) studies, showing the absolute risk reduction (ARR) in stroke at 3, 5, and 8 years relative to
the degree of stenosis at randomization. Note that the maximal benefit was observed in patients with 90% to 99% stenoses, whereas
patients with near occlusion and distal vessel collapse or underfilling (string sign) did not benefit from CEA. (From Rothwell et al.,
2003.)

risk (in fact there was an inverse relationship).
Table 15.1 also summarizes the principal results
from the ACST. Note that the results were very
similar to those of the ACAS. However, the key
finding from ACST was a 50% reduction in fatal
or disabling stroke long term.

Carotid Endarterectomy

Operative Principles

The carotid bifurcation is usually approached
via a longitudinal incision based on the anterior
border of sternomastoid. The upper aspect of
the incision angles posteriorly to minimize
trauma to the greater auricular nerve. Any
superficial veins are ligated and divided. Dissec-
tion continues medial to the sternomastoid to
reveal the common facial vein. This large tribu-
tary of the internal jugular vein often overlies
the carotid bifurcation and is a useful landmark.
The common facial vein is divided. Round-
toothed West retractors open up the space
between the perilaryngeal structures and the
jugular vein. Dissection continues medial to the
jugular vein and the common carotid artery
(CCA). Careful dissection is then continued
superiorly. The external carotid artery (ECA)

can be identified by locating its first branch (the
superior thyroid artery). Occasionally the bifur-
cation is rotated. The surgeon should remember
to mobilize the ECA branches toward the first
assistant.

There are a number of strategies for mobiliz-
ing the bifurcation and distal ICA. Care should
be taken to avoid excessive mobilization of the
bifurcation, as this leads to functional elonga-
tion and distal ICA kinking (predisposing
toward postoperative thrombosis) and an in-
creased risk of procedural embolization. Most
surgeons prefer to mobilize a discrete segment
of ICA well above the bifurcation so as to min-
imize the risks of dislodging an embolus into
the cerebral circulation. The patient is systemi-
cally heparinized and the carotid arteries cross-
clamped. If the surgeon chooses to shunt the
patient, the shunt is inserted now. The plaque is
endarterectomized, tacking sutures inserted if
required, and the ECA origin cleared of plaque
using the eversion technique. The arteriotomy
is closed either primarily or by a patch (vein/
prosthetic). Flow is restored first up the ECA,
then the ICA. Having achieved hemostasis, the
wound is closed with absorbable suture to re-
constitute platysma (usually over a deep suction
drain). Nonabsorbable suture or clips are used
to close the skin.

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VASCULAR SURGERY

Points for Debate

Despite being a relatively straightforward oper-
ation in concept, few operations arouse so much
debate regarding content. A summary of the
principal debating points follows, which high-
lights those of most practical concern.

Stop Antiplatelet Therapy or Not?

There is no evidence that aspirin should be
withdrawn during the perioperative period. An
emerging problem, however, is the effect of the
ADP inhibitor clopidogrel on surgical hemosta-
sis, particularly if the patient is receiving com-
bination antiplatelet therapy. Many surgeons
have anecdotally observed that suture line
bleeding is significantly increased in patients
receiving chronic clopidogrel therapy. In the
Leicester Royal Infirmary, clopidogrel therapy
is stopped 1 week preoperatively and aspirin is
restarted.

Locoregional or General Anesthesia?

The rationale for the use of locoregional anes-
thesia is that the surgeon is immediately aware
of any neurological deficit during the proce-
dure. Accordingly, steps can be taken to treat
this deficit. Advocates of general anesthesia
cite ease of operation, no patient movement,
and lower cerebral metabolic requirements to
counter this deficit. There is no evidence that
either anesthetic technique reduces operative
morbidity or mortality. However, meta-analyses
of nonrandomized trials suggest that locore-
gional anesthesia may be associated with
lower perioperative cardiovascular morbidity.
A further large randomized trial (GALA) is
currently underway in the U.K.

Preincision Infiltration with Local Anesthesia
and Adrenaline?

No randomized trial data are available. The
rationale is to minimize troublesome skin edge
bleeding at the beginning of the procedure.
Advocates need to be aware that subcutaneous
and cutaneous bleeding may occur in the early
postoperative period as the adrenaline effect
wears off.

Longitudinal or Transverse Incision?

No randomized trial data are available. Trans-
verse wounds probably confer a better cosmetic
result, but may be associated with problems
relating to access to the distal ICA. Longitudinal
incisions inevitably divide more cutaneous
nerves, leading to a larger area of anesthesia
under the chin. The latter, however, is the
approach of choice if there is any question of
high carotid disease, especially in male patients
with short fat necks!

Anticipating Distal Disease?

Preoperative preparation is mandatory. Nasola-
ryngeal intubation opens the space between the
ramus of the mandible and the mastoid pro cess.
Nasolaryngeal intubation should probably not
be undertaken in all patients, as there is a not
insignificant risk of retronasal bleeding, which
can predispose to vomiting (and aspiration) in
the early postoperative period. If the surgeon
feels that temporomandibular subluxation may
be necessary (preferable to dislocation), this
must be anticipated in advance and maxillofa-
cial specialists must be involved. This procedure
cannot readily be undertaken once the proce-
dure has started. In the Leicester Royal
Infirmary, >1200 CEAs have been performed
over the last decade without recourse to tem-
poromandibular subluxation. Surgeons unfa-
miliar with dissecting in the upper reaches of
the neck should involve more experienced col-
leagues. High carotid dissections are associated
with an increased risk of operative stroke,
bleeding, and cranial nerve injury.

When Should I Clamp the Internal Carotid
Artery Early?

Transcranial Doppler (TCD) allows the surgeon
to be promptly aware of particulate emboliza-
tion during the dissection phase of the opera-
tion. One or two emboli warn of the likelihood
of an unstable plaque. The dissection technique
is then made even more meticulous, and early
clamping is not usually necessary, provided no
attempt is made to injudiciously dissect around
the bifurcation. Continued embolization (des-
pite modification in operative technique) is a
worrisome phenomenon and merits consid-
eration of early distal ICA clamping. There is

173

CAROTID ARTERY DISEASE

usually more than enough time to complete the
dissection safely and insert a shunt as necessary.

Blocking the Sinus Nerve?

There is no randomized trial evidence that
routine blockade of the sinus nerve with ligno-
caine significantly influences postoperative
cardiovascular morbidity. The rationale is that
sinus blockade minimizes intraoperative hypo-
tension. However, this must be offset against
the potential for postoperative reinnervation
hypertension. In practice, once the ICA has
been clamped, intraoperative hypotension is not
usually a problem.

Should I Ever Abandon a Procedure at
This Stage?

There are few situations warranting abandon-
ment of the operation at this stage. The com-
monest reason is cardiovascular instability
(e.g., electrocardiogram evidence of myocardial
ischemia not controlled with simple therapy,
unstable arrhythmia). Other reasons reflect an
unanticipated change in the risk/benefit ratios
for the patient, that is, the benefits quoted to the
patient preoperatively are now being exceeded
by the potential risks as the procedure becomes
ever more complex. Scenarios might include a
hypoplastic carotid artery extending to the skull
base (this can be evaluated by on-table angiog-
raphy). Controversy then relates to whether the
ICA should be tied off or left alone. Most would
probably leave it alone and start the patient
on warfarin postoperatively. Other examples
include unexpected high disease extension in a
patient with a unilateral asymptomatic stenosis.
As the annual risk of stroke was only about
2% in the AC AS and ACST trials (where high
disease was specifically excluded), it may now be
considered best to abandon the procedure, as
the operative risks will be in excess of what was
quoted preoperatively.

What Dose of Heparin?

Most centers administer 5000 units of intra-
venous heparin before clamping. There is no
evidence that heparin doses tailored to patient
weight influences the balance between anti-
thrombotic and hemorrhagic risk.

Should I Shunt?

This is an ever-enduring controversy. There is
no evidence that a policy of routine shunting,
selective shunting, or never shunting actually
alters the operative risk, largely because the
trials were small and poorly designed. Most sur-
geons are either routine or selective shunters,
with the choice being most likely to reflect the
strategy of their trainer!

What Choice of Shunt?

The most commonly used shunts are the Javid
(less flexible, tapered, requiring external retain-
ing clamps) and the Pruitt-Inahara (softer,
more flexible, smaller caliber, intraluminal
retaining balloons). Alternatives include the
Brener in-line shunt. No large randomized trials
have compared the effect of shunt type on clin-
ical outcome. Evidence suggests that 90% of
patients have flow rates within 10% of preclamp
levels using the Pruitt shunt. High carotid dis-
sections probably benefit from using the Pruitt
shunt, as the Javid requires a further centimeter
or so of distal dissection to position the retain-
ing clamp. This can sometimes be quite difficult
to achieve in the upper reaches of the neck.

Proximal or Distal End of the Shunt in First?

No randomized trial has addressed this issue.
Most surgeons insert the proximal (CCA) limb
first and flush the shunt to clear debris prior to
distal insertion. Allowing the distal ICA to back-
vent before carefully inserting the shunt can
also reduce distal embolism. No force should
ever be applied during shunt insertion. Resis-
tance should encourage the surgeon to dissect
the carotid artery more distally to exclude an
impacting coil.

How Do I Know If the Shunt Is Working?

About 3% of shunts malfunction, usually
because of impaction of the distal limb against
the ICA wall or carotid coil. Unless some form
of monitoring is used, this will go unnoticed.
Simple techniques include awake testing or
TCD. For those without any access to monitor-
ing, the surgeon using the Pruitt shunt can
temporarily clamp the CCA inflow and assess
backflow from the circle of Willis (i.e., is the

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VASCULAR SURGERY

distal channel patent or not) by opening the red
tap on the T limb.

The Shunt Is Working But I Am Still Worried
About Perfusion

Advocates of TCD recommend trying to main-
tain mean middle cerebral artery blood flow
velocity of >15cm per second. This threshold
broadly corresponds to that equivalent to the
level of brain perfusion usually associated with
loss of cerebral electrical activity. Note that this
threshold does not equate to loss of neuronal
function. If flow rates are considered inade-
quate, check that the shunt limbs are neither
impacted nor kinked. If there is no mechanical
problem, the anesthetist can then carefully
elevate the patient's blood pressure pharmaco-
logically, which usually raises the intracranial
blood flow to acceptable levels.

Traditional or Eversion Endarterectomy?

Traditional endarterectomy involves the
removal of the plaque through a longitudinal
arteriotomy extending from the CCA into the
ICA. The plaque is usually transected proxi-
mally and removed with cephalad dissection
using a Watson-Cheyne dissector. The distal
end is feathered or transected. Eversion endar-
terectomy involves transecting the ICA from
the bifurcation. Everting the enclosing media/
adventitia then expels a tube of plaque. The CCA
is endarterectomized and the ICA reimplanted
onto the bifurcation. Potential advantages of
eversion endarterectomy include no need for
patching and the ability to shorten an elongated
ICA. However, neither technique is superior to
the other.

Patch or Not?

This is another of the single-issue subjects that
have characterized carotid surgery. Options
include routine patching, selective patching,
and never patching. No randomized trials have
compared selective with routine patching. How-
ever, a meta-analysis of the six randomized
trials comparing routine patching with routine
primary closure showed that patching conferred
a three- to fourfold reduction in (1) periopera-
tive thrombosis, (2) perioperative stroke, (3) late
stroke, and (4) and late restenosis (Counsell
et al., 1997). Accordingly, there is little evidence
to support continuance with a policy of routine
never patching.

Choice of Patch?

A meta-analysis by the Cochrane collaboration
has shown that patch type does not influence
outcome. There is, however, a perception that
prosthetic patches are probably more thrombo-
genic than vein. A recently published random-
ized trial addressed this issue and observed
no difference in the rates of embolization in
the early postoperative period. In reality, pa-
tient factors seem more likely to mediate
an increased risk of thrombosis than does the
patch type. The Achilles heel of prosthetic
patching is infection, which complicates approx-
imately 1% of procedures. About half become
apparent in the first few months of surgery, the
commonest organisms being staphylococci and
streptococci. Evidence suggests that removal of
the prosthetic material with autologous recon-
struction is associated with the lowest risk of
stroke and late reinfection. Secondary recon-
struction with prosthetic material should be
avoided.

Tack the Intimal Step or Not?

No randomized trial data are available, and atti-
tudes usually reflect the policy of the trainer.
The NASCET observed that tacking sutures
were associated with a higher perioperative risk.
This nonrandomized comparison, however, may
simply reflect the fact that tacking sutures were
more likely to be inserted when the surgeon
encountered a more complex case (e.g., difficult
to achieve a clean, tapering distal end-point in a
thin walled vessel).

Should Vein Be Harvested from Ankle
or Groin?

Vein patches are susceptible to rupture. This
characteristically occurs on the 5th to 7th post-
operative day and is more common in females
and in hypertensives where the vein has been
harvested from the ankle. Current advice, there-
fore, is to use groin saphenous vein for patching
because of its intrinsically stronger structure.
Only about 15% of patients need their saphe-

175

CAROTID ARTERY DISEASE

nous vein for alternative cardiovascular recon-
structions in the next 5 years.

Carotid Bypass?

Carotid bypasses should not be performed rou-
tinely but are indicated if the endarterectomy
zone is too thin after plaque removal, if there
is extensive atheroma and concomitant kink-
ing, or if there is any question of infection. In
common with infrainguinal venous recon-
structions, about 20% of carotid bypasses using
saphenous vein develop a recurrent stenosis
within 24 months. This is significantly higher
than that observed with traditional endarterec-
tomy and patching. Accordingly, bypass patients
require serial duplex surveillance.

Shorten the Carotid or Not?

Following endarterectomy, particularly if there
is a slightly redundant distal ICA, there is a
tendency to observe functional elongation of
the endarterectomy zone. Uncorrected, this may
predispose to perioperative thrombosis. Short-
ening the endarterectomy zone may reduce this.
Options include transection and reanastomosis
(may be difficult in thin-walled, narrow-caliber
vessels in female patients) or eversion plication.
In the latter, stay sutures incorporating the
redundancy on either side of the artery are tied,
causing the excess arterial wall to be everted.
The eversion is then closed with a continuous
6:0 Prolene suture.

Monitor or Not?

There is considerable skepticism as to whether
monitoring reduces stroke risk after CEA.
Options include electroencephalogram (EEG),
somatosensory sensory evoked potentials
(SSEPs), TCD, near-infrared spectroscopy,
jugular venous oxygen saturation, awake test-
ing under locoregional anesthesia, xenon blood
flow measurement, subjective assessment of
backflow, and stump pressure. In practice, the
most commonly used techniques are awake
testing, TCD, and EEG. To date, no randomized
trial has been performed to address this issue.
However, for any form of monitoring to work,
the right questions must be asked. Electroen-
cephalography and SSEP only tell the surgeon
that perfusion has dropped below the threshold
for maintaining electrical function. Awake

testing identifies any neurological deficit
(indicative of perfusion having fallen below the
threshold for neuronal viability), but it requires
additional strategies (e.g., some sort of quality
control) to identify what was actually causing
the underlying problem. It has been the experi-
ence at the Leicester Royal Infirmary that com-
bining a monitoring method (TCD) with quality
control assessment (angioscopy) has been asso-
ciated with a 60% reduction in the operative risk
over the last 10 years.

Quality Control or Not?

Quality control assessment is a slightly different
concept from monitoring. Its use is based on
the observation that the majority of operative
strokes follow inadvertent technical error.
Accordingly, detection of technical error should
(in theory) reduce the risk. Once again, no
randomized trials have evaluated completion
angioscopy, angiography, or duplex ultrasound.
Advocates of monitoring and quality control
assessment have reported significant benefits.
However, such a policy is helpful only if the
choice of technique addresses the appropriate
question. Awake testing does not prevent
embolization during carotid dissection. Awake
testing remains the only "gold standard" for
determining who benefits from selective
shunting, but does not prevent a stroke due
to embolization of luminal thrombus follow-
ing restoration of flow unless something like
angioscopy is employed.

Drain or Not?

Surprisingly, no randomized trial has addressed
this issue. However, most surgeons insert a
suction drain into the neck wound for 12 to 24
hours on the basis that it probably does no
harm. There is certainly no evidence that drains
increase the risk of prosthetic patch infection.

Early Postoperative
Management

Establishing the Neurological Status

Following surgery, the patient must be carefully
monitored for three clinical variables: neurolog-
ical status, wound stability, and blood pressure.

176

VASCULAR SURGERY

If general anesthesia has been used during the
operation, the patient should be closely ob-
served to ensure that cerebral function remains
intact upon awakening. The initial assessment
should include the patient's response to simple
verbal commands and extremity movement.
Once the patient becomes fully alert in the
recovery room, a more detailed assessment
including the vagus and hypoglossal nerve
function can be performed.

that regular review is required as (quite often)
the hypertension is a transient phenomenon
and may require therapy only for 4 to 6 hours.
Sustained postoperative hypertension at 3 to 5
days requires assessment by a cardiovascular
physician. Caution should be exercised in dis-
charging patients before blood pressure is
adequately controlled, as these patients are
probably at higher risk of suffering seizures in
the early postoperative period.

Neck Hematoma

The neck incision should be regularly moni-
tored for swelling. This is usually a result of
hematoma formation, although surprising
amounts of tissue edema can accumulate within
hours of the procedure. Despite achieving com-
plete hemostasis and placing a closed suction
drain in the wound, delayed bleeding result-
ing in hematoma and airway compromise can
occur. Once an expanding hematoma is recog-
nized, the patient should be returned to the
operating room promptly to evacuate the
hematoma and identify the potential bleeding
source. If the patient develops respiratory dis-
tress, the neck incision should be opened at the
bedside to decompress the hematoma followed
by orotracheal intubation to establish an airway
if needed. Alternatively, it is useful to have infil-
trated the neck incision with local anesthetic
agent prior to finishing the procedure. Should
a significant neck hematoma occur, it can be
released without having to reintubate the
patient.

Hypertension and Hypotension

Significant, sustained hypotension is not usually
a problem following endarterectomy and tends
to respond well to colloid replacement. Early
postoperative hypertension is more common
and requires careful monitoring and control.
As a rule, most anesthetists prefer to maintain
blood pressure within 10% of preoperative
levels. There is anecdotal evidence from reports
documenting outcome for carotid surgery
under locoregional anesthesia that postopera-
tive hypertension is less of a problem. Most
cases of early postoperative hypertension
respond to a single bolus or carefully titrated
infusion of beta-blocker (e.g. labetalol). Note

The Patient Suffers a
Neurological Deficit

Intraoperative

An intraoperative stroke is defined as having
occurred if a neurological deficit becomes
apparent as the patient recovers from anesthe-
sia. Usually the first sign is a prolonged delay in
awakening. In the absence of any monitoring
modality, it should be assumed that the patient
has suffered either a carotid thrombosis or
embolization into the cerebral arteries, and
the patient should be reexplored. The aim of
reexploration is to recognize and treat throm-
bosis before an irreversible neurological deficit
occurs. Delay beyond 1 hour is associated with
a progressively worsened outcome. The second
reason is to identify and correct a source of
technical error responsible for platelet accumu-
lation and secondary embolization.

Neurological Deficit Within the First 24 Hours

Focal neurological deficits occurring within the
first 24 hours are still usually thromboembolic.
In the absence of any monitoring techniques, it
is again probably best to return the patient
immediately to the operating room. Intracranial
hemorrhage is extremely rare within the first 24
hours, and a CT scan is probably unnecessary
unless it is done immediately on the way to the
operating room.

In the Leicester Royal Infirmary, we have pre-
viously observed that the majority of early post-
operative neurological deficits were secondary
to carotid thrombosis. Subsequent research
showed that patients at risk of progressing to
thrombosis had a 1- to 2-hour period of increas-
ing embolization on transcranial Doppler
before any neurological deficit became appar-

177

CAROTID ARTERY DISEASE

ent.This association has now been corroborated
in many centers around the world. This phase
of sustained embolization can be arrested by
intravenous infusion of Dextran 40 in saline,
the dose of which has to be increased in 30%
of patients in order to control embolization.
No case of stroke due to early postoperative
thrombotic occlusion has been encountered fol-
lowing 1000 CEAs in the Leicester Unit since
the protocol of 3 hours of TCD monitoring
with selective Dextran therapy was instituted in
1995.

The algorithm in Figure 15.7 summarizes the
current strategy in the Leicester Royal Infirmary
for managing a neurological deficit in the first
24 hours after a successful recovery from anes-
thesia. Patients with hemiplegia/hemiparesis
are more likely to have suffered a major vessel
occlusion and are probably more likely to bene-
fit from reexploration. Patients with a mono-
paresis or isolated dysphasia are highly unlikely
to have suffered major vessel occlusion, and
there is time for more discriminating inves-
tigation and treatment. The aim is to avoid
unnecessary reexploration in patients with a

normal endarterectomy zones and in those who
have suffered embolic occlusion of the middle
cerebral artery mainstem. Note that transcranial
Doppler is used to detect any evidence of
ongoing embolization and can be invaluable in
guiding decisions regarding reexploration.

Neurological Deficit After 24 Hours

Strokes occurring after 24 hours have elapsed
have a greater number of potential underlying
causes. In addition to thromboembolism, the
clinician must now consider the likelihood of
hyperperfusion and intracranial hemorrhage.
Figure 15.8 summarizes the current Leicester
protocol in this situation. The key difference
from the strategy for managing strokes within
the first 24 hours is the importance of perform-
ing an emergency CT scan. Intracranial hemor-
rhage complicates 1% of CEAs and carries a
very poor outcome, with up to 80% of patients
dying or suffering a major disabling stroke.
There is currently very little that can be done
to treat these patients, although vascular sur-
geons may like to ask their neurosurgical

neurological deficit within 24 hours

hemiplegia

TCD and Duplex assessment

I L_

ICA
occ

ongoing
emboli

No MCA
emboli

no improvement
in 30 minutes

deficit
improves

emergency
exploration

Dextran
therapy

monoparesis

MCA main
stem occln

MCA
normal

Conservative management

exclude cardiac sources

CT scan at 3-5 days

Figure 1 5.7. Algorithm for the investigation and management of patients at the Leicester Royal Infirmary who have suffered a neu-
rological deficit within the first 24 hours of CEA, having made a normal recovery from anesthesia. CT, computed tomography; ICA,
internal carotid artery; MCA, middle cerebral artery; TCD, transcranial Doppler.

178

VASCULAR SURGERY

neu.

] eficit after 24 hours

TCD + Duplex + CT scan

no hemorrhage present

emergency
reexploration

intracranial hemorrhage

hyperperfusion

high MCAV

hypertension

seizures

+ /- CT edema

Figure 1 5.8. Algorithm for the
investigation and management
of patients at Leicester who
have suffered a neurological
deficit after 24 hours or more
have elapsed after carotid
endarterectomy (CEA).

conservative Mx
blood pressure control
anticonvulsants

colleagues whether they might ever consider
clot evacuation.

Stroke due to hyperperfusion syndrome is
another poorly understood entity, and there is
considerable controversy as to whether it would
be better renamed the "reperfusion" syndrome.
More recently, there has been renewed debate as
to how much the condition is associated with
high flow as opposed to hypertensive encepha-
lopathy or dysautoregulation. Patients at risk of
hyperperfusion-related stroke tend to have a
history of severe bilateral disease and treated
hypertension. Stroke is often preceded by
seizure and severe hypertension. The main-
stay of management is control of seizures and
careful reduction of blood pressure. Early CT
scans often show changes consistent with an
evolving ischemic infarction, but in fact this is
often white matter edema. Paradoxically, a lot of
the white matter edema is present in the verte-
brobasilar territory.

Late Postoperative Management

There is a surprisingly good transatlantic con-
sensus regarding many of the principal issues
relating to carotid surgery. Two, however, serial
noninvasive surveillance and reintervention for
recurrent stenoses, have aroused considerable
debate.

Serial Surveillance and Recurrent Stenoses

In North America and in many centers in main-
land Europe, follow-up carotid duplex scan-
ning is considered mandatory. The underlying
rationale is to monitor for recurrent lesions, as
well as for progressive disease of the contralat-
eral carotid artery. Patients are recommended
to return for an initial follow-up visit approxi-
mately 1 month following the operation to
ensure that adequate wound healing has taken
place. A carotid duplex scan is performed at that
time to evaluate the carotid reconstruction and
to provide a new baseline for future study com-
parison. This is followed by a subsequent clinic
visit at 6 months, at which time a repeat carotid
duplex scan is performed. If the duplex scan
shows satisfactory results of both carotid arter-
ies, the patient may be seen 1 year following
the operation. A bilateral carotid duplex scan
should be performed at that visit and at all
future annual examinations.

In the U.K., parts of northern mainland
Europe, and Scandinavia, the policy is com-
pletely different. Here patients are reviewed at
4 to 6 weeks, and unless they are part of an
ongoing research program, they are discharged
with instructions to return if any new symp-
toms recur. The rationale underlying this
approach is based on the following observa-
tions. First, the annual risk of stroke after sue-

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CAROTID ARTERY DISEASE

cessful endarterectomy is only about 1% to
2% in the operated hemisphere and 2% in the
contralateral hemisphere. Second, it has been
difficult to determine the actual risk of ipsilat-
eral stroke in patients with a recurrent stenosis,
largely because many of the patients have
already been subjected to a prophylactic redo
CEA. However, in Frerick's recent overview, 10
published series documented the risk of stroke
according to whether the patient had a recur-
rent stenosis or not. Having corrected for the
effects of different lengths of follow-up and
study size, a reanalysis of the data suggests that
the incidence of ipsilateral stroke in patients
with a recurrent stenosis (>50%) is approxi-
mately 5.5% at 3 years (i.e., only about 2% per
annum). For those with no evidence of a re-
current stenosis, the risk of ipsilateral stroke
was 3.3% over 3 years (i.e. only about 1% per
annum). These figures correlate closely with the
follow-up data reported in the international
trials. Third, acute changes in plaque morphol-
ogy tend to precede onset of symptoms rather
than a progressive worsening of stenosis. In
short, if one reviews the results of the last sur-
veillance scan before onset of neurological
symptoms, it rarely enables reliable prediction
of patients at risk of subsequent stroke.

Carotid Angioplasty

Angioplasty is an accepted component of
vascular practice apart from the cerebral cir-
culation. The reason for this discrepancy is
the potential for procedural embolization and
stroke. The first carotid angioplasty was per-
formed in 1980. By 1992, the first overview of
balloon angioplasty in the carotid artery was
published. In a pooled series of 123 patients
from 10 studies, the procedural mortality rate
was 0%, the disabling stroke rate 0%, and the
30-day death and any stroke rate was 0.8%.
This study was thereafter a catalyst for the
increasing interest in the potential for angio-
plasty to replace endarterectomy as the gold
standard treatment for occlusive carotid artery
disease.

However, despite the excellent results from
these pioneers of angioplasty (particularly as
they appeared safer than diagnostic angio-
graphy alone), concerns thereafter were voiced

that balloon angioplasty alone was probably
not safe. This observation was based on con-
cerns that vessel recoil, intimal dissection,
plaque dislodgment, and particulate emboli-
zation were now major potential problems,
despite not having been evident in the original
overview. It was proposed that the insertion
of a stent would avoid the above problems
as well as reduce the rate of re-stenosis. A
subsequent overview of outcomes following
primary stenting revealed a 4.3% death/stroke
rate at 30 days in 2569 patients with either
symptomatic or asymptomatic patients and a
re-stenosis rate of <5%. Interestingly, there is
now a third-generation view that these results
can be improved even further with the use of
cerebral protection devices. These devices
(distal balloon, distal aspiration, distal filters
and umbrellas, and retrograde flow during
balloon insufflation) are currently under devel-
opment or clinical evaluation.

To date, the results from voluntary stent reg-
istries and single centers around the world have
clearly demonstrated that angioplasty is feasible
and accepted by patients. It remains to be seen
when and where it should replace endarterec-
tomy. The situation regarding carotid angio-
plasty, therefore, is analogous to that faced by
the cardiac surgeons in the 1980s when coro-
nary angioplasty was first introduced. Ulti-
mately, the answer will have to be determined
by level I randomized trials, and it is inevitable
that angioplasty will have a role in the manage-
ment of selected patients with cerebral vascular
disease. Evidence suggests that the worst
procedural outcomes are to be encountered in
older patients, symptomatic patients, those with
lesions longer than 10mm, and those with more
severe degrees of stenosis.

An overview of the published literature in
2000 indicated that the results of angioplasty
were generally poorer than surgery in trials
reporting outcomes in symptomatic patients
who should, otherwise, form the mainstay of
current treatment (Golledge et al., 2000). Angio-
plasty cannot simply be justified because it is
effective in predominantly asymptomatic popu-
lations. Using the results of ACAS as a guide,
only 58 ipsilateral strokes would be prevented
per 1000 angioplasties on asymptomatic pa-
tients with 60% to 99% stenoses.

Five randomized trials have now compared
CEA and angioplasty in the treatment of symp-

180

VASCULAR SURGERY

tomatic patients with carotid artery disease.
Four have been published in peer-reviewed
journals, whereas the SAPPHIRE study has only
recently been presented to the American Heart
Association.

The Leicester trial was abandoned after a
small number of patients were recruited
because of an excess risk of stroke in the angio-
plasty group. The WALLSTENT study was aban-
doned after 1 year, again because of a threefold
excess risk of stroke in the angioplasty arm. The
fourth trial was performed in a community
hospital in the U.S. that reported no early or
late strokes at all in either arm. The largest ran-
domized study to date is the CAVATAS. This trial
randomized 504 patients and found that at 1
year there was no significant difference in the
rate of ipsilateral stroke relative to angioplasty
or surgery. However, the re-stenosis rate was
significantly higher in the angioplasty group.
The most worrisome aspect of the CAVATAS
trial was the excessive 30-day risk of stroke or
death in both the CEA (9.9%) and angioplasty
patients (10.0%). The SAPPHIRE study ran-
domized 307 patients to CEA or angioplasty.
The 30-day risks of death/stroke were not
significantly different (4.4% following angio-
plasty versus 6.1% after surgery), but the major
adverse event rate (30-day risk of death/
stroke/Ml) was 5.8% versus 12.6% in favor of
angioplasty (presented at the American Heart
Association in 2002). The inclusion of MI as a
hard end-point is a new development in the
history of performing randomized carotid
surgery trials.

Evidence suggests that following a successful
angioplasty, the risk of recurrent symptoms and
severe re-stenosis are low. A number of centers
have documented a zero incidence of late stroke
with restenosis rates of <5% at 12 months. In
CAVATAS, the rate of re-stenosis at 12 months
was 14%.

In the U.K., angioplasty is generally reserved
for use in randomized trials, although it is
probably the optimum treatment for those few
recurrent stenoses after CEA and particularly
carotid vein bypasses requiring reintervention.
In Europe and the U.S., the indications are prob-
ably more liberal but should remain within
institutional review board control.

Future Perspectives

There are a number of key issues that must be
addressed and implemented in the next 5 years:

• Researchers must ensuring that the popu-
lation-based results are equivalent to those
of the ECST and NASCET.

• Surgeons must know and quote their own
results rather than those from the ECST
and NASCET.

• The aim of treatment is not simply identi-
fying those with operable carotid disease.
Optimal medical therapy must be imple-
mented in everybody.

• High-risk symptomatic and asymptom-
atic patient subgroups must be identified
to optimize clinical benefit and cost-
effectiveness. The simple fact remains that
at 3 years, NASCET and ECST have shown
that 70% of symptomatic patients did not
need surgery (or by inference angioplasty),
whereas ACAS showed that almost 90%
of asymptomatic patients did not need
intervention.

• Randomized trials, as opposed to personal
dogma and interdisciplinary turf wars,
should determine which patients will
benefit from surgery or angioplasty in the
future.

References

Bamford J, Sandercock P, Dennis M, Burn J, Warlow C. ( 1990)

J Neurol Neurosurg Psychiatry 53:16-22.
Bonita R. (1992) Lancet 339:342-4.

CAPRIE Steering Committee (1996) Lancet 348, 1329-39.
Collins R, MacMahon S. (1994) Br Med Bull 50:272-98.
Counsell CE, Salinas R, Naylor R, Warlow CP. (1997) Eur J

Vase Endovasc Surg 13:345-54.
Golledge J, Mitchell A, Greenhalgh RM, Davies AH. (2000)

Stroke 31:1439-43.
Loftus IM, Naylor AR, Bell PR, Thompson MM. (2000) Br J

Surg 89:680-94.
Rothwell PM, Eliasziw M, Gutnikov SA, et al. (2003) Lancet

361:107-16.
Zarins CK, Giddens DP, Bharadvaj BK, Sottiurai VS, Mabon

RF, Glagov S. (1983) Circ Res 53:502-14.

Arch Vessel, Vertebrobasilar, and
Upper Extremity

Eva M. Rzucidlo and A. Ross Naylor

The innominate, proximal common carotid and
upper limb arteries are relatively rare sites for
atherosclerotic disease, arteritis, and trauma.
Accordingly, there is little evidence-based liter-
ature to guide clinical practice. The Joint Study
of Arterial Occlusion reported that the incidence
of severe lesions demonstrated by arteriography
in the innominate and proximal subclavian
artery was 17%. However, of the 2000 operations
performed at the University of California-
San Francisco for supra-aortic disease, only
7.5% were undertaken for innominate, common
carotid, or subclavian artery lesions.

The Innominate Artery

Etiology

Innominate artery (IA) occlusive disease is
uncommon, representing only 1.7% of all
operations performed at the University of
California-San Francisco for occlusive lesions
involving the brachiocephalic trunk, vertebral
arteries, and carotid bifurcation. Most contem-
porary studies report that 61% to 84% of
patients with innominate artery disease have
concomitant arch, vertebral, or carotid bifurca-
tion lesions (Rhodes et al., 2000).

In the United States the most common etiol-
ogy of innominate artery occlusive disease is
atherosclerotic disease (Fig. 16.1). Other impor-
tant etiologies include Takayasu's arteritis
(second most common in the United States),

giant cell arteritis, and radiation-induced ather-
osclerosis. Trauma is relatively uncommon,
but may follow a deceleration injury in major
vehicle accidents or penetrating injury. Innom-
inate artery occlusive disease tends to occur in
patients in their fifth and sixth decades (Azakie
et al., 1998). In the United States, there appears
to be a trend toward the majority being women.
Conversely, in France, Kieffer et al. (1995)
reported that 72% of the 148 patients undergo-
ing innominate artery reconstruction for ather-
osclerosis in their practice were men.

Symptoms

Symptoms largely depend on the underlying
etiology, anatomy, and co-involvement of other
major vessels. For example, in the bovine
anomaly (Fig. 16.2) the innominate and left
common carotid arteries arise from a common
origin, and therefore any symptoms could
involve either the carotid territory or the verte-
bral system. In general, innominate artery
lesions present with symptoms of ischemia of
the right upper extremity, symptoms involving
anterior cerebral circulation, symptoms refer-
able to the posterior circulation, or combined
upper extremity and neurological symptoms.
Upper extremity symptoms occur in 5% to
63% of patients and include claudication due
to hemodynamic compromise or embolic phe-
nomenon from unstable proximal lesions. A
combination of upper extremity and neurolog-
ical symptoms occurs in 30% to 40% of patients.

181

182

VASCULAR SURGERY

Figure 16.1. A: Arch angiogram showing occlusion of the innominate artery and a severe stenosis at the origin of the left common
carotid artery (arrow). B: Delayed films following on from part A.The right subclavian and distal innominate arteries are filled via ret-
rograde flow down the right vertebral artery. The actual innominate occlusion is relatively short.

Figure 16.2. Bovine arch anomaly. The innominate and left
common carotid arteries have a common origin (arrow). There is
a large atherosclerotic lesion causing a severe stenosis of the
bovine origin and total occlusion of the left subclavian artery.

Cerebrovascular symptoms [transient ische-
mic attack (TIA)/stroke] may be due to
thromboembolism into the carotid circulation
(hemisensory/motor signs, monocular blind-
ness, or higher cortical dysfunction) or the
vertebrobasilar system (bilateral sensory/motor
signs, dysarthria, ataxia, nystagmus, homony-
mous hemianopsia, cortical blindness, etc.).
Neurovascular symptoms affect 5% to 90% of
patients with severe innominate artery disease.
Ten percent of patients present with global
ischemia involving both the carotid and verte-
bral territories.

Diagnosis

Many of the clinical features of innominate
artery occlusive disease are of equal relevance to
subclavian and vertebral artery disease and are
reviewed in this section. Atherosclerotic disease
of the supra-aortic trunk is suggested by absent
pulses in the neck (subclavian, carotid) or arm
(axillary, brachial) in one or both sides. Unequal
or abnormally low blood pressures in the upper
extremity should also be noted. Physical exam-
ination should include palpation and ausculta-

183

ARCH VESSEL, VERTEBROBASILAR, AND UPPER EXTREMITY

tion of the proximal and midcervical carotid
pulses and palpation of the superficial tem-
poral, subclavian, brachial, radial, and ulnar
pulses. Carotid or subclavian artery bruits or
thrills suggest innominate artery or other
supra-aortic trunk stenotic lesions. Absent
pulses are suggestive of occlusions.

Blood pressure comparison of both upper
extremities is mandatory. If bilateral upper
extremity blood pressures are determined to be
low, comparison should be made to those in the
lower extremity. The hands should be inspected
for cyanosis, ulcers, subungual splinter hemor-
rhages, or livedo reticularis, which may indicate
ulcerated proximal lesions predisposing to
atheroemboli. In patients with subclavian steal
(see later), a pulse delay may be detected in the
radial artery.

A computed tomography scan of the brain is
an essential part of the workup of any patient
with suspected atherosclerotic disease of the
supra-aortic vessels. About 80% of the cerebral
cortex is clinically silent, and the finding of
areas of infarction (in the absence of any previ-
ous symptoms) may be helpful in planning
management strategies.

Duplex evaluation of the proximal supra-
aortic vessels may not be possible because they
may be out of the scanning range of most
machines. However, an experienced sonogra-
pher will warn the surgeon of damped wave-
forms in the common carotid or subclavian
vessels. This should alert the surgeon to the like-
lihood of inflow disease and the need for
employing other imaging modalities.

Arch arteriography remains the gold stan-
dard for defining the anatomy of the lesion,
extent of disease, and probable etiology (e.g.,
atherosclerosis versus arteritis). A complete
examination should include an arch aortogram,
selected carotid views, vertebral imaging, and
images of the intracranial circulation.

Concomitant coronary artery disease is
present in 40% to 50% of patients with supra-
aortic trunk disease. Inevitably, these patients
have other cardiovascular risk factors including
hypercholesterolemia, history of stroke, TIAs,
peripheral vascular disease, hypertension, dia-
betes, and renal insufficiency. A prior history of
smoking is present in 78% to 100% of patients
with supra-aortic trunk disease. Accordingly,
cardiac evaluation is advisable, especially if any
major reconstructions were planned.

Treatment

Historically, supra-aortic trunk disease was
treated by direct reconstruction. In 1956 Davis
et al. first described transthoracic innominate
endarterectomy. Later, in 1958, DeBakey des-
cribed prosthetic bypass grafting of the great
vessels. In appropriately selected patients, both
forms of direct reconstruction can give excellent
results.

Most patients with supra-aortic trunk ather-
osclerosis have multiple supra-aortic trunk
lesions. Multiple arch vessel involvement occurs
in 61% to 84% of patients. The best operative
repair of this patient population having multi-
ple arch vessel lesions may therefore be directed
reconstruction with bypass grafting.

Bypass grafting has an excellent technical
success rate and good early results with relief of
symptoms in up to 95% of patients. Long-term
relief of symptoms appear equally as good, with
primary patency rates of 95% being evident.
The two largest series were from Berguer et al.
(1998) (100 consecutive patients followed over
16 years) and Kieffer et al. (1995) (148 patients
followed over 20 years). Berguer et al. reported
5- and 10-year cumulative primary patency
rates of 87% and 81%, respectively. Stroke-free
survival rates at 5 and 10 years were 87%
and 81%, respectively. Kieffer et al. reported a
primary patency rate of 98% and 96% at 5
and 10 years, respectively. The probability of
freedom from ipsilateral stroke was 98% and
96% at 5 and 10 years, respectively. Life-table
analysis and perioperative events were used to
calculate the probability of survival, which was
77% and 51% at 5 and 10 years, respectively.
Most patients died from cardiac events.

