Haimovici's Vascular Surgery

Haimovici’s

Vascular Surgery 5th edition

As I assume chief editorship with this edition of Haimovici’s Vascular Surgery, I would like to take this opportunity to recognize my parents, Samuel and Emilia, for their guidance and support throughout my life. Enrico Ascher

Haimovici’s

Vascular Surgery FIFTH EDITION

Editor-in-Chief Enrico Ascher Associate Editors L. H. Hollier D. Eugene Strandness Jonathan B. Towne Co-editors Keith Calligaro K. Craig Kent Gregory L. Moneta William H. Pearce John J. Ricotta Founding Editor Henry Haimovici

Blackwell Publishing

© 2004 by Blackwell Science a Blackwell Publishing company Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5018, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia All rights reserved. No part of this publication may be reproduced in any form or by any electronic or mechanical means, including information storage and retrieval systems, without permission in writing from the publisher, except by a reviewer who may quote brief passages in a review. 05 06 07 08 5 4 3 2 ISBN-13: 978-0-632-04458-0 ISBN-10: 0-632-04458-6 Library of Congress Cataloging-in-Publication Data Haimovici’s vascular surgery. — 5th ed. / editor-in-chief, Enrico Ascher ; associate editors, L.H. Hollier, D. Eugene Strandness, Jr., Jonathan B. Towne ; co-editors, Keith Calligaro . . . [et al.] ; founding editor, Henry Haimovici. p. ; cm. Includes index. ISBN 0-632-04458-6 (hardcover) 1. Blood-vessels — Surgery. [DNLM: 1. Vascular Surgical Procedures. WG 170 H151 2004] I. Title: Vascular surgery. II. Ascher, Enrico. III. Haimovici, Henry, 1907– RD598.5.V39 2004 617.4’13 — dc21 2003011854 A catalogue record for this title is available from the British Library Acquisitions: Laura DeYoung Development: Julia Casson Production: Julie Elliott and Debra Lally Cover design: Hannus Design Associates Typesetter: SNP Best-set Typesetter Ltd., Hong Kong Printed and bound by Sheridan Books in Ann Arbor, MI For further information on Blackwell Publishing, visit our website: www.blackwellmedicine.com Notice: The indications and dosages of all drugs in this book have been recommended in the medical literature and conform to the practices of the general community. The medications described do not necessarily have specific approval by the Food and Drug Administration for use in the diseases and dosages for which they are recommended. The package insert for each drug should be consulted for use and dosage as approved by the FDA. Because standards for usage change, it is advisable to keep abreast of revised recommendations, particularly those concerning new drugs. The publisher’s policy is to use permanent paper from mills that operate a sustainable forestry policy, and which has been manufactured from pulp processed using acid-free and elementary chlorine-free practices. Furthermore, the publisher ensures that the text paper and cover board used have met acceptable environmental accreditation standards.

CONTENTS

Preface

x

PART II

Acknowledgments

xi

Basic Cardiovascular Problems

Editors

xii

Contributors

xiii

Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment,

1

Frank J. Veith and Enrico Ascher

CHAPTER 9 Artherosclerosis: Biological and Surgical Considerations, Bauer E. Sumpio

PART I

CHAPTER 10

Imaging Techniques

Intimal Hyperplasia,

Christopher K. Zarins, Chengpei Xu, Hisham S. Bassiouny, and Seymour Glagov

CHAPTER 2 Ultrasonic Duplex Scanning,

117

David S. Sumner

CHAPTER 1 A Tribute to Henry Haimovici,

CHAPTER 8

7

D. Eugene Strandness, Jr

137

164

CHAPTER 11 Therapeutic Angiogenesis,

K. Craig Kent

176

CHAPTER 3 Duplex Arteriography for Lower Extremity Revascularization, Enrico Ascher and

35

Thrombogenesis and Thrombolysis,

CHAPTER 4

CHAPTER 13 50

Rodney A. White

196

CHAPTER 14 61

Harvey L. Neiman and James Lyons

Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures,

206

John D. Bisognano, Thomas W. Wakefield, and James C. Stanley

CHAPTER 6 Computed Tomography in Vascular Disease, Frederick L. Hoff, Kyle Mueller, and

Etiology of Abdominal Aortic Aneurysm, Ahmad F. Bhatti, Tonya P. Jordan, and M. David Tilson

CHAPTER 5 Fundamentals of Angiography,

183

Donald Silver, Leila Mureebe, and Thomas A. Shuster

Anil Hingorani

Intravascular Ultrasound Imaging,

CHAPTER 12

87

William Pearce

PART III CHAPTER 7 Magnetic Resonance Angiography, Jagajan J. Karmacharya, Omaida C. Velazquez, Richard A. Baum, and Jeffrey P. Carpenter

103

Basic Vascular and Endovascular Techniques CHAPTER 15 Vascular Sutures and Anastomoses,

221

Henry Haimovici

v

vi

Contents

CHAPTER 16

CHAPTER 29

Patch Graft Angioplasty,

Henry Haimovici

231

Retroperitoneal Exposure of the Iliac Arteries, Henry Haimovici

237

CHAPTER 30

348

CHAPTER 17 Endarterectomy,

Henry Haimovici

The Lower Extremity,

CHAPTER 18 Balloon Angioplasty of Peripheral Arteries and Veins, Juan Ayerdi, Maurice M. Solis, and

Henry Haimovici

247

Kim J. Hodgson

PART V

CHAPTER 19

Occlusive Arterial Diseases

Stents for Peripheral Arteries and Veins,

257

Carber C. Huang and Samuel S. Ahn

CHAPTER 31

CHAPTER 20

Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury, Walter N. Durán,

Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis,

354

272

373

Peter J. Pappas, Mauricio P. Boric, and Robert W. Hobson, II

W. Todd Bohannon and Michael B. Silver, Jr.

CHAPTER 32

CHAPTER 21 Role of Angioplasty in Vascular Surgery,

285

Arnold Miller and Charles P. Panisyn

Arterial Embolism of the Extremities and Technique of Embolectomy, Henry Haimovici

388

CHAPTER 33 Fluoroscopically Assisted Thromboembolectomy, Evan C. Lipsitz,

PART IV

409

Frank J. Veith, and Takao Ohki

Surgical Exposure of Vessels

CHAPTER 34 CHAPTER 22 Exposure of the Carotid Artery,

301

Percutaneous Aspiration Thromboembolectomy, Rodney A. White

417

Henry Haimovici

CHAPTER 35

CHAPTER 23 The Vertebrobasilar System: Anatomy and Surgical Exposure, Ronald A. Kline and

304

Ramon Berguer

Asher Hirshberg and

421

Kenneth L. Mattox

CHAPTER 36

CHAPTER 24

Fasciotomy,

Extrathoracic Exposure for Distal Revascularization of Brachiocephalic Branches, Henry Haimovici

308

Calvin B. Ernst, Bruce H. Brennaman, and Henry Haimovici

Ankle and Foot Fasciotomy for Compartment Syndrome of the Foot,

Trans-sternal Exposure of the Great Vessels of the Aortic Arch, Calvin B. Ernst

315

CHAPTER 26 Henry Haimovici

322

CHAPTER 27 Transperitoneal Exposure of the Abdominal Aorta and Iliac Arteries, Henry Haimovici

334

447

Enrico Ascher and Elke Lorensen

PART VI Chronic Arterial Occlusions of the Lower Extremities CHAPTER 38

CHAPTER 28 Retroperitoneal Exposure of the Abdominal Aorta, Calvin B. Ernst

437

CHAPTER 37

CHAPTER 25

The Upper Extremity,

Vascular Trauma,

342

Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity, Henry Haimovici

453

Contents

CHAPTER 50

CHAPTER 39 Nonatherosclerotic Diseases of Small Arteries, Henry Haimovici and Yoshio Mishima

vii

475

Postoperative Surveillance,

Jonathan B. Towne

617

CHAPTER 51 CHAPTER 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases,

Extra-anatomic Bypasses, 499

Enrico Ascher and

David C. Brewster

CHAPTER 52

CHAPTER 41

Popliteal Entrapment and Chronic Compartment Syndrome: Unusual Causes for Claudication in Young Adults,

Percutaneous Interventions for AortoIliac Occlusive Disease, Edward B. Diethrich

522

CHAPTER 53 534

559

Benjamin B. Chang, Paul B. Kreienberg, Philip S.K. Paty, Sean P. Roddy, Kathleen J. Ozsvath, and Manish Mehta

Lumbar Sympathectomy: Conventional Technique, Henry Haimovici

651

CHAPTER 55 Laparoscopic Lumbar Sympathectomy,

CHAPTER 44

657

Armando Sardi and Larry H. Hollier 568

Frank J. Veith, Sushil K. Gupta, Evan C. Lipsitz, and Enrico Ascher

PART VII

CHAPTER 45 Bypasses to the Plantar Arteries and Other Branches of Tibial Arteries, Enrico Ascher and

644

CHAPTER 54

CHAPTER 43

Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage,

Infected Extracavitary Prosthetic Grafts, Sean V. Ryan, Keith D. Calligaro, and Matthew J. Dougherty

and Henry Haimovici

In Situ Vein Bypass by Standard Surgical Technique, Dhiraj M. Shah, R. Clement Darling, III,

637

William Turnipseed

CHAPTER 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment, Frank J. Veith

625

Frank J. Veith

582

William R. Yorkovich

Aortic and Peripheral Aneurysms CHAPTER 56 Thoracic Aortic Aneurysms,

Joseph S. Coselli

663

CHAPTER 46 Extended Techniques for Limb Salvage Using Free Flaps, David L. Feldman and L.

587

CHAPTER 57 Endovascular Repair of Thoracic Aortic Aneurysms and Dissections, Frank R. Arko

Scott Levin

687

and Christopher K. Zarins

CHAPTER 47 Extended Techniques for Limb Salvage Using Complementary Fistulas, Combined with Deep Vein Interposition, Enrico Ascher

592

Thoracoabdominal Aortic Aneurysms,

695

Nicholas J. Morrissey and Larry H. Hollier

CHAPTER 48 Extended Techniques for Limb Salvage Using Vein Cuffs and Patches, Robyn Macsata,

CHAPTER 58

CHAPTER 59 600

Abdominal Aortic Aneurysm,

Alfio Carroccio

703

and Larry H. Hollier

Richard F. Neville, and Anton N. Sidawy

CHAPTER 60

CHAPTER 49 Intraoperative Assessment of Vascular Reconstruction, Jonathan B. Towne

606

Endovascular Repair of Abdominal Aortic Aneurysms, Juan C. Parodi and Luis M. Ferreira

736

viii

Contents

CHAPTER 61 Endovascular Treatment of Ruptured Infrarenal Aortic and Iliac Aneurysms,

CHAPTER 71 744

Nonatherosclerotic Cerebrovascular Disease, Gary R. Seabrook

843

Frank J. Veith and Takao Ohki

CHAPTER 62 Management of Infected Aortic Grafts,

753

G. Patrick Clagett

Visceral Vessels

CHAPTER 63 Isolated Iliac Artery Aneurysms,

PART IX

763

Henry Haimovici

CHAPTER 72 Surgery of Celiac and Mesenteric Arteries,

861

Stephen P. Murray, Tammy K. Ramos, and Ronald J. Stoney

CHAPTER 64 Endovascular Grafts in the Treatment of Isolated Iliac Aneurysms, Frank J. Veith,

767

Mesenteric Ischemia,

Julie A. Freischlag, Michael M. Farooq, and Jonathan B. Towne

Evan C. Lipsitz,Takao Ohki, William D. Suggs, Jacob Cynamon, and Alla M. Rozenblit

875

CHAPTER 74

CHAPTER 65 Para-anastomotic Aortic Aneurysms: General Considerations and Techniques,

CHAPTER 73

775

Renal Artery Revascularization,

887

Keith D. Calligaro and Matthew J. Dougherty

Daniel J. Char and John J. Ricotta

CHAPTER 75 Visceral Artery Aneurysms,

Matthew J.

902

Dougherty and Keith D. Calligaro

PART VIII Cerebrovascular Insufficiency

PART X CHAPTER 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery,

787

Upper Extremity Conditions

Anthony M. Imparato

CHAPTER 76

CHAPTER 67

Vasospastic Diseases of the Upper Extremity, Scott E. Musicant, Gregory L. Moneta,

Eversion Carotid Endarterectomy,

810

R. Clement Darling, III, Manish Mehta, Philip S. K. Paty, Kathleen J. Ozsvath, Sean P. Roddy, Paul B. Kreienberg, Benjamin B. Chang, and Dhiraj M. Shah

James M. Edwards, and Gregory J. Landry

CHAPTER 77 Neurogenic Thoracic Outlet Syndrome,

817

CHAPTER 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction,

Samuel R. Money

940

Richard J. Sanders and Michael A. Cooper

CHAPTER 69 Carotid Stenting: Current Status and Clinical Update, Robert W. Hobson, II

924

Richard J. Sanders and Michael A. Cooper

CHAPTER 68 Complications and Results in Carotid Surgery, Michael S. Conners, III and

915

827

CHAPTER 79 Arterial Thoracic Outlet Syndrome,

949

Frank J. Veith and Henry Haimovici

CHAPTER 70 Vertebrobasilar Disease: Surgical Management, Ronald A. Kline and Ramon Berguer

835

CHAPTER 80 Arterial Surgery of the Upper Extremity, James S.T. Yao

958

Contents

CHAPTER 81

ix

CHAPTER 91

Upper Thoracic Sympathectomy: Conventional Technique, Henry Haimovici

974

Venous Interruption,

Lazar J. Greenfield and

1097

Contemporary Venous Thrombectomy,

1106

Mary C. Proctor

CHAPTER 92

CHAPTER 82 Thoracoscopic Sympathectomy,

981

Anthony J. Comerota

P. Michael McFadden and Larry H. Hollier

CHAPTER 93

PART XI

Endoscopic Subfascial Ligation of Perforating Veins, Manju Kalra and

Arteriovenous Malformation

Peter Gloviczki

1115

CHAPTER 94

CHAPTER 83 Arteriovenous Fistulas and Vascular Malformations, Peter Gloviczki, Audra A. Noel,

991

Venous Reconstruction in Postthrombotic Syndrome, Seshadri Raju

1131

and Larry H. Hollier

CHAPTER 95 CHAPTER 84 Vascular Access for Dialysis,

Harry Schanzer

1015

and Andres Schanzer

1139

Henry Haimovici

CHAPTER 96

CHAPTER 85 Portal Hypertension,

Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene,

James D. Eason and

1030

John C. Bowen

1152

Thomas F. O’Donnell, Jr.

PART XII Venous and Lymphatic Surgery CHAPTER 86 Clinical Application of Objective Testing in Venous Insufficiency, John J. Bergan and

Diagnosis and Management of Lymphedema, Mark D. Iafrati and

1047

PART XIII Amputations and Rehabilitations CHAPTER 97 Amputation of the Lower Extremity: General Considerations, Henry Haimovici

Warner P. Bundens

1171

CHAPTER 87 Varicose Veins,

Mark D. Iafrati and Thomas F. O’Donnell, Jr.

1058

CHAPTER 98 Above-the-knee Amputations,

1175

Henry Haimovici

CHAPTER 88 Superficial Thrombophlebitis,

1073

Anil Hingorani and Enrico Ascher

Postoperative and Preprosthetic Management for Lower Extremity Amputations, Yeongchi Wu

CHAPTER 89 Acute Deep Vein Thrombosis,

CHAPTER 99

1078

Anthony J. Comerota

CHAPTER 100 Prosthetics for Lower Limb Amputees,

CHAPTER 90 Acute Upper Extremity Deep Vein Thrombosis, Anil Hingorani and Enrico Ascher

1183

Jan J. Stokosa 1091

Index

1207

1190

PREFACE

It has been nearly three decades since the late Dr Henry Haimovici (1907–2001) first presented to us his landmark publication Vascular Surgery: Principles and Techniques. Even then he observed that, in this historically brief period of time, we had already experienced momentous developments in the magnitude and scope of our specialty. I believe that, unlike any other period of time and unlike any other surgical specialty, we have also maintained the ability to focus and redirect our craft in tandem with, if not in advance of, the changing needs of our patients and the technological advancements available to us. As a great pioneer of vascular surgery, Dr Haimovici was a principal instrument of our success throughout the infancy and maturation of vascular surgery. He was ever committed to its future beyond measure. Henry was also my mentor and a great friend. I am forever indebted to him for the privilege of assuming editorship of this grand textbook. We are also saddened by the loss of yet another great leader in vascular surgery: D. Eugene Strandness, Jr., MD (1928–2002). Dr Strandness fielded numerous contributions throughout the formative years of noninvasive vascular testing and ultimately established what has now become our most effective asset in the diagnosis of vascular disease — the vascular laboratory. His early work focused on physiologic tests, but he was also responsible for the development and application of direct ultrasonic methods for vascular diagnosis. Working with engineers at the University of Washington, he combined a B-mode imaging system and a Doppler flow detector to create the

x

first duplex scanner. These explorers of science were prolific in their contributions to our specialty through their research, publications, and societal leaderships. It is in their footsteps that the current and successive generations of vascular leaders must walk — and they have left great shoes for them to fill. We are proud to have returning Section Editors Larry Hollier (Aortic and Peripheral Aneurysms), Eugene Strandness (Imaging Techniques), and Jonathan B. Towne (Acute Arterial Occlusions of the Lower Extremities). We are also fortunate to have joining us K. Craig Kent (Basic Cardiovascular Problems), John J. Ricotta (Cerebrovascular Insufficiency), Keith D. Calligaro (Visceral Vessels), Gregory L. Moneta (Specific Upper Extremity Occlusions), and William H. Pearce (Venous and Lymphatic Surgery) as Section Editors. This 5th edition of Haimovici’s Vascular Surgery remains true to its heritage of the comprehensive inspection of the practice of vascular surgery. Innovations in operative technique and reflections on noninvasive diagnostic imaging have been examined and each topic has been updated and expanded. This textbook has now included the most current topics regarding endovascular therapy. Extensive changes have been made to this edition — fully 75 chapters have been revised and 25 new chapters have been added. Enrico Ascher, MD New York, New York 2003

ACKNOWLEDGMENTS

It would be impossible for me to express my gratitude to all those who have labored to see this important endeavor come to fruition. There are so many worthy contributors to this edition, including both the prominent leaders of today and the rising stars of tomorrow, that the author’s index reads like the “Who’s Who?” of vascular surgery. Their roles are of great import not only now, but will extend well into the millennium. Within my own practice, I am grateful to my partner and friend, Dr Anil Hingorani, for permitting me the necessary “protected time” away from the operating room and from the clinic when I needed to focus on this project. I also especially wish to recognize my assistant, Ms Anne Ober, for her perseverance, loyalty, and dedication. Her

coordination of activities and gentle massaging of the many personalities involved, when necessary, are unparalleled and much appreciated. Lastly, I must thank Blackwell Publishing for their continued support of this title. Many have contributed their talents, but particular recognitions are due to Julia Casson, Development Editor, and Kate Heinle, Editorial Coordinator. Their professional expertise and roles in the evolution of this complex undertaking are amply evident in the cohesive production that has evolved. Enrico Ascher, MD New York, New York 2003

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EDITORS

ENRICO ASCHER, MD Professor of Surgery Mount Sinai School of Medicine New York, New York Chief, Vascular Surgery Services Maimonides Medical Center Brooklyn, New York L. H. HOLLIER, MD, FACS, FACC, FRCS (ENG) Julius Jacobson Professor of Vascular Surgery Mount Sinai School of Medicine President The Mount Sinai Hospital New York, New York D. EUGENE STRANDNESS, JR., MD, DMED Former Professor of Surgery University of Washington Former Attending Surgeon University of Washington Medical Center Seattle, Washington JONATHAN B. TOWNE, MD Professor of Surgery Chairman of Vascular Surgery Medical College of Wisconsin Milwaukee, Wisconsin KEITH CALLIGARO, MD Associate Clinical Professor University of Pennsylvania School of Medicine Chief, Section of Vascular Surgery Pennsylvania Hospital Philadelphia, Pennsylvania K. CRAIG KENT, MD Chief Columbia Weill Cornell Division of Vascular Surgery Columbia College of Physicians and Surgeons Weill Medical College of Cornell University New York, New York

GREGORY L. MONETA, MD Professor of Surgery Head, Division of Vascular Surgery Oregon Health and Science University Portland, Oregon WILLIAM H. PEARCE, MD Violet R. and Charles A. Baldwin Professor of Vascular Surgery Chief, Division of Vascular Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois JOHN J. RICOTTA, MD, FACS Professor and Chair Department of Surgery State University of New York at Stony Brook Chief of Surgery Stony Brook University Hospital Stony Brook, New York HENRY HAIMOVICI, MD Former Foreign Corresponding Member French National Academy of Medicine Paris, France Former Clinical Professor Emeritus of Surgery Albert Einstein College of Medicine at Yeshiva University Former Senior Consultant and Chief Emeritus of Vascular Surgery Montefiore Medical Center New York, New York

CONTRIBUTORS

SAMUEL S. AHN, MD, FACS Clinical Professor of Surgery UCLA School of Medicine Attending Surgeon UCLA Center for the Health Sciences Division of Vascular Surgery Los Angeles, California FRANK R. ARKO, MD Director, Endovascular Surgery Assistant Professor of Surgery Division of Vascular Surgery Stanford ENRICO ASCHER, MD Professor of Surgery Mount Sinai School of Medicine New York, New York Chief, Vascular Surgery Services Maimonides Medical Center Brooklyn, New York

W. TODD BOHANNON, MD Assistant Professor of Surgery and Radiology Texas Technical University Health Sciences Center University Medical Center Lubbock, Texas MAURICIO P. BORIC, PhD Departomento de Ciencias Fisiológicas P. Universidad Católica de Chile Santiago, Chile JOHN C. BOWEN, MD Chairman Emeritus, Department of Surgery Ochsner Clinic Foundation New Orleans, Louisiana BRUCE H. BRENNAMAN, MD Director, Noninvasive Vascular Laboratory The Medical Center Surgical Associates of Columbus Columbus, Georgia

JUAN AYERDI, MD Division of Peripheral Vascular Surgery Southern Illinois University School of Medicine Springfield, Illinois

DAVID C. BREWSTER, MD Clinical Professor of Surgery Harvard Medical School Surgeon Massachusetts General Hospital Boston, Massachusetts

HISHAN S. BASSIOUNY, MD Associate Professor of Surgery Medical Director of Noninvasive Laboratories Department of Vascular Surgery University of Chicago Chicago, Illinois

WARNER P. BUNDENS, MD Assistant Clinical Professor of Surgery University of California, San Diego San Diego, California

RICHARD A. BAUM, MD Department of Surgery University of Pennsylvania School of Medicine Philadelphia, Pennsylvania

KEITH D. CALLIGARO, MD, FACS Associate Clinical Professor University of Pennsylvania School of Medicine Chief, Section of Vascular Surgery Pennsylvania Hospital Philadelphia, Pennsylvania

JOHN J. BERGAN, MD, FACS Professor of Surgery University of California, San Diego Professor of Surgery Uniformed Services of the Health Sciences Bethesda, Maryland

JEFFREY P. CARPENTER, MD Associate Professor of Surgery Department of Surgery University of Pennsylvania School of Medicine Philadelphia, Pennsylvania

RAMON BERGUER, MD, PhD Professor and Chief Division of Vascular Surgery Wayne State University/Detroit Medical Center Detroit, Michigan AHMAD F. BHATTI, MD Columbia University and St. Luke’s/ Roosevelt Hospital Center New York, New York JOHN D. BISOGNANO, MD, PhD, FACP, FACC Assistant Professor of Medicine University of Rochester Attending Cardiologist Strong Memorial Hospital Rochester, New York

ALFIO CARROCCIO, MD Resident in Vascular Surgery Division of Vascular Surgery Mount Sinai Medical Center New York, New York BENJAMIN B. CHANG, MD Assistant Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Assistant Professor of Surgery Albany, New York DANIEL J. CHAR, MD Assistant Clinical Instructor of Surgery Division of Vascular Surgery Stony Brook University Hospital Stony Brook, New York

xiii

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Contributors

G. PATRICK CLAGETT, MD Jan and Bob Pickens Distinguished Professorship in Medical Science Professor and Chairman, Division of Vascular Surgery University of Texas Southwestern Medical Center Dallas, Texas ANTHONY J. COMEROTA, MD Professor of Surgery Temple University School of Medicine Chief, Vascular Surgery Temple University Hospital Philadelphia, Pennsylvania MICHAEL S. CONNERS, III, MD Vascular Surgery Fellow Alton Ochsner Clinic Foundation New Orleans, Louisiana MICHAEL A. COOPER Attending Surgeon Rose Medical Center Denver, Colorado JOSEPH S. COSELLI, MD Professor of Surgery Chief, Division of Cardiothoracic Surgery Baylor College of Medicine Houston, Texas JACOB CYNAMON, MD Maimonides Medical Center Brooklyn, New York R. CLEMENT DARLING, III, MD Professor of Surgery Albany Medical College Chief, Division of Vascular Surgery Albany Medical Center Albany, New York EDWARD B. DIETHRICH, MD Medical Director and Chief of Cardiovascular Surgery Arizona Heart Institute Arizona Heart Hospital Director and Chairman Department of Cardiovascular Services Healthwest Regional Medical Center Phoenix, Arizona MATTHEW J. DOUGHERTY, MD, FACS Assistant Clinical Professor University of Pennsylvania Section of Vascular Surgery Pennsylvania Hospital Philadelphia, Pennsylvania WALTER N. DURÁN, PhD Professor of Physiology and Surgery Chief, Division of Microcirculatory Research Department of Physiology University of Medicine and Dentistry of New Jersey New Jersey Medical School Newark, New Jersey JAMES D. EASON, MD, FACS Head, Section of Abdominal Transplantation Ochsner Clinic Foundation New Orleans, Louisiana JAMES M. EDWARDS, MD Associate Professor of Surgery, Division of Vascular Surgery Oregon Health Sciences University

Chief of Surgery, Portland Veterans Affairs Medical Center Portland, Oregon CALVIN B. ERNST, MD Clinical Professor of Surgery University of Michigan Medical School Head, Division of Vascular Surgery Henry Ford Hospital Detroit, Michigan MICHAEL M. FAROOQ, MD Assistant Professor of Surgery University of California, Los Angeles DAVID L. FELDMAN, MD, FACS Assistant Professor of Surgery SUNY Health Science Center at Brooklyn Director, Division of Plastic Surgery Maimonides Medical Center Brooklyn, New York LUIS M. FERREIRA, MD Staff, Vascular Surgery Department Instituto Cardiovascular de Buenos Aires Buenos Aires, Argentina JULIE A. FREISCHLAG, MD Medical College of Wisconsin Milwaukee, Wisconsin SEYMOUR GLAGOV, MD Department of Pathology University of Chicago School of Medicine Chicago, Illinois PETER GLOVICZKI, MD Professor of Surgery Mayo Medical School Chair, Division of Vascular Surgery Director, Gonda Vascular Center Mayo Clinic and Foundation Rochester, Minnesota LAZAR J. GREENFIELD, MD Frederick A. Collier Professor and Chairman of Surgery University of Michigan Medical School Department of Surgery University of Michigan Medical Center Ann Arbor, Michigan SUSHIL K. GUPTA, MD Section Chief Guthrie Clinic Sayre, Pennsylvania HENRY HAIMOVICI, MD Former Foreign Corresponding Member French National Academy of Medicine Paris, France Former Clinical Professor Emeritus of Surgery Albert Einstein College of Medicine at Yeshiva University Former Senior Consultant and Chief Emeritus of Vascular Surgery Montefiore Medical Center New York, New York ASHER HIRSHBERG, MD Associate Professor of Surgery Michael E. DeBakey Department of Surgery Baylor College of Medicine Director of Vascular Surgery Medical Director, Non-invasive Vascular Laboratory Ben Taub General Hospital Houston, Texas

Contributors ANIL HINGORANI, MD Clinical Assistant Professor State University of NY — Brooklyn Attending Surgeon Maimonides Medical Center Brooklyn, New York ROBERT W. HOBSON, II, MD Professor of Surgery and of Physiology Division of Vascular Surgery Department of Surgery University of Medicine and Dentistry of New Jerse New Jersey Medical School Newark, New Jersey FREDERICK L. HOFF, MD Assistant Professor of Radiology Department of Radiology Northwestern University Medical School Chicago, Illinois KIM J. HODGSON, MD Division of Peripheral Vascular Surgery Southern Illinois University School of Medicine Springfield, Illinois L. H. HOLLIER, MD, FACS, FACC, FRCS (Eng) Julius Jacobson Professor of Vascular Surgery Mount Sinai School of Medicine President The Mount Sinai Hospital New York, New York CARBER C. HUANG, MD Endovascular Fellow, Division of Vascular Surgery UCLA School of Medicine Los Angeles, California MARK D. IAFRATI, MD, RVT, FACS Department of Surgery Division of Vascular Surgery New England Medical Center Boston, Massachusetts ANTHONY M. IMPARATO, MD Professor of Surgery New York University School of Medicine New York, New York TONYA P. JORDAN, MD Columbia University and St. Luke’s/Roosevelt Hospital Center New York, New York MANJU KALRA, MBBS FRCSEd Department of Surgery Mayo Clinic Rochester, Minnesota J.J. KARMACHARYA, MD Department of Surgery University of Pennsylvania School of Medicine Philadelphia, Pennsylvania K. CRAIG KENT, MD Professor of Surgery Columbia Weill Cornell Division of Vascular Surgery Columbia College of Physicians and Surgeons Weill Medical College of Cornell University New York, New York SASHI KILARU, MD Vascular Surgery Fellow Weill Cornell Medical College

New York Presbyterian Hospital — Cornell New York, New York PAUL B. KREIENBERG, MD Associate Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Albany, New York RONALD A. KLINE, MD, FACS Associate Professor of Surgery Wayne State University School of Medicine Program Director, Vascular Surgery Harper University Hospital Detroit, Michigan GREGORY J. LANDRY, MD Assistant Professor of Surgery, Division of Vascular Surgery Oregon Health Sciences University Portland, Oregon L. SCOTT LEVIN, MD Chief, Division of Plastic, Maxillofacial, and Reconstructive Surgery Duke University Medical Center Durham, North Carolina EVAN C. LIPSITZ, MD Assistant Professor, Division of Vascular Surgery Albert Einstein College of Medicine Attending Vascular Surgeon Montefiore Medical Center Bronx, New York ELKE LORENSEN, MD Vascular Fellow Maimonides Medical Center Brooklyn, New York JAMES B. LYONS, MD Interventional Radiologist Desert Samaritan Medical Center Mesa, Arizona P. MICHAEL MCFADDEN, MD Clinical Professor of Surgery Tulane University School of Medicine Surgeon and Surgical Co-Director Lung Transplantation Program Ochsner Clinic New Orleans, Louisiana ROBYN MACSATA, MD Resident, Vascular Surgery Washington Hospital Center Georgetown University Washington, DC KENNETH L. MATTOX, MD Professor and Vice Chair Michael E. DeBakey Department of Surgery Baylor College of Medicine Chief of Staff/Chief of Surgery Ben Taub General Hospital Houston, Texas MANISH MEHTA, MD Assistant Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Albany, New York

