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 CAROTID
ENDARTERECTOMY

DK3434_C000a.indd 1 08/22/2006 1:00:16 PM

DK3434_C000a.indd 2 08/22/2006 1:00:16 PM
 CAROTID
ENDARTERECTOMY
Principles and Technique
Second Edition

CHRISTOPHER M. LOFTUS
Temple University
Philadelphia, Pennsylvania, U.S.A.

New York London

DK3434_C000a.indd 3 08/22/2006 1:00:16 PM

 Informa Healthcare USA, Inc.
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International Standard Book Number-10: 0-8247-2832-7 (Hardcover)

International Standard Book Number-13: 978-0-8247-2832-8 (Hardcover)

This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are
indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the
publisher cannot assume responsibility for the validity of all materials or for the consequences of their use.

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Library of Congress Cataloging-in-Publication Data

Loftus, Christopher M.
Carotid endarterectomy : principles and technique / by Christopher M. Loftus.--2nd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN-13: 978-0-8247-2832-8 (hardcover : alk. paper)
ISBN-10: 0-8247-2832-7 (hardcover : alk. paper)
1. Carotid artery--Surgery. 2. Enarterectomy. I. Title.
[DNLM: 1. Endarterectomy, Carotid--methods--Atlases. 2. Carotid Artery Diseases--surgery--Atlases. 3. Endarterectomy, Carotid--
Atlases. WG 17 L829c 2006]

RD598.6.L64 2006
617.4’13--dc22 2006043872

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T&F_LOC_C_Master.indd
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6/14/06 9:09:57
1:00:17 AM
PM
DK3434_Loftus_FM 8/21/06 1:06 PM Page iii

This book is dedicated to the memory of my father,

Angel N. Miranda, M.D.,
who lived to see the first edition, but not the second one.
DK3434_Loftus_FM 8/21/06 1:06 PM Page iv
DK3434_Loftus_FM 8/21/06 1:06 PM Page v

Preface to the Second Edition

It is a privilege to be able to write a second preface for a new edition of Carotid
Endarterectomy: Principles and Technique, twelve years after I wrote the orginal one. As I
had predicted in that first preface, the scientific and epidemiologic universe surround-
ing carotid artery surgery has changed dramatically—and for the better, for both
surgeons and patients—during this time.
Of course I have moved on in the academic world since 1994, first to assume the
Harry Wilkins Chair of Neurosurgery at the University of Oklahoma in 1997 and then
in 2004 to become Professor and Chairman of the Department of Neurosurgery at
Temple University in Philadelphia. Perhaps the only constant is my ongoing fascination
with the scientific background and technical performance of carotid artery surgery.
I have been fortunate to have outstanding neurology and vascular surgery colleagues
at both of these institutions, as I had at Iowa when the first edition was published.
We know so much more now than we did in 1994 about the propriety of carotid
reconstruction based on quality data from credible investigators around the world. For
asymptomatic disease the ACST results have reinforced the strong data from ACAS,
and validate a surgical option in stroke prevention for these patients. The NASCET
data, the early iteration of which we discussed in the first edition, has been expanded
to validate a surgical option for 50% or greater symptomatic stenosis, data which corre-
late well with ECST and VASST.
The endovascular universe has changed as well. Quality devices, with protected
stenting, now offer a viable and seemingly enduring treatment option for patients with
carotid disease who have co-morbidities that preclude a surgical approach. Data
regarding equivalency of endovascular treatment for routine carotid patients do not yet
exist, except perhaps for SAPPHIRE-studied high-risk patients, and I implore the
reader to study that data carefully, as discussed in Chapter 1, and draw your own
conclusions. Clearly there will be new high-quality cooperative trials comparing
endovascular and surgical approaches, and thoughtful surgeons will need to study
these data carefully, and potentially revise their practice patterns, if the data justify a
change at some future time.
The reader will note that we have a new publisher. The publishing rights for
Carotid Artery Surgery: Principles and Technique were sold to Marcel Dekker, Inc. several
years ago, and as part of that transfer I agreed to begin work on this second edition. As
time passed Marcel Dekker was absorbed into Informa Healthcare U.S.A., who have
completed the task with me. They have proved to be wonderful partners, professional,
organized, and efficient, and I hope the reader will find that this book justifies my con-
fidence in them, and theirs in me. In particular, I am indebted to Geoff Greenwood in
England, who made the initial contact and directed the project, Dana Bigelow in New
York, who collated and assimilated all the new materials with me, and Joanne Jay at The
Egerton Group Ltd., who took charge of production.
This book, then, represents twelve years additional experience on my part with
carotid surgery. I have significantly expanded and updated the didactic material in
Chapter 1, and I feel it is quite current. There are many more cases and interesting exam-
ples of anatomical variants, and an expanded section on complications. I retained much
of the old material from the first edition, substituted a few new photographs when
I thought they could be improved upon, but mostly added new material from the store-
house of clinical material that I have been accumulating in the intervening decade (plus).

v
DK3434_Loftus_FM 8/21/06 1:06 PM Page vi

vi PREFACE

As in the first edition I hope the readers find this information useful, educational,
and valid, and that in some small way it advances our knowledge of carotid surgical phi-
losophy and technique. I have been most gratified at the positive worldwide reception
that was afforded to the first edition, and based on that it has been my privilege to train
surgeons from many international centers who have come to visit and observe. It is my
earnest hope that this current offering, which to my mind really offers much greater
depth and experience, will prove to be useful to practicing surgeons as well.
Carotid surgery, performed by skilled surgeons with quantifiable results, prevents
stroke in asymptomatic and symptomatic patients. The facts are unimpeachable.
Our challenge now is to continually refine the techniques to ensure the greatest possible
margins of safety, and to educate surgeons around the world to ensure uniform
standards of care for all deserving patients.

Christopher M. Loftus
DK3434_Loftus_FM 8/21/06 1:06 PM Page vii

Contents
Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
CHAPTER 1 Historical Perspective on Carotid Reconstruction . . . . . . . . . . . . . . . . . . . . . 1
Scientific Foundation for Carotid Artery Reconstruction . . . . . . . . . . . . . . . . . 2
Asymptomatic Carotid Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Symptomatic Carotid Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
Clinical Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Special Surgical Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Technical Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
Anesthesia Choice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
Monitoring Techniques During Carotid Cross-Clamping . . . . . . . . . . . . . . 20
Arteriotomy Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
Surgical Technique of Cervical Carotid Reconstruction . . . . . . . . . . . . . . . . . 30
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Preoperative Studies and Preparation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
Surgical Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
Special Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
Microsurgical Endarterectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
Bilateral Carotid Endarterectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
Complete Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
Acute Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
Postoperative Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
Complications of CEA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
Endovascular Treatment of Carotid Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . 42
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
CHAPTER 2 Radiographic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
2-1 Low Bifurcation of the Carotid Artery with Symptomatic
Plaque Just at the Origin of the Internal Carotid Artery . . . . . . . . . . . 62
2-2 High Bifurcation of the Cervical Carotid Artery . . . . . . . . . . . . . . . . . . 64
2-3 Side by Side . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66
2-4 Focal Internal Carotid Artery Ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68
2-5 Deep Ulceration of a Carotid Plaque . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
2-6 Benign Arteriogram—Bad Ulceration . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
2-7 Ninety-Five Percent Lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
2-8 Extensive Plaque in Common Carotid Artery with
Long Arteriotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
2-9 String Sign . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2-10 X-Ray Identification of an Ascending Pharyngeal
Artery Originating at the Carotid Bifurcation . . . . . . . . . . . . . . . . . . . . 80
2-11 Tandem Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
2-12 Cross Filling into Contralateral Middle Cerebral Artery . . . . . . . . . . . 84
2-13 Can We Predict the Need for Shunting? . . . . . . . . . . . . . . . . . . . . . . . . . 86
2-14 Preoperative External Carotid Artery Occlusion . . . . . . . . . . . . . . . . . . 88
2-15 Internal Carotid Stump . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90

vii
DK3434_Loftus_FM 8/22/06 12:44 AM Page viii

viii CONTENTS

2-16 Carotid Kink . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92

2-17 Carotid Stenosis with Distal Cervical Aneurysm . . . . . . . . . . . . . . . . . 94
2-18 Intraluminal Thrombus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
2-19 Complication—Clot Along Suture Line. . . . . . . . . . . . . . . . . . . . . . . . . . 98
2-20 Complication—Complete Postoperative Occlusion . . . . . . . . . . . . . . 100
2-21 Complication—External Carotid Artery Dissection . . . . . . . . . . . . . . 102
CHAPTER 3 Surgical Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
3-1 Surgical Instruments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
3-2 Surgical Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
3-3 Alternate Incisions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
3-4 Side-by-Side Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
3-5 Incision for High Bifurcation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
3-6 Draped and Ready for Incision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
3-7 Platysma with Michel Clips. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118
3-8 Sternocleidomastoid Muscle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120
3-9 Jugular Vein—Common Facial Vein. . . . . . . . . . . . . . . . . . . . . . . . . . . . 122
3-10 Ligation of Common Facial Vein . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124
3-11 Secure Ligation of the Common Facial Vein. . . . . . . . . . . . . . . . . . . . . 126
3-12 Minor Branches of Facial Vein. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
3-13 Dissection Behind Parotid Gland . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
3-14 First Demonstration of Common Carotid Artery with Control. . . . . 132
3-15 Exposure of Carotid Artery with Retractors . . . . . . . . . . . . . . . . . . . . . 134
3-16 Four Sutures in the Carotid Sheath . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
3-17 Unexpected Internal Carotid Artery Atresia. . . . . . . . . . . . . . . . . . . . . 138
3-18 Major Nerve Structures Potentially Injured During
Carotid Endarterectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
3-19 Other Nerves at Risk During Carotid Endarterectomy. . . . . . . . . . . . 142
3-20 Low Bifurcation with Omohyoid Muscle . . . . . . . . . . . . . . . . . . . . . . . 146
3-21 Division of Omohyoid Muscle to Secure Adequate Low
Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
3-22 Hypoglossal Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
3-23 Sternomastoid Artery—An External Carotid Artery Branch . . . . . . . 152
3-24 High Bifurcation with Digastric Muscle and Hypoglossal
Nerve—Left Carotid Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154
3-25 High Bifurcation with Digastric Muscle and Hypoglossal
Nerve—Right Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
3-26 Side-by-Side Carotid Anatomy—Exposure. . . . . . . . . . . . . . . . . . . . . . 158
3-27 Isolation of Superior Thyroid Artery—Right Carotid Exposure . . . . 160
3-28 Isolation of Superior Thyroid Artery—Left Carotid Exposure . . . . . 162
3-29 Isolation of Ascending Pharyngeal Artery (Left) . . . . . . . . . . . . . . . . . 164
3-30 Isolation of Ascending Pharyngeal Artery (Right) . . . . . . . . . . . . . . . 166
3-31 Tactile and Visual End of Plaque—Left Carotid Exposure. . . . . . . . . 168
3-32 Tactile and Visual End of Plaque—Right Carotid Exposure . . . . . . . 170
3-33 Extensive Plaque Erosion into the Adventitial Layer . . . . . . . . . . . . . 172
3-34 Javid Clamp Around Internal Carotid Artery . . . . . . . . . . . . . . . . . . . 174
3-35 Loftus Shunt Clamps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 176
3-36 Placement of Cross-Clamp Below Rummel Tourniquet . . . . . . . . . . . 178
3-37 Incision Along Common and Internal Carotid Arteries
(Blue Line)—Left Carotid Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180
3-38 Potts Scissors Opening—Left Carotid Exposure . . . . . . . . . . . . . . . . . 182
3-39 Potts Scissors Opening Vessel—Left Carotid Exposure . . . . . . . . . . . 184
3-40 False Plane Demonstrated with Penfield Retractor—Right
Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 186
DK3434_Loftus_FM 8/21/06 1:06 PM Page ix

CONTENTS ix

3-41 Focal Plaque in Proximal Internal Carotid Artery—Left

Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188
3-42 Long, Extensive Common Carotid Artery/Internal Carotid
Artery Plaque. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
3-43 Shunt in Common Carotid Artery/Internal Carotid Artery . . . . . . . 192
3-44 Initial Placement of Shunt Down Common Carotid Artery. . . . . . . . 194
3-45 Securing of Shunt in Common Carotid Artery. . . . . . . . . . . . . . . . . . . 196
3-46 Bleeding and Evacuation of Shunt Before Placement in
Internal Carotid Artery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
3-47 Placement of Shunt in Distal Internal Carotid Artery. . . . . . . . . . . . . 200
3-48 Potential for Intimal Damage from Placement of Shunt. . . . . . . . . . . 202
3-49 Securing of Shunt in Internal Carotid Artery . . . . . . . . . . . . . . . . . . . . 204
3-50 Loftus Type Carotid Shunt in Place—Two Views . . . . . . . . . . . . . . . . 206
3-51 Evaluation of Shunt Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208
3-52 Repair with Shunt in Place . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
3-53 Plaque Removal Begins at Lateral Edge—Left Carotid Exposure. . . 212
3-54 Sharp Transection in Common Carotid Artery—Right
Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
3-55 Plaque Removal from Internal Carotid Artery (Feathered
Edge)—Right Carotid Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
3-56 Plaque Removal from External Carotid Artery—Left
Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 218
3-57 Opening of External Carotid Artery—Inadequate Feathering. . . . . . 220
3-58 Opening of External Carotid Artery—Inadequate Feathering. . . . . . 222
3-59 Opening of External Carotid Artery Because of
Poor Doppler Signal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
3-60 Opening of External Carotid Artery—Repair. . . . . . . . . . . . . . . . . . . . 226
3-61 Completed External Carotid Artery Repair in a Case with
Internal Carotid Artery Hemashield Patch . . . . . . . . . . . . . . . . . . . . . . 228
3-62 Removal of Fragments in Circumferential Fashion—Right
Carotid Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
3-63 Left Carotoid Endarterectomy—Completed Removal,
Sharp Margins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
3-64 Completed Removal, Sharp Margins—Left Carotid Exposure . . . . . 234
3-65 Placement of Tacking Sutures in Internal Carotid Artery. . . . . . . . . . 236
3-66 Anatomic Variant—Atherosclerotic Web on Posterior
Wall of Vessel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
3-67 Repair Beginning in Internal Carotid Artery—Left
Carotid Exposure—No Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
3-68 Microscopic Internal Carotid Artery Repair . . . . . . . . . . . . . . . . . . . . . 242
3-69 Repair Beginning in External Carotid Artery—Right Carotid
Exposure—No Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
3-70 Repair of External Carotid Artery—Left Carotid Exposure—No
Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246
3-71 Second Limb of Repair Coming Up Common Carotid Artery—No
Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
3-72 Suture Sequence and Placement of the Hemashield Roof
Patch Graft on the Internal Carotid Artery . . . . . . . . . . . . . . . . . . . . . . 250
3-73 Removal of Shunt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254
3-74 Tying Together—Evacuation of Air—Right Carotid Exposure . . . . . 256
3-75 Blunt Needle to Evacuate Air and Debris as Final
Step—Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
3-76 Sequence of Clamp Removal at Completion of Arteriotomy. . . . . . . 260
3-77 Doppler Examination of Repair—Left Carotid Exposure. . . . . . . . . . 262
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x CONTENTS

3-78 Completed Dry Repair Without and With Hemashield

Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 264
3-79 Y-Shaped Suture Line—No Patch Graft . . . . . . . . . . . . . . . . . . . . . . . . 272
3-80 Surgicel on Dry Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274
3-81 Closure of Sheath . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
3-82 Closure of Platysma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3-83 Skin and Hemovac . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280
3-84 Skin Closure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282
3-85 Placement of Saphenous Vein Patch Graft . . . . . . . . . . . . . . . . . . . . . . 284
CHAPTER 4 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287
4-1 Acute Postoperative Internal Carotid Artery Thrombosis . . . . . . . . . 288
4-2 Technique for Exploration of Complete Carotid Occlusion . . . . . . . . 290
4-3 Use of Fogarty Catheters to Reopen Thrombosed
Internal Carotid Artery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292
4-4 Postoperative Wound Hematoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294
4-5 Aneurysm Formation Four Years Postoperatively . . . . . . . . . . . . . . . 296
CHAPTER 5 Special Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299
5-1 Treatment of Isolated Common Carotid Artery Stenosis . . . . . . . . . . 300
5-2 Treatment of “Stump” in an Occluded Internal Carotid Artery . . . . 302
5-3 Repair and Straightening of a Large Left Carotid Kink . . . . . . . . . . . 306
5-4 Rapid Recurrence of Stenosis from Myointimal Hyperplasia . . . . . . 308
5-5 Scarring in the Carotid Sheath in a Case of Recurrent Stenosis . . . . 310
5-6 Reoperation in a Case Previously Repaired with a
Saphenous Vein Roof Patch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315
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CHAPTER 1