The excellent outcomes following bypass
grafting of supra-aortic trunk disease, however,
does not come without a price. Perioperative
mortality ranges from 0% to 15%. In the more
recent studies, the rate generally is around 5%
and is mostly attributable to cardiac causes. The
perioperative stroke rate ranges from 0% to 8%
giving a combined stroke and death rate of
almost 16%. Rhodes et al. (2000) have deter-
mined risk factors for early and late complica-
tions in these patients. Patients with serum
creatinine levels of >2 had a significantly higher
combined stroke/death rate when compared to
patients with normal creatinine (50% versus
7%). Similarly, stroke rates were higher in

184

VASCULAR SURGERY

patients with preoperative evidence of a hyper-
coagulable state (33% versus 4%).

Although there have been no randomized
controlled trials, endarterectomy has been
reported to confer the same results as bypass
grafting. Bypass grafting of supra-aortic trunk
lesions requires the use of prosthetic material,
often with multiple limbs, which maybe kinked
after closure of the sternotomy wound.

Endarterectomy has the advantage of recon-
struction without the use of prosthetic material,
but is technically intimidating to surgeons who
have limited experience of operating in that part
of the vascular system. It is essential, therefore,
that patients are selected carefully. Anatomical
features considered contraindications for
endarterectomy include (1) atherosclerosis or
calcification of the aortic arch extending into
the origin of the innominate artery, and (2)
close proximity of the origin of the left common
carotid artery, which prevents safe clamping of
the innominate artery without increasing the
risk of embolization or of compromising cere-
bral blood flow. Endarterectomy would not be
an appropriate option in patients with bovine
arches (Fig. 16.2) as cross-clamping would pre-
dispose to inadequate left hemisphere perfu-
sion. The San Francisco group has long been
proponents of the endarterectomy technique
and has partly overcome the problems imposed
by multiple vessel disease by performing sepa-
rate endarterectomies on each of the affected
vessels (Azakie et al., 1998). Certain diseases
processes (inflammatory arteritis and radiation
arteritis) are best treated with bypass grafting,
as the pathological process is a transmural
process and development of an endarterectomy
plane may be difficult.

The emergence and technical advances in
percutaneous angioplasty, however, have ren-
dered many of these major reconstructions
obsolete. Percutaneous therapy for occlusive
lesions of supra-aortic trunk disease has several
advantages over a surgical approach. These
include its minimally invasive nature, avoidance
of general anesthesia, lower cost, and, most
importantly, the potential for lower morbidity
and mortality. Percutaneous angioplasty for
treatment of supra-aortic trunk lesions was
introduced in 1980. Since that time more than
30 small series have been published regarding
the role of angioplasty or stenting as primary
therapy for supra-aortic trunk lesions in more

than 900 patients. None of the reports are ran-
domized controlled trials (as is also the case
with surgery), and long-term results are still not
available.

A comparative trial of stenting and surgical
intervention for supra-aortic trunk lesions was
reported in 1998 by Whitbread et al. Eighteen
patients with symptomatic arch vessel stenosis
or occlusion were treated with angioplasty and
stenting, and the data compared with the pub-
lished results following surgical procedures. The
primary success rate was 100%, with no major
procedural complications, and at 17-month
follow-up all patients were asymptomatic with
100% primary patency. The incidence of stroke
and death was 3% and 2%, respectively. The
authors therefore concluded that stenting
should now be considered the first-line therapy
for brachio cephalic obstruction. A review of the
available literature suggests that the initial
success rate is higher with stenoses (98%), as
opposed to occlusions (46%). Both types of
lesions were treated with minimal mortality
(0.2% for stenoses and 0% for occlusions), the
stroke rate was commendably low (0.3% for
stenoses, 0% with occlusion), and with no
reports of arm embolization. Recurrence of
stenoses was similar for both stenotic lesions
and occlusions. With a mean follow-up period,
63 months, the incidence of recurrent stenosis
was identical: 11% in originally stenotic lesions,
9% for occlusions.

Although the initial results following angio-
plasty of supra-aortic trunk lesions are well
documented, there is a relative lack of reports
describing the long-term results. There are,
however, reports of endovascular treatment of
patients with supra-aortic trunk lesions with 9-
and 15-year follow-up (Henry et al., 1999). These
follow-up results are longer than most pub-
lished surgical series. Cumulative primary
patency was 91% to 95% at 5 years and 81% to
84% at 10 years. Sullivan et al. (1998) prospec-
tively studied acute and long-term results of
angioplasty and stenting in occlusive lesions of
the supra-aortic trunk. The initial technical
success rate was 94%, and 80% of the technical
failures were due to an inability to cross occlu-
sive lesions. With initial failures included, life
table analysis revealed 84% patency at 35
months. None of the patients required reinter-
vention or surgical conversion for recurrent
symptoms. The authors concluded that angio-

185

ARCH VESSEL, VERTEBROBASILAR, AND UPPER EXTREMITY

Figure 16.3. A: Severe stenosis in the right subclavian artery immediately distal to the vertebral artery (arrow). This produced arm
symptoms only and no subclavian steal. This was successfully treated by angioplasty (B).

plasty and stenting of the supra-aortic trunk
vessels could be performed with relative safety
and satisfactory midterm success.

Endovascular treatment of supra-aortic
trunk lesions began prior to the advent of arte-
rial stents. Some groups have advocated the
routine use of stents, whereas others use them
only when angioplasty produces technically
inadequate results. The routine use of stents
is supported by nonrandomized evidence
documenting improved early and long-
term patency rates, especially when treating
occlusions.

One further role for endovascular interven-
tion is in the management of the critically ill
patient with innominate disruption or false
aneurysm formation following trauma. The
whole procedure can be undertaken via direct
exposure of the right common carotid artery
with retrograde cannulation of the carotid and
innominate arteries.

subclavian artery disease was only found in
4.3%. Isolated subclavian artery stenosis (Fig.
16.3) is most commonly found in patients with
systemic vascular disease. The true prevalence
of subclavian artery disease, however, is difficult
to estimate because most patients are asympto-
matic. Only 24% of patients with disease of the
subclavian artery arteriography have symp-
toms. The left subclavian artery, arising directly
from the aortic arch, tends to be affected three
to four times more frequently than the right.

Other important causes of subclavian artery
disease include aneurysm, radiation arteritis,
Takayasu's arteritis, and the thoracic outlet syn-
drome. Thoracic outlet syndrome is due to com-
pression of one or more components of the
neurovascular bundle (subclavian artery, sub-
clavian vein, and brachial plexus) by a cervical
rib (Fig. 16.4), fibrous band, first rib, and clavi-
cle and anatomical anomalies of the scalene
musculature.

The Subclavian Artery

Etiology

Subclavian artery lesions are relatively uncom-
mon, but are encountered more frequently than
innominate or proximal common carotid artery
lesions. The most common cause is atheroscle-
rosis. In 4748 angiograms performed for signs
and symptoms of ischemic cerebrovascular
disease, the prevalence of stenosis greater than
30% was 21%, whereas the prevalence of occlu-
sion was 3%. Out of nearly 2000 great vessel
reconstructions by Wylie and Effeney (1979),

Figure 16.4. Three-dimensional magnetic resonance tomo-
graphic image of cervical rib with connection on to first rib.

186

VASCULAR SURGERY

Symptoms

As with the lower limb, symptoms can be acute
or chronic. Thromboembolism from a subcla-
vian artery aneurysm can cause acute upper
limb ischemia or more focal digital ischemia.
The latter may also originate from poststenotic
dilatation distal to (1) an atherosclerotic proxi-
mal subclavian stenosis or (2) a damaged artery
in patients with thoracic outlet syndrome. The
latter is a surgical emergency and must be rec-
ognized and treated promptly.

Chronic symptoms depend on the location
of the disease. Lesions distal to the origin of the
vertebral artery present with forearm claudica-
tion with exercise. No neurological signs or
symptoms are elicited from the history. Occlu-
sive/stenotic disease proximal to the origin of
the vertebral artery produces the subclavian
steal syndrome. Here forearm exercise increases
the need for increased blood flow, which is pro-
duced via reversed flow in the ipsilateral verte-
bral artery.

Subclavian steal is a vertebrobasilar neuro-
logic symptom that occurs with ipsilateral arm
exercise. With the use of the affected arm, the
demand for blood flow increases and the arm
"steals" blood from the cerebral circulation
through the ipsilateral vertebral artery. Interest-
ingly, even if there is reversed blood flow in the
ipsilateral vertebral artery on imaging, symp-
toms of vertebrobasilar insufficiency may rarely
be apparent, and the risk of posterior circula-
tion cerebral infarction is extremely low
(Hennerici et al., 1988) A rich collateral blood
supply is the likely reason why symptoms may
not become apparent.

Patients with atherosclerotic subclavian
artery disease tend to have a good prognosis,
with <20% suffering significant disease pro-
gression within 2 years of diagnosis. Moreover,
nearly one quarter of patients who presented
with steal (i.e., indicating marked hemody-
namic impairment) and who were then treated
conservatively became asymptomatic over the
next 42 months of follow-up (Schillinter, 2002),
indicating the potential for developing a collat-
eral circulation in this situation.

A second type of steal, again peculiar to the
subclavian artery, is the coronary-subclavian
steal syndrome. This phenomenon specifically
occurs in patients who have had coronary
revascularization using the internal mammary

artery. If thereafter they should develop a severe
stenosis or occlusion of the proximal subclavian
artery, arm exercise can steal blood away from
the heart. Most patients present with recurrent
angina symptoms or cardiac failure. Treatment
(angioplasty or carotid subclavian bypass) pro-
duces significant improvements in blood flow to
the heart. Clearly, cardiac surgeons should be
aware of the potential for this problem and
arrange for imaging of the subclavian arteries if
there is any evidence of dizziness with arm exer-
cise, forearm claudication, unequal blood pres-
sures in the upper limbs, or weak radial pulses
on palpation. Any significant lesion can there-
after be treated (usually with angioplasty) or
alternative conduits considered (contralateral
internal mammary, radial artery, saphenous
vein).

Thoracic outlet syndrome is characterized by
symptoms attributable to compression of the
subclavian artery, vein, or brachial plexus.
Arterial compression can cause claudication
with exercise, Raynaud's phenomenon, digital
microembolization, and even acute upper limb
ischemia. Arterial symptoms are usually associ-
ated with bony anomalies (e.g., cervical rib) or
compression between the clavicle and first rib.
Arterial symptoms secondary to thoracic outlet
compression must be treated urgently. Com-
pression of the subclavian vein causes heavi-
ness/blueness of the arm and can predispose to
subclavian vein thrombosis (Paget-Schroetter
syndrome). Venous compression/thrombosis in
this syndrome is often seen in patients partici-
pating in demanding fitness regimes. The
neurological component of thoracic outlet
syndrome depends on whether there is com-
pression of the lower (C8/T1) or upper (C5/C6)
trunks of the brachial plexus. Pain or paresthe-
sia predominate, but in severe cases muscle
wasting can occur.

Diagnosis

Duplex ultrasound is now the principal imaging
modality for examining the subclavian artery.
Although the origin of this vessel may be
difficult to image directly, an experienced ultra-
sonographer will be alert to a damped inflow
waveform suggestive of significant disease. If
required, a corroborative or diagnostic mag-
netic resonance angiogram (MRA) or digital

187

ARCH VESSEL, VERTEBROBASILAR, AND UPPER EXTREMITY

subtraction angiography (DSA) can be
undertaken.

Symptoms suggestive of arterial compression
(cold arm, fluctuating radial pulse with arm
movements, forearm claudication, microem-
bolization) require careful x-rays of the thoracic
inlet to look for a cervical rib or a prominent
transverse process on C8. The latter suggests
that a fibrous band may be present. More
modern tomographic imaging can demon-
strate the size and location of any cervical rib
(Fig. 16.4).

Management

Revascularization of the chronically occluded
subclavian artery is possible with either angio-
plasty or surgery. Surgical options include (1)
carotid-subclavian bypass, (2) carotid-axillary
bypass, (3) axillary-axillary bypass, and (4)
subclavian-carotid transposition. The choice of
technique reflects local expertise, clinician pref-
erence, and patient presentation.

Primary patency rates following carotid-
subclavian bypass have been reported to be
94%, with 87% symptom-free survival at 10
years (Vitti et al., 1994). The principal advantage
of subclavian transposition is that no prosthetic
material is used. Here the proximal subclavian
artery is mobilized, transected, and reanasto-
mosed end-to-side onto the common carotid
artery. It is reported to have similar outcomes to
carotid-subclavian bypass (primary patency at 5
years, 98%; freedom from recurrent symptoms,
95%). However, these types of revascularization
are not without risk: thoracic duct injury (2%),
nerve injury (11%), stroke (6%), and wound
hematoma (1%). The long-term durability of
axillary- axillary bypass is inferior to carotid-
subclavian bypass or transposition but may be
the treatment of choice in a high-risk patient
because it can be performed under local anes-
thesia. For obvious reasons, this type of recon-
struction should be avoided in any patient who
might subsequently a median sternotomy.

Angioplasty is the preferred option in the
United Kingdom and most European countries.
There is, however, no consensus as to whether
stents should be routinely used. Angioplasty of
the subclavian artery carries a 2% to 3% risk of
procedural stroke. This risk can be minimized
by passing a protective balloon up the brachial
artery and up into the ipsilateral vertebral

artery. This is inflated while the main subclavian
lesion is angioplastied, and deflated once it is
completed. It is of interest to note that following
successful subclavian artery angioplasty, flow
reversal in the vertebral artery is not instanta-
neous. The reason for this delayed reversal of
flow is not known.

The Proximal Common
Carotid Artery

Etiology

Proximal common carotid disease occurs much
less frequently than carotid bifurcation disease,
but 1% to 2% of patients with severe bifurcation
disease also have significant proximal common
carotid disease. Lesions of the right common
carotid artery are rare in the absence of innom-
inate artery disease and are rarer compared to
left common carotid disease. The principal
underlying pathologies include atherosclerotic
disease (most common), Takayasu's arteritis,
and, rarely, radiation-induced atherosclerosis.

Symptoms

Proximal common carotid lesions present with
thromboembolic symptoms that are identical to
those of disease at the carotid bifurcation
(hemisensory/motor signs, temporary monocu-
lar blindness, higher cortical dysfunction).

Diagnosis

The proximal common carotid artery is not
within the scanning range of current Duplex
technology. However, as with proximal subcla-
vian disease, significant disease at its origin
causes significant damping of the waveform and
turbulence. If there is any evidence of this (or if
the patient is being considered for bifurcation
angioplasty), he/she will need to undergo either
MRA or DSA. Other emerging alternatives
include computed tomography (CT) angiogra-
phy. Clearly the choice reflects the unit's experi-
ence, access, and preference.

Management

In the past, proximal common carotid disease
required partial sternotomy and either endar-

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VASCULAR SURGERY

terectomy or bypass off the aortic arch. Other
options included carotid-carotid bypass or
carotid transposition. However, this is another
situation where on-table angioplasty (following
exposure of the mid-common carotid artery)
affords a balance between minimal risk and
prevention of embolization. Venting blood into
a sheath or up the external carotid artery can
prevent the latter. One advantage of on-table
angioplasty is that it can be combined with
synchronous bifurcation endarterectomy

The Vertebral Artery

Etiology

The vertebral arteries arise from the proximal
subclavian arteries. The first segment extends
from its origin to where it enters the transverse
cervical vertebral processes. The second seg-
ment is intraspinal. The third segment starts at
the upper border of the transverse process of C2
and passes up to the atlanto-occipital mem-
brane. The fourth segment is intradural to its
confluence with the contralateral vertebral to
thereafter form the basilar artery. The com-
monest pathology is an atherosclerotic stenosis
or occlusion of the proximal vertebral artery
(Fig. 16.5). Alternative (less common) patholo-
gies include fibromuscular dysplasia or
dissection.

Symptoms

Classical vertebral territory symptoms (verte-
brobasilar symptoms) include varying com-
binations of unsteadiness of gait, diplopia,
bilateral motor/sensory impairment, nystag-
mus, ataxia, bilateral blindness, and dysarthria.
These symptoms can be due to either thrombo-
sis or embolism (often very difficult to tell), but
the consensus view is that the majority is prob-
ably hemodynamic. Tomographic imaging can
sometimes help in the difficult task of discrim-
inating between the two etiologies.

There is much controversy about whether
nonhemispheric symptoms (isolated diplopia,
isolated dizziness, isolated vertigo, syncope,
etc.) can be attributed to disease in the verte-
brobasilar system. To date, there is no com-
pelling evidence that they are attributable

Figure 16.5. Occlusion of the proximal vertebral artery with
distal refilling via collaterals. The most likely pathology is throm-
bosis secondary to atherosclerotic disease.

unless they definitely coexist with other, more
typical vertebrobasilar territory symptoms. One
other myth is the concept of "nipping of the
intraspinal vertebral arteries causing dizziness
on head movement." At the Leicester Royal
Infirmary, a number of these patients have been
examined with transcranial and extracranial

189

ARCH VESSEL, VERTEBROBASILAR, AND UPPER EXTREMITY

duplex imaging, and none have ever been noted
to have any change in flow or direction of flow
with head movements. All were subsequently
found to have inner ear pathologies. There is
also no evidence that coils or kinks in the prox-
imal vertebral artery are responsible for cere-
brovascular symptoms unless a coexistent
stenosis is present.

Diagnosis

Duplex imaging identifies evidence of damped
flow, hypoplastic arteries (not uncommon), and
inflow stenoses. It is not, however, particularly
good at imaging the entire length of the artery.
Accordingly, patients suspected of having verte-
brobasilar insufficiency should undergo MRA
or intraarterial DSA.

Treatment

The treatment of vertebral artery stenoses/
occlusions is to first address the anterior circu-
lation. If there is significant internal carotid
artery disease, carotid endarterectomy should
be employed first. Some centers have reported
huge series of vertebral reconstructions.
At Leicester (apart from carotid-subclavian
bypass), only three vertebral reconstructions
have been performed over the last 8 years, all
involving segment 1. Angioplasty is currently
the emerging treatment of choice, although
some surgeons remain strong advocates of
surgical revascularization of segment 2 (endar-
terectomy and patch, bypass, transposition onto
the carotid artery).

Technique

All interventions should be undertaken in a spe-
cially equipped operating room with dedicated
fluoroscopic/angiographic capabilities. As one
of the risks for endovascular treatment of the
supra-aortic trunk is distal embolization, local
infiltrative anesthesia supplemented with intra-
venous sedation is optimal. This type of anes-
thesia allows for continuous monitoring of the
patient's neurologic status.

Due to the risk of distal embolization, com-
mon carotid lesions are best treated through a
limited surgical incision in the neck. This allows

for distal control of the common carotid artery
and the ability of flushing the artery of athero-
sclerotic emboli. Flow through the external
carotid artery is usually sufficient for cerebral
perfusion. If concomitant bifurcation disease
is present (around 2% of patients), then the
common carotid lesion should be treated first.
Once the artery is exposed, intravenous heparin
is given prior to obtaining proximal control,
placement of the sheath, and crossing the lesion.
The artery is accessed with a Potts-Cournand
18-gauge needle in a retrograde fashion and a
0.035-mm wire in advanced with the help of
fluoroscopy into the aortic arch. A 35-cm-long
sheath maybe placed to allow for more distance
between the surgeon and radiation field,
decreasing exposure to the surgeon's hands.
Access of the femoral artery allows for place-
ment of a flush catheter in the aortic arch and
more precise localization of the ostium of the
vessel. Selection of the innominate artery and
selected oblique views to define the right
common carotid and right subclavian origin is
imperative for precise stent placement. The true
location of the ostium is imperative to deter-
mine optimal stent placement, with 1 to 2 mm of
the stent protruding into the lumen of the aortic
arch. Occlusions should be predilated to avoid
stent dislodgment during crossing of the lesion
or to allow for safe passage of self-expanding
stents across the lesion. Whether balloon
expandable stents or self-expanding stents are
better is unknown, as there are no compara-
tive studies. It would seem logical that if the
lesion is tortuous or crosses the clavicle, a self-
expanding stent, which is more flexible, would
be preferred. Cerebral protection devices may
change the need for surgical control of the
common carotid artery. These devices could be
used for stenoses, but not for occlusive lesions.
As in internal carotid artery stenting, the lesion
is crossed with the low-profile cerebral protec-
tion devise prior to any manipulation of the
lesion. This would be impossible with an occlu-
sive lesion. Other limitations of the cerebral pro-
tection device use would be common carotid
size, not allowing for good apposition of the
device to the artery. The device, therefore,
would need to be placed in the internal carotid
artery.

Subclavian lesion maybe treated both from a
femoral and brachial approach. Again, a com-
bined brachial-femoral approach allows for

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VASCULAR SURGERY

placement of a flush catheter in the aorta and
therefore more precise placement of the stent.
With occlusive lesion, the brachial approach
allows for more pushability to cross the lesion.
The caveat to this approach is risk of dissection
into the aortic arch. In general, stenting allows
for tacking of the dissections. Other considera-
tions are posterior circulation embolization. It
is therefore imperative to determine flow direc-
tion in the vertebral artery by duplex ultra-
sonography. Antegrade vertebral flow is delayed
from 20 to 240 seconds, serving as an effective
protective mechanism against embolism in the
posterior circulation. Brachial artery cutdown
allows for direct repair of the artery after com-
pletion of the stenting, thus decreasing the
risk of atherosclerotic emboli (allowing for
flushing of the artery) and avoiding risk
of hematoma.

References

Azakie A, McElhinney DB, Higashima R, Messina LM, Stoney

RJ. (1998) Ann Surg 228:402-10.
Berguer R, Morasch MD, Kline RA. (1998) J Vase Surg 27:

34-41; discussion 42.
Hennerici M, Klemm C, Rautenberg W. (1988) Neurology

38:669-73.
Henry M, Amor M, Henry I, Ethevenot G, Tzvetanov K, Chati

Z. (1999) J Endovasc Surg 6:33-41.
Kieffer E, Sabatier J, Koskas F, Bahnini A. (1995) J Vase Surg

21:326-36; discussion 336-7.
Rhodes JM, Cherry KJ Jr, Clark RC, et al. (2000) J Vase Surg

31:260-9.
Sullivan TM, Gray BH, Bacharach JM, et al. ( 1998) J Vase Surg

28:1059-65.
Vitti MJ, Thompson BW, Read RC, et al. (1994) J Vase Surg

20:411-7; discussion 417-8.
Whitbread T, Cleveland TJ, Beard JD, Gaines PA. (1998) Eur

J Vase Endovasc Surg 15:29-35.
Wylie EJ, Effeney DJ. (1979) Surg Clin North Am

59:669-80.

Aneurysmal Disease

Philip Davey and Michael G. Wyatt

Arterial aneurysmal disease has been recog-
nized now for over 4000 years, with the expres-
sion "aneurysm" deriving from the Greek word
aneurysma, meaning "a widening." Historical
review charts a condition in which initially
observational experiences of aneurysms have
been gradually replaced with the established
treatment regimes we see in clinical practice
today. Advances made in aneurysm manage-
ment reflect not only improved surgical acumen
and the appliance of innovative technology but
also the progress made in our basic scientific
knowledge, clinical experience, diagnosis, peri-
operative care, anesthesia, and follow-up of
the disease. Aneurysmal disease constitutes a
substantial component of the vascular surgeon's
work load, and this chapter reviews the
common pathology with reference to contem-
porary opinion in pathogenesis, diagnosis, and
management.

Classification of
Arterial Aneurysms

The aneurysm is defined as an abnormal,
focal dilatation of a blood vessel. An artery is
empirically considered aneurysmal when its
diameter becomes 50% larger than its normal
vessel segment. This diagnosis is distinct from
ectasia, which refers to a dilated vessel that
has not yet reached this threshold. Similarly,
the conditions of arteriomegaly and multiple

aneurysms must not be confused. In the former,
generalized dilated vasculature (>50%) is ob-
served but, unlike the latter condition, normal-
caliber vessel segments do not distinguish these
conditions.

Aneurysmal disease may be classified as
follows:

1. By nature: true aneurysms relate to a dis-
tinct pathological process involving all
three layers of the arterial wall. False or
pseudoaneurysms do not reflect a gen-
uine aneurysmal process at all but rather
clinical mimicry true disease. They are, in
fact, a vessel-associated contained blood
collection and typically result from
trauma.

2. By morphology: saccular aneurysmal
disease is present if only part of the vessel
circumference is diseased. Entire circum-
ferential involvement is termed fusiform.

3. By etiology: aneurysms are frequently
referred to with respect to an antecedent
disease process. The list, which is not
exhaustive, includes

a. Degeneration (e.g., atherosclerosis,
fibromuscular dysplasia)

b. Infection (e.g., syphilis, bacterial,
fungal)

c. Trauma (e.g., iatrogenic, penetrating,
blunt)

d. Inflammation (e.g., Takayasu's or
Kawasaki disease, polyarteritis nodosa)

191

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VASCULAR SURGERY

e. Connective tissue disorders (e.g.,
Marfan syndrome, Ehlers-Danlos
syndrome)

f. Congenital (e.g., tuberous sclerosis,
Turner syndrome)

4. By location: for example, abdominal aortic,
popliteal, femoral, subclavian, thoracoab-
dominal, etc.

Pathogenesis of
Aneurysmal Disease

Despite extensive research, the exact mecha-
nisms underlying aneurysm pathogenesis
remain unclear. It appears the process is multi-
factorial, involving variable components of
altered biochemistry, immunological, mechani-
cal, and genetic importance (Wassef et al.,2001).
Much of our understanding of the disease
relates to work performed on the abdominal
aorta, and it is assumed that nonaortic aneurys-
mal disease results from a similar pathological
sequence of events.

Aneurysmal disease ultimately results follow-
ing gradual proteolytic degradation of arterial
vessel walls. Structural integrity of arterial wall
is dependent on adequate functional connective
tissue elements including elastin and collagen.
Loss of these elements weakens the vessel wall
and thus predisposes to aneurysm formation.
Research into abdominal aortic aneurysms
(AAAs) has discovered local increased levels of
matrix metalloproteinases (MMPs) that result in
this observed connective tissue breakdown.
Four MMP subtypes are thought to be of impor-
tance in this process: gelatinases (MMP-2 and
MMP-9), matrilysin (MMP-7), and macrophage
elastase (MMP-12). In addition to this increased
local expression, altered levels of circulating
proteases may play a role, and research con-
tinues into the contributions to aneurysmal
disease from various plasminogen activators,
serine elastases, and cysteine proteases (cathep-
sins S and K). Abnormally low levels of protease
inhibitors are suggested to exert the same path-
ogenic effects, and this has also been the focus
of much recent work. Preliminary research into
the most abundant serine protease inhibitor,
cystatin c, has confirmed that in patients with
aneurysmal disease corresponding levels of this
protein are indeed lower than normal.

Chronic inflammation plays an important
role in aneurysmal disease. Much of the vessel
wall destruction is undoubtedly mediated by the
inflammatory infiltrate composed of T cells,
macrophages, B lymphocytes, and plasma cells,
but the antecedent trigger for this cellular
migration remains unclear. It has been sug-
gested that aneurysmal disease is in fact an
antigen-driven immune disease from work
analyzing AAA disease. Proposed antigenic
activators to subsequent inflammation include
elastin, interstitial collagen, oxidized low-
density lipoprotein, cytomegalovirus, and
artery-specific antigenic proteins such as
AAAP-40. Following T-cell antigen recognition,
the inflammatory cascade begins, ultimately
resulting in vessel wall degradation and pro-
gression to aneurysmal disease.

Arterial wall biomechanical stress is also
accepted as being of considerable importance
in both aneurysm progression and rupture.
Model analysis of wall stress variation in differ-
ent anatomical locations implies that altered
hemodynamic profiles may explain the varying
susceptibility of an arterial wall to become
aneurysmal (e.g., increased disease incidence
in abdominal as opposed to thoracic aorta).
It is suggested that mechanical failure from
excessive stress initiates and promotes ane-
urysmal pathogenesis first by the aggregation
of humoral factors, and then by a consequent
focal inflammatory response and finally wall
breakdown.

The familial clustering of aneurysmal
disease has led to interest in determining a
possible genetic explanation for the process.
Supporting evidence is derived from observa-
tions regarding the altered disease charac-
teristics of "familial" and "spontaneous"
aortic aneurysmal disease. Cases of familial
AAA present significantly younger, carry a
greater rupture risk (especially in females)
and are 18 times more likely to be present in
other family members than is seen with sponta-
neous pathology. Affected sibling pair DNA
linkage studies aims to identify the putative
AAA-susceptibility gene, whose expression or
mutation promotes progression to aneurysmal
disease. This approach to pathogenesis may
eventually form the basis of genetic testing
of specific increased-risk populations,
allowing more focused surveillance and early
intervention.

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ANEURYSMAL DISEASE

Abdominal Aortic Aneurysms

In the 16th century the anatomist Vesalius first
recognized aneurysmal disease affecting the
infrarenal aorta. Limited progress was made
over the following centuries in the treatment of
AAA, and it was not until 1952 that Dubost
reported the first successful treatment of the
condition by surgical repair. In the past 50 years,
increased experience and advancement of sur-
gical techniques have rendered elective AAA
repair a routine albeit major operative proce-
dure with expected mortality rates of less than
5% (Hallin et al., 2001). Exciting developments
in the endovascular arena over the last decade
have offered further options for treatment in
elective AAA disease and promises to revolu-
tionize management for many patients.

The natural history of AAA is to gradually
expand and eventually rupture. Ultimately, the
aim of elective surgery is to prevent this from
happening by excluding the aneurysm from the
circulation by means of either prosthetic graft
insertion or endovascular stent deployment.
Unfortunately, even with improved periopera-
tive management and operative technique, the
great advances made in elective AAA repair
have not been witnessed in the emergency
setting for AAA rupture, and consequently mor-
tality rates remain high at approximately 50%.

Definition

Aneurysms are arbitrarily defined as a segment
of vessel dilatation that is at least 50% larger
than the expected normal vessel diameter. In
practical terms this diameter refers to the nona-
neurysmal adjacent vessel segment. We accept a
"normal" abdominal aorta to be approximately
20 mm in diameter, and therefore an aorta wider
than 30 mm would suggest aneurysmal disease.

Epidemiology

In all epidemiological analysis, statistical varia-
tion can exist as a result of inconsistent
definitions of disease, and AAA is no exception.
Population screening surveys and postmortem
studies have been used to estimate a current
prevalence of AAA of between 1.3% and 12.7%
in England (Wilmink and Quick, 1998). Marked
increases in the prevalence of the disease are

seen if the definition of AAA is relaxed to even
1 mm less than stated earlier (30mm), but little
difference exists between the two methods of
prevalence estimation in this condition.

The incidence of asymptomatic AAA has
been reported at 3 to 117 per 100,000 person-
years. These estimations are derived from the
number of hospital admissions for elective
asymptomatic AAA repair and have been
observed to increase by 7% to 26% over the past
15 years. This basically reflects changes in
improved disease awareness, referral patterns,
and diagnosis, more specifically the increased
availability and use of ultrasound scanning in
recent years. The reported incidence of rup-
tured AAA is much more inaccurate due to high
prehospital mortality, but quoted values are
between 1 and 21 per 100-000 person-years.
Data also suggests that this value is continuing
to increase by 2.4% per year. In the United
Kingdom, ruptured aortic aneurysms have been
reported as the 13th commonest cause of death
accounting for 1.2% of male and 0.6% of female
mortality.

Abdominal aortic aneurysm is typically a
disease of the male population, being five times
more common than in women. A sharp
increased incidence is seen after the age of 50
years, rising to apeak at 80 years of age. Abdom-
inal aortic aneurysm in females does not tend
to occur until about 10 years later than in men,
and then increases linearly from the age of 60.

In a more general sense, 5% of the over-60
population will have an AAA, and at the age of
67 a man is ten times more likely to die from a
ruptured AAA than is a woman.

Risk Factors for Abdominal
Aortic Aneurysm

Factors associated with an increased risk of
aneurysmal development in the infrarenal aorta
include increasing age, male sex, ethnic origin,
family history, smoking, hypercholesterolemia,
hypertension, and prior vascular disease.
Studies suggest that of these, male sex and
smoking are the most important, increasing
the chances of AAA development by 4.5 and 5.5
times, respectively. A positive family history
(first-degree relative affected) alone doubles the
risk of AAA presentation and is more likely if
the affected relative is a female. Interestingly,

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VASCULAR SURGERY

diabetes mellitus, which is a major risk factor
for occlusive arterial disease, is associated with
less risk (compared to nondiabetics) in the
development of aortic aneurysmal disease.

Clinical Features

The vast majority of AAAs are asymptomatic,
and the diagnosis is usually made on clinical
abdominal examination or following ultra-
sound investigation for other pathology. If
symptoms are present, they usually relate to
the complications of infra-aortic aneurysmal
disease both locally and systemically

Abdominal or back pain may be experienced,
and this must alert the clinician to the possibil-
ity of posterior erosion of the aneurysm into the
neighboring vertebral bodies. Classically in this
situation, the history of pain follows a non-
specific and indolent course. Appropriate subse-
quent investigations should distinguish erosion
from the diagnosis of inflammatory AAA (see
later). Sudden onset of severe abdominal or
back pain in a patient with a known AAA
who is hemo dynamically unstable suggests
aneurysm rupture. The pain may radiate into
the hips, and the patient will be pale, anxious,
clammy, tachycardic, and hypotensive. An
aneurysm rupture that is contained within the
retroperitoneum is often seen with a similar but
less pronounced symptom profile, affording
more time for preoperative optimization than
uncontained ruptures.

Symptoms of distal ischemia may result
directly from the presence of AAAs. Emboliza-
tion of contents from the aneurysmal sac may
present with acute or chronic limb ischemia,
whereas a similar picture may be witnessed if
the AAA thromboses in situ. In the latter case
one would expect symptoms of bilateral leg
ischemia.

Less common presentations of infra-renal
aortic aneurysmal disease relate to fistulation.
Cases of aortoduodenal fistulas present classi-
cally with intermittent, unexplained gastroin-
testinal bleeding and melena or massive
uncontrollable hematemesis. The diagnosis is
confirmed by upper gastrointestinal endoscopy
prompting urgent surgical repair. Isolated aor-
tocaval fistulas are rare but present with symp-
toms of high output cardiac failure. More
commonly, an aortocaval fistula results as a con-
sequence of aneurysm rupture, and the opera-

tive finding at laparotomy is that of massive
venous hemorrhage requiring rapid control to
avert on-table death due to exsanguination.

Detection of an AAA can potentially be made
by careful abdominal palpation during clinical
examination. The reliability of this technique
alone is questionable, its sensitivity governed by
a variety of factors such as aneurysm size, exam-
iner's skill, patient's body habitus, and the
purpose of the clinical examination itself. Even
after acknowledgment of these variables, a
correct diagnosis is achieved in only approxi-
mately 50% of cases. Smaller aneurysms and
obesity increase the likelihood of a missed
diagnosis, whereas an false-positive diagnosis of
AAA may be made in thin patients, tortuous
aortas, or in those with more prominent vessels
as a consequence of lumbar lordosis. Similarly,
the success of manual examination in the
assessment of aneurysm size and proximal
extent in relation to the renal arteries is poor.
Subcutaneous fat and overlying intestine tend to
cause an overestimation of size, and the ability
to admit an examining hand between the costal
margin and pulsatile mass will not indicate
infrarenal disease in all cases.

Investigations for Abdominal
Aortic Aneurysm

Plain Film Radiography

Plain abdominal x-rays are cheap and widely
available but of little use in the routine diagno-
sis of the AAA. Occasionally, calcification may
be observed in the wall of the aneurysmal vessel
or there may be loss of the psoas major shadow.
In the preoperative setting their use is limited
to exclusion of an alternate diagnosis to AAA.
They do, however, play an important role fol-
lowing endovascular stent graft repair of AAA
for observation of long-term outcome and graft
integrity.

Ultrasonography

Abdominal ultrasound examination is responsi-
ble for the detection of the majority of asymp-
tomatic AAAs and it is also used to confirm
the suspected clinical diagnosis (Fig. 17.1). In
addition, this modality is employed to observe
aneurysmal expansion in patients with disease

195

ANEURYSMAL DISEASE

L«08. 6 JJg

*■**>

■

Figure 17.1. An abdominal ultrasound showing an aortic
aneurysm.

under surveillance. Ultrasound is cheap, rela-
tively quick, widely available, and noninvasive.
Visualization of the aorta is achieved in 97%
of patients, and current figures demonstrate
minimal interobserver variability. The avail-
ability of mobile ultrasound machines allows
assessment of the critically ill patient who
ideally should not be transferred to the radiol-
ogy department.

Ultrasound, however, does have its limita-
tions. Unfortunately, cases of suprarenal, vis-
ceral artery aneurysmal disease and iliac vessel
extension cannot be accurately assessed by
ultrasound. In obese, ventilated patients, or
those patients with excessive bowel gas, this
unreliability is further exaggerated. Further-
more, this modality is poor at confirming the
presence of aneurysm rupture and hence plays
no role in the emergency setting.

Computed Tomography Scanning

Computed tomography (CT) scanning remains
the investigation of choice for the most accurate
assessment of AAA disease. The procedure
allows visualization of the upper extent of the
aneurysm and its nature (i.e., noninflammatory
or inflammatory), and provides reliable infor-
mation regarding iliac artery involvement.
Interobserver variation in the measurement of
aneurysm size is superior to ultrasound, with
over 90% of studies exhibiting a discrepancy
of less than 5 mm. Computed tomography
scanning with 3-mm cuts can also be used to
determine if the patient is a candidate for

endoluminal stent grafting. The imaging,
however, is invasive, time-consuming, and
expensive, and it entails substantial radiation
exposure for the patient. It is therefore restricted
for preoperative assessment in those suspected
to be imminent candidates for surgical repair,
follow-up of endovascular stent graft repairs,
and for patients with suspected AAA rupture
who are stable enough for deferment of
laparotomy.

The advent of spiral CT scanning in some
centers has led to increased speed of assess-
ment (a single breath hold) with the ability to
reconstruct CT images in a three-dimensional
manner, resulting in a more user-friendly and
informative imaging. The use of CT scanning
must be judicious in patients with a prior
history of contrast reaction, high blood pres-
sure, and preexisting renal impairment. As with
ultrasound, CT scanning cannot detect visceral
artery involvement or the presence of renal
artery stenosis, and this must be remembered in
assessment of the generated images.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) for AAA
offers comparable results to CT scanning in
terms of assessment of aneurysm size, proximal
extent, iliac extension, and etiology (e.g.,
inflammatory), and has the added advantage of
being noninvasive and safe because no contrast
administration is required. The procedure,
however, is not well tolerated by claustrophobic
patients, and its limited availability and expense
have relegated its use to a second-line investi-
gation for AAA, reserved for those patients for
whom CT scanning is inappropriate (e.g.,
iodinated contrast allergy, chronic renal failure,
or claustrophobia).

Angiography

Contrast arteriography offers little information
regarding the possible diagnosis or sizing of an
AAA, as it is only the vessel lumen (not the
aneurysmal sac) that is delineated in this exam-
ination. For these reasons, this investigation
plays little role in the management of the
routine infrarenal AAA. It does, however, offer
detailed information with respect to possible
visceral or renal artery disease, and allows ade-
quate vessel anatomy analysis for planning prior

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VASCULAR SURGERY

to surgical repair. Indications for arteriography,
therefore, include aneurysms with possible
suprarenal involvement or suspected visceral
artery disease, renal stenosis, and in patients
with coexistent peripheral vascular or nonaor-
tic aneurysmal disease (e.g., popliteal). Again,
the investigation is invasive, involves the use of
substantial amounts of contrast agent, and
carries with it the risks of embolic and renal
complications.

Screening for Abdominal
Aortic Aneurysm

There is currently much debate about the merits
about introducing a national screening program
for the detection of aneurysmal disease affect-
ing the abdominal aorta (Table 17.1). The nature
of AAA is such that the majority of patients have
the condition silently, until they present at the
hospital under the most extreme circumstances:
aneurysm rupture. Because the prevalence of
this disease is relatively high (5% of the over-60
population), it has been suggested that a simple
ultrasound-screening test at about this age
would uncover the asymptomatic pathology at
an early stage. Appropriate follow-up and elec-
tive repair could then be planned, thus dimin-
ishing the frequency of ruptured aneurysm
presentation and its inherent cost implications.
Recent studies in the U.K. have shown that a
screening program would indeed fulfill these
expectations, observing a reduction in the AAA
rupture rate by 50%. Other groups suggest a
screening program would have a greater diag-
nostic yield and hence prove more cost-effective
if only the specific, high-risk populations were
targeted, such as elderly male smokers. What-
ever the proposal, it would certainly appear that
a timely ultrasound examination may be
beneficial in the early management of AAA, but
a large multicenter trial is needed to obtain

Table 1 7.1 . Why screen for aneurysms?