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Contributors

ARNOLD MILLER, MD Associate Clinical Professor of Surgery Harvard Medical School Boston, Massachusetts Chief Department of Surgery Leonard Morse Hospital MetroWest Medical Center Natick, Massachusetts YOSHIO MISHIMA, MD Professor and Chairman of Surgery Tokyo Medical and Dental University Tokyo, Japan GREGORY L. MONETA, MD Professor of Surgery Chief, Division of Vascular Surgery Oregon Health Sciences University Portland, Oregon SAMUEL R. MONEY, MD, FACS, MBA Clinical Associate Professor Tulane School of Medicine Head, Section of Vascular Surgery Ochsner Clinic Foundation New Orleans, Louisiana NICHOLAS J. MORRISSEY, MD Assistant Professor of Surgery Division of Vascular Surgery Mt. Sinai School of Medicine New York, New York KYLE MUELLER, MD Resident, General Surgery Northwestern University Medical School Chicago, Illinois LEILA MUREEBE, MD Assistant Professor, Department of Surgery University of Missouri — Columbia Staff Surgeon, Department of Surgery University of Missouri Health Care Columbia, Missouri STEPHEN P. MURRAY, MD Inland Vascular Institute Spokane, Washington Assistant Clinical Professsor, Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland SCOTT E. MUSICANT, MD Resident in Surgery Oregon Health Sciences University Portland, Oregon HARVEY L. NEIMAN, MD Executive Director, American College of Radiology Reston, Virginia Professor of Radiology Temple University School of Medicine Philadelphia, Pennsylvania RICHARD F. NEVILLE, MD Associate Professor of Surgery Georgetown University Chief Vascular Surgery Georgetown University Medical Center Washington, DC

AUDRA A. NOEL, MD Assistant Professor of surgery Mayo Medical School Consultant Division of Vascular Surgery Mayo Clinic Rochester, Minnesota THOMAS F. O’DONNELL, Jr., MD Andrews Professor and Chairman of Surgery Tufts University School of Medicine Surgeon-in-Chief Chief of Vascular Surgery New England Medical Center Boston, Massachusetts TAKAO OHKI, MD Associate Professor of Surgery Albert Einstein College of Medicine Chief, Vascular and Endovascular Surgery Montefiore Medical Center Bronx, New York KATHLEEN J. OZSVATH, MD Assistant Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Albany, New York CHARLES P. PANISYN, MD Assistant Clinical Professor of Surgery Tufts Medical School Boston, Massachusetts PETER J. PAPPAS, MD Division of Vascular Surgery Department of Surgery University of Medicine and Dentistry of New Jerse New Jersey Medical School Newark, New Jersey PHILIP S. K. PATY, MD Associate Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Albany, New York JUAN C. PARODI, MD Vice Director of the Post-Graduate Training Program in Cardiovascular Surgery of the University of Buenos Aires Chief, Vascular Surgery Department Instituto Cardiovascular de Buenos Aires Director, Instituto Cardiovascular de Buenos Aires Buenos Aires, Argentina WILLIAM PEARCE, MD Violet R. and Charles A. Baldwin Professor of Vascular Surgery Department of Surgery Northwestern University Medical School Chicago, Illinois SANJEEV PRADHAN, MD Resident, Department of Surgery Yale University School of Medicine New Haven, Connecticut MARY C. PROCTOR, MS Department of Surgery University of Michigan Medical School Ann Arbor, Michigan

Contributors TAMMY K. RAMOS, MD Creighton University Medical Center Department of Surgery Omaha, Nebraska SESHADRI RAJU, MD, FACS Emeritus Professor of Surgery and Honorary Surgeon University of Mississippi Medical School Jackson, Mississippi JOHN J. RICOTTA, MD Professor and Chairman of Surgery Department of Surgery Stony Brook University Hospital Stony Brook, New York SEAN P. RODDY, MD Assistant Professor of Surgery Albany Medical College Attending Vascular Surgeon Albany Medical Center Hospital Albany, New York ALLA M. ROZENBLIT, MD Maimonides Medical Center Brooklyn, New York SEAN V. RYAN, MD Surgical Resident Pennsylvania Hospital Philadelphia, Pennsylvania RICHARD J. SANDERS, MD Clinical Professor of Surgery University of Colorado School of Medicine Rose Medical Center Denver, Colorado ARMANDO SARDI, MD, FACS Chief Surgical Oncology Medical Director, Clinical Research Center St. Agnes HealthCare Baltimore, Maryland ANDRES SCHANZER, MD Surgical Resident, Department of Surgery University of California at Davis UCD Medical Center Sacramento, California HARRY SCHANZER, MD, FACS Clinical Professor of Surgery Mount Sinai School of Medicine Attending Surgeon Mount Sinai Hospital New York, New York GARY R. SEABROOK, MD Professor of Vascular Surgery Medical College of Wisconsin Milwaukee, Wisconsin DHIRAJ M. SHAH, MD Director, The Vascular Institute Professor of Surgery Associate Professor of Physiology and Cellular Biology Albany Medical College Albany, New York THOMAS A. SHUSTER, DO Vascular Surgery Fellow, Department of Surgery University of Missouri — Columbia Vascular Fellow, Department of Surgery

xvii

University of Missouri Health Care Columbia, Missouri ANTON N. SIDAWY, MD, MPH Professor of Surgery George Washington University Georgetown University Chief, Surgery Service VA Medical Center Washington, DC MICHAEL B. SILVA, Jr., MD Vice-Chairman, Department of Surgery Professor & Chief, Vascular Surgery and Vascular Interventional Radiology Texas Tech University Health Sciences Center Attending Surgeon University Medical Center Lubbock, Texas DONALD SILVER, MD Professor Emeritus, Department of Surgery University of Missouri — Columbia Medical Director, Surgical Services University of Missouri Health Care Columbia, Missouri MAURICE M. SOLIS, MD Chief, Vascular and Endovascular Surgery Macon Cardiovascular Institute and Mercer University School of Medicine Macon, Georgia WILLIAM D. SUGGS, MD Maimonides Medical Center Brooklyn, New York JAN J. STOKOSA, CP Stokosa Prosthetic Clinic East Lansing, Michigan RONALD J. STONEY, MD Professor of Surgery University of California, San Francisco, School of Medicine San Francisco, California D. EUGENE STRANDNESS, Jr., MD, DMed Former Professor of Surgery University of Washington Former Attending Surgeon University of Washington Medical Center Seattle, Washington DAVID S. SUMNER, MD Distinguished Professor of Surgery, Emeritus Chief, Section of Peripheral Vascular Surgery Southern Illinois University School of Medicine Springfield, Illinois BAUER E. SUMPIO, MD, PhD Professor and Vice Chairman of Surgery Chief, Vascular Surgery Yale University School of Medicine Chief, Vascular Service Yale — New Haven Hospital New Haven, Connecticut JAMES C. STANLEY, MD, FACS Professor of Surgery University of Michigan Head, Section of Vascular Surgery University of Michigan Hospital Ann Arbor, Michigan

xviii

Contributors

M. DAVID TILSON, MD Ailsa Mellon Bruce Professor of Surgery (Columbia University) Director Emeritus Department of Surgery St. Luke's/Roosevelt Hospital New York, New York JONATHAN B. TOWNE, MD Chief of Vascular Surgery Froedtert Memorial Lutheran Hospital Professor of Surgery Medical College of Wisconsin Milwaukee, Wisconsin WILLIAM TURNIPSEED, MD Professor of Surgery Section of Vascular Surgery University Hospital Madison, Wisconsin FRANK J VEITH, MD, FACS Professor of Surgery Albert Einstein College of Medicine The William J. von Liebig Chair in Vascular Surgery Montefiore Medical Center New York, New York OMAIDA C. VELAZQUEZ, MD Department of Surgery University of Pennsylvania School of Medicine Philadelphia, Pennsylvania THOMAS W. WAKEFIELD, MD S. Martin Lindenauer Professor of Surgery Section of Vascular Surgery University of Michigan Medical Center Staff Surgeon University of Michigan Hospital and Ann Arbor Veterans Administration Medical Center Ann Arbor, Michigan

RODNEY A. WHITE, MD Associate Chair Department of Surgery Harbor — UCLA Research and Education Institute Chief, Vascular Surgery Division of Vascular Surgery Harbor — UCLA Medical Center Torrance, California YEONGCHI WU, MD Associate Professor of Physical Medicine and Rehabilitation Northwestern University Medical School Director, Amputee Rehabilitation Rehabilitation Institute of Chicago Center for International Rehabilitation Chicago, Illinois CHENGPEI XU, MD Stanford University School of Medicine Division of Vascular Surgery Stanford, California JAMES S.T. YAO, MD, PhD Magerstadt Professor of Surgery Northwestern University Medical School Attending Surgeon Northwestern Memorial Hospital Chicago, Illinois WILLIAM R. YORKOVICH, RPA Physician Assistant Division of Vascular Surgery Maimonides Medical Center Brooklyn, New York CHRISTOPHER K. ZARINS, MD Chidester Professor of Surgery Stanford University School of Medicine Chief, Division of Vascular Surgery Stanford University Medical Center Stanford, California

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 1 A tribute to Henry Haimovici: September 7, 1907, to July 10, 2001 Frank J. Veith and Enrico Ascher

On July 10, 2001, vascular surgery lost one of its founding fathers, Henry Haimovici, whose interesting life was dramatically altered by the upheavals associated with World War II, and who brought scholarly excellence to our specialty. Henry Haimovici was born on the banks of the Danube in Romania on September 7, 1907. After early schooling in Tulcea, Romania, not far from the Black Sea, young Henry, at the age of 20, went to Marseille, France, for his medical education and residency training—first in all specialties and then in general surgery. He was a distinguished student and scholar from the beginning. He developed an early interest in vascular surgery, and the title for his thesis for his medical degree, only awarded upon completion of his training, was “Arterial Emboli to the Limbs.” His thesis was of such high quality that Henry’s chief at the time, Professor Jean Fiolle, suggested that it be published as a monograph. It was, with a preface by another pioneer in vascular surgery, René Leriche, who had become one of Henry’s earliest admirers and supporters. This book was of sufficient quality that it attracted the attention of another vascular surgery pioneer, Geza de Takats, who recommended that it be translated into English so that “this splendid piece of work be available to everyone.” While still in training, Haimovici developed an interest in venous gangrene. He published one of the first case reports on this condition and subsequently a classic monograph on what he termed “ischemic venous thrombosis”, a condition also known under the more popular name, phlegmasia cerula dolens.

Immediately after his residency training, Dr Haimovici was selected by the dean of his medical school to direct a new institute of neurology and neurosurgery which was planned as a joint project by the Rockefeller Foundation. To qualify for this new chief’s position, Dr Haimovici was sent to the United States to study neurophysiology under Dr Walter B. Cannon of Harvard University, regarded as the most prestigious physiologist in America. During his year’s fellowship with Dr Cannon, Henry published key papers on the effects of motor and sympathetic denervation and regeneration. He always considered Dr Cannon to be his most exceptional mentor and his time with him to be his most productive. While in the US, Dr Haimovici also met with all the neurosurgical leaders in North America and had planned further training in neurosurgery before returning to his prestigious appointment in Marseille. However, World War II had broken out, and all of Dr Haimovici’s plans were disrupted. He was drafted into the French Army, but after France surrendered he decided to accept Dr Cannon’s invitation and return to the US. However, his escape from occupied France involved many adventures and lasted two years, by which time Dr Cannon had retired. So Dr Haimovici returned in 1942 to Boston and the Beth Israel Hospital, where he worked with outstanding scientists such as Rene Dubos and Jacob Fine on infections, toxic shock, and the effect of gelatin in preventing thrombosis of injured veins. After two highly productive years in Boston, Dr Haimovici moved to New York, where he married a young PhD biochemist, Nelicia Maier. He and his new

1

2

Introduction

wife combined their interests in studying the metabolism of atherosclerotic arteries, a field to which he would continue to contribute for the rest of his career. In New York City, Dr Haimovici held an appointment in vascular surgery at Mount Sinai Hospital before being

FIGURE 1.1 Henry Haimovici.

appointed chief of vascular surgery at Montefiore Medical Center in 1945. While at these two institutions, he continued to write important articles relating the physiology of the autonomic nervous system, its mediators and its blocking agents, to vascular conditions such as Buerger’s disease and atherosclerosis. His work was published in the leading medical and physiology journals of the time. Dr Haimovici’s scholarly activity extended well beyond his high-quality original investigations. In addition to writing over 200 journal articles and book chapters, Dr Haimovici authored or edited more than 10 books. His monograph on metabolic complications of acute arterial occlusion and related conditions, published in 1988, is now considered a classic. In addition, Haimovici’s Vascular Surgery: Principles and Techniques, first published in 1976, is regarded as one of the finest texts in the vascular surgery field and was also published in a Spanish edition. The first four editions of this important text were edited by Dr Haimovici himself. Despite all these accomplishments, Henry Haimovici’s crowning achievement was his role in founding the International Society of Cardiovascular Surgery (ISCVS). In March 1950, Dr Haimovici, who was editor of the journal Angiology, took the initiative of organizing the International Society of Angiology. He discussed his plans with René Leriche, who became the organization’s first president. A number of the most prominent vascular surgeons from around the world signed on as charter members. Dr Haimovici became the organization’s first secretary-general and drafted its original bylaws, which created regional chapters for this worldwide vascular society. In 1952, the first meeting of the North American chapter of the ISCVS (now the American Association for

FIGURE 1.2 Haimovici at the Harvard Medical School Department of Physiology, 1939 (second row, fifth from left).

Chapter 1 A Tribute to Henry Haimovici

FIGURE 1.3 Haimovici (center) in the French Army, 1940.

3

Vascular Surgery) was held in Chicago. Emile Holman was elected the first president and Henry Haimovici the first secretary-treasurer of the chapter. Meanwhile, he held the post of secretary-general in the international organization from 1950 to 1963. In this position, Dr Haimovici was a major force in organizing the Society’s first four biannual international congresses, in changing the name of the Society in 1957 to the International Society of Cardiovascular Surgery, and in establishing its journal, the Journal of Cardiovascular Surgery. He served as the founding co-editor of this publication from 1960 to 1973 and was a consulting editor until his death. Henry Haimovici was honored with the presidency of the North American chapter of the ISCVS in 1959 and 1960. He served as a visiting professor around the world and was awarded nine honorary degrees. In 1986 he was elected a corresponding member of the French National Academy of Medicine, a truly unique honor for an American surgeon. In his 93 years, Henry Haimovici made his scholarly mark on surgery around the globe. He helped to establish vascular surgery as a true specialty, and he contributed greatly to its scientific underpinnings. He was a leading vascular surgeon in at least two countries and was widely known and well respected everywhere. He was a true surgeon-scholar with an encyclopedic knowledge of the vascular literature. He was a talented editor and writer, and he had organizational skills possessed by few vascular surgeons. Henry Haimovici was a colleague and a friend who will be sorely missed, even though his mark will long remain on vascular surgery.

FIGURE 1.4 Haimovici (second from right) at the French National Academy of Medicine, 1986.

PART I

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

Imaging Techniques

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 2 Ultrasonic Duplex Scanning D. Eugene Strandness, Jr

The past decade has seen a dramatic increase in the ability to assess vascular disease wherever it occurs. This has been in large part due to the development of ultrasonic duplex scanning (1,2). This modality, which combines imaging with pulsed Doppler ultrasound, permits access to all major vascular beds, providing information that is relevant to how patients are managed. For some conditions, such as deep venous thrombosis, this method has essentially replaced venography as a diagnostic tool. This method is also beginning to replace arteriography for many areas such as the carotid and peripheral circulation (see Chapter 3). This represents a major advance that, with time, will expand into other areas as well. This chapter addresses the major areas in which ultrasonic duplex scanning can be applied not only for diagnosis, but also for follow-up. The modern duplex scanner combines two basic modalities that can be used in concert to provide the necessary diagnostic information (3). The essential elements of the device are as follows.

Imaging Ultrasound is reflected from tissue interfaces, making it possible to localize and characterize structures of differing acoustic impedance. The transducer consists of piezoelectric crystals that convert an electrical voltage into an ultrasonic vibration. The sound that is reflected back from tissue is again translated into an electrical voltage that is detected by the receiver in the instrument. Those from the more superficial structures return sooner, those from deeper tissues return later. The exact time of return is

determined not only by the distance from the energy source but also by the speed of sound in tissue, which tends to vary somewhat depending on the tissue being interrogated. In medical ultrasound, 154,000 cm/s is used as the average speed of sound in soft tissue. The brightness of the return echo is determined by the strength or amplitude of the sound reflected from the tissues being interrogated. The most common problem that occurs with imaging is refractive distortion (4). The pulsed imaging process assumes that the ultrasound sent into tissue returns along the same line in which the transducer is pointed. However, because of differences in sound speed in tissue, the sound may bend and cause structures to appear in the wrong location, particularly when viewed in the lateral region of the image. If the ultrasound beam is perpendicular to the object, this type of distortion does not occur. It is important to understand this when one examines any images generated by ultrasound. The best resolution will always be seen in those tissues that are perpendicular to the sound beam. For example, as noted in Figure 2.1, the clearest images are seen in the mid-portion rather than the lateral areas of the field scan. The scan format must be understood to appreciate the images that are generated (4). Two of the various possible approaches are shown in Figure 2.2. With the raster scan format, all transmission lines of the beam are parallel, whereas with the sector scan format, all lines emanate from a point source. The scan lines in the raster format are generally generated by a linear array transducer. The potential advantages of the raster format are shown in Figure 2.3. If the blood vessel being imaged is parallel to the skin

7

8

Part I Imaging Techniques

FIGURE 2.3 With the raster scan format and the artery parallel to the skin surface, the double line on the posterior wall of the artery, which represents the combined thickness of the intima and media, can be visualized throughout the length of the scan. FIGURE 2.1 In this ultrasound image of a common carotid artery, the best resolution is in the midportion of the scan. At this point, the tissues of the arterial wall are perpendicular to the sound beam.

(Reproduced by permission from Beach KW, Appendix. In Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 285.)

FIGURE 2.2 With the raster scan format (top), all scan lines are parallel and all of the image planes are also parallel. The scan lines originate from a different point along the tranducer’s crystal. With the sector scan format (bottom), the scan lines originate from a small region of the transducer. (Reproduced by permission

sector format, the optimal image area is more limited, as shown in Figure 2.4. Both of these formats have certain advantages that vary depending upon the intended applications. There are also innumerable variations on how the transducers function. These range from electronic beam steering to curved and concave linear array transducers, each of which has specific advantages for some applications. No single transducer design will satisfy all applications. Readers interested in more details are urged to consult the more complete coverage of this subject by Beach (4). Although the scan format used is important, it is also necessary to understand the role of the transmitting frequency, its application, and its effect on the performance of the system (4). Attenuation of the signal is directly related to the transmitting frequency. The goal is to obtain signals (images) with the maximum possible resolution. For superficial structures a high transmitting frequency of 5 MHz is satisfactory, but for deeper structures, such as the renal arteries, a much lower transmitting frequency of 2.0–3.5 MHz may be needed. There is less attenuation of the ultrasound signal with the lower frequencies, making them better for visualizing deeper structures.

from Beach KW, Appendix. In: Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 284.)

Doppler

and at right angles to the scan lines, optimal images are obtained. However, if a vessel begins to deviate from this parallel path, image quality may begin to degenerate and some structures such as the double line representing the thickness of the intima–media are no longer seen. With the

The Doppler ultrasound used in nearly all modern systems is pulsed, making it possible to selectively sample flow from any point along the sound beam (5). As with the imaging, knowing the speed of sound in tissue makes it possible to range gate return signals to assess flow velocity at any depth that is reachable by the ultrasound frequency used. The size of the sound packet (the sample volume)

RASTER SCAN

SECTOR SCAN

Chapter 2 Ultrasonic Duplex Scanning

9

FIGURE 2.5 The area in tissue insonated by a continuous wave Doppler is contrasted with that insonated by a pulsed system. As noted, the width of the sample volume can be varied by the degree of focus provided. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 20.)

FIGURE 2.4 With the sector scan format, the double line that represents the intima and media is seen only in a limited portion of the scan plane as shown. (Reproduced by permission from Beach KW, Appendix. In: Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 285.)

for all pulsed systems can be varied considerably depending upon the intended application. The sample volume has both length and width. Its length is determined by the duration of the sound burst and its width is determined by the focusing characteristics of the transducer (Fig. 2.5). The size of the sample volume can be adjusted by the user, so it is important to review how it might be used and the problems that one might encounter with improper use (6). 1.

When examining arteries such as the carotid or femoral, one would like to use as small a sample volume size as possible. If one widens the sample volume to encompass the entire artery, the received signal will be identical to that obtained with continuous wave Doppler ultrasound. Figure 2.6 illustrates the basis for this observation. Near the normal arterial wall, the velocity gradients are very steep, resulting in the recording of a broad range of frequencies. This broadens the velocity spectrum (7,8). As noted, spectral broadening is not seen with a small sample volume placed in the center stream of the common carotid artery. This can be confusing if one attempts to use spectral broadening as a parameter for diagnosing carotid artery stenosis. This will be covered in detail later.

2.

A large sample volume is of benefit when one is examining arteries that experience a great deal of movement with respiration. The best examples of these are the renal, celiac, hepatic, splenic, and mesenteric arteries. With the large sample volume, flow can be monitored during an entire respiratory cycle, avoiding the intermittent loss of the signal due to movement of the sample volume in and out of the artery.

One important difference between pulsed and continuous wave systems is the problem of aliasing (4). Nyquist noted that, in order to faithfully record frequencies, it was necessary to have at least one sample taken for every peak and one for every valley of a waveform. This is the reason that the sample rate [the pulse repetition frequency (PRF)] must be at least twice the transmitting frequency of the pulsed Doppler. Thus, if one needed to record Dopplershifted frequencies of 5 kHz, it would be necessary to use a pulse repetition frequency of 10 kHz. If the Doppler shift were to exceed this limit, the frequencies that exceeded the 5 kHz level would appear beneath the zero frequency line (Fig. 2.7). There are ways to circumvent this problem. One is to simply increase the PRF of the instrument. Another is to reduce the transmitting frequency of the transducer. Finally, it is possible to combat aliasing by baseline shifting, which moves a portion of the reverse flow display to the forward flow location. This method is very commonly used in the currently available systems. The methods used for signal processing of the Doppler data are one of the most important advances in the field. For the velocity data that are recorded to be useful, they must be analyzed in a format that displays all of the pertinent information in the Doppler spectrum. The

10

Part I Imaging Techniques

FIGURE 2.7 Aliasing of a spectral waveform when pulsed Doppler ultrasound is used and the recorded frequencies exceed the pulse repetition frequency (PRF) of the pulsed system. On the left, there is foldover of the peak velocity, which is corrected by doubling the pulse repetition frequency shown on the right. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 20.)

FIGURE 2.6 These velocity recordings are an ensemble average of 16 heart beats taken as the sample volume is moved from close to the anterior wall of the common carotid artery to the vessel lumen and to the posterior wall region. Near the walls, the spectrum is “filled in” (spectral broadening) owing to the very steep velocity gradients near the wall. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: SG.)

most versatile method in use is fast Fourier transform (FFT) spectrum analysis (4,8). This method has become the standard for displaying all Doppler data with both continuous wave and pulsed systems. The display has frequency (velocity) on the ordinate and time on the abscissa. It also provides information relative to the intensity of the backscattered ultrasound, but for most clinical purposes this information is not used. From a practical standpoint, the most useful clinical data relate to velocity since they are the most sensitive to change in vessel dimensions. As will be shown, velocity criteria are the most commonly used to detect and grade the degree of narrowing of arteries (3,9). The other commonly used parameter is spectral broadening. If blood flow is laminar and the recording is taken from the center stream of the artery, the area beneath the systolic peak will be clear (6–8). On the other hand, if there is turbulence, the red blood cells are no longer moving at a uniform

velocity and the systolic window will be filled (10). However, spectral broadening is being used less because of its qualitative nature. To interpret it properly, it is necessary to know precisely from which regions in the artery the flow is being detected, as well as the size of the sample volume being used (see Fig. 2.6). If one uses continuous wave Doppler ultrasound, all velocity data in the path of the beam will be recorded (6). Since the velocity of flow near the wall of an artery is slower, one will record all velocities up to and including the peak, which is usually in the center stream of the artery. On the other hand, with pulsed Doppler ultrasound, if a large sample volume were employed that encompassed the entire cross-sectional area of the artery, its output would be identical to that of a continuous wave Doppler ultrasound and would provide similar types of FFT displays. It is also clear that, depending upon the intended application, the technologist will vary the sample volume size used. For example, in the case of the carotid artery, it is preferable to use as small a sample volume as possible (10). In contrast, studies of the renal artery often require a larger sample volume for the velocity data to be continuously recorded throughout each respiratory cycle (11). If a small sample volume were used, the artery would move in and out of the sample volume with respiration. In theory, it is possible to record absolute velocities with Doppler methods; therefore, it is important to review briefly some of the concerns and problems that can occur with this method. The major factors that determine the recorded velocity are the transmitting frequency and the angle of the sound beam with the velocity vectors that are encountered (12). The choice of transmitting frequency

Chapter 2 Ultrasonic Duplex Scanning

will depend upon intended application. For superficial vessels, a higher transmitting frequency (5–10 MHz) is used; for deeper vessels, lower frequencies (2.0–3.5 MHz) are used. The angle of incidence is the most difficult variable to control for transcutaneous use. The ideal would be to have the sound beam directed down the center stream of the artery parallel to the velocity vectors. When this is possible, the incident angle of the sound beam is zero, giving a cosine value of 1. Because this is rarely possible in clinical use, one must estimate the angle of incidence of the beam, which can then be used to calculate the angle-adjusted velocity. This is done automatically by the duplex scanners currently in use. However, even with this approach there can be problems that must be appreciated. One of the most difficult is the problem of nonparallel velocity vectors, which are continually changing the angle of the incident sound beam (12). Nonparallel velocity vectors are common in the arterial system and are always found in the vicinity of branch points and bifurcations (7). Also, once the velocity vectors begin to deviate from what one might expect, a finite distance from the source of the velocity disturbance must be traversed before the vectors again assume a laminar flow pattern. A few examples of this problem and the need for its understanding are shown in Tables 2.1 and 2.2. In Table 2.1, velocities were recorded from the common carotid artery using different angles of incidence of the sound beam. In theory, this should make no difference in the recorded velocity, particularly if the velocity vectors were parallel to the wall. However, as noted, there are variations in the calculated velocities that must be related to directional changes in the flow vectors. In Table 2.2, the recordings were made from the superficial femoral artery,

TABLE 2.1 Doppler frequency and angle-adjusted velocity from common carotid artery Incident Angle (%) 40 50 60 70

Doppler Frequency (kHz)

Angle-adjusted Velocity (cm/s)

4.732 4.299 3.726 3.180

97 105 117 145

and an entirely different situation was found. Here, changing the incident angle of the sound beam had very little effect on the angle-adjusted velocity. In this situation, flow is much more stable (laminar), thus permitting a more realistic estimate to be made. This clearly illustrates the differences that can be found depending upon the sampling site within the arterial system. These types of data also emphasize the importance of using a constant Doppler angle for all studies in patients whenever that is possible. We prefer to use 60∞, which is quite easily obtained in most situations (12). However, if this angle of incidence is not obtainable, the technologist must record the angle used. In addition, if follow-up studies are to be performed, the same angle must be used. This will provide consistency among the data obtained. Although most manufacturers refer to the use of anglecorrected velocities, we prefer the term angle-adjusted velocity as representing a more realistic situation for daily clinical practice (4). It is also clear that, because we rarely have the ideal situation for making recordings, the velocity data we obtain is, in general, an estimate. FFT depictions of velocity data have become standard for nearly all instruments, but now “color Doppler” and “power Doppler” have added an entirely new dimension to ultrasound studies (13–15). The color can be obtained with a variety of transducer systems. The Doppler image is formed by analyzing the phase changes between echoes from each scan line. In order to generate one scan line, a series of echoes is required. For each depth, the phase change from echo to echo is measured to determine the frequency shift. A color is assigned to the corresponding depth according to its direction and velocity. In practice, shades of red and blue are used, although this is arbitrary. Color has great appeal because it provides a nearly instantaneous presentation of the velocities, which has the following advantages (14): 1. 2. 3. 4. 5.

1. 2.

Incident Angle (%)

3.

40 50 60 70

Angle-adjusted Velocity (cm/s)

3.561 2.906 2.292 1.524

73 71 72 70

The local vascular anatomy is immediately displayed. The relation of flow to the wall is apparent. Areas of narrowing and turbulence may be detected. The direction of flow is detected. Regional changes in velocity can be seen.

Even given all of the advantages of color, there are problems that need to be faced because they can adversely affect how the data are generated and interpreted. Some of the problems are as follows:

TABLE 2.2 Doppler frequency and angle-adjusted velocity from superficial femoral artery Doppler Frequency (kHz)

11

4.

Aliasing can occur with color. Changes in the direction of the velocity vectors will result in a change in the hue of the color, which may be misinterpreted as an absolute velocity change. The frequency shift information referable to the color bar and velocity should not be construed as representing a true value. The velocity data obtained with color are mean values (4). The temptation to make direct measurements of the degree of stenosis as an index of the degree of narrow-

12

Part I Imaging Techniques

ing must be resisted. Simply changing the gain can drastically alter what one might consider to be the lumen of an artery. Power Doppler does not display the frequency change at the site of interrogation. It reflects the amplitude of the backscattered frequencies—not the Doppler shift. This has certain advantages, particularly when one is interested in the arterial anatomy or the geometry of a stenosis. It is a valuable adjunct to the other aspects of duplex scanning.

Medical Applications of Ultrasonic Duplex Scanning Ultrasonic duplex scanning has reached such a level of maturity that it is now possible to draw some conclusions about its use in cardiovascular medicine (3). There are few technologies currently available as cost-effective or generally as useful as duplex scanning in clinical medicine. As will become evident, no other diagnostic instruments have the versatility found with duplex scanning. Nearly every area of clinical interest and need can be studied with this method.