Historical Perspective on
Carotid Reconstruction

1
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2 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

The first mention of carotid artery surgery occurred in 1793 and is credited to
Hebenstreit, who performed a carotid artery ligation for carotid injury (1). However,
the first deliberate ligation of the carotid artery occurred in 1798 and was performed
by John Abernathy (2). The ligation was performed on a patient whose carotid artery
had been torn by the horn of a cow. In 1805, Sir Astley Cooper performed a cervical
carotid ligation for treatment of a cervical carotid aneurysm. Unfortunately, the patient
died of sepsis following surgery. Undaunted by this complication, Cooper performed
his first successful ligation of the carotid artery in 1808 on another patient with a cer-
vical carotid aneurysm. The patient suffered no untoward effects from the ligation and
lived until 1821 (3).
In the 19th century, a number of carotid ligations were performed by various sur-
geons for the treatment of various diseases such as cervical carotid aneurysms and
other vascular malformations. Benjamin Travers reported a case of carotid ligation in a
patient who presented with carotid-cavernous sinus fistula in 1809 (1). In 1868, Pilz
published a series of 600 cases of carotid ligation for hemorrhage or cervical aneurysm
with an overall mortality of 43% (1).
Carrea et al. reported the first successful carotid reconstruction procedure in
Buenos Aires in 1951 (4). The patient presented with symptoms of a stroke, and arteri-
ography demonstrated a stenosis of the internal carotid artery (ICA). Carrea performed
a direct anastomosis of the external carotid artery (ECA) to the distal ICA following
resection of the stenotic segment.
The surgical technique of thromboendarterectomy was first introduced to the
United States by Wylie in 1951 (5). He documented use of this technique for the removal
of atherosclerotic plaques in the aortoiliac segments. The success of this procedure on
the large vessels of the abdomen and lower extremities set the stage for the application
of this technique to the cervical carotid vessels.
DeBakey performed the first successful carotid endarterectomy (CEA) in 1953 (6).
The patient presented with symptoms of a frank stroke. Angiogram confirmed the pres-
ence of a total occlusion of the left ICA. Postoperatively, arteriography confirmed the
presence of flow in the ICA (7).
Carotid reconstruction for the treatment of carotid occlusive diseases and tran-
sient ischemic attacks (TIAs) was presented by Eastcott et al. in 1954 (8). They reported
the case of a 66-year-old woman who presented with episodes of TIAs that had been
getting progressively worse. Angiography demonstrated the presence of near occlusion
of the left ICA. She underwent direct anastomosis of the common carotid artery (CCA)
to the ICA following resection of the diseased portion of the ICA. She tolerated the pro-
cedure quite well and suffered no further attacks of ischemia or infarction related to the
left ICA. This case represented the beginning of the exploration of carotid artery recon-
struction as a primary treatment for the carotid occlusive diseases. It is a source of great
satisfaction to neurovascular surgeons that at the present time this elegant and enjoy-
able operation, nearly 40-years-old, has now been unequivocally shown to prevent
stroke in well-chosen patients with clear and unambiguous clinical findings.

SCIENTIFIC FOUNDATION FOR CAROTID

ARTERY RECONSTRUCTION

Diseases of the carotid circulatory system can be divided into asymptomatic (always
and still the subject of great debate) and symptomatic forms. Patients with asympto-
matic carotid diseases include those with asymptomatic carotid bruits, symptoms refer-
able to one carotid territory with radiographic demonstration of clinically silent
contralateral carotid stenosis or ulceration, and those who are found to have ausculta-
tory or radiographic evidence of carotid pathology while being prepared for their major
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 3

surgical procedures (most commonly coronary or peripheral vascular surgery).

Symptomatic carotid disease encompasses a spectrum of presentations from TIAs to
stroke in evolution and completed stroke, and includes acute or subacute carotid occlu-
sion as well as the so-called “stump syndromes.” In the last decade, several domestic
and international government funded multicenter randomized cooperative trials have
changed the practice of carotid reconstruction for both asymptomatic and symptomatic
patients. Clearly, the scientific rationale for carotid artery reconstruction differs from
the principles outlined in the first edition of this book (9), and we should carefully ana-
lyze the class 1 evidence trial data for both types of clinical presentation.

Asymptomatic Carotid Disease

Asymptomatic Bruit
Surgery for asymptomatic carotid disease has long been controversial. At the time of the
first edition of this book, no level 1 evidence was in place to justify asymptomatic
carotid reconstruction. The results of the Asymptomatic Carotid Atherosclerosis Study
(ACAS) and Asymptomatic Carotid Surgery Trials (ACST) (10,11) have changed many
opinions and have validated the practice of CEA for asymptomatic disease in selected
cases. It seems unlikely that trials such as ACAS/ACST will ever be repeated, consid-
ering the definitive results of the study; consequently, in my practice we have tailored
surgical recommendations to comply with ACAS findings, and we have devised strate-
gies to deal with and address the questions (such as the status of women) that ACAS
did not answer. Let us first examine the data on which we based clinical decisions prior
to ACAS, and then re-evaluate that data in the light of the ACAS/ACST evidence.
Carotid bruits are heard in 3% to 4% of the asymptomatic U.S. population over 45
years of age and are present in 10% to 23% of patients in referral populations with symp-
tomatic atherosclerosis in other arterial distributions. Many major studies advocated sur-
gery for asymptomatic carotid bruits (12,13). These two referenced studies followed a
group of unoperated patients with asymptomatic bruits and reported higher rates of neu-
rologic sequelae (with stroke rates of 15–17%) as compared to operated controls. Neither
report, however, documented the relationship of the neurologic events to the territory of
the carotid bruit (e.g., ipsilateral or contralateral), nor was it reported which of the patients
suffering acute cerebrovascular accident (CVA) had experienced a warning TIA prior to
that event (which would have justified prophylactic endarterectomy in most centers).
These questions have been addressed, however, in several subsequent population studies
(14,15). The first study reported on a series of 72 patients with carotid bruits, 10 of whom
went on to develop strokes, but in whom the strokes occurred mostly in different vascular
territories (14). In the second report, data from the Framingham study confirmed that
asymptomatic bruit predicted an increased risk of neurologic events, but that the majority
of these events were either in other cerebrovascular territories or were etiologically related
to noncarotid factors, e.g., aneurysms, lacunar infarcts, or emboli following myocardial
infarction (MI) (15). Both studies confirmed that patients with asymptomatic bruit are at
increased risk for cerebrovascular and/or cardiac problems, but could not provide justifi-
cation for prophylactic surgery for the asmyptomatic bruit alone.
There was some evidence to suggest that silent, small cerebral infarction [seen on
computed tomography (CT)] may justify CEA in otherwise asymptomatic patients.
Norris and Zhu (16) reported a significantly higher incidence of silent infarcts ipsilat-
eral to high-grade (>75%) carotid stenosis compared to lower grades. Based on this evi-
dence, we considered (and still do) lacunes of this type combined with severe stenosis
to be a relative indication for prophylactic carotid reconstruction.
The question of surgery for critical high-grade asymptomatic stenosis remained
open and was the subject of considerable debate among vascular surgeons, neurosur-
geons, and neurologists. Hemodynamic studies suggested that critical reductions in
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4 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

cerebral blood flow may not be reached until 75% to 84% diameter stenosis has
occurred, indicating that stenosis must be of a very high grade to be significant (17).
One group, using prospective noninvasive studies, showed a higher propensity for
neurologic events or acute carotid occlusion in lesions found to be 80% or more stenotic
(18), and another documented the protective effect of surgery in these patients (19). On
the basis of these reports, many surgeons felt justified in correcting such severe but other-
wise asymptomatic lesions. Chambers and Norris, on the other hand, reported that in
asymptomatic patients with stenosis of all degrees, the risk of cardiac ischemia was
higher than that of stroke. In their series, although the risk of cerebral ischemic events
was highest in patients with severe carotid artery stenosis, in most instances these
patients did not have strokes without some sort of warning event (20). More recently,
Norris et al. (21) followed 696 patients for a mean of 41 months with noninvasive stud-
ies. While the combined TIA/stroke rate for patients with >75% stenosis was a signifi-
cant 10.5%, the ipsilateral stroke rate (without warning TIA) was 2.5% for patients with
>75% stenosis, and 1.1% with <75% stenosis. These data reemphasized the need for sur-
gical action in symptomatic high-grade stenosis patients, but did not identify a high-
risk asymptomatic subgroup (21). Many reviews on this subject recommended medical
management of the patient with asymptomatic carotid bruit or stenosis with
antiplatelet aggregating therapy (ASA) and attention to contributing risk factors
(hypertension), with surgical intervention deferred until such time as frank TIAs
develop (22–25).
The continuing controversy over asymptomatic carotid disease spawned several
large clinical trials. Prospective, randomized trials comparing medical and surgical
therapies in patients with asymptomatic ICA stenosis include the Carotid Artery
Stenosis with Asymptomatic Narrowing Operation Versus Aspirin (CASANOVA)
study, the Mayo Asymptomatic Carotid Endarterectomy Trial (MACE), the Veterans
Administration Cooperative Trial on Asymptomatic Carotid Stenosis (VAAST), and the
ACAS. Three of these four trials were negative for a surgical benefit in stroke preven-
tion, but the fourth trial (ACAS) was positive and authoritative, and no further North
American trials are planned or likely to be done. The largest, and most recent asympto-
matic carotid surgery randomized trial— the ACST— trial was just completed in the
United Kingdom and Europe (26). Gratifyingly, this trial also supports asymptomatic
carotid reconstruction, just as the ACAS did (11).
The CASANOVA study randomized patients from the general population to
immediate surgery versus antiplatelet therapy alone and best medical management.
The stenosis criterion was 50% to 90% by noninvasive testing or angiography. Both
arms received best medical management including aspirin (1000 mg/d) and dipyri-
damole (225 mg/d). The follow-up was three years and the study size was 410 patients.
Endpoints were death and stroke. Two-hundred-and-six patients were randomized to
immediate surgery and 204 patients were randomized to antiplatelet therapy alone.
One-hundred-and-eighteen of the 204 patients in the nonsurgical arm had delayed
endarterectomy during the follow-up period secondary to TIA, progressive severe
stenosis (>90%), bilateral stenosis (>50%), or contralateral stenosis (>50%). The study
found no statistically significant difference in outcome between the surgical and non-
surgical arms (10.7% and 11.3%, respectively). The unusual study design of
CASANOVA limits its statistical validity (27). By its very design, excluding high-risk
patients from the medical arm and allowing crossovers, the CASANOVA trial was
biased against surgery from the onset.
The MACE study enrolled 71 patients with >50% stenosis by noninvasive testing.
The planned follow-up was two years. The nonsurgical arm received best medical man-
agement and aspirin (80 mg /d). The surgical arm did not receive aspirin. Only Mayo
Clinic patients were randomized to the treatment arms. The study was terminated pre-
maturely because of increased frequency of MI in surgical arm patients (who did not
receive aspirin). At termination, too few patients were enrolled to assess statistical
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 5

significance. The major finding of MACE was that aspirin was appropriate for the peri-
operative and postoperative period unless contraindicated (28).
The Veterans Administration Asymptomatic Stenosis Trial (VAAST) enrolled only
men from VA centers and randomized them to surgical and nonsurgical arms, both of
which received best medical management and aspirin (1300 mg/d). The stenosis crite-
rion for entry and randomization was >50% by angiography. The follow-up was five
years and the study population was 444 patients (211/444 surgical and 233/444 non
surgical). Participating centers were screened and required to demonstrate a perioper-
ative morbidity and mortality of <3%. At four year follow-up, the combined incidence
of ipsilateral TIA or stroke was 8% and 20.6% for the surgical and nonsurgical arms,
respectively (p < 0.001). The sample size was not large enough to show statistical signif-
icance for stroke alone; the recommendation was that surgery was effective in prevent-
ing subsequent TIAs in asymptomatic patients (29).
The second largest of the asymptomatic trials was the ACAS. The trialists random-
ized 1659 patients (834 treated medically and 825 patients treated surgically) between
ages 40 and 79 years with 60% to 99% ICA stenosis to 325 mg of aspirin plus risk-factor
management or endarterectomy plus medical therapy. The trial was stopped prema-
turely because of a demonstrated benefit for surgery in all patients with >60% linear
stenosis. (It would be considered unethical to continue randomization of patients in the
face of a known surgical benefit.) After median follow-up of 2.7 years, the aggregate
estimated risk over five years for ipsilateral stroke or perioperative stroke or death was
5.1% for patients who underwent surgery and 11% for patients treated medically. CEA
reduced the estimated five-year risk for ipsilateral stroke by 1% per year. The benefit
did not extend to major stroke alone and could not be demonstrated in women as a sub-
group, probably because of the small numbers and premature closure of the trial. [There
was also a higher perioperative complication rate for women in ACAS; two later stud-
ies, however, have shown that no true gender-related risk exists (30,31).] The success of
the ACAS trial, and of the operative procedure, depended on maintenance of a periop-
erative morbidity and mortality of less than 3% (10).
Finally, ACST randomized 3120 patients during 1993–2003 to either CEA or indef-
inite deferral (medical management). The perioperative 30-day stroke/death rate was
3.1%. Five-year stroke risk in the CEA group was 3.8% and in the medical group 11%, a
statistically significant benefit for surgery. Unlike ACAS, benefit was shown independ-
ently for both males and females. The trialists recommended CEA for all patients
<75-years-old with 70% or greater ultrasound confirmed carotid stenosis, with the
conviction that surgery halved the risk of subsequent stroke, even after perioperative
stroke/death rate was factored in (11).
We can say with confidence that the indications for surgical reconstruction in
asymptomatic patients have been confirmed by level 1 clinical trials evidence since
the first edition of this book went to press. My surgical policy follows directly from the
ACAS/ACST guidelines. I offer surgery to patients with a five-year life expectancy who
have 60% or greater stenosis, including women. For women I explain the details of the
data and the weaker evidence that a protective benefit may apply to them as a sub-
group. Most patients, in my experience, choose surgery when informed and educated
in this way. The latest iteration of the American Heart Association (AHA) Guidelines
for CEA confirms this surgical approach for patients with surgical risk <3% and a five-
year life expectancy (32).

Contralateral Carotid Stenosis

A number of clinical studies, primarily retrospective, were undertaken with the goal of
ascertaining the risks of long-term neurologic sequelae in patients with contralateral
carotid stenosis managed nonoperatively. The critical point, much as in the follow-up
of asymptomatic bruits, was to determine what percentage of these patients progressed
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6 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

to frank stroke in the appropriate carotid distribution without warning TIAs. Most of
the studies specified 50% stenosis of the contralateral carotid as the criterion for signif-
icant disease (33–37). In three of these reports, no patients followed up for contralateral
asymptomatic lesions developed a stroke without warning TIAs (35–37). In two other
reports, a few patients did develop such strokes, but the incidence was invariably less
than 3%, and thus less than the accepted risks of surgical morbidity and mortality (33,
34). A single study included all patients with contralateral stenosis from 1% to 99% and
reported the incidence of direct stroke in unoperated patients to be 3%; these authors
recommended prophylactic surgery on this basis, and also concluded that the percent
stenosis did not correlate with the risk of neurological sequelae (38). Aside from this
group’s findings, however, no authors could demonstrate that prophylactic surgery for
contralateral lesions of greater than 50% stenosis had any protective effect in the
absence of clinical symptoms referable to that lesion.
The question of progression to 80% or greater on the contralateral side was specif-
ically addressed by Roederer et al. (19). In noninvasive follow-up, they found that the
rate of neurologic events significantly increased once an 80% lesion developed. They
argued that these asymptomatic stenoses of >80% should be reconstructed. Their data
seem prescient now in view of the ACAS and ACST results discussed above, and it is our
policy to recommend surgical reconstruction for contralateral silent stenosis opposite
either an asymptomatic or symptomatic lesion, assuming that baseline ACAS/ACST
criteria are satisfied.