Abdominal aortic aneurysms (AAA) are asymptomatic

Major complication of AAA is rupture

Morbidity and mortality of repair of ruptured AAAs:

50% to 70%; elective AAAs, 1% to 5%
Patients who survive repair have a similar life

expectancy as the general population
Ultrasound is inexpensive and noninvasive

adequate numbers of patients with the power
to demonstrate the cost-effectiveness of this
approach to AAA disease.

Management of the Elective
Abdominal Aortic Aneurysm

The basic goal underpinning the management
of the asymptomatic and symptomatic non-
ruptured AAA is to avert the presentation of
aneurysm rupture. As with all surgery, a surgeon
must balance the risks of the required major
operation in terms of mortality and morbidity
against that of a possible rupture-related death
with nonoperative "conservative" management.
With appropriate case selection and surgical
expertise, mortality following elective AAA
repair should be between 2% and 5%. Important
issues to be taken into account, which enable the
surgeon to make the correct decision whether or
not to operate, are discussed in the following
subsections.

Aneurysmal Size

The maximum diameter of AAA is without
doubt the most important factor in predicting
the ruptured risk of an aneurysm. The 5-year
rupture risk of an aneurysm less than 4 cm in
diameter is approximately 15%, and this rises to
nearly 95% if the aneurysm grows to 7 cm in
diameter. Unfortunately, vascular surgery is not
an exact science, however, and small aneurysms
will continue to rupture and many people with
large aneurysms will outlive the disease and die
of an unrelated cause.

The recently completed U.K. small aneurysm
trial aimed to provide guidelines regarding
when to offer elective surgery on the basis of
aneurysm size (Lancet, 1998). Comparison of
surgical repair of small aneurysms (4 to 5.5 cm)
with nonoperative ultrasound surveillance sug-
gested that there was no survival benefit to be
gained from operative management of the AAA.
The trial researchers recommended that
aneurysms should be considered for surgical
repair when the maximal diameter exceeded
5.5 cm or the aneurysm became symptomatic or
tender. It was at this stage the operative risk of
repair was less than the risk of rupture associ-
ated with nonoperative management.

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ANEURYSMAL DISEASE

Treatment protocols for small aneurysms
remain less clear-cut, but as a general rule all
AAAs greater than 30 mm in diameter should be
kept under ultrasound surveillance. Aortas less
than 40 mm in diameter should probably be
monitored with annual ultrasound scans,
whereas if there is growth to between 40 and 55
mm the frequency of observations should
increase to every 6 months. Other measures in
management include encouragement to stop
smoking, aggressive blood pressure control,
and possibly the administration of propranolol
unless contraindicated (see later). If an
aneurysm under surveillance appears greater
than 50 mm in diameter, a CT scan should be
obtained to formally size and delineate aneurys-
mal anatomy in preparation for operative repair.
At some centers, it is at this stage that the patient
may be considered for endovascular treatment
as opposed to open repair of their aneurysm.

Expansion Rate

Aneurysmal expansion rate is considered an
important factor as it enables the clinician to
estimate the timing of elective surgery governed
by the size of the AAA. Much evidence suggests
that the larger the aneurysm, the quicker the
expansion rate, so that aneurysmal growth
can be considered as exponential function of
aneurysm size. Small aneurysms between 40
and 60 mm are expected to expand "normally"
at an annual rate of around 10% (4 to 5 mm).
Growth patterns that exceed this reflect unpre-
dictable pathology and may warrant earlier sur-
gical intervention. It is generally accepted that if
the aneurysm expansion rate is greater than 10
mm, this is an indication for operative repair,
regardless of the aneurysm size.

The exact reasons for the vast differences wit-
nessed in aneurysm expansion remain unclear.
Studies have shown that smoking, advancing
age, cardiac disease, and hypertension are all
independent predictors of an increased expan-
sion rate, and that administration of certain
beta-blocker drugs may reduce this phenome-
non. Recently, much interest has been directed
toward the medical management of small
aneurysms with the drug propranolol, which is
observed to reduce the rapid expansion of AAA
by nearly 40%. The exact mechanism of this
finding could simply be explained by improved
blood pressure or heart rate control, but some

groups suggest that since propranolol blocks
circulating tissue plasminogen activator (tPA),
there is a direct effect on the aortic wall by
diminished plasmin-mediated MMP activation
and therefore reduced expansion rate. Whatever
the pharmacological explanation, it would cer-
tainly appear that unless contraindicated (e.g.,
asthma, severe cardiac failure), a good argument
can be made for the administration of propra-
nolol while the aneurysm is under surveillance.

Proximal Extent of Abdominal
Aortic Aneurysm

The relationship of the aneurysm to both the
renal and visceral arteries must be elicited prior
to surgical repair. Juxtarenal aneurysms com-
mence immediately below the renal arteries
and thus do not permit a clamp to be placed
infrarenally, as is also the case with suprarenal
aneurysms, which may or may not involve the
superior mesenteric artery or coeliac axis. If the
pathology commences higher than the coeliac
trunk, the aneurysm is deemed to be thora-
coabdominal. Repair of all these aneurysms
carries significantly increased patient mortality
or morbidity with requirement for higher levels
of surgical expertise. Hence, referral to a terti-
ary vascular center is mandatory and repair
should not be attempted at a district general
hospital.

Patient Comorbidity

Full patient assessment prior to proposed AAA
surgery should aim to identify medical factors
to be addressed in the preoperative workup.
Aneurysmal surgery is obviously not appropri-
ate in those patients with widespread advanced
malignancy and limited life expectancy or those
with neurological degenerative disease. Other
conditions that do not preclude surgery should
be appropriately treated in order to optimize the
patient for the operating room and so minimize
the risks of aneurysm repair. Specific preopera-
tive conditions associated with poor outcome
following elective AAA surgery include renal
dysfunction, cardiac failure, myocardial
ischemia, and respiratory impairment. The
presence of one or more of these conditions may
indicate the need for extensive preoperative
investigation and appropriate referral to other
medical specialties.

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Individual Surgeon's Audited Results

In the current climate of clinical governance
and accountability, it is no surprise that the
decision to operate in AAA does not entirely
depend on the patient but also on the ability of
the operating surgeons themselves. Advances in
operative technique and vascular anesthesia in
major centers have been reflected in a fall of
operative mortality following elective AAA
repair to around 2% to 5%. Unfortunately, the
death rate at some district general hospitals
after the same operation by personnel without
specialist knowledge has been reported in
excess of 10% and poses the question of whether
this surgeon-specific discrepancy warrants the
shift of all elective AAA repairs to be performed
at recognized major vascular centers.

Aneurysmal Symptomatology

Symptomatic and suspected ruptured aortic
aneurysms are usually in themselves an indica-
tion for surgical intervention. The rationale for
this decision is explained by the high mortality
rate of a presumed imminent rupture, and pre-
dicted morbidity following embolism from the
aneurysmal sac.

Preoperative Assessment of the
Elective Abdominal Aortic Aneurysm

One of the cornerstones of the successful man-
agement of the elective AAA is adequate preop-
erative preparation. An extensive patient history
and full examination should be performed,
followed by a set of basic investigations for all
patients. These measures should aid the deci-
sion of whether or not operative intervention
is appropriate and may uncover any subclinical
pathologies that can be corrected, or at least
optimized prior to surgery. We consider the
required analysis as of two distinct types, exam-
ining both general health status with quality of
life and also aneurysm-specific factors.

General Health Status

After initial assessment of an apparently med-
ically fit patient, it is essential to gain an appre-
ciation of that person's quality of life. This loose
term is difficult to define but encapsulates all
aspects of the patient's daily living, involving

not only physical status but mental and social
aspects also. Operation for AAA should both
prolong and preserve quality of life. Due to the
nature of the disease, it is unlikely that AAA
repair will lead to any physical improvement in
the preoperative condition with the risk of a
drastic deterioration in health. On the other
hand, for many, quality of life is still vastly
improved by elimination of the cause of much
psychological torment that was the "time bomb"
ticking in their abdomen. There is little doubt
that issues pertaining to a subject's quality of life
can raise difficult and emotive questions. The
astute clinician should enlist help with manage-
ment decisions from not only the patient but
also the family, nursing staff, and caregivers.

Basic laboratory investigations to be per-
formed on all patients considered for AAA
surgery include a full blood count, erythrocyte
sedimentation rate (ESR), blood glucose, serum
urea, and electrolytes. Hematological disorders
and anemia may well be uncovered at this stage,
prompting further investigation before surgery.
An elevated ESR might be the only indicator of
an inflammatory AAA or even reflect ongoing
chronic infection or inflammation elsewhere.
Hyperglycemia may expose the unknown dia-
betic and has implications for both peri- and
postoperative patient care. Silent renal or
endocrine dysfunction is suggested with abnor-
mal urea and electrolyte values, and these would
necessitate further investigation and optimiza-
tion before surgery.

In addition to these tests a 12-lead electro-
cardiogram (ECG), chest x-ray, arterial blood
gas analysis, and pulmonary function tests
should be performed. These reflect the impor-
tance of adequate cardiorespiratory reserve
on the successful outcome of AAA surgery.
Depending on the results obtained, it may well
be the case that further investigations such as an
exercise ECG, echocardiography, and even coro-
nary angiography should be performed before
surgery. The presence of significant cardiac
disease may indeed require significant inter-
vention such as angioplasty, stenting, or even
bypass grafting before the patient is considered
fit enough elective AAA repair.

Aneurysm-Specific Factors

It is most likely that by this stage an ultrasound
scan will have been performed confirming the

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ANEURYSMAL DISEASE

presence of an AAA. Unless contraindicated, the
aneurysm should now be imaged by means of
CT scanning for accurate sizing, proximal and
distal extension, relationships to other abdomi-
nal vasculature, and possibly an assessment for
endovascular stenting. In those patients where
CT scanning is not an option, MRI offers an
alternative method of gaining the required pre-
operative information.

In the majority of cases, this constitutes all
that is required radiologically to appropriate
plan operative intervention. However, in
juxtarenal or suprarenal aneurysms, or patients
with peripheral vascular disease or aneurysmal
disease elsewhere, angiography should be
considered.

Operative Management
of the Elective Abdominal
Aortic Aneurysm

Assuming the patient workup is completed and
the patient is suitably optimized, elective AAA
repair can now be attempted. Broadly speaking,
there are two techniques used for aneurysm
repair, and consideration will be given to each
in turn.

Open Repair of Elective Abdominal
Aortic Aneurysm

It is now over half a century since the first
reported successful open repair of an AAA, and
the technique remains well established today.
Informed patient consent for the procedure is
obtained and adequate (8 to 10 units) type-
specific blood is cross-matched before surgery.
Invasive monitoring is mandatory in AAA
repair, requiring insertion of a urinary catheter
and also arterial and central venous cannula-
tion. A nasogastric tube is inserted for stomach
decompression, and the anesthetist may decide
to float a pulmonary artery catheter (Swan-
Ganz) in those patients with significant cardiac
disease. It is at this stage that an epidural
catheter maybe inserted to minimize postoper-
ative pain. A single bolus dose of a wide-
spectrum antibiotic (e.g., cefuroxime 1.5 g) is
usually given to reduce the risk of prosthetic
graft infection and this dose maybe repeated in
long operative procedures. The general anes-
thetic is administered and the airway is secured

by endotracheal intubation so that artificial ven-
tilation can commence. Once the vascular anes-
thetist is satisfied, the stable patient is then
transferred into the main operating room.

Elective AAA repair may proceed by either a
transabdominal or retroperitoneal approach as
long as adequate exposure to gain proximal and
distal control is achieved. The patient is thus
appropriately positioned, draped, and prepped.
A relative indication for retroperitoneal access
is the case of a "hostile" abdomen either due to
adhesions from a previous laparotomy or the
presence of an abdominal wall stoma. In the
majority of elective repairs, however, it is a stan-
dard transperitoneal approach that is preferred.
Laparotomy is performed by standard full-
length midline incision offering a generous
exposure, although some surgeons advocate a
transverse incision in cases with no iliac
aneurysmal involvement. Advantages of the
latter are a better cosmesis and a decreased inci-
dence of respiratory complications postopera-
tively as a result of reduced wound pain.
Long-term wound disorders, however, are seen
more frequently with a transverse incision.

Following skin incision the peritoneum is
divided from a point just left to the base of the
small bowel mesentery extending distally as far
as the iliac artery. A self-retaining retractor is
then positioned so that the surgeon has ade-
quate exposure of the aneurysm, with the small
bowel usually "stored" in a sterile bag for pro-
tection and facilitation of access. The neck of the
aneurysm is dissected free followed by each of
the iliac arteries prior to application of vascular
clamps. Intravenous heparin is given just before
aortic cross-clamping in order to reduce the risk
of thrombotic complications, and this dose may
be repeated in prolonged procedures.

After allowing enough time for systemic anti-
coagulation, the clamps are applied in a manner
so that the possibility of distal complications are
minimized. In practice this requires clamping of
the least-diseased vessels first, taking care to
avoid vessel damage and mural plaque disrup-
tion. The proximal clamp should be as close to
the renal arteries as possible so that the resid-
ual native infrarenal aortic segment is minimal,
therefore limiting the risk of subsequent
aneurysmal recurrence. Once proximal and
distal control has been achieved, the sac of the
aneurysm is incised longitudinally along its
anterior surface, taking care not to damage the

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inferior mesenteric artery (IMA) that arises just
to the left of midline from the aorta. Problem-
atic bleeding may be encountered at this stage
from patent lumbar arteries, and these are over-
sewn by vascular sutures. Back-bleeding from
the IMA should be temporarily controlled with
a small vascular clamp (e.g., bulldog clamp)
during aneurysm repair, and the need for pos-
sible reimplantation should be assessed later in
the operation.

An appraisal can now be made regarding the
type of graft to be used and appropriate sizing
performed. In 60% of cases a straight "tube"
synthetic inlay graft may be used, requiring
aorto-aortic anastomosis. The remainder of
cases require a bifurcated graft due to either
iliac extension of aneurysmal disease or con-
comitant occlusive pathology. In this situation
the distal anastomosis should be performed into
a normal vessel, distal to the affected artery. This
usually requires iliac anastomosis, but if there
is extensive iliac artery disease or technical
difficulties, a femoral anastomosis must be con-
sidered. It should be remembered in the latter
scenario that the patient will be at an increased
risk of infection and false aneurysm formation
as a result of opening the groin. The graft is
sutured with 2-0 or 3-0 nonabsorbable stitches,
ensuring to take deep-enough bites in the prox-
imal anastomosis for adequate strength. In cases
of friable aortic tissue, the surgeon may wish to
consider the use of pledgets in the suture line in
order to reinforce the anastomosis. Integrity
of the proximal anastomosis is confirmed by
careful release of the proximal clamp against
resistance offered by prior application of a
clamp across the graft. Minimal bleeding sug-
gests successful anastomosis, and the proximal
clamp is reapplied to its original position so
that attention can now be given to the run-off
vessel(s).

Distal anastomosis should be to the appro-
priate vessel as outlined earlier, with the aim to
preserve at least internal iliac artery for mainte-
nance for colonic and neural blood supply. After
completion of the first iliac (or distal aortic)
anastomosis, blood flow into the supplied limb
should be restored after confirmation of anas-
tomotic integrity. Close lesion with the anes-
thetic team is required at this stage, and release
of the distal clamp should be very gradual.
Sudden clamp release could lead to precipitous
falls in blood pressure ("declamping hypoten-

sion") as a result of rapid volume redistribution
into the large dilated distal ischemic vascular
beds. This phenomenon is further exaggerated
by systemic release of accumulated vasoactive
metabolites from the clamped limb, and there-
fore timely intravenous fluid "loading" is neces-
sary following surgical alert before clamp
release.

With the graft in situ and hemostasis
ensured, attention returns to the IMA. In the
majority of cases the IMA maybe simply ligated
with a vascular suture. This practice, however,
requires at least one patent internal iliac artery,
a disease-free superior mesenteric artery, pink
healthy large bowel, and finally good back-
bleeding on release of the bulldog clamp. If
these criteria are not met or colonic perfusion
appears suboptimal at the end of the procedure,
the IMA may have to be reimplanted into the
graft by means of a Carrel patch.

Assuming IMA reimplantation is not neces-
sary, the native aneurysm sac is closed over the
graft and loosely sutured, providing physical
graft protection from other intraabdominal
structures. The bowel is released from the tem-
porary storage bag and a final examination is
made to ensure adequate organ perfusion and
also to allow correction of any iatrogenic injury.
The patient's limbs are also assessed to ensure
adequate distal perfusion and exclude immedi-
ate graft thrombosis or embolism that would
require prompt surgical correction. The self-
retaining retractor is removed and the abdomen
closed in routine fashion.

Following the operation the patient should be
transferred to an intensive care or high depend-
ency unit for close monitoring. Return to the
ward is usually possible the following day if
there have been no complications.

Discharge following elective AAA repair is
variable but can be expected at between 7 and
14 days depending on preoperative comorbidity,
operative difficulty, patient determination, and
postoperative complications.

Complications Following Open
Abdominal Aortic Aneurysm Repair

Despite extensive preoperative workup and
improvements in anesthesia and surgical tech-
nique, complications following elective open
repair of AAA still occur. All possible measures

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ANEURYSMAL DISEASE

must be taken to minimize them, as often mor-
bidity following aneurysm repair can translate
to mortality. An acceptable mortality rate of less
than 5% justifies prophylactic AAA repair in
appropriate aneurysms as compared to the risk
of rupture and subsequent near- 100% mortality
with a conservative approach. The nonfatal
complications are considered as early or late.

Early Complications

Cardiorespiratory

Cardiorespiratory complications account for
25% to 30% of all morbidity following elective
open AAA repair. The majority of cardiac
ischemic events take place in the initial 48 hours
postoperatively, myocardial infarcts accounting
for a third of these. Measures that can be taken
by the surgical team to reduce the incidence of
these complications include appropriate fluid
management to optimize preload and reduce
myocardial stress, administration of oxygen
therapy, and adequate postoperative pain relief.
Chest infections complicate approximately 5%
of AAA repairs and can be minimized by appro-
priate analgesia without sedation, chest physio-
therapy, and early mobilization.

Hemorrhage

Problematic hemorrhage intraoperatively is
usually due to bleeding from the proximal
suture line or inadvertent iatrogenic vessel
injury. The renal and iliac veins are particularly
susceptible to damage during initial exposure,
and all attempts should be made to address this
before proceeding to aneurysm repair. Difficult
dissections in freeing the iliac arteries for
clamping are probably best managed with intra-
luminal balloon occlusion rather than poten-
tially hazardous clamp application.

Generalized postoperative hemorrhage is
most often due to an acquired coagulopathy
rather than a direct consequence of surgery.
Massive transfusion and hypothermia lead to
clotting factor deficiencies, low platelet counts,
an impaired coagulation cascade, and altered
platelet function. Appropriate blood product
and platelet transfusion with rewarming is nec-
essary to reverse these problems and should be
guided by serial laboratory coagulation studies
and hematology advice.

Renal

Impaired renal function post open AAA repair
accounts for 5% to 12% of all early complica-
tions, and of these nearly half require renal
replacement therapy with dialysis. These figures
reflect a substantial decrease in the incidence
of renal morbidity and are attributed to the
improvements made in its pre- and periopera-
tive management. Advancing knowledge and
understanding of radiological contrast-induced
nephrotoxicity has led surgeons to defer surgery
following such investigations in order to allow
renal recovery. Current perioperative fluid
management regimes that are guided by sensi-
tive invasive indicators of circulating volume
(e.g., Central Venous Pressure (CVP) lines) have
also improved the perioperative maintenance of
a normal cardiac output and renal blood flow.
The exact cause of renal failure despite these
measures after AAA repair remains unknown. It
is highly probable that the damage is a conse-
quence of debris embolizing from the diseased
aortic wall that is dislodged during proximal
aortic cross-clamping. Meticulous preoperative
image analysis may highlight this potential
complication before surgery and thus allowing
modification of the surgical technique.

Patients presenting for elective open AAA
repair with known renal impairment are at the
greatest risk of postoperative renal failure.
Administration of renoprotective agents such as
mannitol, frusemide, or dopexamine in these
patients may limit this risk, but substantial evi-
dence for this is lacking.

Limb Ischemia

Limb ischemia attributable to AAA surgery is
seen in 1% to 4% of cases. This is due to
either distal embolization of debris from the
aneurysm sac or more rarely graft thrombosis.
The microemboli released following AAA repair
are usually too small for surgical intervention to
be warranted, triggering a variety of limb symp-
toms such as persistent pain, cold, and blue toes.
Rarely, larger emboli may cause postoperative
problems, and in this situation operative explo-
ration is mandatory.

Gastrointestinal

A degree of intestinal dysmotility after laparo-
tomy ("ileus") is very common and usually

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VASCULAR SURGERY

settles with bowel rest and fluid management.
Removal of the nasogastric tube should not
be too premature, and reintroduction of a
normal diet must not occur until there is objec-
tive evidence of returning bowel function (e.g.,
flatus).

The most severe gastrointestinal following
open AAA surgery is colonic ischemia. This con-
dition, fortunately, occurs much less often then
ileus, in about 1% of open AAA repair. The
cause of this potentially fatal complication is
explained by inadequate colonic perfusion via
the IMA or internal iliac artery. It may occur
due to inappropriate IMA ligation (see earlier),
inadvertent collateral vessel damage during
IMA ligation distant from its origin, or internal
iliac artery thrombosis or embolism. Sinister
postoperative symptoms include bloody diar-
rhea, left iliac fossa pain, and an explained high
intravenous fluid requirement.

In cases of colonic ischemia, urgent
colonoscopy is indicated, and management is
dependent on the findings. Patchy areas of
partial bowel wall ischemia and sloughing may
well settle with conservative bowel rest and
intravenous antibiotics. Severe bowel ischemia,
which is evident as a full-thickness infarction,
requires urgent resection of the affected colon
with end-colostomy

Venous Thromboembolism

The incidence of deep venous thrombosis
(DVT) and pulmonary embolism following
open AAA surgery is less than is seen with other
general surgical operations. This is probably
explained by the intraoperative heparin antico-
agulation administered during surgery. Never-
theless, DVT still occurs in 8% of patients,
and that risk should be addressed with sub-
cutaneous prophylactic low-molecular-weight
heparin, compression stockings, and early
patient mobilization where appropriate.

Neurological

The most devastating and feared complication
after open AAA repair is that of paraplegia. For-
tunately, this is a rare event in infrarenal surgery
as compared to thoracoabdominal aneurysm
repair. It results following ligation of an abnor-
mally low accessory spinal artery (of
Adamkiewicz), which is usually found in a

descending thoracic or upper abdominal aorta.
Interruption of spinal blood flow through col-
lateral vessels by compromising internal iliac
artery perfusion may also result in paraplegia,
but this is more frequently seen in conjunction
with systemic hypotension as experienced
during ruptured AAA.

Careless dissection may damage the impor-
tant autonomic neural pathways found on the
left side of the infrarenal aorta. The true inci-
dence of impotence and retrograde ejaculation
after elective AAA surgery is unknown, but may
approach 20%.

Late Complications

Delayed complications arising from open AAA
surgery are infrequent and can be classified as
graft or wound related.

Graft-related late complications include false
aneurysms (0.2% to 1.2% at 3 years) due to
anastomotic disruption, graft infection, and
aortoenteric fistulas. Data suggest that the com-
bined likelihood of infection or fistula at 10
years is approximately 5% and is much more
likely if a femoral anastomosis is used.

Long-term wound disorders such as poor
cosmesis requiring revision or hernia depend
on both surgical technique and perioperative
factors such as wound infection, nutritional
status, diabetic management, etc. Surgical atten-
tion is not required in the vast majority of cases,
and each presentation should be assessed indi-
vidually on its merits.

Endovascular Repair of Abdominal
Aortic Aneurysm

The first successful treatment of an AAA by
transfemoral endoluminal repair was reported
over a decade ago. Since that time, advances in
endovascular surgery coupled with a greater
experience and understanding of this technique
has led to possibly a viable alternative to open
repair in aneurysm management (Woodburn et
al., 1998). The basic principle of endovascular
management is the exclusion of the AAA from
the systemic circulation by means of a pre-
operatively sized deployed stent graft, thus
preventing further aneurysm expansion
and elimination of the rupture risk. For this
to be achieved, a self-expanding or balloon-

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ANEURYSMAL DISEASE

expandable device is advanced into the abdom-
inal aorta to be released at a position so that
the seal is generated both proximal and distal to
the aneurysmal segment. Depending on the type
of repair, the procedure may or may not require
a combined surgical bypass for successful
treatment.

Suitability for endovascular intervention
depends on extensive preoperative investigation
of aneurysm morphology, and the limitations of
currently available stent graft devices mean that
this approach is not an option in all elective or
ruptured cases. At present, about 50% to 60% of
all elective AAAs could potentially be considered
for stenting,but this figure is extremely variable
as much debate continues regarding the exclu-
sion criteria for the procedure. With current
devices it is generally agreed that the most
important morphological features in assessing
aneurysms' suitability for stenting are as follows:
an adequate length (>15mm) of infrarenal
aneurysm neck with a maximal neck diameter
of 30 mm to ensure a good proximal seal; limited
vessel tortuosity, defined as vessel angulation
(60 degrees at the neck of the aneurysm and 90
degrees at the iliac arteries); and iliac arteries of
sufficient caliber (>7 to 9mm) to tolerate the
passage of the graft as it is admitted into the
infrarenal aorta. Features that are severe as rel-
ative contraindications to the procedure include
short (<25mm) and wide (>14mm) common
iliac arteries and the presence of mural throm-
bus in the aneurysmal sac. Funnel-shaped necks
and excessive calcification are absolute con-
traindications to endovascular repair.

The exciting advances in this arena offer a less
invasive approach to AAA management so that
some patients considered unfit for open surgery
may well be candidates for endoluminal repair.
Results of endovascular intervention as com-
pared to open repair are currently being
assessed with prospective trials such as the
ongoing Endovascular Arterial Reconstruction
(EVAR) project. At this stage it would appear
that endovascular repair offers mortality and
morbidity rates similar to those of open surgery,
but stenting has the advantage of a markedly
reduced length of total in-hospital stay and
diminished requirement for intensive care and
high dependency support. The financial advan-
tage of this, however, is offset by the major draw-
back of this approach, which is the cost of the
stent graft itself.

Type of Endovascular Procedure

Three distinct endovascular prostheses are cur-
rently available for AAA repair. All the manu-
factured devices form the proximal seal in the
infrarenal aortic segment, but differences exist
in the location of their distal "landing site." The
aorto-aortic straight graft resides entirely in the
abdominal aorta but is only suitable in 5% of
cases amenable to endovascular repair. Bifur-
cated stents can be used in 30% of patients, with
the distal seals formed in the iliac vessels. The
remainder (65%) of suitable aneurysms may be
repaired with aorto-uniiliac stent graft devices.
This latter method requires a combined surgi-
cal crossover procedure (usually femoro-
femoral) for maintenance of contralateral lower
limb blood supply following radiological
embolization or surgical occlusion of the non-
graft common iliac artery.

Perioperative Management

The patient should be assessed and prepared for
endoluminal intervention as discussed earlier
for open repair. Adequate appropriate radiol-
ogical imaging should be obtained to enable
calibration of both aneurysm and related
vasculature for graft sizing. Informed consent
should include the known specific complica-
tions associated with endovascular repair and
also mention the possibility of conversion to
open surgery if necessary. The operating room
should be equipped with a C-arm or equivalent
for intraoperative imaging, and adjunctive input
is required from both the resident surgical and
interventional radiology team.

After anesthesia induction, the patient is
appropriately positioned, prepped, and draped.
The procedure commences by surgical cut-
down to the femoral artery to gain access to the
arterial circulation. The device is admitted
through the exposed artery and advanced prox-
imally under radiological control until deploy-
ment of the appropriate site for aneurysm
exclusion. Correct graft position and the
absence of endoleak is confirmed by on-table
angiography, and the groin is closed in a routine
fashion unless a surgical crossover graft is to be
performed. At the end of the procedure, the
lower limbs should be assessed for evidence of
graft thrombosis or embolism before transfer to
the recovery area. The patient can be mobilized

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VASCULAR SURGERY

gently the day after surgery, and discharge can
be expected at 5 to 7 days in uncomplicated
cases with a satisfactory early postoperative CT
scan. Follow-up guidelines currently advise 6-
month CT and plain lumbar spine imaging in
the first year and then annually thereafter.

Complications of Endovascular Abdominal
Aortic Aneurysm Repair

Endovascular AAA repair unfortunately carries
with it a distinct spectrum of specific complica-
tions in addition to "routine" causes of postop-
erative morbidity.

Iatrogenic Vessel Injury

The introduction of guidewires, large-bore
catheters, and a stent graft poses the risk of arte-
rial and proximal vessel injury such as rupture
or dissection. Delayed manifestations of iatro-
genic vessel damage may present later, with the
development of a false aneurysm at the cannu-
lation site, and requires prompt surgical repair.

Endoleak

Endoleak refers to the persistence of arterial
flow of blood into the "excluded" aneurysm sac
but outside the lumen of the deployed stent
graft. It represents one or more of the following
processes: incomplete sealing of the proximal or
distal landing sites (type I); continued blood
flow into the sac by collateral and lumbar vessels
(type II); an incomplete seal at junctions of
overlapping graft components or ruptured graft
fabric (type III); or leakage of blood through a
porous graft membrane (type IV). The inci-
dence of endoleak is approximately 20% and
may be further classified as immediate, early,
or late. Without treatment, the aneurysm may
continue to expand, thus carrying the risk of
rupture, although most cases seal spontaneously
with thrombosis. Bearing this in mind, the
majority of vascular surgeons initially manage
an endoleak with simple observation. If, after a
prescribed time period, the endoleak persists or
rapid aneurysm expansion is observed, further
interventions such as endoluminal graft exten-
sion deployment, band ligation of the aortic
aneurysmal neck, or even open repair may be
indicated.

Embolization

Endoluminal stent graft deployment carries
the risk of distal embolization of debris from
the aneurysmal sac. This is particularly true in
cases of extensive mural thrombosis, and there-
fore the benefits of endovascular repair should
be questioned in these circumstances. Shower-
ing of microemboli may result in renal failure
and leg ischemia requiring amputation.

Graft Migration, Dislocation,
and Displacement

Long-term follow-up of endoluminal stenting
has shown that the stent devices may migrate,
resulting in endoleak, dislocating, and jeopard-
izing the seal and kink, with potential thrombo-
sis. The advent of second-generation devices has
attempted to address these problems with rein-
forcement of graft struts and the introduction
of suprarenal uncovered fixation.

Postimplant Syndrome

Well described in the literature, postimplant
syndrome refers to the presence of early back
pain and fever without leukocytosis following
endoluminal AAA repair. It lasts for up to 1 week
after insertion. The condition is self-limiting
and is managed conservatively.

Conversion to Open Repair

Failure of endovascular management of AAA
may require conversion to open repair, occur-
ring in 2% of cases. Indications for such
measures include aortic rupture during a
primary stenting procedure, persistent endoleak
with failed secondary intervention, and graft
infection.

Ruptured Abdominal
Aortic Aneurysms

Ruptured aortic aneurysms are uniformly fatal
without operative intervention, explaining the
emphasis of AAA management of early detec-
tion and elective repair. Unfortunately, the vast
improvements in outcome following elective
AAA repair have not simultaneously been wit-
nessed in the emergency situation, and opera-

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ANEURYSMAL DISEASE

tive mortality under these circumstances has
remained static over the last 20 years at between
40% and 70%. Even this estimation can be con-
sidered conservative, as the figure does not take
into account community prehospital deaths,
and therefore an overall mortality following
AAA rupture is probably in the region of 80%
to 90%.

The exact process that triggers rupture of
an AAA remains unknown. Several factors
(discussed earlier) are known to suggest an
increased likelihood of rupture and the most
important of these is aneurysm size.

Clinical Presentation

A high index of suspicion is paramount in
clinching the diagnosis. Any patient with a
known AAA who presents with sudden severe
abdominal or back pain has a ruptured
aneurysm until proven otherwise. The difficulty
arises in atypical presentations of patients with
unknown aneurysmal disease leading to detri-
mental delays in surgical management. Rup-
tured AAA should feature in the differential
diagnosis of any patient who presents with
unexplained hypertension, severe abdominal
pain, or cardiac arrest with no prior history of
myocardial disease or trauma.

Clinical symptoms of rupture are varied, but
classically comprise sudden back or abdominal
pain with an episode of collapse, fainting, and
maybe nausea. Examination reveals a pulsatile
mass on abdominal palpation that may or may
not be tender. The patient may be pale, irritable,
clammy, tachycardic, and hypotensive. Mainte-
nance of a normal blood pressure may indicate
a contained rupture, affording the clinician time
to confirm the diagnosis with appropriate
imaging prior to surgery. This luxury is not
offered in an uncontained ruptured AAA when
the patient should be taken to the operating
room for operative repair without delay.

Operative Repair of a Ruptured Abdominal
Aortic Aneurysm

Perioperative management is aimed at stabiliz-
ing the precarious hemodynamic status of the
patient. After an initial brief history and exam-
ination, venous access should be secured with
at least two large-bore cannulae and blood

samples withdrawn for biochemistry, hematol-
ogy, and urgent crossmatch (at least 10 units) of
packed red cells and blood products.

Arguments persist regarding the optimal goal
of fluid resuscitation in cases of ruptured AAA.
It has been suggested that overzealous fluid
management runs the risk of a sudden increase
in blood pressure and hence converting a con-
tained leak into a frank rupture. Management
strategies should aim to keep a systolic blood
pressure of 90 mm Hg by infusion of intra-
venous fluids until operative repair can be per-
formed. Patient response should be assessed
with continuous hemodynamic monitoring and
a urinary catheter inserted. Early involvement of
both the surgical and anesthetic team is desir-
able in order to optimize patient status and min-
imize operative delay.

In some stable presentations of suspected
AAA rupture, radiological imaging may be per-
formed to confirm the diagnosis and delineate
aneurysmal anatomy. The investigation of
choice remains CT scanning. Ultrasound is of
little benefit due to its inability to reliably dis-
tinguish a ruptured AAA.

Operative management for leaking AAA is by
open repair by midline laparotomy. Although
some centers have reported encouraging results,
endovascular management currently plays little
role in the management of ruptured AAA.
Surgery should be expedient, performed by the
most senior available member of the vascular
team. Following incision, brisk but careful dis-
section should proceed with placement of the
clamp in the infrarenal aorta, avoiding damage
to the left renal vein. Temporary supraceliac
clamping maybe performed to initially control
problematic bleeding and facilitate dissection
for later re-siting in the infrarenal aortic
segment. In extreme circumstances, the sur-
geon's fingers or an intra-aortic balloon maybe
used to gain proximal control. Intravenous
antibiotics should be administered to limit graft
infection, but unlike in elective cases, intra-
venous heparin is not routinely given. Once the
aorta is cross-clamped, the operation is then
performed as is described for elective AAA.

Outcome Following Repair of a Ruptured
Abdominal Aortic Aneurysm

Significant postoperative morbidity following
repair of ruptured AAA occurs in 50% to 70%

206

VASCULAR SURGERY

of cases (Heller et al., 2000). This figure repre-
sents both suboptimal patient preparation for
major surgery and the sequelae of prolonged
hypotension experience pending operative
repair. Cardiorespiratory disorders and renal
impairment are the most commonly encoun-
tered complications, closely followed by
ischemic colitis. The latter condition carries a
subsequent mortality of 25% and results from
gut hypoperfusion secondary to aneurysm
rupture. The clinician should anticipate its
diagnosis.

Assuming operative survival, patients with a
ruptured AAA enjoy a long-term prognosis as
governed by their other comorbidities. Repair
has not been shown to diminish the patient's
quality of life postoperatively, and no different
exists in outcome should the aneurysm have
been repaired electively

Inflammatory Abdominal
Aortic Aneurysms

An important subdivision of infrarenal aortic
aneurysmal disease is the inflammatory aortic
aneurysm (Rasmussen and Hallett, 1997).
Inflammatory AAAs were not classified per se
until the early 1970s, and even today their
nature in terms of being a distinct clinical and
pathological entity is still disputed.

Definition of the inflammatory AAA depends
on the presence of a triad of factors: a thickened
aneurysmal wall, marked perianeurysmal/
retroperitoneal fibrosis, and dense adhesions
involving adjacent abdominal viscera to the
aneurysm. These aneurysms comprise 5% to
10% of all AAAs, and the typical patient is a
male in his sixth decade. Females are rarely
affected by the disease (male-to-female ratio of
20 : 1). Interestingly, the average age at diagnosis
is about 10 years younger than those patients
presenting with noninflammatory aortic
aneurysms. Postulated risk factors that are
specific for the development of inflammatory
AAA include cigarette smoking and a genetic
predisposition.

There is currently much debate regarding the
etiology and pathogenesis of the inflammatory
AAA. Until recently, it was generally upheld that
these aneurysms were of a distinct exclusive
nature and therefore to be considered different
from their noninflammatory counterpart. This

belief is now being challenged. An early hypoth-
esis suggesting the periaortic fibrosis was sec-
ondary to retroperitoneal blood leakage from
tiny perforations in a previously noninflamma-
tory aneurysm has been rejected. Similarly,
other theories of an initial prodromal athero-
sclerotic AAA developing into an aneurysm of
inflammatory type remain unproven. The sug-
gested mechanism for this transformation is by
either lymphatic vessel compression by the
expanding aneurysm resulting in stasis, edema
and subsequent fibrosis, or as a direct conse-
quence of an inflammatory reaction between
blood in the aneurysmal sac and the aortic
wall. Viral infection with herpes simplex or
cytomegalovirus has also been proposed as a
causal factor, with evidence of their presence
in the aortic wall proven by DNA polymerase
reactions.

A more convincing theory regarding inflam-
matory AAA development is that it is the result
of a specific inflammatory process. This process
is responsible for both inflammatory and
noninflammatory AAAs, and thus we are not
to consider the two pathologies as distinct
pathological entities; rather, the former is an
"inflammatory variant" of the latter. There
seems to be good evidence for this theory.
Initially, histological analysis revealed the
presence of a chronic inflammatory infiltrate
present in the walls of inflammatory and
noninflammatory aortic aneurysms, with the
only difference being an augmented level of
inflammatory response in the putative inflam-
matory AAA. This finding was then supported
by serial observations of a progressive inflam-
matory response from the initial atherosclerotic
to the inflammatory AAA proven both under
the microscope and radiologically It is sug-
gested that there is a primary inflammatory
reaction to an antigen present in the aortic wall
whereby there is gradual infiltration of B lym-
phocytes, T lymphocytes, and macrophages.
Subsequent cytokine production from the
infiltrate triggers a proteolytic cascade with
increased turnover of MMPs, elastin, and colla-
gen. With time the aortic wall begins to degrade,
losing tensile strength, and the aneurysm
begins to develop. It is proposed that this
inflammatory response is accentuated further
in smokers and those with a genetic pre-
disposition, explaining an earlier presentation
of aneurysmal disease.

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ANEURYSMAL DISEASE

Clinical Features

The inflammatory AAA is typically sympto-
matic with only 20% cases being discovered
incidentally. Classically, the presence of abdom-
inal or back pain, weight loss, and an elevated
ESR in patients with a known AAA confers
a diagnosis of inflammatory aneurysm until
proven otherwise. Clinical examination may
reveal a pulsatile mass on abdominal palpation
and generalized evidence of weight loss. Specific
blood tests to be taken if an inflammatory AAA
is suspected are an ESR, which will be raised in
70% cases signifying the acute phase response,
and less reliably a white cell count. Serum elec-
trolytes and creatinine should also be taken to
look for evidence of obstructive uropathy and
associated chronic renal failure (10% to 20% of
patients).

Diagnosis

Despite symptomatology and available labora-
tory investigations, the inflammatory AAA still
tends to be a diagnosis that is made at opera-
tion. Preoperative CT scanning can sensitively
detect aneurysm wall thickening and peri-
aneurysmal fibrosis but depends on the radiol-
ogist's awareness to make the diagnosis.
Although ultrasound remains useful in routine
AAA surveillance, it is less helpful than CT in
distinguishing the inflammatory variant. If
there is any suspicion of ureteric involvement by
the retroperitoneal fibrosis, an intravenous pyel-
ogram should be requested.