The Carotid Artery The first area in the circulation to be studied by duplex scanning was the carotid artery (16). This was done for several reasons: first, its proximity to the skin makes it easily accessible to ultrasound; and, second, disease in this location is common and is frequently studied by contrast arteriography. This made it possible to validate the accuracy of duplex scanning in detecting the presence of disease and estimating its severity. It is now clear that arteriography is not a good gold standard for this purpose. Atherosclerosis commonly affects the extracranial circulation but has the highest incidence at the level of the bulb. The carotid bulb is a unique area in the circulation owing to its geometry. It is the only region of the arterial system where a regional dilation is found. The geometry of the bulb creates peculiar flow patterns that can be a source of great confusion if their presence is not recognized (8). It has been theorized that this geometry and the resulting flow patterns explain the localization of the atheroma to this region. As all vascular surgeons recognize, the disease rarely extends beyond the distal limit of the bulb itself, which is one reason that carotid endarterectomy is feasible. The flow changes in the normal bulb that are unique are referred to as boundary layer separation (8). As the flow enters the bulb, that flow near the flow divider will be antegrade at all times in the pulse cycle, while that in the posterolateral region will reverse. The area of reverse flow is the region of boundary layer separation (8). The size of this region varies during the pulse cycle. As flow leaves

the bulb, a helical flow pattern will be generated that is propagated for varying distances into the internal carotid artery. The presence of boundary layer separation can be demonstrated both with FFT displays and with color (Fig. 2.8). The dramatic nature of the flow changes during a single pulse cycle can be seen in the FFT display. The importance of understanding boundary layer separation is that it does not occur when an atheroma fills the posterolateral region of the bulb; that is, it is only seen with a normal bulb. In clinical medicine we must deal with the relation between the extent of disease and the clinical outcome, so it is important to develop criteria that can be used to dictate how the patient should be treated. Over the past several years, we have developed categories of disease involvement detectable by duplex scanning that are of great practical value. These can be summarized as follows (10): 1. 2. 3. 4. 5.

normal; <50% diameter reducing stenosis; 50–79% diameter reduction; 80–99% diameter reduction; total occlusion.

With the publication of the results of the North American Symptomatic Carotid Endarterectomy trial (NASCET) (17,18) and the European Carotid Surgery Trial (ECST) (19), the relationship between the degree of diameter reduction and stroke became clear. The degree of

FIGURE 2.8 In the normal bulb, an area of recirculation is found in the posteriolateral aspect of the bulb. In this area, flow will be both antegrade and retrograde. With the sample volume near the flow divider, all flow is antegrade. However, with the pulsed Doppler sample volume moved to the lateral aspect of the sinus, both forward and reverse flow components are seen. This is referred to as boundary layer separation. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 113–157.)

Chapter 2 Ultrasonic Duplex Scanning

risk is clearly associated with how much narrowing is present. The highest risk is in the 80% to 99% diameter reduction category. After the early reports that only the 70% diameter reducing lesions were significant, we began to use another velocity-derived parameter to classify this degree of diameter reduction. The algorithm for its detection is easily adapted to the criteria already in common use (19). The diagnostic criteria for determining the degree of diameter reduction are related to two ultrasound features (Fig. 2.9): peak systolic velocity and end-diastolic velocity. We have stopped using spectral broadening except in special circumstances. They are used in the following fashion:

3.

4.

5. 1. 2.

Normal bulb. The major diagnostic finding is boundary layer separation. Diameter reduction <50%. Disease is seen in the bulb on imaging but it does not increase the peak systolic flow velocity across the bifurcation.

13

Diameter reduction >50% but <79%. There is an increase in the peak systolic velocity at the stenosis that exceeds 125 cm/s. Diameter reduction 80% to 99%. The end-diastolic frequency now is greater than 145 cm/s. This is the lesion that is most likely to proceed to total occlusion. Of course, the peak systolic velocity will be much higher. To classify a lesion in the >70% diameter reducing range, it is necessary to divide the peak systolic velocity at the site of the stenosis by the peak recorded from the common carotid artery. If this ratio exceeds 4.0, there is a 90% chance that the lesion exceeds this cutoff value (19). Total occlusion. No flow will be detectable in the internal carotid artery. However, there are other clues that are useful in suspecting this finding. These include the following: 1) end-diastolic flow in the common carotid artery will often go to zero; in 34 cases of total occlusion, end-diastolic flow went to zero in 32;

FIGURE 2.9 The spectral criteria used for detecting varying degrees of stenosis of the carotid artery are shown. The major features, with increasing degrees of narrowing, include the peak systolic velocity, the end-diastolic velocity, and spectral broadening (see text).

14

Part I Imaging Techniques

2) flow in the contralateral carotid artery will be doubled as it now supplies both hemispheres, which results in a marked increase in the end-diastolic velocity; 3) as the sample volume is positioned close to the occlusion, a “thumping” sound may be heard that is very distinctive of total occlusion; and 4) there will be no flow in the internal carotid beyond the bulb—although one might think that color flow would be the best method of detecting a total occlusion, this has not been verified to date. It should be noted that flow in the contralateral carotid will be much higher so it may be necessary to downgrade the degree of narrowing there by one category (3). Because a total occlusion removes the patient from surgical consideration, this diagnosis is of paramount importance. In many cases, it will be necessary to obtain an arteriogram to render the final judgment, but even here there can be problems if the residual flow channel in the stenosis is very narrow and the flow very slow. The accuracy of duplex scanning as a method of detecting and classifying the degree of stenosis has been well established (10). Its sensitivity is in the range of 98% with a specificity that is in the 95% range, which makes it satisfactory for screening populations with either a high or low prevalence of disease (20). Screening Before Intervention The majority of patients with extracranial arterial disease who develop ischemic episodes will do so secondary to disease within the bulb. Although there is no doubt that lesions at the level of the aortic arch can lead to transient ischemic events and strokes, this is very uncommon. However, precise criteria for grading the degree of narrowing of the arteries at the level of the arch have not been worked out with the same precision. It is possible to detect turbulent flow patterns in the proximal common carotid artery that are a clue that problems exist at that level (21). Clearly, for lesions in the innominate and subclavian artery, arm pressures must be measured along with direct insonation of the subclavian arteries. This can be helpful in detecting clinically significant disease. A systolic pressure gradient of more than 15 mmHg between the two arms could be significant. Another area that has been of concern is the carotid siphon (22). It is well known that lesions can develop in this region that might be a cause of ischemic events. This area cannot be studied by duplex scanning. However, the studies that have been performed examining the role of the siphon have not supported the impression that lesions here are a cause of ischemic events. This region can now be evaluated by transcranial Doppler ultrasound, but there is not yet sufficient information to determine if this method is of any value for this purpose. As duplex scanning is an accurate screening test for lesions of the bulb (23,24), could it be used as the sole diagnostic test before carotid endarterectomy? The concern is that the information obtained by duplex scanning alone

might not prove sufficient to proceed safely with the operation. To address this issue, it is necessary to consider the problems that could occur to negate the use of duplex scanning alone: 1.

2.

3.

The key element is a properly performed duplex scan that accurately assesses the location and extent of the involvement In the results of the NASCET and ECST studies, the degree of stenosis was the only factor that determined the need for endarterectomy (17–20). The published results from good laboratories would suggest that a well-done test is as accurate as arteriography in determining the degree of narrowing. This means that vascular surgeons must have confidence in the laboratory doing their testing procedure. This means good quality control and experience (21–23). Does arteriography provide additional information that would preclude operation or suggest a different approach? There are obvious lesions, particularly at the intracranial level, that would, or could possibly, change the approach. These include aneurysms, tumors, and occlusive lesions in the distribution of the middle cerebral artery. Mass lesions would be discovered by the computed tomography (CT) scan, but occlusive lesions would not. Lesions at the level of the aortic arch may dictate a different approach because if undiscovered they may lead to failure of the carotid endarterectomy. This possibility can be avoided by a careful examination of the flow patterns at the level of the aortic arch (24). Interestingly, lesions in the siphon do not appear to contribute to the outcome after endarterectomy. The lesions which occur in the siphon are not generally due to atherosclerosis but are known as intimal cushions, which are smooth and do not appear to ulcerate (25).

We have carried out two prospective studies to assess the role of duplex scanning alone for the selection of patients for endarterectomy (26,27). Over a 29-month period, the vascular surgeons involved in the study had to make decisions relative to the management of 103 patients who were being considered for carotid endarterectomy (111 carotid arteries). For each case, the surgeon recorded his plan before the arteriography. Nine patients were excluded because arteriography was not carried out, or was performed before the surgeon’s evaluation. The duplex scans were diagnostic in 87 (93%) of the 94 cases. The carotid lesion was inadequately evaluated by duplex scan in seven patients because the disease was not limited to the distal common carotid artery or bulb (four cases), anatomic or pathologic features of the carotid artery interfered with imaging or Doppler analysis (one case), or a lesion could not be distinguished with certainty as an occlusion (two cases). When the duplex scan was adequate, the arteriography contributed information that was of additional value in only one case (1%). This patient had a middle cerebral artery stenosis distal to a

Chapter 2 Ultrasonic Duplex Scanning

high-grade stenosis. Operation was withheld because of this intracranial stenosis. Later, he sustained a completed stroke that might well have been secondary to the carotid bifurcation stenosis. We concluded that duplex scanning could be used as the sole preoperative study as long as a satisfactory, complete duplex scan had been performed. Our data suggest that a perfectly satisfactory outcome could be achieved by this approach. In fact, there are clinical trials under way that accept duplex scanning alone as the method used for selecting patients for endarterectomy. Postoperative Studies In the early postoperative period (first week), testing can be done but is generally used to determine the patency of the internal carotid artery. Because of the fresh wound and the patient’s discomfort, it is not always possible to carry out a complete study. However, within 7 to 10 days, a more complete examination can be done if it is deemed necessary. During the follow-up period, the major lesion that develops is myointimal hyperplasia (28,29). This is a smooth lesion that will develop within the first 12 months, and is not a common cause of ischemic events. Some of these lesions can proceed to total occlusion, but this appears to be very uncommon. The progression to internal carotid artery occlusion after operation was found in 4% of the 200 consecutive patients we have followed prospectively (28).

15

Doppler ultrasound, a great deal is known about the normal arterial flow patterns and their use in documenting both the presence and extent of disease. The most important fact to understand is that the velocity patterns are dictated by the vascular resistance offered by the tissue supplied and its metabolic activity at the time of study. There are some generalizations that are useful. The organs and systems that are low-resistance vascular beds are the brain, liver, spleen, and kidney. These organs demand high levels of blood flow at all times during the day. In the supplying arteries, the end-diastolic velocity should always be above the zero baseline (Fig. 2.10). The high-resistance arterial beds are the upper and lower extremities under resting conditions (35,36). At rest, a reverse flow component of the velocity waveform will be prominent until the resistance to flow decreases, such as occurs with and immediately after exercise (Fig. 2.11). The upper limb velocity patterns are more variable because some individuals will not show a reverse flow component even at rest. In the lower leg arteries, reverse flow should always be seen when the patient is at rest. There are arteries supplying tissues of intermediate resistance. The most common and frequently studied by duplex scanning is the superior mesenteric artery. Under fasting circumstances, a small

The Peripheral Arterial System The most widely used noninvasive test for peripheral arterial disease is the measurement of the ankle–arm index (AAI), followed in some instances by exercise testing (30–34). This provides the necessary objective baseline values for both establishing the diagnosis and following the progress of the disease with and without interventional therapy. If the patient is a candidate for intervention, the next diagnostic study performed is arteriography. This study provides the necessary road map for the surgeon in reconstructing the arterial system. Is this approach adequate or can we make significant progress by adding duplex scanning for specific cases (34,35)? The issue of using duplex scanning alone prior to operation will be considered in greater detail in Chapter 3. In order to determine the place for duplex scanning in diagnosis, it is necessary to establish its accuracy compared with arteriography, which is still considered to be the gold standard. Progress in the implementation of duplex scanning for the peripheral arteries had to await the necessary technological improvements that guaranteed access to all arteries of interest. For clinical purposes, it is necessary to scan the arterial system from the level of the abdominal aorta to the ankle arteries and, in the upper extremity, from the level of the subclavian artery to those at the wrist. Based upon previous experience with physiological studies and those conducted with continuous wave

FIGURE 2.10 With a low-resistance type of waveform, the end-diastolic velocity is always above zero. This waveform was taken from the mid-portion of the right renal artery (RRA). Ao, aorta. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 200.)

16

Part I Imaging Techniques

A

B

FIGURE 2.11 The high-resistance waveform typically has a reverse flow component as shown here from tracings taken from the external iliac artery (EIA), the common femoral artery (CFA), and the proximal superficial femoral artery (SFA-p). (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 166.)

amount of reverse flow is seen in the superior mesenteric artery. Within 20 minutes of eating, this pattern begins to change, with a loss of the reverse flow component and an increase in the end-diastolic velocity as the volume blood flow to the gut increases to meet the metabolic demands of digestion (Fig. 2.12). Interestingly, this same phenomenon is seen with the inferior mesenteric artery, but the flow velocity change occurs only when the material ingested is handled by the colon. The blood flow in the inferior mesenteric artery does not appear to change when foods ingested are handled primarily by the stomach and small bowel. Given these considerations, it is possible to utilize velocity data as diagnostic aids in assessing the status of the arterial system. Documentation of an abnormality depends upon demonstrating flow velocity changes that deviate from this normal pattern. As with other arterial beds, the extent to which the patient becomes symptomatic depends upon both the location and, most importantly, the degree of narrowing that is present. In the

FIGURE 2.12 Changes that occur with vasodilation of the mesenteric vascular bed after food ingestion are shown (top). Taken during fasting and (bottom) after food ingestion. There is a dramatic increase in both the peak and end-diastolic velocities noted. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 69.)

peripheral arterial circulation, patients will become symptomatic only when the pressure and flow beyond the lesion begin to decrease, making it impossible to maintain adequate nutritional flow either with exercise or at rest. In general, the level of narrowing that is sufficient to do this is a 50% or greater degree of diameter reduction. This is often referred to as a critical stenosis (37). However, some stenoses that narrow the artery by less than this amount can become hemodynamically significant under conditions of increased blood flow (38). In this case the increase in flow across the narrowed segment will induce turbulence that accentuates the normal pressure gradient. When there is a decrease in pressure and flow during exercise, the patient may develop intermittent claudication. Given the above, it is clear that if duplex scanning is to partially or completely replace arteriography, it will have to be able to detect and grade lesions of all levels of severity (39). There are also other considerations that are relevant to this question.

Chapter 2 Ultrasonic Duplex Scanning

1.

2.

3.

4.

5.

6.

The studies have to be done at the sites of disease involvement. This means, of course, that long lengths of the arterial system will have to be scanned. The changes in flow velocity across the stenotic lesions should be a reflection of the degree of narrowing. The information must have clinical relevance for the physician in his or her management of the patients and their problems. The testing will have to be cost-effective and not just another test providing information that is already available from existing and, in some cases, less expensive tests. The testing should provide data that can be used for follow-up comparisons. It has become increasingly clear that accurate, objective follow-up is very useful in making sure that the benefits of therapy can continue. Several examples of this will be covered later in this chapter. Technologists should be capable of performing the tests.

For study purposes, the systems used must be state-ofthe-art, with color Doppler ultrasound and a variety of transducers with different transmitting frequencies. Because the arteries in the abdomen are deeper than those in the leg, lower transmitting frequencies in the range of 2.0 to 3.5 MHz for imaging may be required. For most applications, a 5-MHz system is adequate for Doppler studies. The scanning commences in the upper abdominal aorta, proceeding distally to the arteries at the level of the ankle. The technologist is testing for areas where the peak systolic velocity increases from one segment to another. The criteria that have emerged can be considered in two categories, each of which is very dependent upon the other. The role of color/power alone is reviewed below, but it cannot be divorced from the simultaneous use of the FFT real-time spectral analysis. Color/power Doppler ultrasound provides certain advantages related primarily to rapid identification of the vessels of interest as well as the sites of the lesion(s) and a rough estimate of their severity (13–15). Color Doppler alone must not be used to quantitate the absolute velocity values. It provides data only on the means and not the absolute values for the peaks (4). Power Doppler is based on the amplitude of the backscattered ultrasound and not the velocities. With experience, color has been useful in the following ways: 1.

2.

The normal flow pattern of triphasic flow can be recognized by the transient appearance of blue (reverse flow), which becomes apparent during late systole and early diastole (14,36). With a stenosis there are two changes that suggest that it may be a lesion with more than 50% diameter reduction (15). The first is the appearance of turbulence, which is seen as an admixture of colors just

3.

4.

17

distal to the stenosis. The other indirect sign is the appearance of a bruit. This is recognized as the appearance of spontaneous bursts of color outside the arterial wall. This represents arterial wall vibration. It is only seen at and distal to a stenosis, which is consistent with the clinical observation that bruits are always transmitted downstream of the area of narrowing. An occlusion is recognized by two features (15). One is the lack of color flow at sites where it should be found. The other is the appearance of collateral vessels that take their origin at right angles to the artery. Since this dramatic change in direction of flow, which is now either toward or away from the transducer, the color change at the site of origin of the collaterals will be dramatic. In most cases, the color will be a very light shade of red, or even white, reflecting this dramatic change in the direction of flow. Power Doppler is particularly useful in identifying the anatomy of the segments being examined. For example, the tortuosity seen in the internal carotid artery may be difficult to sort out, but power Doppler makes this much easier.

These color changes are important, but, as mentioned earlier, the best method of determining the actual velocity at suspected sites of narrowing is to make use of the single sample volume of the pulsed Doppler and the FFT to give an accurate measurement of the true velocities at areas of narrowing. Although the color provides the road map, we still must rely on the velocity changes as follows (Fig. 2.13): 䊏

䊏

䊏

䊏

Normally, there should not be a detectable change in peak systolic velocity in short segments of arteries. However, it is well recognized that there is a gradual decrease in peak systolic velocity as one moves down the limb from the level of the abdominal aorta to the tibial arteries at the ankle (36). With roughening of the arterial wall but without a measurable degree of narrowing, the only detectable change will be some spectral broadening (36). For this category we have labeled the disease as being in the 1% to 19% category of diameter reduction. As the lesions progress there will be a progressive increase in the peak systolic velocity (32,33). For stenoses in the 20% to 49% category of diameter reduction, the peak systolic velocity will increase between 30% and 100% over that in the preceding segment. Most importantly, there will be spectral broadening but the reverse flow component is generally preserved. These are not a clinical problems when the patient is at rest. However, in some cases with the increase in flow that accompanies exercise, turbulence can develop which can lead to a pressure drop. For the pressure and flow-reducing lesions (> 50% diameter reduction), the peak systolic velocity within

18

Part I Imaging Techniques

䊏

FIGURE 2.13 The spectral criteria used to separate the varying degrees of involvement of the peripheral arteries are shown. (A) With the normal artery the triphasic waveform without spectral broadening is seen. (B) With 1–19% wall roughening, reverse flow is retained but some spectral broadening can be noted. (C) In the lesions with 20–49% diameter reduction, the peak systolic velocity will increase by 30% to 100% from that of the preceding segment, with spectral broadening noted. Reverse flow may be preserved. (D) In the lesions with 50% to 99% diameter reduction, the peak systolic velocity increases by more than 100% from that of the preceding segment. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders. 2nd edn. New York: Raven Press, 1993: 169.)

the stenotic segment will increase by more than 100% over that in the preceding segment, with a loss of the reverse flow component and the development of marked spectral broadening (35,36). Total occlusion is recognized by the absence of flow.

These criteria have been prospectively tested against arteriography, with the results shown in Table 2.3. When one examines the accuracy of duplex scanning and compares its results against those of arteriography, the ultrasonic method does quite well. The comparison between duplex scanning and the reading of a single arteriographer does not tell the entire story because there is another element of variability in the reading of the arteriograms. To evaluate the interobserver variability, we compared the results when the films were read by two radiologists (see Table 2.3) (36). Because only the stenoses with diameter reductions of less than or more than 50% are clinically relevant, this subset of stenoses was chosen for comparison. In this study, both radiologists used calipers to measure diameter reduction. The senior radiologist was arbitrarily used as the gold standard. The results for this study are summarized in Table 2.4 for the positive and negative predictive values for the segments studied. These types of data reinforce the belief that the gold standard also has limitations, as does duplex scanning. However, this does not negate the potential role for the ultrasonic method. Either method must be used in the context of the clinical presentation. For example, if the patient has intermittent claudication and a superficial femoral occlusion but there is also a suggestion of an iliac artery stenosis, a negative duplex scan of the feeding iliac artery would appear to be sufficient to direct attention to the femoral artery lesion alone. Screening Before Intervention The patients for whom we have reserved duplex scanning are those considered candidates for intervention, be it endovascular or surgical (40). To prospectively test the role of duplex scanning, we conducted a study that included 122 patients who had undergone both duplex scanning and arteriography. There were 110 arteriograms that

TABLE 2.3 Duplex scanning versus arteriography for a stenosis of less than or greater than 50% diameter reduction Arterial Segment Aorta Iliac Common femoral Superficial femoral Profunda femoral Popliteal All segments

Sensitivity (%)

Specificity (%)

Positive Predictive Value (%)

Negative Predictive Value (%)

100 90 67 84 67 75 82

100 90 98 93 81 97 92

100 75 80 90 53 86 80

100 96 96 88 88 93 93

Chapter 2 Ultrasonic Duplex Scanning TABLE 2.4 Comparison of two radiologists in classifying arterial lesions into categories of less than or more than 50% diameter reduction

Arterial Segment Iliac Common femoral Superficial femoral (proximal) Superficial femoral (middle) Superficial femoral (distal) Popliteal All segments

5.

Positive Predictive Value (%)

Negative Predictive Value (%)

94 100 100 100 78 100 88

96 91 88 93 94 95 93

The senior radiologist was arbitrarily used as the “gold standard.”

were preceded by duplex scans. Of this group, 45 were scheduled for angioplasty on the basis of the results of the duplex scan. Angioplasty was performed in 47 of these cases. In one patient, the lesion was felt to be too dangerous to dilate. In a second patient, a significant pressure gradient was not found across the area of stenosis. In a third patient, a stenosis in the superficial femoral artery distal to a total occlusion was missed. Is this approach worthy of the extra effort and time? At present, there are several reasons why these appear to be acceptable. First, if duplex scanning is as accurate as two radiologists reading the same films, why not apply it as a screening test? Second, it is likely that the number of arterial punctures was reduced because the radiologists knew before the procedure where the lesions were to be found. Third, this method is likely to reduce the total number of arteriograms obtained. It appears that many radiologists and surgeons use arteriography as the initial diagnostic procedure, then decide what approach should be used at a later time. Finally, this is a very satisfactory approach in that patients can be made aware of the proposed form of therapy and the likelihood of success. Vein Mapping The saphenous vein is the most satisfactory bypass graft for peripheral arterial occlusive disease, so it is important to determine its adequacy before surgery. The advantages of preoperative ultrasonic assessment are as follows (41). 1. 2.

3.

4.

Anatomic variants are not uncommon, being found in 30% to 70% of patients. Double systems are not uncommon. It is worthwhile to scan patients who have had a vein stripping because a duplicate system that may be usable can occasionally be found. Areas of scarring or occlusion within the vein may be found, which will require the modification of the procedure. The size of the vein may be estimated, providing some confidence as to its suitability as a conduit. In general,

19

a vein with an internal diameter of 2 mm is suitable for bypass purposes. Alternative sources for veins can be determined in those patients in whom the greater saphenous is either absent or inadequate.

In the prospective studies that have been done, the sensitivity of duplex scanning was found to be in the 93% to 96% range. The positive predictive value was also in this range. The specificity is not as high, being in the range of 60% to 70%. In some cases, it is necessary to explore the suspicious venous segments to be certain of their status. In some patients whose lower limbs do not have suitable veins, it may be necessary to screen the arms for a possible conduit. In order to do the study, it is necessary to use a highresolution B-mode system. The linear array transducers (7–10 MHz) have an advantage in that long segments of vein can be seen in the field, which makes the scanning time faster. To facilitate the examination, it is best to do the study with the leg in a dependent position, which can either be the reverse Trendelenburg or the standing position. This provides maximal venous dilation, which is important both for visualizing the vein and for determining its diameter. The scanning procedure takes 20 to 30 minutes, and the technologist can then mark the course of the vein, along with large branches that might be of concern. Follow-up Once the surgical or endovascular procedures is completed and the patient has left the hospital, the long-term outcome is dependent upon two major factors. One is the problem of myointimal hyperplasia (42). This interesting lesion may develop when there has been some injury to the vessel wall. The lesion, in its most simple terms, is an overgrowth of smooth muscle that may significantly narrow the artery or graft at the site of development. If the narrowing becomes sufficiently severe, the procedure may fail. The exact incidence of myointimal hyperplasia is not known, but it has been estimated that up to 30% of those with arterial reconstructions will develop this complication. The lesion will nearly always develop during the first year following the therapy. The other common cause of failure of many reconstructions is disease progression. This can occur either proximal or distal to the site of therapy. Until recently, it was not common practice to follow patients prospectively after surgery, but rather to simply await the appearance of new symptoms. This was not proper, as we now know from the prospective studies that have been done. Regular surveillance of the reconstruction appears to be very important, particularly for vein grafts, to detect new lesions before thrombosis occurs. Surveillance permits early correction of the complication with prolongation of the life of the graft (43,44). For vein grafts, the most suitable method of follow-up has been color Doppler ultrasound with real-time spectral analysis. This permits a complete survey of the graft in-

20

Part I Imaging Techniques

cluding the inflow and outflow arteries as well. The criteria that have been developed relate to the extent of the degree of stenosis and the peak systolic velocity in the graft itself, which can also reflect changes in both the inflow and outflow from the graft. Although the criteria used by different investigators have varied somewhat, the following guidelines would appear to work well for follow-up purposes. Arterial Inflow Most of the grafts being followed have their origin from the common femoral artery, but some will be placed at a lower level, depending on the extent of the occlusive disease. Regardless of the site of origin, there are velocity criteria that can provide information that is useful. These are as follows: a triphasic waveform (forward–reverse–forward flow). This is reassuring that inflow to that point is adequate. The finding of a monophasic waveform at any point proximal to the origin of a vein graft is certain evidence that there is proximal disease that is hemodynamically significant. If one desires to further scan the inflow to localize the site of involvement and estimate its significance, the procedure as described earlier in this chapter should be followed. The Vein Graft Before beginning the scanning procedure, the examiner must be aware of the type of graft used (in situ versus reversed). With the in situ graft, the proximal portion of the graft is larger, and the opposite is found with the reversed graft. With the in situ graft the peak systolic velocities will increase as one approaches the distal anastomosis; the opposite will be seen with the reversed vein graft. There are several points to consider in determining how well a graft is functioning. The areas that are of specific interest are as follows: First is the proximal anastomosis. The geometry of an end–side anastomosis is complex. It is impossible to provide firm guidelines to be used with regard to absolute values for peak systolic and end-diastolic velocities across such unions. However, because follow-up studies permit comparisons from one visit to another, it is possible to document the development of an anastomotic stenosis when changes are found. Second is the vein graft itself. Problems can also develop at sites of valve cusps (4,5). Most myointimal lesions are generally very well localized, as noted in Fig. 2.14. These discrete areas will produce changes in peak systolic velocity, the magnitude of which depends on the degree of diameter reduction. Arteriovenous fistulas may also be present in the in situ graft and are easily recognized by the very high end-diastolic velocities recorded proximal to the fistula. The findings during follow-up that are important can be summarized as follows. The velocities in a graft without any obvious sites of narrowing will be dependent upon several variables including the size of the vein graft and the nature of the outflow. Low velocities (<45 cm/s) can be found in an otherwise normal graft, particularly if the graft is large (6 mm or greater). However, if velocities below 45 cm/s

FIGURE 2.14 This B-mode picture is of a stenotic lesion in a vein graft that developed secondary to myointimal hyperplasia. Arrows indicate site of lesion.

are seen in a vein graft without any obvious sites of stenosis, then it is either secondary to an inflow or outflow problem. For velocities at sites of narrowing within the body of the graft, the problem is not in detecting the site of narrowing, but in estimating its severity and, most importantly, its present and future effect on graft function. If the lesion narrows the graft by more than 50%, it will most likely lead to a fall in distal pressure and flow, which could compromise graft function. The problem is further complicated by trying to predict on the basis of diameter reduction which grafts will thrombose if left alone. This is, of course, the most important issue because vein graft patency, along with preservation of function, is the major goal of a surveillance program. The efforts in this regard have been led by Bandyk (43,44), followed by others who have carried out similar surveillance programs in an attempt to detect those lesions that need prompt intervention in contrast to those that can be safely followed. While there are some differences in the end points used for intervention, the published studies have in general shown an improvement in assisted primary patency of the vein grafts by instituting such a program. Bandyk has proposed that the indications for graft revision be based on the severity of the hemodynamic impairment of the graft rather than the duplex scan findings alone (40,41). He has recommended graft revision for the following situations: 1) a low peak systolic velocity (<45 cm/s) in the distal graft; 2) a decrease in peak systolic velocity of more than 30 cm/s associated with a decrease in the AAI of more than 0.15; and 3) a correctable lesion within the vein graft. Bandyk’s program has achieved an assisted primary patency rate of 85% at 2 years by following this protocol.