Carotid Risks in Noncarotid Preoperative Patients

Randomized cooperative trial data (class 1 evidence) is definitive, and clearly has suf-
ficient power to change surgical practice. It should be clear by now that the
ACAS/ACST trials superseded a substantial number of smaller clinical series, many of
which could not demonstrate a surgical benefit. One such clinical issue that was exten-
sively studied was the proper management of preoperative patients who are found to
have auscultatory or radiographic evidence of otherwise silent carotid artery disease. A
number of studies addressed this problem. One early group performed prophylactic
endarterectomies in 34 surgical patients and was able to demonstrate low morbidity
and good long-term survival following the procedure (39). It was not clear, however,
that their patients were at increased risk for cerebrovascular events, and thus whether
these prophylactic procedures, albeit safe in their hands, were necessary. This point was
addressed further by a series of retrospective studies of surgical patients identified to
have asymptomatic bruits but followed without carotid surgery (40–43). These studies
established the incidence of asymptomatic bruits in random preoperative patients to be
near 15%. Although they documented a perioperative stroke rate of about 1% in their
patient groups, none of these investigators could find a correlation between presence or
location of carotid bruits and risk of perioperative stroke. Further investigations (44–47)
prospectively examined asymptomatic bruit patients with noninvasive carotid studies
in an attempt to correlate percent stenosis with risk of perioperative stroke. Although
some of their reports documented higher perioperative mortality in the carotid steno-
sis groups (44,45), these deaths were primarily attributable to an increased risk of MI,
and once again no correlation could be demonstrated between bruit or stenosis and
perioperative stroke risk. In one prospective study of preoperative patients with
asymptomatic bruits only, 14% incidence of bruits in this group was confirmed, and all
strokes (0.7% of patients) were found in patients having coronary bypass surgery (48).
The concept that the increased risk of perioperative stroke in coronary bypass patients
arises from femoral arterial cannulation rather than incidental carotid disease with
carotid embolization and/or hypoperfusion was supported by a Canadian study that
found femoral cannulation to be the only statistically significant common denominator
among a group of bypass patients with embolic stroke (49). Furlan (50) studied patients
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 7

undergoing coronary artery bypass graft (CABG) who had angiographically documented
asymptomatic stenosis greater than 50% and showed that stroke risk was not increased
in patients with either <90% stenosis or with total ICA occlusion. There was an insuffi-
cient number of patients in the 90% -to- 99% group to allow statistical conclusions.
While ACAS/ACST validate carotid reconstruction for asymptomatic stenosis,
the timing issue vis-a-vis other planned surgery is not as clear. Our previous policy of
“watchful waiting” for patients with silent stenosis undergoing other surgical procedures
is no longer appropriate, and we reconstruct silent carotid disease when it is identified
in patients scheduled for noncarotid surgery. Whether a staged or a reverse-staged
operative strategy is best has not been answered, and remains the judgment of the indi-
vidual surgeon taking all patient factors into account.

Hollenhorst Plaque
In 1961, Hollenhorst described 31 patients with orange-yellow or copper colored
plaques observed ophthalmoscopically at bifurcations of the retinal arterioles. Twenty-
seven of these patients had occlusive disease in the carotid tree and four in the verte-
bral basilar tree. He also described five patients who underwent CEA and subsequently
were found to have showers of these plaques in the retina postoperatively. Hollenhorst
felt that these plaques represented cholesterol emboli from the extracranial circulation
and that their presence warranted aggressive investigation of the cardiovascular and
cerebrovascular system for surgically correctable disease (51). The atheromatous nature
of this embolic material was confirmed by David’s pathologic report in 1963 (52).
It is important to distinguish symptomatic retinal plaques from asymptomatic
ones. Multiple authors have reported plaques associated with either amaurosis fugax or
retinal artery occlusion with visual field deficits and there is little doubt that these rep-
resent symptomatic carotid lesions (53–55). Russell classifies these refractile cholesterol-
containing flakes as his third type of retinal emboli, and points out that they
customarily disappear from the retina within a few weeks, with or without leaving a
permanent field deficit. Once again these symptomatic lesions certainly deserve active
investigation for carotid origin embolization.
In 1973, Hollenhorst’s group reported on 208 consecutive patients observed to
have retinal cholesterol emboli who had been followed up for at least six years. This
group was mixed and many of them had visual symptoms associated with their choles-
terol emboli. This group of patients had significantly decreased survival compared to a
heterogeneous comparison group with a survival rate 13% less than expected in the first
year increasing to 80% less than expected by the eighth year of observation. The cause
of death in many of these patients was related to diffuse vascular disease with MI being
the greatest factor. Hollenhorst concluded on the basis of these data that these plaques
warrant aggressive cardiac and cerebrovascular investigation (56).
Patients with truly asymptomatic retinal cholesterol emboli represent a much more
unusual and smaller group. Very little data are available as to the natural history and
prognosis of these patients. Bruno et al. (57) recently studied 70 consecutive men with
asymptomatic retinal cholesterol emboli and compared them to a control group of 21 ran-
domly selected subjects without retinal emboli. Patients in their study group had a signif-
icantly higher prevalence of hypertension and smoking history than did the control
group. The prevalence of carotid stenosis
50% ipsilateral to the embolus was only 13%,
however, and this was not significantly different from that in control subjects. However,
carotid stenosis
50% on either side was more common in patients with asymptomatic
retinal cholesterol emboli. According to Bruno’s data, asymptomatic retinal cholesterol
emboli do indicate a higher prevalence of systemic vascular disease and of ischemic heart
disease, similar to that reported by Pfaffenbach and Hollenhorst (56). Their data,
however, do not support the concept that asymptomatic retinal cholesterol emboli are the
harbingers of cerebrovascular events or of the presence of an unstable carotid
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8 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

atherosclerotic plaque. In keeping with this, it should be noted that asymptomatic retinal
cholesterol emboli were not considered entry criteria for the North American
Symptomatic Carotid Endarterectomy Trial (NASCET).
What then can be said about the presence of Hollenhorst plaques? Certainly, any
identifiable retinal lesion with visual symptoms must be considered a symptomatic
carotid event until proven otherwise and warrants full investigation. I have performed
CEA on many patients whose initial presentation was visual loss from central retinal
artery occlusion. The significance of asymptomatic lesions in the retina is more obscure
and not as extensively studied. Available small series data imply that these patients do
not represent a high-risk group. Notwithstanding, it has been my inclination to actively
investigate these patients on the few occasions when absolutely no visual symptoms
can be elicited and I have been aggressive in the management of these lesions, consis-
tent with my standard approach to asymptomatic disease. I am pleased that ACST and
ACAS data support this, and validate carotid reconstruction in such patients when an
appropriate degree of stenosis is confirmed.

Symptomatic Carotid Disease

Symptomatic disease in the carotid circulation encompasses a spectrum of presenta-

tions from classical carotid TIAs to frank embolic or thrombotic stroke. It is at times
paradoxical, in that the degree of collateral circulation may allow severe carotid
pathology to present with only minimal symptomatology (e.g., there is a finite inci-
dence of carotid occlusion presenting with TIAs alone). Whereas the discussion of
asymptomatic carotid disease involved primarily a comparison of operated patients
versus unoperated control groups, any consideration of surgery for symptomatic
carotid disease must be based on objective comparison of surgical morbidity and
results of both the natural history of the disease process and the best available medical
therapy. The surgical risk in elective CEAs performed in major centers approaches 3%,
as previously mentioned, and this figure should be used for evaluation of therapeutic
choices. Guidelines for acceptable surgical morbidity and mortality have been
published by both the AHA Stroke Council (58) and the American College of
Physicians (59). Evidence-based guidelines for asymptomatic and symptomatic
carotid reconstruction have been elegantly revised by an AHA working group, and
should be considered definitive (32).

Transient Ischemic Attacks

Three well-accepted studies have documented that the risk of stroke following a first
classical carotid TIA approximates 5% per year (60–62). Equally important are data
showing that 51% of all such strokes occur in the first year following initial TIA and that
21% occur in the first month following such an event (63). It is only after the first six
months that the risk of stroke falls to, and remains, 5% annually. This malignant natural
history has prompted approaches to medical therapy. Anticoagulation has proven diffi-
cult to control in an outpatient population. Such therapy has also been shown to be asso-
ciated with a high risk of intracranial hemorrhage which, in one series of patients aged
55 to 74, was eight times greater than in a control group (64). Furthermore, all studies of
anticoagulant therapy in TIAs failed to demonstrate differences in mortality between
treated and untreated groups. The consequent decline in use of anticoagulation as pri-
mary therapy for TIAs was paralleled by a great interest in antiplatelet-aggregating
agents. In the American controlled study of aspirin therapy for cerebral ischemia (65),
antiplatelet-aggregating therapy was shown to decrease the incidence of recurrent TIAs
but did not significantly decrease the long-term incidence of stroke in treated patients.
The Canadian study of aspirin and sulfinpyrazone, however, did show a significant
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 9

31% decrease in long-term risk of stroke or death (66). This risk reduction was sex
dependent, and in males a 48% risk reduction was demonstrated. Dipyridamole has not
supplemented aspirin’s effect on risk reduction of stroke after TIA (67). Assuming a 5%
annual risk of stroke in untreated patients then, the best medical therapy presently avail-
able reduces this risk by nearly one half, to 2 1⁄2% per year.
Much like asymptomatic carotid disease, symptomatic carotid disease became the
focus of several randomized cooperative trials in the late 1980s. An European Carotid
Surgery Trial (ECST) of symptomatic patients in all subgroups from 0% to 99% stenosis
was paralleled by two trials in North America, the NASCET and the VA Cooperative
Trial of Symptomatic Carotid Disease (VASST). On February 22, 1991, the entry of
patients with greater than 70% stenosis into the NASCET trial was stopped because an
endpoint was reached in which it was clearly demonstrated that surgical treatment of
these patients was superior to medical management (68,69). The NASCET trial contin-
ued entry and follow-up of patients from 30% to 69% stenosis who were clinically
symptomatic. Later analysis of the NASCET data showed a surgical benefit, albeit more
modest, for patients with angiographic stenosis of 50% or more (70).
Concurrent with release of data from the NASCET trial, a similar release by the
European group (coincidentally during the same week) reported that a clear surgical
benefit was found in patients with 70% to 99% stenosis in that trial as well (71). At the
same time these investigators declared that medical therapy was clearly superior for
symptomatic patients with stenosis less than 30% (a group not studied by NASCET). The
European trial also continued to enter patients with between 30% to 70% stenosis; para-
doxically, they were not ultimately able to demonstrate a surgical benefit in the moder-
ate stenosis group (72). This contradiction can be explained and reconciled by the more
rigorous angiographic measurement system employed in the NASCET; many “high-
grade” stenosis ECST patients were considered only “moderate grade” when measured
with the NASCET system (where N is the linear diameter at the area of greatest narrow-
ing, and D is the greatest diameter of the normal artery distal to the carotid bulb.

Percent (%) stenosis  (1  N/D)  100

and moderate-grade ECST patients (in whom a surgical benefit was not demonstrated)
fall below the 50% NASCET criterion. When imaging data were later normalized so that
the NASCET and ECST groups could be directly compared, ECST also showed a mod-
est benefit for surgery in 50% to 69% stenosis patients (73).
The VASST was terminated early secondary to preliminary results from the two
aforementioned trials. Though 5000 patients were screened at 16 participating VA cen-
ters, only 193 men were randomized to best medical management (98 men) and surgical
(91 men) treatment arms (74). Angiography was performed on all patients and greater
than two-thirds of the population had >70% stenosis. There was a mean follow-up of 11.9
months. The risk of stroke or crescendo TIA was 7.7% versus 19.4% (surgical vs. nonsur-
gical, p  0.028). There was a significant surgical benefit in patients with >70% stenosis.
Sample size at 50% to 69% stenosis was too small to draw any statistically significant
conclusions. Surgical benefit was appreciated as soon as two months status post-
randomization and was maintained throughout follow-up. Total perioperative risk was
5.5% (perioperative morbidity of 2.2% plus perioperative mortality of 3.3%).
The exciting data from the NASCET, European, and VASST trials showed that sur-
gical treatment is the best option in patients with classical carotid TIAs and greater than
50% stenosis demonstrated by arteriography.

Acute Neurological Deficit

Surgical intervention via CEA is often not a consideration in cases of acute stroke, for sev-
eral reasons. First, many patients presenting with acute neurologic deficits have as their
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10 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

primary problem a noncarotid event such as hypertensive hemorrhage or cardiogenic

emboli. Second, even those patients identified to have carotid embolic disease as the
cause of their neurologic deterioration have fared poorly when subjected to emergency
carotid surgery. In one early study, more than 50% of such patients suffered a fatal
intracranial hemorrhage within 72 hours of emergency endarterectomy (75). Other inves-
tigators have reported moderate success, however, with emergency surgery in patients
fulfilling strict preoperative criteria. These criteria include crescendo TIAs (attacks
abruptly increasing in frequency to at least several per day) in patients with severe steno-
sis; stroke following angiography; stroke following endarterectomy if thrombosis is pres-
ent; and disappearance of a previously auscultated bruit in patients awaiting elective
carotid surgery (presumably indicating acute occlusion) (76–79). Subsequently, encourag-
ing results were reported by two groups performing emergency surgery for crescendo
TIAs and stroke in evolution clinically and radiographically localized to one carotid
artery (79,80). Goldstone and Moore (79) emphasized, however, that patients with
depressed levels of consciousness or acute fixed deficits were excluded from their surgi-
cal series, and agree with other authors that such findings must be taken as absolute
contraindications for emergency CEA.
The retrospective series of Walters et al. (81) from the Massachusetts General
Hospital confirmed many of these conclusions. In their 64 patients (a mixed series
including 16 total occlusions), clinical results were best in patients with mild to moder-
ate deficit and a rapid course from onset of deficit to surgery. Like previous authors,
they recommended surgery for patients who had loss of bruit or deficit following
angiography and/or endarterectomy. They also recommended emergency surgery for
crescendo TIAs in patients with angiographic severe stenosis and distal flow delay, ICA
stenosis with intraluminal filling defect, or demonstrated acute complete occlusion (81).
A study of acute carotid occlusion and profound neurologic deficit was reported by
Meyer et al. (82) in a series of 34 patients with complete occlusion who had emergency
CEA. All patients had profound neurologic deficit including hemiplegia and aphasia.
Patency was restored in 94% of cases and they documented nine patients (26.5%) with nor-
mal postoperative neurological function, four patients (11.8%) with minimal neurological
deficit, 10 (29.4%) with moderate hemiparesis but improved from preoperative level, four
(11.8%) with unchanged hemiplegia, and seven (20.6%) dead. The authors of this study felt
that these results compared favorably with the natural history of complete acute carotid
occlusion with profound deficit and suggested that the presence of favorable collateral cir-
culation on angiography was a positive prognostic sign for neurologic recovery (82).
At present, then, emergency CEA is indicated only in a specific subpopulation of
stroke patients, that is, those with documented carotid etiology for a progressive but
nondebilitating ischemic event, or those in whom evidence of acute thrombosis is pres-
ent and who can be operated upon within several hours of the event (18).
It should be mentioned that a fine line of distinction is drawn between emergency
and urgent carotid artery surgery. The data from the NASCET study clearly show that
surgery is the best treatment for symptomatic patients with ipsilateral stenosis greater
than 50% (69,70). When such patients, particularly those with high-grade or preocclu-
sive stenosis, are identified in my practice, and they are neurologically stable, we con-
sider them urgent cases, and perform surgery as soon as possible, customarily the day
after angiography. Almost all of these patients are managed with systemic heparin anti-
coagulation, which is continued up to and throughout the surgical procedure (as dis-
cussed later). Tretter et al. (83) have elegantly analyzed their risk factors in a large
Cleveland Clinic series of “nonelective” CEA; the demonstrated increased risk is attrib-
utable to cardiopulmonary risk factors rather than neurologic events.
There are new data addressing the combination of intravenous thrombolysis for
stroke (tPA) and urgent carotid reconstruction. McPherson et al. (84) operated within 48
hours of tPA administration on five patients without complications when a high-grade
residual stenosis was identified, demonstrating feasibility and safety with this
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 11

approach. Eckstein reports a mixed series of 14 patients with either cervical ICA or
intracerebral major vessel occlusions (MCA, ACA) or both, who received either staged
tPA followed by CEA (3 cases), or in 11 cases emergency CEA with concurrent intraop-
erative angiographic selective urokinase injection intracranially (85). In these patients,
all of whom had a severe preoperative neurological deficit, four made a complete recov-
ery and six more had only minor residual strokes. This is a complex strategy, but it does
indicate that aggressive and individually tailored approaches to stroke, which infold
CEA as a treatment arm, are appropriate.