Management

Although inflammatory aneurysms are usually
larger than their atherosclerotic counterpart, it
is generally accepted that the risk of rupture is
lower. Presumably this is due to the paradoxical
strengthening of the periaortic tissue by fibrotic
change. Some clinicians advocate administra-
tion of oral corticosteroids in an effort to atten-
uate the inflammatory aneurysmal response,
but there is no evidence to support this. In fact
there is a body of opinion that suggest steroid
therapy may actually increase the risk of
inflammatory AAA rupture by a reduction in
the protective fibrosis. Ultimately, surgery
remains the treatment of choice for inflamma-
tory AAA.

Surgical Intervention for Inflammatory
Aortic Aneurysms

At laparotomy the inflammatory AAA is easily
recognized with its thickened aortic wall and
shiny, smooth white appearance. There is
periaortic and retroperitoneal change with
adhesions invariably involving the duodenum
and less commonly the inferior vena cava and
left renal vein. Disease affecting the ureters
occurs in 20% to 40% of cases, which may neces-
sitate a team approach with both the vascular
surgeon and urologist.

Aneurysm repair should proceed with as
little dissection as possible. The propensity of
these aneurysms to bleed compounded by the
high risk of iatrogenic damage to neighboring
structures poses potentially high surgical mor-
bidity. Early inflammatory AAA surgery with
futile attempts at periaortic adhesiolysis were
complicated by needless duodenal enterotomies
and inadvertent venous and ureteric injury, and
this approach to repair has now been discarded.
The method of surgical repair is otherwise
as previously described for noninflammatory
infrarenal AAAs, and operative mortality rates
for elective inflammatory AAA repair should be
comparable (3% to 4%).Ureterolysis at the time
of AAA repair remains a controversial issue.
Over half of inflammatory AAAs demonstrate
ureteric involvement on preoperative CT scan-
ning. We advise that such ureteric surgery be
reserved for those exhibiting signs or symptoms
of obstruction or proven incipient uropathy on
preoperative investigation. Early consultation
with the urology team is advisable in these
circumstances.

Thoracoabdominal
Aortic Aneurysms

Aneurysmal diseases affecting both the abdom-
inal and thoracic aorta are known collectively as
thoracoabdominal aortic aneurysms (TAAAs).
In clinical practice these essentially refer to
aneurysms arising above the celiac axis. Previ-
ously considered as quite a rare condition,
recent advances in clinical diagnostic capability
by methods such as angiography, CT, and MRI
suggest that these aneurysms in fact account for
up to 10% of the aortic aneurysm population.
The management of these patients is complex

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VASCULAR SURGERY

and indeed may fall into the realm of both the
vascular and cardiothoracic surgeon. It is there-
fore suggested that these aneurysms are best
dealt with at a tertiary referral center with
appropriate expertise and not routinely at the
district general hospital.

Etiology

Atherosclerosis is the most commonly impli-
cated factor in the development of TAAA
disease. The classical fusiform aneurysm that
results is typically seen in men over the age of
50 years, usually with evidence of arterial
atherosclerotic pathology elsewhere. In fact,
over half of TAAA presentations are subse-
quently discovered to have coexistent aneurys-
mal disease at an alternative site including the
infrarenal aorta and femoral and popliteal
arteries. Other causal factors to be excluded are
thoracic dissection with secondary aneurysm
formation, cystic medial necrosis (e.g., Marfan
syndrome, Takayasu disease, trauma leading to
false aneurysm), and infection. Previously the
most common cause of this type of aneurysm,
syphilitic aortitis leading to the classical Craw-
ford type I (see later) saccular TAAA, has now
thankfully declined and is rarely seen nowadays
in non-Third World practice.

Clinical Features

Clinical presentation of TAAA can be catego-
rized as asymptomatic, symptomatic but not
ruptured, and ruptured.

Asymptomatic Thoracoabdominal
Aortic Aneurysm

The vast majority of TAAAs are without
symptoms. Unlike infrarenal and peripheral
aneurysms, it is also improbable that routine
clinical examination will yield the diagnosis. In
these patients it is the review of the chest radi-
ograph that initially arouses clinical suspicion
of TAAA, for further investigations to confirm.

Symptomatic Nonruptured
Thoracoabdominal Aortic Aneurysm

Symptomatic TAAAs usually result from local
pressure effects, and this most commonly man-

ifests as chest pain. The pain is central and radi-
ates through to the upper back, depending on
the neighboring anatomy (e.g., spinal nerves or
vertebral column erosion). Irritation of the
recurrent laryngeal nerve and bronchial struc-
tures may result in voice changes, stridor,
and dyspnea. Gradual unexplained orthopnea,
paroxysmal nocturnal dyspnea, and ankle
swelling all indicate a failing myocardium, and
this may be due to a compromised pulmonary
circulation by TAAA compression. Occasionally,
if the abdominal component of the TAAA is
large enough, the clinician or even the patient
may discover a pulsatile mass. Occult symptoms
of distal embolization should always arouse sus-
picion of an ongoing proximal aneurysmal
process, thus necessitating appropriate investi-
gation for exclusion of TAAA.

Ruptured Thoracoabdominal
Aortic Aneurysm

A TAAA rupture can be varied in its clinical
presentation. There is usually a history of acute
severe chest pain, and examination may reveal a
hemodynamically unstable patient requiring
vigorous resuscitation. The site of rupture
and possible involvement of other thoracic
structures govern other associated symptoms.
Massive hematemesis may result if rupture
occurs into the esophagus, whereas hemoptysis
and dyspnea suggests the possibility of rupture
into the tracheobronchial tree. Hemorrhage into
the pleural cavity or retroperitoneal space can
often result in a more delayed and profoundly
hypovolemic presentation.

Diagnosis

Examination of a standard chest radiograph
may reveal a widened mediastinum, loss of tho-
racic aorta outline, or a "mass" extending into
the left hemithorax. Calcification in the wall of
the aorta is seen in about one third of patients.
In cases of TAAA rupture into the pleural space,
evidence of a hemothorax should be seen.
Confirmation of the diagnosis is achieved by
spiral CT scanning, which usually gives all the
required preoperative information regarding
aneurysm size, visceral artery relation, and
proximal extent of aneurysm. Magnetic
resonance imaging techniques are equally

209

ANEURYSMAL DISEASE

instructive, but their availability and cost limits
their use. Unlike investigation of infrarenal
aneurysms, ultrasound for TAAAs offers unreli-
able and poor quality results; hence, it plays no
role in either radiographic diagnosis or surveil-
lance. Angiography is indicated only if CT scan-
ning does not give sufficient information
regarding relationships to visceral (especially
renal) arteries and for the evaluation of possi-
ble visceral artery stenoses.

Classification

Classification of thoracoabdominal aneurysms
is into one of four types as described by Craw-
ford:

Type I: Aneurysm involves the descend-
ing thoracic aorta as far as visceral
artery branches

Type II: Aneurysm extends from the aortic
arch, just distal to the left sub-
clavian artery as far as the aortic
bifurcation (involves visceral
arteries)

Type III: Aneurysm commences in the
midthoracic aorta and extends to
the aortic bifurcation

Type IV: Aneurysm starts at or just below
the diaphragm but above the renal
arteries and extends as far as the
aortic bifurcation

Of the four types, surgical repair is carried out
most often on type IV.

Management of Thoracoabdominal
Aortic Aneurysm

As in all surgery a balance must be struck
between the high morbidity and mortality of
operative repair, with a reported 5-year survival
of 20% in nonoperative management. Aneurys-
mal size is important, and as general rule,
asymptomatic aneurysms are not considered
for intervention unless maximal diameter
exceeds 6 cm. This threshold may be reduced in
saccular pathology due to the increased propen-
sity to rupture.

Extensive preoperative preparation is man-
datory in order both to exclude patients with
insufficient physiological reserve to survive
operation and to allow adequate planning of

proposed surgery. Required investigations are as
outlined in the workup for AAA repair, with an
emphasis on rigorous optimization of car-
diorespiratory and renal status.

Open Repair of Thoracoabdominal
Aortic Aneurysm

Following appropriate patient positioning,
draping, and skin preparation, a left-sided
thoracoabdominal incision is performed. In
high aneurysms (types I and II) some surgeons
advocate the use of extracorporeal circulation
with atriofemoral or femorofemoral cardiopul-
monary bypass to reduce the increased after-
load and left ventricular strain induced by
thoracic aorta cross-clamping. If this maneuver
is not performed, the requirement for expedient
surgery is further augmented. The thoracic and
abdominal aorta are dissected out to enable
proximal and distal control through nona-
neurysmal aortic (and possibly iliac) cross-
clamping. Under normal circumstances heparin
is not routinely given prior to clamp application
to avoid unacceptable blood loss. An appropri-
ately sized inlay prosthetic graft is introduced
after opening the aneurysmal sac, and the prox-
imal anastomosis is performed by continuous
Prolene suture end-to-end with the thoracic
aorta distal to the left subclavian artery. After
confirmation of proximal anastomosis integrity,
the visceral vessels (celiac axis, superior mesen-
teric, and renal arteries) are then reimplanted
into the graft with sequential clamping in order
to minimize organ ischemic time. Most high
intercostal arteries are oversewn, but those in
the region of T10 to L2 must be reimplanted for
preservation of spinal cord blood supply. After
verification of successful vessel anastomosis
with evidence of perfusion, the distal anasto-
mosis is formed at the level of the aortic bifur-
cation or iliac vessels. The aneurysm sac is
closed over the graft and the patient closed in
routine fashion. Postoperatively, the patient is
transferred to the intensive care unit for close
observation.

The nature of type I and type IV thoracoab-
dominal aneurysms may permit modifications
to the outlined surgical technique in operative
management. In certain low type IV aneurysms,
a "rooftop" abdominal incision can be used for
a total transabdominal access without the
need for thoracotomy. The abdominal aorta is

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VASCULAR SURGERY

approached retroperitoneally with mobilization
of the spleen, left kidney, and bowel to the con-
tralateral side. A vascular clamp can then be
applied to the suprarenal aorta to allow an
oblique proximal anastomosis to be performed,
incorporating a tongue of native aorta from
which the celiac axis and superior mesenteric
and renal arteries emerge. Once achieved, the
clamp is reapplied infrarenally to allow organ
perfusion following minimal ischemic time.
Certain type I aneurysms may be approached
with the need for thoracotomy only. In a similar
manner to type IV repair, the distal anastomo-
sis can be obliquely fashioned to incorporate a
reversed tongue of native vessel from which the
visceral arteries originate and so limit organ
ischemic time.

Perioperative spinal fluid drainage is sug-
gested as an adjunctive measure to lessen the
risk of neurological complication. The tech-
nique aims to optimize spinal cord perfusion by
enabling regulation of the increases in spinal
fluid pressure that result from aortic cross-
clamping. A fine-bore intrathecal catheter con-
nected to a pressure transducer is introduced
between the fourth and fifth lumbar vertebrae.
If a potentially deleterious rise in spinal fluid
pressure are observed, fluid drainage by a tap is
performed to correct it. The catheter is removed
once normal neurological function is confirmed
in the early postoperative period.

Endovascular Repair of Thoracoabdominal
Aortic Aneurysm

Endoluminal stent grafting may treat suitable
descending thoracic aneurysms without vis-
ceral artery involvement. The principles of graft
deployment were discussed earlier, with the
exception that the aneurysmal neck is ideally
situated at least 25 mm distal to the left subcla-
vian artery. More proximal pathology may still
be considered in the knowledge that compro-
mised upper limb perfusion due to subclavian
artery occlusion would require either operative
reimplantation into the carotid artery or a
carotid-subclavian bypass procedure.

Outcome of Thoracoabdominal
Aortic Aneurysm Repair

As with AAA repair, cardiorespiratory morbid-
ity remains the most frequently encountered

complications postoperatively. Renal failure
requiring replacement therapy with dialysis
occurs in 10% and is more likely in those with
preoperative renal dysfunction.

Postoperative paraplegia and paraparesis
remain the most feared legacy of thoracoab-
dominal aneurysmal surgery. In spite of the out-
lined operative measures to reduce this risk,
type I and II repairs are associated with a 15%
to 20% chance of paraplegia compared to 5% to
10% occurring after types III and IV surgery. In
general terms, higher thoracic aorta clamping
equates to an increased risk of paraplegia, and
this is supported by reported paraplegia rates
of<l% for low type IV repairs performed by a
total abdominal approach. Informed patient
consent must include detailed discussion with
respect to these risks prior to operative repair.
If paraplegia does result from surgery, the clini-
cian should make immediate referral to the local
spinal rehabilitation team for early physiother-
apy and patient support.

Mortality rates following TAAA repair are
variable. Assuming appropriate case selection
and sufficient surgical expertise, acceptable
operative mortality rates of 10% to 15% for
types I and II aneurysms and 5% to 8% for types
III and IV are observed. Attempted repair
of ruptured TAAA transmits inferior results,
and postoperative death rates are reported as
between 40% and 60%. If operative survival is
accomplished, the patients' long-term prognosis
is good and nearly two thirds of operated
patients are alive at 5 years.

Peripheral Arterial Aneurysms

Aneurysmal disease affecting the nonaortic
arterial vasculature may occur in isolation or
more commonly as part of a generalized
systemic arterial dilatation. It is for this reason
that a thorough examination of all susceptible
vessels should be performed after the
initial assessment of the presenting peripheral
aneurysm.

Popliteal Arterial Aneurysms

Popliteal aneurysms are the commonest
nonaortic aneurysms, accounting for 70% of all
diagnosed peripheral aneurysms (Dawson and
van Bockel, 1997). Defined as an external diam-

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ANEURYSMAL DISEASE

eter of one and a half to two times the normal
proximal vessel, the true prevalence and inci-
dence of the disease remains unknown. That
said, it is estimated currently that approximately
five patients present to a major vascular center
on an annual basis with such lesions. Males in
their sixth and seventh decades are most fre-
quently affected, and the aneurysms are bilat-
eral in around half of patients; 6% to 12% of
presentations have a coexistent AAA.

The majority of popliteal aneurysms are
associated primarily with atherosclerosis but
other etiologies include trauma, infection, and
popliteal artery entrapment syndrome. These
should always be considered, especially in the
younger patient. The aneurysms occur above
the knee joint and are either fusiform or saccu-
lar in nature. The beaded fusiform popliteal
aneurysms tend to be smaller (2- to 3-cm diam-
eter) than the saccular variety with diameters
reached of 4 to 6 cm.

Clinical Features

About one third of all popliteal aneurysms are
asymptomatic; the diagnosis is made only after
investigation of a lump in the popliteal fossa
found on a routine clinical examination. The
remaining two thirds are symptomatic and
reflect the complications of these aneurysms:
limb ischemia, rupture, or local pressure effects.

Limb ischemia remains the commonest pres-
entation and is due to either aneurysmal sac
thrombosis or distal embolization of intraa-
neurysmal clot. The emergence of ischemia
(acute or chronic) is dependent on the presence
of an established collateral circulation. In the
more frequent case of acute thrombosis, such a
circulation is usually poorly developed, and
presentation is typically that of acute severe
ischemia with threatened limb viability. Chronic
thrombosis of popliteal aneurysms affords more
time to the surgeon, resulting in one or more of
symptoms of claudication, rest pain, blue-toe
syndrome, or gangrene.

Local pressure effects of popliteal aneurysms
may cause edema by compression of the adja-
cent popliteal vein and even local or referred
pain by irritation of the neighboring sciatic
nerve or its derivatives. Rupture of popliteal
aneurysm is a rare presentation, necessitating
immediate surgical attention in order to pre-
serve the limb.

Diagnosis

The diagnosis of popliteal aneurysm should be
suspected if an exaggerated pulsation is discov-
ered on palpation behind the knee during clin-
ical examination. A firm pulseless mass in the
popliteal fossa may indicate a thrombosed
aneurysm, especially if an aneurysm is found on
examination of the contralateral limb. Further
information regarding the lump should then be
obtained by appropriate imaging.

Arterial duplex scanning is cheap, easily
available, and therefore ideal for diagnosis
confirmation, sizing, and subsequent popliteal
aneurysm surveillance. Arteriography is of less
use in the estimation of aneurysm size, but is
paramount in the assessment of the regional
vasculature for determination of planned surgi-
cal intervention. Computed tomograph and
MRI can offer detailed assessment of the
popliteal fossa contents and the nature of the
intravascular thrombus content, but their
expense and limited availability renders them of
little use in the management of the routine
popliteal aneurysm.

Management of Symptomatic
Popliteal Aneurysms

Acute Ischemia and Rupture

Presentation of a pale, pulseless, cold, and pares-
thetic leg signifies an immediate threat to limb
viability, and prompt intervention is needed to
avert primary amputation. There are a variety
of surgical procedures with adjuvant therapy
(thrombolysis) for repair, depending on the
aneurysm's size, embolic potential, and the
status of proximal and distal vessels.

Ideally, a preoperative angiogram should be
obtained and the patient taken for arterial recon-
struction without delay. The aim of surgery is
limb preservation and popliteal aneurysm exclu-
sion. After adequate exposure by either the
medial or the posterior approach (see later), the
aneurysm is excluded by means of ligation
and bypass grafting, inlay grafting, or resection
with primary anastomosis. There should be a
low threshold for performing an additional fas-
ciotomy as indicated by the individual clinical
picture.

Bypass grafting after proximal and distal
aneurysm ligation remains well established and

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VASCULAR SURGERY

is the usual technique employed. The conduit
may be prosthetic graft or preferably autoge-
nous saphenous vein if available. Improved
distal run-off can be achieved by the intra-
operative use of balloon-tipped embolectomy
catheters, and enhanced perfusion following
surgery should be confirmed by an on-table
angiogram. The commoner complications of
this surgery include graft thrombosis, infection,
and deep vein thrombosis. Resection of
popliteal aneurysms is indicated only in the
larger, saccular type that involves a short
segment of popliteal artery, so the resultant end-
to-end anastomosis can be performed without
tension. Great care must be taken in resection to
avoid damage to the adjacent popliteal vein, and
for this reason some surgeons avoid this method
of aneurysm repair.

Thrombolysis has an important role to play in
the management of acute symptomatic popliteal
aneurysmal disease. In thrombosed aneurysms
with acute ischemia, a percutaneous trans-
femoral arterial catheter can be inserted and
lodged in the aneurysmal thrombus. Infusion of
thrombolytic agent [recombinant tissue-type
plasminogen activator (rtPA), streptokinase, or
urokinase] is commenced at an appropriate
dose, and check angiograms are performed at
suitable intervals (every 4 to 6 hours) to confirm
the clinical observations of improved blood
supply. Angiographic demonstration of ade-
quate run-off is an indication to stop throm-
bolytic infusion and proceed to bypass grafting.
Long periods of thrombolysis carry the risks of
bleeding and embolization of released intraa-
neurysmal thrombus. Strict observation for
excessive hemorrhage and worsening foot
ischemia must be adhered to during treatment,
and they mandate cessation of the infusion if
they occur. In advanced ischemia with loss of
sensation and muscle power, attempts at surgi-
cal revascularization should not be delayed, and
thrombolysis should be restricted to intraoper-
ative use in an effort to clear tibial and peroneal
vessel run-off.

Chronic Ischemia

Symptoms of chronic ischemia in popliteal
aneurysmal disease may be due to thrombosis
or distal embolization. A conservative nonoper-
ative approach maybe considered in the case of
thrombosed popliteal aneurysm, as an acute

deterioration is unlikely due to the established
collateral circulation. Distal embolization, on
the other hand, involves a persistent blood flow
through the aneurysm (unlike thrombosis),
putting the patient at risk of further embolic
episodes and worsening limb ischemia unless
the aneurysm is surgically excluded.

Management of Asymptomatic
Popliteal Aneurysms

Discovery of these aneurysms is usually on
examination following diagnosis of aneurysmal
disease elsewhere such as the abdominal aorta
or contralateral popliteal artery. Subsequent
treatment remains a controversial issue with as
yet no clear guidelines for surgical intervention.
The recent trend of aggressive repair in the
majority of asymptomatic popliteal aneurysms
is currently under review in an effort to balance
the inherent surgical morbidity of repair and
the fact that for many patients their popliteal
aneurysm will be associated with no long-term
adversity. Review of the literature suggests that
following factors favor elective surgery: ane-
urysm size >2 cm, the presence of mural throm-
bus (potential embolic source), autogenous
conduit availability, absent ankle pulses (indi-
cating possible "silent" embolization), and a
long life expectancy. Classical popliteal ane-
urysm exclusion and bypass as described earlier
is the operation of choice in this situation.
Endovascular procedures have been described
in the treatment of popliteal aneurysms but the
long-term patency rates and outcomes are at
present unknown.

Surgical Approach in Popliteal
Artery Aneurysms

Access to the popliteal artery in aneurysmal
surgery is achieved by either the medial or pos-
terior approach.

In the medial approach the knee is partially
flexed and the skin incision follows the course
of the long saphenous vein, taking care to pre-
serve the vein for later harvest. The adductor
muscles are retracted, allowing entry to the
popliteal space with decent exposure and better
access to the superficial femoral and tibial arter-
ies than with the posterior approach. A further
advantage of this method is that the incision

213

ANEURYSMAL DISEASE

may be easily extended without the need for
patient repositioning.

The posterior approach requires the patient
to be prone, and the incision is made between
the heads of the gastrocnemii extending proxi-
mally Excellent exposure of the popliteal artery
is achieved, but access to more proximal or
distal vessels proves more problematic. Further-
more, unless the short saphenous vein is to be
used for bypass, this approach compels a second
incision for vein harvest.

Femoral Arterial Aneurysms

Femoral arterial aneurysms can be divided
simply into true or false aneurysms. Due to its
ease of accessibility and the trend for more inva-
sive medical investigation and treatment (e.g.,
cardiac catheterization, intra-aortic balloon
pumps), iatrogenic injury of the femoral artery
leading to false aneurysm is a relatively com-
mon occurrence. This chapter discusses only
true femoral aneurysms, and false aneurysms
are considered in detail elsewhere.

Although rare, true femoral aneurysms are
the second commonest peripheral aneurysm
after those affecting the popliteal artery. They
occur in between 2% and 3% of patients with
aortic aneurysms and tend to be a disease of
elderly men (male-to-female ratio of 30:1). The
condition is frequently bilateral and similar to
popliteal aneurysms; a coexistent generalized
aneurysmal process may be manifest in other
anatomical sites such as the aortoiliac or
popliteal arteries. Multiple factors are impli-
cated in their development including athero-
sclerosis, turbulent blood flow (at proximal
major vessel bifurcations and infrainguinally),
and repeated hip flexion. Other etiologies to
exclude are infection, inflammation (e.g., sys-
temic lupus erythematosus, Takayasu's disease),
trauma, and connective tissue disorders (e.g.,
Marfan syndrome).

Classification

True femoral aneurysms are distinguished by
the Cutler and Darling classification:

Type 1: aneurysm involves common
femoral artery (CFA) only, not the
bifurcation

Type 2: aneurysmal disease of the bifurca-
tion, the commencement of the
profunda femoris (PFA), or the
superficial femoral artery (SFA)

Clinical Features

Femoral aneurysms may be symptomatic or
asymptomatic. The latter group is usually dis-
covered incidentally on clinical examination of
a patient with an aneurysm elsewhere or suffer-
ing symptoms of chronic limb ischemia. Pre-
sentation of a symptomatic femoral aneurysm
can include a pulsatile groin mass (which may
or may not be painful), leg swelling (in large
aneurysms due to femoral vein compression
and deep vein thrombosis), or features associ-
ated with chronic ischemia attributable to
aneurysm thrombosis/embolization.

Diagnosis

Once clinical suspicion has been aroused, the
diagnosis should be confirmed with a duplex
scan. If surgery is being considered (e.g., in
CFA thrombosis or embolization), preoperative
angiography is desirable for further informa-
tion regarding the proximal and distal vessels.

Management of Femoral Aneurysms

Symptomatic femoral aneurysms are them-
selves an indication for surgical intervention. As
with popliteal disease, the management of the
asymptomatic case is less clear. It is generally
accepted, however, that if aneurysms are >4cm
or aortoiliac disease is present (with indicated
surgery), then operative repair is warranted.

Surgical Repair of Femoral Aneurysms

The skin incision extends from a point approx-
imately 4 cm proximal to the inguinal ligament,
following the course of the artery (and thus
aneurysm) to a point just distal to the CFA
bifurcation. Once proximal and distal control is
achieved, heparin and intravenous antibiotics
are administered so that aneurysmal repair
can be performed. In Type 1 aneurysms, the
CFA-restricted disease, may be addressed by
aneurysm resection and insertion of an inter-
position graft [polytetrafluoroethylene (PTFE)/
Dacron]. Repair of type 2 aneurysms is by graft

214

VASCULAR SURGERY

(autogenous saphenous vein or prosthetic)
interposition with an end-to-end technique
between the nonaneurysmal CFA and the larger
of the bifurcated vessels (SFA or PFA). The
smaller vessel is then reimplanted into the side
of the graft directly, or by the use of a second
graft. Patency rates following repair are good,
80% to 85% at 5 years with a low operative mor-
tality and morbidity.

Iliac Artery Aneurysms

Isolated iliac aneurysms are rare with a reported
incidence of only 1% to 2% of all aortoiliac
aneurysmal disease. The aneurysms tend to be
large (4 to 8 cm), with annual expansion rates
comparable to that of AAAs. Males over the age
of 70 years are most frequently affected, with the
atherosclerotic process implicated in the vast
majority of cases. Other reported etiologies
include infection (TB, syphilis), trauma (pelvic
fractures and iatrogenic during surgery),
inflammation, and pregnancy.

Clinical Features

Iliac aneurysmal disease may be asymptomatic
or symptomatic. Human pelvic anatomy
accounts for the fact that even very large iliac
aneurysms may remain "silent" until an inci-
dental diagnosis. Any symptoms experienced
are typically due to local effects on neighboring
structures including the ureter, small bowel,
iliac vein, and femoral or sciatic nerve.

Abdominal examination may reveal the diag-
nosis but is usually normal. Palpation of a pul-
satile mass on rectal or vaginal examination
should alert the clinician to the possibility of
iliac aneurysmal disease.

Diagnosis

Duplex ultrasound scanning is cheap, readily
available, and thus the preliminary investigation
of choice in diagnosis confirmation. Conven-
tional angiography is extremely informative,
but due to contrast load and radiation exposure
its use is restricted to preoperative instruction.
The cost and availability of spiral CT and mag-
netic resonance angiography negates their
use routinely, but the quality of information
obtained remains impressive.

Management of Iliac Aneurysms

Management strategies are outlined depending
on whether the common iliac (CIA) or internal
iliac (IIA) artery is involved.

Common Iliac Aneurysms

Small CIA aneurysms (<3cm) do not require
surgery and can be managed conservatively. If
the maximal aneurysm diameter lies between 3
and 4 cm, patients should be kept under ultra-
sound surveillance (every 6 months) and oper-
ation offered if expansion to >4 cm. Isolated CIA
aneurysms may be repaired by means of an
interposition graft and oversewing of the IIA
origin. Alternatively, the CIA aneurysm can be
ligated (proximally and distally) with execution
of an iliofemoral or femorofemoral crossover
graft.

Internal Iliac Aneurysms

Unilateral IIA aneurysms can be addressed
by either radiological or operative techniques.
Coil embolization of the IIA successfully ex-
cludes the aneurysm from the circulation with
minimal long-term sequelae. Surgical inter-
vention requires simple proximal and distal
aneurysm ligation for treatment in these cases.
Bilateral IIA aneurysms pose an interesting
problem as bilateral aneurysm ligation or
embolization is not a viable option to preserve
adequate colorectal and perineal blood supply.
In this scenario an attempt at surgical revascu-
larization should be made. The bypass graft
runs from the nonaneurysmal CIA to the distal
IIA with proximal aneurysm ligation. Extensive
hemorrhage can often be encountered in this
difficult procedure for which the surgeon should
be prepared.

Visceral Artery Aneurysms

Aneurysmal disease involving the visceral arter-
ies is uncommon but an important cause of
vascular admission. As imaging techniques con-
tinue to improve, there will no doubt be a cor-
responding increase in the diagnostic yield of
these aneurysms, so it is hoped that manage-
ment strategies can be applied to the elective
rather than the emergency presentation.

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ANEURYSMAL DISEASE

Splenic Artery Aneurysms

The splenic artery is the most common visceral
artery to be affected by aneurysmal disease,
accounting for 60% of all visceral aneurysms.
They are the second most common abdominal
aneurysm after the aorta, with an estimated
population incidence of 1%. Vessel dilatation is
usually minimal (<2 cm) and about one fifth of
these aneurysms are multiple. Contrary to
aneurysmal disease elsewhere, it is multiparous
women who are classically affected. The etiol-
ogy of splenic artery aneurysm is unknown, but
theories include the vascular sequelae of multi-
ple pregnancies, altered flow dynamics in portal
hypertension, and multifactorial vessel wall
degradation.

Eighty percent of splenic artery aneurysms
are asymptomatic. The remaining proportion
may present with a nonspecific pain in the left
hypochondrium or epigastrium that can radiate
to the left flank or be referred to the left shoul-
der by diaphragmatic irritation. As aneurysmal
progression continues, the symptoms worsen
and are further aggravated by excessive move-
ment. Abdominal examination is usually
normal, although splenomegaly is detected in
20% of patients. Rupture occurs in 5% to 10% of
splenic artery aneurysms, and in these cases the
patient presents with severe upper abdominal
pain, hypotension (volume loss), and frank peri-
tonism. Nearly all ruptures occur during preg-
nancy, and associated mortality rates are high
(75% mother, 95% fetus).

Diagnosis of splenic artery aneurysms is
usually incidental on imaging modalities such
as plain abdominal radiographs (calcification),
angiogram, spiral CT, or MRI scanning. Alter-
natively, these lesions may be discovered during
laparotomy for other pathology. Management
planning in splenic aneurysms tends to be
dependent on whether symptoms exist. As a
general rule, the majority of asymptomatic
aneurysms maybe treated conservatively, but in
those experiencing symptoms, surgical inter-
vention is indicated at an early stage. Operative
procedure is governed by the anatomical loca-
tion of disease within the splenic artery. Proxi-
mal aneurysms (in the first third of the splenic
artery) are treated by either ligation or excision
and grafting after an approach through the
lesser sac. Ligation is indicated in aneurysms
affecting the middle third of the artery, whereas

either splenectomy or aneurysmal excision (for
splenic conservation) is advocated for distal
disease. Coil embolization performed by a
member of the resident interventional radiol-
ogy team may be successfully used to treat
appropriate splenic aneurysms in high-risk
patients.

Hepatic Artery Aneurysms

Aneurysmal disease involving the hepatic artery
accounts for approximately one fifth of visceral
aneurysms. They occur more often in the male
population with an average age at presentation
of 40 years, somewhat lower than is observed in
other aneurysmal processes. Site of aneurysm
formation is either intrahepatic (25%) or extra-
hepatic (75%), the latter aneurysms being
usually solitary affecting the common hepatic
artery (60%). Isolated involvement of the right
and left hepatic arteries is less frequent, but if
present, a predilection for the right hepatic
artery is seen (seven times more common). The
cause of extrahepatic aneurysm is normally ath-
erosclerosis, but factors such as infection,
trauma, and cystic medial degeneration must be
considered. Conversely, intrahepatic disease
tends to be false aneurysms resulting from
trauma.

Nonruptured hepatic aneurysms are usually
asymptomatic but may present with discomfort
in the right hypochondrium or epigastrium. As
its size increases, the pain radiates into the back.
Sudden development of acute abdominal pain,
hypotension, and peritonism indicates rupture
of the aneurysm, occurring in 20% of cases.
Unless the aneurysm has indeed ruptured, clin-
ical examination is invariably normal, although
detection of a pulsatile mass and bruits have
been reported.

Prerupture clinical diagnosis of hepatic
aneurysm is problematic. Elevated serum
amylase, bilirubin, and white cell counts may be
observed, but more often than not diagnosis
depends on ultrasound and CT findings. Once
suspected, the investigation of choice for
hepatic aneurysm is selective celiac and supe-
rior mesenteric angiography.

Due to high rates of rupture-related mor-
tality of approximately 40%, proven hepatic
aneurysms merit aggressive management. The
exact surgical procedure is again guided by
anatomical location of aneurysms: for extra-

216

VASCULAR SURGERY

hepatic aneurysms proximal to the gastroduo-
denal artery, simple aneurysm ligation should
be performed (hepatic blood supply maintained
by gastroduodenal and right gastric arteries); if
the aneurysm location is distal to the com-
mencement of the gastroduodenal artery, then
an excision and graft procedure should be
attempted. Intrahepatic aneurysm repair is
more difficult. Both embolization and limited
liver resections have been performed, but not
all aneurysms are suitable for coil deployment,
and operative mortality in these cases remains
high.

Renal Artery Aneurysms

Renal artery aneurysms are about as common
as hepatic aneurysms, accounting for one fifth
of all visceral aneurysms. The true incidence of
these aneurysms lies between 0.3% and 1.3%,
with less than 10% of those affected exhibiting
symptoms. They occur in both sexes, with
women of childbearing age considered to be of
highest rupture risk. Etiologies of renal artery
aneurysms are varied, but the majority (80%
to 85%) are caused by the degradation of the
internal elastic lamina at the renal arteriolar
divisions leading initially to microaneurysm
formation that then progresses into frank
aneurysmal disease. Other factors to consider in
aneurysm development include previous renal
trauma and generalized arteritis. As already
mentioned, the vast majority of these
aneurysms are clinically silent, but if present,
symptoms include flank pain on the affected
side, hematuria, and systemic hypertension.
Clinical examination may reveal a bruit on aus-
cultation. Rupture is manifest by acute localized
pain and hypovolemia due to either retroperi-
toneal hemorrhage or rupture into the neigh-
boring renal vein, resulting in a high-output
arteriovenous fistula.

Diagnosis is usually made at laparotomy for
a different abdominal pathology or incidentally
on radiographic imaging such as CT scanning,
angiography, or MRI. Management of asympto-
matic, low-risk renal artery aneurysms should
be nonoperative, as the procedure carries a
significant (5%) risk of nephrectomy. On the
other hand, "high risk" asymptomatic popula-
tions (defined as women of fertile age) and
symptomatic patients should proceed to
aneurysm repair irrespective of aneurysmal

size. Operative procedures include excision with
direct end-to-end arterial anastomosis, graft
interposition (prosthetic or autogenous vein),
and nephrectomy. Suitable aneurysms may be
treated with embolization, but these techniques
carry a significant risk of parenchymal damage.

Superior Mesenteric Artery Aneurysms

These aneurysms are rare, representing approx-
imately 8% of all visceral aneurysms. Both sexes
are equally affected, with infection implicated as
the causal factor in two thirds of cases. Other
etiologies include atherosclerosis and trauma.
Age at presentation is variable, mycotic
aneurysms being more common before 50 years
of age, whereas atherosclerotic aneurysms
usually present later (over 60 years of age).
Superior mesenteric artery aneurysm man-
agement tends to be aggressive, as there is a
high rate of rupture whatever the size of the
aneurysm. Surgery should attempt to ligate the
aneurysm without reconstruction or excision
due to the high risk of damaging adjacent struc-
tures. Again, embolization may be considered,
but it carries the potentially fatal complication
of intestinal ischemia.

Celiac Artery Aneurysms

Celiac aneurysms are even less common than
those affecting the superior mesenteric artery,
representing 3% to 4% of all visceral
aneurysms. There is an equal sex distribution,
and most are due to atherosclerosis and medial
degeneration. The majority are without symp-
toms, but if present they include epigastric pain,
nausea, and vomiting. A bruit may be heard on
clinical examination. Diagnosis is confirmed by
CT scanning or abdominal ultrasound, and sub-
sequent management involves surgical excision
(for small aneurysms) or reconstruction.

Gastroduodenal, Pancreaticoduodenal, and
Pancreatic Artery Aneurysms

Aneurysms of these arteries are extremely rare,
collectively accounting for 3% of visceral
aneurysms. The patient is usually a man in his
sixth decade with a prior history of pancreati-
tis. Symptoms, if present, are of epigastric pain
radiating through to the back, and angiography

217

ANEURYSMAL DISEASE

or CT scanning reveals the diagnosis. Rupture-
related death rates are high (about 50%); there-
fore, a low threshold should exist for surgical
repair. Operation is by aneurysm ligation, or
in suitable cases coil embolization may be
appropriate.

Jejunal, Ileal, and Colic Artery Aneurysms

Together these aneurysms constitute 2% to
3% of all visceral aneurysms. Sex distribution
appears to be equal, with an average age at pres-
entation of 75 years. These aneurysms tend to
be small, isolated, and asymptomatic until
rupture. Diagnosis is invariably made at sub-
sequent laparotomy, where repair is by either
aneurysm ligation or excision. Concomitant
limited bowel resection may have to be per-
formed if the vascular repair threatens an
inadequate intestinal blood supply.

Axillary and Subclavian
Artery Aneurysms

Aneurysmal disease affecting the upper extrem-
ity is rare but remains of importance due to the
severity of possible sequelae associated with the
disease. Ideal management, therefore, aims at
early diagnosis and repair in order to minimize
this potential morbidity. Pathology in this
region is divided anatomically into one of three
types, each with a distinct etiology.

Subclavian Artery Aneurysms

Subclavian aneurysms (SCAs) are arbitrarily
classified as proximal or distal in reference to
the location of diseased arterial segment. Prox-
imal aneurysms are totally confined to the
parent artery and are usually caused by degen-
erative disease, trauma, or infection. They occur
more commonly in men and over the age of 60
years. In contrast, distal subclavian aneurysms
tend to occur in the younger female population.
Clinical features associated with SCA can be
considered as local or distant. The patient may
complain of a painless pulsatile mass in the
lower neck, whereas acute aneurysm expansion
or rupture causes pain experienced in the chest,
neck, or shoulder. Local symptoms due to com-
pression are common and include neuropathic
pain (which may be referred) due to brachial

plexus irritation, an ipsilateral Horner syn-
drome from sympathetic chain compression,
hoarseness due to recurrent laryngeal nerve
pressure, stridor due to partial extrinsic tra-
cheal obstruction, and upper limb edema
caused by venous outflow obstruction. Pul-
monary erosion by the aneurysm explains any
hemoptysis, whereas distant manifestations of
the condition can include acute or chronic limb
ischemia from thromboembolism and Raynaud
syndrome. Examination may reveal a supraclav-
icular pulsatile mass with an audible bruit. An
assessment of full upper limb neurovascular
status is mandatory, which classically reveals
normal pulses in the evidential face of prior
microembolism and altered neurology in the
corresponding segment of brachial plexus or
sympathetic chain.

Duplex or CT scanning confirms the diagno-
sis of SCA, but angiography is also required to
plan appropriate intervention. Proximal SCA
management is by resection with end-to-end
anastomosis for (small aneurysms) or by surgi-
cal resection with interposition arterial graft.
Proximal vascular control can be difficult,
and occasionally sternotomy (right SCA) or
extended thoracotomy (left SCA) is required.
Surgical correction of the distal SCA adheres to
the same principles as for proximal pathology,
with the advantage that adequate exposure is
achieved by simple supraclavicular incision.

Axillosubclavian Artery Aneurysms

These aneurysms involve the junction between
the terminal subclavian and proximal axillary
arteries at the border of the first rib. They are
invariably poststenotic aneurysms from a tho-
racic outlet syndrome caused by either a cervi-
cal rib or fibrous band. The disease is more
common in younger females, probably because
it is this population that has the highest inci-
dence of cervical rib.

Symptoms are similar to those outlined for
isolated subclavian aneurysms, but it is worth
noting that there is an increased frequency of
embolic phenomena. Investigation of axillosub-
clavian disease is initially by duplex ultrasonog-
raphy, but arteriography is advised for all cases
to be considered for surgery. Exact management
depends on both aneurysmal size and the pres-
ence of distal thromboembolic complications.
Large (defined as more than twice the arterial

218

VASCULAR SURGERY

diameter) or symptomatic aneurysms require
arterial repair by means of excision and graft
interposition with synchronous removal of the
antecedent cause (e.g., excision of cervical rib or
division of fibrous band). Small, asymptomatic
aneurysms may well recede once the thoracic
outlet syndrome has been surgically corrected
so that arterial reconstruction is often not
required.