Chapter 2 Ultrasonic Duplex Scanning

Idu et al., in a prospective study of 201 vein grafts, reported that for 58 grafts with stenotic graft lesions that were not treated, the following outcome was noted (45): none of the grafts with a 30% to 49% diameter reduction failed; occlusion occurred in 57% of the non-revised grafts with a 50% to 69% diameter reduction, as compared with only 90% of the revised grafts; and grafts with a 70% to 99% stenosis all failed if not treated, as compared with 10% for the revised grafts. By following such a protocol, the primary assisted patency at 48 to 60 months for grafts with lesions not treated at the time of detection was 72%. In contrast, for those in which intervention was performed, the rate during the same time interval was 88%. Mattos et al., over a 39-month period, studied 170 limbs with vein grafts (46). These grafts were studied at 3, 6, and 12 months and then yearly. There were 110 stenoses detected in 62 (36%) of the vein grafts. Of these stenoses, 27% were at anastomoses and 65% were in the graft itself. A total of 77% were detected within the first year. Of this group, 39% of the grafts with lesions were revised. For those grafts with negative scans, the primary patency was 90% at 1 year and 83% at 2 to 4 years. In contrast, the patency rates with grafts that had a stenosis of more than 50% diameter reduction that were not corrected, the patency was 66% at 1 year and 57% for years 2 through 4. Mattos et al. concluded that color duplex scanning was effective in detecting those lesions of more than 50% diameter reduction, which were associated with a high failure rate (46). The criterion for detecting such a stenosis in a vein graft was finding a peak systolic velocity ratio of 2. The ratio is the peak systolic velocity in the stenosis divided by that recorded just proximal to the stenosis. Our studies are quite similar to the above. We have noted that duplex scan velocity measurements are valid predictors of impending graft stenosis. The best predictors of outcome were a velocity ratio of 3.5 or more and a mean graft velocity of <50 cm/s. We recommend repair of correctable graft lesions that fall into this category. Grafts that do not have detectable lesions in the inflow, the graft or outflow regardless of the mean graft velocity may be safely followed (47–50). Most of the changes that require revision will develop within the first few months but the surveillance program must still be followed. The time intervals for study vary somewhat from center to center but are most frequent in the first year. If the graft remains patent without problems at one year, the intervals of study can be every 6 months. If a new problem develops at any time the follow-up interval will have to be shortened to document the stability of the lesion.

important as methods of screening and follow-up after intervention, be it surgical or endovascular. Mesenteric Circulation The two most common events involving the mesenteric circulation are acute mesenteric ischemia and mesenteric angina. In the case of acute ischemia with occlusion of the superior mesenteric artery, the clinical presentation and urgency for a prompt diagnosis are such that duplex scanning has a small role to play. The success of the outcome depends upon the rapidity with which therapy is applied to prevent bowel necrosis, which is associated with a very high mortality rate. Chronic mesenteric ischemia is often difficult to diagnose. Although the clinical presentation of fear of food because it produces abdominal pain and diarrhea accompanied by marked weight loss is typical for the syndrome, the symptoms are often not specific. Often other causes for the symptom complex need to be sorted out. Prior to the availability of duplex scanning, aortography with lateral views of the celiac and superior mesenteric arteries was the only method of establishing with certainty the involvement of these arteries, which is required for the syndrome to develop. It is now well known that all three of the major arteries supplying the small bowel must be involved for this syndrome to develop. This is because the collateral circulation that can develop is normally very extensive. For example, it is possible for the celiac and superior mesenteric arteries to be totally occluded yet the blood supply to the small bowel be entirely normal via the inferior mesenteric artery. Thus, in theory if duplex scanning is to play a diagnostic role, it should be used to investigate all three sources of blood supply to the small bowel. Until recently, most attention has been paid to the celiac and superior mesenteric arteries (51–55). The inferior mesenteric artery, owing to its size and location, has been more difficult to study, but this is now also possible. The guidelines that have been used for the diagnosis of chronic mesenteric ischemia have evolved to include the following (53,54). 1. 2.

3.

The Visceral Arteries With the availability of low-frequency transducers, it has become possible to study flow in the hepatoportal circulation, the mesenteric arteries and the renal arteries. From the standpoint of the vascular surgeon, these have become

21

4.

The criteria used are based on changes in the peak systolic velocity. The normal peak systolic velocities in the abdominal aorta in the region of the origins of the celiac and superior mesenteric arteries are in the range of 100 ± 20 cm/s. As the sample volume of the pulsed Doppler is moved from the aorta to the first portion of the celiac and superior mesenteric arteries, the peak systolic velocity will increase. To establish the normal range for the detected velocities, Moneta et al. studied 100 patients with lateral aortograms as a part of a workup for peripheral arterial disease (54).

22

Part I Imaging Techniques

The peak systolic velocities for celiac and superior mesenteric arteries with a diameter reduction of less than 70% were compared with those noted to have highergrade lesions. Values of less than 275 cm/s for the celiac artery and less than 200 cm/s for the superior mesenteric artery were sufficiently accurate to rule out the highergrade lesions. They considered the higher-grade lesions as potential contributors to the syndrome of chronic mesenteric ischemia as long as both were involved. In practice, the clinical presentation and a finding of high-grade stenoses or occlusions of these two major inputs to the gut are generally sufficient to make the diagnosis and institute therapy. If the inferior mesenteric artery is also studied and found to be normal, it may be necessary to carry out a food challenge to test the ability of the available blood supply to meet normal nutritional needs. Moneta et al. published a case report of a patient whose small bowel was entirely supplied by the inferior mesenteric artery. In this patient, it was shown that the blood flow increase with a food challenge was entirely normal (55). With regard to the response of the blood flow in the superior mesenteric artery to feeding, the normal patterns are now well known. Before detailing the response to a food challenge, it is necessary to review briefly the normal blood flow patterns during fasting. Under fasting conditions, the velocity patterns in the celiac, superior, and inferior mesenteric circulations have been well characterized. The celiac artery supplies the liver and spleen, which are low-resistance organs. This means that the end-diastolic velocity will always be above zero, much as is seen with the internal carotid artery. On the other hand, the mesenteric arteries supplying the gut have a much different pattern. Under fasting conditions, the resistance to flow is high, which results in an enddiastolic velocity that goes to zero and in some cases is associated with a reverse flow component similar to that seen with the arteries supplying the lower limbs. With the ingestion of a mixed meal (Ensure®). there are dramatic changes in the flow in the superior mesenteric artery with little or no change in the flow in the celiac artery. After eating, flow rapidly increases in the first 20 min, reaching a maximal level in 30 to 60 min (56). The changes are in both the peak systolic and end-diastolic velocity, reflecting the increase in volume flow that is required (Fig. 2.15). The response of the inferior mesenteric artery is entirely different. The blood flow to the colon will not change with ingestion of materials destined to be handled by the stomach and small bowel. However, if the material taken by mouth is handled entirely by the colon, flow in the inferior mesenteric artery will increase, but only after the material reaches the colon. One such substance is lactulose, which is handled entirely by the colon. When it is ingested, there is no change in the flow in the superior mesenteric or celiac arteries until 45 minutes later when the material reaches the colon. Then the peak systolic and end-diastolic velocities will increase in the inferior mesen-

FIGURE 2.15 The dramatic changes in the enddiastolic velocities recorded from the superior mesenteric artery after ingesting a variety of meals are shown. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 69.)

FIGURE 2.16 Example of the changes in the velocity patterns from the inferior mesenteric artery after ingestion of lactulose. Left: fasting; right: after lactulose (see text).

teric artery (Fig. 2.16). These studies clearly show how the small and large bowel respond to different food challenges. However, it has not been possible to use the “food challenge” as a test for mesenteric insufficiency. It has not proven useful for separating cases with marginal disease of the mesenteric arteries from those that truly lead to the full-blown syndrome. Follow-up The success of intervention can easily be monitored using duplex scanning. Because the site and nature of the intervention are known, it is a simple matter to reexamine the area to assess the outcome. Although no group has experience with a large number of these patients, we have had the opportunity of using duplex scanning to detect problems with reconstructions that could be corrected before there was irretrievable loss of the repair. A few examples of how this can be done are in order. Case no. 1 This 49-year-old woman had a classic history of chronic mesenteric angina. A duplex scan revealed a high-grade stenosis of both the celiac and superior mesenteric arteries (Fig. 2.17). This was treated by a saphenous vein graft from the origin of the celiac artery to the superi-

Chapter 2 Ultrasonic Duplex Scanning

or mesentetic artery distal to the pancreas. The graft worked well and the patient was free of symptoms for 9 months, when they returned. A repeat duplex scan showed that there was no flow in the graft. However, it was possible to carry out a transluminal angioplasty of the superior mesenteric artery with complete relief of her symptoms. Case no. 2 This 65-year-old woman experienced marked weight loss associated with the fear of food. Every time she ate she developed abdominal pain and diarrhea. A duplex scan confirmed the presence of a high-grade celiac artery stenosis with occlusion of the superior mesenteric artery near its origin. A reversed saphenous vein graft was placed from the left common iliac artery to the superior mesenteric artery below the level of the pancreas. This worked very well for about 9 months, when the patient returned with recurrence of her symptoms. A repeat duplex scan showed the vein graft to be patent but with a tight stenosis noted at the origin of the vein graft. It was possible to correct this with a transluminal angioplasty at the site of the narrowing, with marked improvement in the velocities across this segment and relief of her symptoms (Fig. 2.18).

Renal Arteries The renal arteries are of great interest for two reasons: hemodynamically significant lesions are a common cause of hypertension, and bilateral lesions can be an important cause of renal failure. One of the problems with regard to this area of the circulation is that the renal arteries are difficult to access by almost any method. Several noninvasive tests have been designed to detect renovascular lesions, but these have been largely ineffective due to the high rate of false-positive and false-negative tests (57,58).

23

While renal artery stenosis has been considered to be uncommon, it appears to be more prevalent then previously thought. Because arteriography was the only available imaging method, it was applied in only very select cases. To give an accurate estimate of the numbers of patients with renal stenosis within the community of patients with hypertension is not possible, but there are some figures that are considered reasonably accurate. For example, within the entire population of patients with hypertension, it is estimated that 1% to 3% will harbor a lesion in the renal artery as the cause. However, if screening is limited to selected subgroups of hypertensive patients, the prevalence of a renal artery problem increases markedly. If screening is limited to patients who have blood pressure that is out of control, have malignant hypertension, or are in renal failure, the diagnostic yield will be in the range of 30% to 45%. Because of the location of the renal arteries, it is necessary to use much lower transmitting frequencies (2.0–3.5 MHz) to reach these arteries. Our own progress in this area has gone through several phases, each of which was important in helping us refine the method. These are as follows: 1.

2.

3. 4. 5.

Determine the feasibility of studying the renal circulation —we found that by studying normal subjects and patients in a fasting state to minimize the presence of bowel gas, complete studies could be done in up to 90% of patients (59,60). Develop diagnostic criteria that could be used to categorize normal renal arteries and those affected by both atherosclerosis and fibromuscular dysplasia. Develop algorithms that would characterize the degrees of narrowing into clinically useful categories. Prospectively test the algorithms against conventional arteriographic methods. Document the potential for using duplex scanning as a method of follow-up for patients who are being treated medically or by some form of intervention. In this regard, we were interested in determining which parameters might be most useful for documenting disease progression.

Diagnostic Algorithms

FIGURE 2.17 This lateral aortogram shows very tight stenoses in the celiac and superior mesenteric arteries of a patient with chronic mesenteric ischemia. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 96.)

Although it was relatively simple to develop criteria for the documentation of narrowing and estimating the degree of stenosis for arteries that are superficially placed, this is not the case for the renal arteries. By virtue of their location, size and tortuosity, it is often difficult to determine precisely the angle of incidence of the sound beam with the artery. This becomes critical if one is to estimate the degree of narrowing or to utilize these studies for follow-up. From our studies of normal subjects, we found that the normal values for peak systolic velocities for the renal arteries was in the range of 100 ± 20 cm/s (11). If these values were used as absolute cutoff levels for documentation of disease, this might lead to an unacceptably

24

Part I Imaging Techniques FIGURE 2.18 The high-grade stenosis near the origin of the saphenous vein graft from the left iliac artery was treated successfully by balloon angioplasty. (Reproduced by permission from Strandness DE, Jr. Duplex scanning in vascular disorders, 2nd edn. New York: Raven Press, 1993: 224.)

high false-positive level, resulting in unnecessary arteriograms being performed. To avoid this potential problem, we elected to use a cutoff level of 180 cm/s, which is approximately 2.5 standard deviations above the normal range. Any detected peak systolic value below this level would be considered normal. With regard to “significant” stenoses, what level of narrowing is sufficient to activate the renin–angiotensin system and lead to the development of hypertension? The study by Haimovici and Zinicola has provided information in this regard (61). These authors found that, in a dog model, the renal artery had to be narrowed by 60% or more to produce a pressure drop and cessation of urine flow. It was this cutoff level of narrowing that we attempted to estimate by the duplex findings. Kohler et al., in our first retrospective study, found that one of the most useful parameters was the renal/aortic ratio (RAR) (59). This defines the ratio of the peak systolic velocity at the site of narrowing in the renal artery to that recorded from the aorta. If this ratio exceeded 3.5, it appeared to provide a satisfactory cutoff point for the detection of a stenosis of more than 60% diameter reduction (60).

By using the above criteria, the following results were obtained in prospective studies comparing duplex scanning against arteriography (11). 1.

2.

For detection of renal artery stenosis without consideration of the degree of narrowing, the sensitivity of the examination was 95% [95% confidence interval (CI) 90–100%]. The specificity was 90% (95% CI 71–100%). For the detection of a stenosis of more than 60% diameter reduction, the sensitivity was 90% (95% CI 84–99%). The specificity was 62% (95% CI 43–80%). Of the 74 sides with arteriographic confirmation, 10 sides were labeled by duplex scanning as having a stenosis of less than 60% diameter reduction. Only one of these arteries was normal by arteriography. The remaining disagreements were not about the presence or absence of disease but about the precise degree of narrowing. This type of disagreement is not unusual given the uncertainty of interpreting the degree of stenosis by arteriography.

Chapter 2 Ultrasonic Duplex Scanning

3.

4.

For the detection of a total occlusion of the renal artery, the absence of a detectable flow signal combined with a kidney length of less than 9 cm proved to be quite accurate. A total occlusion was detected in 10 of 11 cases. One of the early problems that duplex scanning has largely overcome is the detection of accessory renal arteries. With the availability of color/power Doppler, these are being recognized with increasing frequency. There is no doubt that an accessory renal artery with a pressure and flow-reducing lesion can be the cause of hypertension.

Screening Before Intervention The most important role for screening of patients with hypertension is to detect those cases with renal artery stenosis that might be treatable by endovascular or surgical methods. One additional benefit is to provide referring physicians with a firm diagnosis on which they can base their therapy. Another important and emerging indication is the patient who may be at risk of developing ischemic renal failure. This problem is becoming recognized as increasingly important. It has been estimated that up to 150,000 patients may be on chronic renal dialysis secondary to atherosclerotic involvement of both renal arteries. Our experience to date indicates that up to 25% of patients referred for a screening study will be found to have a stenosis of more than 60% diameter reduction. Two diseases are commonly found as a cause of renal artery stenosis. The most common is atherosclerosis, which commonly affects the origin and first portion of the renal artery. The other is fibromuscular dysplasia, which is primarily a disease found in women and tends to involve the mid and distal renal artery. These are multiple lesions (like a string of beads), which make it difficult to estimate arteriographically the hemodynamic effects of these lesions. The lesions are discovered only when they are the cause of hypertension. If they are successfully treated by either angioplasty or surgery, the blood pressure will either be improved or be cured. We have found that if an RAR of 3.5 or greater is not lowered to below 3.5 by angioplasty, the patient’s hypertension will not be improved. Natural History of Renal Artery Stenosis The relation between renal artery stenosis and hypertension is well known, but the natural history of the atherosclerotic lesions, including-their long-term outcome, is not well understood. This is due to the lack of accurate, safe, and repeatable testing procedures such as duplex scanning. Before considering the long-term outcome, it is necessary to review the types of studies that have been done, the type of information that can be obtained, and its interpretation. Long-term outcome is determined by the rate of progression of atherosclerosis. For our studies we did not include fibromuscular dysplasia since the number of these

25

patients is quite small. Ideally, we would like to document the rate of disease progression by noting the transition from lesser to higher grades of stenosis and total occlusion. This is feasible within rather broad categories, as follows: normal; diseased but less than 60% diameter reduction; greater than 60% diameter reduction; and total occlusion. However, we have documented a method using peak systolic velocity alone to suggest that progression has occurred when the degree of stenosis falls into the 60% to 99% category (62). We have shown conclusively the relationship between the degree of stenosis and loss of renal mass. More about the data shortly (62,63). The patients recruited into the study were from those referred to the Vascular Diagnostic Service at the University of Washington Medical Center. A patient found to have a renal artery stenosis was invited to participate in our long-term surveillance program. In addition to the criteria developed for the grading of disease in the renal artery, we found that renal length (a reflection of mass) is also an important parameter to measure as well as flow patterns and resistance to flow in the cortex of the kidney (8,9,56). There were 170 patients who entered the study, 85 men and 85 women. These patients were discovered by duplex scanning. If the lesions occupied the mid to distal renal artery and the patient was a female, she was excluded from follow-up. There were 295 eligible renal arteries for long-term follow-up. The mean duration of follow-up was 33 months (range 33 months to 7.2 years). In these long-term studies we were interested in several factors: 1) the relationship between the degree of narrowing and kidney length; 2) the relationship between the degree of stenosis and renal failure; 3) the rate of progression of renal artery stenosis; 4) those factors that appeared to be predictive of progression and outcome; and 5) the correspondence between disease of the renal arteries and other sites commonly affected by atherosclerosis. It is important to note that there were no kidneys with loss of length of more than 1 cm in the normal group or the stenosis group with less than 60% diameter reduction. When the loss of renal mass is considered by extent of disease (unilateral vs. bilateral), the patients with bilateral stenoses with more than 60% diameter reduction had three times the risk of developing a smaller kidney (43% vs. 13%, p < 0.02). The progressive loss of renal mass as related to time is shown in Fig. 2.19. With the increasing interest in endovascular therapy of renal artery stenosis and the use of stents, to what extent can ultrasound be used to not only visualize the stent but detect the development of recurrent stenosis and occlusion? Fig. 2.20 illustrates a renal stent that is protruding into the aorta. This will be quite common when the periaortic lesions are being treated. Although the initial evaluation of the long-term outcome focused on the loss of renal mass, a larger number of patients were subsequently included in the follow-up program, permitting a better picture of the problem of disease progression and associated risk factors with the renal

26

Part I Imaging Techniques

FIGURE 2.19 The loss of renal mass (length) as related to baseline degree of disease. (Reproduced by permission from Caps MT, Zierler RE, Polissar NL, et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998; 53: 735–742.)

artery lesions. In our latest follow-up data there were a total of 170 patients each having at least one abnormal renal artery (62–66). The breakdown of these patients is as follows. There were 85 men and 85 women, of mean age 68 years. The follow-up interval was every 6 months. The mean follow-up duration was 33 months (range 3 months to 7.2 years). From the total of 295 eligible arteries, 45 were excluded either for prior intervention or for nondiagnostic studies. From the 295 sides available for follow-up, the renal artery was normal in 56, had a stenosis of less than 60% reduction in 96, a stenosis of more than 60% reduction in 143, and was totally occluded in 21. The loss of renal mass as related to the initial degree of disease is shown in Fig. 2.19. Interestingly, the incidence of progression to occlusion was 10%. As noted, there was a statistically significant relationship between the baseline level of disease and progression. The estimated 3-year cumulative incidence of progression was 18%, 28%, and 49% for renal arteries classified as normal, < 60%, and > 60%. The therapeutic implications of these studies will require more time to evaluate; however, it is clear that atherosclerosis, as in other areas of the circulation, continues to progress in an unpredictable fashion. Of course, if the progression occurs in both renal arteries, the outcome could be renal failure. It is here that earlier intervention by surgical or endovascular means may improve renal function and prevent the patient from going on to dialysis.

The Venous System Acute Deep Vein Thrombosis The most common vascular disorder that develops in the hospital is acute deep vein thrombosis (DVT). The disease

FIGURE 2.20 This color Doppler longitudinal view of the abdominal aorta at the level of the renal arteries clearly shows the presence of a stent which has protruded into the aorta. Stents are readily seen by duplex scanning.

can occur at all levels of the venous system, but its localization must be taken into account when reviewing outcome. For example, the early studies done with 125Ilabeled fibrinogen showed that the earliest sites for the development of venous thrombi were the sinuses in the soleal muscle and the sinuses of the venous valves (67). At this stage the thrombi did not produce symptoms or signs. However, if left untreated, up to 20% of the thrombi progressed to involve the posterior tibial and peroneal veins up to, and often including, the popliteal vein. However, this is not the pattern of involvement that is seen when patients present with symptoms and signs secondary to the development of DVT. More about this later. The term thrombophlebitis is commonly used to describe the involvement of the deep venous system, but it is not appropriate because the process is usually bland and does not lead to a marked inflammatory reaction in the vein or surrounding tissues. This is in sharp contrast to the process seen in the superficial veins, where the inflammatory response is very prominent and is one of its distinguishing features. It is my opinion that these two processes are separate and distinct and should not be considered in the same category. The treatment and potential for future complications is also entirely different for these two components of the venous system. Bedside Diagnosis There is no doubt that acute DVT can lead to the development of pain, swelling, and the appearance of prominent superficial venous collaterals. However, these are not specific enough to make them a reasonable set of guidelines for the diagnosis to be made (68, 69). It is also well known that the process is usually bland without producing any symptoms or signs. One of the most misleading historical factors that has led to confusion in the field is the use of Homans’ sign, which is positive when there is pain in the

Chapter 2 Ultrasonic Duplex Scanning

calf with forceful dorsiflexion of the foot, but is very nonspecific and must not be used at all in the course of an examination. The only situation in which the bedside diagnosis is adequate is with phlegmasia cerulea dolens (massive iliofemoral venous thrombosis). When this develops, the limb is massively swollen from the level of the thigh to the ankle. There is also severe pain, cyanosis, and in rare cases, a marked reduction in arterial inflow to the point where limb viability may be in question. No further diagnostic tests are needed for this syndrome to be recognized. The patients that should be scanned for acute DVT include the following: any patient suspected of having the disease; those with suspected or proven pulmonary emboli; those with unexplained leg swelling after orthopedic, pelvic, or vascular surgery; and patients with chronic leg swelling of uncertain etiology. Four ultrasound criteria are used to establish the diagnosis of DVT (70): 1) thrombus visualization; 2) incompressibility of the vein; 3) absence of spontaneous flow; and 4) loss of flow phasicity. Thrombus visualization is an obvious and certain way of making the diagnosis. However, the method is 92% specific but only 50% sensitive. The low sensitivity is due to the fact that some thrombi are not echogenic enough to be seen. In addition, it is not yet certain during which phases of their development thrombi are most likely to be echogenic. One of the most widely applied diagnostic methods is compression of the venous segment with the head of the transducer (62). This is always done with the vein visualized in a transverse view. If the two walls of the vein cannot be totally coapted with pressure, the test is positive. This maneuver has a sensitivity of 79% and a specificity of 67%. The problems with this method relate to those sites that are not readily compressible and include the inferior vena cava, the common iliac veins, and the superficial femoral vein in the adductor canal. Some investigators suggest that the ultrasound test only involve the common femoral and popliteal vein—use only compression and not include the calf veins or those proximal to the inguinal ligament. This also does not include the use of color/ power Doppler or the flow patterns that can be of use (71). This cannot be accepted as state-of-the-art and is, in fact, dangerous since it ignores key parts of the venous system. Today, with the advances in color/power Doppler combined with spectral analysis, we are able to identify with certainty the tibial/peroneal veins, the gastrocnemial veins and the soleal sinuses. The information obtained with pulsed Doppler ultrasound is very useful in establishing the diagnosis (70). Normally, venous flow is spontaneous in all proximal veins. In the veins below the knee, it may or may not be detected depending upon factors such as the ambient temperature. In a cool environment with vasoconstriction, cutaneous blood flow may be markedly reduced, leading to an overall reduction to the below-knee region. When spontaneous venous flow is not detected particularly from the tibial/peroneal veins, it is necessary

27

to augment flow by foot compression to be certain that the vein being studied is patent. The absence of spontaneous flow is highly specific to venous thrombosis involving the veins from the popliteal vein to the inferior vena cava. Of interest is the fact that the anterior tibial vein is rarely the site of venous thrombosis for reasons that are poorly understood. The anterior tibial vein is not routinely examined for the presence of thrombi. Because flow in the veins of the lower limb is normally dominated by respiratory events, the phasicity of flow is also a very useful parameter. Normally, with inspiration and descent of the diaphragm, intraabdominal pressure increases and venous flow will decrease. The opposite occurs with expiration. The absence of phasic flow is 92% sensitive and is specific for the diagnosis of DVT in the proximal venous segments. As noted above, this may not apply to the veins below the knee where the absence of spontaneous flow is not synonymous with acute DVT. Duplex scanning has largely replaced venography as the diagnostic test of choice. There are some circumstances in which the duplex method cannot be used, for example, when patients are in long leg casts. Another area of some difficulty is the patient with a past history of DVT who is suspected of having another acute episode. If the patient had been previously studied by duplex scanning, the problem would not be difficult, but in most instances this is not the case. As the previous DVT may have led to some chronic changes in the lumen and wall of the vein, it is often difficult to be certain that the findings are specific enough to warrant the diagnosis of recurrent DVT. In this setting it may be necessary to resort to venography, but even here it may be difficult unless dye is seen sleeving around a thrombus—the so-called railroad track sign. However, it is known that a major vein that is the site of an acute DVT will have a larger diameter than its companion in the opposite leg. When the vein has been irreversibly damaged by a previous episode of DVT, its diameter will be smaller than its companion in the opposite leg (72). Chronic Venous Disease Patients who fall into the chronic venous disease group are easily separated into those with primary and those with secondary venous disease. In general, the patients with primary venous disease have varicose veins without associated involvement of the deep venous system. Those patients who have a previous history of DVT and then go on to develop further problems are placed in the secondary category—the post-thrombotic syndrome. The presentation and problems with these two groups of patients are different. However, for both groups of patients, the studies are directed to the assessment of both residual obstruction and valve function. Evaluation of Valve Function The evaluation of valve function is difficult; therefore, it is necessary to review how this is done and the type of information that can be obtained. From a physiologic

28

Part I Imaging Techniques

standpoint, venous valves will close when a reverse transvalvular pressure gradient is produced (73). A small amount of reflux can and will normally occur before valve closure is completed. At present duplex scanning is the only method that can be used to examine specific venous segments in both the superficial and deep venous system. The problems with this and other methods of study relate to the manner in which reflux is induced and how it can be quantified. Most studies in the clinic or at the bedside are with continuous wave Doppler ultrasound. With this simple hand-held device, directional changes in venous blood flow are easily detected when a reverse transvalvular pressure gradient has been created. However, the manner in which the transvalvular gradient is created is a source of some uncertainty. In practice, most physicians have used the Valsalva maneuver and limb compression to induce reverse flow. In addition, most studies are performed with the patient in the supine position, which is not ideal. The veins should be maximally dilated to obtain the optimal results and this can only be realized if the patient is upright or nearly 50 (74). We have conducted a series of studies to develop and document the optimal method of study for the patient with chronic venous disease. It is my view that studies of this type must become standard if we are to make any sense out of many aspects of these difficult and often perplexing problems. First, while the Valsalva maneuver can induce reflux in most cases, there can be problems that greatly limit its application. For example, if there is a competent valve in the iliac or common femoral veins, reflux in the superficial femoral vein cannot be detected. In addition, the farther one moves away from the inguinal area, the less effective the Valsalva maneuver becomes. Limb compression is another method of suddenly increasing the transvalvular pressure gradient but, like the Valsalva maneuver, it has serious problems. It is very ineffective at the thigh level but is fairly good below the knee, where a forceful compression is much easier to perform. To get around many of the problems with Valsalva and limb compression, we developed the cuff inflation–deflation method for documenting reflux at all levels of the venous system, superficial and deep (64). The patients are studied in the upright position to ensure maximal venous filling. The pneumatic cuffs used vary in size from 24 cm for the thigh, to 12 cm for the calf, and 10 cm for the ankle. These cuffs are inflated by an automatic cuff inflator. The pressures used are 80 mmHg for the thigh, 100 mmHg, for the calf and 120 mmHg for the foot. The cuffs are rapidly inflated in 3 seconds, but most importantly, the cuff is completely deflated in less than 0.3 seconds. To determine valve incompetence, the transducer of the duplex scanner is placed less than 5 cm cephalad to the end of the cuff. As the cuff inflates, the vein beneath the cuff is emptied. With rapid cuff deflation, blood will reflux into the emptied venous segment if the valves within that region are incompetent. This method works well for both

the superficial and deep veins from the level of the pelvis to the ankle. It is the only method that provides objective, numerical data that can be referenced to normal values. In our early studies with the cuff method, we were able to determine that normal venous valves will close in less than 0.05 s in 95% of the normal venous segments (Fig. 2.21) (74). If one cannot use the cuff method, it is possible to use a minus 10 degrees Trendelenburg and use the Valsalva maneuver for the proximal veins and limb compression for the distal venous segments. When this is used, normal valve closure time is 2 s or less. With these normal studies as the background, we conduced several prospective studies in patients with acute DVT who were willing to be placed in a follow-up program. From these prospective and long-term studies, we have characterized many of the changes that take place after an episode of DVT. Many of the changes that we have documented explain a good deal about the natural history of patients with DVT. With regard to the problem of the post-thrombotic syndrome, it is not yet possible to predict who will develop the advanced changes that are commonly associated with this problem. Two outcomes are possible after an episode of DVT. One is the development of chronic venous obstruction and the other is the development of venous valve incompetence. Both processes can be present, but venous valvular incompetence is more common.

FIGURE 2.21 Venous valve closure times in normal subjects. The reflux duration was the time to valve closure after cuff deflation. Measurements were from the common femoral vein (cfv), superficial femoral vein (sfv), profunda femoris vein (prf), popliteal vein (pop), posterior tibial at calf level (ptc), and posterior tibial at the ankle (pta). (Reproduced by permission from van Bemmelen PS, Bedford G, Strandness DE, Jr. Ouantitative segmental evaluation of venous valvular reflux with ultrasonic duplex scanning. J Vasc Surg, 1989; 10: 425–431.)

Chapter 2 Ultrasonic Duplex Scanning

The consequences of chronic venous obstruction are different from those associated with valvular incompetence. Venous claudication may develop in patients who have chronic obstruction of the iliofemoral venous segment. They often have patent veins and competent valves distal to this level. With exercise, which has to be quite severe, the marked increase in arterial flow cannot be emptied in a normal manner. This leads to venous congestion of the thigh, which is very painful (75). The patient complains of a bursting pain that can be relieved only by elevation of the limb. Beginning with the studies of Killewich et al., we have been interested in the relation between spontaneous lysis of venous thrombi and venous valvular reflux (76). Several things have been learned from these prospective studies. The major finding can be summarized as follows: lysis starts early after the DVT and is progressive in most patients; recanalization of the occluded venous segments is common (76); and the time of recanalization (lysis) is important in determining which valves will become incompetent. We found that the earlier lysis takes place, the more likely it is that valve function will be preserved (77–80). Valves in veins not involved in the thrombotic process rarely become incompetent during follow-up; and after complete recanalization, the vein diameter will return to a level comparable to that of the noninvolved vein in the other leg. On the other hand, if the thrombus is not completely lysed, the diameter of the vein will be less than that of its partner in the contralateral limb; if recanalization occurs (partial or complete), the ability of the vein to dilate in response to a Valsalva maneuver remains normal (81).