Complete Carotid Occlusion

Complete carotid occlusion, like many of the carotid syndromes, may present without
symptoms, with TIAs or fluctuating neurologic deficit, or with frank stroke. Some over-
lap exists, therefore, in the literature dealing with complete occlusion and in that
addressing emergency endarterectomy for stroke. Aside from the acute nondebilitating
neurologic deficits previously discussed, surgery for subacute carotid occlusion has
been performed both to restore blood flow to the ipsilateral hemisphere and to prevent
emboli originating from the stump of an occluded ICA from propagating distally. The
ability to reestablish flow in such situations is dependent upon the duration of the
occlusion, with several authors reporting 100% success in reopening these arteries
within 7 days (86,87). Delayed surgery has been less promising (87,88), and successful
restoration of flow in late surgical cases (5 weeks) appears to be dependent upon the
degree of collateral filling present from intracavernous and intrapetrous carotid
branches (86,89). One study has documented 58% patency at six months by follow-up
angiography (90), while a more recent study by McCormick et al. (91) reported 88%
wide patency and only one reocclusion at a mean 28 months follow-up. In one recent
series of surgery for documented acute ICA occlusion, patency was established in 83%
of cases and 74% of patients had neurological improvement at three to six months (92).
In another series, Paty et al. (93) were able to open 30% of carotids explored within two
weeks; in the rest an ECA endarterectomy was combined with ICA stump ligation.
Surgical intervention for complete carotid occlusion appears indicated in an
extremely limited group of patients who present with either acute nondebilitating
deficit directly attributable to such occlusions, or with ischemic symptoms referable to
embolization from an occluded stump. In these highly selected cases, thrombo-
endarterectomy carries a low surgical risk and, depending on the duration of occlusion
and degree of collateral filling, has a reasonable chance of achieving long-term patency.

Stump Syndromes
As mentioned previously, in recent years attention has focused on the importance of the
often-found “stump” of an occluded ICA as a possible source for ipsilateral embolic
phenomena (94,95). The presumed mechanism for these TIAs is through embolization
of debris from the stump through external carotid–ophthalmic artery collaterals. This
mechanism has been documented angiographically (95,96). Obviously, before the
carotid stump can be implicated as the etiologic source, the presence of major collater-
als and the absence of other significant atheromatous disease must be documented with
four-vessel angiography. In cases where this etiology seems clear, however, and where
reopening of the internal carotid cannot be achieved, I surgically ligate and oversew
(from the inside out) the offending stump, with concurrent open endarterectomy of the
CCA and ECA, and, for the past several years, placement of a common to external roof
patch Hemashield angioplasty (97). (See Section 5-2 for details.) I monitor these patients
with the same EEG criteria as an internal CEA, and am prepared to shunt the external
carotid if changes are noted. In my experience, by using strict selection criteria, this
procedure has been an effective therapy for recurrent neurologic phenomena, and has
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12 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

the added benefit that an occasional stump exploration may lead to backbleeding
and the reestablishment of anterograde internal carotid flow. I feel strongly that treat-
ment of such stumps in appropriate patients is as important for stroke prevention as is
treatment of any other symptomatic carotid lesion.

Special Considerations with Recent Stroke

Finally, it should be noted that a number of authors who customarily advocate selective
shunting have found intraoperative monitoring to be unreliable in patients who have
had recent reversible ischemic neurologic deficit (RIND) or stroke. These groups recom-
mend empirical shunt placement in all such cases (98,99). Likewise, although many
cerebrovascular surgeons empirically recommend a three to six weeks delay prior to
performing CEA in patients with fresh but nondebilitating strokes, especially those
with CT or magnetic resonance imaging (MRI) findings of large infarct and mass effect
(and thus with presumed defective autoregulation), three later studies have shown that
patients who are neurologically stable probably are at no greater surgical risk in the
early poststroke period than TIA patients, and that the high-risk subgroup is that of
patients who remain neurologically unstable at the time of surgery (100–102).

Clinical Evaluation

Patients present to the cerebrovascular surgeon in many different ways. Asymptomatic

patients are customarily elective and seen in the office or clinic. Patients with TIAs may
present likewise or may be seen as hospital consults. Patients with crescendo TIAs,
frank stroke, and/or acute occlusion will no doubt be seen as emergencies while in hos-
pital. The latter patients may or may not be heparinized and may be in various states
of neurologic deterioration.
Elective patients undergo a rapid workup with the goal of performing surgery as
soon as possible. I continue to prefer formal angiography in most cases including arch
and selective injection of both common carotids. Attention to intracranial cross filling is
also useful in assessing collateral patterns and I request biplane cervical angiography in
order to determine the anatomical relationship of the ECAs and ICAs. It is helpful to
have bony landmarks imaged on the lateral angiographic films to ascertain the height
of the carotid bulb in relation to the cervical spine, the angle of the mandible, and the
hyoid bone. Although I use duplex scanning as a screening procedure and for postop-
erative follow-up, I do not believe it is routinely needed if patients have already under-
gone magnetic resonance angiography (MRA) or angiography.
A topic of current interest is that of operating on patients based on MRA or CT
angiography alone (103,104). This has become a common practice among neurovascu-
lar surgeons seeking to avoid the small but finite risk of angiography, nearly 1% in
ACAS (10). Many surgeons have accepted MRA alone for surgical decision making and
planning, although there is to my mind no question that the anatomical detail is not as
rich. I do not operate on patients on the basis of duplex scanning alone. There is
compelling evidence to suggest that noninvasive studies alone are inferior for surgical
decision making if low-risk angiography is available (105).
Patients who are seen for potential carotid surgery are customarily on aspirin or
some form of anticoagulation; if they are not, they are started on aspirin at the time of
first visit. I do not stop preoperative aspirin therapy in preparation for surgery, but I do
discontinue ticlopidine or clopidrogel at least one week preoperation. Likewise in
patients who are heparinized for crescendo TIAs, I customarily maintain full anticoag-
ulation up to, and throughout, the surgical procedure. In such patients, we check the
activated clotting times (ACT) value in the operating room at the beginning of the case;
most often the anticoagulation is too low despite continuous heparin and a small bolus
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 13

must be given. As mentioned, I have no hesitation to operate on fully heparinized

patients, and in special cases (bilateral crescendo TIAs, mechanical heart valves), I have
maintained full heparinization postoperatively then converted to warfarin without any
gap; the risk of this is postoperative wound hematoma, and in my series I have encoun-
tered two of these (see Fig. 4-4), both in patients with mechanical valves treated with
constant anticoagulation therapy.
The remainder of the preoperative evaluation is standard. A careful neurologic
examination is performed and a history is carefully obtained for stereotypic TIAs in any
carotid distribution. A history of cardiac disease warrants cardiology consultation and
patients who smoke are advised to quit as far in advance of the surgical procedure as
possible.

Special Surgical Considerations

Several special situations in carotid patients were previously considered relative con-
traindications to successful reconstruction but these have become more acceptable with
recent advances in radiologic, surgical, and anesthetic techniques.

Plaque Ulceration
The correlation of plaque ulceration with ischemic neurologic symptoms and need for
surgery is difficult for several reasons. First, studies have shown interobserver variability
either on ultrasound or arteriographic examinations, and poor correlation between patho-
logic specimens and radiographically demonstrated ulceration. Second, in symptomatic
patients, deep ulceration is most commonly found in conjunction with significant degrees
of carotid stenosis, and it becomes difficult to separate clinical symptomatology between
these two findings (106,107). The most recent data from the NASCET study, however,
shows that in medically treated patients with 70% to 99% stenosis (now proven to be
unequivocal surgical candidates), the presence of plaque ulceration in conjunction with
stenosis significantly increases the risk of stroke (108).
The significance of intraplaque hemorrhage as a predictor of ischemic symptoms
is unclear. Although Gomez (106) suggested that intraplaque hemorrhage was found
much more commonly in patients with symptomatic carotid disease, other studies sug-
gest that there is a low correlation between ischemic symptoms and plaque hematoma
in CEA patients (109).

Critical Stenosis
The question of critical stenosis has recently been well addressed. Critical stenosis need
no longer be debated. Surgery is appropriate and proven by class 1 evidence for 50% or
greater symptomatic lesions and for 60% or greater asymptomatic lesions. In light of
these data, “critical” stenosis now only indicates a need for expeditious surgery and in
many cases for preoperative systemic anticoagulation.

Intraluminal Thrombus
The problem of surgical timing in patients with angiographically demonstrated propa-
gating intraluminal thrombus remains an open question among cerebrovascular experts.
There are two types of thrombus seen on imaging studies: the small “bullet type”—
localized to the area of critical stenosis, and the longer “propagating type”—extending
far up the internal carotid, sometimes into the supraclinoid region (see Fig. 2-18). For the
bullet type, which can be easily controlled by cross-clamping above the thrombus at
open surgery, we do not hesitate to proceed. The best management for the propagating
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14 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

type is less clear. Several authors have documented that an increased risk of periopera-
tive or intraoperative stroke must be accepted when operating on patients who have
propagating clot that may extend beyond the area of internal carotid cross-clamping or
that is more friable and prone to dislodgment than the usual carotid plaque (110–112).
Review of the literature suggests that a period of observation with full heparinization
prior to undertaking surgical therapy may reduce the morbidity and mortality in these
patients (110,112,113). Clearly, the choice of therapy must be tailored for individual
cases. It is equally clear, however, that intraluminal thrombus is a therapeutic emer-
gency but not necessarily a surgical emergency, rather the identification of propagating
thrombus should provoke a careful and measured response to the situation. As one
author has suggested, heparinization should probably be instituted in every case fol-
lowed by consideration of endarterectomy in patients who are neurologically stable,
and by a delayed surgical plan following a period of expectant observation in neurolog-
ically unstable patients or those with serious intercurrent illness or hypercoagulable
state (113). In patients who present with TIAs (which in my experience have always
resolved with anticoagulation) and an intraluminal thrombus, I have opted for delayed
surgery (at six weeks, following repeat angiography) in nearly every case, and have
never seen a negative outcome from intercurrent embolization once heparin is insti-
tuted (112). Likewise, there is a small subset of patients with postoperative neurologic
events (most often TIA) following CEA who are found to have a fresh thrombus adher-
ent to the suture line (see Fig. 2-19), partially occluding the artery, and which is presum-
ably the source of embolic phenomena. If there is no other angiographic evidence of
technical inadequacy, I manage these patients conservatively as well, with full antico-
agulation and six weeks follow-up arteriography (or, in the current era, MRA). In every
case, the thrombus has resolved and there have been no negative neurologic outcomes
in my series with this plan of management. Despite the surgeon’s natural inclination to
fix a problem with bold action, I have found that a measured conservative approach
yields good results in cases of fresh or propagating thrombus and in my experience out-
weighs undertaking a high-risk surgical procedure.

Contralateral Carotid Occlusion

Early reports of surgery in the face of contralateral carotid occlusion were dismal (114),
but with advances in surgical and anesthetic techniques, most surgeons currently have
little or no hesitation to approach symptomatic carotid lesions with contralateral occlu-
sion. Surgeons who employ selective shunting based on intraoperative monitoring do
report a higher incidence of shunt-dependent cases in this group (115,116), and several
studies have reported higher rates of postoperative neurologic deficits in this subgroup
when shunts were not used (117,118). Several series dealing exclusively with this prob-
lem have been published, and all reported satisfactory results. Interestingly, three
groups employed universal shunting in dealing with contralateral carotid occlusion
(119–121), while the fourth reported excellent results in patients who were never
shunted (122). It has been my policy to approach these cases with EEG monitoring and
selective shunting, much as routine carotid procedures are performed, although
unquestionably the need for intraluminal shunting has been greater in this subgroup.
In my series where the shunt rate is ~15%, 25% of patients with contralateral occlusion
have required shunts based on full-channel EEG criteria (123).
Notwithstanding my personal opinions on the safety of carotid surgery in patients
with contralateral occlusion, we must note that NASCET data identified contralateral
occlusion as an independent risk factor for poor outcome in reconstruction of sympto-
matic carotid disease (124). These data have been extensively cited in support of carotid
stenting, as opposed to open surgery, for these purported “high-risk” patients.
There is new and compelling evidence to suggest that contralateral CEA is bene-
ficial to both hemispheres in patients with symptomatic ICA occlusion. Rutgers and
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 15

co-workers (125) showed that transcranial Doppler (TCD) flow increased bilaterally,
basilar artery antegrade and ophthalmic artery reverse flow decreased, brain lactate
levels decreased, and CO2 reactivity increased following contralateral CEA when an
occluded carotid was identified.

Tandem Lesions of the Carotid Siphon

The presence of carotid siphon disease has been proposed as a contraindication to CEA
because of both the inability to pinpoint the symptomatic source and the reputed
increased possibilities of postoperative occlusion from decreased carotid flow velocity.
At least two surgical series have refuted these contentions (126,127). In both of these
studies, no significant association between postoperative complications or recurrent
symptoms could be demonstrated in patients undergoing CEA in the face of known
“inaccessible” siphon disease. Several other interesting reports on this problem have
been published. Day et al. (128) documented two cases of siphon disease resolution fol-
lowing ipsilateral CEA (128). Little et al. (129) described a similar entity of angiographic
“pseudotandem stenosis,” which likewise resolved in two cases following endarterec-
tomy. The presence of a tandem lesion does not appear to contraindicate successful
CEA if the indications and surgical risks are otherwise justified.
Intracranial atherosclerotic disease (IAD) was studied as an offshoot of NASCET.
IAD was found to be an independent risk factor for stroke in medically treated
NASCET patients and CEA reduces this risk (130).

Concurrent Carotid Disease and Intracranial Aneurysm

Several studies have focused on the repair sequencing of symptomatic carotid disease
and silent intracranial aneurysm discovered on carotid angiography. Although one
report documents rupture of an intracranial aneurysm six months following carotid
reconstruction for tight stenosis (131), most other authors recommend repair of the
symptomatic lesion first, which in most cases will be symptomatic carotid artery steno-
sis (132,133). These authors conclude that CEA is unlikely to precipitate rupture of
intracranial aneurysm during the perioperative period.
A clever and elegant solution to the carotid/aneurysm dilemma, using a com-
bined approach to both lesions at one operation, has been described by Hodge (134).
This approach solves the waiting problem and merits consideration by surgeons with
the ability to perform both techniques.