Axillary Artery Aneurysms

Isolated axillary artery aneurysms are very rare
but typically affect young males as a conse-
quence of trauma. Repeated blunt trauma to
the axillary artery, classically due to long-term
crutch-use, may result in aneurysm develop-
ment and the subsequent complicating symp-
toms of acute or chronic upper limb ischemia.
Penetrating trauma tends to result in false
aneurysm formation. A rich collateral blood
supply in this region may lead to delayed and
atypical presentations, so a high index of suspi-
cion is needed to make the diagnosis.

Investigation is by duplex ultrasound fol-
lowed by arteriography, and appropriate
surgery is aneurysm resection and arterial
reconstruction by interposition autogenous
vein graft (saphenous vein). Prosthetic grafts
have been successfully used but are associated
with inferior long-term patency rates. Recently,
successful management with axillary endovas-
cular stent grafts has been reported, but the
long-term results of this intervention are
presently unknown.

Carotid Artery Aneurysms

Extracranial carotid aneurysmal disease requir-
ing vascular surgical expertise is extremely rare.

True carotid aneurysms are located either in
the carotid bifurcation, internal carotid system
or external carotid, in decreasing frequency of
that order. Etiological factors are varied, but the
most common include atherosclerosis, trauma,
previous carotid surgery (e.g., endarterectomy),
and carotid artery dissection. Historically,
infection used to be the major culprit causing
disease, but widespread antibiotic availability
has rendered this mechanism responsible in
only a minority of cases.

The patient may present with an awareness of
a pulsatile mass in the neck that may or may not

be painful. Other symptoms are attributed to
local compression and include dysphagia as a
result of pharyngeal proximity, deafness or
facial pain due to cranial nerve compression,
and hoarseness caused by vagus nerve impinge-
ment. Distal central nervous neurological symp-
toms such as stroke, amaurosis fugax, or
transient ischemic attack (TIA) indicate throm-
boembolic complications from the carotid
aneurysm and are in fact the most common pre-
senting feature of the disease. Large aneurysms
have also been implicated in posture-related
transient neurology as a result of limitation and
even occlusion of blood flow through the neigh-
boring internal carotid artery. Ruptured carotid
aneurysms are fortunately rare but are usually
fatal if they occur.

It is interesting that despite the paucity of
the disease, carotid aneurysms remain over-
diagnosed. True aneurysms must be distin-
guished from the much commoner reality of
tortuous or coiled carotid vessels, and other
diagnoses such as cervical lymphadenopathy,
carotid body tumors, and branchial cysts. In the
majority of cases history and clinical examina-
tion alone should be sufficient to expose the
bona fide aneurysm, but confirmation can be
obtained with duplex or CT scanning. If inter-
vention is being contemplated, an angiogram
must also be obtained.

The aim of management is ultimately pre-
vention of the neurological complications
associated with carotid aneurysmal disease.
Current opinion regarding preferred treatment
is divided between surgical and endovascular
methods. In the former, the aneurysm is
resected, arterial reconstruction is performed,
and cerebral blood flow is maintained during
carotid clamping with an operative shunt. The
adequacy of this maneuver is assessed by some
surgeons with the use of intraoperative tran-
scranial Doppler or electroencephalography in
order to confirm distal perfusion. Surgery is
notoriously perilous in proximal internal
carotid disease and in larger aneurysms where
"distal" control can be difficult to secure. The
most feared complication of carotid aneurysm
surgery is disabling stroke, occurring in 6% to
10% of cases, which may result from cerebral
hypoperfusion or intraoperative dislodgment of
debris from the vessel wall. Another specific risk
of surgery is cranial nerve palsy, resulting from
local tissue handling or careless dissection. The

219

ANEURYSMAL DISEASE

condition affects 20% of patients and is usually
temporary, but must nonetheless be mentioned
to the patient preoperatively while obtaining
informed consent.

Endovascular approaches to carotid
aneurysm management may soon render
surgery as second-line treatment for extracra-
nial carotid aneurysmal disease. Graft stenting
and coil embolization of such lesions is reported
to be as effective as surgical repair, without
the need for operation. These techniques may
be especially appropriate in large aneurysms,
revisional surgery, or the case of high carotid
aneurysm close to the base of skull so that
access is problematic. The risk of neurological
complications following the procedures re-
mains, but these cerebrovascular events appear
less common in this approach to treatment. Still
in its infancy, these initial encouraging results
may be tempered as we await the longer term
results of endoluminal intervention.

Controversial Issues

• Should there be a national screening
program for the detection of AAA?

• Are all elective AAA repairs best per-
formed at tertiary referral centers?

Is open repair preferable to endovascular
therapy in elective AAA repair?
What is the optimal management of type I
and type III endoleaks?
Does routine uterolysis have a role in the
management of the inflammatory AAA?
Do all high (Crawford types I and II) tho-
racoabdominal aneurysm repairs mandate
the use of cardiopulmonary bypass and
spinal fluid drainage?
What is the best treatment for the asymp-
tomatic popliteal aneurysm?
When should carotid aneurysms be
repaired with endovascular methods?

References

Dawson I, Sie RB, van Bockel JH. (1997) Br J Surg 84:

293-9.
Hallin A, Bergqvist D, Holmberg L. (2001) Eur J Vase

Endovasc Surg 22:197-204.
Heller JA, Weinberg A, Arons R, et al. (2000) J Vase Surg

32:1091-100.
Rasmussen TE, Hallett JW Jr. (1997) Ann Surg 225:155-64.
Wassef M, Baxter BT, Chisholm RL, et al. (2001) J Vase Surg

34:730-8.
Wilmink AB, Quick CR. (1998) Br J Surg 85:155-62.
Woodburn KR, May J, White GH. (1998) Br J Surg 85:

435-43.

Renovascular Hypertension and
Ischemic Nephropathy

Sherry D. Scovell

Renovascular hypertension is a relatively
uncommon cause of hypertension and is only
seen in 5% to 10% of the hypertensive popula-
tion. However, this translates to at least 600,000
people in the United States alone when consid-
ering that nearly 60 million people in the United
States have some degree of hypertension. Renal
artery stenosis (RAS) often produces an unclear
clinical picture. Patients maybe asymptomatic.
However, they may also present with severe,
uncontrolled hypertension referred to as reno-
vascular hypertension or with evidence of renal
insufficiency, otherwise known as ischemic
nephropathy. This chapter focuses on the clini-
cal characteristics that may be helpful in iden-
tifying those patients who may be at risk for
RAS, how to accurately diagnose RAS, and how
to correlate RAS with the symptoms of uncon-
trolled hypertension or ischemic nephropathy.
It also outlines the options available for treat-
ment, including medical management, endo-
vascular correction of RAS via angioplasty
with or without stenting, and open surgical
revascularization.

Characteristics

With renovascular disease being responsible
for only 5% to 10% of the hypertensive popu-
lation, it would be helpful to define certain
clinical characteristics that are prevalent in
this population to aid in screening patients.
Typically, renovascular hypertension produces

severe diastolic hypertension, which is defined
as diastolic blood pressure greater than 115mm
Hg. In a blood pressure screening program 137
patients with new-onset hypertension were
diagnosed in a shopping center. Further workup
consisted of angiography followed by renal
vein renin measurements and split renal func-
tion tests in patients with evidence of critical
renal artery stenosis. None of the 102 patients
with a diastolic blood pressure between 90
and 115mmHg had evidence of renovascular
hypertension. However, nine of the 35 patients
(26%) with a diastolic blood pressure of 115 mm
Hg or higher did have evidence of renovascular
hypertension. With respect to race, none of
the African-American patients had renovascu-
lar hypertension, whereas nine of the 22 (41%)
Caucasian patients did have renovascular
hypertension.

Renovascular hypertension has also been
described as having a bimodal age distribution,
with patients at the two extremes of age carry-
ing the highest incidence of having renovascu-
lar disease responsible for their hypertension.
It is typically seen in children younger than 5
years old and in patients over 60 years of age.

Based on observations such as these, addi-
tional characteristics thought to be associated
with renovascular hypertension were postulated
to include recent onset of hypertension, young
age, lack of family history of hypertension, and
the presence of an abdominal bruit. The most
comprehensive study used to compare these
characteristics in hypertensive patients both

221

222

VASCULAR SURGERY

with and without RAS was the Cooperative
Study of Renovascular Hypertension (Simon,
1972). One of the ultimate conclusions of this
study was that neither the above four criteria
nor any other clinical criteria could accurately
predict the presence of renovascular hyperten-
sion. Indeed, the majority of patients with ren-
ovascular hypertension do not present with
what were once thought to be the "classic" char-
acteristics delineated above. As a result of these
studies, it is necessary to maintain a high index
of suspicion in patients whose hypertension is
difficult to control with medical management
and to rely on screening examinations in
patients with severe diastolic hypertension.

Etiology

The etiology of RAS is primarily atherosclerotic
in approximately 90% of patients. The second
most common etiology is fibromuscular dyspla-
sia (FMD). Other less common causes of RAS
include aortic dissection, vasculitis, emboli,
radiation, and extrinsic compression from
masses or tumors.

Atherosclerotic renal artery stenosis is seen
predominantly in males. The majority of these
lesions are believed to be ostial encroachment
of an aortic plaque on the orifice of the renal
artery or arteries. As a result, 50% of the time
these lesions are bilateral. As well, these lesions
are typically eccentric and irregular luminal
stenoses. It is well known that atherosclerotic
disease is progressive and the renal artery in not
an exception. RAS will be progressive in 30% to
70% of cases. Approximately 11% of the time,
patients with a greater than 60% stenosis of the
renal artery will progress to total occlusion
within a 2-year period (Zierler, 1994).

The stenoses caused by FMD are primarily
nonostial and often extend into the branches
of the renal arteries. Fibromuscular dysplasia
may be divided into three types: medial fibro-
dysplasia, perimedial dysplasia, and intimal
fibroplasia.

Medial fibro dysplasia is the most common
type, accounting for 85% of all FMD lesions.
Women are predominantly affected, usually
between 25 and 45 years of age. In 55% of
patients, the disease is bilateral. If it is unilateral,
it is more likely to affect the right renal artery
when compared to the left renal artery. The

angiographic appearance is that of a string of
beads. There are two distinct types of medial
fibrodysplasia — diffuse and peripheral.

Perimedial dysplasia is seen in only about
10% of patients with FMD. This subtype is again
seen most often in women in the fourth or fifth
decades of life. This type may be more progres-
sive when compared to medial fibrodysplasia.

Finally, intimal fibroplasia is seen in 5% of
patients with FMD. These lesions are long, irreg-
ular, tubular regions of stenosis. They tend to
progress more rapidly than those caused by
medial fibrodysplasia.

Pathophysiology

Any comprehensive review of renovascular
hypertension must cite Goldblatt's (1934) classic
experiments. He described both the two-kidney,
one-clip model of unilateral RAS in the setting
of a normal contralateral kidney, as well as the
one-kidney, one-clip model that represents uni-
lateral RAS in a patient with only one kidney.

In the two-kidney, one-clip model, one renal
artery is clamped while the other one is left
open. In this model, there is decreased renal
blood flow seen by the ipsilateral juxtaglomeru-
lar apparatus. This leads to increased secretion
of renin by the clipped kidney. Through the
renin-angiotensin-aldosterone system, there is
mild sodium retention as a result of increased
aldosterone and increased blood pressure sec-
ondary to angiotensin II-related vasoconstric-
tion. The contralateral kidney then suppresses
its release of renin to compensate. When an
angiotensin-converting enzyme (ACE) inhibitor
is administered to a patient in the two-kidney,
one-clip model acutely, there is a dramatic
reduction in blood pressure. This demonstrates
that the elevation in blood pressure is primarily
angiotensin II-dependent.

In the one-kidney, one-clip model of reno-
vascular disease, a clip is applied to the renal
artery supplying a single kidney. In this case,
there is an initial elevation in renin. This initial
rise in the renin leads to activation of the renin-
angiotensin-aldosterone system, and there is
peripheral vasoconstriction as well as an
increase in sodium and water retention. Blood
pressure rises as a result of both of these mech-
anisms. This model is both an angiotensin-
dependent system as well as a volume-driven

223

RENOVASCULAR HYPERTENSION AND ISCHEMIC NEPHROPATHY

system and produces a more persistent form of
hypertension.

Diagnostic Evaluation

The patients who are well served by renal revas-
cularization are those with severe RAS in the
setting of either uncontrolled hypertension or
ischemic nephropathy. Patients without an asso-
ciation between the anatomical stenosis and
these symptoms are not well served by correc-
tion of the RAS. Therefore, it is necessary to
establish a correlation between the anatomical
RAS and the uncontrolled hypertension or
ischemic nephropathy to determine who will
benefit from an attempt at revascularization.
This is done primarily through the combination
of both anatomical screening tests as well as
studies that document associated physiological
consequences. Anatomical tests are those that
delineate RAS and document associated hemo-
dynamic data. Physiological tests attempt to
establish an association between the anatomical
stenosis and the alterations in the renin-
angiotensin-aldosterone axis.

Anatomical Tests

Duplex Ultrasound

Duplex examination of the kidneys and the
renal arteries is an extremely useful screening
modality as it is a noninvasive examination. The
only preparation necessary is an overnight
fast, and it is not necessary to discontinue anti-
hypertensive medications for reliable results.
Renal artery duplex examination is able to iden-
tify hemo dynamically significant renal artery
lesions. It offers information on renal length
as well as on the renal artery blood flow. The
resistive index (RI) indicates the degree of
renal artery resistance and should be calculated.
It is defined as the peak systolic shift minus
the minimum diastolic shift over the peak sys-
tolic shift. A normal RI is less than 0.70. The RI
may be predictive of outcome with respect
to renal revascularization (Radermacher et al.,
2001). However, caution should be taken in
the interpretation of RI as it may also be in-
creased in patients with intrinsic renal disease,
decreased cardiac output, or perinephric fluid
collections.

The degree of RAS is typically calculated
based on the renal-to-aortic ratio (RAR) as well
as the peak systolic velocities in the renal artery.
The RAR is the ratio of the peak systolic veloc-
ity of the renal artery to the aortic peak systolic
velocity. If the RAR is less than 3.5 with a peak
systolic velocity of greater than 180 cm/sec,
there is a less than 60% stenosis. If the RAR is
greater than 3.5 and the peak systolic velocity
is greater than 180 cm/sec, this is diagnostic
of a greater than 60% stenosis. If there is no
detectable renal artery signal with a kidney
length of less than 9 cm, the renal artery is con-
sidered occluded.

Although this is an excellent screening test
to detect the presence of renal artery stenosis,
duplex examination is unable to accurately
predict the clinical response of either the hyper-
tension or renal insufficiency following correc-
tion of the RAS. It is also unable to accurately
identify all accessory branches of the renal
artery and their contribution to the clinical
picture. This is, however, an appropriate nonin-
vasive screening test to evaluate for RAS and is
useful for following the patient with serial
examinations after intervention.

Angiography/Digital
Subtraction Angiography

The gold standard for the identification of RAS
still remains angiography, although it is an inva-
sive test and not an optimal screening tool. It
serves to define the presence, severity, and loca-
tion of intraluminal anatomical defects in the
renal artery. It facilitates a full evaluation of
the abdominal aorta as well as the renal artery
orifices and the accessory branches of the renal
artery. Multiple accessory renal arteries exist in
up to 25% of patients and are well defined with
angiography. It is able to define a nephrogram.
It is still controversial whether angiography
should be utilized as a screening test for reno-
vascular disease. It is likely best used as an
adjunct when duplex examination is unable to
visualize the renal arteries, or smaller accessory
branches are suspected of contributing to severe
renovascular hypertension.

Technically, the renal arteries usually arise
posterolaterally from the aorta and require
oblique views for adequate visualization of their
orifices. Peak systolic pressure gradients across
the lesion of >20mmHg or mean gradients of

224

VASCULAR SURGERY

10 mm Hg have been used as objective criteria to
define a significant reduction in blood flow.

It has been well documented that angiogra-
phy may exacerbate renal failure in patients
with baseline renal insufficiency. Nonionic, low-
osmolar contrast material is recommended
for the evaluation of the renal arteries and is
associated with a lower incidence of contrast-
induced nephropathy (Barrett and Carlisle,
1993). In patients with an elevated creatinine,
C0 2 or gadolinium may be substituted without
an increase in contrast-induced nephropathy. As
well, preintervention hydration is critical as is
acetylcysteine in select patient groups.

The calculation of R AS is determined by com-
parison of the narrowest segment of the renal
artery to the normal diameter of the renal artery
either proximal to the stenosis or distal to any
region of poststenotic dilatation. Poststenotic
dilatation is common in many cases of long-
standing arterial stenosis.

Patient Selection

Renal artery stenosis alone, in the absence of
symptoms, does not mandate repair. The coex-
istence of RAS and hypertension does not
establish a causal relationship. For this reason,
it is essential to determine the functional
significance of the anatomical stenosis.

Patients with RAS and symptoms attributable
to that stenosis are considered for treatment and
correction of the anatomical lesion. Symptoms
of hypertension, renal insufficiency, or pul-
monary edema in the setting of a greater than
60% RAS serve as criteria for repair. Clinical cri-
teria for revascularization have been defined
recently in the Guidelines for Reporting on
Renal Artery Revascularization in Clinical Trials
(Rundback, 2002). Based on these guidelines,
hypertension was classified as either accelerated
with sudden worsening in the setting of previ-
ous control, refractory hypertension resistant to
medical management with three or more anti-
hypertensive medications including a diuretic,
or malignant hypertension with evidence of
severe end-organ damage as a result. The pres-
ence of hypertension in the setting of a unilat-
erally shrunken kidney was also used as an
indication for intervention. With respect to
renal insufficiency, the clinical criteria for inter-
vention were defined as unexplained worsening
of renal function or a decrease in renal function

with the addition of an ACE inhibitor, as well as
renal dysfunction not attributable to another
obvious etiology. Finally, recurrent episodes
of "flash" pulmonary edema not able to be
explained on the basis of severe left ventricular
dysfunction in the setting of RAS was also con-
sidered an indication for revascularization. The
value of prophylactic renal artery revasculariza-
tion in asymptomatic patients is unproven at
this point, and that is why physiological tests are
significant in these patients.

Physiological Tests

When a unilateral RAS is defined by anatomical
studies, the functional significance must be
determined. In the past, many different tests
were attempted in order to define this correla-
tion including intravenous urography, nuclear
medicine studies, conventional angiography,
computed tomography, and magnetic resonance
imaging. More recently, this is accomplished
through the use of renal vein renin assays or by
isotope renography. The value of these tests is
not as great in patients with severe bilateral
renal disease or RAS in a solitary kidney when
compared to unilateral renal disease and a func-
tioning contralateral kidney.

Physiologically, there is a functional increase
in plasma levels of renin from the affected
kidney, which is characteristic in the setting of
RAS. Originally, systemic levels of renin were
obtained in an attempt to establish a diagnosis.
However, utilizing this method, the rate of false-
negative and false-positive results were high,
43% and 34%, respectively, in patients with
confirmed renovascular hypertension. As well,
roughly 20% of patients with essential hyper-
tension had an elevated plasma renin level. The
value of selective renal vein sampling of renin,
although an invasive procedure, has been found
to be more sensitive and specific. This test com-
pares the renin levels between the ipsilateral
and contralateral kidneys. If the renal vein/renin
ratio is greater than 1.5, there is lateralization of
renin secretion. This, as well, seems to be pre-
dictive of improvement following renal revascu-
larization. However, the failure to demonstrate
lateralization does not reliably predict failure of
revascularization procedures. In addition, there
are unfortunately strict prerequisite guidelines
required prior to performance of this test. Anti-
hypertensive medications must be held for up to

225

RENOVASCULAR HYPERTENSION AND ISCHEMIC NEPHROPATHY

3 weeks prior to the test, which is not without
clinical consequences.

For these reasons, other physiological tests
became more favorable. Initially, isotope renog-
raphy was developed as a screening procedure
for renovascular hypertension. The theory was
that the underperfused kidney would have
delayed uptake and excretion of solute when
compared to the normal, well-perfused con-
tralateral kidney. Various nucleotides were uti-
lized; however, this test still yielded a high rate
of false-negative results. More recently, the
results of this functional test have improved
through the use of the ACE inhibitor captopril.
Angiotensin II is elevated in patients with RAS,
and this elevation leads to selective vasocon-
striction of the efferent arterioles in an attempt
to maintain glomerular filtration. The use of
captopril blocks angiotensin II production, and
thus filtration drops precipitously. The finding
of a decrease in the uptake and excretion of the
tracer is more pronounced in patients after cap-
topril in the setting of clinically significant RAS.
Through the use of captopril, this study has
most recently demonstrated a 92% sensitivity
and a 94% specificity.

Therapeutic Options

The options for the treatment of symptomatic
RAS include medical management utilizing
multiple antihypertensive medications, the
endovascular approach including angioplasty
with or without the placement of a stent, or open
surgical management.

Medical Management of
Symptomatic Renal Artery Stenosis

The medical management of symptomatic RAS
is accomplished using a variety of antihyper-
tensive medications in an attempt to control the
hypertension. Control of the hypertension in
itself is critical, as uncontrolled hypertension is
a major risk factor for myocardial infarction,
cerebrovascular accident, and chronic renal
insufficiency. Thus, the goals of medical man-
agement of symptomatic RAS are to reduce the
blood pressure, to control cardiovascular risk
factors, and ultimately to prevent end-organ
damage from sustained hypertension.

However, the natural history of uncorrected
RAS is not benign. It has previously been docu-
mented that 11% of patients with a greater than
60% stenosis of the renal artery progress to
occlusion within a 2-year period. As well, over
40% of patients with a critical stenosis of the
renal artery will have a decrease in glomerular
filtration by greater than 25% with progressive
deterioration in renal function being common
in this group of patients.

As a result of these findings, there have been
numerous studies designed to evaluate medical
management for symptomatic RAS compared to
both open surgical repair as well as endovascu-
lar management.

Hunt and Strong (1973) orchestrated a com-
parative analysis examining drug therapy com-
pared to operative therapy to treat symptomatic
RAS; 114 patients were in the medical treatment
arm and 100 patients were in the surgical treat-
ment arm. The follow-up was over the course of
7 to 14 years. Overall, 84% of patients were alive
in the surgical group compared to 66% alive in
the group treated medically. Of those alive in the
surgical group, 93% were cured or significantly
improved, whereas of those patients in the
medical treatment group, 21% subsequently
required surgical intervention for uncontrolled
hypertension. Another seven patients from that
group continued to have uncontrolled hyper-
tension but were not taken to surgery. In addi-
tion, death was twice as common in the
medically treated group. These differences were
statistically significant (p < .01) for both ather-
osclerotic and FMD lesions. This study demon-
strated that in patients with renovascular
hypertension, there is a need to treat sympto-
matic lesions surgically. Indeed, in this series,
surgical intervention offered better sympto-
matic relief of hypertension, which translated to
a lower incidence of end-organ damage.

Webster and colleagues (1998) performed the
first prospective randomized trial comparing
medical management with renal artery angio-
plasty in 55 patients. All patients were hyper-
tensive and showed evidence of >50% RAS on
angiography. They found that only patients with
bilateral RAS demonstrated a significant
decrease in blood pressure with angioplasty.
There was no significant improvement in renal
excretory function. Otherwise, there was no sta-
tistical difference between the two groups. This
study suggested that there might be a significant

226

VASCULAR SURGERY

benefit to be derived from the endovascular
management of symptomatic RAS over medical
management of these patients, which ultimately
led to the validation of this therapeutic option.
Based on the results of the above studies as
well as other smaller studies, it became clear
that intervention, either endovascular or open
surgical, should play a significant role in the
treatment of symptomatic RAS.

Endovascular Repair of Renal
Artery Stenosis

In addition to open surgical repair for sympto-
matic RAS, renal artery angioplasty with or
without stenting offers a less invasive method to
correct the anatomical stenosis. Although still a
matter of great debate, it is clear that angio-
plasty with or without stenting may offer at least
short-term improvement in blood pressure
and, in certain circumstances, renal function.
Although this option is especially appealing for
patients, it is certainly necessary to further eval-
uate and better define what the role of endovas-
cular management of symptomatic RAS should
be through a multi-institutional randomized,
prospective trial.

There is much debate regarding the need to
place a stent in the renal artery compared to
angioplasty alone. Typically, renal artery angio-
plasty alone is utilized for fibrodysplastic
lesions and lesions that do not involve the origin
of the renal artery. However, as mentioned pre-
viously, RAS that is atherosclerotic in etiology is
often an extension of aortic plaque. For this
reason, angioplasty alone is not as durable. It
has been demonstrated that atherosclerotic
lesions of the renal artery seem to have lower
rates of re-stenosis following angioplasty and
placement of a stent for this reason. In addition,
it is clear that if there is a residual stenosis fol-
lowing initial angioplasty or evidence of dissec-
tion, a stent should be placed at that time.

There has been some concern that renal
artery angioplasty and stenting may make oper-
ative intervention difficult or impossible sec-
ondary to postangioplasty periarterial fibrosis.
This is especially true for transaortic renal
endarterectomy. In the case of a previously
placed renal stent placement, renal artery
bypass grafting to a site on the renal artery
distal to the stent may be the best option.

However, in certain cases, endarterectomy may
still be feasible (Pak, 2002).

Although it is widely practiced at most insti-
tutions, renal artery angioplasty and stenting is
a topic that is still the subject of modest debate.
There are only a few prospective randomized
controlled trials that compare medical therapy,
endovascular management, and open surgical
repair of symptomatic RAS.

Weibull and associates (1993) prospectively
and randomly assigned 58 patients with symp-
tomatic RAS to either renal angioplasty or sur-
gical renal revascularization. Percutaneous
transluminal angioplasty (PTA) was initially
technically successful 83% of the time, whereas
surgical management was successful 97% of the
time. The primary patency rate after 2 years was
75% in the PTA group compared to 96% in the
surgical group. Secondary patency was 90%
versus 97%, respectively, in the PTA and surgi-
cal patients. Hypertension was improved in 90%
after PTA and 86% following open surgical renal
revascularization, and improvement in renal
function was seen in 83% and 72%, respectively.
The authors concluded that PTA is a reasonable
option when compared to surgical revascular-
ization. Indeed, the primary patency was lower
in the endovascular group, but the secondary
patency was comparable. Patients treated with
angioplasty of RAS clearly require close surveil-
lance and often subsequent procedures to main-
tain patency.

Martin and colleagues (2003), as well, have
demonstrated a 30% incidence of re-stenosis
following initially technically successful renal
artery angioplasty. This high incidence of re-
stenosis with respect to renal artery ostial
lesions is likely due to the fact that these lesions
represent extension of an aortic plaque. The
idea of placing stents in the renal arteries as a
method of preventing re-stenosis was intro-
duced by Palmaz in 1976, initially in animal
models and subsequently in humans. Currently,
the indications for the placement of a stent in a
renal artery following renal artery angioplasty
include substantial elastic recoil, resistance of
the plaque, or dissection.

Bush and colleagues (2001) retrospectively
examined the results of renal artery stenting in
73 consecutive patients over a 7-year period. In
this study, the majority of stents were placed
for residual stenosis following angioplasty or
dissection. The technical success rate was

227

RENOVASCULAR HYPERTENSION AND ISCHEMIC NEPHROPATHY

89%, with one patient requiring thrombolytic
therapy for intrastent thrombus. The complica-
tion rate was 9.1% with renal artery thrombo-
sis, extravasation, and hematoma. In this study,
the authors noted a significant decrease in both
systolic and diastolic blood pressures (p < .001)
as well as a decrease in the number of medica-
tions required to treat the hypertension (p <
.01). Over the course of an average of 20 months'
follow-up, serum creatinine levels decreased
by more than 20% in 22% of patients. It
remained unchanged in 48% of patients and
deteriorated in 25% of patients. Of the 25% of
patients who had an increase in serum creati-
nine, 12% eventually required hemodialysis.
Five of these patients had a preoperative creati-
nine level over 4.0mg/dL. Over the course of
approximately 11 months' follow-up, 10 patients
had evidence of re-stenosis in a total of 14 renal
arteries. Overall, this retrospective study estab-
lished the safety of endovascular management
with respect to these lesions as an alternative to
open surgical repair.

Attempts to validate the endovascular man-
agement of symptomatic RAS seem to be
beneficial, at least in the short term. This
method of treatment, although less invasive
than open surgical repair, appears not to be as
durable over the long term. This group of
patients needs close post-angioplasty and stent
surveillance to detect re-stenosis and subse-
quent intervention to have results that are com-
parable to open surgical repair. However, this
still remains an option that is feasible for the
treatment of these lesions and attractive for the
patients. It is hoped that through the use of a
well-constructed trial, more data will be avail-
able to formulate more solid conclusions on
angioplasty and stenting of symptomatic renal
artery stenosis.

Open Surgical Renal
Revascularization

Open surgical repair or reconstruction of symp-
tomatic renal artery lesions still remains the
gold standard in treatment. Options for direct
open surgical repair include aortorenal bypass,
reimplantation of the renal artery, and throm-
boendarterectomy Indirect renal revasculariza-
tion may be accomplished via splenorenal or
hepatorenal artery bypass. This option is espe-

cially useful because aortic cross-clamping may
be avoided. The conduits available for use
include autologous vein grafts, synthetic polyte-
trafluoro ethylene (PTFE) and Dacron pros-
thetic grafts, and autologous hypogastric artery.
Nephrectomy, as well, may be considered in
patients with unreconstructable renal disease
with a nonfunctioning ipsilateral kidney.

The operative approach may be through a
midline xiphoid to pubis incision, a supraum-
bilical transverse incision, an extended flank
incision, or a subcostal incision. The midline
approach is useful for atherosclerotic lesions as
well as lesions combined with aortic proce-
dures, whereas the subcostal or flank incisions
are efficacious for fibrodysplastic lesions or
splanchnorenal bypass. When combined with
mesenteric artery bypass grafting, the extended
flank incision may be useful. Thromboen-
darterectomy may be easily accomplished via a
retroperitoneal trapdoor approach.

With respect to exposure of the distal renal
artery, the left renal artery lies posterior to the
left renal vein. The vein must be sufficiently
mobilized with division of the gonadal and
adrenal veins. The renal vein may be retracted
either cephalad or caudad to expose the renal
artery. There is also a lumbar vein that enters the
posterior aspect of the renal vein that may be
easily avulsed if not carefully identified and
ligated. Distal exposure of the renal artery is
essential to clearly identify the extent of the
atheroma, and the renal artery should be dis-
sected free distal to the atherosclerotic plaque.
Silastic loops may be used for distal arterial
control, as they are less traumatic compared to
metal clamps.

The aortic anastomosis is typically per-
formed utilizing an aortotomy that is two to
three times the diameter of the conduit. The
anastomosis is usually placed on the anterolat-
eral aspect of the aorta. It is essential to prevent
the graft from kinking. For right-sided revascu-
larizations, the aortorenal graft is typically
placed in a retrocaval position, although this
must be individualized. With respect to left-
sided revascularizations, the graft is usually
placed beneath the left renal vein.

Subsequently, the renal anastomosis is com-
pleted. This is typically anastomosed in an end-
to-end fashion with spatulation of both the graft
and renal artery. Spatulated anastomoses are
ovoid and less prone to the development of

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VASCULAR SURGERY

strictures. Intraoperative evaluation of blood
flow is typically accomplished using a direc-
tional Doppler device. Intraoperative angiogra-
phy is usually unnecessary; however, many
surgeons advocate baseline angiography prior
to discharge to establish a baseline and to
confirm the adequacy of repair.

Hansen and colleagues (1992) retrospectively
reviewed the data on 200 patients who under-
went open surgical renal revascularization over
a 54-month period. There was a mortality rate
of 2.5% and only a 1.4% primary failure rate at
30 days. In this series, the hypertension was
cured in 21% of patients and improved in
another 70%. Of the patients with ischemic
nephropathy, 49% demonstrated an improve-
ment in glomerular filtration; 36% of these
patients remained stable and only 15% wors-
ened. This study clearly demonstrates that open
surgical renal revascularization is a safe option
that is successful in treating the underlying clin-
ical manifestations of the RAS in the majority of
patients.

Recently, Cherr and associates retrospectively
reviewed the clinical outcome of 500 consecu-
tive patients with renovascular hypertension.
The perioperative mortality was 4.6% at 30 days.
The hypertension was cured in 12%, improved
in 73%, and unchanged in only 15%. With
respect to ischemic nephropathy, 43% had an
improvement in renal function, 47% were
unchanged, and 10% became worse. Interest-
ingly, of the 43% of patients who demonstrated
an improvement in renal function, 28 patients
were removed from dialysis dependence. These
data confirm the findings of Hansen and asso-
ciates and once again demonstrate that open
surgical repair of severe, flow-limiting, sympto-
matic RAS is efficacious in improving hyper-
tension and ischemic nephropathy in the
majority of patients. It adds the point, however,
that if there was a blood pressure cure or an
improvement in renal function, there was an
association with dialysis-free survival. This has
a significant impact on patient lifestyle as well
as on health care dollars.

At this time, there is significant controversy
regarding the optimal treatment in patients
with symptomatic RAS. It is important that a
multicenter, prospective, randomized clinical
trial be organized in an effort to further define
the best possible treatment options for these
patients.

Conclusions

Renovascular hypertension is an uncommon
cause of hypertension in the general population.
However, it may cause considerable morbidity
with respect to end-organ damage from uncon-
trolled hypertension as well as progression of
ischemic nephropathy. It appears as if duplex
ultrasound is at least a reasonable screening tool
in patients suspected of having hypertension
that is renal in origin. However, there clearly
needs to be correlation between the anatomical
stenosis and the physiological effect. For this
purpose, there is not a clearly optimal test,
although captopril renography seems to offer
the best results at this time.

Once diagnosed and found to be functionally
significant, there are several options for the
treatment of RAS, including medical manage-
ment, endovascular angioplasty with or without
stent placement, or open surgical revasculariza-
tion. From the data that are available, it is
clear that there is a patient population that
does benefit from revascularization, either
endovascular or surgical. Surgical revascular-
ization is more durable, and long-term success
has been previously demonstrated. Angioplasty
with or without stent placement is indeed less
durable over the long-term; however, with close
surveillance and secondary intervention, it may
offer results comparable with open surgical
repair.

Although there have been a multitude of
attempts to define which patients with sympto-
matic RAS would benefit from renal revascular-
ization, both surgical and endovascular, there is
still no clear consensus at the present time.
Recently, the American Heart Association
released the guidelines for the reporting of renal
artery revascularization in clinical trials. This
document serves to clearly outline criteria and
definitions for randomized, controlled clinical
trials, which are needed to further dictate the
optimal management of symptomatic RAS. At
this time, it is clear that certain patients do
benefit from restoration of blood flow to the
kidney, but a multicenter, prospective, random-
ized, controlled study will be better able to
define which patients benefit from surgical
repair compared to endovascular management
and which patients, if any, should merely be
treated medically.

229

RENOVASCULAR HYPERTENSION AND ISCHEMIC NEPHROPATHY

References

Barrett BJ, Carlisle EJ. (1993) Radiology 188:171-8.

Bush RL, Najibi S, MacDonald MI, et al. (2001) J Vase Surg

33:1041-9.
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Radiol 14:5297-310.
Pak LK, Kerlan RK, Mully TW, Messina LM. (2002) J Vase

Surg 35:808-10.
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344:410-17.

Rundback JH, Sacks D, Kent KC, et al. (2002) J Vase Intervent
Radiol 13:959-74.

Simon N, Franklin SS, Bleifer KH, Maxwell MH. (1972)
JAMA 220:1209-18.

Webster J, Marshall F, Abdalla M, et al. (1998) J Hum Hyper-
tens 12:329-35.

Weibull H, Bergqvist D, Bergentz SE, Jonsson K, Hulthen L,
Manhem P. (1993) J Vase Surg 18:841-50; discussion
850-2.

Zierler RE, Bergelin RO, Isaacson JA, Strandness DE Jr.
(1994) J Vase Surg 19:250-7; discussion 257-8.

Visceral Ischemic Syndromes

George Geroulakos, Peter A. Robless, and
William L. Smead

The disorders of the visceral circulation are
infrequent mainly because of the very extensive
and efficient collateral system connecting the
celiac, superior mesenteric, and inferior mesen-
teric arteries. However, there is a lot of interest
in the optimal management of these conditions,
because of their catastrophic outcomes that are
usually associated with a high morbidity and
mortality. Over the last two decades there has
been a greater awareness of these conditions,
which was followed by the introduction of new
diagnostic and therapeutic techniques such as
duplex ultrasound, computed tomography (CT),
magnetic resonance angiography (MRA), and
angioplasty/stenting.

Visceral ischemic syndromes can be classified
as acute or chronic. Acute ischemic syndromes
are the result of embolic or thrombotic occlu-
sion of a visceral branch of the infradiaphrag-
matic aorta. In addition, it could be the result of
mesenteric venous thrombosis. Chronic visceral
ischemia is usually caused by stenotic or occlu-
sive atherosclerotic lesions involving two or
more visceral vessels.

Acute Mesenteric Ischemia

Acute mesenteric ischemia (AMI) is a life-
threatening condition seen in 1 per 1000 hospi-
tal admissions with mortality rates ranging
between 60% and 100% despite advances in
operative technique and perioperative manage-
ment (Bradbury et al., 1995). Early diagnosis

and aggressive management are essential.
However, the relative rarity of this condition,
along with the nonspecific physical findings
makes early diagnosis difficult and is often
delayed. Furthermore, patients with AMI are
often elderly, malnourished, and have signi-
ficant comorbidity that increases the risk of
major surgical intervention.

The most common causes of AMI are supe-
rior mesenteric artery embolization (50%) or
thrombosis (25%), nonocclusive mesenteric
ischemia (20%), and acute mesenteric venous
thrombosis (5%). Rarer causes include vas-
culitis, fibromuscular dysplasia, dissection,
trauma, and mesenteric aneurysm rupture or
thrombosis.

Pathophysiology

Two thirds of mesenteric blood flow supplies
the gut mucosa. Splanchnic autoregulation fails
when perfusion pressure falls below 40mmHg,
and prolonged gut ischemia results in anaerobic
metabolism. The extent of injury is related to
the duration and the anatomical extent of
mesenteric ischemia. At the cellular level,
adenosine triphosphate (ATP) is depleted with
a buildup of catabolic products and lactate.
Mucosal and vascular permeability increases
and tissue injury occurs. Hemorrhagic necrosis
follows with mucosal sloughing, bowel wall
edema, and intestinal hemorrhage (Table 19.1).
The bowel wall becomes permeable to gut bac-
teria once the mucosa is shed. Peritonitis results

231

232

VASCULAR SURGERY

Table 19.1. Pathophysiology of mesenteric ischemia

Mucosa — villous sloughing
Increased capillary permeability — Edema
Submucosal hemorrhage
Transmural necrosis

from transudation of microflora across the
intestinal wall. Septicemia develops as the
organisms enter the portal circulation. Massive
fluid shifts into the bowel wall and peritoneum
follow, resulting in hemoconcentration, oliguria,
and hypotension. Serum levels of lactate dehy-
drogenase (LDH), serum glutamic oxaloacetic
transaminase (SGOT), and creatine kinase (CK)
become markedly elevated with the death of
intestinal cells.

Ischemia reperfusion injury due to free
radical production through the xanthine
oxidase pathway may result from subsequent
reperfusion of the acutely ischemic gut. There is
a high mortality rate from the ensuing multior-
gan dysfunction syndrome.

Acute Mesenteric Embolism

The main presenting symptom is usually the
sudden onset of severe central abdominal pain.
The severity of the pain is usually out of pro-
portion to the physical findings. This may be
accompanied by vomiting or diarrhea.

Mesenteric emboli can originate from the
heart or the supradiaphragmatic aorta and most
frequently occur in patients with cardiac arry-
thmias, valvular disease, or following myocar-
dial infarction. If the embolus disintegrates and
travels distally, the resulting ischemia may be
patchy, typically affecting the duodenum, prox-
imal jejunum, and colon. The majority of emboli
lodge in the superior mesenteric artery (SMA)
distal to the origin of the middle colic artery,
often sparing the proximal jejunum and ascend-
ing/transverse colon. Owing to the lack of ade-
quate collaterals, this may lead to reactive
vasoconstriction, thereby reducing existing col-
lateral blood flow and increasing the ischemic
injury.