Who Should Be Studied? There are compelling reasons for studying patients with a variety of vascular conditions, but there is little agreement as to which patients with chronic venous disease should be studied and for what purpose. My own approach is as follows.

29

The distinction between the primary and secondary forms of venous disease is important. Because the deep venous system is rarely involved with primary disease, it is very rare for these patients to develop the signs and symptoms of the post-thrombotic syndrome. Post-thrombotic Syndrome While there is little disagreement as to what can lead to the development of the syndrome, there are several unanswered questions that may be answered by the more widespread use of duplex scanning (80). For example, up to one-half of patients with the classic findings of the postthrombotic syndrome provide no historical clues as to why they sustained damage to the deep veins of the leg. There is no history of a previous episode of DVT. This is not surprising because DVT can be bland and produce few or no symptoms. Interestingly, the duplex ultrasound findings in patients with deep vein damage but without a history of DVT are nearly identical to those in patients with a definitive history of the problem (80). The similar findings suggest that extensive venous valvular damage can occur even in patients who have DVT but who never develop symptoms from the process. Which valves are of importance? As duplex scanning can be used to characterize all of the major veins, both superficial and deep, it is possible to relate the extent of the venous damage to patient outcome. The venous valves increase in number as one proceeds toward the foot. In fact, in the inferior vena cava there are no valves. In the iliac veins, valves are not invariably present, but as one moves in a caudal direction to the proximal superficial femoral vein, the greater saphenous, and profunda femoris veins, valves are commonly found. Two to three valves are often found in the superficial femoral vein, but again, this is extremely variable. One or two valves may be found in the popliteal vein. Below the knee there are hundreds of valves, which says a great deal about the importance of this region for continued and useful function of the leg.

Primary Varicose Veins If one accepts the fact that primary varicose veins generally involve only the superficial veins, there would be little need to study them unless some form of intervention were planned. Even then, what might be accomplished by a preoperative duplex scan? If one is contemplating a vein stripping, it is important to determine whether the entire greater saphenous vein will have to be removed. It is possible to restrict the procedure to only the involved veins if one has precise information about the status of the superficial system from the level of the groin to the ankle. Other valuable information that might not be anticipated is the finding of valvular incompetence in the deep system. When this is found, the patient should probably be placed in the secondary category even though there may be no history of a previous episode of DVT.

Transcranial Doppler Ultrasound Aaslid et al., in 1982, first reported the use of transcranial Doppler (TCD) methods for the study of the intracranial circulation (82). This method used a pulsed system of 2 MHz that could successfully penetrate the skull to provide flow information relative to the basal arteries. It was also shown that several anatomic ports could be used to access these arteries. These include the orbit, the transtemporal region, and the foramen magnum. The method as originally developed made use of the hand-held TCD unit, but it is now available with nearly all duplex scanners. The advantage of the use of TCD as a duplex method is clear, but there have been no studies that have shown it to be superior in terms of the information obtained or its use clinically. This will require much more work before its role can be clearly identified. The method

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Part I Imaging Techniques

has been proposed as useful for the following states: the detection of intracranial stenoses and occlusions; estimating the effect of extracranial lesions on flow velocity in the basal arteries; documentation of flow direction in the basal arteries; monitoring flow changes in the basal arteries during carotid endarterectomy; detection of arteriovenous malformations; monitoring flow velocity after subarachnoid hemorrhage to document the course of vasospasm; detection of microemboli; documentation of the ability of the brain to autoregulate in the presence of severe extracranial arterial disease; and documentation of brain death. Examination Method For a complete review of the method employed to interrogate the basal arteries with TCD, the reader is urged to review the work of Otis and Ringelstein (83). The windows chosen will determine which arteries can be detected and the information that is desired. Fig. 2.22 shows the arteries that can be detected along with the nomenclature used. 1.

2.

3. 4.

The transtemporal approach is used to detect flow in the M1 and N2 segments of the middle cerebral arteries (MCA). For the detection of these arteries, the anterior orientation of the sound beam is used. In addition, the C1 segments of the carotid siphon, the A1 segment of the anterior cerebral artery, and often the anterior communicating artery can be detected. With the beam directed in a posterior direction, the P1 and P2 segments of the posterior cerebral and the most anterior portion of the basilar artery may occasionally be detected. The important posterior communicating artery may also be studied in some patients. The transorbital approach is used to study the anterior cerebral circulation. From this site, the ophthalmic artery and the C3 segment of the carotid siphon can be detected. The suboccipital approach is the view used to screen the vertebral and basilar arteries. The submandibular approach is used if one wishes to track the distal internal carotid artery. With this window, it is possible to detect flow in the distal internal carotid artery. This approach is not very commonly used.

Study Parameters A direction-sensing pulsed Doppler is used for transcranial studies, so the parameters include the peak systolic and mean velocity and the direction of blood flow. The dimensions of the basal arteries cannot be measured, so it is not possible to measure volume flow by this approach. To estimate the functional reserve of the brain, the changes in blood flow velocity with hypocapnia and hypercapnia are determined. For the neurosurgeon, this may be the best method to determine which patients are most likely to benefit from extracranial-to-intracranial bypass grafting when the internal carotid arteries are occluded. The values of velocities for the middle cerebral, anterior cerebral,

FIGURE 2.22 The arteries that can be examined by TCD ultrasound and the position of the probe to insonate both tile anterior (A) and posterior (B) aspects of the circle of Willis. In A, the line XX¢ indicates the frontal plane that runs through placement of the probe on either side and perpendicular to the sagittal midline plane of the skull. Z¢ indicates the position of the intracranial carotid bifurcation. The X¢Z¢ distance is generally 63 ± 5 mm. The angle μ is the angle at which the probe is angled anteriorly to obtain signals from the middle and anterior cerebral arteries. The angle is in the range of 6° ± 1.1°. The angle w indicates the angle that is used to insonate the top of the basilar artery (T) and the P1 segments (P¢) on both sides. This angle was found to be in the range of 4.6° ± 1.2°. The basilar artery bifurcation could be detected at depths of 78 ± 5 mm corresponding to the distance XT or X¢T. Y indicates the fictional point at which the sound beam transits the contralateral skull, which is about 2–3 cm posterior to the external acoustic meatus. The P2 segments can also be insonated if the beam is directed even more posteriorly and caudally (X¢P). W lies approximately 5 cm behind the contralateral external acoustic meatus. (C) Basal and cerebral arteries of the circle of Willis. OA, ophthalmic artery; CS, carotid siphon (C1–C3); ICA, internal carotid artery, ACA, anterior cerebral artery (A1¢A2); ACoA, anterior communicating artery; MCA, middle cerebral artery (M1M2); PCA, posterior cerebral artery (P1P2) PCoA, posterior communicating artery; BA, basilar artery, VA, vertebral artery. (Reproduced by permission from Otis SM, Ringelstein EB. Transcranial Doppler sonography. In Zweibel WJ. Introduction to vascular ultrasonography, 3rd edn, Philadelphia: WB Saunders, 1992: 149.)

Chapter 2 Ultrasonic Duplex Scanning

posterior cerebral, and basilar arteries in normal subjects are quite constant and reproducible and tend to decrease with age (85).

Clinical Applications Detection of Intracranial Arterial Stenosis and Occlusion Not surprising, the findings that signify arterial narrowing of intracranial arteries are very similar to those found elsewhere: increased flow velocity at the site of narrowing and spectral broadening (85,86). Although these changes are specific for detection of narrowing, it is not yet possible to estimate the degree of stenosis in these small arteries. It must also be recognized that other lesions can lead to an increase in flow velocity such as arteriovenous malformations. However, in this case the flow changes will not be focal as they will with a stenosis. Occlusions are recognized by the absence of flow. The pitfalls associated with these findings are outlined by Otis and Ringelstein (83).

Assessment of Flow in the Basilar Arteries A potential benefit of TCD is that the effects of varying degrees of extracranial arterial disease on flow velocity in the basilar arteries and the potential contribution of the various components of the circle of Willis. For example, with a very tight internal carotid artery stenosis or occlusion, it is possible to determine by which route and from which arteries the middle cerebral artery receives its flow (83–86). In many cases these findings are quite specific, but it is not yet clear under what circumstances the information can be used from a diagnostic standpoint. For example, if a patient presented with an ischemic event and was found to have no extracranial arterial lesions, but a stenosis was found or suspected in the MCA or siphon, one might assume that this is the responsible vessel. How should TCD be used for patients with suspected extracranial arterial disease? My recommendation is that it be done only if there is no detectable disease in the carotid bulb or the disease found is not sufficient to explain the clinical presentation. There is no justification for doing this examination on all patients having a duplex scan study of the extracranial arterial circulation.

Assessment of Flow in the Posterior Circulation One of the most difficult areas to evaluate clinically is the basilar circulation. Vascular surgeons are often asked to see patients who are suspected of having the subclavian steal syndrome (87,88). These patients are suspected largely because of the nature of the clinical presentation, which varies considerably due to the nonspecific nature of the symptomatology. In general terms, these patients may be dizzy, have drop attacks, and, on very rare occasions,

31

present with exercise-induced dizzy spells (76,78). The patients are initially suspected when by duplex scanning a high-grade stenosis or occlusion of the subclavian artery is found with reversal of flow in the vertebral artery. In our laboratory, we identified 43 patients with reversal of flow in the vertebral artery. Only 7% of this group had symptoms that were compatible with the subclavian steal syndrome. However, the problem is less difficult if the innominate artery becomes involved (89). When this occurs, and there is either a very high-grade stenosis or occlusion, the patients are very likely to become symptomatic with exercise of the ipsilateral arm. Given the above, it is not yet clear what role TCD might play in unraveling this problem. Clearly, duplex scanning can provide the clue as to the site of disease, but this must be combined with a compatible clinical picture (79). We have used TCD to see if it might help sort out some diagnostic dilemmas with the posterior circulation, but unfortunately it has been of little assistance.

Monitoring During Carotid Endarterectomy One area of great potential appeal for TCD is the monitoring of patients undergoing the very common procedure of carotid endarterectomy. It is a relatively simple matter to continuously monitor flow velocity in the MCA during the operation (90–92). There are two areas in which the procedure might have merit. One is with regard to those who need a shunt to avoid a perioperative stroke. Another intriguing area is the detection of emboli during endarterectomy, and their sequelae (91). There is no doubt that TCD can detect emboli and may with more time and experience permit some conclusions as to their size, nature, and potential for causing problems. A study reported by Ackerstaff and Schroeder of 55 patients who were continuously monitored during endarterectomy documented 75 embolic episodes (91). However, in only one case could this be related to the development of a stroke. While it is difficult to prove that one can reduce the stroke rate associated with endarterectomy, there is information combined with intraoperative duplex examination of the endarterectomized segment that can be of assistance.

Vasospasm After Subarachnoid Bleeding Somewhere between 4 and 14 days after an episode of subarachnoid bleeding, cerebral vasospasm can develop. This can have a severe effect on cerebral blood flow and may lead to death if not corrected. It has been noted that TCD is a useful method of monitoring these blood flow changes, permitting intervention before the changes are irreversible (93).

Autoregulation of Cerebral Blood Flow The cerebral circulation can maintain cerebral blood flow within a normal range even with mean blood pressures as

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Part I Imaging Techniques

low as 50 mmHg. One method of testing this response is to use TCD to test the functional reserve of the cerebral arteries. The most convenient stimulus to use is carbon dioxide. In order to do this, it is necessary to monitor the MCA while having the subject breathe increasing concentrations of CO2 (2%, 3%, 4%, and 5%). Since CO2 mainly affects the small cortical vessels and not the MCA itself, any changes in velocity should be a reflection of a change in volume flow (94). If there is no response or a limited increase in blood flow to increasing amounts of CO2, it is presumed that the autoregulatory mechanism has broken down. Study of this response to CO2 may be of importance in selecting patients who could be candidates for the extraintracranial bypass grafting. Although this operation was discarded as being of little value in patients with internal carotid artery occlusion, there was no attempt to separate those patients who were able to autoregulate normally from those who were not. This may well be the only way to select potential candidates for extra-intracranial bypass grafting. The theory is that, if there is no longer any vasomotor reserve, any further reduction in pressure or flow is likely to precipitate an ischemic event.

References 1. Barber FE, Baker DW, et al. Ultrasonic duplex echo Doppler scanner. IEEE Trans Biomed Eng 1974; 21: 109–113. 2. Barber FE, Baker DW, et al. Duplex scanner II for simultaneous imaging of artery tissues and flow. Ultrason Symp Proc IEEE 1974; 74CH0896-ISU. 3. Strandness DE Jr. Duplex scanning in vascular disorders, 3rd edn. New York: Lippincott/William Wilkins, 2001, 1993. 4. Beach KW. Physics and instrumentation for ultrasonic duplex scanning. In: Strandness DE Jr, ed. Duplex scanning in vascular disorders, 3rd edn. New York: Lippincott/Williams Wilkins, Appendix, 2001. 5. Baker DW. Pulsed ultrasonic Doppler blood flow sensing. IEEE Trans Biomed Eng 1970; 17: 170–185. 6. Knox RA, Phillips DJ, et al. Empirical findings relating sample volume size to diagnostic accuracy in pulsed Doppler cerebrovascular studies. J Clin Ultrasound 1982; 10: 227–232. 7. Phillips DJ, Greene FM, et al. Flow velocity patterns in the carotid bifurcations of young presumed normal subjects. Ultrasound Med Biol 1983; 9: 19–49. 8. Ku DN, Giddens DP, et al. Hemodynamics of the normal human carotid bifurcation. I. Flow visualization. Ultrasound Med Biol 1985; 11: 13–26. 9. Kremkau FW. Diagnostic ultrasound, principles, instruments, and exercises. Philadelphia: WB Saunders, 1989. 10. Langlois YE, Roederer GO, Strandness DE Jr. Ultrasonic evaluation of the carotid bifurcation. Echocardiography 1987; 4: 141–149. 11. Hoffman U, Edwards JM, et al. Role of duplex scanning for the detection of athrosclerotic renal artery disease. Kidney Int 1991; 39: 1232–1239.

12. Phillips DJ, Beach KW, et al. Should results of ultrasound Doppler studies be reported in units of frequency or velocity? Ultrasound Med Biol 1989; 15: 205. 13. Zierler RE, Phillips DJ, et al. Noninvasive assessment of normal carotid bifurcation hemodynamics with colorflow ultrasonic imaging. Ultrasound Med Biol 1987, 13: 471–476. 14. Hatsukami TS, Primozich J, et al. Color Doppler characteristics in normal lower extremity arteries. Ultrasound Med Biol 1992; 16: 167–171. 15. Hatsukami TS, Primozich J, et al. Color Doppler imaging of lower extremity arterial disease: a prospective validation study. J Vasc Surg 1992; 16: 527–533. 16. Phillips DJ, Powers JE, et al. Detection of peripheral vascular disease using duplex scanner III. Ultrasound Med Biol 1980; 6: 205–218. 17. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325: 445–453. 18. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators [see comments]. N Engl J Med 1998; 339: 1415–1425. 19. European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70–99%) or with mild stenosis. Lancet 1991; 337: 1235–1243. 20. Farrell B, Fraser A, Sandercock P, Slattery J, Warlow CP, Eur Carotid Surg Trial Collaborat Group. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European carotid surgery trial (ECST). Lancet 1998; 351: 1379– 1387. 21. Moneta GL, Edwards JM, et al. Correlation of North American Symptomatic Carotid Endarterectomy Trial (NASCET) angiographic definition of 70% to 99% internal carotid artery stenosis with duplex scanning. J Vasc Surg 1993; l7: 152–160. 22. Fujitani RM, Mills JWLM, et al. The effect of unilateral internal carotid occlusion upon contralateral duplex criteria for accurate interpretation. J Vasc Surg 1992; 16: 459–468. 23. Roederer GO, Langlois YE, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984; 15: 605–613. 24. Grosvel WJHM, Lawson JA, et al. Clinical and hemodynamic significance of innominate artery lesions evaluated by ultrasonography and digital angiography. Stroke 1988; 19: 958–962. 25. Roederer GO, Langlois YE, et al. Is siphon disease important in predicting the outcome of carotid endarterectomy? Arch Surg 1983; 118: 1177–1181. 26. Dawson DL, Zierler RE, Kohler TR. Role of arteriography in the preoperative evaluation of carotid artery disease. Am J Surg 1991; 161: 619–624 27. Dawson DL, Zierler RE, et al. The role of duplex scanning and arteriography before carotid endarterectomy; a prospective study. J Vasc Surg 1993; 18: 673–683. 28. Healy DA, Clowes AW, et al. Immediate and long-term results of carotid endarterectomy. Stroke 1989; 20: 1138–1142.

Chapter 2 Ultrasonic Duplex Scanning 29. Nicholls SC, Phillips DJ, et al. Carotid endartetectomy: relationship of outcome to early restenosis. J Vasc Surg 1985; 2: 375–381. 30. Carter SA. The relationship of distal systolic blood pressures to healing of skin lesions in limbs with arterial occlusive disease, with special reference to diabetes mellitus. Scand J Clin Lab Invest 1973; 31(Suppl 128): 239–243. 31. Strandness DE Jr., Bell JW. Peripheral vascular disease: diagnosis and objective evaluation using a mercury strain gauge. Ann Surg 1965; 161(Suppl): 1–35. 32. Strandness DE Jr. Exercise testing in the evaluation of patients undergoing direct arterial surgery. J Cardiovasc Surg 1970; 11: 192–200. 33. Strandness DE, Bell JW. Ankle blood pressure responses after reconstructive arterial surgery. Surgery 1966; 59: 514–516. 34. Strandness DE Jr., Carter SA. Outcome criteria in patients with peripheral arterial disease. Ann Vasc Surg 1993; 7: 491–496. 35. Kohler TR, Nance DR, et al. Duplex scanning for diagnosis of aortoiliac and femoropopliteal disease: a prospective study. Circulation 1987; 76: 1074–1080. 36. Jager RA, Phillips DJ, et al. Noninvasive mapping of lower limb arterial lesions. Ultrasound Med Biol 1985; 11: 515–521. 37. May AG, VandeBerg L, et al. Critical arterial stenosis. Surgery 1963: 54: 250–259. 38. Carter SA. Response of ankle systolic pressure to leg exercise in mild or questionable arterial disease. N Engl J Med 1972; 287: 578–582. 39. Kohler TR, Andos G, et al. Can duplex scanning replace arteriography for lower extremity arterial disease? Ann Vasc Surg 1990; 4: 280–287. 40. Edwards JM, CoIdwell DM, et al. The role of duplex scanning in the selection of patients for translunimal angioplasty. J Vasc Surg 1991; 13: 69–74. 41. Leather RP, Kupkinski AM. Preoperative evaluation of the saphenous vein ad a suitable graft. Semin Vasc Surg 1988; 1: 51. 42. Clowes AW. Arterial wall response to injury and healing. J Vasc Surg 1989; 9: 373–375. 43. Bandyk DF, Schmitt DD, et al. Monitoring functional patency of in situ saphenous vein bypasses: the impact of a surveillance protocol and elective revision. J Vasc Surg 1989; 9: 286–296. 44. Bandyk DF. Postoperative surveillance of infrainguinal bypass grafts. Surg Clin North Am 1990; 70: 71–75. 45. Idu MM, Blankenstein JD, et al. Impact of color-flow duplex surveillance program on infrainguinal graft patency: a five year experience. J Vasc Surg 1993; 17: 42–53. 46. Mattos MA, van Bemmelen PS, et al. Does correction of stenoses identified by color duplex scanning improve infrainguinal graft patency? J Vasc Surg 1993; 17: 54–66 47. Vesti BR, Primozich J, Bergelin RO, Strandness DE, Jr. Follow-up of valves in saphenous vein bypass grafts with duplex ultrasonography. J Vasc Surg 2001; 33: 369–374. 48. Tullis MJ, Primozich J, Strandness DE Jr. Detection of “functional” valves in reversed saphenous vein bypass grafts: identification with duplex ultrasonography. J Vasc Surg 1997; 25: 522–527. 49. Gibson KD, Caps MT, Gillen D, Bergelin RO, Primozich J, Strandness DE, Jr. Identification of factors predictive of

50.

51. 52.

53.

54.

55.

56.

57. 58.

59.

60.

61.

62.

63.

64.

65.

66.

67.

68.

33

lower extremity vein graft thrombosis. J Vasc Surg 2001; 33: 24–30. Caps MT, Cantwell-Gab K, Bergelin RO, Strandness DE, Jr. Vein graft lesions: Time of onset and rate of progression. J Vasc Surg 1995; 22: 466–475. Jager KA, Fortner GS, et al. Noninvasive diagnosis of intestinal angina. J Clin Ultrasound 1984; 12: 588–591. Jager KA, Bollinger A, et al. Measurement of mesenteric blood flow by duplex scanning. J Vasc Surg 1986; 3: 462–469. Nicholls SC, Kohler TR, et al. Use of hemodynamic parameters in the diagnosis of mesenteric insufficiency. J Vasc Surg 1986; 3: 507–510. Moneta GL, Lee RW, et al. Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg 1993; 17: 79– 86. Moneta GL, Cummings C, et al. Duplex ultrasound demonstration of postprandial mesenteric hyperemia in splanchnic circulation collateral vessels J Vasc Tech 1991; 15: 37–39. Moneta GL, Tayler DC, Helton WS Duplex ultrasound measurement of postprandial intestinal blood flow: effect of meal composition. Gastroenterology 1988; 95: 1294–1301. Treadway KK, Slater EE. Renovascular hypertension. Ann Rev Med 1984; 35: 665–691. Grim GE, Loft FC, Weinberger MH. Sensitivity and specificity of screening tests for renal vascular hypertension. Ann Intern Med 1979; 91: 617–622. Kohler TR, Zierler RE, et al. Noninvasive diagnosis of renal artery stenosis by ultrasonic duplex scanning. J Vasc Surg 1986; 4: 450–456. Taylor DC, Kettler MD, et al. Duplex ultrasound in the diagnosis of renal artery stenosis: a prospective evaluation. J Vasc Surg 1988; 7: 363–369. Haimovici H, Zinicola N. Experimental renal artery stenosis: diagnostic significance of arterial hemodynamics. J Cardiovasc Surg 1962; 3: 259–262. Caps MT, Perissinotto C, Zierler R, Pollisar NL, Bergelin RO, Tullis MJ, Cantwell-Gab K, Davidson RC, Strandness DE Jr. Prospective study of atherosclerotic disease progression in the renal artery. Circulation 98: 2866–2872. Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K, et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998; 53: 735–742. Edwards JM, Zaccardi MJ, Strandness DE Jr. A preliminary study of the role of duplex scanning in defining the adequacy of treatment of patients with renal artery fibromuscular dysplasia. J Vasc Surg 1992; 15: 604–609. Guzman RP. Progressive renal atrophy with renal artery stenosis: a prospective evaluation with duplex ultrasound. Hypertension 1994; 23: 346–350. Zierler RE, lsaacson JA, et al. Natural history of renal artery stenosis: a prospective study with duplex ultrasound. J Vasc Surg 1994; 19: 250–258. Kakkar VV, Howe CT, et al. Natural history of postoperative deep venous thrombosis. Lancet 1969; 2: 219–232. Haeger K. Problems of acute venous thrombosis: I. The interpretation of symptoms and signs. Angiology 1969; 20: 219–223.

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69. Cranley JJ, Canos AJ, Sull WJ. The diagnosis of deep venous thrombosis: fallibility of clinical symptoms and signs. Arch Surg 1976; 111: 34–36. 70. Killewich LA, Bedford GR, et al. Diagnosis of deep venous thrombosis: a prospective study comparing duplex scanning to contrast venography. Circulation 1989; 79: 810–814. 71. Lensing AWA. Prandoni P, et al. Detection of deep vein thrombosis by real time B-mode ultrasonographv. N EugI J Med 1989; 320: 342–345. 72. Tullis MJ, Meissner MH, Bergelin RO, et al. The relationship of venous diameter to reflux, cephalad thrombus and cephalad reflux following deep venous thrombosis. Thromb Haemost 1997; 77: 462–465. 73. van Bemmelen PS, Beach KW, et al. The mechanism of venous valve closure: its relationship to the velocity of reverse flow. Arch Surg 1990; 125: 617–619. 74. van Bemmelen PS, Bedford G, Strandness DE Jr. Quantitative segmental evaluation of venous valvular reflux with ultrasonic duplex scanning. J Vasc Surg 1989; 10: 425–431. 75. Killewich LA, Martin R, et al. Pathophysiology of venous claudication. J Vasc Surg 1984; 1: 507–511. 76. Killewich LA, Bedford GR, et al. Spontaneous lysis of deep venous thrombosis: rate and outcome. J Vasc Surg 1989; 9: 89–97. 77. Markel A, Manzo RA, et al. Valvular reflux after deep vein thrombosis: incident and time of occurrence. J Vasc Surg 1992; 15: 377–384. 78. Meissner MH. Manzo RA, et al. Deep venous insufficiency: the relationship between lysis and subsequent reflux. J Vasc Surg 1993; 18: 596–608. 79. van Ramshorst B, van Bemmelen PS, et al. Thrombus regression in deep venous thrombosis: quantification of spontaneous thrombolysis with duplex scanning. Circulation 1992, 86: 414–419. 80. van Bemmelen PS, Bedford G, et al. Status of the valves in superficial and deep venous system in chronic venous disease. Surgery 1991; 9: 730–734. 81. Meissner MH, Manzo RA, Bergelin RO, Strandness DE, Jr. Venous diameter and compliance after deep venous thrombosis. Thromb Haemost 1994; 72: 372–376. 82. Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow

83.

84.

85.

86. 87.

88.

89.

90.

91.

92. 93.

94.

velocity in the basal arteries. J Neurosurg 1982; 57: 769–774. Otis SM Ringelstein FB. Transcranial Doppler sonography. In: Zweibel WJ, ed. Introduction to vascular ultrasonography. Philadelphia: WB Saunders 1992: 145–171. Ringelstein EB, Zeumer H, et al. Transkranielle Dopplersonographie der hirnversorgenden arterien: Atraumatische diagnostic von stenosed and verschluessen des carotissiphons und der a cerebri media. Nevenartz 1985; 56: 296. Ringelstein EB. A practical guide to transcranial Doppler sonography. In: Weinberg J, ed. Noninvasive imaging of cerebral vascular disease. New York: Alan R Liss, 1989: 75. Spencer MP, Whisler D. Transorbital diagnosis of intracranial arterial stenosis. Stroke 1986; 17: 916–921. Reivich M, Hollins HE, et al. Reversal of blood flow through the vertebral artery and its effects of cerebral circulation. N Engl J Med 1961; 265: 878–885. Bornstein NM, Norris JW. Subclavian steal syndrome: a harmless hemodynamic phenomenon. Lancet 1986; 2: 303–305. Grosveld WJHM, Lawson JH, et al. Clinical and hemodynamic significance of innominate artery lesions evaluated by ultrasonography and digital angiography. Stroke 1988; 19: 958–962. Ackerstaff RGA, Grosveld WJHM, et al. Ultrasonic duplex scanning of prevertebral segment of the vertebral artery in patients with cerebral atherosclerosis. Eur J Vasc Surg 1988; 2: 387–393. Ackerstaff RGA, Schroeder TV. Intraoperative monitoring with transcranial Doppler sonography. In: Bernstein EF; ed. Vascular diagnosis. St. Louis: CV Mosby, 1993: 361–366. Bernstein EF. Role of transcranial Doppler in carotid surgery. Surg Clin North Am 1990; 70: 225–234. Harders A, Gilsbach JM. Time course of blood velocity changes related to vasospasm in the circle of Willis measured by transcranial Doppler ultrasound. J Neurosurg 1987; 66: 718–728. Markwalder TM, Grolimund P, et al. Dependency of blood flow velocity in the middle cerebral artery on end-tidal carbon dioxide partial pressure—a transcranial Doppler study. J Cereb Blood Flow Metab 1984; 4: 368–372.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 3 Duplex Arteriography for Lower Extremity Revascularization Enrico Ascher and Anil Hingorani

Contrast arteriography (CA) is still considered the gold standard imaging modality for patients in need of lower extremity revascularization procedures. However, it continues to be associated with local and systemic complications, and patients in general are demanding less invasive alternatives. Encouraged by recent technological advances in duplex ultrasonography, several authors have expressed an increasing interest in the use of duplex arteriography (DA) as a potential replacement of preoperative standard CA for peripheral arterial imaging. Thus, it is not surprising that DA is being investigated for this purpose (1–3). Although some authors have demonstrated an acceptable correlation between arteriography and DA (4–12), others have been less than enthusiastic and continue to advocate preoperative or pre-bypass arteriography (13–16). Some of the factors that may explain these discrepant results include: 1) use of older duplex equipment; 2) inexperience of the vascular technologist(s); 3) lack of formal training and protocols for DA; 4) less commitment in terms of time and effort to perfect the technique; 5) reluctance of the surgeon to give up the visual effect of a complete, uninterrupted study as provided by arteriography; and 6) severe calcification preventing adequate vessel insonation, and other local barriers making DA less feasible in some of these patients. In an effort to explore the use of DA for patients undergoing lower extremity revascularizations, we have used DA during a 4-year period in 466 patients. In addition, some of the techniques that we have used to obtain adequate data from DA for the lower extremity revascularization even in disadvantaged situations are considered.

Material and Methods From January 1, 1998 to May 31, 2001, 466 patients, of whom 262 (56%) were men, underwent 485 lower extremity revascularization procedures at our institution. Preoperative imaging consisted of DA alone in 449 procedures and DA and CA in 36. An attempt to image from the distal aorta to the pedal arteries was made in all the patients. The selection of optimal inflow and outflow anastomotic sites was based on a schematic drawing following DA examination. Inflow disease and the conduit were also assessed by intraoperative pressure gradient (IPG) between the distal anastomosis and radial arteries.

Duplex Scan Examination Two registered vascular technologists performed all duplex scan examinations using either ATL HDI 3000 or 5000 scanners. The protocol included mapping of the arterial system from the mid-abdominal aorta to the pedal vessels. The test starts by placing the patient in the lateral decubitus position opposite to the side of interest, with slight ipsilateral knee and hip flexure for insonation of the distal aorta and the ipsilateral common and external iliac arteries. This position improves the ultrasound field of view by shifting the gas-containing bowel away from the probe (Figs. 3.1–3.3). Next, the patient is placed in the supine position, with mild genuflection and thigh abduction for visualization of the common, superficial, and deep femoral arteries. Still in this position, the aboveknee popliteal artery segment is evaluated from a medial

35

36

Part I Imaging Techniques FIGURES 3.1–3.3 Duplex arteriography of the iliac arteries.