Recurrent Carotid Stenosis

A small but finite incidence of recurrent carotid stenosis occurs following primary CEA.
Most authors quote a symptomatic recurrence rate of approximately 4% to 5%, and in
one study of noninvasive follow-up after carotid surgery, a 4.8% recurrence rate of
symptomatic carotid restenosis was documented with an additional 6.6% silent resteno-
sis rate (135). Piepgras et al. (136) have quoted somewhat lower figures with their use
of patchgraft repair (1% symptomatic, 4–5% total at two year follow-up).
Aside from technical inadequacies, it is difficult to identify risk factors associated
with recurrent carotid stenosis, although continuation of smoking habits following
endarterectomy proved to be a significant risk factor in one study whereas hyperten-
sion, diabetes mellitus, family history, lipid studies, aspirin use, and coronary disease
were not found to be significant risk factors by this group (137,138).
Reoperation for carotid stenosis is a technically more difficult procedure than pri-
mary operation. Most surgeons feel that the stroke risk in redo CEA is associated with
significantly higher risks than primary endarterectomy [4.8% vs. 0.8% in one recent
series (139), 3.4% in another (140)], and the risk of cranial nerve injury is clearly
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16 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

increased as well. Piepgras et al. (136) carefully documented a reoperation CEA compli-
cation rate of 10.5%—four times their customary figure. At my institution, the possibil-
ity of reoperation for carotid stenosis is entertained for patients who present with
angiographically proven disease and classical neurologic symptoms referable to the
appropriate artery. In addition, since the ACAS data became available, we have rou-
tinely followed patients with noninvasive studies and recommended reoperation for
high-grade recurrent stenosis when it is identified. Recurrent stenosis, however, was
significantly reduced in my practice following the adoption of primary universal
Hemashield patch angioplasty. We do see cases from other surgeons in which primary
repair has failed, and we evaluate these patients in light of the ACAS data, taking spe-
cial care to educate them of the higher risks associated with reoperative surgery when
they make their surgical decision. The Mayo group likewise feels that changing bruits
or rapidly progressive silent stenosis justifies surgical intervention (136).
Data from the SAPPHIRE trial now suggest that stenting should be considered as
an equivalent therapy for “high-risk” carotid patients such as those with recurrent dis-
ease. It remains to be seen what paradigm will ultimately emerge regarding the
endarterectomy/stenting balance for high-risk cases (141).

Concurrent Coronary/Carotid Disease

It is well established that patients with extracranial carotid artery disease have a higher
than normal incidence of coronary disease as well as other peripheral vascular prob-
lems. Indeed, the risk of perioperative MI exceeds the risk of perioperative stroke in
many clinical series of CEA. Several major questions arise when planning treatment for
concurrent coronary/carotid disease. First—what is the risk of coronary revasculariza-
tion in a patient with a high-grade asymptomatic stenosis or bruit; second—in patients
with symptomatic carotid disease, what is the appropriate workup of the coronary cir-
culation; and third—if both symptomatic carotid artery and coronary artery disease are
identified, what is the appropriate surgical management of this patient: staged carotid
followed by coronary revascularization, combined procedure, or “reverse-staged” coro-
nary revascularization followed by delayed CEA.
The first of these questions regarding asymptomatic bruit in symptomatic coro-
nary patients has been dealt with earlier in this chapter. We accept the ACAS evidence
that suggests that carotid reconstruction is an appropriate choice for patients with 60%
or greater stenosis. It is less clear whether carotid surgery is needed first for the asymp-
tomatic bruit in patients about to undergo surgical procedures of a different type. In
such cases, a reverse-staged strategy is appropriate. We reemphasize that symptomatic
carotid disease is the harbinger of stroke in patients who are candidates for other sur-
gery, and in cases of this type we recommend staged surgery with the carotid first.
The second question regarding appropriate workup of coronary disease in symp-
tomatic carotid artery patients is a more difficult one. In this situation, workup is cus-
tomarily guided by the patient’s history and symptomatology. I obtain cardiology
consultation for any patient with a history of angina, known heart disease, or abnormal
resting electrocardiogram (ECG). The workup proceeds with a thallium stress test with
exercise or dipyridamole, and if there is any evidence of myocardial ischemia, coronary
angiography is performed (142,143).
When the results of cardiac evaluation indicate the need for coronary revascular-
ization, the question becomes one of timing of the surgical procedures. I prefer to do
staged procedures whenever possible. With careful hemodynamic monitoring and good
anesthetic technique, I am routinely able to perform safe unilateral CEAs prior to coro-
nary revascularization. The risks of combined procedures are high; Medicare population
studies have documented a combined 17.7% stroke/death rate for combined
CEA/CABG surgery, even though the majority of patients had asymptomatic carotid
disease (144). An occasional patient with severe unstable angina may require a combined
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 17

procedure, but clearly this entails a significantly higher surgical risk and I, like others
with extensive experience, attempt staged procedures whenever possible (142,145).
Most series dealing with “reverse stage” coronary carotid procedures (i.e., the coro-
nary artery revascularization first with delayed CEA) discuss these in the context of
asymptomatic carotid disease (146). In the first edition of this book I stressed my prac-
tice of not offering prophylactic revascularization to asymptomatic patients with or
without concurrent coronary disease (9). Clearly, the ACAS/ACST results have
changed our approach, and we now consider reverse-staged procedures an appropri-
ate and effective strategy for risk reduction in patients who meet the ACAS criteria for
prophylactic CEA (147).

TECHNICAL CONSIDERATIONS

Anesthesia Choice
The choice of anesthetic type for carotid reconstruction, whether local, regional, or gen-
eral, is highly individualized by surgeon. It is also important to remember that moni-
toring, shunt philosophy, and anesthetic choice are intimately intertwined, and that the
choice of local or regional anesthetic technique, at least in previous decades, implied the
surgeon’s belief that direct observation was an effective and probably the most accurate
monitoring strategy to document cross-clamp ischemia and the consequent need for
placement of an intraluminal shunt. In early reported series, however, failure to toler-
ate cross-clamping under regional anesthesia (RA) caused the procedure to be aborted
(in 10% of cases), with a reoperation under general anesthesia (GA) and universal
shunting 24 to 48 hours later (148). The current standard technique for local anesthesia
(LA)/RA has evolved significantly, and this delay practice is no longer reported.

Local/Regional Anesthesia
It is difficult to ascertain with certainty the prevalence of LA/RA in carotid reconstruc-
tion. Despite a growing and renewed interest in the local/regional techniques, I think
we can safely assume that GA remains the most common practice for carotid recon-
struction across all specialties. In the NASCET randomized trial of symptomatic carotid
disease (including both vascular and neurosurgeons), the majority (>95%) of patients
underwent GA (149), and surprisingly only 55% were neurologically monitored. The
later work of Cheng et al. (150) presents a survey of the members of the Society of
Neuroanesthesia and Critical Care (SNACC). Of those who responded (50.7% of the
surveyed group), 84.7% administered GA for CEA, while 16.7% used regional block
anesthesia, and 2.8% reported either LA or a regional/general combination in their
practices. These decisions, of course, were primarily made by the surgeon, but the data
still should reflect accurately current neurosurgical practice since an anesthesia team
will be present for all cases. Although the data are probably valid for neurosurgical
CEA, it is unclear whether it can be extrapolated to the larger vascular/cardiothoracic
population of surgeons, and whether the prevalence of LA/RA (which I suspect would
be higher still) differs in those groups.
A discussion of local or regional carotid anesthesia is mostly academic for this
author since I almost never use it in my practice (9,123,147,151–168). This is primarily
because like many surgeons I am hesitant to deviate from a standardized operative plan
(the use of essentially universal GA with full-channel EEG monitoring in my case)
which has yielded good results. I have, on several occasions, performed successful
CEAs under LA when the patients had pulmonary problems so severe that postopera-
tive ventilator dependence was a risk.
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18 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

Popular opinion on the use of LA changes in different surgical generations.

External forces mandating decreased cost and length of stay by whatever means neces-
sary may drive the surgical choice. Some have suggested that carotid surgery be per-
formed essentially as an outpatient procedure (169) although I have reservations to this
approach, particularly in patients with associated risk factors. I think we must say in
fairness that the data reported by Harbaugh and Harbaugh (170) and Allen et al. (171)
would indicate that significantly decreased morbidity, increased patient satisfaction,
and complication rates equal to or better than the best general anesthetic series can now
be demonstrated by surgeons committed to the local/regional anesthetic technique.
Since the first edition of this book was published, compelling evidence has demon-
strated that locoregional anesthesia is associated with significantly less perioperative
hemodynamic instability than GA (172), and in a second, randomized trial, that LA
patients with known ischemic heart disease had half the rate of perioperative myocar-
dial ischemia as GA patients (173).
General anesthetics versus regional anesthetics have been directly compared in
several recent series from single institutions (171,174–177). Forssell et al. (175) reported
a randomized series of 101 patients in which 56 received LA and 55 received GA. There
was no significant difference in stroke rate, but the rate of intraluminal shunt use (based
on stump pressure for GA and neurologic observation for LA) was five-times higher in
GA patients. LA patients, on the other hand, experienced significantly higher systemic
blood pressure during cross-clamping (210 mmHg vs. 173 mmHg mean systolic) (175),
Corson et al. reported 252 GA endarterectomies and 157 RA cases at Albany Medical
Center (174). Monitoring in GA cases consisted of stump pressure and visual assess-
ment of backbleeding; many patients under GA were shunted empirically. The stroke
rate was significantly higher in the GA cases, and there was a higher incidence of labile
blood pressure and the need for vasoactive drugs in the GA group. Five patients under
RA required conversion to a general anesthetic. Allen et al. (171) made a strong case for
the use of the regional technique. Their study compared 361 general anesthetic cases
and 318 regional cases on the vascular surgical service at Washington University. There
was no difference in stroke rate between anesthetic groups or between asymptomatic
and symptomatic patients. Significantly more (42.1% vs. 19.2%) patients were shunted
in the GA group than in the RA group. (Monitoring consisted of EEG plus stump pres-
sure in GA cases and neurologic status observation in RA cases; patients with contralat-
eral occlusion or recent stroke were shunted empirically in many cases.) RA patients
had significantly shorter operative times, fewer perioperative cardiopulmonary com-
plications, and shorter hospital stays. Shah et al. (178) revised and updated the earlier
Albany series. In their study, RA reduced mean ICU stay from 1.4 to 0.7 days and hos-
pital stay from 5 to 3 days. Palmer’s community hospital study by a single surgeon
using the two techniques disputes the length of stay and complications data, being
unable to show a statistical difference (179).
It appears now that experienced surgeons who choose RA can apply it to all
carotid patients they come across. This was not the case in earlier reports. There is good
evidence from Harbaugh’s series that the RA technique can be applied universally,
eliminating the need, at least in his cases, for emergency intubation and/or procedure
termination that complicated older reported series (170,180). Most current reports doc-
ument little or no conversion to GA in patients operated with local/regional technique
(181). It would appear that those rare cases where emergency induction of GA is
required are primarily cases where airway control is inadequate following a severe neu-
rologic change (unconsciousness) at cross-clamping, or for seizure occurring at cross-
clamping (178). In Shah’s report, 1.1% of patients required GA conversion, half for
inadequate analgesia, and half for the aforementioned neurologic problems (178).
The implication of LA/RA is that the patient can be continually examined by either
the anesthetist or surgeon or be required to perform some motor task (such as squeezing
a child’s toy with the contralateral hand) (182) to confirm adequate ipsilateral perfusion
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 19

during cross-clamping. Groups with large experience in the technique report that the
risk of patient disorientation from ischemia with subsequent movement and contamina-
tion of the operative field can be minimized by careful monitoring and sedation by the
anesthetist (182–186). Proponents of LA stress the advantages of patient response to
questioning as a superior monitoring technique in assessing the need for shunt place-
ment, primarily because of dissatisfaction with the use of stump pressure measurements
(186) or EEG monitoring (185) in the anesthetized patient. Other advocates of LA, includ-
ing some who shunt routinely (184), report a 2% to 5% incidence of undetected shunt
malfunction during endarterectomy (either from cephalad migration of the shunt with
distal abutment against the ICA wall or from intraluminal thrombosis), and feel that
direct observation of the awake patient is the most reliable indicator of shunt function
(184,187). Perhaps, the most interesting data from the LA series are that of Steed et al.
(183) who analyzed the causes of stroke during CEA in a series of 345 LA procedures.
They found that intraoperative neurologic deficit was most often associated with dissec-
tion around the carotid (for exposure) or clamp reopening, and only rarely with carotid
cross-clamping. Their data support the theory (also championed by those who never
shunt) that most neurologic deficits are embolic rather than ischemic in nature.
We have recently analyzed our own institutional data, comparing the incidence of
EEG changes and the need for shunting between two surgeons; a vascular surgeon who
uses only LA/RA with EEG, and myself, using GA with EEG (176,177). In this series,
the incidence of EEG changes and shunt placement was less with LA. There was no dif-
ference, however, in stroke rate, complications outcome, or length of stay.
The potential drawbacks of LA/RA for carotid reconstruction have been enumer-
ated by Michenfelder (188). These include patient discomfort, the perceived need for
hasty surgery and/or shunt placement, loss of patient cooperation if cross-clamp
ischemia produces confusion, panic, or seizures, the possibility of a delayed deficit
occurring at some time beyond the initial test period, the inability to administer cere-
bral protective (anesthetic) agents, and the inability to optimize blood gases and blood
pressure to augment cerebral perfusion. It is difficult to document or discern from pub-
lished reports the number of patients who are unable to tolerate the local/regional tech-
nique, but surgeons with great experience universally point out that extensive
preoperative counseling and a skilled experienced anesthetist are the keys to prevent-
ing panic or lack of cooperation.
Either sequential infiltration of the cervical layers with 1% lidocaine or regional
block anesthesia may be used for awake CEA. Hafner and Evans (189), reporting a
series of 1200 CEAs, preferred local infiltration, with the feeling that regional block was
not always successful in eliminating pain during cross-clamping. Other authors are sat-
isfied with percutaneous cervical block anesthesia, although complications such as
extension of anesthetic effect to the brachial plexus with transient monoparesis and
generalized seizure (presumably from intra-arterial injection) have been documented
(180,181). Mild sedation with midazolam hydrochloride is often added (189), and the
need for block augmentation with local anesthetic infiltration is often mentioned (190).
A complete description of the technique and its advantages can be found in Harbaugh’s
recent article (180).
Seizures at the time of cross-clamping, although rare, have been reported, leading
to abandonment of the procedure (190) or as mentioned above conversion to a general
anesthetic (178).

General Anesthesia
GA remains the technique of choice for carotid artery surgery in many centers for a
number of reasons. Certainly, many surgeons prefer the more controlled surgical envi-
ronment afforded by GA. It is my personal feeling that GA facilitates resident educa-
tion, a fact that cannot be discounted. A light general anesthetic, mostly narcotic/N20
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20 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

with a low concentration of inhalational agent, is commonly used. All commonly

selected inhalational anesthetic agents, and intravenous barbiturates, significantly
reduce CMRO2 (191), providing a theoretical advantage in brain protection during
ischemia. In addition, GA provides for accurate manipulation of respiratory parameters
and arterial pCO2, and facilitates rapid intraoperative control of blood pressure
changes.
Manipulation of arterial pCO2 to optimize cerebral protection has been the subject
of great study and some debate. Intraoperative hypercapnia was initially felt to provide
cerebral protection through vasodilation and increased global regional cerebral blood
flow (rCBF) (192). Later investigations, however, showed that hypercapnia has no effect
on either ipsilateral stump pressure (193) or rCBF (measured by gaseous washout)
(194), and that indeed it may be deleterious (195). Hypocapnia, through the “inverse
steal” effect (196–198), may be more effective in enhancing rCBF in ischemic areas (193,
195,196). One clinical study, however, in which patients were randomized into hyper-
capneic or hypocapneic techniques, could show no statistically significant difference in
neurologic outcome between the two groups, although the hypocarbic group did have
fewer neurologic complications (199). In view of these findings, patients undergoing
carotid artery surgery are currently managed at normocapneic levels, or with only mild
hyperventilation, avoiding extremes of arterial pCO2 (191,200).
Data concerning induced-intraoperative hypertension is much more consistent.
Significant increases in both local rCBF (194) and in stump pressure (191) have been
documented with pharmacologically induced hypertension in patients undergoing
carotid cross-clamping. Many surgeons, who shunt based on intraoperative monitor-
ing, first attempt to reverse ischemic changes with a controlled elevation of arterial
pressure. Cheng’s data show that a majority of SNACC members use intraoperative
hypertension (61.1%) routinely in carotid surgical anesthesia (150). Current anes-
thetic management in carotid surgery aims at maintenance of normotensive levels
with tolerance of systolic pressure up to 20% higher before antihypertensive meas-
ures are instituted (19l). Certainly, it is also clear that intraoperative hypotension is
to be avoided.