Mesenteric Artery Thrombosis

Thrombosis of the SMA or celiac axis occurs
as a result of underlying mesenteric atheroscle-

rotic stenosis progressing to occlusion. This
usually occurs at the origin of the vessel. Other
causes include systemic vasculitic and pro-
thrombotic syndromes. Less common causes
include aortic and visceral artery aneurysms
or dissection. Some patients may describe pro-
dromal symptoms compatible with chronic
mesenteric ischemia. These patients often have
coexisting multilevel atherosclerotic disease.
Unlike acute mesenteric embolism, the onset of
pain is often gradual, with nonspecific central
abdominal pain. The extent of infarction usually
involves the duodenum to the transverse colon
and is typically more extensive than that seen
with acute embolism.

Nonocclusive Mesenteric Ischemia

Nonocclusive mesenteric ischemia (NOMI)
develops in patients with low-cardiac-output
states, especially in the presence of digoxin or
vasoconstrictors. Secondary mesenteric vaso-
constriction results in segmental vasospasm of
the secondary and tertiary branches of the SMA.
It is not caused by underlying atherosclerosis or
venous obstruction. Causes of low-flow states
include cardiac failure, shock, and hypovolemia.
The use of vasoconstricting agents that affect
the splanchnic circulation such as digoxin,
cathecholamines, angiotensin II, vasopressin,
beta-blockers, and cocaine has been associated
with NOMI.

Diagnosis

Acute mesenteric ischemia presents classically
with acute onset of abdominal pain out of pro-
portion to the physical findings. Central abdom-
inal pain occurs as a result of mid-gut ischemia
and spasm. Gastrointestinal emptying, with
emesis and bloody diarrhea may occur. Labora-
tory findings including leukocytosis, acidosis,
hyperkalemia, raised hematocrit, LDH, SGOT,
and CK occur later. However, no single labora-
tory investigation or combination of tests has
proved to be sensitive or specific enough to
enable the early diagnosis of AMI.

Early recognition of AMI is crucial, as bowel
necrosis develops in many patients by the time
of surgery and investigations should not pro-
duce unnecessary delays in revascularization.

Plain abdominal x-rays may show nonspecific
findings of intestinal dilatation, gasless abdo-

233

VISCERAL ISCHEMIC SYNDROMES

men, or other signs of ileus. Occasionally mural
"thumb printing" is caused by submucosal
edema or hemorrhage. Pneumoperitoneum or
portal vein pneumatosis may be seen in
advanced cases with transmural infarction.
Ultrasonography in patients with AMI may
reveal a thickening of the bowel wall, signs of
ileus with distended bowel loops, intraperi-
toneal fluid, or air in the portal vein. Ultra-
sonography is also helpful in excluding other
causes of an acute abdomen.

Ultrasound and plain x-rays are not very
specific in diagnosing AMI and other imaging
modalities such as CT, MRA, and contrast
angiography play a major role in the diagnosis.
Computed tomography angiography is sen-
sitive for the diagnosis of mesenteric occlusion
or bowel ischemia. Computed tomography
scanning also facilitates the identification of
nonvascular causes of acute abdominal pain.
Computed tomography angiography with three-
dimensional reconstruction may facilitate iden-
tification of vascular anatomy and pathology
with good enough detail for diagnosis and oper-
ative planning (Fock et al., 1994).

Differentiation of the three forms of mesen-
teric arterial occlusion can be done with aor-
tography and it facilitates planning of
treatment. Selective mesenteric angiography
remains the most reliable and definitive diag-
nostic tool for AMI. Endovascular interven-
tions or catheter-directed vasodilator therapy
can be started immediately after angiography
(Park et al., 2002).

Thrombotic occlusion of the SMA produces a
sudden cut-off at the vessel origin or within 1 to
2 cm of the SMA trunk. Extensive collaterals in
the distal SMA indicate a chronic occlusion.
Mesenteric arterial emboli produce a sharp,
rounded filling defect with a typical meniscus
sign on angiography. Vasospasm maybe present
with mesenteric thrombosis or embolism.
Angiographic criteria for NOMI include a
diffuse narrowing of the SMA and its branches,
alternating areas of narrowing and dilatation of
the SMA branches (string of sausages sign),
spasm of the peripheral vascular arcades,
impaired filling of the intramural vessels, and a
sluggish flow with reflux of contrast during
selective SMA injection. Increased vessel diam-
eter following papaverine infusion and the
absence of atherosclerotic disease on angiogra-
phy supports the diagnosis of AMI.

Treatment

Regardless of the etiology of the AMI, the goals
of surgical treatment are to reestablish good
pulsatile flow to the SMA, to restore adequate
blood flow to the ischemic but viable gut, and to
resect the necrotic bowel. Adequate volume
resuscitation and correction of acid base and
electrolyte imbalance must also be undertaken.
Cardiac output has to be optimized, and any
arrhythmias treated. Broad-spectrum antibi-
otics are given if signs of peritonitis are present.

The single factor in improving the results
of surgical treatment of acute mesenteric
insufficiency has been the addition of tran-
scatheter intraarterial vasodilator infusion peri-
operatively (Boley et al., 1981).

The decision to undertake second-look
laparotomy is made at the time of the initial
laparotomy. It allows the reassessment of bowel
viability and to decide if further bowel resection
is required. Bowel viability can be assessed by
physical examination, handheld Doppler scan
examination, and intravenous injection of
fluorescein (Ballard et al., 1993).

Acute Mesenteric Artery Embolism

Surgical revascularization in the presence of an
embolism is performed with balloon embolec-
tomy usually with p atch angioplasty of the SMA.
Patients with chronic proximal occlusion or
stenosis undergo revascularization with bypass
grafting. Autogenous vein is the graft material
of choice if resection of necrotic bowel is nec-
essary. Resection of the infarcted bowel is per-
formed following revascularization.

Acute Mesenteric Artery Thrombosis

The thrombotic process occurs in a severely ath-
erosclerotic proximal SMA. Therefore, these
patients require placement of a bypass graft to
the SMA distal to the occlusive segment. Ante-
grade or retrograde bypass may be performed
depending on anatomical considerations or
according to surgeon preference.

Thrombolytic therapy is a potential consider-
ation in patients with acute thrombosis and no
clinical signs of peritonitis. Successful lysis
returns the mesenteric circulation to its chronic,
stable state. Subsequent operative revasculari-

234

VASCULAR SURGERY

zation or balloon angioplasty of the stenotic
vessel can be undertaken electively. How-
ever, this does not allow inspection for bowel
viability following reperfusion and may delay
operative revascularization if thrombolysis is
unsuccessful. Thrombolysis in AMI therefore
should be reserved for selected patients (Park
et al, 2002).

Nonocclusive Mesenteric Ischemia

The treatment of NOMI is primarily nonsurgi-
cal. A metabolic cause of the problem should be
identified and corrected. The SMA is selectively
catheterized, and vasodilating agents such as
papaverine (or tolazoline hydrochloride) are
administered. Resection of nonviable bowel
may be required (Park et al., 2002).

Chronic Visceral Ischemia

Clinical Presentation

The most common pattern of symptoms is
chronic abdominal pain that is associated with
involuntary weight loss. The pain is usually epi-
gastric, dull, or colic. The patient experiences
the pain 15 to 30 minutes after eating, and it
lasts for 1 to 3 hours before disappearing. The
pain becomes so severe that soon the patient
develops fear of food and limits the oral intake.
This results in a pronounced weight loss.
Absence of weight loss may put in doubt the
diagnosis of chronic visceral ischemia. Other
gastrointestinal complaints may include diar-
rhea, nausea or vomiting, and constipation. The
most typical feature of the clinical presentation
is that the symptoms are atypical. We and others
have shown that the majority of the patients
affected are women in their sixth decade of life.
The reasons for this sex predilection remain
undetermined. On examination, the patient
looks emaciated, mimicking a patient with
advanced malignant disease. These is often an
epigasric bruit present.

Untreated patients with symptoms of chronic
visceral ischemia are at an increased risk of
death from complications of acute visceral
ischemia. In a large series of patients presenting
with acute mesenteric ischemia over a period of
10 years, 43% had prior chronic symptoms.

Investigations

Gastrointestinal contrast studies, endoscopy,
and computed tomography are not essential to
the diagnosis but are important in eliminating
other sources of abdominal discomfort.
Microulceration of the gastric mucosa and atyp-
ical colonic mucosa ulceration are uncommon
endoscopic findings.

Duplex ultrasound examination of the celiac
and the superior mesenteric artery origin can
be successfully obtained in 80% to 95% of the
cases, and in these it is a reliable screening test
for chronic visceral ischemia. To obtain optimal
visualization of the celiac and superior mesen-
teric arteries, patients should be on a clear
liquid diet on the day before the examination
and should refrain from oral intake for 6 hours
before the study. Lateral views of biplane aor-
tography remains the primary diagnostic
modality in demonstrating visceral occlusive
lesions compatible with the diagnosis. In a
typical patient there is involvement of two or all
three visceral arteries. Aortography also reveals
the meandering mesenteric artery (arch of
Riolan or arch of Treves), a large collateral tor-
tuous vessel of uniform caliber residing in the
left upper quadrant of the abdomen. It connects
the middle colic artery with the patent trunk of
the inferior mesenteric artery.

Treatment

Angioplasty

Mesenteric percutaneous transluminal angio-
plasty (PTA) is a valuable treatment option in
patients with chronic visceral ischemia who are
considered high operative risk. The initial tech-
nical success rate is good, with the majority of
patients having symptomatic improvement and
continuous relief of symptoms at short-term
follow-up. However, long-term patency results
are unknown. Allen et al. (1996) presented a
series of 19 patients treated by PTA. The only
technical failure resulted in mesenteric artery
dissection, thrombosis, bowel infarction, and a
fatal outcome. Complete symptomatic relief was
attained in 15 patients. Recurrent symptoms
developed in three patients (20%) at a mean
interval of 28 months. Percutaneous translumi-
nal angioplasty may also be used for the man-
agement of recurrent symptoms following the

235

VISCERAL ISCHEMIC SYNDROMES

development of a stenosis in the aortomesen-
teric bypass.

Surgery

A variety of techniques have been developed
to correct atherosclerotic obstruction of the
major visceral branches of the thoracic aorta.
Techniques of revascularization include tran-
section of the mesenteric artery and reimplan-
tation on the aorta, bypass grafting, and
thromboendarterectomy There is no consensus
regarding the best surgical approach for the
treatment of chronic visceral ischemia. Bypass
grafting is the most common type of visceral
revascularization performed today. It provides
immediate restoration of flow and may origi-
nate from several different locations that
include the suprarenal aorta (antegrade recon-
struction) or the infrarenal aorta and the
common iliac arteries (retrograde reconstruc-
tion). The distal thoracic aorta is usually free of
atherosclerosis and is an excellent origin of a
short bypass placed in the direction of normal
flow. This design eliminates the possibility of
kinking and thrombosis by compression or
traction from the overlying mesentery, which
may be observed with retrograde grafts. The
distal thoracic aorta may be approached from
the abdomen or via a thoracoabdominal inci-
sion. The retrograde bypass has the advantage
that its origin is in a more familiar territory,
but it is more commonly affected by atheroscle-
rotic or aneurysmal disease. Park et al. (2002),
in a large series of 98 reconstructions for
chronic visceral ischemia, reported a 5-year
symptom-free survival of 92%. The rate of
recurrence was unaffected by the number of
vessels revascularized or the orientation of the
bypass. In contrast, others have reported that
revascularization of as many visceral vessels
as possible is important in reducing the risk
of recurrent intestinal ischemic symptoms
(Rheudasil et al., 1988). Thus the number of
vessels that need to be revascularized remains a
controversial issue.

Thromboendarterectomy has been used by a
small number of groups with excellent results.
The aorta is approached via medial visceral
rotation. For the majority of ostial stenoses, a
"trapdoor" arteriotomy is made around the
celiac and superior mesenteric arteries as they
emerge from the aortic wall. A retrograde

endarterectomy facilitates direct removal of the
aortic plaques. Duplex scanning should be
routinely used at the end of the procedure to
document the technical result at the distal end
point of the endarterectomy in the mesenteric/
celiac artery. A comparison of antegrade bypass
(n =004 26) and transaortic endarterectomy
(n = 48) showed the same incidence of periop-
erative mortality and 5-year recurrence-free
survival for both groups (Cunningham et al.,
1991).

Mesenteric Venous
Thrombosis

Mesenteric venous thrombosis is a rare but
potentially lethal form of intestinal ischemia
that accounts for 5% to 15% of all cases of
mesenteric vascular events. Improved survival
depends on early recognition and appropriate
treatment of this entity.

Etiology

Low-flow states in the mesenteric venous circu-
lation that may be produced by liver cirrhosis,
portal hypertension, and congestive heart
failure could lead to mesenteric venous throm-
bosis. Intraabdominal infections from organs
that drain to the mesenteric venous system such
as appendicitis, diverticulitis, pelvic abscess,
and pancreatitis can be associated with mesen-
teric venous thrombosis. Other conditions that
may predispose to mesenteric venous thrombo-
sis include hypercoagulable states associated
with malignancy, oral contraceptives, and recent
operations, particularly splenectomy followed
by thrombocytosis. Thrombophilia is common
in this group of patients. In a series of 31
patients, 13 (42%) were diagnosed to have a
hypercoagulable state. Twelve patients were
found to have protein C, protein S, or antithrom-
bin III deficiency. A single patient had activated
protein C resistance. Six patients had prior
thrombotic episodes, including deep venous
thrombosis (« = 5) or arterial thrombosis (n =
l).Four patients had a history of cancer, and five
patients had previously undergone a splenec-
tomy (mean platelet count 487,000) (Morasch
et al.,2001).

236

VASCULAR SURGERY

Clinical Presentation

The most common presenting symptom is
abdominal pain. The pain is constant, colicky,
and poorly localized. Often the complaints of
abdominal pain are out of proportion to the
clinical findings. Other symptoms include vom-
iting, diarrhea, and constipation. In a series of
patients with mesenteric venous thrombosis,
upper and lower gastrointestinal bleeding
occurred in 10% and 19% of the patients,
respectively. Physical findings in patients who
had gradual onset of abdominal symptoms may
reveal low-grade pyrexia, abdominal distention,
increased bowel sounds, and generalized
abdominal tenderness. When the pain is local-
ized, it may be located in either the upper or
lower quadrants of the abdomen.

Peritoneal signs such as guarding and
rebound are present when infarction of the
bowel has occurred.

Investigations

Plain abdominal films are abnormal but not
specific in the majority of the patients. Edema-
tous and dilated small bowel loops are the most
common finding.

Contrast-enhanced CT scanning is the most
sensitive tool in detecting acute mesenteric
venous thrombosis. The presence of a mesen-
teric venous filling defect is diagnostic of this
condition. Other CT findings include free fluid;
an enlarged, dilated superior mesenteric vein;
mesenteric edema or stranding; bowel wall
thickening or edema; and dilated small bowel
loops. Selective mesenteric angiography may
show intense spasm of the arterial branches
supplying the involved part of the bowel, pro-
longed opacification of the thickened bowel
wall, contrast extravasation into the lumen of
the bowel, visualization of the venous thrombus,
or nonvisualization of the venous phase. Cur-
rently, angiography is not recommended as the
initial investigation.

Treatment

Patients with mesenteric venous thrombosis
and no signs of peritonitis are treated with fluid
resuscitation, prophylactic antibiotic therapy,

and intravenous heparin. Close clinical and
hemodynamic monitoring is indicated, prefer-
ably in an intensive care unit. If peritoneal signs
are present, a laparotomy should be performed
and the infarcted bowel should be resected. An
ileostomy should be considered if there is exten-
sion of the macroscopic involvement at the
resection margins. The macroscopic features of
the affected part of the bowel are striking, and
consist of a dark red coloration and thickening
of the bowel. It is often difficult to distinguish
viable from nonviable bowel. In a recent series
82% of patients who underwent bowel resection
(about 100 cm length) did not have transmural
necrosis. Bowel viability assessment by direct
inspection may be improved by Doppler ultra-
sound techniques or fluorescein examination
under a Wood's lamp. Several case reports have
been published indicating that thrombolysis
may be a useful treatment option for patients
with no signs of peritonitis. Antegrade transar-
terial thrombolysis via the superior mesenteric
artery has been effective in a small number of
cases in lysing the thrombus and providing
good symptomatic relief (Antoch, 2001). Post-
operatively, patients should be anticoagulated to
prevent recurrent episodes of thrombosis. The
duration of anticoagulation is determined by
the expected duration of the predisposing
factors.

References

Allen RC, Martin GH, Rees CR, et al. (1996) J Vase Surg

24:415-21; discussion 421-3.
Antoch G, Taleb N, Hansen D, Stock W. (200 1 ) Vase Endovasc

Surg 20:471-2.
Ballard JL, Stone WM, Hallett JW, Pairolero PC, Cherry KJ.

(1993) Am Surg 59:309-11.
Boley SJ, Feinstein FR, Sammartano R, Brandt LJ, Sprayre-

gen S. (1981) Surg Gynecol 153:561-9.
Bradbury AW, Brittenden J, McBride K, Ruckley CV. (1995)

Br J Surg 82:1446-59.
Cunningham CG, Reilly LM, Rapp JH, Schneider PA, Stoney

RJ. (1991) Ann Surg 214:276-87; discussion 287-8.
Fock CM, Kullnig P, Ranner G, Beaufort-Spontin F, Schmidt

F. (1994) Eur J Radiol 18:12-14.
Morasch MD, Ebaugh JL, Chiou AC, Matsumura JS, Pearce

WH, Yao JS. (2001) J Vase Surg 34:680-4.
Park WM, Gloviczki P, Cherry KJ Jr, et al. (2002) J Vase Surg

35:445-52.
Rheudasil JM, Stewart MT, Schellack JV, Smith RB 3rd, Salam

AA, Perdue GD. (1988) J Vase Surg 8:495-500.

Endovascular Approaches and Techniques

Steven M. Thomas, Kong T. Tan, and Mark F. Fillinger

This last chapter describes the equipment com-
monly used during endovascular procedures;
some of the commonly used endovascular tech-
niques, beginning with arterial access tech-
nique; and the endovascular interventions for
arterial occlusive disease and aneurysmal
disease. Embolotherapy is also discussed.

Equipment for Access,
Angiography, and
Vascular Intervention

Needles

In general terms, there are two types of needles
available for obtaining vascular access: one-part
and two-part. The one-part needle has a sharp
cutting bevel, whereas the two-part needle has
a sharp inner stylet with a blunt outer needle.
The two-part needle is preferred by many for
vascular access at the femoral artery, because it
reduces the risk of vascular damage at the access
point, either due to movement of the needle tip
or passage of the guidewire into the subintimal
plane (see Access Technique, below). The most
commonly used needle calibers are 18 and 19
Stubs needle gauge (18 being the larger and
equivalent to about 1.25 mm in outer diameter).
For most purposes the 19-gauge needle suffices,
though it does not accommodate an 0.038-inch-
diameter guidewire if required. A newer variant
of the one-part needle designed to reduce arte-

rial injury is the 20- or 22-gauge needle typically
used as part of a "micropuncture" set. The
micropuncture technique uses a 0.014- or 0.018-
inch guidewire and standard Seldinger tech-
nique to introduce a short 4-French sheath,
which is then used to place the typical 0.035-
inch guidewire.

Wires

Guidewires are integral to successful catheteri-
zation; they support the catheter and allow the
catheter to be steered to its intended location.
Guidewires come in many diameters and
lengths, and degrees of stiffness, slipperiness,
and steerability All wires have a softer, more
flexible, curved, or "floppy" leading end to min-
imize damage to the vessel as it is advanced,
though the length of the flexible segment may
vary. This is because a long flexible segment may
be useful if a vessel is extremely tortuous, or a
very short flexible segment may be needed to
allow maximum support for an advancing
catheter or sheath.

Diameter

Most standard guidewires are 0.035 inch in
diameter, though some very stiff wires are 0.038
inch in diameter. It is important to ensure that
the wire used is compatible with the lumen
diameter of the catheter to be placed over it. If
small-caliber catheters are used, small-diameter
wires such as 0.014 or 0.018 inch are required.

237

238

VASCULAR SURGERY

However, many of these wires do not have the
same stiffness as larger diameter wires, and
hence may kink or result in poor tracking of the
catheter. If a kink is produced, it is usually very
difficult to pass a catheter over the wire, and a
new wire is required. The hydrophilic Terumo
(Terumo, Leuven, Belgium) guidewire has a
nitinol core and is difficult to kink.

Length

The usual length of guidewire required is about
150 cm, and this is adequate for most diagnostic
imaging. However, in some circumstances
longer wires are required, usually ranging from
200 to 300 cm. This is particularly the case in a
peripheral location, where the catheter has to be
changed, or a guiding catheter, angioplasty
balloon, or stent has to be introduced. When
using monorail balloon catheters or stents for
intervention, this is usually less of a problem
compared to systems that are fully over the wire.
This is because in a monorail system the wire
passes through the wire guide for only about 30
cm from the tip of the catheter or device, rather
than through the whole length of the catheter or
device as occurs in a fully over-the-wire system.
Aortic stent-graft interventions also tend to
require long (260 cm) guidewires due to the
length of the delivery system for most aortic
stent grafts. However, systems tend to be manu-
facturer-specific, as some newer aortic stent-
graft systems require only 180-cm guidewires.

Stiffness

The degree of guidewire stiffness varies consid-
erably (Table 20.1). It is generally easier to track
a catheter or device over a stiffer guidewire;
however, a very stiff guidewire may be more
difficult to manipulate into a vessel origin or
through a diseased vessel. Exchanging wires is
often necessary for different parts of a proce-
dure, but a stiff wire should always be placed
through a catheter that has been positioned
using a more conventional wire to prevent
damage to the vessel during advancement of the
stiff wire.

Slipperiness

Some wires (e.g., Terumo Glidewire or Cook
Nimble guidewire), have a hydrophilic coating
that, once lubricated, becomes very slippery and

Table 20.1. Variation in guidewire stiffness

Floppy

Bentson

Movable core

Standard J or straight

Hydrophilic
More supportive

Heavy duty J or straight

Stiff hydrophilic

Wholey
Stiff

Amplatz super stiff

Amplatz extra stiff

TAD

Flexfinder
Very stiff

Meier

Lunderquist

nearly frictionless. They are very useful for
negotiating tortuous vessels and crossing
stenoses and occlusions. They can be difficult to
handle because when slippery, the wire may slip
back through the operators hands during
catheter exchanges, and if allowed to become
dry, can stick to the operator's gloves and are
then easily pulled out inadvertently. These prob-
lems can be minimized by keeping hydrophilic
wires moist, handling the wires with a damp
gauze to allow slightly more friction than a
glove, using a "torque device" when manipulat-
ing the wire, and using caution when moving
the wire in or out of the patient.

Steerability

A completely straight wire and a J wire have
little or no inherent steerability. A straight wire,
to which a curve has been introduced, can be
directed using the curve, and this is enhanced if
a directional catheter is also used. Many wires
have tips that can be deformed into a curve or
even into a J if required. Some hydrophilic wires
have a preformed curve or angle, and if the core
is made of nitinol (an elastic nickel-titanium
alloy with "memory"), this cannot be changed.
This gives more torque control and makes the
wire very steerable.

Catheters

There are a plethora of catheters available, to be
placed over the guidewire to facilitate arteriog-

239

ENDOVASCULAR APPROACHES AND TECHNIQUES

raphy, selective entry to branch vessels, device
delivery, and so on. The size of catheter is
denoted using the French (F) system, which
describes the outer circumference (external
diameter of 3F = 1mm external diameter).
Smaller caliber catheters have the advantage
that the access puncture site can be kept small,
although the turning ability or torque control is
often compromised. For nonselective angio-
grams this is not usually a problem, and 3F or
4F catheters can be used, but if a selective
catheterization is required, then larger caliber
catheters may be required.

It must be remembered that catheters are
thrombogenic to some extent, and should
always be regularly flushed with heparinized
saline while in the patient. In the case of guide
catheters, this is often best achieved using a bag
of heparinized saline (using a pressure bag)
connected via a side arm.

Most catheters are reasonably radiopaque,
though hydrophilic-coated "glide catheters"
and smaller caliber catheters can be relatively
radiolucent. Some catheters have radiopaque
material added to them toward the tip, or a
radiopaque band at the tip to enhance visibility.

Catheter Types

Most catheters can be divided into two main
groups: nonselective and selective.

Nonselective Catheters

These are used to inject large volumes of con-
trast at high rates into large vessels. They have
multiple side-holes to allow high injection rates
and reduce the risk of subintimal injection by
the end-hole jet of contrast. The most com-
monly used nonselective catheter is the pigtail
catheter, the workhorse of diagnostic angiogra-
phy. If the vessel is too small to accommodate
the pigtail loop, a straight multi-side-hole
catheter can usually be used instead.

Selective Catheters

These are shaped catheters that have directional
properties that aid selective catheterization of
side branch vessels. Some, such as the Multi-
purpose, Cobra, Berenstein, and Sidewinder
catheters, can be used for a variety of selective
examinations, whereas others such as the inter-

nal mammary or renal double-curve catheters
are designed to aid catheterization of particular
vessels. In practice, most angiographers prefer
to have a range of catheters available and some-
times many may be used to achieve a difficult
selective arterial position. Probably the six
most commonly used selective catheters are
Berenstein (or similar Kumpe), Cobra,
Sidewinder, Headhunter, Sos Omni, and Multi-
purpose. Catheters such as the Sidewinder and
Cobra come in a range of sizes designated 1 to
3 dependent on the degree of catheter curve or
loop. These are useful for varying the degree of
angulation at the catheter tip, and the ease of
manipulation as the diameter and tortuosity
varies substantially in large vessels. When using
a Sidewinder catheter in the aorta, if the loop is
too large, the catheter tip will be held away from
the aortic wall and will not engage branch
vessels. This may be modified by introducing a
guidewire into the apex of the catheter curve,
but this often means that a smaller Sidewinder
or a Sos Omni catheter should be used instead.

Most of these catheters can be used as soon
as the wire is removed from them, and will
engage side branches if advanced or retracted.
The Sidewinder and smaller Sos-Omni catheters
need to be re-formed so that the reverse curve
of the catheter can be used to engage side
branch vessels. The Sos Omni, being of a smaller
curve than the Sidewinder catheters, can usually
be re-formed in the aorta. The Sidewinder
catheter usually has to be re-formed using a
variety of techniques. The simplest and safest is
to place a guidewire over the iliac bifurcation
using a pigtail catheter and re-form the
sidewinder in the lower aorta. If this is not pos-
sible, it can usually be easily reformed in the
aortic arch by twisting and advancing the
unformed catheter. Once formed, the catheter is
pulled back to engage the origins of arterial side
branches.

When choosing a catheter, it is important first
to select the appropriate gantry angle to view
the origin of the vessel and its "true" degree of
angulation relative to the parent vessel. The
angle of origin of the vessel being catheterized
often dictates which catheter is most likely to
successfully engage the arterial origin, so, for
example, vessels that are angled back toward the
site of access are often best approached with a
Sidewinder or similar catheter. There are also
catheters that have hydrophilic coatings, and

240

VASCULAR SURGERY

these are often very useful for tracking a
catheter to peripheral locations, particularly for
embolization.

Microcatheters

These are coaxial catheters that are only 2F to
3F in diameter that will pass through the 0.035-
or 0.038-inch lumen of the selective catheters
mentioned above. They were originally devel-
oped for cerebral catheterization and inter-
vention, but can be useful for superselec-
tive catheterization of visceral or peripheral
vascular beds, particularly for embolization
procedures.

Sheaths

Sheaths are used to establish a secure pathway
from the skin to the arterial lumen. This allows
catheters and devices, such as balloons and
stents, to be exchanged in an atraumatic
manner. The sheath is a plastic tube with a
hemostatic valve and an attached side arm to
allow flushing. The size designation of the
sheath refers to the size of catheter that will pass
through it (i.e., the internal diameter). Hence, a
7F sheath allows the passage of a 7F catheter or
device. As a result the external diameter of any
sheath is approximately IF larger than its desig-
nated size for smaller sheath sizes, and 2F to 3F
larger when the sheath size is in the 12F to 25F
range. The thickness of the sheath is also some-
what dependent on its length and intended
application, generally thicker for longer sheaths
intended to pass stents or stent grafts through
tortuous arteries. If the puncture is at a steep
angle or in obese patients, the smaller sheaths
may kink, particularly with an antegrade punc-
ture. There are reinforced sheaths that are resist-
ant to kinking, but they have an external
diameter IF to 2F greater than standard sheaths.
Most sheaths are short, but longer sheaths
and guiding catheters can be useful during
interventional procedures to provide stability to
aid selective catheterization and delivery of bal-
loons or stents. Guiding catheters are larger
than standard catheters, often 6F to 7F, because
they are designed to work with a standard
catheter within. Because they are catheters, it is
important to remember that their size is desig-
nated by the external diameter, unlike a sheath,
despite similarities in appearance. Guiding

catheters come in a variety of lengths and
shapes to aid introduction into the vessel
ostium, allowing conventional catheters to be
introduced through them for more distal
catheterization. Guiding catheters can perform
a similar role to sheaths, but they do not usually
have an integral hemostatic valve, and their
internal lumen is smaller. Thus, in some cases a
guiding catheter may be placed within a short
sheath with a hemostatic valve, or used in com-
bination with a Y adapter and a Tuohy-Borst
valve for hemostasis.

Commonly Used Medications

When performing vascular interventions, a
number of medications are frequently required.
Examples in a number of broad groups are pro-
vided, but this is not a comprehensive descrip-
tion. Practioners should be familiar with local
guidelines for medication use, and if in doubt
should consult standard sources to check
dosages and interactions.

Local Anesthetics

Local anesthetic is used for nearly all diagnos-
tic and interventional procedures. The most
commonly used agent is lignocaine hydrochlo-
ride (lidocaine in the United States). It has a low
incidence of side effects when used as a local
anesthetic, but a total dose of 200 mg (20 mL of
1% solution) should not be exceeded, as over-
dosage may lead to central nervous and cardio-
vascular system toxicity. Alternative agents
are prilocaine hydrochloride or bupivacaine
hydro chloride, which are longer acting and may
be useful in certain circumstances. Depending
on the agent, some adjustments may be advised
for renal impairment, primarily related to
metabolites that are renally excreted, or hepatic
impairment. For any of these agents, direct
intraarterial or intravenous injection should be
avoided, due to risk of seizure and other poten-
tial immediate systemic effects.

Heparin

Heparin is added to saline flushes and used rou-
tinely in higher doses during interventional
procedures. In both cases it helps prevent peri-
catheter or vessel thrombosis during the pro-

241

ENDOVASCULAR APPROACHES AND TECHNIQUES

cedure. For flushes, it is used in a dose of
about 5000 IU per liter of normal saline. For
interventional procedures, doses of between
3000 and 5000 IU are given depending on the
size of the patient and the proposed length of
the procedure. For aortic stent-graft procedures,
the sheaths may be totally occlusive, and sys-
temic heparinization is commonly used. Sys-
temic heparinization is also common in carotid
stent procedures, due to the risk of emboli and
to prevent thrombosis related to distal protec-
tion devices. As the half-life of heparin is 45 to
60 minutes, further doses should be considered
if a procedure is prolonged. During longer
cases or for systemic heparinization, dosing
may be based on the activated clotting time
(ACT), with target levels in the 250 to 300 s range
depending on the procedure, the degree of vas-
cular occlusion by devices, and the throm-
boembolic risk.

Vasodilators

Vasodilators are used for prophylaxis or treat-
ment of vascular spasm, and during intraarter-
ial pressure measurements, to augment distal
flow and give a better assessment of the
significance of a pressure drop across a lesion.
Commonly used intraarterial agents are glyc-
eryl trinitrate (GTN, 100 jj,g) (nitroglycerin in
the U.S., 50 to 100|J,g) and papaverine (30 mg).
Of course, vasodilators may produce significant
hypotension, so attention should be paid to
patient hydration status and coexisting cardiac
disease. Vasodilators should not be used in
patients with significant aortic stenosis, as
they may produce severe hypotension in this
circumstance. Nifedipine (10 mg) can be given
orally prior to a procedure if significant spasm
is likely, such as embolization of the testicular
vein.

Atropine/Glycopyrronium Bromide

These agents are given routinely during carotid
stenting to reduce the risk of bradycardia and
hypotension during balloon inflation in the
carotid bulb. Glycopyrronium bromide (600 (J,g)
is preferred in patients with a history of cardiac
disease because it has a better side effect profile
(U.S. equivalent is glycopyrrolate, adult dosage
100 jj,g IV repeated every 2 to 3 minutes as nec-
essary with a reasonable upper limit of 600 (J,g).

Sedation/Analgesia

Sedation is rarely required for vascular proce-
dures, short of aortic stent grafts. Patients with
limb ischemia should have their pain adequately
controlled prior to investigation, as patients in
severe pain can rarely lie still for prolonged
periods. If sedation is required, small doses of
short-acting benzodiazepines such as midazo-
lam (2 to 10 mg IV) are preferred, with the aim
being to relax, not anesthetize, an agitated
patient. If anesthesia is produced, an anesthetist
must be in control of it, but if oversedation does
occur, the effects of the benzodiazepine can be
reversed (temporarily) with flumazenil (200 ng
over 15 s and then 100 |J,g every 60 s up to a total
dose of lmg). If analgesia does become neces-
sary, opiates such as morphine or pethidine (25
to 100 mg) can be given IV, or an appropriate
oral opiate can be given, though the onset of
action may be considerably delayed. In all cases
with analgesia and sedation, IV administration
is preferred, as IM absorption is unpredictable
and cumulative effects can result in sudden
overdosage.

Antibiotics

When and which antibiotics are used varies
according to local policy. Common indications
are when prosthetic graft material is likely to be
punctured during a procedure, when prosthetic
material is to be placed (especially aortic stent-
grafts), or for some embolization procedures.

Antiplatelet Agents

All patients with peripheral vascular disease
should be advised to take antiplatelet agents,
predominantly for their cardioprotective effect.
Dosages of aspirin likely need be no higher than
75 mg daily, although the precise optimal dosage
has not been definitively determined. If the
patient is intolerant of aspirin then dipyri-
damole (25 to 50 mg) or clopidogrel (75 mg) are
alternative agents. In our practice, patients are
given clopidogrel 75 mg at least 3 days prior to
and for 30 days following carotid stent inser-
tion. If the patient has not taken a dose prior
to the day of the procedure, a loading dose of
300 mg is given on the day of procedure. In the
U.S., most centers use both aspirin and clopido-
grel for carotid stents.

242

VASCULAR SURGERY

Drugs for Treating
Contrast Reactions

It is imp erative to b e aware of the risk of a severe
contrast reaction and its treatment. The drugs
to do this should be readily available on the
resuscitation trolley in the angiography suite.
All centers should have a protocol for treatment
of severe contrast reactions. This should be
prominently displayed and usually involves
the use of some or all of the following: chlor-
pheniramine (10 to 20 mg IV); adrenaline or
epinephrine (0.5 mL of 1:1000 solution subcu-
taneous or 0.1 mL of 1:10,000 solution IV),
usually given if there is severe anaphylactic
shock; hydrocortisone (200 mg IV), though its
effects are not immediate; cimetidine (300 mg
IV), may be useful as a second-line drug follow-
ing adrenaline; atropine (500 (J,g to 1 mg IV) can
be used for severe bradyarrhythmia.

Devices for Vascular
Intervention

Various devices may be required to perform
vascular interventional procedures, such as
balloon catheters and stents for treating arterial
occlusive disease, or coils for embolization. The
specifics of these devices are described during
discussion on their use elsewhere in this
chapter.

Closure Devices

Arterial puncture site closure devices aim to
eliminate or reduce the need for manual com-
pression of the puncture site, reduce the time
to patient mobilization, and reduce the risk
of significant bleeding, especially when using
larger sheath sizes. For most centers it is the
increased throughput of patients and the ability
to perform intervention as a day case that
justifies their use.

There are a number of devices available,
divided into two main groups: "stitchers" and
"pluggers." The Closer (Perclose, CA) device is
the original "stitcher." It percutaneously places a
suture through the artery at the puncture site,

and the patient can be fully mobilized immedi-
ately. It can be used for closure of up to a 10F
sheath size. Another suture-based device,
Prostar XL (Perclose), has been used success-
fully for closure of 24F femoral artery access.
One of the authors has personally used these
devices with good success for totally percuta-
neous endovascular aortic aneurysm repair,
both abdominal and thoracic. The primary
issues are vessel size and calcification, which can
affect the ability of the device to capture the
sutures properly. Obesity and prior surgery or
dense scar can also affect these devices. The
vessel can be immediately reaccessed if neces-
sary and other than the suture, there is no other
residual material to cause problems if surgery is
required at the access site. There are a number
of plugging devices, such as the Angioseal (St.
Jude Medical, St. Paul, MN), the Duett (Vascular
Solutions Inc., Minneapolis, MN), and the
Vasoseal (Datascope Corp., Montvale, NJ).
The authors are also quite familiar with the
angioseal. This is quick and simple to use and
comes as a 6F or 8F device. An absorbable shoe
remains inside the artery and a collagen plug is
deployed over the puncture site outside the
artery. The device now uses a knot mechanism
to hold the collagen plug in position, and the
patient can mobilize in 2 to 4 hours. The
primary issues with this device are vessel size
and the size of the arterial access device used for
the procedure.

Access Technique

Before any diagnostic or interventional proce-
dure can begin, vascular access has to be estab-
lished. The basic technique remains the same as
that described by Seldinger:

• Vessel puncture

• Guidewire introduction

• Placement of the catheter over the
guidewire

Vessel Puncture

For the purposes of this chapter, only arterial
access is discussed; venous access is discussed
in Chapter 13. In general, which vessel to punc-
ture is dictated by the site of disease to be inves-

243

ENDOVASCULAR APPROACHES AND TECHNIQUES

Table 20.2. Arterial access sites

Access site

Main indications

Ipsilateral common femoral artery (CFA)

All accessible stenotic/occlusive lesion

Contralateral CFA

Occluded ipsilateral CFA

Lesion to be treated close to ipsilateral groin

Scarred groin

Low superficial femoral artery (SFA)

Percutaneous transluminal angioplasty (PTA) of ipsilateral CFA (rare), SFA
origin or proximal graft anastomosis but contralateral femoral puncture
not possible

Profunda femoris (PF) artery

PTA of PF origin

PTA of CFA (rare) if SFA occluded and contralateral approach not possible

Direct graft puncture

Arteriography in patients with graft crossing both groins

Intervention at graft anastomoses

Occluded graft, to allow accelerated thrombolysis

Popliteal artery

PTA of occlusions involving the origin of the superficial femoral artery
Failure of guidewire passage antegrade, often due to steep, large collaterals
at the proximal site of an occlusion

Brachial artery

Bilateral aortoiliac occlusions

PTA of a supraaortic branch occlusion or stenosis

Severe aortoiliac disease and vascular tortuosity

Axillary artery (brachial approach preferred)

As above

Radial artery

Arteriography as above; limited intervention possible

tigated or treated, and the strength of the arte-
rial pulses at various sites. The commonly used
arterial puncture sites are shown in Table 20.2.
For most purposes, the common femoral
artery is used, as it is a relatively easy artery to
puncture, the artery is readily compressed over
the femoral head, and most vascular beds are
easily within reach. The vessel is punctured at
the point of maximal pulsation, not by means
of external anatomical landmarks. At this point
the vessel is over the femoral head. The site is
first cleaned and draped, and local anesthetic
inserted. A two-part needle is preferred for most
access as this avoids the risk of damaging the
vessel if the tip of the needle has to be reposi-
tioned. There is also a reduced risk of the wire
passing into a subintimal position. This can
occur because the long bevel of a one-part
needle may imply the needle tip is in the center
of the lumen of the vessel, when it is only par-
tially through the wall of the artery. The needle
is guided at about 45 degrees to the skin surface
toward the pulse, and the vessel is speared. The
central stylet is then removed and the needle

gently withdrawn until the tip is felt to flick into
the lumen of the artery, and this should be
accompanied by the free pulsatile backflow of
arterial blood.

Bony landmarks for the femoral artery on
fluoroscopy can also be used, namely the medial
aspect of the femoral head, but direct palpation
is preferable. If there are difficulties gaining
access or if the pulse is weak or absent, then gen-
erally the best approach is to use ultrasound to
directly visualize the arterial target. This is par-
ticularly useful for antegrade femoral artery
punctures, as it often avoids the need to use
fluoroscopy to guide a wire into the superficial
femoral artery (SFA) for distal intervention, and
hence reduces the risk of irradiating the hands
of the operator. In cases of difficult access, a
micropuncture set is commonly used to reduce
the risk of arterial injury, and in most of these
sets the guidewire is specifically designed with
an echogenic tip to aid visualization of the small
0.018-inch wire. Once arterial access is obtained
with a short 4F introducer, an exchange is made
for a larger guidewire and 5F sheath.