1

2

3

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

approach and the below-knee segment from a posterior approach. The examination continues by moving the probe medially to insonate the posterior tibial artery and its plantar branches. The patient is then returned to the original position for visualization of the tibioperoneal trunk and peroneal arteries, as well as the origin of the anterior tibial artery. This is accomplished by placing the probe just posteriorly to the lower border of the fibula. The remainder of the anterior tibial artery is visualized by positioning the probe between the tibia and the fibula. Lastly, the dorsalis pedis artery and its metatarsal branches are insonated with the patient in the supine position (Figs 3.4–3.8). During DA, we routinely perform a venous mapping to identify usable veins for harvest, thereby avoiding the additional time and energy needed in pursuit of vein of good quality and caliber. If no usable vein is identified and a bypass to the tibial vessels is required, the diameter and quality of the tibial veins may be measured for a possible prosthetic bypass with a distal fistula. Finally, examination of the subclavian-axillary segment may be performed as a possible inflow source for debilitated patients with severe aorto-iliac disease. This is accomplished without the risk of an additional thoracic aortogram or the time needed for an additional thoracic magnetic resonance angiography (MRA) scan. A variety of scanheads is utilized to obtain highquality B-mode, color, and power Doppler images as well as reliable velocity spectra. Curvilinear 5–2 MHz and phased-array 3–2 MHz probes are used for aorto-iliac scanning. A linear 7–4 MHz probe is used for visualization of the femoral, popliteal, and tibial vessels. High resolution of compact linear 10–5 or 15–5 MHz scanhead allows better visualization of superficial arteries on the ankle and foot. A peak systolic velocity (PSV) ratio ≥2 reflects a lesion ≥50% stenosis, a PSV ratio ≥3 is used to confirm a ≥70% stenosis. Any discrepancies are communicated to the operating surgeon. The arterial segments are classified as normal or mildly diseased (< 50%), significantly stenosed (≥50%), occluded or not visualized. Vessel wall thickness and degree of calcification are reported to aid in the choice of anastomosis sites. A more precise evaluation of arterial size, length, and degree of narrowing, as well as of plaque characteristics, is performed for single focal or sequential lesions suitable for balloon angioplasty and/or stent placement. A color-coded map of the arterial tree is drawn to facilitate reading by the surgeon (8,12). In general, however, color and power Doppler are used primarily, and B-mode and velocity spectra are used to supplement these data, especially in the presence of long lesions or multiple lesions. Since the status of the branches of the arteries can also add valuable data for the surgeon, visualization of as many tibial and pedal branches as possible, including malleolar, plantars, tarsals, deep plantar arteries, and branches of the named vessels, is also performed during DA. We found that the high-frequency probe (10–15 MHz) can be especially useful in this portion of the protocol.

37

Contrast Arteriography In our series, standard percutaneous preoperative CA with digital subtraction arteriography (DSA) was obtained when DA was not able to provide adequate imaging of arterial segments essential for limb revascularization (n = 36). During this time period, these were the only CA images obtained by our service. Patients generally underwent arterial reconstruction the day after CA if there was no worsening of renal function. Patients who underwent mapping but had not undergone revascularization (53 refused, two not needed, six too ill for revascularization) or who were mandated to have a preoperative angiogram by study or training protocols (n = 7) were excluded from this series.

Intraoperative Evaluation Completion arteriography was performed in 210 (43%) cases to evaluate patency of the distal anastomosis and runoff status. All of the infrapopliteal interventions and any bypasses with difficult anastamoses or conduits underwent completion angiography (Figs. 3.9–3.15). The aortoiliac segment was evaluated at the completion of the procedure by measuring the pressure gradient between the distal anastomosis and radial arteries in patients undergoing infrainguinal bypasses. A gradient > 20 mmHg of systolic pressure warranted on-table angiography and repair of the inflow lesions and assessment of the conduit.

Results Indications for surgery were severe claudication in 91 (19%) limbs, tissue loss in 197 (40%), rest pain in 113 (23%), acute ischemia in 46 (10%), popliteal aneurysm in 18 (4%), superficial femoral artery aneurysm in one, abdominal aortic aneurysm in one, and failing graft in 18 (4%). Age ranged from 30 to 97 years [mean 72 ± 12 (SD) years] and risk factors such as diabetes, hypertension, use of tobacco, coronary artery disease, and endstage renal disease were present in 45%, 45%, 44%, 44%, and 13% of the patients respectively. A total of 121 (25%) limbs had at least one previous ipsilateral revascularization. During this time period, the distal anastomosis was to the popliteal artery in 173 cases (100 to the below knee popliteal) and to the tibial and pedal arteries in 255. Inflow procedures to the femoral arteries, embolectomy, thrombectomy, balloon angioplasty, and patch angioplasty accounted for the remaining 57 cases. The specific procedures performed in these patients are shown in Tables 3.1 and 3.2. The mean DA time was 66 ± 20 (SD) min (15–150 min). Owing to difficulties in evaluating some of the arterial segments using DA alone (Table 3.3), additional preoperative imaging (CA) was deemed necessary in 36 cases (7%) as a result of extensive ulcers (4), edema (8), severe arterial wall calcification (4), uncooper-

38

Part I Imaging Techniques FIGURES 3.4–3.8 Duplex arteriography of the infrapopliteal vessels.

4

5

6

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

39

FIGURES 3.4–3.8 (continued)

7

8

ative patient (4), low flow (4), obesity (8), multiple previous surgeries (13), poor visualization of the origin of anterior tibial artery (1), and very poor runoff (18). Table 3.4 demonstrates differences found between intraoperative findings and preoperative DA. Twelve-month primary patency for femoral above-knee popliteal artery bypass with PTFE was 95%, femoral below-knee popliteal bypass with vein 95%, femoral below-knee with PTFE was 90%, femoral distal with vein was 80% and femoral distal with PTFE was 77%. Overall, 6, 12, and 24 months’ secondary patency rates were 86%, 80%, and 66% respectively. During the entire time period, 34 grafts closed and 21 underwent revision for failure.

The Technology The turn of the millennium has been marked by an accelerated technological progress that stimulated the

development of less invasive treatment and diagnostic procedures. Accordingly, CA has been challenged by the development of MRA and duplex ultrasonography. In the last few years, computer technology improvements related to the ultrasound industry have produced scanners with higher definition B-mode image and more refined color-flow features. Nonetheless, duplex ultrasonography’s most popular feature remains the hemodynamic assessment by velocity spectral waveform PSV ratio, which directly measures the degree of arterial narrowing. However, the presence of collateral branches, tapering or dilation of adjacent arterial segments, arterial bifurcation or tortuosity, presence of close sequential lesions, and inaccuracies in the Doppler angle may affect the velocity-waveform spectra. Therefore, a combined B-mode/color-flow and hemodynamic assessment is desirable. Power Doppler helps to outline the residual lumen and quantify the degree of arterial narrowing, par-

40

Part I Imaging Techniques

10

9

11

FIGURES 3.9–3.15 Arterial mapping and completion angiography.

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

41

12

14

13

FIGURES 3.9–3.15 (continued)

42

Part I Imaging Techniques FIGURES 3.9–3.15 (continued)

15

TABLE 3.1 Infrainguinal procedures

Femoral popliteal bypass Bypasses to infrapopliteal vessels Superficial femoral, tibioperoneal or popliteal artery balloon angioplasty Thrombectomy Embolectomy

TABLE 3.2 Inflow procedures performed

Vein

PTFE

Total

64 100

109 155

173 255

Iliac angioplasty and stent Axillofemoral bypass Femorofemoral bypass Iliofemoral bypass Aortofemoral

63 11 12 1 2

16 10 7

The other procedures not included on this list include suprainguinal procedures not performed with an infrainguinal procedure or balloon angioplasties.

TABLE 3.3 Areas that were difficult to evaluate with DA (n = 67 patients)

Calcification Iliacs SFA Popliteal Tibials

4 4 1 24

Gas interposition

Pain

Obesity

Uncooperative Patient

12

1

9

8

Low Flow

Open Ulcer

Tortuous

Edema

Total

9

35 5 1 49

1 1

1

2

ticularly in the presence of color bleeding, exacerbated color flashing produced by tight stenosis, or low-flow situations. Inflow and outflow site selection of infrainguinal bypass based on CA involves visualization of an adequate inflow with unobstructed runoff. Thereby, precise estimation of intervening sequential stenoses may be irrelevant for surgical decision-making. Similarly, the information obtained by duplex ultrasonography can be drawn into a diagram to aid surgeons’ visualization of significant lesion and formulation of revascularization strategy.

2

4

6

1

Prior Studies Prior literature examining DA primarily focused on comparing DA with CA (17–20). However, most of these studies attempted to compare the predicted bypass based on DA with that predicted by angiography. Since the variation in the choice of procedure between surgeons given the same angiography data has been well documented, the conclusions that can be drawn from these comparison studies between DA and CA remain questionable (21). In addition, since the vascular technologists performing these examinations in these studies would not

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

43

TABLE 3.4 Differences between DA and intraoperative findings (completion angiography or graft pressure measurements) Problem

Cause

Change in Outcome

Peroneal, thought to be closed, was open More disease in distal PT More disease in distal PT Not able to see iliac

Heavy calcification Very low flow Very low flow Heavy calcification

No change—had femoral DP bypass None—no other alternative available None—no other alternative available Balloon angioplasty/stent of EIA lesion, stent graft of CIA aneurysm

Distal posterior tibial artery thought to be open

Very low flow distal posterior tibial artery, large distal collateral Did not see (60%) stenosis well in proximal CIA Calcification Did not see stenosis well in proximal CIA Did not see iliacs well Obesity

CIA thought to be open Distal anterior tibial artery thought to be open CIA thought to be open CIA thought to be open EIA thought to be open

be experienced with insonation of the tibial and pedal arteries and have no opportunity to learn from the angiogram or intraoperative findings, the very basis of these comparison studies remains unrealistic and artificial.

Limitations Poor visualization of vessels with extremely calcified vessel walls, skin quality problems such as severe dermatitis, open ulcers, heavy scarring, severe lymphedema, and severe hyperkeratosis are some of the problems associated with DA, as well as rest pain, noncompliant patients, and excessive edema. Additionally, we encountered difficulty visualizing the iliac arteries, owing to colostomy, marked iliac tortuosity, recent abdominal surgery, ascites, morbid obesity, or gas interposition in a few of our patients. To circumvent the problem of severe calcification, we have found increasing the gain, persistence and sensitivity, and using power Doppler and SonoCT technology quite useful. Lack of patient cooperation may be one limitation to accurate DA, particularly for the iliac and infrapopliteal segments. In fact, a small percentage of patients are uncooperative because of altered mental status, inability to position the leg, severe, ischemic pain, or spinal condition. The inclusion of pain medications for severe pain, sedation or having a family member in the laboratory to calm the confused patient was also found very helpful. In certain instances, we re-attempted the examination after a few days of elevation to decrease the edema and attempted overnight fasting prior to the examination to reduce bowel gas. Often, with limited visualization of the iliacs but with normal common femoral waveforms, it was elected to proceed to revascularization, realizing that an intraoperative balloon angioplasty of the iliacs may be needed. Nevertheless, a small number of our patients were not able to have adequate information derived from DA and did require preoperative contrast angiography despite these attempts.

Jump to plantar Stent of CIA Jump to dorsalis pedis Stent of CIA Stent of CIA Stent of EIA

Our evolving experience also demonstrates some of the nuances of the DA examination. We have noted that failure of visualization of all segments of the arterial tree in every patient has not posed a significant issue. Incomplete visualization of the iliac vessels has led to a graft–radial artery pressure gradient that resulted in an intraoperative balloon angioplasty and placement of a stent in the iliac arteries from the proximal anastomosis of the bypass in five instances. In these five patients, no common femoral artery waveform abnormalities were detected, consistent with our prior published data, suggesting that these are not reliable (3). These patients also had SFA disease, making other noninvasive techniques less reliable for detection of these occult iliac lesions. Nevertheless, because of this limitation, the surgeon using DA as a sole preoperative imaging tool needs to be able to perform these endovascular procedures during the revascularization if needed. Since our policy is to perform the inflow angioplasty at the same time as the lower extremity revascularization, and the expertise and tools necessary to perform endovascular procedures are readily available, this has not been an issue at our institution. Furthermore, incomplete visualization of the crural and pedal vessels does not always have a major impact on the course of the procedure. For example, if a surgeon prefers to perform a bypass to the distal anterior tibial artery rather than to the distal peroneal, and the distal peroneal was too calcified to insonate, the lack of data on the distal peroneal may have little impact on the planning of the procedure. In general, our policy to not perform a femoral distal bypass for claudication means that, in the presence of severe SFA disease with at least one vessel runoff and insignificant iliac artery disease, a femoral popliteal bypass will be planned even if the other two tibial arteries could not be completely evaluated. Nevertheless, when difficulties in the evaluation of the crural and pedal vessels are encountered, and the status

44

Part I Imaging Techniques

of these vessels is necessary, additional techniques can be used. In very low flow situations (PSV of < 20 cm/s) such as in the tibial vessels with acute ischemia or cardiogenic shock, setting the pulse repetition frequency at 150 to 350 Hz and using the low wall filter, the highest persistence and highest sensitivity for the color flow imaging can be beneficial. At times, distal compression can augment flow and demonstrate patency of tibial vessels. When the tibial vessels are severely calcified, we have found power Doppler and Sono CT to be useful. In addition, examining the vessels in transverse section, changing the angle, and increasing the gain can at times allow visualization of the vessel. The depth of the tibioperoneal trunk, origin of the proximal peroneal and posterior arteries, and the superificial femoral artery at Hunter’s canal may necessitate the use of a lower frequency probe for visualization. However, this tends to sacrifice details and the resolution, and can make these areas difficult to interpret. In these cases, velocity spectral analysis can also be a useful adjunct. In difficult arterial segments, manipulation of the leg, using a different probe, or utilizing a variety of approaches may be necessary. For example, the medial approach may help to visualize the proximal peroneal, the medial or posterior approach may assist in visualizing the mid-peroneal artery, and the lateral or posterior approach may facilitate the imaging of the distal peroneal and its branches. Thus, the tibial vessels can be adequately evaluated by using a variety of approaches and angles. The most difficult infrapopliteal segments to visualize that we encountered were the first portion of the anterior tibial artery and the bifurcation of the tibioperoneal trunk. We believe this difficulty is due to the depth of the areas. Overall, most of the nonvisualized segments were localized between two occluded segments. Therefore, nonvisualization of these segments was not relevant for surgical decision-making. Contrary to the belief that the peroneal artery is difficult to image, we were able to visualize it using a variety of techniques. Using these techniques, even its continuation from the tibioperoneal trunk can be assessed. The origin of the anterior tibial artery deserves special attention as collaterals in this area may be mistaken for a patent proximal anterior tibial artery. Careful examination of the origin of the vessels and tracing the vessels distally often can solve some of these issues. In addition, identification of the two adjacent veins can help distinguish between a large collateral and the vessel. Despite these techniques, if patency of vessels that were not visualized well is deemed crucial, an angiogram will need to be obtained before the procedure is attempted.

Advantages Invasive contrast angiography remains the gold standard imaging modality in planning these revascularizations even though this modality may not detect outflow vessels

that may be more clearly visualized with duplex or MRA, as occurs in very low flow situations with acute or severe chronic ischemia (10,22). Conversely, DA has the capability to detect these vessels with very low flow (< 20 cm/s). The visualization of these outflow vessels may result in the performance of lower extremity revascularizations that ultimately achieve limb salvage. Moreover, since biplanar arteriography is not the standard for the entire arterial tree, eccentric lesions, especially in the iliacs, may go undetected utilizing contrast angiography. Finally, while MRA does have certain clear advantages over CA, we have noted that as many as 25% of patients are unable to complete their preoperative MRAs due to scheduling difficulties, claustrophobia, metal implants, or pacemakers. The advantages of DA compared with other imaging tools include the identification of the softest portion of the vessel wall that can be marked on the skin before the intended procedure. Skin marking of the most suitable site for outflow anastomosis, particularly for infrapopliteal segments, may limit incision size and eliminate extensive arterial dissection in search of a soft arterial segment. Information of a noncalcified arterial segment is promptly conveyed to the surgeon, important arterial braches may be spared, and long-incision-related complications reduced. While a target vessel may be patent using luminally-based imaging tools, the vessel may be severely calcified in long segments, as in the diabetic and end-stage renal disease population. We have found that preoperative localization of the softest portion of the vessel by DA can accurately identify the most advantageous anastomotic site, thus decreasing the risk of damage to the artery by clamping or incomplete proximal control with a tourniquet due to concomitant severe SFA calcification. Thus, DA can be an invaluable aid to the surgeon in determining the anastomotic site of choice. Since DA is not just a luminal technology, it can be used to assess the actual disease of the vessel. Highresolution duplex imaging can assess the luminal diameter and thickness of the wall down to approximately 1/10th of a millimeter. While a vessel may appear to have a patent lumen with MRA and contrast angiography, the actual thickness of the wall is not evaluated via these techniques. This visualization by DA may change the site for the anastomosis. In addition, DA has the ability to more accurately assess the chronic nature of an occlusion. Therefore, it is possible to differentiate between an isolated chronic SFA occlusion and an acute embolism with little underlying disease, or acute thrombosis with severe underlying atherosclerotic disease. In addition, aneurysmal vessels with partial thrombosis may have little to no luminal dilation and may be undetectable by CA. Similarly, ulcerated and irregular plaques that may be a source of embolization are also poorly assessed with CA. Highresolution DA more clearly visualizes these plaques. Consequently, we have found this imaging modality particularly valuable in determining patient management compared with other technologies.

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

Furthermore, the hemodynamic information obtained using DA may alter patient management. Volume flow and velocity measurements can help assess whether the visualized lesion is hemodynamically significant, and determine whether repair of the lesion may be beneficial. For example, a poorly visualized iliac plaque with little change in the ratio of peak systolic velocities (< 2) may suggest that the lesion may not be of clinical significance. On the other hand, lesions that are poorly visualized because of severe calcification with elevated ratios distal to the obscured lesion suggest a hemodynamically significant lesion. Other luminal imaging modalities do not readily furnish these details. The portability of the duplex machine should be mentioned. Because the DA can be performed at the bedside, in the operating room, or in the holding area, time spent transporting the patient, and the personnel required, is significantly reduced. Additionally, obtaining the CA or MRA images and their interpretation can entail a delay in the definitive treatment of a severely ischemic limb in a debilitated patient, as well as take a toll on the operative team. With DA, once the patient is identified as needing urgent revascularization, the machine and technician can be brought to any part of the hospital for an abbreviated directed examination.

The DA Team While prior studies have demonstrated the reliability of DA (8,12,13), it is highly operator dependent. We require an experienced technician whose capabilities are well known to the surgical staff. Our DA technicians are MD/RVTs (registered vascular technologists) who each undergo a specialized training protocol including examination of the patient by DA and angiography. The variances encountered between both modalities are then reviewed. In addition, any differences in DA and intraoperative completion angiography are analyzed by all of the surgeons and technologists, resulting in a close relationship. Prior to each procedure, each case is discussed to afford the surgeon a complete picture of the findings, rather than to have the surgeon merely review the mapping. Thus, the intricacies and nuances of the actual quality of the arteries and veins are presented to the surgeon as an adjunct to the mapping and images taken during the examination. For example, the thickness and characteristics of the target vessels can be more effectively communicated by verbal exchange rather than written details or a drawing. This type of data serves to further accentuate the advantages of DA over luminally-based imaging modalities, as this sort of information is not available otherwise. Areas that are not well visualized should be identified as such for the surgeon to decide if this area is crucial. DA demands a high level of technical proficiency, an understanding by the technician of the anatomy and hemodynamics, and appreciation of the intended revascularization. Knowledge and experience of the technolgist play an important role. Details of the exact location of

45

disease with relation to the surgical anatomy are also necessary. For example, identifying disease in the above-, behind-, and below-knee popliteal artery is a concept that must be mastered for DA to be effective. To facilitate these goals, DA technologists at our institution freely visit the operating room to gain insight into the operative procedures. In an attempt to develop a training period at our institution, the first 25 examinations by a new technologist are confirmed with CA or repeated DA examination by an established DA technologist. In the initial stages, a prospective comparative study needs to demonstrate that the DA examinations being performed are as effective as invasive CA in delineating the arterial anatomy (1). In an effort to facilitate the advancement of our DA protocol, every completion angiogram is reviewed with the technologist who performed the examination, as are the iliac angioplasties. The characteristics of the proximal and distal arteries, vein conduit, or tibial vein in the case when an adjunctive arteriovenous fistula is performed, are discussed and any discrepancies are reviewed. DA technologists visit the operating room to witness the intraoperative findings first-hand. In this manner, the constant feedback becomes the cornerstone for the continual improvement in the quality of the DA examinations. This confirms our previous belief that DA can also be used as the only preoperative imaging technique for patients with lower limb ischemia when performed by a well-qualified, experienced registered vascular technologist under the supervision of a vascular surgeon. This is an operator-dependent test that demands the use of different scanners and constant optimization of the image by an operator who has mastered ultrasound technology and hemodynamics.

Shortened Protocol The role of a shortened focused protocol also needs to be explored. Is it necessary to visualize all of the vessels from the aorta to the pedal vessels in every case? For example, the need to scan all the tibial vessels of a patient with claudication and severe iliac disease with no significant femoral disease may be questioned if the surgeon will only perform an inflow procedure for this type of patient. Thus, the DA protocol needs to be tailored for each surgeon, as a complete examination may not be absolutely necessary or additional examinations may need to be performed in certain types of patients, depending on the clinical approach of the operating team. In the presence of a previous patent bypass graft, DA focuses on identifying significant lesions above the proximal anastomosis, evaluating the graft itself for significant lesions, and assessing the best patent artery available for a possible revision. Scanning of the arterial segments between the proximal and distal anastomosis adds very little useful information and may be omitted. Previous occluded bypass grafts are registered, and a complete mapping is performed.

46

Part I Imaging Techniques

Machines DA has further emphasized the need to keep up with rapidly advancing duplex technology, as older machines seem to have decreased resolution, less penetration, increased error on the diameter reduction measurements, lack power imaging, and demonstrate more artifacts. Some earlier investigators attempted to perform DA with less than adequate technology, which may have affected the results (9,11,13–15). As the technology and our knowledge have advanced, so too have our results (5,15,19,23). Therefore, our experience with DA in this patient population continues to evolve as the available technology advances (24).

Renal and Diabetic Patients It has been well documented that patients with diabetes mellitus and/or chronic renal insufficiency are at an increased risk for developing contrast-induced nephropathy when subjected to CA, despite the use of nonionic contrast media (25–28). Although the renal function in most patients with contrast-induced renal failure will return to baseline, a few patients may require hemodialysis and most will have their proposed arterial reconstruction delayed. In modern series, up to 10% of diabetic patients will have contrast-induced renal failure and up to 12% of patients with chronic renal insufficiency will significantly worsen their renal function following CA (3,29,30). In addition, the significant osmotic load associated with dye injection poses a risk for fluid overload for the patients on hemodialysis. Yet, the gold-standard imaging modality for lower limb ischemia continues to be invasive CA even in the presence of diabetes mellitus and chronic renal failure. More recently, several investigators have attempted to validate duplex arterial mapping as a reliable alternative to CA (1,14,16,31). Although some of these studies achieved excellent correlation between DA and CA, few surgeons have actually performed infrainguinal bypasses without preoperative or pre-bypass CA (3). In an effort to examine revascularization without a preoperative dye study, we will focus on our experience with DA in 145 patients who had 180 lower limb arterial bypasses and who were at risk for developing or worsening their renal failure if given nonionic contrast media. From January 1998 to November 2000, lower extremity DA was performed on 145 patients with diabetes mellitus and/or chronic renal failure prior to 180 arterial reconstructions. A total of 121 procedures were performed on 97 patients with diabetes alone, 41 on 33 patients with diabetes and chronic renal insufficiency (CRI), and 18 on 15 patients with CRI alone. Patient ages ranged from 45 years to 98 years (mean 73 ± 10 years). Indications for surgery were severe claudication in 20 (15%), rest pain in 28 (21%), nonhealing ischemic ulcers in 39 (30%) and limb gangrene in 45 (34%). Preoperative CA was performed in 16 procedures, owing to extremely poor runoff based on DA and limited visualization of outflow

vessels. Adequacy of the inflow was confirmed by intraoperative pressure measurements. Post-bypass CA or duplex imaging was obtained to verify the patency of the runoff. The DA procedure time averaged 50 ± 12 min (range 35–90 min). The distal anastomosis was to the popliteal artery in 65 cases (49%) and to the tibial and pedal arteries in 67 (51%). Cumulative patency rates at 1 and 3 months were 94% and 83% respectively. Intraoperative findings confirmed the preoperative DA findings, with the exception of one case in which the distal anastomosis was placed proximal to a significant stenosis, requiring an extension graft. The use of high-quality arterial ultrasonography presents a safe and reliable option to preoperative lower extremity CA for many patients with diabetes or impaired kidney function. The ease of use and favorable patient outcomes achieved by this imaging modality may rival the use of contrast angiography for these patients. This imaging modality can offer results comparable to those achieved with conventional invasive CA while at the same time reducing associated risks. The advantages of avoiding or limiting the use of CA to decrease the incidence of post-procedure renal insufficiency for the diabetic patient and those patients with CRI are self-evident. This complication also results in substantially increased lengths of stay, additional specialty consults and higher costs. In addition, it can also produce suffering for the patient and their family. Moreover, an analysis of natural history studies indicates that 23–63% of patients with diabetes will have progressive renal insufficiency with 10% to 35% winding up on dialysis (32–36). Of the patients with CRI, up to 28% will require eventual dialysis (37,38). It remains unclear whether the administration of intra-arterial dye may result in additional long-term complications in these high-risk patients with peripheral vascular disease.

Acute Ischemia Over the last three decades, the management of acute lower limb ischemia has evolved from simple embolectomies performed with local anesthesia to highly challenging arterial reconstructions. Some of the factors accounting for this dramatic change include a more aggressive approach at limb salvage in the elderly patient by well-trained vascular surgeons, decreased prevalence of rheumatic heart disease, and a substantial increase in the use of warfarin sulfate for cardiac arrhythmias. Accordingly, many of these patients presenting with acutely ischemic limbs will have underlying multisegmental occlusive arterial disease rather than a simple embolus obstructing a healthy vessel. Although the clinical diagnosis of an ischemic leg can often be made without difficulties, the anatomical pattern of the inflow, the outflow, and the occluded arterial segment may at times be impossible to ascertain by standard preoperative imaging modalities. Although invasive CA has been advocated by some authors for patients presenting with acute ischemia (39,40),

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization

it has some limitations, particularly when compared with duplex ultrasound: 1. 2. 3. 4. 5.

It delineates the patent arterial lumen only. It misses thrombosed popliteal aneurysms. It fails to visualize an outflow source in very low-flow situations. It requires potentially nephrotoxic agents. It delays prompt treatment.

Moreover, there are few retrospective reports on the importance of preoperative arteriography in patients with acute ischemia. Conversely, relying solely on a medical history and a physical examination without any preoperative imaging technique may subject patients to unnecessary attempts at embolectomies or thrombectomies and may significantly prolong the operation. This would be quite undesirable in this often high-risk population with multiple cardiovascular risk factors. Furthermore, avoidance of nephrotoxic agents, visualization of low-flow arteries and a more expeditious examination are some of the advantages of DA that are particularly important in these often sick patients presenting with acute lower limb(s) ischemia. The purpose of this section was to focus on whether DA can also be used effectively in the setting of acute ischemia. From January 1998 to February 2001, 68 patients were admitted to our institution with 87 instances of acute lower limb(s) ischemia and underwent 87 operations. There were 34 men and 34 women, whose age ranged from 51 to 95 years (mean 72 ± 12.5 years). There were 44 cases of acute arterial occlusions and 43 cases of bypass graft thromboses. In the former group, the most proximal occluded site was the aorta in one case, common iliac in four cases, external iliac in 15 cases and infrainguinal arteries in 24 cases. In the latter group, there were four suprainguinal grafts, 24 bypasses to the popliteal artery, and 15 bypasses to infrapopliteal arteries. All patients had DA as their initial diagnostic study. The initial duplex protocol varied according to the pulse examination. In patients with a good femoral pulse but absent popliteal pulse, attempts were made to visualize the ipsilateral femoral–popliteal segment and the proximal third of the infrapopliteal arteries. This was extended to the distal tibials vessels and pedal arteries when needed. When the femoral pulse was absent, the protocol started with visualization of the distal aorta, bilateral iliac, and common femoral arteries. This examination was extended into the deep and superficial femoral–popliteal segments in cases of proximal occlusion. None of these cases had preoperative or pre-bypass CA. Intraoperative arterial pressures to confirm the adequacy of the inflow tract and arteriography to assess the runoff were performed in 78% of the cases at the end of the procedure. DA was not completed in 5 of the 87 cases because of severe arterial calcification (3), patient uncooperativeness (1), or obesity (1). DA correctly predicted the extent of the occluded arterial segment in 80 of 82 cases (98%). Of the 44 cases of arterial occlusions, seven were treated by

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thromboembolectomies alone, thromboembolectomies and patch angioplasties in 14 cases, thromboembolectomies and iliac balloon angioplasties with stents in four cases. In the remaining 19 cases a variety of bypasses were required to restore unobstructed flow after an attempted embolectomy. DA correctly identified all seven cases (100%) that required embolectomy alone and 13 of the 14 cases (93%) of thrombectomy and patch angioplasty, two of four cases (50%) of thromboembolectomies with iliac balloon angioplasty and stents. In addition, DA predicted the necessity for bypass operations in 15 of 16 cases (94%) with significant underlying occlusive disease and for three of three (100%) thrombosed popliteal aneurysms. The 1-month arterial patency rate for the 25 embolectomy cases was 65% and 1-month graft patency rates were 59% for 15 femoral–popliteal bypasses and 62% for 24 infrapopliteal bypasses. The time spent to perform DA varied from 20 min to 50 min (mean 30 min). A well-performed DA offers several practical advantages over CA in this subset of patients: 1. 2. 3. 4.

5.

6.

7.

It is noninvasive. It does not require nephrotoxic agents. It is portable and it can be done expeditiously. Color flow and waveform analysis provide a better estimation of the hemodynamic significance of occlusive disease. It allows direct visualization of the entire artery and not only of the lumen, thus enabling plaque characterization. With color flow and power Doppler techniques it is possible to identify patent arteries subjected to very low flow states. It can detect occluded arterial aneurysms, thereby avoiding unnecessary attempts at thromboembolectomies.