Monitoring Techniques During Carotid Cross-Clamping

The decision to perform endarterectomy, in my mind, implies that the surgeon will
become familiar with and learn to rely on one specific monitoring technique to deter-
mine the need for shunt placement. (Basically, this is true for LA/RA as well, with the
exception that the choice of monitoring style may not be quite as varied.) This opinion is
not universally held. Some surgeons will shunt routinely, whether monitoring is used or
not, and some will never shunt under the same conditions. There is, in my mind, no stan-
dard of care referable to the need for monitoring or the placement of a shunt.
Nonetheless, in the ongoing attempt to reduce morbidity and mortality in carotid artery
surgery under GA, a variety of intraoperative monitoring techniques have been devel-
oped to assess the need for increased cerebral protection, whether by induced hyperten-
sion or by intraluminal shunting. These techniques fall into two broad categories: (i) tests
of vascular integrity, such as direct observation of backbleeding, stump-pressure meas-
urements, xenon rCBF studies, TCD, intraoperative OPG, Doppler/duplex scanning,
angiography, and near-infrared spectroscopy (NIRS), and (ii) tests of cerebral function,
such as EEG, EEG derivatives, and/or SSEP monitoring. Monitoring techniques com-
mon to both LA/RA and GA include the cruder tests of vascular integrity (visual assess-
ment, stump pressure) and the EEG/SSEP tests of neurologic function, as well as TCD.
Direct assessment of patient response is of course only available under local/regional
technique. Cheng’s data indicate that 90% of SNACC responders used intraoperative
neuromonitoring, with EEG being the most common method (67.5%) (150).
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 21

Monitoring Techniques Under GA

Vascular Evaluations

Visual Assessment of Backbleeding. Surgeons who may not have access to more
sophisticated techniques of monitoring, and who choose to practice selective shunting,
may rely on visual assessment of retrograde bleeding from the isolated ICA based on
their experience. Although I make a quick assessment of backbleeding, my own prac-
tice is to assess the need for shunting based on EEG data.

Stump Pressure. Measurement of residual “stump” pressure in the isolated distal CCA
or ICA following clamping of the proximal CCA and ECA was proposed as a simple
and reliable indicator of the need for intraluminal shunting. The technique as described
by Moore measured mean internal carotid back pressure, and most authors have sub-
sequently adhered to this standard. In Moore’s initial studies, mean stump values of
greater than 25 mmHg were felt to represent the safe level for carotid back pressure
(99,201), and they continue to advocate this method (202). Hays et al. and others later
reported similar good results with this monitoring technique, but revised the safe level
of mean arterial back pressure to 50 mmHg (203) or even as high as 70 mmHg (204).
Others have emphasized that isolated stump-pressure measurements are not adequate,
and recommend interpretation of such values in relation to the patient’s resting blood
pressure (205) or when jugular venous pressure was concurrently measured and the
calculated cerebral perfusion pressure (CPP) was greater than 18 mmHg (206). Stump-
pressure monitoring has come under criticism when evaluated simultaneously with
other monitoring techniques. In two series of LA procedures, 6% to 9% of patients lost
consciousness and required shunting despite stump pressures greater than 50 mmHg
(207,208). In several general anesthetic series, stump pressures did not correlate well
with either ischemic changes on EEG or with intraoperative rCBF measurements
(209–213), and in one case, the incidence of ischemic changes on EEG despite stump
pressures greater than 50 mmHg was 22% (209). At present, stump-pressure measure-
ments, if taken, are usually augmented by evaluation of physiologic function in intra-
operative evaluation of the need for shunting.

Intraoperative rCBF. Several centers have performed intraoperative rCBF analyses

with intracarotid injection of 133 Xe; in some this remains a routine technique of assess-
ment during carotid artery surgery (214–216). These studies have provided valuable
information concerning both the lower limits of tolerable rCBF and concerning the cor-
relation of rCBF values with EEG monitoring and stump-pressure data. Boysen origi-
nally felt that rCBF values of 30 cc/100 g/min represented the critical threshold for
irreversible intraoperative ischemia (210). Later series, however, including Sundt’s
extensive experience, have revised this figure downward to 18–20 cc/100 g/min (213,
215–217). In most of these series, a good correlation has existed between failure of ipsi-
lateral rCBF and slowing or flattening of the EEG, but several authors have stressed the
lack of such correlation between rCBF and ipsilateral stump pressures (213,210). It is
clear that most surgeons using rCBF determinations opt for intraluminal shunting at
values below 18–20 cc/100 g/min. A single study, however, of patients in whom shunts
were never used reports uneventful neurologic outcomes in some patients with intra-
operative rCBF as low as 9 cc/100 g/min (218). These investigators are credible sur-
geons and their data must be taken seriously. Intraoperative rCBF studies have
certainly provided valuable insights into cerebrovascular physiology, and in certain
specialized centers continue to serve as a routine monitoring technique. Their value to
the majority of carotid surgeons is limited by lack of availability of equipment and
personnel trained in this methodology.
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22 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

Transcranial Doppler. Continuous online recording of systolic and mean TCD veloci-
ties in the ipsilateral middle cerebral artery (MCA) during CEA is gaining increasing
favor in the neurovascular surgical community. The advantages of TCD for carotid
monitoring are several. These include the ability to predict the need for shunting by
virtue of measuring a decrement in MCA velocities (MCAV), the ability to assess func-
tion of the shunt both after insertion (with an increase in MCAV) and during arterial
repair (where presumably a shunt malfunction would manifest as a profound decrease
in MCAV), and finally the ability to detect particulate embolization through audible
TCD monitoring either during the procedure or in the postoperative period. We will
examine each of these monitoring considerations in turn.
TCD may have the ability to predict preoperatively the need for shunting. Benichou
et al. divided 91 patients into two groups. Group A patients had TCD identification of a
functional anterior communicating and either one or two posterior communicating arter-
ies preoperatively whereas Group B patients had no such communicating arteries identi-
fied. Group B patients had a significantly higher incidence of stump pressures <50 mmHg
at surgery and clinical need for shunting. They found that the clinical need for shunting
based on these preoperative criteria was correct in 95.6% of cases (219). Schneider et al.
had likewise reported a similar statistically significant ability to predict decreased MCAV
and shunt need in a somewhat smaller series of 23 patients (220). Sufficient experience
with TCD now exists to allow the technique to be compared to other methods of intraop-
erative CEA monitoring. A number of papers have compared TCD monitoring with intra-
operative stump-pressure measurements, customarily using a stump pressure of less than
50 mmHg as an indication for shunting (220–225). A good correlation with stump pres-
sure and TCD monitoring has been reported although as one would suspect, TCD
appears to be somewhat more sensitive and to be a more direct reflection of the status of
intracranial circulation. Halsey studied TCD and rCBF in eight patients but found consid-
erable variability in the relationship between the two (226). Thiel et al. studied TCD meas-
urements and correlated these with intraoperative SSEP recordings. They used MCAV
reduction of greater than 60% as their criterion for significant change in 78 patients. This
degree of TCD decrease occurred 11 times, however, in only six of these patients did rel-
evant SSEP changes occur simultaneously and one patient with critical SSEP changes did
not have a significant MCAV reduction. The four patients, however, who did have tran-
sient neurological deficits postoperatively, had both critical MCA reduction and critical
SSEP findings (227).
The correlation of intraoperative EEG with TCD has likewise been evaluated.
Schneider et al. (220) showed that EEG changes occurred during cross-clamping in their
patients with an MCAV of 14.7 compared with an MCAV of 24.1 in patients with nor-
mal intraoperative EEG tracing (220). Jorgensen (222) showed that a Vmeanclamp: Vmean
pre-clamp ratio below 0.4 was 97% effective in detecting essentially all patients with
EEG flattening (222).
What is the value of TCD in predicting intraoperative cross-clamp ischemia and
the need for shunting during carotid surgery? In the recent retrospective study by
Halsey (228), 11 centers contributed 1495 CEAs monitored with TCD. The cases were
divided into severe, mild, and no ischemia groups and both shunt use and periopera-
tive stroke rates were assessed in these groups. Ischemia was defined as being severe
if mean velocity in the first minute was 0% to 15% of pre-clamp value, mild if 16% to
40%, and absent if greater than 40%. Severe ischemia occurred in 7.2% of cases but
cleared spontaneously in half. Persistent severe ischemia without shunt was associated
with a high rate of severe stroke; this appeared to be prevented by shunt placement.
As has been shown by Prioleau et al. (229), the stroke rate was actually higher with
shunting in cases without severe ischemia (empirical shunting). A recent report by
Jansen et al. likewise documented 130 consecutive operations in which severe ischemia
(defined as a reduction of
70% MCAV) occurred in 16 patients. Concurrent severe
EEG changes occurred in nine and were corrected by shunt use in eight and profound
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 23

hypothermia in one (in a combined coronary/carotid procedure). These authors were

encouraged by the value of TCD in predicting neurological outcome and the need for
shunt placement (230).
Aside from the value of MCAV in predicting cross-clamp ischemia, acoustic feed-
back from the TCD is useful to assess continuing passage of intracranial emboli. TCD
monitoring for circulating solid cerebral emboli with automated detectors has potential
application in identifying patients with active but clinically silent extracranial embolic
sources (cardiac, aortic, or carotid) who may then be treated prophylactically with war-
farin or surgery, depending on the source (231). Transhemispheric passage of embolic
material has been shown by TCD in patients with an active carotid plaque and con-
tralateral carotid occlusion; the signals disappeared following CEA (232). Detection of
intracranial embolization during various points of the carotid procedure has been
discussed primarily by Spencer et al. who differentiate between air-bubble emboli and
formed-element emboli, and likewise make a distinction between transient effects
and ongoing emboli during long-term recording. Thirty-eight percent of their patients
demonstrated air-bubble emboli at release of CCA cross-clamps. This was felt to be a
relatively benign finding. Formed-element emboli were acoustically identical
to air-bubble emboli but were defined as emboli that occurred during periods where no
air-bubble emboli would be expected, i.e., not during release of cross-clamps or other
similar operative times. Formed-element emboli were identified in 25% of patients and
were associated with strokes and cerebral infarction when they persisted for several
hours postoperatively, indicating presumably an arterial source for consistent platelet
fibrin thrombi (233). Jansen et al. have also shown a significant relation between the
number of embolic signals by TCD during surgical dissection of the carotid artery and
the occurrence of intraoperative infarcts (234).
Finally, TCD has proven utility in preventing technical errors at surgery including
malfunction of an indwelling shunt. A decrement in MCAV during the shunted portion
of the endarterectomy with subsequent revision of shunt and return of velocity has
been documented (235). Likewise, a case of perioperative restenosis due to intimal flap
detected by MCAV decrease has been also reported (236). Powers and Smith (237) have
also reported the utility of postoperative TCD recordings in documenting the course of
a patient with severe carotid stenosis and thus a dysautoregulated hemisphere who
developed hyperperfusion syndrome in the postoperative period (237).
Audible TCD signal can be used as an educational tool. Ackerstaff et al. docu-
mented higher audible embolic signals during various stages of CEA, and recommend
that surgeons modify and refine their dissection and shunting techniques by using con-
tinuous audible feedback to reduce embolic events (238). Spencer documented signifi-
cant reduction in operative stroke rates (7% decreasing to 2%) in a series of 500 patients
where continuous TCD was used as an educational feedback tool (239).
In conclusion, increasing experience with TCD shows it to be an effective method
of intraoperative monitoring, which has the potential to address several questions.
These include cross-clamp ischemia and the need for shunting, evaluation of shunt
function, and elimination of technical errors that yield particulate embolization during
the surgical procedure. It would appear that the ability of TCD to evaluate perfusion
pressure intracranially rather than at the carotid stump is a more accurate measure of
the need for shunting.

Perioperative Retinal Arterial Pressure. Gee et al. studied retinal pressures intraoper-
atively to evaluate the efficacy of shunt placement. They showed clearly that an
indwelling shunt appreciably elevated the ipsilateral ophthalmic systolic pressure over
that noted during carotid clamping (240). Pearce et al. (241,242) have described a tech-
nique of supra orbital photoplethysomography that is said to provide immediate feed-
back concerning intraoperative shunt malfunction. In their small series (15 procedures),
20% of indwelling shunts were repositioned because of decreased intraoperative supra
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24 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

orbital artery flow. To my knowledge, however, neither of these plethysomographic

methods is currently in common use.

Intraoperative Angiography. A single intraoperative common carotid angiogram can

be obtained following arterial closure and has been long championed by several groups
(243–247). The methodology has been well described and involves puncture of the
proximal CCA with hand injection of 10 mL of contrast while a single portable image is
obtained (243). Radiographic defects requiring revision of the arterial suture line are
demonstrated in 2.5% and 8% (246,247) of procedures in these series, and the authors
feel neurologic sequelae have been markedly reduced by the ability to immediately
assess the surgical site. The educational value of routine intraoperative angiography is
also useful for facilitating error recognition and promoting continuous refinement of
surgical technique (246,248).
The primary disadvantage of intraoperative angiography is one of time and con-
venience. All authors emphasize that these factors are reduced with consistency of radi-
ographic personnel and increased experience on the surgeon’s part. One group also
feels that the risk of subintimal injection and consequent thrombosis outweighs the ben-
efits of the technique in routine cases, and recommends that the arteriogram be
reserved only for use when some question exists about the status of the arterial repair
(such as distal intimal tacking, obvious external stenosis, or difficult distal shunt place-
ment) (249). This position has been challenged by Blaisdell (243), who routinely uses
arteriography and has not encountered a subintimal injection problem. At present,
intraoperative completion arteriography seems to enjoy favor among surgeons familiar
with the technique, but is not the standard of care.
A potential application of intraoperative angiography has been suggested in cases
where patients awaken with a new neurological deficit. The patient is returned to the
operating room, the wound is opened, and a hand injection of contrast media is per-
formed while taking a single cervical x-ray. Gross technical errors or thrombosis can be
identified by this technique without the need for reopening the vessel or the delay of
proceeding to the angiographic suite.

Intraoperative Doppler Scanning. Informal use of sterilized Doppler probes applied to

all vessels in the arteriotomy tree is commonly employed as a qualitative measure of
postarteriotomy patency. I have used this method to demonstrate audible patency fol-
lowing carotid reconstruction, and like others (250) have used the Doppler to auscultate
flow through an indwelling shunt. Formal Doppler or duplex scanning intraoperatively
is also used. One study of Doppler spectrum analysis in 45 carotids imaged both pre-
and postendarterectomy was useful in detecting technical errors and in predicting the
need for intraoperative arteriography (251). In two others, intraoperative Doppler
analysis demonstrated ICA defects in 4.3% to 4.5% of arteries and ECA abnormalities in
8.7% to 9% (187,252).