244

VASCULAR SURGERY

Guidewire Introduction

Once the needle is in position, a guidewire is
introduced through it. For most purposes a
standard 3-mm J wire is used to secure access
and to allow initial introduction of catheters
and sheaths. The wire should pass smoothly and
easily into the artery. If any resistance is felt,
fluoroscopy should be used to ensure the wire is
following an appropriate course and is running
freely. If the wire does not pass beyond a certain
point, then a limited angiogram may be
required to identify the problem, but this
requires that at least some wire is within the
arterial lumen to allow the introduction of a
sheath or dilator. If the wire does not pass out
of the needle, then there is probably an arterial
plaque at the puncture site. The needle tip can
often be repositioned without losing an intraar-
terial position, but sometimes re-puncture is
necessary, perhaps using ultrasound to guide
the optimal site for puncture.

Catheter Placement

Once the wire has been advanced into a suitable
position, a catheter or sheath can be introduced
over it. The wire is held under slight tension as
the catheter is introduced, as this helps to avoid
the wire kinking in the soft tissues and makes
tracking the catheter easier. Once the catheter
has been advanced into position, the guidewire
can be removed, the catheter flushed, and the
intraluminal position verified with a test injec-
tion of contrast.

If the site of insertion has dense scar from a
prior procedure, then insertion of even a small
sheath or dilator may be difficult. If this is the
case, then it is often prudent to use a stiffer
guidewire initially or to change to one through
a 4F dilator and then place a sheath for use
during the rest of the procedure. Current
micropuncture sets also have stiff versions for
these cases. Although not needed frequently,
these stiffer versions can be quite helpful.

Endovascular Techniques for
Arterial Occlusive Disease

The mainstay of vascular intervention for arte-
rial occlusive disease remains balloon angio-
plasty, though arterial stenting also has an

important role to play. Some techniques, such as
laser treatments, have come and gone. Atherec-
tomy has a limited role for occlusive disease,
predominantly for graft or stent re stenosis, and
stent grafts are being evaluated for occlusive
disease to see if the expense can be justified over
simple angioplasty or stenting.

Angioplasty

The technique of balloon angioplasty is used
extensively to treat arterial stenoses and occlu-
sions, and the principles and equipment are
largely the same regardless of where they are
applied. The basic principle is to place a
guidewire through an arterial narrowing and
over this to position an appropriately sized
angioplasty balloon. The balloon is then inflated
to high pressure, disrupting the stenotic arterial
plaque. The luminal area, therefore, is increased
and blood flow improved.

As with all vascular intervention, planning is
important and consideration should be given to
the following:

Access site: Access should usually be as near
to the site to be treated as possible. This
optimizes tactile control of wires and
catheters, minimizes a tortuous approach
to a lesion, and may help avoid an awkward
approach to a vessel origin. For distal lower
limb intervention, this usually means an
antegrade femoral artery puncture.

Crossing the lesion: The guidewire has to
lie in an intraluminal position above and
below the site to be treated (even in cases
of subintimal angioplasty). For simple
stenoses, the lesion is crossed intralumi-
nally, often using a directional catheter,
such as a Cobra and a curved wire, with or
without a hydrophilic coating. Particularly
when treating occlusions, the wire may
pass (intentionally or otherwise) into the
subintimal space within the diseased
section. The wire usually buckles on itself
when this happens, and if a hydrophilic
wire is then used, a loop is formed with it.
The wire must then reenter in an intralu-
minal position in the more normal distal
vessel before balloon dilatation is per-
formed. This often occurs by advancing the
wire loop in the subintimal space, with
reentry occurring where a collateral arises

245

ENDOVASCULAR APPROACHES AND TECHNIQUES

or at a vessel bifurcation — the basis of
subintimal angioplasty. A Berenstein or
other directional catheter can also be used
to direct the wire back into the true lumen,
and as with other steps in subintimal
angioplasty, this should be performed with
caution to avoid vessel perforation. New
intravascular ultrasound catheters with
wire guides and over-the-wire "spreading"
devices have recently been produced to
help cross-total occlusions, but are typi-
cally needed only in difficult cases.
Dilatation of the lesion: Angioplasty balloons
fall into two main groups — compliant
and noncompliant. Noncompliant balloons
inflate to only one size, regardless of pres-
sure, up to their burst rating. Compliant
balloons vary in size, dependent on the
pressure/volume of fluid within them. Most
interventionists prefer noncompliant bal-
loons because they often can be inflated
to higher pressure and the risk of over-
sizing of the balloon for the vessel is
smaller. The size of balloon chosen is
dependent on the size of the adjacent
normal vessel, though most operators use
an approximate guide based on experience
and scale the size up or down for individ-
ual patients (e.g., petite elderly women
have small, fragile vessels). Inflation of the
balloon can be performed by hand or using
an inflation device. The latter has the
advantage of a pressure gauge, allowing
more control of the pressure and less like-
lihood of exceeding the maximum balloon
inflation pressure. Inflation is performed
with a contrast/saline mix and the balloon
should fully inflate with no "waist." Some
operators inflate for a short period, others
for 2 to 3 minutes, and some initially at
high pressure, reducing to a prolonged low-
pressure inflation. The basis for this is to
reduce the risk of distal embolization and
significant dissection. However, the evi-
dence that these strategies achieve these
aims is lacking.

Following angioplasty a completion angio-
gram should be performed to assess the appear-
ance of the treated segment and the "runoff."

Of primary importance is exclusion of vessel
rupture with contrast extravasation, particu-
larly in the iliac arteries. If there is arterial

rupture, reinsertion of the balloon and inflation
under low pressure proximal to the site of
rupture should stop or minimize further bleed-
ing. This may suffice for a small hole. It is
prudent to inform a vascular surgeon of the
problem. An angiogram should be performed
after a trial of low-pressure balloon inflation.
If extravasation continues, then the balloon
should be immediately reinflated, and, if avail-
able, an appropriately sized stent graft inserted.
If this is not possible, then surgical repair of the
arterial tear is required.

If there is no injury and the treated segment
remains significantly stenosed, then it may be
that the balloon was undersized, in which case
increasing the balloon size is often all that is
required. In the iliac arteries, a pullback pres-
sure can be performed through the lesion to
assess if there is a significant pressure gradient
at the site treated. This is usually taken to be
a peak systolic pressure drop of lOmmHg
across the lesion following administration of a
distal vasodilator, such as GTN or papaverine.
At other sites, for example, in the SFA, pres-
sures are often not useful, as the catheter has to
cross the treated segment for a pressure read-
ing to be obtained distally, and this may in
itself produce a pressure drop if the lumen is
small. A normal distal pressure, however, is reas-
suring that the stenosis has been treated ade-
quately. If there is still a significant pressure
drop in the iliac arteries after apparently ade-
quate balloon inflation, then secondary stenting
is warranted. If elastic recoil seems to be occur-
ring on balloon deflation, again, stenting should
be considered, depending on the site of the
lesion.

Often following angioplasty, a local dissection
is visualized; however, most of these will
remodel and do not require further treatment.
If there is evidence of flow limitation, then there
is a risk the segment will acutely occlude, and
further investigation/treatment is warranted.
Again a pressure measurement can be per-
formed. For further treatment a long low-pres-
sure inflation may tack back the dissection,
but if this is unsuccessful, stenting may be
required.

Imaging the runoff vessels ensures that there
has been no distal embolization. If this has
occurred and the embolus is in an important
vessel or producing poor flow/limb ischemia,
then thrombo-aspiration should be performed

246

VASCULAR SURGERY

using an appropriate-size catheter for the
occluded vessel and a sheath with a removable
hemostatic valve.

Stenting

Intravascular stenting places a metallic scaffold
inside the vessel to hold open the lumen. Stents
were developed as an adjunct to balloon angio-
plasty in recognition that angioplasty alone was
occasionally unsuccessful. In this circumstance,
the role of stenting is secondary to the primary
treatment of angioplasty and is used to salvage
a failed angioplasty. However, there are occa-
sions when stenting is the initial treatment, so-
called primary stenting. Examples include the
treatment of ostial lesions, such as ostial renal
artery stenosis (Fig. 20.1); most iliac occlusions;
and carotid stenosis. The basis for stenting is to
reduce problems caused by elastic recoil or
distal embolization. Stents are generally avoided
below the inguinal ligament, as there is no evi-
dence they are superior to balloon angioplasty
alone in this location. In these lower flow
vessels, stents may result in early thrombosis
and thus are reserved for bailout situations after
angioplasty.

There are a huge number of types of stents
available for intravascular use, and choice of
stent is usually at the discretion of the practi-
tioner. The common types of stent are described

here, with some examples given of those with
which the authors are most familiar.

Types of Stent

Stents fall into two main groups: balloon-
mounted or self-expanding. Balloon-mounted
stents are usually made of stainless steel and
are positioned on an angioplasty balloon for
expansion and deployment. There is usually
little shortening with expansion, and balloon-
mounted stents are particularly useful where
positioning of the stent is critical, enhanced
by their radiopacity Larger balloon-mounted
stents, for example, unmounted Palmaz stents,
shorten considerably when expanded on a
large-diameter balloon, making their place-
ment more difficult. As these stents are quite
inflexible, they may be difficult to position
through tortuous vessels. Their rigidity, how-
ever, gives them good radial strength, but if
deformed once placed, for example, in superficial
locations, or near joints, they will remain de-
formed and may themselves cause vascular
obstruction. Most of these stents now come pre-
mounted on an angioplasty balloon ready for
deployment, for example, Bridge stent (Medtonic
AVE, Santa Rosa, CA), Genesis, or premounted
Palmaz (Cordis, Miami Lakes, FL). Others have
to be manually crimped to an appropriate
balloon prior to use, for example, SAXX (C.R.

Figure 20.1. Renal artery stenting. Gadolinium-enhanced magnetic resonance imaging (A) showing a tight stenosis in the solitary
kidney, confirmed by catheter angiography (B) and successfully stented with a balloon-mounted stent (C). Note the left renal artery
is occluded (arrow).

247

ENDOVASCULAR APPROACHES AND TECHNIQUES

Bard, Murry Hill, NJ, USA) and the unmounted
Palmaz (Cordis). The premounted stents are less
prone to dislodgment from the balloon. This can
occur as the stent is passed through the sheath
and into its position for use, or during balloon
inflation if a "dumbbell" is not formed around
the stent as the balloon is initially inflated, in
which case the stent may be squeezed off the
deploying balloon. The latter problem is caused
by movement of the stent from the center of the
balloon or poor initial positioning so that one
end of the balloon inflates first. Care is therefore
required when using these stents, and if the stent
has moved on the angioplasty balloon prior to
deployment, it should not be used.

Self-expanding stents all have an inherent
ability to expand to a predetermined length
and/or diameter. They are compressed onto the
delivery catheter and are typically constrained
by a covering sheath. As this sheath is with-
drawn, the stent expands and is deployed. Being
self-expanding, the stent continues to exert an
expansile force on the vessel wall once deployed,
and will show some flexibility and recovery to
their expanded shape if compressed or kinked.
Stents such as the Wallstent (Boston Scientific,
Boston, MA) are made of surgical grade stain-
less steel and rely on their design to be self-
expanding. Newer stents tend to be made from
nitinol, for example, the Memotherm Luminex
(C.R. Bard), or the SMART stent (Cordis).
Nitinol is a highly elastic nickel-titanium alloy
that displays the property of thermal memory,
returning to its preformed shape when released
in the body. The "memory" properties of nitinol
can be made to be more or less sensitive to tem-
perature, which can be an advantage in certain
situations.

The Wallstent shortens considerably as it
expands, with its final length governed by the
diameter achieved in the vessel. This can make
accurate placement difficult. It is very flexible,
but has a relatively low expansile force once in
place. Nitinol stents show considerably less
shortening during expansion, and though
nitinol is poorly radiopaque, many stents now
have gold or platinum markers on their proxi-
mal and distal struts to aid accurate placement.

All stents come in a range of diameters and
lengths to suit their use in different-sized vessels
and different lesion lengths. Placement of a stent
usually requires a larger sheath to allow entry of
the stent into the vascular system, though many

self-expanding and balloon-mounted stents can
now be introduced through 5F to 6F sheaths.

The basic principles of stenting are analogous
to those of angioplasty, in the approach to the
lesion and use of guidewires and catheters to
cross the lesion. If there are difficulties tracking
the stent to the lesion, a stiffer guidewire maybe
required than for balloon angioplasty alone. The
size and length of stent are selected for the size
of vessel and the length of the lesion. For self-
expanding stents the diameter of the stent is
usually oversized by 1 to 2 mm, compared to the
vessel diameter. Use of fluoroscopic road-
mapping techniques help ensure that the stent
is appropriately positioned, both prior to and
during deployment, but this may require the use
of a guiding catheter or catheter positioned
from another access site to perform angiogra-
phy. Many self-expanding stents, as they deploy,
move away from the operator. Gentle back trac-
tion on the delivery system and continuous
screening during deployment should be used to
maintain the position of the stent markers. Fol-
lowing deployment of self-expanding stents,
balloon dilatation can be used to ensure ade-
quate expansion and apposition to the vessel
wall. In some circumstances, for example, small
external iliac arteries, ballooning to the desired
vessel diameter may not be possible because the
patient may experience pain, and there is a risk
of arterial rupture. In these circumstances it is
prudent to use a self-expanding stent, and in
most cases the stent will expand adequately over
the next few days with no adverse outcome. As
with angioplasty, check angiography with
runoff views should be performed.

Atherectomy

As with many new interventions, there was
initially much enthusiasm for atherectomy.
However, the lack of evidence that the technique
was superior to simple balloon treatment for
atheromatous disease has meant there is now
limited use for this technique. Pending data
from newer devices and techniques, the role of
atherectomy is mainly limited to removal of
neointimal hyperplasia from graft anastomoses
or from within stents. Such lesions tend to be
elastic and resist balloon angioplasty alone.
Stenting is often counterproductive as it may
exacerbate the hyperplastic process (at least
pending data using new drug-eluting stents in

248

VASCULAR SURGERY

this role). However, the obstructing material can
often be removed percutaneously using atherec-
tomy devices.

Stent Grafting

Stent grafts are predominately used in the
domain of aneurysmal disease. They have been
advocated as an alternative to angioplasty
and/or stenting for occlusive disease, often as a
form of endovascular bypass procedure. As yet
the technique has not shown superior effec-
tiveness compared to angioplasty or conven-
tional stenting in the iliac arteries, and studies
on their use for long occlusions elsewhere are
ongoing.

Thrombolysis/Thrombectomy

Thrombolysis may be considered if there is
acute critical limb ischemia due to thrombosis.
Thrombolytic agents have the potential to break
down the clot, restore perfusion, and reveal the
underlying abnormality that led to thrombosis
in the first instance. The thrombolytic agents
with which there is most experience for periph-
eral use for limb ischemia are recombinant
tissue-type plasminogen activator (rtPA), strep-
tokinase, and urokinase. Urokinase was with-
drawn for some time, but has recently been
returned to commercial availability.

Thrombolysis is indicated only if there is crit-
ical limb ischemia, and only then if the limb is
salvageable, there is sufficient time for lysis to be
instigated, and there are no contraindications to
giving lytic agents. Its use is usually limited to
the following clinical situations:

• Graft thromboses

• Native vessel thromboses

• Thrombosed popliteal aneurysm with
occluded runoff

In general terms the fresher the thrombus, the
more likely the thrombolysis is to be successful.
Many clinicians do not consider thrombolysis if
the thrombus is more than 2 weeks old, based
partly on the STILE trial data that suggested
that surgery is associated with a better outcome
for more chronic ischemia (Weaver et al. 1996).
When considering thrombolysis, access
should be as close as possible to the thrombosed

segment. This may mean performing a prelimi-
nary ultrasound to identify the upper extent of
clot if a distal graft or the SFA is thrombosed, to
ensure ipsilateral access is possible. This allows
easy access to the thrombus and aids adjunctive
procedures such as angioplasty or thrombo-
aspiration if necessary. Use of a single arterial
wall puncture technique is preferred, and once
access is achieved the guidewire traversal test
should be performed. If the wire does not
pass through the thrombus, the success rate
for thrombolysis is reduced, as the thrombus
is likely to be organized. A catheter and/or
infusion-type wire should be placed through
the thrombus and lytic agents delivered into the
thrombus. If the catheter is positioned above the
thrombosed segment, lytic agents are usually
carried away by collaterals and the only lytic
effect will be systemic. A number of infusion
techniques are available; the most commonly
used is bolus lacing of the thrombus (e.g., 5mg
of rtPA or 100,000 to 250,000 units of urokinase)
followed by a low-dose (e.g., 0.5 mg/h of rtPA, or
10,000 units/h urokinase) infusion of lytic agent
with the catheter embedded in the proximal
extent of the thrombosed segment. There is
no evidence that a high-dose technique (e.g.,
5 mg/h of rtPA) or pulse spray techniques
improve outcomes. However, it may be neces-
sary to use these techniques if the degree of
ischemia does not allow time for a low-dose
approach, because although they are labor
intensive, they do achieve lysis more quickly.

The catheter and sheath should be secured
using a suture to minimize the risk of displace-
ment. Loss of the sheath at the groin may result
in hemorrhage, and if the catheter is pulled
back, the effectiveness of the lytic infusion will
be lost. Patients undergoing lysis are in danger
of a number of complications, predominantly
those of hemorrhage and the effects of reperfu-
sion injury, and should be monitored in a high-
dependency area. Analgesia should be given
IV and the amount required reviewed regularly,
as reperfusion injury may also cause pain. The
effect of the lytic regime is checked angio-
graphically after an appropriate period, and if
necessary the catheter position changed and
lysis continued. If there has been no effect after
a reasonable period, then lysis is deemed to have
failed and alternative surgical strategies may
be considered. Complications may lead to the
procedure being abandoned. If the thrombus

249

ENDOVASCULAR APPROACHES AND TECHNIQUES

clears, partially or completely, then adjunctive
endovascular or surgical treatment may still be
necessary.

There is usually an underlying cause for
graft or vessel thrombosis, and to maintain
patency these should be treated immediately
after they are revealed, usually with angio-
plasty and/or stenting. If clot clearance is only
partial, it may be appropriate to attempt percu-
taneous thrombectomy. This can be simple
aspiration of clot using a large-caliber catheter
through a removable hemostatic valve, or using
specialized mechanical thrombectomy devices
such as the Amplatz Thrombectomy Device
(Microvena, White Bear Lake, MN) or the
Hydrolyser (Cordis). Mechanical thrombectomy
devices macerate the thrombus, with the residue
either aspirated or small enough to pass through
the capillary circulation. Surgical intervention
may be required even if lysis is apparently suc-
cessful, for example, fasciotomy for reperfusion
effects, though more commonly it is needed if
lysis is only partially successful, with treatments
such as graft revision or surgical thrombectomy.

Endovascular Techniques for
Aneurysmal Disease

The aim of stent grafting is to line the aneurysm
and adjacent normal arterial segments with
graft material, therefore excluding the aneurys-
mal segment. There are now many commercially
produced devices, manufactured using a variety
of stent and graft materials, usually as a fully
supported device with a metal frame covered by
graft material.

Much of the focus in recent years has been on
the use of stent grafts to treat abdominal aortic
aneurysms (AAAs). In these circumstances,
special modular bifurcated devices are the most
frequently used to exclude the aneurysmal
infrarenal aorta and allow flow into both iliac
arteries. As with any stent graft procedure, it is
necessary to have a segment of normal-caliber
vessel above and below the aneurysm to anchor
the device and produce exclusion of the sac
from pressure (and preferably flow as well).
Initially, only about 5% of infrarenal AAAs
could be treated with this technique, but this
expanded to 25% to 30% of infrarenal AAAs
with the advent of bifurcated and aorto-uniiliac

grafts. At the present time, 50% or more of
infrarenal AAAs fulfill the necessary criteria to
allow stent grafting depending on device avail-
ability and the criteria applied for iliac access
and sealing. Common reasons for unsuitability
are an inadequate aortic "neck" below the renal
arteries; poor access, with small-caliber or tor-
tuous iliac arteries; and extensive iliac aneurys-
mal disease. To some extent, problems with iliac
access can be dealt with by using iliac or
iliac-femoral conduits, but this diminishes
some of the advantages with regard to morbid-
ity and recovery time. Extensive iliac aneurys-
mal disease can also be handled by coiling or
covering the internal iliac arteries, but this
is not without some risk of added morbidity
compared to standard endovascular repair.
Although undoubtedly a feasible technique with
good short-term outcomes, concerns about the
long-term results, especially the durability of
the devices, mean that patients require lifelong
surveillance, and in the United Kingdom the
technique is offered only as part of an ongoing
study. Lifelong surveillance and participation in
organized data collection or a clinical trial are
also recommended in the U.S., but commercial
use of stent grafts for endovascular aneurysm
repair has been accepted in most parts of the
country following Food and Drug Adminis-
tration (FDA) approval of the first devices in
1999.

Although most commonly applied to
infrarenal AAAs, stent grafts can be used for
a number of other applications: to exclude an
aneurysmal section of a single vessel such as the
iliac artery or the thoracic aorta; to treat vessel
rupture, including partial aortic transection fol-
lowing deceleration injury, or iatrogenic rupture
from balloon angioplasty; and to treat the acute
ischemic complications of thoracic aortic dis-
section. In the case of thoracic aortic dissection,
this is achieved by stent grafting the true lumen
covering the entry tear, which usually lies just
beyond the origin of the left subclavian artery.
As a result there is a shift of blood flow from the
false to the true lumen and a resolution of many
of the ischemic complications that frequently
occur due to compression of the true lumen by
a high-pressure false lumen. Although coverage
of the entry tear achieves the acute objectives,
stable long-term fixation of the device should
be in the normal aorta proximal and distal to
the dissection to prevent erosion of the device

250

VASCULAR SURGERY

through the weakened segment of the aortic
wall. Treatment of acute dissections requires a
thorough understanding of the physiology
related to flow in the false lumen, and may
require adjunctive techniques such as balloon
fenestration of the dissection distally or stent-
ing of branch vessels.

The endovascular techniques used during
stent grafting are essentially those of stenting
generally. Devices are sized in terms of length
and diameters to ensure adequate anchorage
and to produce a seal proximally and distally
and to cover the aneurysmal section of vessel,
according to manufacturer guidelines. Appro-
priate selection of patient anatomy, device type,
device diameter, and length are all crucial to the
success of the procedure (Broeders et al., 1997;
Fillinger, 1999; Wyers et al, 2003). Being large,
most stent graft devices have to be introduced
through an arterial cutdown at the groin,
although recently the successful use of arterial
closure devices for total percutaneous repair
have been described. Also, as the devices are
often bulky and fairly rigid, very stiff
guidewires, such as the Amplatz Superstiff, Lun-
derquist (Cook Inc., Bloomington, IN) or Meier
(Boston Scientific, Boston, MA), are used to
facilitate tracking of the device into position for
deployment (Fillinger, 1999; Wyers et al, 2003).
Accurate deployment is vital to ensure that renal
or internal iliac arteries are not inadvertently
covered by the graft material, and this usually
requires adjusting the gantry angle for the
aortic neck angle. Deployment for most systems
involves the unsheathing of the device, but
deployment mechanisms may include self-
expansion (e.g., Medtronic AneuRx or Talent), a
release mechanism for a self-expanding device
(e.g., Gore Excluder), a combination of these
(e.g., Cook Zenith), or balloon expansion after
retraction of the sheath (e.g., Edwards Lifepath).
Most devices require adjunctive or optional
balloon inflation to seat the device within the
vessel. In part this is because hooks or some
other attachment device may be present to
help anchor the proximal or distal stents.
For modular devices, the different parts are
deployed separately, reducing the size of the
individual delivery systems.

At completion, angiography is performed to
ensure that there is no evidence of leak into the
aneurysm sac. The key for completion angiog-
raphy is to confirm the absence of type I (attach-
ment site) or type III (stent-graft junction)

endoleaks, which are the most dangerous and
should be treated prior to leaving the endovas-
cular suite if at all possible. Type IV "graft
porosity" endoleaks should seal spontaneously
in 24 hours, and type II [lumbar artery or infe-
rior mesenteric artery (IMA) branch] endoleaks
usually seal spontaneously as well, over a period
of weeks to months. Care should be taken not to
assume that the endoleak is a more benign
variety, but to confirm the source prior to
removing guidewires and catheters. Confir-
mation may require maneuvers such as retro-
grade injection near the distal end point,
injection within the graft at the location of a
modular junction, or other techniques.

Following endovascular aneurysm repair
(EVAR) it is essential that adequate imaging sur-
veillance be performed, as set out in Chapter 4.
This should enable late complications to be
detected with a view to appropriate treatments,
as necessary, whether by endovascular or con-
ventional surgical means.

Embolotherapy

Embolization techniques involve the deliberate
blocking of blood vessels. This may be neces-
sary to stop arterial hemorrhage, to exclude
an aneurysm or pseudoaneurysm, to occlude
a branch vessel that may contribute to an
"endoleak" as part of endovascular aneurysm
repair, or to treat vascular tumors and arteri-
ovenous malformations. It is beyond the scope
of this chapter to describe the use of emboliza-
tion in detail for all these indications, but
some general principles and techniques are
described.

In all cases of embolization there are four
main considerations:

• What is the anatomy?

• What needs embolizing?

• What embolic material should be used?

• Maintain patient safety.

Usually noninvasive testing or the clinical sce-
nario will indicate the likely answers to the
above considerations. However, an understand-
ing and knowledge of the vascular anatomy is
vital. This can usually be helped by high-quality
angiography, which should be performed before
embolization begins, during embolization as
flow dynamics may change, and at completion.

251

ENDOVASCULAR APPROACHES AND TECHNIQUES

Once the anatomy becomes clear, then the target
for embolization should also become clear. It
may be a whole vascular bed or a single inflow
vessel. The type of embolic material is dictated
by the embolization site and whether perma-
nent or temporary occlusion is required. During
embolization procedures, a separate trolley
should be used for the preparation of the
embolization material. In addition, to avoid
accidental injection of the material, all contam-
inated syringes, contrast, and saline should be
discarded and replaced.

Before starting, consideration should be
given to the approach to the embolization site.
The shortest, straightest route is usually the
best. Preliminary angiography may reveal the
need for equipment, such as guiding catheters
or microcatheters. Single end-hole catheters
should always be used, and a guide catheter may
be used to help ensure that a stable catheter
position is achieved. When embolizing, always
consider the effects of collaterals, as they may
carry embolic material away from their target
and damage normal tissues, in which case the
catheter position needs to be closer to the target.
When embolizing a vessel that is not an end
artery, it is important to "close the back door" to
prevent potential back-filling once the entry
vessel is occluded. If this is not done, then a
lesion will not have been effectively treated, and
as the "front door" has been closed, further
access for embolization will be impossible.

The main embolic agents to choose from are
the following:

Particles: for example, Gelfoam, polyvinyl

alcohol (PVA) microspheres
Mechanical devices: for example, coils and

balloons
Liquids: for example, sclerosants, glues

When particles are injected they flow into
distal vessels, occluding the vessels according to
the age of the particles used. Correct selection
of the size of the particles is important; small
particles may pass through a lesion, causing
undesirable embolization, whereas large parti-
cles may not successfully occlude the vascular
bed. Gelfoam is a temporary embolic material,
most commonly used by cutting up a sheet of
Gelfoam into pledgets about 1 mm X 1 mm, that
when mixed with contrast can be injected
through a conventional catheter. PVA is a per-
manent embolic agent that comes in a range of

sizes from 150 to 1000 |J.m in diameter. When
injecting particles, it is important to ensure that
full stasis is not obtained before all embolic
material in the catheter has been injected; oth-
erwise further injection will produce significant
reflux. Flush the embolic material mixed with
contrast from the catheter with saline, and then
it is safe to perform angiography.

Coils are permanent embolic agents that act
as a focus for thrombosis within the vessel. They
are metallic, but covered by thrombogenic
threads. They are best used to occlude a single
vessel or number of discrete feeding vessels to
isolate a vessel or area of the circulation. Coils
come in a variety of sizes. The wire diameter
varies from 0.014 to 0.038 inch and is important
to consider, as a large gauge will not pass down
a small-lumen catheter, such as a micro catheter.
Coil length also varies, with shorter coils being
most easily managed. The formed coil diameter
dictates the size the coil will form in the vessel
and should be appropriate for the location being
embolized: too small and the coil may migrate;
too large and it may not form well in the vessel.
Always check the stability of the catheter posi-
tion prior to deploying the first coil. This is done
by advancing the pusher wire to the end of the
catheter and ensuring the catheter tip does not
recoil or advance. The appropriate wire is stiff
enough to push the coil but not so stiff as to
dislodge the catheter. A Wholey wire has a
straight flexible tip with a prominent radio-
paque mark on the tip to distinguish it from the
coil being pushed. If this wire is too stiff, a
Bentson or other more flexible wire might
be preferable. The coil is introduced into the
catheter by pressing the coil introducer into the
catheter hub and using the appropriate pusher
wire to push the coil into the catheter, then out
the distal end of the catheter, deploying the coil
in the appropriate place.

Liquid agents are permanent agents and the
most potent. They have the potential to rapidly
produce hemodynamic changes resulting in
inadvertent embolization and can be difficult to
control in this respect. As such, their use should
be limited to those with the most experience.
Absolute alcohol causes immediate thrombosis
as it enters a vessel. It is the ultimate permanent
embolic agent and produces so much pain that
patients usually require general anesthesia. Its
principal use is for vascular malformations.
Glues, such as cyanoacrylate, solidify on contact
with ionic substances in blood, and are injected

252

VASCULAR SURGERY

with lipiodol and dextrose solutions to ensure
they do not solidify in the catheter. Once again,
it is an unforgiving material but can be useful
and does not produce the severe pain likely with
other liquid agents. In general, liquid agents are
best mixed with a contrast agent if they are not
already radiodense, so the amount of injection
and extent of delivery can be detected under
continuous fluoroscopic guidance.

References

Broeders IA, Blankensteijn JD, Olree M, Mali W, Eikelboom

BC. (1997) J Endovasc Surg 4:252-61.
Fillinger ME (1999) Surg Clin North Am 79:451-75.
Weaver FA, Comerota AJ, Youngblood M, Froehlich J,

Hosking JD, Papanicolaou G. (1996) J Vase Surg 24:

513-21.
Wyers MC, Fillinger MF, Schermerhorn ML, et al. (2003) J

Vase Surg 38:730-8.

Index

Abdomen, vascular injuries to, 128-130
Abdominal aortic aneurysms, 12, 13, 193-207
clinical features of, 194
complications of, 204
definition of, 193
diameter of, 196-197
endovascular repair of, 202-204, 249-250

anesthesia for, 67

long-term costs of, 25
epidemiology of, 193
familial, 192
inflammatory, 206-207
non-ruptured (elective), management of, 196-204

anesthesia for, 66

aneurysmal expansion rate in, 197

aneurysmal size in, 196-197

complications of, 200-202

endovascular repair technique, 202-204

open repair technique, 199-202

patient comorbidity in, 197

preoperative assessment in, 198-199

proximal extent of aneurysm in, 197

surgeon's audited results in, 198
pathogenesis of, 192
radiological investigations of, 29, 35-36
risk factors for, 193-194
ruptured

gender differences in, 193

leaking, 205

as mortality cause, 193,204-206

operative repair of, 198, 204-206

in peripheral arterial disease patients, 53

symptoms of, 205
screening for, 196
Accreditation Council for Graduate Medical
Education (ACGME), 153

Acrocyanosis, 79

Activated clotting time (ACT), 41

Activated partial thromboplastin time (aPTT),41,

43
Activated protein C resistance (APCR), 48
Acute mesenteric ischemia (AMI), 231-234
Adrenaline, 172
P-Adrenergic antagonists, 59
Advanced Trauma Life Support (ATLS), 129
Afterload, cardiac, aortic cross-clamping-related

increase in, 68
Agency for Healthcare Research and Quality

(AHRQ), 149
Alternative medical therapy, for lower limb

ischemia, 95
Amaurosis fugax, 161, 163
Ambulatory venous pressure (AVP), 107
American Board of Surgery, 153
Amputations

Buerger's disease-related, 87

combat injuries-related, 125

concomitant vascular and nerve injuries-related,
130

in diabetic patients, 58

lower limb ischemia-related, 95, 97-98, 100

peripheral vascular disease-related, 53
Analgesia, 241
"Anatomical snuffbox"

as arteriovenous fistula access site, 142

pulse in, 13
Anesthesia, for vascular surgery, 65-72, 241

for carotid endarterectomy, 69-70, 172, 176

for endovascular interventions, 66-67

general, 65-66, 67-69, 69, 172, 176

local anesthesia, 240

in carotid endarterectomy, 172

for lower extremity vascular surgery, 70-71

253

254

INDEX

Anesthesia, for vascular surgery {cont.)

for upper extremity vascular surgery, 71-72
locoregional, for carotid endarterectomy, 172
regional, 65-66, 69-70, 71-72

contraindications to, 71
risks associated with, 65-66
tumescent, 67
Aneurysms, 191-219. See also Pseudoaneurysms
aortic. See Aortic aneurysms
axillary arterial, 218
axillosubclavian arterial, 218-219
"berry," 88
carotid arterial, 218-219

false, 158

true, 158, 159
classification of, 191-192
definition of, 191
false, 158,202
femoral arterial, 213-214
iliac arterial, 214
mesenteric arterial, 34, 35, 216
pathogenesis of, 192
popliteal arterial, 13, 210-213

duplex imaging evaluation of, 22-23

as limb ischemia cause, 101, 104

management of, 211-213

popliteal pulse in, 93

ruptured, 211-212
rupture of, 192,211-212
subclavian arterial, 185, 186,218
traumatic, 13
visceral arterial, 214-217
Angiitis, cutaneous leukocytoclastic, 85
Angina, mesenteric, 34-35
Angiogenic therapy, for limb ischemia, 98
Angiography

of abdominal aortic aneurysms, 195-196
in blunt abdominal trauma patients, 129
carotid, 156, 159, 165, 178-179, 188

of the carotid arch, 25
catheter, 26-28

of abdominal aortic aneurysms, 35-36

complications of, 29

of endoleaks, 36

of peripheral vascular disease, 31

pulmonary, 33
complications related to, 140
computed tomography

of peripheral vascular disease, 31

of the proximal common carotid artery, 187

pulmonary, 25
contrast

of carotid disease, 165

of lower limb ischemia, 95
of cystic adventitial disease, 89
digital subtraction, 26

of carotid artery disease, 156, 159

of the proximal common carotid artery, 187

of the subclavian artery, 186-187
for endoleak detection, 36, 250
magnetic resonance, 30
of carotid disease, 165, 166
of the mesenteric arteries, 35
of the proximal common carotid artery, 187
of pulmonary embolism, 33
of the renal arteries, 35
of the subclavian artery, 186-187
post-angioplasty, 245

of renal artery stenosis, 35, 223-224
of subclavian arterial aneurysms, 217
of thoracoabdominal aortic aneurysms, 209
Angioplasty

percutaneous transluminal

as fibromuscular dysplasia treatment, 88
mesenteric, 234-235
as renal artery stenosis treatment, 226
as supra-aortic trunk disease treatment,
184-185
as renal artery stenosis treatment, 225-226
of the subclavian artery, 187
techniques in, 244-246
Angioplasty balloons, 245
Angiotensin-converting enzyme inhibitors, 88,

222
Angiotensin II, captopril blockage of, 225
Angiotensin II receptor antagonists, 78
Ankle block, 71

Ankle-brachial index (ABI), 19, 150-151
in chronic venous insufficiency, 109
definition of, 15
in diabetes mellitus, 19
effect of exercise testing on, 20
in lower limb ischemia, 93, 94, 95
in peripheral arterial disease, 53, 58
Antibiotics, indications for use of, 241
Anticoagulation therapy, 66, 99-100, 127
Antihypertensive therapy, guidelines for, 59
Antineutrophil cytoplasmic antibodies (ANCAs), 79,

80,83
Antioxidant therapy, 8
Antiphospholipid antibody syndrome, 50
Antiplatelet therapy, 1, 54-56, 166-167, 172
Antiplatelet Trialists Collaboration, 56, 166, 167
Antithrombin III deficiency, 48
Aorta

abdominal

aneurysms of. See Abdominal aortic aneurysms
diameter of, 193
palpation of, 14
thoracic, trauma-related disruption of, 128
traumatic injuries to, 37, 128
Aortic aneurysms

abdominal. See Abdominal aortic aneurysms
thoracoabdominal, 207-210
Aortic dissection, 36-37, 100
Aortic reconstruction, complications of, 137

255

INDEX

Aortic surgery, open

anesthesia for, 67-69

pharmacological considerations for, 68-69
Aortitis, 81,208

Aortobifemoral bypass, long-term results of, 96
Aortofemoral bypass, 68, 101-102, 102
Apolipoproteins, 4-5

L-Arginine, as lower limb ischemia treatment, 95
Arterial bypass. See also specific types of arterial
bypass

as limb ischemia treatment, 101-102
Arterial pressure index (API), Doppler, 126
Arterial reconstruction, complications of, 134-135
Arteriography. See also Angiography

of abdominal aortic aneurysms, 195-196

arch, of innominate artery occlusive disease, 183

of axillary artery aneurysms, 218

of popliteal arterial aneurysms, 21 1
Arteriovenous access grafts

autogenous. See fistulas, arteriovenous

nonautogenous, 141, 143
complications of, 145-146
Arteriovenous malformations, pulmonary, 33-34
Arteritis

giant cell, 80, 160, 163, 181

radiation, 160, 185

Takayasu's, 32, 80-81, 157, 159, 163, 181, 185
Artery of Adamkiewicz, ligation of, as paraplegia

cause, 202
Aspirin, as hemorrhage risk factor, 39, 40
Aspirin therapy, 54-55, 76, 166, 167, 241
Asymptomatic Carotid Atherosclerosis Study

(ACAS), 169, 170-171, 173, 179
Asymptomatic Carotid Surgery Trial (ACST), 169,

170-171,173
Atherectomy, 247-248
Atheroma, 5-6
Atherosclerosis, 1-8

of the carotid artery, 156-157

clinical history of, 10

epidemiology of, 1-2

of the innominate artery, 181

lipid metabolism in, 3-5

lipid profiles in, 59

as lower limb ischemia cause, 91, 92, 93

pathogenesis of, 5-7

prevention of, 7-8

radiation-induced, 181

regression of, 6-7

risk factors for, 2-5

of the subclavian artery, 185

as systemic vascular disorder, 53

theories of, 5-7

as thoracoabdominal aortic aneurysm cause, 208
Atherosclerotic plaques, 5-7

carotid, 157-158

fibrous, 5

fibrous cap of, 5, 157

rupture of, 7, 157-158

stable versus unstable, 7
Atrial fibrillation, 156, 167-168
Atriofemoral bypass grafting, 68
Atrophie blanche, 105, 108
Atropine, 241
Auscultation, 14
Axillary artery

cystic adventitial disease of, 89

traumatic injuries to, 130

as vascular access site, 243
complications of, 140
Axillary artery/vein dissection, anesthesia for, 71
Axillobifemoral bypass, in abdominal trauma

patients, 130
Axillofemoral bypass, 66, 68, 71, 102
Axillosubclavian artery aneurysm, 217
Azathioprine, as giant cell arteritis treatment, 160

Bandaging, multilayer lymphedema (MLLB), 120,

121
Banding, of arteriovenous fistulas, 145
Benzodiazepines, 241

Benzpyrenes, as lymphedema treatment, 122
Beta blockers, use in peripheral arterial disease

patients, 59
Bleeding disorders, 39-42. See also Coagulation

disorders
Blood flow

mesenteric, 231

normal venous, 106-107
Blue digit syndrome, 31
Blunt trauma, 125

abdominal, 128-129

to the carotid artery, 127

to the extremities, 130, 131

to the neck, 127, 160
Bovine branch anomaly, 182
Brachial artery

distal, cystic adventitial disease of, 89

as vascular access site, 243
Brachial plexus, traumatic injuries to, 126, 130

clinical assessment of, 128
Brachial plexus blocks, 71-72
Breast cancer, mortality rate in, 54
Breast cancer treatment, as lymphedema-related

pain cause, 120
British Hypertension Society, 59
Bruits

carotid, 14, 93, 164-165, 183

subclavian, 183

vascular injury-related, 126
Buerger, Leo, 86
Buerger's disease, 31, 86-87, 91
Buerger's test, 14
Bullets, velocity of, 126
Bupivacaine, 66, 240