Most of the patients in this series had their DA performed during regular hours since it was not possible to have the technologist(s) available at all times. Except for the time of day, there was no other factor differentiating those patients with acute ischemia who underwent DA from those who did not. Regardless of its obvious limitations, this experience demonstrates the advantages of DA in helping the surgeon plan the surgical approach and avert unnecessary thrombectomies and embolectomies that can further contribute to the high mortality and morbidity in patients with acute lower limb ischemia.

Conclusions This experience correlates with our belief that highquality arterial ultrasonography performed by a highly skilled and well-trained vascular technologist may represent an alternative to conventional arteriography for patients in need of primary or secondary lower extremity revascularization. The technologist needs to be trained to

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understand vascular pathology, hemodynamics, and ultrasound technology to perform an accurate DA. Limitations inherent to the technique and very poor runoff observed on ultrasonographic examination may necessitate additional preoperative imaging modalities in certain patients. Despite these techniques, there were two cases in which a jump graft was performed owing to a missed distal lesion. One stenosis in the distal anterior tibial artery was missed, and a large collateral was mistaken for the distal posterior tibial artery in a patient with extremely low flow. Both of these occurred early in the course of our experience, were detected by routine completion angiography, and were remedied with a jump graft. Both patients seemed to have no complications from the procedures. While these cases help illustrate the limitations of DA, the cases seem quite infrequent. These types of limitation need to be weighed against the potential benefits of the DA protocol and the limitations of CA. Nevertheless, further investigation is warranted to resolve the issues that are raised by this experience and to support the use of DA as a viable preoperative imaging tool in place of CA for lower extremity revascularization procedures.

References 1. Mazzariol F, Ascher E, et al. Values and limitations of duplex ultrasonography as the sole imaging method of preoperative evaluation for popliteal and infrapopliteal bypasses. Ann Vasc Surg 1999; 13: 1–10. 2. Ascher E, Mazzariol F, et al. The use of duplex ultrasound arterial mapping as an alternative to conventional arteriography for primary and secondary infrapopliteal bypasses. Am J Surg 1999 Aug; 178(2): 162–5. 3. Mazzariol F, Ascher E, et al. Lower-extremity revascularisation without preoperative contrast arteriography in 185 cases: lessons learned with duplex ultrasound arterial mapping. Eur J Vasc Endovasc Surg 2000; 19: 509–15. 4. Sensier Y, Hartshorne T, et al. A prospective comparison of lower limb colour-coded Duplex scanning with arteriography. Eur J Vasc Endovasc Surg 1996; 11: 170–5. 5. Ligush J Jr, Reavis SW, et al. Duplex ultrasound scanning defines operative strategies for patients with limbthreatening ischemia. J Vasc Surg 1998; 28: 482–90. 6. Sensier Y, Fishwick G, et al. A comparison between colour duplex ultrasonography and arteriography for imaging infrapopliteal arterial lesions. Eur J Vasc Endovasc Surg 1998; 15: 44–50. 7. London NJ, Sensier Y, Hartshorne T. Can lower limb ultrasonography replace arteriography? Vasc Med 1996; 1: 115–19. 8. Polak JF, Karmel MI, et al. Determination of the extent of lower-extremity peripheral arterial disease with colorassisted duplex sonography: comparison with angiography. AJR Am J Roentgenol 1990; 155: 1085–9. 9. Moneta GL, Yeager RA, et al. Accuracy of lower extremity arterial duplex mapping. J Vasc Surg 1992 Feb; 15(2): 275–83.

10. Wilson YG, George JK, et al. Duplex assessment of runoff before femorocrural reconstruction. Br J Surg 1997 Oct; 84(10): 1360–3. 11. Karacagil S, Lofberg AM, et al. Value of duplex scanning in evaluation of crural and foot arteries in limbs with severe lower limb ischaemia—a prospective comparison with angiography. Eur J Vasc Endovasc Surg 1996; 12: 300–3. 12. Koelemay MJ, Legemate DA, et al. Can cruropedal colour duplex scanning and pulse generated run-off replace angiography in candidates for distal bypass surgery. Eur J Vasc Endovasc Surg 1998; 16: 13–18. 13. Cossman DV, Ellison JE, et al. Comparison of contrast arteriography to arterial mapping with color-flow duplex imaging in the lower extremities. J Vasc Surg 1989 Nov; 10(5): 522–8. 14. Larch E, Minar E, et al. Value of color duplex sonography for evaluation of tibioperoneal arteries in patients with femoropopliteal obstruction: a prospective comparison with anterograde intraarterial digital subtraction angiography. J Vasc Surg 1997; 25: 629–36. 15. Lai DT, Huber D, et al. Colour duplex ultrasonography versus angiography in the diagnosis of lower-extremity arterial disease. Cardiovasc Surg 1996; 4: 384–8. 16. Wain RA, Berdejo GL, et al. Can duplex scan arterial mapping replace contrast arteriography as the test of choice before infrainguinal revascularization? J Vasc Surg 1999 Jan; 29(1): 100–7. 17. Proia RR, Walsh DB, et al. Early results of infragenicular revascularization based solely on duplex arteriography. J Vasc Surg 2001; 33: 1165–70. 18. Elsman BH, Legemate DA, et al. Impact of ultrasonographic duplex scanning on therapeutic decision making in lower-limb arterial disease. Br J Surg 1995 May; 82: 630–3. 19. Pemberton M, Nydahl S, et al. Colour-coded duplex imaging can safely replace diagnostic arteriography in patients with lower-limb arterial disease. Br J Surg 1996; 83: 1725–8. 20. Sarkar R, Ro KM, et al. Lower extremity vascular reconstruction and endovascular surgery without preoperative angiography. Am J Surg 1998; 176: 203–7. 21. Kohler TR, Andros G, et al. Can duplex scanning replace arteriography for lower extremity arterial disease? Ann Vasc Surg 1990; 4: 280–7. 22. Carpenter JP, Owen RS, et al. Magnetic resonance angiography of peripheral runoff vessels. J Vasc Surg, 1992; 16: 807–13. 23. Pemberton M Nydahl S, et al. Can lower limb vascular reconstruction be based on colour Duplex imaging alone? Eur J Vasc Endovasc Surg 1996; 12: 452–4. 24. Salles Cunha S, Andros G. Preoperative duplex scanning prior to infrainguinal revascularization. Surg Clin North Am 1990; 70: 41–59. 25. Waugh JR, Sacharias N. Arteriographic complications in the DSA era. Radiology, 1992; 182: 243–6. 26. Lautin EM, Freeman NJ, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors. Am J Roentgenol, 1991 157: 49–58. 27. Gussenhoven MJ, Ravensbergen J, et al. Renal dysfunction after angiography; a risk factor analysis in patients with peripheral vascular disease. J Cardiovasc Surg (Torino), 1991; 32: 81–6.

Chapter 3 Duplex Arteriography for Lower Extremity Revascularization 28. Martin Paredero V, Dixon SM, et al. Risk of renal failure after major angiography. Arch Surg 1983; 118: 1417–20. 29. Rudnick MR, Goldfarb S, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. Kidney Int 1995; 47: 254–61. 30. Parfrey PS, Griffiths SM, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320: 143–9. 31. Wilson YG, George JK, et al. Duplex assessment of runoff before femorocrural reconstruction. Br J Surg 1997; 84: 1360–3. 32. Humphreys P, McCarthy M, et al. Chromosome 4q locus Associated with insulin resistance in Pima Indians. Studies in three European NIDDM populations. Diabetes 1994; 43: 800–4. 33. Nelson RG, Knowler WC, et al. Determinants of endstage renal disease in Pima Indians with type 2 (noninsulin-dependent) diabetes mellitus and proteinuria. Diabetologia 1993; 36: 087–93. 34. Nelson RG, Newman JM, et al. Incidence of endstage renal disease in type 2 (non-insulin-dependent)

35.

36.

37.

38.

39. 40.

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diabetes mellitus in Pima Indians. Diabetologia 1988; 31: 730–6. Perneger TV, Brancati FL, et al. End-stage renal disease attributable to diabetes mellitus. Ann Intern Med 1994; 121: 912–8. Ismail N, Becker B, et al. Renal disease and hypertension in non-insulin-dependent diabetes mellitus. Kidney Int 1999; 55: 1–28. Maschio G, Alberti D, et al. Effect of the angiotensinconverting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. The Angiotensin-Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group. N Engl J Med 1996; 334: 939–45. Kshirsagar AV, Joy MS, et al. Effect of ACE inhibitors in diabetic and nondiabetic chronic renal disease: a systematic overview of randomized placebo-controlled trials. Am J Kidney Dis 2000; 35: 695–707. Dale WA. Differential management of acute peripheral arterial ischemia. J Vasc Surg 1984; 1: 269–78. Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity. Its natural history contrasted with arterial embolism. Arch Surg 1984; 119: 784–7.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 4 Intravascular Ultrasound Imaging Rodney A. White

Intravascular ultrasound (IVUS) has developed rapidly in the last few years. By providing an accurate luminal and transmural image of vascular structures, IVUS displays vascular pathology and illustrates immediate results of interventions. In addition to obvious diagnostic applications, the potential significance of IVUS has become even more apparent owing to the simultaneous development of minimally invasive catheter-based therapeutic techniques, including balloon angioplasty, atherectomy, laser angioplasty, and intravascular stents. The thrust of current development is to incorporate IVUS as an adjunct to peripheral and coronary angioplasty procedures. It is probable that IVUS will become a critical component of future interventional devices, and an understanding of the technique will be essential for those involved in the management of patients with cardiovascular disease.

Device Development and Imaging Configurations A major advantage of diagnostic ultrasound is that it avoids ionizing radiation and intravenous administration of contrast agents. Conventional transcutaneous ultrasound has limited ability to assess structures obscured by bone or air, and to obtain fine resolution of deep-lying tissues. Attaching the ultrasound transducer to an intraluminal catheter and increasing the frequency of the ultrasound energy enhances the interrogation and resolution of organs that are poorly accessible to transcutaneous ultrasound.

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Intravascular Ultrasound Catheter Design The first IVUS catheter prototypes were used to measure intracardiac dimensions and cardiac motion in the 1950s, utilizing A-mode transducers fixed to large intraluminal catheters (1,2). Various devices (A-, B-, and M-mode) were developed for both intravascular and transesophageal imaging of vascular structures, but it was not until the early 1970s that true intraluminal, crosssectional imaging of vessels was reported using a multielement array transducer (3–6). To obtain a 360° cross-sectional image, the ultrasound beam must be scanned through a full circle, and the beam direction and deflection on the display must be synchronized. This can be achieved by mechanically rotating the imaging elements, or by using electronically switched arrays (Fig. 4.1). Current multiple-element IVUS catheters utilize frequencies in the range of 15 to 25 MHz. The plane of imaging is perpendicular to the long axis of the catheter and provides a full 360° image of the blood vessel. A problem of the early phased-array devices was the electronic noise caused by the multiple wires within the catheter itself, as each of the 32 elements was an independent minitransducer needing its own connections. This problem was later overcome by incorporating a miniature integrated circuit at the tip of the catheter, which provided sequenced transmission and reception without the need for numerous electrical circuits traveling the full length of the catheter. As well as reducing the electronic noise, this modification simplified the manufacturing and improved the flexibility of the catheter. A problem of these imaging

Chapter 4 Intravascular Ultrasound Imaging

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FIGURE 4.1 (A) Diagram of a mechanical ultrasound device with rotating (1) and fixed (2) elements. Either the transducer or the mirror may be fixed with the other element in a rotating position. (B) Diagram of a phased-array device with the elements arranged circumferentially around the tip of the catheter. (Reproduced by permission from White RA. Indications for fiberoptic angioscopy and intraluminal ultrasound. Comp Ther 1990;16:23–30.)

catheters, common to all high-frequency ultrasound devices to some extent, is the inability to image structures in the immediate vicinity of the transducer, i.e., in the “near field.” Because the imaging crystals in a phased-array configuration are in almost direct contact with the structure being imaged, a bright circumferential artifact known as the “ring down” surrounds the catheter. The ring-down artifact can be electronically removed, but structures within the masked region will not be seen. Mechanical transducers, the most frequently used type of IVUS catheters, have one of two basic configurations: either the transducer itself or an acoustic mirror is rotated at the tip of the catheter using a flexible, hightorque cable that extends the length of the device. Some catheters use a transducer that is angled slightly forward of perpendicular, which produces a cone-shaped ultrasound beam and results in an image of the vessel slightly forward or in front of the transducer assembly. Devices that utilize a rotating acoustic reflector have the mirror set at a 45° angle to the rotating shaft, producing an image that is perpendicular to the axis of the catheter. In both rotating transducer and rotating mirror devices, ultrasound frequencies between 12.5 and 30 MHz generally are used, although some experimental devices using frequencies up to 45 MHz have produced excellent images of human arteries in vitro (7). In the rotating mirror devices, the ultrasound energy produced by the fixed transducer at the distal tip of the catheter is directed toward an angled mirror placed a short distance proximally. This configuration avoids the necessity for rotating the transducer, and the necessary distance between the transducer and the rotating mirror partially eliminates the ring-down image artifact and the poor resolution near-field of the scan. Both these problems are substantially reduced by allowing the ultrasound energy to travel a short distance in the imaging chamber filled with saline. The scan converter in the image-

FIGURE 4.2 Cross-sectional intravascular ultrasound image of common femoral artery, produced by a rotating mirror mechanical device. a, Artifact caused by the transducer electrical wire; double arrows, fibrous plaque; arrows, arterial media, u, ultrasound catheter void. (Reproduced by permission from Tabbara M, et al. In-vivo human comparison of intravascular ultrasound and angiography. J Vasc Surg 1991;14:496– 504.)

processing unit compensates for this nonimaging portion of the beam and generates images beginning at the surface of the catheter. In the rotating transducer and multiplearray devices, a part of the ring-down region and nearfield zone of the beam occur outside the catheter, so that it is not possible to image clearly in this area. However, both types of mechanical imaging catheters suffer less image loss due to these problems than the phased-array transducers (8). In devices with a distally placed transducer and proximal rotating mirror, it is necessary for an electrical connecting wire to pass along the side of the imaging assembly. This wire produces an artifact that occupies approximately 15° of the image cross-section (Fig. 4.2). A similar artifact is generated in any device in which a wire passes along the side of the imaging element. An interesting modification of the mechanical catheter design involves rotation of both the transducer and the mirror, eliminating any electrical wire artifact. Current disposable mechanical catheters utilize a saline- or water-filled imaging chamber that must be rendered and maintained bubble-free to allow adequate imaging. Miniaturization of the moving parts of the mechanical systems is a major limitation that may ultimately separate these devices from phased-array catheters in their utility in smaller-caliber vessels. On the other hand, as phased-array catheters are used in progressively smaller

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vessels, the problems of ring-down and near-field imaging become more apparent. The smallest currently available mechanical catheters (2.9 Fr. or 0.9 mm in diameter) approximate the size of diseased coronary arteries and, when used with higher-frequency ultrasound, may prove to be superior in most applications.

Computerized Three-dimensional Image Reconstruction Three-dimensional (3-D) intravascular ultrasound imaging has developed as a result of advances in digital computer graphics technology and mass data storage capabilities of personal computers. Algorithms of 3-D image reconstruction can be classified as either surface or volume rendering; currently available 3-D IVUS imaging utilizes surface rendering. Object surfaces are explicitly formed before being depicted on a two-dimensional (2-D) screen using techniques such as hidden-part removal, shading, translucency, dynamic rotation, and stereo projection (9). With this technology, a longitudinally aligned set (up to 300 images per set) of consecutive 2-D images obtained during a “pullback” through a vessel segment is assembled in sequence to produce the 3-D image (Image

Comm, Inc., Santa Clara, CA) (10) (Fig. 4.3). The “pullback” is performed by withdrawing the imaging catheter at a uniform rate using a mechanical device at a rate of 1 cm every 4 seconds. The 2-D IVUS dataset from a 5-cm vessel segment is therefore represented by a 20-s “pullback,” which can be recorded on videotape or reconstructed online. The images are then sampled in digital format following analog-to-digital conversion, at rates of up to 7.5 frames per second (150 frames for a 20-s “pullback”). Currently, most processing is accomplished using datasets recorded on magnetic videotape. Preacquisition of these data allows the user to select the most suitable segments for reconstruction and to adjust screen cropping parameters to electronically eliminate the artifact of the IVUS catheter and other unwanted image data. Approximately 12 seconds of computer processing time is required for the initial reconstruction of a highresolution gray-scale, 2-D longitudinal view of the vessel segment (Fig. 4.4). Before final 3-D reconstruction, the image density threshold is adjusted to optimize differentiation of structures. This step is particularly important when it is necessary to separate tissues of similar echodensity, e.g., soft plaque and thrombus. The 3-D image is then displayed in multiple orientations to allow inspection of

FIGURE 4.3 The 2-D images labeled A, B, and C (center) are “stacked” by the computer, and correspond to the sites labeled with the same letters on the 3-D image (right) and longitudinal section of the 3-D image (left). The longitudinal section of the 3-D image is displayed on the computer monitor to allow optimal adjustments of the image density threshold and viewing orientation. (Reproduced by permission from Cavaye DM, et al. Three-dimensional vascular ultrasound imaging. Am Surg 1991,57:751–756.)

Chapter 4 Intravascular Ultrasound Imaging

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FIGURE 4.4 High-resolution, gray-scale, 2-D longitudinal view of an atherosclerotic human superficial femoral artery. The ultrasound catheter void (u) is seen within the lumen at right and abutting soft plaque (s) at left. C, calcium; single arrows, media. (Reproduced by permission from Cavaye DM, et al. Three-dimensional intravascular ultrasound imaging of normal and diseased, human and canine arteries. J Vasc Surg 1992;16:509–519.)

FIGURE 4.5 Three-dimensional image of the vessel in Figure 4.4. The reconstructed image is viewed in a longitudinal hemi-section to allow complete examination of the luminal surface in this projection. c, Calcium; single arrows, media. (Reproduced by permission from Cavaye DM, et al. Three-dimensional intravascular ultrasound Imaging of normal and diseased, human and canine arteries. J Vasc Surg 1992;16:509–519.)

the arterial segment in all possible projections both from within the lumen and from the adventitial surface (Fig. 4.5). Other parameters such as image sharpness, contrast, and ambient light can be altered to improve the resolution of particular features being examined in the reconstructions. Images of the luminal volume alone can also be produced by removing vessel wall signals. Although it has been shown that 2-D cross-sectional IVUS and gray-scale longitudinal reconstructions provide accurate luminal and transmural dimensions, the accuracy of currently available 3-D imaging has not been established. By viewing all three image formats simultaneously on a screen, however, the location of the 2-D image site along the length of the 3-D image can be identified using a linear cursor, and the dimensions of a site on the 3-D image can be estimated. A continuing problem associated with many 3-D imaging techniques is the near-field effect of the ultrasound imaging catheters at frequencies of 20 to 30 MHz, resulting in bright imaging of the blood immediately surrounding the catheter. As the 3-D imaging software has improved, it has allowed manipulation of the image data to reduce the blood artifact, but this problem still remains in some images because of the inherent features of the imaging catheter.

Forward-looking Intravascular Ultrasound An exciting recent advance is the development of forward-looking IVUS, utilizing acoustic beams that radiate in the shape of a cone from the front of a 7.5-Fr. catheter (Echo Cath, Ltd, Princeton, NJ) (Fig. 4.6). A 27MHz transducer fills a 60° divergent cone with 2000 sequential beams, each comprising 64 axially aligned acoustic measurements. The result is a 3-D image of a volume shaped like a truncated cone, with the near surface located 5 mm from the catheter tip and extending forward 9 mm to the most distant surface. Although this system is experimental, it provides new and unique imaging data that may be critical for guidance of endoluminal devices in treating occlusive vascular lesions.

Intravascular Ultrasound Imaging Techniques Intravascular ultrasound catheters can be introduced percutaneously or through a standard arterial access sheath (7 to 9 Fr.) or through an opening in a vessel during

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A

ization. Image quality is best when the catheter is parallel to the vessel wall—i.e., the ultrasound beam is directed at 90° to the luminal surface—while minor angulations may affect the luminal shape and dimensional accuracy. Eccentric positioning causes the vessel wall nearer the imaging chamber to appear more echogenic than the distant wall, producing an artifactual difference in wall thicknesses. Positioning the catheter in the center of the lumen is especially difficult in tortuous vessels and is often best achieved as the catheter is withdrawn rather than during advancement. Luminal flushing with saline or radiographic contrast agent has been reported to improve delineation of acoustic interfaces in medium and small-sized vessels (11,12).

Clinical Utility of Intravascular Ultrasound Disease Distribution and Characterization

B

FIGURE 4.6 (A) Schematic of forward-looking IVUS catheter. The transducer fills a 60° cone with 200 sequential beams, resulting in an image shaped like a truncated cone, with the near surface located 5 mm from the catheter tip and the far surface extending back a total of 14 mm. (B) Display screen showing the volume image, catheter icon, and cursor (upper left), and representative cross-sections below. (Reproduced by permission from Cavaye DM, White RA, eds. Intravascular ultrasound imaging. New York: Raven Press, 1992.)

a surgical procedure. If large vessels proximal to the arteriotomy are imaged (e.g., iliac artery imaging via a femoral cutdown), a hemostatic access device should be used to reduce blood loss and prevent catheter damage during insertion. Most devices can be passed over a guidewire, which allows more controlled maneuvering of the device within the lumen of the vessel from a remote introduction site, particularly in tortuous or tightly stenotic vessels. It is important to orientate the IVUS catheter within the vessel so that anteroposterior accuracy can be achieved. The best ways to maintain orientation are to use the image artifact produced by the transducer’s connecting wires, and to establish correct initial alignment at the point of catheter insertion. For example, when imaging the aortoiliac segments via a femoral puncture site, rotational alignment can be confirmed by the relative position of anatomical landmarks such as the aortic and iliac bifurcation. Because the catheters are rotationally rigid, there is very little loss of orientation with torquing and manipulation during imaging. Careful positioning of the catheter tip within the vessel and appropriate size matching of the device to the artery caliber are essential to optimize visual-

Several studies have reported that IVUS is accurate in determining the luminal and vessel wall morphology of normal or minimally diseased arteries both in vitro and in vivo (13–18). In muscular arteries, distinct sonographic layers are visible and the media appears as an echolucent layer sandwiched between the more echodense intima and adventitia (see Fig. 4.2). The precise correlation between the ultrasound image and the microscopic anatomy of the muscular artery wall is still uncertain. The internal and external elastic laminae and adventitia are considered to be the backscatter substrates for the inner and outer echodense zones (13,19). The adventitia may be difficult to measure precisely unless the vessel is surrounded by tissues of differing echogenicity such as echolucent fat. Even small intimal lesions such as flaps or intimal tears are well visualized because of their high fibrous tissue content and the difference between the echoic properties of these structures and those of the surrounding blood. The three-layer appearance of muscular arteries is not readily seen in larger vessels such as the aorta, because of the increased elastin content in the media. Intravascular ultrasound devices are sensitive in differentiating calcified and noncalcified vascular lesions. Because the ultrasound energy is strongly reflected by calcific plaque, it appears as a bright image with dense acoustic shadowing behind it (Fig. 4.7; see Figs 4.4 and 4.5). For this reason, the exact location of the media and adventitia cannot be seen in segments of vessels containing heavily calcific disease, and dimensions must be estimated by interpolating adjacent size data. Gussenhoven et al. have described four basic plaque components that can be distinguished using 40-MHz IVUS in vitro (19): echolucent, lipid deposit, or lipid “lake”; soft echoes, fibromuscular tissue, or intimal proliferation including varying amounts of diffusely dispersed lipid; bright echoes, collagen-rich fibrous tissue; and bright echoes with acoustic shadowing, calcified tissue.

Chapter 4 Intravascular Ultrasound Imaging

Numerous investigations have compared angiography and IVUS for determining luminal and transmural dimensions of normal and moderately atherosclerotic human arteries (18,20,21). The cross-sectional areas calculated from biplanar angiograms and measured from IVUS correlate well for normal or minimally diseased

FIGURE 4.7 Intravascular ultrasound image of atherosclerotic human iliac artery. A large calcified plaque (arrows) produces a bright luminal line with acoustic shadowing behind it: u, ultrasound catheter void; a, imaging artifact. (Reproduced by permission from Tabbara M, et al. In-vivo human comparison of intravascular ultrasound and angiography. J Vasc Surg 1991; 14:496–504.)

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peripheral arteries in vivo. Most studies reveal that IVUS and angiography also correlate well when used to image mildly elliptical lumens but, when used to derive dimensions from severely diseased vessels, the angiogram tends to underestimate the severity of disease. By offering a method to define the luminal and transmural morphology and dimensions, IVUS provides a new perspective from which to investigate arterial disease. Recent studies have compared 2-D and 3-D IVUS with angiography and 3-D computed tomography (CT) for imaging abdominal aortic aneurysms (22). Each modality provides unique information regarding the anatomy of the aorta and the distribution of components of the aneurysm (Fig. 4.8). In the case that is illustrated, the aortogram confirmed that the aneurysm was confined to the infrarenal aorta and documented the patency of adjacent branch arteries. The luminal morphology imaged on the angiogram underestimated the size of the aneurysm although displacement of the right ureter suggested a larger dimension. In addition, the angiogram did not provide precise cross-sectional and volumetric data regarding the dimensions of the neck of the aneurysm, quantity of thrombus, aortic wall characteristics, and other findings that were apparent on CT and IVUS. Views of cross-sections of the aneurysm acquired by CT and IVUS enabled accurate sizing of luminal and wall dimensions and correlated closely at various levels along the aorta. Surrounding anatomic structures and characteristics of the vessel wall were highlighted using each method (Fig. 4.9). The IVUS images demonstrated the origin of visceral vessel (superior mesenteric and renal arteries) in relation to the aneurysm and displayed areas of calcification compared with thrombus and fibrous wall components. Calcification was clearly identified by IVUS as hyperechoic areas with shadowing beyond the lesion. Calcification of the wall of the aorta was more readily apparent by IVUS than by angiography or CT. Although

FIGURE 4.8 Left to right: Aortogram, longitudinal gray-scale IVUS, surface-rendered 3-D IVUS, and 3-D CT of the external surface of the aortic aneurysm. The images are of comparable lengths of the aorta with similar magnifications to enable comparison of the methods. (Reproduced by permission from White RA, et al. Innovations in vascular imaging angiography, 3D CT and 2D and 3D intravascular ultrasound of an abdominal aortic aneurysm. Ann Vasc Surg 1994;8:285–289.)

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the 2-D cross-sectional CT and IVUS images corresponded closely for determining the luminal and vessel wall dimensions, the 3-D IVUS reconstructions demonstrated some variation in the shape and topography of the wall surface along the longitudinal axis of the aneurysm compared with the 3-D CT. The 3-D CT outlined the external surface of the aorta, while the IVUS visualized the lumen and transmural wall characteristics. Development of future interventional methods such as intravascular graft deployment will utilize specific applications of each method to enhance precision of endovascular repairs. In particular, IVUS is being used to size and assess the characteristics of the aortic wall and aneurysm before deployment, to precisely place the device during the procedure, and to assess the accuracy of the graft positioning. Conventional angiography has been unable to provide adequately sensitive data regarding the effects of endovascular therapies. For meaningful critical assessment of these new methods, plaque consistency and distribution of residual lesions following intervention must be known. Intravascular ultrasound imaging provides the

ability to accurately measure stenoses produced by comparing luminal dimensions with normal-appearing adjacent reference vessels. This is due in part to the restrictions of single or biplanar arteriography, but also to the fact that an angiogram is a luminal silhouette rather than a transmural image. Three-dimensional IVUS can be used to demonstrate atherosclerotic lesion volume, distribution, and tissue characteristics, and is particularly relevant to investigation of the natural history of atherosclerotic disease and to volumetric plaque studies before and after endovascular interventions. Lesion volume is measurable using 3-D IVUS imaging, but data regarding its accuracy are not currently available. Plaque volume estimation is based on the concept of differing cylindrical volumes, in that the inner (smaller) cylinder is represented by the vessel lumen and the outer (larger) cylinder is confined by the adventitia. By creating a surface-rendered luminal image and a complete cylindrical adventitial reconstruction of a vascular segment, these two volumes can be displayed (Fig. 4.10). The difference between the two cylinders represents the “volume” occupied by the arterial wall elements, either normal or pathologic. If this volume is measured before and after an intervention such as atherectomy, the difference in the volumes represents the amount of actual lesion removed. This information is required to delineate the mechanisms of angioplasty failure, because the roles of residual stenosis and recurrent stenosis have not been adequately defined using currently available angiographically determined data. Intravascular ultrasound provides information essential in the investigation of arterial wall dissections by determining the size, location, and extent of intimal flaps (Fig. 4.11). Because IVUS imaging is a dynamic, real-time imaging modality, the movement of arterial flaps with systolic–diastolic blood flow can be seen. The precise location and orientation of the flap is important as it may determine the need for excision and grafting, stenting, or repair. Intravascular ultrasound has been used to identify the location and severity of dissections and flaps, and may enable endovascular assessment and treatment alone (23–26). Three-dimensional IVUS imaging is especially useful in this role, because aortic dissection commonly results in a spiral or complex-shaped flap that is difficult to appreciate in three dimensions using alternative imaging modalities. Three-dimensional reconstruction allows determination of the dissection entry site, the extent of the flap, and the relation of the false lumen to major visceral branches, and it plays a vital role in experimental endoluminal stenting of aortic dissections.

FIGURE 4.9 Comparison of views by IVUS (top) and CT (bottom) of the aneurysm at the same location. I, Aortic lumen; t, thrombus in the aneurysm; c, calcification; IVC, inferior vena cava; v, vertebral body.

Intravascular Ultrasound as an Adjunct to Endovascular Interventions

(Reproduced by permission from White RA, et al. Innovations in vascular imaging angiography, 3D CT and 2D and 3D intravascular ultrasound of an abdominal aortic aneurysm. Ann Vasc Surg 1994;8:285–289.)

Recent studies have indicated that in percutaneous transluminal angioplasty (PTA), balloon size is often underestimated when selection is made using quantitative angiography, and that optimal balloon size is more accu-

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A

FIGURE 4.11 Intravascular ultrasound image of the distal abdominal aorta in a patient with an acute dissecting aortic aneurysm confirms dissection extending to this level. Dissection flap (double arrows), aortic wall (single arrow), true (T) and false (F) lumens are seen. (Reproduced by permission from Cavaye DM, et al. Intravascular ultrasound imaging of an acute dissecting aortic aneurysm: a case report J Vasc Surg 1991;13:510–512.)