Functional Evaluations

EEG Monitoring. Intraoperative assessment of the EEG has withstood the test of time
as a popular, readily available, and reliable method for determining cross-clamp
dependent ischemia and the need for indwelling shunt. While early investigators
merely correlated EEG changes observed at surgery (in non-shunted patients) with
postoperative neurological deficits (253), EEG monitoring rapidly gained favor and was
shown by several groups to correlate well with the need for shunting in both awake
(254) and anesthetized (217,250,255–257) patients. The number of patients who show
EEG changes during carotid clamping has varied according to different series: being as
low as 8.5% (257) or as high as 31% (253). In my own series, 15% of patients have EEG
changes and shunt placement. This increases to 25% if contralateral carotid occlusion is
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 25

present (9,163–166). The ability of angiographic findings to predict intraoperative EEG

changes has been low (258,259), and even patients with contralateral carotid occlusion,
although appearing to require shunts more often than routine cases, have shown EEG
changes in only 17% and 42%, respectively, in two series (115,116).
The EEG changes associated with intraoperative ischemia have been well docu-
mented, and consist most often of generalized slowing and decreased amplitude in the
ischemic hemisphere (217,253,256,260). Chiappa has proposed that attenuation of anes-
thetic-induced fast rhythms may be more significant than ipsilateral slowing of the EEG
and recommends that the electroencephalograph sensitivity be sufficient to monitor
this fast activity (261). Trojaborg and Boysen (217) also measured simultaneously the
intraoperative EEG and ipsilateral rCBF. They showed that EEG slowing correlated
with rCBF values of 16 to 22 mL/100 g/min (227), whereas flattening of the EEG
occurred with values of 11 to 19 cc/100 g/min. Several groups have documented EEG
changes developing with intraoperative hypotension and have stressed avoidance of
this complication (255,257).
Despite the inclination of many surgeons to shunt patients who have so-called
moderate EEG changes as defined by Blume et al. (262), it should be recognized that
there are investigators who do not share this viewpoint. Blume et al. studied 176 con-
secutive patients undergoing CEA without shunt. Nineteen percent of their patients
had moderate EEG changes and 22 had “major EEG changes.” Despite their lack of
shunt use, there were no postoperative strokes in either the EEG unchanged or EEG
moderately changed groups. Nine percent of patients with major clamp-associated EEG
changes did develop postoperative strokes in their study.
Computerized EEG processing techniques have been developed to quantitate the
information the EEG contains and display it in a format readily accessible to the surgi-
cal and anesthetic teams, eliminating the necessary presence in the operating room of
personnel trained in electroencephalographic interpretation. Such displays typically
provide trend analysis and provide rapid evaluation of the EEG under intraoperative
conditions. Most computerized EEG analysis techniques convert the EEG from the time
domain to the frequency domain. In the conversion process, amplitude, measured in
voltage, is changed to a derivative of voltage—power. Compressed spectral array (CSA)
and density-modulated spectral array (DSA) are two ways of displaying this power
spectrum analysis. Several parameters have been derived to simplify the description
and interpretation of these complex displays of frequency and power data. The three
most commonly used are the median power frequency (MPF), the frequency at the
median of the power spectrum; the peak power frequency (PPF), the frequency com-
prising the largest single component of the power spectrum; and the spectral edge fre-
quency (SF) the highest frequency in the power spectrum in which there is activity.
These systems are attractive, appear to yield good results, and will certainly undergo
continuing refinement (261,263–267).

SSEP Monitoring. Considerable interest has been generated in the use of median nerve
generated SSEP as predictors of cerebral ischemia, reflected both as the need for intra-
operative shunting or as a predictor of poor neurologic postoperative outcome. Several
important questions exist regarding SSEP monitoring during CEA. These include the
criteria to be used for SSEP prediction of neurologic events, questions regarding
the false positive and false negative rate of the technique, and finally whether the tech-
nique is sufficient to supersede the more standard electrophysiologic technique of
online EEG discussed previously.
SSEP criteria for cross-clamp cerebral ischemia include either prolongation of the
central conduction time (latency) or reduction in amplitude of the SSEP. Most authors
have used 50% amplitude reduction of the N20-P25 SSEP as their criterion for specifying
significant cerebral ischemia (200,268–276). Others have used a bimodal technique
whereby either a prolongation of central conduction time or a decreased SSEP amplitude
DK3434_Loftus_Ch01 8/21/06 1:07 PM Page 26

26 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

represent event criteria (277). No matter which criteria are used to determine the need
for shunting, however, it is clear that complete loss of amplitude, i.e., flat SSEP is associ-
ated with a profound postoperative neurological deficit in 100% of cases where
responses do not return with or without shunting (268,269,278). The entire subject of
SSEP monitoring during carotid surgery has been well reviewed by Markand (260).
The literature varies widely regarding the rates of false positive and false negative
results with the use of the SSEP technique. Several authors report a false positive rate
of zero when SSEP flattening is the criterion (i.e., as mentioned, all patients with irre-
versible SSEP loss had a neurologic deficit) (269–272,279), whereas at 50% amplitude
decrease level, Lam et al. reported many false positives (275). False positives exist with
many monitoring techniques, however, and are not unique to SSEP recording. The more
serious question of whether or not false negatives exist is also debated. Although
Amantini et al. (268,269) reported no false negatives (i.e., no cases in which neurologi-
cal deficit ensued with normal SSEP tracings throughout), some false negative out-
comes (admittedly rare) have been reported by others including De Vleeschauwer (270)
in 3/177 cases, Horsch (272) in 4/586 cases, and Haupt (271) in 1/994 cases. Two recent
articles elucidate best the current level of the debate regarding SSEP monitoring during
CEA. The study of Tiberio et al. (276) included 264 surgical procedures with criteria for
shunt insertion being central conduction time prolongation greater than 1 msec and/or
N20-P25 amplitude decrease of at least 50%. Eighty-nine percent of cases had normal
SSEP and 11% had abnormal SSEP. A shunt was used in 9% of cases and no patient had
a permanent neurological deficit. These authors argue strongly that SSEP is a highly
reliable predictor of the need for shunting and use it as their primary monitoring tech-
nique. In direct contradistinction to this is the recent article by Kearse et al. (274), who
monitored simultaneously the EEG and SSEP in 53 CEAs. Rather than using neurolog-
ical outcome as an endpoint, their SSEP criteria were measured against EEG as a “gold
standard,” and in their 23 patients with EEG evidence of ischemia following cross-
clamping, 10 had prolongation of the central conduction time but only one had an
amplitude decrease of 50% or greater. It was their strong conclusion that SSEP was not
sufficiently sensitive to reliably identify compromised cerebral perfusion that was read-
ily discernible by EEG in these cases (274).
We should finally mention one interesting case report by Gautier et al. in which
online monitoring of SSEP showed a loss of amplitude during head positioning in
preparation for CEA (280). In this case, SSEP disappeared eight minutes following head
positioning consisting of neck extension and rotation of the head to the right. Return of
the head to a neutral position resulted in a normalization of SSEP and the surgical pro-
cedure was then completed uneventfully.

NIRS Measurement. The latest monitoring technique introduced is continuous moni-

toring of cerebral hemoglobin oxygen saturation by NIRS techniques (281,282). This
technique uses a simple probe applied to the forehead to measure oxyhemoglobin (oxy-
Hb), deoxyhemoglobin (deoxy-Hb), and total hemoglobin continuously, with special
attention paid to changes in their ratio during cross-clamping, clamp release, and with
or without shunt insertion. Kirkpatrick et al. (281) reported good correlation between
increased deoxy-Hb, decreased oxy-Hb, and a rapid fall in MCAV by simultaneous
TCD measurement at the time of cross-clamping (281). Kuroda et al. (282) correlated
NIRS with rCBF [by single photon emission computed tomography (SPECT)] and with
SSEP measurements. They describe two classes of patients; in the first, initial decrease
in oxy-Hb/increase in deoxy-Hb corrects rapidly and spontaneously in the first few
minutes after cross-clamping, these patients do not show SSEP or rCBF changes. In the
second group, the NIRS changes are more rapid and sustained following clamping, and
are associated with profound decreases in rCBF and loss of N20 amplitude on SSEP; in
this group the changes do not reverse until an indwelling shunt is placed (282). Clearly,
the technique of NIRS measurement to determine the need for shunt placement holds
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 27

promise, but further validation studies will need to be performed before it is widely
available or accepted. Kirkpatrick has discussed NIRS and its potential weaknesses in
great detail (281,283,284).

Intraoperative Shunting
The necessity for indwelling arterial shunt during CEA is one of the most widely
debated and long-standing controversies in neurovascular surgery. Carotid surgeons
generally group themselves into three; those who use shunts in every case, those who
employ shunting when indicated by some form of intraoperative monitoring, and those
who never shunt no matter what the clinical or monitoring situation. My personal pref-
erence is to use a custom shunt of my own design (285) (Loftus shunt, Integra
Neuroscience, Plainsboro, NJ), which is secured in the ICA with a special encircling
type clamp (Loftus shunt clamp, Scanlan Medical Instruments, St. Paul, MN). Aufiero
et al. (286) have discussed the performance characteristics associated with different
shunt choices in detail (286).
Monitoring is most critical for surgeons who practice selective (monitoring-
dependent) shunt placement, as I do. For those who have chosen to shunt every case,
or for those who never place a shunt, intraoperative monitoring, while interesting, will
not customarily affect treatment decisions, and may not be used at all. Likewise, sur-
geons who prefer shunting may practice in settings where monitoring is not available,
and may thus choose universal shunting to afford maximum theoretical protection
against cross-clamp ischemia.
Proponents of universal shunting argue that their technique is benign, assures
the maximum degree of cerebral protection in every case, and eliminates depend-
ence on specialized intraoperative monitoring techniques (120,287–291). They
emphasize the relaxed surgical environment afforded by shunt flow and feel that
extra time can be taken to ensure meticulous attention to the intimal dissection and
arteriotomy repair. Some also point out the value of the shunt tubing as a stent to aid
arterial closure (287).
Those who argue against routine intraluminal shunting do so on several
grounds. They feel strongly that shunt placement is not nearly so benign, and carries
with it the risks of distal particulate embolization. In one series, the stroke incidence
in shunted cases was actually far higher than in a nonshunted control series (229).
Occult shunt malfunction, whether from thrombosis, distal clamping, or distal abut-
ment against the internal carotid wall, has been mentioned by several authors and
may be more common than generally realized (182,184,292), and with few exceptions
(292) there are currently no effective direct means available to monitor shunt flow.
The possibility of distal intimal damage from the shunt end leading to embolization
or carotid dissection is also present (293). Because of these risks, numerous nonshunt-
ing series have been accumulated and published. Gross et al. (294) successfully sub-
stituted barbiturate-induced burst suppression for shunt placement in cases where
EEG changes did not respond to hypertensive therapy, but this method has not been
accepted widely (294). Spetzler has likewise reported excellent nonshunted results
with a strategy of intraoperative barbiturates and microsurgical technique (295).
Several large series have been presented where good surgical results are obtained
without shunt placement under any circumstances (117,296–303). These authors do
not deny the existence of postoperative stroke, but they feel strongly that neurologic
deficits from carotid surgery are invariably embolic rather than hemodynamic in
nature, and that intraoperative monitoring and/or shunt placement will not further
reduce the already low morbidity in their series (298). Ferguson (301), who has been
perhaps the foremost advocate of nonshunting, has indicated that he does feel shunt-
ing may be of value in a very small percentage of cases with “severe” EEG changes
and stump pressures of 25 mmHg or less.
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28 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

Nearly all authors, even those who shunt routinely, agree that shunts are probably
not required in the majority of carotid procedures (304). The merits and wisdom of selec-
tive shunting based on intraoperative monitoring criteria, and the impressive results with
this technique in a large series of patients, have been well documented by Sundt (214,216).
It should finally be noted that a number of authors who customarily advocate selec-
tive shunting have found intraoperative monitoring to be unreliable in patients having had
recent reversible ischemic neurologic deficit (RIND) or stroke. These groups recommend
empirical shunt placement in all such cases (98,99,305). On the contrary, Green et al. (306)
reviewed their series of selective shunting, and felt that the benefit of EEG monitoring was
in protecting the patient from the risky insertion of a shunt. They argued that there was no
benefit from selective shunting (over nonshunting) unless the patient had sustained a
recent stroke prior to surgery (306).

Is the Shunt Needed?

It should be clear that shunt use is an individual surgeon’s choice. The need for intra-
operative shunting, as discussed more extensively above and as described by published
monitoring techniques, can be summarized as follows:
■ Awake: deficit within 60 seconds
■ Stump: carotid stump back pressure <50 mmHg
■ CPP: stump-IJP <18 mmHg
■ rCBF: 18–20 mL/100 g/min
■ TCD: MCAV 0% to 15% preclamp
■ EEG: unilateral attenuation 8–15 Hz fast or 2 increase l Hz delta
■ SSEP: 50% amplitude decrease or 5% to 20% latency increase in central conduction time
■ NIRS: rapid increase in deoxy-Hb, decrease in oxy-Hb, without return.

Insertion of the Shunt

The technique for insertion of an indwelling shunt varies among surgeons and is based on the
type of shunt used. The basic principles I use to place a shunt can be summarized as follows:
■ Total exposure above plaque
■ Shunt in CCA first
■ Evacuation of shunt
■ Gentle ICA insertion
– Backbleeding allowed
– Shunt open to distend ICA lumen
■ Doppler of shunt to auscultate flow
■ Monitoring must return

These techniques are discussed and illustrated in detail in the second section (see
Fig. 3-43 to 3-52).

Is the Shunt Working?

Similarly, the shunt, once placed, needs to carry blood and ensure cerebral perfusion.
This can be ascertained in several ways, depending on the monitoring technique cho-
sen by the surgeon, as follows:
■ Functional evaluations—recovery of EEG, SSEP, or NIRS
■ Vascular evaluations—return of MCAV by TCD, return of rCBF, Doppler
auscultation of shunt.

MCAV and TCD criteria with specific shunt types have been elegantly addressed by Hayes
et al. (307), who feel that performance is optimized by the Pruitt–Inahara design (307).
Whether a complete return of MCAV to baseline during shunting is needed is less clear.
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 29

Arteriotomy Techniques

Some areas of controversy exist concerning technical performance of the carotid arterial
repair. Objective data on these subjects is scarce owing to the difficulty of attributing
success or failure in large series of patients to skill variance among surgeons. A few top-
ics, however, are worthy of mention.

Patch Grafting
Most surgeons favor patch grafting the internal carotid repair in cases of recurrent
stenosis, and many employ patch grafts selectively in a primary repair where the inter-
nal carotid lumen has been sufficiently narrowed to cause concern about postoperative
stenosis and possible thrombosis. The routine use of patch grafts has been advocated
by Little et al., who present data that show a statistically significant decrease in post-
operative occlusion between grafted and nongrafted groups (308). Since the first edi-
tion of this book was published, several new studies provide further compelling
evidence for the superiority of primary patch graft angioplasty versus simple primary
closure. This evidence includes individual case series from experienced surgeons such
as Archie, who reports a statistically significant decrease in restenosis/reoperation
when patch grafting is used (309), multivariate analysis of multistate Medicare out-
come data, in which patch grafting, intraoperative Heparin, and perioperative aspirin
produced statistically better outcomes (310), and at least one randomized clinical trial,
in which patch closure was less likely to cause ipsilateral stroke, TIAs, or recurrent
carotid stenosis (311,312).
The choice of material, whether venous or synthetic, appears to be of little conse-
quence. Yamamoto et al. felt strongly that synthetic materials were superior to sapenous
vein because of the fear of aneurysm formation and central vein patch rupture (313).
Several other studies have shown no effective difference between synthetic and vein
patch in postoperative stroke rate; admittedly these studies did not address the ques-
tion of central patch rupture (312,314,315). One recent randomized trial does appear to
show an advantage in prevention of perioperative stroke, carotid thrombosis, and early
restenosis when polytetraflouroethylene (PTFE) patches are used instead of collagen-
impregnated Dacron (Hemashield); one offsetting disadvantage is the longer time to
hemostasis needed for PTFE (316).
Although I previously reserved patch grafting for reoperative carotids, I have now
adopted a policy of universal roof patch angioplasty with the Hemashield graft. Since
adoption of this policy about eight years ago, and with routine postoperative interval
duplex scanning, my incidence of significant (amenable to surgery) recurrent stenosis
under observation has dropped to almost nothing.