256

INDEX

Calcitonin gene-related peptide, 74, 78-79
Calcium channel blockers, as Raynaud's

phenomenon treatment, 76, 77-78
Calf muscle, venous blood pumping function of,

106-107
Capillaroscopy, 76
Capillary refill test, 13
CAPRIE (Clopidogrel versus Aspirin in Patients at

Risk of Ischemic Events) study, 56, 167
Captopril, 225

Carbon dioxide, as vascular contrast media, 27-28
Cardiac failure, high-output, 145
Cardiovascular disease, as mortality cause, 1
Carotid arteries

aneurysms of, 218-219
false, 158
true, 158, 159
dissection of, 127, 129, 158-159, 163
external, in carotid endarterectomy, 171
internal

in carotid endarterectomy, 171, 172-173
elongation and kinking of, 158
fibromuscular dysplasia of, 158
occlusive disease of, vertebral artery occlusive

disease-associated, 189
thrombosis of, as stroke cause, 156
proximal common, occlusive disease of, 187-188
stenosis of, 22, 182
tortuous, 33, 158
traumatic injuries to, 127, 160
Carotid artery disease, 155-180
clinical presentation of, 161-163
epidemiology of, 155
investigation of, 164-166
management of, 166-175
medical, 166-168
surgical, 169-175
pathology of, 157-160
postoperative management of, 175-179
prognosis of, 164

radiological investigations of, 32, 33
Carotid body tumors (CBTs), 32, 160
Carotid bypass, 175
Carotid-sub clavian bypass, 187
Carotid surgery, anesthesia in, 69-70
Catheterization

central venous, 141, 142
epidural, 66

equipment for, 237-240
as vascular injury cause, 126
Catheters, 238-240

central venous, 141, 142, 143-144, 146-147

complications related to, 140, 146-147

for embolotherapy, 251

flushing of, 101, 147,239,240-241

placement of, 244

types of, 239-240

CAVATAS study, 180
Cavography, 109
Celiac artery

aneurysms of, 216

duplex ultrasound examination of, 234
Cerebral perfusion pressure (CPP), 69
Cervical plexus block, 69, 70
Cervical rib, 76, 185, 187, 217
Charles operation, for lymphedema, 122
Chest, vascular injuries to, 128
Chewing tobacco, as Buerger's disease cause, 86
Cholesterol, hepatic production of, 3
Churg, Jakob, 84
Churg-Strauss syndrome, 84-85
Chylomicrons, 3, 4
Cilostazol (Pletal), 61-62, 95
Claudication

as amputation cause, 95

chronic limb ischemia-related, 10

cystic adventitial disease-related, 88

exercise testing evaluation of, 20

innominate artery occlusive disease-related, 181

intermittent, 60

drug therapy for, 61-62

dyslipidemia-related, 58

effect of smoking cessation on, 2

exercise programs for, 60

lower limb ischemia-related, 53, 91, 92-93, 95,

98
medical management of, 54
natural history of, 53
risk factors for, 55, 58
of the jaw, 163
neurogenic, differentiated from vascular

claudication, 92-93
thoracic outlet syndrome-related, 186
upper-limb, 1 1
venous, 108
Clinical status, 150-151
Clopidogrel, 56, 166, 167,241
Clopidogrel versus Aspirin in Patients at Risk of

Ischemic Events (CAPRIE) study, 56
Closure devices, arterial, 25, 26, 242
Clotting disorders. See Coagulation disorders
Coagulation cascade, 42
Coagulation disorders
acquired, 46-47

complications related to, 139-140
inherited, 42-46
Cogan's syndrome, 81-82
Coils, embolic, 251
Colic artery, aneurysms of, 217
Colonic ischemia, postoperative, 202, 206
Colonoscopy, 202

Colorectal cancer, mortality rate in, 54
Common femoral artery, orthopedic surgery-related

injuries to, 126
Compartment pressures, measurement of, 103

257

INDEX

Compartment syndrome, 102-103, 103, 130
Compression injuries, abdominal, 128-129
Compression therapy, 110-111, 121
Computed tomography (CT), 28-30. See also
Angiography, computed tomography

of abdominal aortic aneurysms, 36, 195, 199,
205

of arteriovenous fistulas, 123

of carotid disease, 165-166

of inflammatory abdominal aortic aneurysms,
207

of innominate artery occlusive disease, 183

of lower limb ischemia, 93, 95

of lymphedema, 119

of popliteal arterial aneurysms, 21 1

of subclavian arterial aneurysms, 217

of thoracic trauma, 128

of thoracoabdominal aortic aneurysms, 208
Congestive heart failure, incidence of, 2
Connective tissue disorders, Raynaud's

phenomenon-related, 75, 76
Continuous quality improvement (CQI), 152-153
Contrast agents, 26, 27-28

first use of, 25-26

nephrotoxicity of, 27, 33, 95, 224

reactions to, 242
Cooperative Study of Renovascular Hypertension,

221-222
Corona phlebectatica (ankle/malleolar flare), 105,

108
Coronary artery disease (CAD)

carotid disease-related, 65

cholesterol as risk factor for, 6

incidence of, 2

as mortality cause, 1

peripheral arterial disease-related, 53

postoperative, 133

prevention of, with cholesterol-lowering therapy,
7,8

supra-aortic trunk disease-associated, 183
Coronary-subclavian steal syndrome, 186
Corticosteroids, as giant cell arteritis treatment, 80,

160
Cost outcomes, in vascular surgery, 152-153
Cranial nerve palsy, 159, 218-219
C-reactive protein, in giant cell arteritis, 80
Critical closing pressure (CCP), in lower limb

ischemia, 93
Cross-clamping, aortic, effect on cardiac afterload,

68
Crush injuries, 126, 128
Cryoglobulinemia, essential mixed, 85
Cryoglobulins, 85-86
Cyanoacrylate, 252

Cyanosis, Raynaud's phenomenon-related, 75
Cyclophosphamide, 84, 160
Cystic adventitial disease, 88-89
Cytokines, 6, 157

Debridement, 22, 130
Deceleration injuries, 126, 128-129
Decongestive lymphedema therapy (DLT), 120
Deep venous reconstruction, as varicose veins

treatment, 112-113
Deep venous thrombosis

abdominal aortic aneurysm repair-related, 202

chronic venous insufficiency-related, 107

hypercoagulability-related, 61

as lymphedema cause, 118

medical management of, 54
Dense granule deficiency, 46
Dermatitis, chronic venous insufficiency-related,

105,108,110
Diabetes mellitus

ankle-brachial index (ABI) in, 19

as atherosclerosis risk factor, 1,2

hypertension management in, 59, 167

lower limb ischemia associated with, 91, 97

negative correlation with abdominal aortic
aneurysms, 193-194

peripheral arterial disease associated with, 55, 58,
59
Dialysis Outcomes and Practice Patterns Study

(DOPPS), 142
Dialysis patients, vascular access in, 141-148
Diazepam, 66-67

Digital pressures, measurement of, 20
Diphenhydramine, 66-67
Dipyridamole, 56, 166, 241
Distal revascularization-interval ligation (DRIL),

145
Dorsalis pedis artery, absence of, 19
Dressings, for chronic venous insufficiency

management, 109-110
Drug injection, intraarterial, adverse effects of,

16-17,131
Drugs. See also names of specific drugs

as bleeding risk factor, 39, 40
Dysarthria, 163
Dysfibrinogenemias, 49
Dyshypoplasminogenemias, 49
Dyslipidemia, management of, 58-59
Dysphagia, 163
Dysplasia, fibromuscular, 87-88

of the internal carotid artery, 158

radiological investigations of, 35

as renal artery stenosis cause, 222, 225

as stroke cause, 157

subtypes of, 158

Eczema, 105, 108, 120
Edema

chronic venous insufficiency-related, 108-109

pulmonary, "flash," 224
Ehlers-Danos syndrome, 158-159

258

INDEX

Elastases, 7

Elastic bandages, 110-111, 121
Elderly patients, brachial emboli in, 12
Electrocardiography, preoperative, 198
Elephantiasis, as lymphedema cause, 118
Embolectomy. See also Embolotherapy

as lower limb ischemia treatment, 100-101, 103
Embolic agents, 251-252
Embolism

cardiac, as ischemic stroke cause, 156
cholesterol, 161, 162
common sources of, 11
distal, of the supra-aortic trunk, 189
endovascular abdominal aortic aneurysm repair-
related, 204
as lower limb ischemia cause, 98-99, 100-101,

103,104
mesenteric, 232, 233
pulmonary, 32-33, 202
as upper limb ischemia cause, 16, 17
as upper limb vascular disease cause, 1 1
Embolotherapy, 250-252
Endarterectomy
carotid, 169-179

anesthesia for, 66, 69-70
atherocsclerotic plaque excision in, 157
bifurcation, of the proximal common carotid

artery, 188
cerebral protection in, 69
comparison with carotid angioplasty, 179-180
effect on stroke risk, 169-171
monitoring during, 66
neurological deficits associated with,

176-178
operative principles of, 171-175
postoperative management of, 175-179
preoperative hypertension control for, 167
traditional versus eversion, 174
in vertebral artery stenosis/occlusion, 189
transaortic renal, 226
transthoracic innominate, 183, 184
Endoleaks, 36, 204, 250

Endothelin-1, in Raynaud's phenomenon, 74-75
Endovascular approaches and techniques, 237-252.
See also Embolotherapy; Stenting; Stent
grafting
for abdominal aortic aneurysms, 67, 202-204

conversion to open repair, 204
access techniques, 242-244
anesthesia in, 66-67
for aneurysmal disease, 249-250
for arterial occlusive disease, 244-249
for arterial trauma, 131
for carotid aneurysms, 218, 219
equipment for, 237-240
medications used in, 240-242
radiological investigations with, 25-26
for renal artery stenosis, 226-227

for supra-aortic trunk disease, 184-185

for Takayasu's arteritis, 81

for thoracoabdominal aortic aneurysms, 210

vascular intervention devices for, 242
Epidural anesthesia, 66, 71
Errors, medical, 149

Erythrocytes, in Raynaud's phenomenon, 75
Erythrocyte sedimentation rate, 80, 83, 198
Eryfhromelalgia, 79
Estrogen, 39, 75

European Carotid Surgery Trial (ECST), 169-170
EuroQol, 152
Exercise

health benefits of, 60

lymphedema-exacerbating effects of, 122
Exercise testing, 20

in lower limb ischemia patients, 94-95
Exercise therapy

for lower limb ischemia patients, 95

for peripheral arterial disease patients, 60

Factor deficiencies, 42-45
Factor inhibitors, 46-47
Fasciotomy, 102-103, 130
Fatty streaks, 5
Femoral arteries

aneurysms of, 13,213-214

superficial

aneurysms of, 13

distal, occlusive disease of, 96

as hemodialysis access conduit, 147

traumatic injuries to, 130-131

as vascular access site, 243
Femoral artery punctures, complications of, 131, 140
Femoral-femoral bypass, 96, 101-102
Femoral-popliteal bypass, 96
Femoral shaft fractures, 126
Femoral-tibial bypass grafting, 97
Fentanyl, 67
fibrinogen, 41

fibrinogen abnormalities, 45
filiariasis, as lymphedema cause, 118
fistulas

aortocaval, 194

aortoduodenal, 194

arteriovenous, 123, 124, 128, 131, 141, 142-143
complications of, 144-145

carotid-cavernous sinus, 128
flavonoids, as lymphedema treatment, 122
fluid management, perioperative, in patients with

ruptured aortic aneurysms, 201
Framingham Study, 6
Functional status, 151-152

Gadolinium chelate, 28

Gangrene, 17, 91, 92, 93, 94, 96-97, 131

259

INDEX

Gastroduodenal artery, aneurysms of, 216-217

Gingko, 40, 95

Glomerulonephritis, Wegener's granulomatosis-
related, 84

Glucocorticoids, as Takayasu's arteritis treatment,
81

Glucose tolerance test, 58

Glues, embolic, 252

Glyceryl trinitrate, 241

Glycopyrronium bromide, 241

Grafts, peripheral vascular. See also Stent grafting
complications related to, 134-139
infrainguinal, duplex imaging of, 22
lower limb, occlusion of, 100, 136-137
as lower limb ischemia risk factor, 91
polytetrafluoroethylene, 96, 97, 102, 135,

136
prosthetic, complications of, 137-139
in supra-aortic trunk disease, 183-184

Granulomatosis, Wegener's, 83-84

Gray platelet syndrome, 46

Greater saphenous vein, radiofrequency or laser
ablation of, 67

Greater saphenous vein grafts, 135

Growth factor therapy, for limb ischemia, 98

Guidewires, 237-238, 244-245

introduction through needles, 244

Gunshot wounds, 126, 129

Hand surgery, anesthesia for, 72

Health Plan Employer Data and Information Set

(HEDIS), 151
Heart Protection Study, 58, 59
Hemangiomas, 123
Hematomas

of neck incisions, 176

retroperitoneal, 129

vascular injury-related, 126, 127, 129
Hemianopia, homonymous, 162, 163
Hemophilia, 42-43
Hemorrhage

abdominal, trauma-related, 129

chronic venous insufficiency- related, 109

femoral artery puncture-related, 131

intracranial, carotid endarterectomy-related,
177-178

perioperative, in abdominal aortic aneurysm
patients, 201

thrombolytic therapy- related, 248

vascular injury-related, 126, 127

venous, trauma-related, 130
Henoch, Edouard, 85
Heparin

in catheter saline flushes, 101, 147,239,240-241

as contraindication to epidural catheter use,
66

as hypercoagulability treatment, 47, 48

intraoperative administration of, 173,240-241

as thrombocytopenia cause, 50-51
Hepatic artery, aneurysms of, 215-216
Hepatitis C virus, 85, 86
Herbal remedies, as hemorrhage risk factor, 39,40,

41
Hexopal (inositol nicotinate), 61-62
High-density lipoprotein, 2, 4, 168
Hollenhorst plaques, 161
Homan operation, for lymphedema, 122
Homocysteine, 3, 48-59
Homocystinemia, 61
Horner syndrome, 163

partial, 159
Human immunodeficiency virus (HIV) infection,

118
Hunter, William, 125
Hydro thorax, 37

3-Hydroxy-3-mefhylglutaryl coenzyme (HMG CoA)
reductase, inhibition of, 3, 5. See also Statin
therapy
5-Hydroxytryptamine. See Serotonin
Hypercholesterolemia, 1,6, 193
Hypercoagulable disorders

acquired, 47, 50-51, 60-61

inherited, 47, 48-50, 60, 61

as ischemic stroke cause, 157

peripheral arterial disease-associated, 60-61

supra-aortic trunk disease-associated, 183-184

as vascular thrombosis cause, 139-140
Hyperhomocystinemia, 47, 48-49
Hyperhomocystinuria, 48-49
Hyperlipidemia, 2, 168

Hyperperfusion syndrome, as stroke cause, 178
Hyperplasia, myointimal, 135
Hypertension

as abdominal aortic aneurysm risk factor, 193

as atherosclerosis risk factor, 1, 3

diabetes mellitus-related, 2
management of, 59, 167

drug therapy guidelines for, 59

fibromuscular dysplasia-related, 88

incidence of, 2

as peripheral arterial disease risk factor, 59-60

postoperative, endarterectomy-related, 176

renovascular, 22 1 -229

diagnostic evaluation of, 223-224
pathophysiology of, 222-223
renal artery stenosis-related, 225-226
treatment of, 225-228

as stroke risk factor, 3, 167
Hypotension

endarterectomy-related, 176

vascular injury-related, 126, 128

Ileal artery, aneurysms of, 217
Ileus, laparotomy-related, 201-202

260

INDEX

Iliac arteries

aneurysms of, 214

cystic adventitial disease of, 89

external, orthopedic surgery-related injuries to,
126
Iloprost, 76, 78

Imaging. See Radiological investigations
Impotence, abdominal aortic aneurysm repair-
related, 202
Infections

arteriovenous access graft- related, 146

arteriovenous fistula-related, 145

central venous catheter-related, 144, 146-147

prosthetic graft-related, 137-139
Inferior mesenteric artery, in abdominal aortic

aneurysm repair, 199-200,202
Inferior vena cava

as hemodialysis access conduit, 147

traumatic injuries to, 130
Inflammation

as aneurysmal disease cause, 192, 206

as atherosclerosis cause, 6
Infrainguinal bypass, as acute ischemia treatment,

102
Innominate artery

occlusive disease of, 181-185

traumatic injuries to, 128
Inositol nicotinate (Hexopal), 61-62
Institute of Medicine, "To Err is Human" report, 149
Intercostal arteries, in thoracoabdominal aortic

aneurysm repair, 209
Intermediate-density lipoprotein, 3, 4-5
Internal jugular veins, traumatic injury to, 127
Internal mammary artery revascularization, as

coronary-subclavian steal syndrome cause,
186
International normalized ratio (INR), 41
International Society for Cardiovascular Surgery,

151
Interscalene technique, of deep cervical plexus

block, 70
Intravenous immunoglobulin, as Kawasaki's disease

treatment, 82
Ischemia

colonic, postoperative, 202, 206

limb. See Limb ischemia

mesenteric, 16, 231-234

popliteal arterial aneurysm-related, 211-212

Raynaud's phenomenon-related, 76

visceral. See Visceral ischemic syndromes
Itching, chronic venous insufficiency- related, 108

Jejunal artery, aneurysms of, 217

Kaposi's sarcoma, 118
Kawasaki, Tomisahu, 82

Kawasaki's disease, 82

Ketanserin, 78

Klippel-Trenaunay- Weber syndrome, 117

Knee injuries, 126, 131

Kocher maneuver, 130

Korean War, vascular surgery during, 125

Lacunar infarcts, 156, 164

Language disorders, carotid disease-related, 163

Laparotomy, as ileus cause, 201-202

Laser ablation, of the greater saphenous vein, 67

Leap Frog Group, 149-150

Lecithin- cholesterol acetyltransferase, 4

Letessier-Meige syndrome, 117

Lidocaine, 66, 67, 240

Lifestyle risk factors, clinical evaluation of,

10
Limb ischemia

lower. See Lower limb ischemia
upper limb

clinical examination of, 16-17
radiological investigations of, 32
vascular injury-related, 126
Limb pressures, segmental, 19-20, 21
Limb reduction procedures, as lymphedema

treatment, 122
Limbs, vascular injuries to, 130-131
Limb salvage, in acute lower limb ischemia,

103
Lipedema, 119

Lipid-lowering therapy, 7, 8, 58-59
Lipid metabolism, 3-5
Lipid profile, "diabetic," 58
Lipodermatosclerosis, 105, 108
Lipoprotein (a), 2, 4
Lipoprotein lipase, 4
Liver, cholesterol production in, 3
Local anesthesia, 240

in carotid endarterectomy, 172

in lower extremity vascular surgery,

70-71
in upper extremity vascular surgery,
71-72
Long saphenous vein, 106
Long saphenous vein surgery, for varicose veins,

111-112
Lorazepam, 67
Low-density lipoprotein, 1,2,3, 4-5, 168

small-density, 2, 4
Lower limb(s), pallor of, 14
Lower limb ischemia, 91-104
acute, 98-104

clinical examination of, 16
diagnostic studies of, 99
five P's of, 99
outcomes of, 103-104
patient history of, 98-99

261

INDEX

physical examination of, 99
treatment of, 99-103
chronic, 10, 92-98

abdominal aortic aneurysm-related, 194
clinical examination of, 16
diagnostic studies of, 94-95
outcomes of, 98
patient history of, 92-93
physical examination of, 93-94
treatment of, 95-98
critical, 97
acute, 10, 54
amputations in, 97-98
hypertension treatment in, 59, 60
in peripheral vascular disease patients, 53
thrombolytic therapy for, 248
etiology and presentation of, 91-92
postoperative, in abdominal aortic aneurysm

patients, 201
subclavian artery aneurysm-related, 217
treatment of

amputation, 97-98
medical, 95

revascularization, 95-97
Lung cancer, mortality rate in, 54
Lupus anticoagulant, 50
Lymph, formation of, 121-122
Lymphadenitis, 118
Lymphangiography, 119
Lymphangioma circumscriptum, 116
Lymphangioma diffusum, 116
Lymphangiomas, 116
Lymphangiosarcoma, 116, 119
Lymphangitis, 118
Lymphatic drainage, manual lymphatic (MLD), 120,

121
Lymphatic system, anatomy and functions of,

113-114
Lymphedema, 113-122

acute inflammatory episodes (AIEs) associated

with, 118, 121
clinical assessment of, 115-116
definition of, 114
differential diagnosis of, 115
epidemiology of, 1 1 5
etiological classification of, 109
factitious, 119
familial, 117

lymphatic system in, 114
management of, 120-122
pathophysiology of, 114
primary, 114, 116-118
relationship with chronic venous insufficiency,

118-119
secondary, 114, 118-119
Lymphedema congenita, 117
Lymphedema praecox, 117
Lymphorrhea, 120-121

Macrophages, 6, 157, 192
Magnetic resonance imaging (MRI). See also
Angiography, magnetic resonance

of abdominal aortic aneurysms, 195

of carotid disease, 165-166

of popliteal arterial aneurysms, 211

of thoracoabdominal aortic aneurysms, 208-209
Mannitol, 69

Marfan syndrome, 46, 158-159
Matrix metalloproteineases, 157, 158, 192
Mean arterial pressure (MAP), during carotid

endarterectomy, 69
Medical Outcomes Short Form 36 (SF-36), 151-152
Mesenteric arteries

aneurysms of, 34, 35, 216

radiological investigations of, 34-35

superior

aneurysms of, 216

duplex ultrasound examination of, 234
embolization of, as ischemia cause, 231
thrombosis of, as ischemia cause, 231, 233
traumatic injuries to, 129-130

thrombosis of, 231, 232, 233-234
Mesenteric ischemia, acute, 231-234
Mesenteric venous thrombosis, 235-236
Midazolam, 241
Middle cerebral artery, 156
Milroy's disease, 117
Morphine, 241

Motor deficits, carotid disease-related, 162-163
Multiple Risk Factor Intervention Trial (MRfiT), 2
Mupirocin, 146

Muscle death, acute limb ischemia-related, 99, 100
Myocardial infarction, 7, 53, 201
Myxedema, pretibial, 119

Naftidrofuryl (Praxilene), 61-62

National Committee for Quality assurance (NCQA),

151
National Veterans Administration Surgical Quality

Improvement Program (NSQIP), 149
Neck

anatomic zones of, 127
innervation of, 69-70
traumatic injuries to, 126, 127-128, 160
Neck incisions, hematoma of, 176
Nephropathy

contrast agent-induced, 27, 33, 95, 224
diabetic, lower limb ischemia associated with, 91
ischemic, 221, 223, 228
Nerve injuries, vascular injuries-associated, 126,

130
Neurological deficits, post-carotid endarterectomy,

176-178
Neurological examination, of vascular injury
patients, 126

262

INDEX

Neuropathy
diabetic, 71
ischemic, 104
Neutrophils, in Raynaud's phenomenon

pathophysiology, 75
Nicotine replacement therapy (NRT), 57
Nifedipine, 76,241
Nitroglycerin, 68-69, 78, 241
Nitroprusside, 68, 69
Nonsteroidal anti-inflammatory drugs, as

hemorrhage risk factor, 39, 40
Noone-Milroy syndrome, 117
North American Symptomatic Carotid

Endarterectomy Trial (NASCET), 166,

169-170,174

Obesity

adverse health effects of, 57-58

management of, 57

in peripheral arterial disease patients, 58
Ocular disorders, carotid disease-related, 161-162
Ocular-ischemia syndrome, 161, 162
Opiates, 241

Optic nerve, ischemia of, 161, 162
Orthopedic injuries, treatment for, 130
Orthopedic procedures, as vascular injury cause, 126
Osier- Weber-Rendu disease, 46
Ostial lesions, stenting of, 246
Outcome measures, in vascular surgery, 149-154
Ovarian vein reflux, imaging of, 109
Oxfordshire Community Stroke Project, 164
Oxypentifylline (Trental), 61-62

Padma Basic, 95

Pallor, 14, 16, 75,99

Palpation, 13-14, 194, 207, 211

Pancreatic artery, aneurysms of, 216-217

Pancreaticoduodenal artery, aneurysms of, 216-217

Papaverine, 241

Paralysis, acute limb ischemia-related, 99

Paraplegia, 128, 202

Paresthesia, acute limb ischemia-related, 99

Patching, in carotid endarterectomy, 174-175

Patient satisfaction, 151

Penetrating trauma, 125

abdominal, 128

to the extremities, 130

to the neck, 127

thoracic, 128

weapon-related, 125
Pentoxifylline, 95

Perforator ligation, as venous disease treatment, 112
Peripheral vascular disease

asymptomatic, in diabetic patients, 58

atherosclerosis risk factor treatment in, 1

cholesterol-lowering therapy for, 7

as coronary artery disease risk factor, 65

diabetes mellitus associated with, 58

evaluation instruments for, 152

as lower limb ischemia cause, 91

medical management of, 53-63

vascular risk factor modification, 53-61

mortality rate in, 53, 54

radiological investigations of, 31
Pethidine, 241
Phleboliths, 123
Physicians' Health Study, 56
Platelet-derived growth factor, 54, 135
Platelet disorders, 45-46
Platelet factor, 4, 54
Platelets, in Raynaud's phenomenon

pathophysiology, 75
Pletal (cilostazol), 61-62
Plethysmography, 21, 109
Pneumothorax, 37

tension, 128
Poiseuille's law, 95
Polyangiitis, microscopic, 85
Polyarteritis nodosa, 82-83, 85
Polytetrafluoroethylene grafts, 96, 97, 102, 135, 136
POPADAD (Prevention of Progression of Arterial

Disease in Diabetes), 55, 58
Popliteal artery

aneurysms of, 13,210-213

duplex imaging evaluation of, 22-23
as limb ischemia cause, 101, 103
management of, 211-213
popliteal pulse in, 93
ruptured, 211-212

cystic adventitial disease of, 89

occlusive disease of, surgical treatment of, 96

orthopedic surgery-related injuries to, 126

traumatic injuries to, 131

as vascular access site, 243
Popliteal pulse, in popliteal aneurysm, 93
Postimplant syndrome, 204
Postthrombotic syndrome (PTS), 107
Praxilene (naftidrofuryl), 61-62
Prazosin, 74
Prednisolone, as Wegener's granulomatosis

treatment, 84
Pregnancy, "white leg" of, 107
Prevention of Progression of Arterial Disease in

Diabetes (POPADAD), 55, 58
Prilocaine hydrochloride, 240
Primary valvular incompetence (PVI), 107
Pringle's maneuver, 129
Prostate cancer, mortality rate in, 54
Proteases, 7

Protein C deficiency, 49
Protein S deficiency, 49
Prothrombin time (PT),41
Pseudoaneurysms

of arterial puncture sites, 131, 140

263

INDEX

arteriovenous access graft-related, 146

carotid, 127-128
Pulmonary arteries, imaging of, 32-34
Pulmonary disease

implication for anesthesia, 71

postoperative, 133-134
Pulseless disease. See Arteritis, Takayasu's
Pulselessness, acute limb ischemia-related, 99
Pulselessness, vascular injury-related, 126
Pulses

abdominal, 14

carotid, 13-14

lower limb, 13

subclavian, 13

ulnar, 13

upper limb, 13
Pulse volume recordings (PVRs), 20-21
Purpura, Henoch-Schbnlein, 85

Quality-adjusted life years (QALYs), 153

Quality analysis (QA), 153

Quality Interagency Coordination Task Force, 149

Radial arteries

distal, cystic adventitial disease of, 89
traumatic injuries to, 130
as vascular access site, 143, 243
Radiation, as arteritis cause, 160, 185
Radiofrequency ablation, of the greater saphenous

vein, 67
Radiological investigations, 25-38. See also specific
radiological imaging modalities in
complications of, 140
controversies in, 25
radiation safety during, 30-31
of trauma, 37

of vascular diseases, 31-37
Radionuclide investigations, mesenteric, 34
Raynaud, Maurice, 73
Raynaud's phenomenon, 73-79
primary, 73, 75

differentiated from secondary, 75-76
secondary, 73, 74, 75-76
thoracic outlet syndrome-related, 186
treatment for, 76-79
Recombinant tissue-type plasminogen activator, 248
Renal arteries

aneurysms of, 216
radiological investigations of, 35
resistive index (RI) in, 223
stenosis of, 221-229
bruits associated with
diagnostic evaluation of, 223-224
etiology of, 222

experimental models of, 222-223
medical management of, 225-226

natural history of, 225
pathophysiology of, 222-223
renal-to-aortic ratio (RAR) for, 223
surgical management, 223, 224, 225-228, 246
traumatic injuries to, 130
Renal function, postoperative, in abdominal aortic

aneurysm patients, 201, 206
Renal insufficiency. See also Nephropathy, ischemic
contrast agent-related exacerbation of, 95, 224
in lower limb ischemia patients, 97
renal artery stenosis-related, 224
Renal-to-aortic ratio (RAR), 223
Renal vein, left, operative exposure of, 227
Renal vein renin assays, 224-225
Renography, isotope, 225
Reperfusion syndrome, as stroke cause, 178
Residency training programs, outcomes measures

competency requirement in, 153
Resistive index (RI),in the renal artery, 223
Rest pain, 10, 11,92,93,98
Resuscitation, in abdominal vascular injury

patients, 129
Retinal artery, occlusion of, 161, 162
Rheumatoid arthritis, as lymphedema cause,

119
Rib fractures, 128
Rubor, 14, 15,75

Saline, heparinized, 101, 147,239,240-241
Saphenofemoral junction, incompetence of, 14-16,

16
Saphenopopliteal junction, ligation of, 112
Saphenous vein, as carotid endarterectomy patch,

174-175
SAPPHIRE study, 180
Schonlein, Johann, 85
Sclerotherapy, for chronic venous insufficiency,

111
Scottish Intercollegiate Guidelines Network (SIGN),

59
Sedation, 241
Seldinger technique, 26
Selective serotonin reuptake inhibitors, as

Raynaud's phenomenon treatment, 78
Sensory deficits, carotid disease-related, 162-163
Serotonin, 54, 75
Serotonin antagonists, as Raynaud's phenomenon

treatment, 78
Short saphenous vein, 106
Short saphenous vein surgery, for varicose veins,

112
Shunting, in carotid surgery, 69, 173-174
Simvastatin, 8, 59

Sinus nerve, in carotid endarterectomy, 173
Sistrunk operation, for lymphedema, 122
Skin perfusion pressure (SPP), 21-22
"Slipped heart syndrome," 12

264

INDEX

Smoking

as abdominal aortic aneurysm cause, 193

as atherosclerosis cause, 1,2

as Buerger's disease cause, 86, 87

by occlusive vascular disease cause patients, 12

as peripheral arterial disease cause, 1, 57

as stroke cause, 167

by supra-aortic trunk disease patients, 183
Smoking cessation

cardiovascular health benefits of, 2

effect on stroke risk, 167

in lower limb ischemia patients, 95

methods, 57

in peripheral arterial disease patients, 1, 57

as weight gain cause, 58
Society for Vascular Surgery, 151
Speech disorders, carotid disease-related, 163
Splenic artery, aneurysms of, 215
Stab wounds, 126
Starling's forces, 114
Statin therapy, 7-8, 59
Steal, vascular, 145, 146
Stemmer's sign, 115-116
Stent grafting, 248

of abdominal aortic aneurysms, 202-204, 249-250
migration of stent in, 204

of carotid artery aneurysms, 219

devices for, 249, 250

postimplantation imaging of, 36

types of stents, 246-247
Stenting

intravascular, 246-247

of renal artery stenosis, 226-227

of supra-aortic trunk disease, 184-185

techniques in, 246

of thoracoabdominal aortic aneurysms, 210
Sticky platelet syndrome, 49
Strauss, Lotte, 84
Streptokinase, 101,248
"String of sausages" sign, 233
Stroke

atrial fibrillation-related, 167-168

in carotid endarterectomy patients, 176-178

in carotid territory. See Carotid artery disease

completed, 161

definition of, 155

in evolution, 161

hemorrhagic, 156

incidence of, 2

investigation of, 164-166

ischemic, 156-157, 164

as mortality cause, 164

perioperative, in supra-aortic trunk disease
patients, 183-184

peripheral arterial disease-related, 53

prevention of

with antiplatelet therapy, 166-167
with carotid endarterectomy, 169-179

with risk factor modification, 167-168
vertebrobasilar symptoms of, 161, 163, 188-189
Subclavian arteries

aneurysms of, 185, 186,217

as arteriovenous fistula access site, 142

occlusive disease of, 185-187

cerebrovascular symptoms of, 1 1
revascularization of, 187
right, stenosis of, 185
traumatic injuries to, 128, 130
Subclavian steal, 186
Subclavian vein, compression of, 186
Subfascial endoscopic perforator surgery (SEPS),

duplex ultrasound-guided, 112
Suction drains, 175
"Sunset foot," 14

Sympathectomy, as Raynaud's phenomenon
treatment, 74, 76-79

Takayasu, Mikito, 80

Thiazides, 59

Thompson operation, for lymphedema, 122

Thoracic outlet syndrome, 185, 186,217

Thoracic spine, traumatic injuries to, 128

Thoracotomy

emergent, in thoracic vascular injury patients,
128

in thoracoabdominal aortic aneurysm repair, 209,
210
Thrombectomy, 249
Thrombin inhibitors, 47

Thromboangiitis obliterans. See Buerger's disease
Thromboasthenia, Glanzmann's, 45, 75
Thrombocytopenia, heparin-induced, 50-51
Thromboembolism. See also Deep venous
thrombosis

carotid artery aneurysm-related, 218

as ischemic carotid territory stroke cause, 156

subclavian artery fhromboembolism-related, 185

venous, hypercoagulability-related, 48
Thromboendarterectomy, 227, 235
p-Thromboglobulin, 54
Thrombolytic therapy, 101, 248-249
Thrombophilia

acquired, 60-61

inherited, 60, 61, 105-106

mesenteric venous thrombosis-related, 235

peripheral arterial disease-related, 60-61
Thrombophilia screen, 41
Thrombophlebitis, superficial venous, 118
Thrombosis. See also Deep venous thrombosis

as acute lower limb ischemia cause, 98-99, 104

arteriovenous access graft- related, 146

arteriovenous fistula-related, 145

central venous catheter-related, 147

of chronic arterial stenosis, 10

of collateralized chronic stenosis, 16

265

INDEX

hypercoagulability- related, 139-140

post-endarterectomy, 176-177
Thromboxane A 2 , 54, 75
Tibial nerve, traumatic injuries to, 131
Ticlopidine, 166-167
Tissue factor, 42
Tobacco use. See also Smoking

as Buerger's disease cause, 86, 87
Toe-brachial index (TBI), in lower limb ischemia, 94
Topical agents

for chronic venous insufficiency-related
dermatitis, 110

for lymphedema-related eczema, 120
Trancutaneous oxygen testing (TcP0 2 ), 97-98
Transient ischemic attacks (TIAs), 161

definition of, 155

epidemiolgy of, 155

innominate artery occlusive disease-related, 182

types of, 161
Trauma

as acute upper limb vascular disease cause, 11-12

as axillary artery aneurysm cause, 218

as carotid artery aneurysm cause, 218

as innominate artery occlusive disease cause, 181

as mortality cause, 125

vascular. See Vascular injuries
Trendelenburg test, 14-15
Trental (oxypentifylline), 61-62
Triglycerides, 4, 58

Ulceration

chronic venous, 109

epidemiology of, 105-106

management of, 113

physical therapy for, 110
foot/lower limb

differential diagnosis of, 14

ischemia-related, 91, 92, 93-94, 96-97

skin perfusion pressure evaluation of, 21-22
lymphedema-related, 116
Ulnar arteries

distal, cystic adventitial disease of, 89
traumatic injuries to, 130
Ultrasonography

of abdominal aortic aneurysms, 194-195, 198-199
Doppler

of arterial disease, 15-16, 19-20,21

of arteriovenous fistulas, 123

fixed waved, 15-16

waveform analysis in, 21
duplex, 22-23, 150-151

of arteriovenous fistulas, 123

of axillary artery aneurysms, 218

carotid, 32, 164-165

of chronic venous insufficiency, 109

of cystic adventitial disease, 89

of popliteal arterial aneurysms, 211

post-carotid endarterectomy, 178

of the renal artery, 223

of subclavian arterial aneurysms, 217

of the subclavian artery, 186

of upper limb vascular disease, 32
of inflammatory abdominal aortic aneurysm, 207
United Kingdom Prospective Diabetes Study group,

167
University of Iowa, 67
Ureterolysis, 207
Urokinase, 101,248

Varices, pelvic, imaging of, 109
Varicose veins, 12

arteriovenous fistula-associated, 123

clinical evaluation of, 14-15

epidemiology of, 105-106

physical examination of, 108

radiofrequency or laser ablation treatment of, 67

recurrent, surgical treatment of, 112

secondary, 107

surgical treatment of, 111-113
Vascular access, 141-148

complications of, 144-147

desperate, 147-148

equipment for, 237-240

principles of, 141

standards for, 141-142

techniques in, 242-244

for thrombolytic therapy, 248

types of, 142-144
Vascular disease. See also Peripheral vascular
disease

clinical evaluation of, 9-18
clinical examination in, 12-18
clinical history in, 9-12
patient's characteristics, 9
radiological studies in, 18

diabetes mellitus-related, 2

lipoproptein (a) as risk factor for, 4

nonatherosclerotic, 73-89

miscellaneous disorders, 86-89
vasculitis, 79-86
vasospastic disorders, 73-79

noninvasive examination of, 19-23

upper limb occlusive, 11-12
Vascular examination, noninvasive, 19-23
Vascular injuries, 125-132

abdominal, 128-130

combat-related, 125

diagnosis of, 126

of the extremities, 126, 130-131

iatrogenic, 126, 131

imaging of, 37

mechanism of injury in, 126

in the neck, 126, 127-128

thoracic, 128

266

INDEX

Vascular surgery. See also specific surgical
procedures
complications of, 133-140
Vasculitis, 79-86

cryoglobulinemic, 85-86
large-vessel, 80-82
medium-vessel, 82-83
small-vessel, 83-85
Vasoconstriction, Raynaud's phenomenon-related,

73
Vasodilation, erythromelalgia-related, 79
Vasodilators, 241

Vasospasm, Raynaud's phenomenon-related, 73
Vasospastic disorders, 73-79
Vein grafts, historical background of, 125
Velocity analyses, 22
Venoarteriolar reflex, lymphedema-related loss of,

116
Venous disease

chronic, clinical evaluation of, 17
deep, symptoms of, 12
superficial, symptoms of, 12
symptoms of, 12
Venous function, normal, 106-107
Venous insufficiency
chronic, 17, 105-113

classification of, 105, 106
clinical assessment of, 107-109
epidemiology of, 105-106
nonsurgical management of, 109-111
pathophysiology of, 107
relationship with lymphedema, 118-119
surgical management of, 111-113
symptoms of, 108
Venous systems, deep and superficial, 106-107
Vertebral arteries

effect of subclavian stenosis on, 11
occlusive disease of, 188-190

traumatic injuries to, 128
Vertebrobasilar symptoms, of stroke, 161, 163,

188-189
Very-low density lipoprotein (VLDL), 2, 3, 4
Veterans Administration, Surgical Quality

Improvement Program (NSQIP), 149
Vietnam Vascular Registry, 125
Vietnam War, vascular surgery during, 125
Visceral arteries, aneurysms of, 214-217
Visceral ischemic syndromes, 231-236

acute mesenteric ischemia, 231-234

chronic visceral ischemia, 234-235

mesenteric venous thrombosis, 235-236
Visuospatial neglect, 163
von Willebrand disease, 43-44
von Willebrand factor, 41

Walking Impairment Questionnaire (WIQ), 152

WALLSTENT study, 180

Wegener, Friedrich, 83

Wegener's granulomatosis, 83-84

Weight gain, smoking cessation-related, 58

Weight-loss programs, 57, 58

World Wars I and II, vascular surgery development

during, 125
Wound healing, evaluation of, 21-22

Xanthelasma, 12

X-ray exposure, safety precautions for, 30-31

X-rays

abdominal, of abdominal aortic aneurysms,
194

chest, of traumatic injuries, 37, 128

Yellow-nail syndrome, 117

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