Tacking Sutures
The use of tandem sutures to secure the distal intima in the internal carotid has been
deemed unnecessary by some (289,299,317) yet has been cited by others as one of the
major technical improvements in reducing carotid surgical morbidity (288). Although
such sutures have the potential to narrow the internal carotid lumen, this risk seems low
in comparison to the possibility of intimal dissection if a loose flap is left behind.
Patterson (120) and Ferguson (299), among others, point out that tacking sutures become
unnecessary if the ICA is carried far enough to visualize normal intima distal to the
plaque. These arguments are reasonable; however, experienced carotid surgeons agree,
even with excellent ICA exposure, that in some cases a clean distal endpoint cannot be
achieved, and if there is any question of potential subintimal dissection, I place distal
tacking sutures (in approximately 10% of cases), usually at the 4- and 8 O’clock positions.
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30 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

Heparinization
Intravenous heparin is routinely administered at some point prior to arterial cross-
clamping and repair. The dose, which may vary from 2500 to 10,000 units, is a matter of
individual preference. One group has suggested a weight-based dosing schedule of
85 mg/kg with good results (318). Many surgeons (317) reverse the intraoperative anti-
coagulation with protamine at the conclusion of surgery, and Chandler has shown that
reversal of this heparinization does not produce increased carotid thrombogenicity in
dog carotids (319). Others, including myself, do not reverse the anticoagulation.
There is no evidence that this single dose of anticoagulant contributes to intraop-
erative or postoperative bleeding any more than the preoperative antiplatelet or antico-
agulant agents most carotid patients receive, and there is compelling evidence that
protamine use increases the stroke rate (320). Indeed, Gross et al. (294) validated a com-
mon practice when they reported a series of patients with threatened stroke in whom
endarterectomy was performed under full systemic anticoagulation; no untoward
problems with the arterial repair were encountered (294). I do not hesitate to operate
with full heparinization throughout the procedure in patients with crescendo TIAs.
For several years, we have adopted a policy of checking intraoperative ACT dur-
ing anesthesia induction in patients who are heparinized preoperatively. Almost invari-
ably the anticoagulation is subtherapeutic and an additional tailored bolus dose is
required at cross-clamping time.

SURGICAL TECHNIQUE OF CERVICAL

CAROTID RECONSTRUCTION

Only surgeons with excellent perioperative morbidity and mortality results can offer
carotid patients an outcome superior to the best available medical management. In this
section, a technical scheme for CEA is presented that has yielded a combined morbid-
ity and mortality of 2% (inclusive of patients in all risk grades including recent stroke)
in my hands, and which allows me to confidently recommend carotid surgery to appro-
priate patients. I fully recognize that different techniques have proven successful for
individual surgeons, and eschew a dogmatic approach to carotid surgery. It has proven
valuable in my practice, however, to perform all carotid surgery with a uniform techni-
cal approach, thereby avoiding oversights or the necessity of hurried intraoperative
decisions, and I present here an overview of the methods I have found most useful.
Refer to part 3 for an illustrated, step-by-step description of the technique.

Indications

I have summarized earlier the data from the major randomized carotid indications tri-
als. My policy regarding indications for surgery is to follow the recommendations of the
large randomized cooperative trials and of the most recent AHA Guidelines (32). I pro-
pose surgery for all asymptomatic patients with linear stenosis of
60%, since this was
the group that was shown to benefit from surgery in the ACAS trial (10). The benefit is
not as great for women, and the benefit depends on the ability to perform surgery with
a combined morbidity/mortality of less than 3%. Patients need to have an expected sur-
vival of five years following surgery to benefit from CEA if they are asymptomatic; for
this reason patients with malignancies or other life-threatening conditions should not
be offered surgery.
Patients with symptomatic carotid stenosis, whether evident as TIA or stroke,
benefit from surgery if their arteriogram shows
50% linear stenosis as measured by
the NASCET method (69,70) (see below). This benefit is greatest in men who are non-
diabetic (diabetes clearly increases the surgical risk). According to several carotid
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CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION 31

trials (69,71,74), the benefit is realized immediately, so there should be no delay in

operating on such patients. The benefit of surgery is also greatest in patients who
have hemispheric symptoms instead of amaurosis fugax, and patients with plaque
ulceration are at higher risk than those with smooth plaques (Fig. 1). We offer sur-
gery to nearly all patients with symptoms and
50% linear stenosis.
It is still unclear what treatment is best for ulcerated plaques (which intuitively
would seem more dangerous) of less than 50% and for recurrent stenosis, whether
symptomatic or asymptomatic. We sometimes offer surgery for deep ulcers of less
than 50% stenosis, especially if they have hemispheric symptoms. We offer surgery
for recurrent stenosis when symptoms are present, and also for patients who rapidly
progress to high-grade stenosis while being followed with serial noninvasive stud-
ies. The risk of surgery is of course higher in cases of recurrent stenosis, and the
patient must be informed of this. In the current era, an endovascular approach
should also be considered for recurrent disease, although the results are unproven.

Preoperative Studies and Preparation

Patients with acute ischemic strokes or TIAs undergoing workup for their stroke
etiology should have bilateral carotid duplex studies or MRA. Asymptomatic patients
who on clinical evaluation are noted to have a carotid bruit or significant atherosclerotic
disease should undergo similar testing. The population of patients with a documented
lesion in either study should proceed to a tailored arteriogram (arch and both carotids,
cervical and cranial), which at our institution still remains the gold standard for preop-
erative evaluation for CEA. The stenosis is defined from the NASCET criteria, where
N is the linear diameter at the area of greatest narrowing, and D is the greatest diame-
ter of the normal artery distal to the carotid bulb.

Percent (%) stenosis  (1  N/D)  100

Preoperative evaluation also involves aggressive workup of any patients with car-
diac symptoms before CEA is performed.
Patients taking aspirin preoperatively are instructed to continue their therapy with-
out interruption. Patients taking clopidrogel (Plavix®) or ticlopidine (Ticlid®) are switched
to a daily aspirin one week before surgery (this strategy markedly reduces intraoperative
oozing associated with these drugs). Patients on warfarin anticoagulation therapy for
artificial heart valves, TIAs, and other indications (crescendo TIAs or critical stenosis)
should be preoperatively admitted to the hospital and have their iatrogenic coagulopathy
converted to IV heparin therapy. The heparin should be continued to the operating room
and is stopped when the arterial closure is complete. As mentioned, some patients require
postoperative heparin infusion for mechanical cardiac valves; these patients should be
considered high-risk patients. We do not use protamine for reversal of anticoagulation.

Surgical Technique

In my opinion, there are several cardinal principles for carotid reconstruction

■ Complete knowledge of the patient’s vascular anatomy.
■ Complete vascular control at all times.
■ Anatomical knowledge to prevent harm to adjacent structures.
■ Assurance of a widely patent repair free of technical errors.

It is our feeling that the meticulous anatomical dissection and identification of

vital cervical structures needed to minimize postoperative complications can be
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32 CHAPTER 1: HISTORICAL PERSPECTIVE ON CAROTID RECONSTRUCTION

achieved only with a bloodless field. Accordingly, we do not consider elapsed time to
be a factor in the performance of carotid surgery. On our service, CEA requires from two
to two-and-a-half hours of operating time and the average cross-clamp time is between
30 and 40 minutes. No untoward effects from the length of the procedure have been
observed in any patients and we are convinced that the risk of cervical nerve injury or
postoperative complications related to hurried closure of the suture line are signifi-
cantly reduced by meticulous attention to detail.
The author has developed a complete set of custom carotid instruments (see
Fig. 3-1) (Scanlan Instruments, St. Paul, MN), which we use in every case. The improve-
ments in this set include two sizes of well-balanced vascular pickups, special dissecting
scissors for coarse and fine work, and specialized cross-clamps, shunt clamps, and nee-
dle drivers. Microring-tip forceps are included as well to clean small fragments from the
artery prior to repair. The beauty of a single set that includes everything needed for the
operation cannot be overstated.
Two surgeons trained in the procedure are always present during carotid surgery.
Both surgeons may stand on the operative side, the primary surgeon facing cephalad
and the assistant facing the patient’s feet (this is our preference), or the surgeons may
stand on either side of the table. The operative nurse may stand either behind or across
the table (in our setup) from the primary surgeon. The patient is positioned supine
on the operating room table with the head extended and turned away from the side of
operation. Several folded pillowcases are placed between the shoulder blades to facili-
tate extension of the neck and the degree of rotation of the head is determined by the
relationship of the external and ICA on preoperative angiography. The carotid vessels
are customarily superimposed in the antero-posterior plane, and moderate rotation of
the head will swing the internal carotid laterally into a more surgically accessible posi-
tion. In those patients where the internal carotid can be seen angiographically to be lat-
erally placed, the head rotation need not be that great. On the other hand, occasional
patients will demonstrate an internal carotid that is rotated medially under the external
carotid, and in such cases no degree of head rotation will yield a satisfactory exposure.
In these cases, the surgeon must be prepared to mobilize the external carotid more
extensively and swing it medially to expose the underlying internal carotid (even tack-
ing it up to medial soft tissues if necessary) (see Figs. 3-4 and 3-26).
The position of the carotid bifurcation has been likewise determined before sur-
gery from the angiogram and the skin incision is planned accordingly. We always use a
vertical type linear incision along the anterior portion of the sternomastoid muscle. This
may go as low as the suprasternal notch and as high as the retro-aural region depend-
ing on the level of the bifurcation. The skin and subcutaneous tissues are divided
sharply to the level of the platysma, which is always identified and divided sharply as
well. Hemostasis often requires generous use of electrocautery. Self-retaining retractors
are then placed and the underlying fat is dissected to identify the anterior edge of the
sternocleidomastoid muscle. Retractors are left superficial at all times on the medial
side to prevent retraction injury to the laryngeal nerves, but laterally may be more
deeply placed. Dissection proceeds in the midportion of the wound down the ster-
nomastoid muscle until the jugular vein is identified. Care must be taken under the
sternomastoid muscle, however, to prevent injury to the spinal accessory nerve, which
can be inadvertently transected or stretched.
We emphasize that the jugular vein is the key landmark in this exposure and com-
plete dissection of the medial jugular border should always be carried out before proceed-
ing to the deeper structures. [A fascinating retrojugular approach to the carotid has been
described; I personally have not tried this technique (321).] In some corpulent individu-
als, the vein is not readily apparent and a layer of fat between it and the sternomastoid
must be entered to locate the jugular itself. If this is not done, it is possible to fall into an
incorrect plane lateral and deep to the jugular vein. As soon as the jugular is identified,
dissection is shifted to come along the medial jugular border (antejugular approach) and
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Fin du Tome second.

 TABLE
DES CHAPITRES
Contenus dans ce Volume.

Chapitre premier. Le Docteur Slop va aussi son petit train. Page

1
Chap. II. Il faut y veiller. 4
Chap. III. Le chagrin rend injuste. 8
Chap. IV. Il sait enfin où elle est. 9
Chap. V. Je n'en sais rien. 14
Chap. VI. Cela est vrai. 16
Chap. VII. Mon père pourroit bien avoir raison. 17
Chap. VIII. Ce seroit le goût de bien des Dames. 19
Chap. IX. Les plus grands exemples ne persuadent pas
toujours. 20
Chap. X. Eh bien! on attendra. 23
Chap. XI. Le Docteur Slop n'y est plus. 25
Chap. XII. Cela seroit à souhaiter. 28
Chap. XIII. Réflexions fort sensées. 29
Chap. XIV. Un rien nous déconcerte. 31
Chap. XV. Monsieur un tel et tant d'autres n'agissent pas de
même. 32
Chap. XVI. Le pauvre bonhomme! 35
Chap. XVII. Mon oncle Tobie argumente à sa mode. 37
Chap. XVIII. La précaution. 39
Chap. XIX. Hélas! il n'est plus temps. 41
Chap. XX. Ce qui fixe nos idées. 44
Chap. XXI. Grand événement. 45
Chap. XXII. Consolation. 48
Chap. XXIII. L'Excommunication. 53
Chap. XXIV. Il en manque encore. 64
Chap. XXV. Fin de l'excommunication. 67
Chap. XXVI. Ma manière de voir. 68
Chap. XXVII. Elle est renversée. 74
Chap. XXVIII. Oh! ma Mère! 76
Chap. XXIX. Dissertation sur l'éloquence. 78
Chap. XXX. Le Docteur Slop manque son coup. 79
Chap. XXXI. Rien. 81
Chap. XXXII. L'effet en est ostensible. ibid.
Chap. XXXIII. L'Enigme. 83
Chap. XXXIV. Ni moi non plus. 85
Chap. XXXV. Mes offres. ibid.
Chap. XXXVI. Le chapitre trente-quatre continue. 86
Chap. XXXVII. Quel dommage! 90
Chap. XXXVIII. Ils vont donc m'abandonner! 91
Chap. XXXIX. Préface de l'Auteur. 93
Chap. XL. Je rentrerai bientôt dans la carrière. 110
Chap. XLI. M'y voilà. 112
Chap. XLII. Emportement de mon Père. 112
Chap. XLIII. L'Invocation inutile. 116
Chap. XLIV. Le Prélude. 119
Chap. XLV. Le Type. 120
Chap. XLVI. La Promenade nocturne. 122
Chap. XLVII. Je m'égare. 127
Chap. XLVIII. Ce qu'on devroit faire quand on n'est pas
instruit. 129
Chap. XLIX. Je vais bientôt naître. 133
Chap. L. Je suis né. 134
Chap. LI. Mon propre désespoir. 135
Chap. LII. On parle bien souvent sans en dire autant. 136
Chap. LIII. Ad libitum. 138
Chap. LIV. Les prétentions de ma bisaïeule. 139
Chap. LV. La définition. 141
Chap. LVI. Suite du chapitre cinquante-quatre. 144
Chap. LVII. Hélas! 145
Chap. LVIII. Ce que c'est que la propriété. 149
Chap. LIX. On n'est pas toujours en faveur. 153
Chap. LX. Prenez-y garde. 155
Chap. LXI. Mon père se brouille avec Erasme. 156
Chap. LXII. Il se console avec Slawkembergius. 158
Chap. LXIII. La prise de Strasbourg, conte. 163
Chap. LXIV. Le Chef-d'œuvre. 196
Chap. LXV. Si j'avois le pinceau de Greuze! 198
Chap. LXVI. La Rechute inopinée. 199
Chap. LXVII. Générosité de mon oncle. 200
Chap. LXVIII. Pourquoi pas? 202
Chap. LXIX. Préparatifs de mon Père. 203
Chap. LXX. Cela ne réussit pas bien. 204
Chap. LXXI. Encore moins. 206
Chap. LXXII. Mon chapitre des hasards. 207
Chap. LXXIII. Mon chapitre des chapitres. 209
Chap. LXXIV. L'Art de marcher. 212
Chap. LXXV. La double entente. 216
Chap. LXXVI. L'utilité des journaux. 217
Chap. LXXVII. Les quatre événemens. 221
Chap. LXXVIII. La leçon. ibid.
Chap. LXXIX. J'obtiens enfin un nom dans le monde. 223
Chap. LXXX. Je vous mets à mieux faire. 224
Chap. LXXXI. Question facile à résoudre. 225
Chap. LXXXII. Où va-t-il aller? 227
Chap. LXXXIII. Avis aux médecins. 229
Chap. LXXXIV. Assaut de valeur. 232
Chap. LXXXV. Préliminaires effrayans. 235
Chap. LXXXVI. Déploration de mon Père. 236
Chap. LXXXVII. Ma manière d'agir. 241
Chap. LXXXVIII. On se résout à partir. 243
Chap. LXXXIX. La lacune. 245
Chap. XC. La lacune justifiée. 246
Chap. XCI. L'humeur s'en mêle. 250
Chap. XCII. Les fausses conjectures. 253
Chap. XCIII. La précaution utile. 258
Chap. XCIV. Mes lamentations. ibid.
Chap. XCV. A quoi l'attribuer? 259
Chap. XCVI. Extrême inquiétude. 262
Chap. XCVII. On sait enfin ce que c'est. 265
Chap. XCVIII. Qu'en va-t-il faire? ibid.
Chap. XCIX. Nouvelles conjectures. 266
Chap. C. Remède pour la brûlure. 268
Chap. CI. Dialogue. 273
Chap. CII. Solution. 277

Fin de la Table du Tome second.

 Note du transcripteur.
On a conservé l'orthographe de l'original, avec ses
incohérences (par ex. Makai/Makay, vuides/vides,
abîme/abyme, etc.). Les erreurs clairement introduites par
le typographe ont été corrigées.
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