B

FIGURE 4.10 (A) Complete cylindrical vessel reconstruction, with the outer boundary formed by the adventitia. (B) Luminal reconstruction from the same vessel. By subtracting the volume of the luminal cylinder from the volume of the complete vessel cylinder the volume of the vessel wall (pathologic or normal) can be derived. (Reproduced by permission from Cavaye DM, et al. Three-dimensional vascular ultrasound imaging. In Cavaye DM, White RA, eds. A text and atlas of arterial imaging: modern and developing technologies. London: Chapman & Hall, 1993:143–147.)

rately determined by IVUS (27). Other findings suggest that the angiographic success of balloon angioplasty is more likely when hard lesions are disrupted with dissections extending into the media of the vessel, while angiographic failure is seen in lesions that are not displaceable or when circumferential dissections or intimal flaps occur (28). Angiographic success in soft lesions is associated with superficial fissures or fractures of the luminal surface, while vessel recoil and luminal disruption or thrombosis at sites of plaque rupture lead to failure. Intravascular ultrasound is capable of imaging all these features and may be invaluable in providing information that will be used to choose lesions suitable for balloon therapy.

By combining information about plaque and vessel wall consistency with lesion location data such as eccentricity, and by quantitating residual stenosis and dissections, IVUS is ideally suited as a screening and guidance method to improve results of balloon angioplasties (29,30). The balloon ultrasound imaging catheter (BUIC; Boston Scientific, Watertown, MA) has been used clinically with promising results. It has been confirmed that single-plane images can be obtained through the midsection of the angioplasty balloon at all times during the course of the angioplasty procedure, and preinflation, inflation, and postinflation luminal features such as plaque fracture and elastic recoil can be monitored with real-time IVUS (31,32). Peripheral balloon angioplasty has been monitored with IVUS and has been especially useful in identifying and assessing the effect of intimal flaps (9). Preliminary studies have utilized IVUS to localize and treat coarctation of the aorta both experimentally and clinically (33). Intravascular ultrasound clearly shows the coarctation and accurately measures the adjacent normal aortic lumen for balloon sizing. Following dilation, IVUS displays the appearance of the dilation including documentation of dissections. Intravascular ultrasound has been used as a method to study the mechanism of action and function of atherectomy devices, lasers, and stents (34–36). For each type of interventional device, the combination of the guidance

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FIGURE 4.12 Intravascular ultrasound image shows the entire length of a coronary artery segment after rotational atherectomy and balloon dilation. Nine cross-sectional images are shown that are 3 mm apart on center. The most distal images are on the left and show dissection of a circumferentially calcific plaque. There is heavy circumferential and longitudinal calcium, especially at the narrowest residual lumen, which measures 2.3 ¥ 2.7 mm. The largest burr used was 2.15 mm, the adjunct balloon size was 3.0 mm. (Reproduced by permission from Mintz GS, et al. Intravascular ultrasound evaluation of the effect of rotational atherectomy in obstructive atherosclerotic coronary artery disease. Circulation 1992;86:1383–1393.)

FIGURE 4.13 (A) Intravascular ultrasound image of a stent in an artery that appeared fully deployed by fluoroscopic examination, but required further balloon inflation using real-time IVUS before full deployment was achieved; (B) stent struts (single arrow), arterial wall (double arrow).

and lesion assessment capabilities of IVUS with an interventional technique may produce specific benefits for a particular type of approach. Figure 4.12 demonstrates the utility of IVUS imaging in choosing the size of atherectomy and balloon devices for the treatment of coronary lesions (351). Intravascular ultrasound also provides a method to guide deployment and assess the effect of intravascular stents in peripheral vessels. It allows selection of the correct stent size for a particular vessel and is useful in identifying the most appropriate site for stenting. Two- and

three-dimensional IVUS are ideally suited to assessing vascular segments before and after stent deployment. Also, unique information regarding the adequacy of deployment and changes in morphology produced by the stent can be seen (Fig. 4.13).

Developing Applications of Intravascular Ultrasound Intravascular ultrasound is an invasive technique requiring intravascular puncture and catheter insertion. The

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FIGURE 4.14 Fundamentals of tissue characterization. The image on the left is constructed from raw radiofrequency information. One line of this information is shown on the right, with the corresponding tissue elements labeled. The image is created from the amplitude envelope of this signal. More information about specific tissue types, however, is available from computer analysis of the raw signal. The image and signal are from a prototype system (Cardiovascular Imaging Systems, Inc., Sunnyvale, CA) that provides combined imaging and tissue characterization. (Reproduced by permission from Yock PG, et al. Clinical applications of intravascular ultrasound imaging. In: Bernstein EF, ed. Vascular diagnosis, 4th edn. Chicago: Mosby Year Book Medical Publishers, 1993: 994–1000.)

diagnostic applications are useful when combined with invasive studies such as peripheral angiography or cardiac catheterization, or as a guidance method during therapeutic procedures including angioplasty and stent deployment. Developing potentials of the method range from improved localization of vascular tumors before surgery (37) or imaging the long-term function of vena caval filters (38) to possible application as the primary guidance method for laser angioplasty (39). A priority in the development of IVUS technology is the need for further miniaturization and cost-effective manufacturing. Current devices are relatively expensive, and, if the technique is to be of clinical benefit as a component of a disposable catheter system for diagnostic or therapeutic intervention, the price of individual units must be justified by the benefits of IVUS imaging. Future angioplasty guidance devices may combine the benefits of angioscopy and IVUS in a single delivery system suitable for incorporating mechanical or laser ablation devices. Angioscopy would allow visual inspection of the lumen, with ultrasound determining the vessel wall characteristics and dimensions. An added benefit of this type of guidance device would be the ability to select an appropriate ablation method for particular plaque types or volumes. Tissue characterization by analyzing the raw radiofrequency ultrasound signal shows promise for differentiating plaque types (Fig. 4.14). Intravascular ultrasound also provides exciting opportunities for vascular research including investigation of blood vessel compliance, dynamic changes in the vascular wall caused by disease or pharmacologic intervention, and the natural history of atherosclerosis.

References 1. Bom N, ten Hoff H, et al. Early and recent intratuminal ultrasound devices. Int J Card Imaging 1989;4:79–88. 2. Cieszynski T. Intracardiac method for the investigation of structure of the heart with the aid of ultrasonics. Arch Immunol Ther Dow 1960;8:551–557. 3. Kossof G. Diagnostic applications of ultrasound in cardiology. Australas Radiol 1966;10:101–106. 4. Carleton RA, Sessions RW, Graettinger JS. Diameter of heart measured by intracavitary ultrasound. Med Res Eng 1969;May:28–32. 5. Frazin L, Talano JV, et al. Esophageal echocardiography. Circulation 1976;54:168–171. 6. Bom N, Lancee CT, Van Egmond FC. An ultrasonic intracardiac scanner. Ultrasonics 1972;10:72–76. 7. Lockwood CR, Ryan LK, Foster FS. High frequency intravascular ultrasound imaging. In Cavaye DM, White RA, eds. Arterial imaging: modern and developing technologies. London: Chapman & Hall, 1993;125–129. 8. Yock PG, Linker DT, Angelsen BAJ. Two-dimensional intravascular ultrasound: technical development and initial clinical experience. J Am Soc Echocardiogr 1989;2(4): 296–304. 9. Heffernan PB, Robb RA. A new method for shaded surface display of biological and medical images. IEEE Trans Med Imaging 1985; MI-4:26–38. 10. Cavaye DM, Tabbarra MR, et al. Three dimensional vascular ultrasound imaging. Am Surg 1991;57:751–755. 11. van Urk H, Gussenhoven WJ, et al. Assessment of arterial disease and arterial reconstructions by intravascular ultrasound. Int J Card Imaging 1991;6:157–164. 12. Burns PN, Goldberg BB. Ultrasound contrast agents for vascular imaging. In: Cavaye DM, White RA, eds. Arterial imaging: modern and developing technologies. London: Chapman & Hall, 1993:61–67.

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13. Gussenhoven WJ, Essed CE, Lancee CT. Arterial wall characteristics determined by intravascular ultrasound imaging: an in-vitro study. J Am Coll Cardiol 1989; 14:947–952. 14. Kopchok CE, White RA, et al. Intraluminal vascular ultrasound: preliminary report of dimensional and morphologic accuracy. Ann Vasc Surg 1990;4:291–296. 15. Kopchok GE, White RA, White G. Intravascular ultrasound: a new potential modality for angioplasty guidance. Angiology 1990;41:785–792. 16. Mallery JA, Tobis JM, et al. Assessment of normal and atherosclerotic arterial wall thickness with an intravascular ultrasound imaging catheter. Am Heart J 1990;119: 1392–1400. 17. Nissen SE, Grines CL, et al. Application of new phasedarray ultrasound imaging catheter in the assessment of vascular dimensions. Circulation 1990;81:660–666. 18. Nissen SE, Gurley JC, et al. Intravascular ultrasound assessing of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation 1993;88:1087–1099. 19. Gussenhoven WJ, Essed CE, et al. Intravascular echo-graphic assessment of vessel wall characteristics: a correlation with histology. Int J Card Imaging 1989;4: 105–116. 20. Tabbara MR, White RA, et al. In-vivo human comparison of intravascular ultrasound and angiography. J Vasc Surg 1991;14:496–504. 21. Tobis JM, Mahon D, et al. The sensitivity of ultrasound imaging compared to angiography for diagnosing coronary atherosclerosis [abstract]. Circulation 1990;82 (Suppl III):439. 22. White RA, Scoccianti M, et al. Innovations in vascular imaging: angiography, 3D CT and 2D and 3D intravascular ultrasound of an abdominal aourtic aneurysm Ann Vasc Surg 1994;8:285–289. 23. Cavaye DM, French WJ, et al. Intravascular ultrasound imaging of an acute dissecting aortic aneurysm: a case report. J Vasc Surg 1991;13:510–512. 24. Pandian NG, Fries A, et al. Intravascular high frequency two-dimension detection of arterial dissection and intimal flaps. Am J Cardiol 1990;65:1278–1280. 25. Neville RF, Yasuhara H, et al. Endovascular management of arterial intimal defects: an experimental comparison by arteriography, angioscopy and intravascular ultrasonography. J Vasc Surg l991;13:496–502. 26. Cavaye DM, White RA, et al. Usefulness of intravascular ultrasound for detecting experimentally induced

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

aortic dissection in dogs and for determining the effectiveness of endoluminal stenting. Am J Cardiol 1992;69: 705–707. Cacchione J, Nair R, Hodson J. Intracoronary ultras ound is better than conventional methods for determining optimal PTCA balloon size [abstract]. J Am Coll Cardiol 1991;17:112A. Leon M, Keren G, et al. Intravascular ultrasound assessment of plaque responses to PTCA helps to explain angiographic findings [abstract]. J Am Coll Cardiol 1991;17:47A. Davidson CJ, Sheikh KR, et al. Intracoronary ultrasound evaluation of interventional procedures [abstract]. Circulation 1990;82(Suppl III):440. Gurley J, Nissen S, et al. Comparison of intravascular ultrasound following percutaneous transluminal coronary angioplasty [abstract]. Circulation 1990;82: 90. Crowley RJ, Hamm MA, et al. Ultrasound guided therapeutic catheters: recent developments and clinical results. Int J Card Imaging 1991;6:145–156. Isner JM, Rosenfield K, et al. Combination balloonultrasound imaging catheter for percutaneous transluminal angioplasty. Circulation 1991;84:739–754. Sanzobrino B, Gillam L, et al. A direct clinical role for intravascular ultrasound: utility in the assessment of coarctation of the aorta [abstract]. J Am Coll Cardiol 1991;17:68A. Smucker ML, Scherb DE, Howard PF. Intra-coronary ultrasound: How much “angioplasty effect” in atherectomy? [abstract]. Circulation 1990;82(Suppl):676. Mintz G, Potkin B, et al. Intravascular ultrasound evaluation of the effect of rotational atherectomy in obstructive athereroscierotic coronary disease. Circulation 1992;86:1383–1393. Cavaye DM, Tabbara MR, et al. Intravascular ultrasound assessment of vascular stent deployment. Ann Vasc Surg 1991;5:241–246. Barone GW, Kahn MB, et al. Recurrent intracaval renal cell carcinoma: the role of intravascular ultrasonography. J Vasc Surg 1990;13:506–509. Greenfield LJ, Tauscher JR, Marx V. Evaluation of a new percutaneous stainless steel Greenfield filter by intravascular ultrasonography. Surgery 1991;109: 722–729. White RA, Kopchok GE, et al. Intravascular ultrasound guided holmium:YAG laser recanalization of occluded arteries. Lasers Surg Med 1992;12:239–245.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 5 Fundamentals of Angiography Harvey L. Neiman and James Lyons

Angiography has undergone considerable change in the last four decades since Seldinger’s pioneering description of coaxial catheterization technique (1). Numerous technical innovations have introduced a remarkable degree of safety, and diagnostic efficacy and therapeutic breadth. Newer imaging modalities, such as computed tomography (CT), ultrasound (CT), and magnetic resonance imaging (MRI), have refined rather than refuted the crucial role angiography plays in patient management. In fact, these newer imaging tools frequently add impetus for a subsequent, more specialized, arteriographic examination; often a therapeutic intervention. Angiography/interventional radiology is a problemoriented discipline that requires diagnostic acumen, an understanding of pathophysiology of vascular disease, technical skills, and a broad knowledge of management of vascular disease. These skills allow the interventionalist to participate in the diagnosis and treatment of patients with vascular disease and to offer techniques when less invasive therapy is warranted.

History of Angiography The foundations of angiography were developed in the excitement generated by Roentgen with his report of the discovery of x-rays in 1895 (2). The first angiographic examination was performed by Haschek and Lindenthal in the month following Roentgen’s classic description. These authors injected a chalk-containing solution (Teichmann’s mixture) into the blood vessels of an amputat-

ed hand (3). Radiographs of both arteries and veins were first made in live patients by Berberich and Hirsch in 1923 using a 20% solution of strontium bromide (4). The first medical application occurred in 1924 when Brooks proposed angiographic criteria for limb amputation (5). In 1928, Moniz and Diaz reported the first attempt to visualize the cerebral circulation by injecting an intensely radioactive suspension of thorium oxide into a surgically exposed carotid artery (6). McPheeters and Rice, in 1929, used iodized poppy seed oil (Lipiodol) to visualize lower extremity veins (7). The emerging disciplines of arteriography and venography were seldom used, however, until the introduction of organic iodinated contrast materials and the development of rudimentary catheterization techniques. In 1929, Moses reported the use of an organic iodide called Uroselectan for intravenous urography, that was much better tolerated than sodium iodide (8). Uroselectan was subsequently superseded by the improved materials diodrast (Diodone) and neo-iopax (Uroselectan B) (9). During the same year, Forssmann inserted a catheter into his own antecubital vein and obtained a radiograph to confirm his impression that the catheter had reached the right atrium (10). In 1931, Moniz and his colleagues succeeded in visualizing the right heart and pulmonary vessels of a patient using Forssmann’s technique (11). The usefulness of intravenous injection of contrast material for arterial opacification became appreciated when Castellanos et al., in 1937, published results on their experiences (12). Their examinations focused on diagnoses of congenital cardiac anomalies. Studies were limited because of their inability

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to opacify the left heart and because the density of the images after intravenous injection was frequently inadequate. Robb and Steinberg, in 1939, expanded the technical aspects of cardiac imaging when they reported the technique of rapid sequence exposure (13). In 1935, Zeides des Plantes suggested that photographic image subtraction be used to separate contrast material densities from those produced by bone or other normal anatomic structures (14). Application of this concept using computerized digital subtraction techniques has revolutionized the field of arteriography today. Retrograde brachial aortography was described in 1939 by Castellanos and Pereiras (15). In 1941, Farinas reported the retrograde passage of a catheter from the femoral artery into the abdominal aorta for aortography (16). However, the modern era of angiography began with Seldinger’s description, in 1953, of a percutaneous transfemoral method of catheter placement over a guidewire (1). Subsequent major advances include the development of coronary arteriography, pharmacoangiography for the diagnosis and management of gastrointestinal hemorrhage or ischemia, renal, pancreatic and hepatic angiography, as well as other techniques too numerous to describe. Parallel changes of equal importance involve technical advances such as the development of the rapid film changer, biplane imaging, computerized digital subtraction, catheter material technology, low-osmolarity contrast media, balloon catheters, stents, and stent–grafts. Computerized digital subtraction allows the display of isolated vascular anatomy without superimposed anatomic structures. Increased contrast resolution is thus achieved (Fig. 5.1).

Technical Principles Angiographic Equipment The standard angiographic room must contain a high quality fluoroscopic system with video monitoring. Procedures should never be carried out without fluoroscopic guidance. Fluoroscopic monitoring assures increased safety and facilitates procedure efficiency and timeliness. Modern fluoroscopic systems are digitized allowing options such as decreased dose, filmless image acquisition, road mapping and real-time image processing and three-dimensional reconstructions (17). A high capacity three-phase generator of constant load output and a rating of at least 100 kW at 100 kV is also necessary to assure optimum kilovoltage levels at minimum exposure times. Full generator output and voltage stability during the examination require a welldesigned power source free of line interference from other hospital equipment. Automatic line voltage compensation should also be integral to the x-ray generator. Rapid film changers are a further necessity for all types of conventional film-screen angiographic examinations. However, current equipment allows for digital

acquisition and output with display on a high-resolution workstation, negating the need for film. Local and wide area networking are then possible—including the operating room, with image storage on some form of an archive jukebox. Biplane capabilities can be helpful, since image acquisition in a single projection may not accurately demonstrate the abnormality. Sequential filming in a second plane is often required when biplane equipment is unavailable. This, however, increases both the time of the procedure and the amount of contrast media used. For lower extremity arteriography, a programmable stepping tabletop should be available. The stepping tabletop or moving gantry can be used in conjunction with a standard film changer and specialized computer-driven equipment that allows the unit to move at preselected intervals. However, automatic stepping is also available for digital subtraction angiography (18). We have utilized this technique for many years with excellent results. In fact, in our department we are entirely filmless. The angiographic catheterization table should have a floating top to facilitate the carrying out of procedures. If possible, this table should also be able to move up and down for both ease of examination and for proper positioning of the patient. The x-ray tube and image intensifier should operate independently to permit magnification views. The latter two units should be mounted on a “C” or “U” arm for ease of use and optimal filming capabilities. Cine capability is necessary only if cardiac catheterizations are performed in the same room. It is obligatory that every angiographic room have ECG and pulse oxygenation monitoring capability and that all patients be so monitored (19). Intra-arterial pressure monitors are extremely important in evaluating the hemodynamic significance of stenoses, the results of angioplasty, and portal vein pressures. Intravascular pressure determination is also essential in pulmonary angiography before the injection of contrast material. An instrument to measure activated clotting times is also essential. Contrast medium injections are performed with automatic mechanical pressure injectors that provide delivery of a given amount of contrast at a predetermined rate and pressure. Hand injections, however, are utilized for testing the placement of catheters during fluoroscopy and during some digital subtraction applications. The former allows for careful monitoring of the catheter injection site to prevent inadvertent mechanical delivery of contrast into the subintimal space or into an unintended vessel. If film is used instead of digital archival, a laser processor should be in close proximity to the catheterization room for proper management of examinations, since the next “run” often depends on information derived from the previous sequence. Each examination must be tailored to the unique needs of a particular patient. Finally, a well-trained team of angiographic technologists and nurses is invaluable and essential for carrying out high-quality examinations with safety and efficiency. Because of the specialized nature of these procedures, only those staff members most familiar with the examinations

Chapter 5 Fundamentals of Angiography

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B

D

FIGURE 5.1 Digital subtraction arteriogram performed with a stepping table. “Real-time” digital subtraction images are produced. This examination was completed with 85 mL of contrast material to visualize the vascular system from the diaphragm to the feet. (A) Mild atherosclerotic disease of the abdominal aorta with a single renal artery bilaterally (arrows). At least partial patency of the celiac and superior mesenteric arteries. (B) Occlusion of the left superficial femoral artery at its origin (arrow). (C) View of thighs with moderate atherosclerotic disease of the right’s uperficial femoral artery and occluded left superficial femoral artery. (D) Reconstitution of the left popliteal artery at the adductor canal (arrow).

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F

G

FIGURE 5.1 (continued) (E) Image at the knees demonstrating moderate stenosis of the left popliteal artery at the knee joint (arrow). Occlusion of the left tibial peroneal trunk (curved arrow). Occlusion of the right popliteal artery (arrowheads) below the level of the knee joint. (F) Lateral view of the left leg demonstrating two-vessel runoff. The peroneal artery is significantly diseased. (G) Lateral view of the right leg demonstrating single-vessel runoff. (H) View of ankles and feet with slight misregistration because of minimal patient motion.

Chapter 5 Fundamentals of Angiography

should perform them on a regular basis. Routine rotation of all departmental personnel into the angiographic suite should be discouraged.

Catheters and Guidewires Improvement in catheter and guidewire design has been one of the most significant recent advances in angiography. Size 5 Fr. catheters have essentially replaced the 6.5 and 7 Fr. catheters used in previous years. Improvements in catheter surface material have dramatically reduced thrombotic and embolic complications. Wall material has been developed that will allow these smaller-diameter catheters to deliver the high-flow, high-volume injections that are necessary for aortography while maintaining the torquability and trackability needed for selective vessel catheterization. Torquable guidewires are also available which facilitate catheter mobility. Catheterization of previously inaccessible vessels is now possible with the development of 3 Fr. catheters and 0.014- to 0.018-inch guidewire combinations, which are particularly useful in visceral angiography and neuroangiography (63). Specialized catheters have been designed for infusion and pulse-spray delivery of thrombolytic agents over a relatively long segment of vessel. Improvements in guidewire technology have allowed the introduction of hollow guidewires through which infusions can be performed (64). These wires are particularly useful for thrombolytic therapy. Guidewires are also available with balloon tips for remote vessel angioplasty (65).

Contrast Material Low- versus High-osmolarity Agents Virtually all modern angiographic contrast agents are iodinated, monomeric or dimeric substituted benzene derivatives. Iodinated compounds are used primarily because of the ability of the relatively massive iodine atoms to absorb x-rays, producing “positive” contrast without the marked toxic effects seen when other heavier elements are used (9). Carbon dioxide is another angiographic contrast agent that has received some attention because of its economy and low associated morbidity (46,47). Unlike iodinated contrast agents, carbon dioxide facilitates the transmission of x-rays, thereby producing “negative” contrast. Carbon dioxide angiography has become a viable imaging technique with the development of digital subtraction angiography, tilt tables, and closed delivery systems (140,141). Until recently, the most commonly used contrast media were the ionic tri-iodo compounds, diatrizoate and iothalamate. These agents are hyperosmolar and cause localized pain on injection in about 60% of patients. The pain is partly related to the sodium content (23). For these reasons, sodium-free contrast agents such as meglumine diatrizoate or meglumine iothalamate are available. In the last 10 years, there has been explosive growth in the use of

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a new family of relatively low-osmolar iodinated contrast agents. These include the nonionic monomers iopromide, iohexol, ioversol, and iopamidol, and the low-osmolarity ionic dimer, ioxaglate. Universal use of these compounds is limited only by their higher cost. Angiography with these agents is associated with considerably less discomfort than that caused by high osmolarity compounds (23,24). These materials have also been shown to be less nephrotoxic and less injurious to the central nervous system and myocardium (24). However, the nonionic compounds have a lower anticoagulant effect than the ionic agents (24,25), and there have been reports of increased thrombotic complications related to nonionic contrast media usage (26,27). Therefore, many authors recommend adding heparin to nonionic agents, especially for elderly or hypercoagulable patients or for those patients undergoing coronary angiography and/or angioplasty (26,28). Cardiovascular Toxicity Iodinated contrast media produces vasodilation of arteries resulting in increased blood flow. A decrease in systemic pressure is seen with injection of contrast media into the right or left heart, aorta or peripheral arteries (27,28). Other cardiovascular responses to contrast injection are an increase in cardiac output, heart rate, stroke volume, chamber pressure, and circulating blood volume. Contrast media also induces a toxic depressive effect on myocardium. Ventricular fibrillation or other severe arrhythmias occur in up to 0.75% of patients undergoing selective coronary arteriography (29,30). Pulmonary hypertension and systemic hypotension occur with contrast injections into the right heart or pulmonary arteries (31). Low-osmolarity contrast agents are associated with a less pronounced cardiovascular response (22,27). Neurotoxicity Experimentally, injection of contrast media into the carotid artery alters the blood–brain barrier by increasing endothelial permeability, which allows the contrast agent to diffuse into the surrounding tissues (22,32). In humans and animals, meglumine salts have been shown to cause less neurotoxicity than sodium salts (33). CNS side effects of contrast injection include seizures, aphasia, cortical blindness, encephalopathy and amnesia (34,35). Direct injection of contrast media into the artery of Adamkiewicz may result in paraplegia. However, most spinal cord complications are transient and clear within 24 hours (36). The use of low-osmolarity contrast agents appears to be associated with fewer neurological side effects (22,27). Nephrotoxicity Iodinated contrast media is excreted almost entirely by the kidneys. Less than 1% of the administered dose is excreted by the biliary and digestive systems (22). As a result, the kidney is the primary target organ for contrast media toxicity. Contrast-induced nephropathy is thought

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to be due to both the direct chemotoxic effects and the elevated osmolality of contrast media (37). Implicated mechanisms include reduced renal blood flow, glomerular and tubular injury, and complement activation (37). The nephrotoxic effects of contrast media appear to be particularly amplified by azotemia (27). Other less important risk factors include diabetes (especially insulindependent type I), dehydration, blood dyscrasias (including sickle-cell anemia and multiple myeloma), advanced age and generalized infirmity (27,37). Although there is a wealth of experimental and laboratory data which indicate that low-osmolarity contrast media is less nephrotoxic than high osmolarity agents, it is not clear whether this benefit is clinically significant for those patients who are not at increased risk for contrast-induced nephropathy (22,27,38,39). Adverse Experiences Adverse experiences related to contrast media administration can be divided into those that are physiologic, chemotoxic, and anaphylactoid (22). Physiologic reactions commonly include heat and pain located in proximity to contrast agent injection as well as associated nausea and vomiting. Although physiologic reactions are typically mild, these reactions interfere with patient compliance and, therefore may compromise examination quality. Low-osmolarity contrast media has a markedly reduced incidence of these responses (22,27). The chemotoxic effects of contrast media administration have been previously discussed and include direct cardiovascular, renal, and neurological injury. Anaphylactoid reactions are an unusual complication of contrast infusion and a great deal of controversy exists regarding the pathogenesis of this type of response. Implicated mechanisms are thought to be immunologic and include histamine release, complement activation, and antibody–antigen reactions, none of which are mutually exclusive (22,40). These frequently devastating reactions occur unpredictably and are independent of the dose of agent administered (40). Pretesting has not been shown to be a useful predictor of severe reactions (41). The overall incidence of severe, life-threatening reactions is between 0.05% and 0.10% (41) while the risk of death from these reactions ranges from one in 75,000 (42) to one in 169,000 (43). Allergic patients have twice the risk for anaphylactoid reactions, while those patients with asthma or with a history of previous severe reaction may have their risk increased by a factor of five (40). Low-osmolarity contrast media significantly reduces the incidence of severe and potentially life-threatening reactions to contrast administration (22,27,40,43). Pretreatment of high-risk patients with 32 mg of intravenous methylprednisolone 12 hours and 2 hours before administration of contrast media has been shown to reduce the risk of mild, moderate, and severe reactions by 23% to 86% (44). Supplementation with oral H1 or H2 (histamine) blockers and substitution of 50 mg of oral prednisone for methylprednisolone has also been advocated (45).

Preparation of the Patient Ideally, evaluation of the patient should be performed by the angiography staff on the day before a planned angiographic procedure. This will allow ample time for appropriate pre-procedure tests or treatments including additional laboratory evaluation and the initiation of prophylactic steroid therapy for documented contrast allergy. A particular note is made of the patient’s hematologic, renal, cardiac, allergic, and neurologic status. Preangiographic orders include clear liquids after midnight and IV fluid to optimize hydration. Platelets, prothrombin time, partial thromboplastin time and INR should all be in the acceptable range. Coumadin use is a relative contraindication to performing an elective procedure. Heparin infusions should be stopped several hours before the procedure when feasible. Other relative contraindications to angiography are listed in Table 5.1. The popularity of outpatient arteriography places a severe stress on laboratory and other pre-procedure patient studies (138,139). However, the temptation to accept an inadequate preprocedure workup in favor of economy and convenience should be avoided. Informed consent is obtained from all patients at the time of pre-procedure evaluation. Details of the procedure and its risks and benefits, as well as possible alternatives, should be discussed at length. Additionally, the use of conscious sedation must be discussed fully with the patient and informed consent obtained. Almost all catheterizations are performed with both local and intravenous analgesia. Peripheral arterial injections are associated with a varying degree of pain and heat, and these reactions are further exacerbated by patient anxiety. As a result, we are very liberal with the use of intravenous sedation. In our department, we use the narcotic analgesic fentanyl in combination with the sedative midazolam. These agents are administered intravenously immediately prior to the examination and as needed during its course. They have been shown to be both safe and efficacious and their short half-life allows for rapid patient recovery (59). Use of these agents should be limited to those settings where proper monitoring with pulse oximetry and continuous ECG tracing can be perTABLE 5.1 Relative contraindications to arteriography (adapted from reference 61) Recent myocardial infarction or significant arrhythmia History of serious reaction to contrast material Significant hypertension—diastolic pressure greater than 110 mmHg Bleeding diathesis, e.g., prothrombin time greater than twice the control, platelets less than 50,000 Impaired renal function Inability to lie supine on angiography table, e.g., congestive heart failure Retained barium from recent examination

Chapter 5 Fundamentals of Angiography

formed by properly trained and available staff. With the exception of children and for aortic stent–grafting in adults, there is little indication for general anesthesia in angiography. Even a TIPS procedure is performed with conscious sedation. Spinal and epidural anesthesia is rarely indicated. Routine systemic heparinization is not utilized during arteriography unless significant disease is encountered during the passage of the guidewire or catheter or when either of these two instruments results in vessel occlusion when crossing a high-grade stenosis. A bolus of 3,000 to 5,000 units of heparin is administered intra-arterially when these situations are encountered. The routine use of systemic heparinization for angiographic procedures has been advocated in the past (60). However, with the use of standard coaxial guidewire and catheter technique and with frequent flushing of indwelling catheters, routine heparinization is rarely necessary. Following the procedure, patients are sent back to their hospital room or are referred to an area where outpatient monitoring can be performed before discharge. We require at least 6 hours of bedrest in these settings. During this time, a member of the angiography staff should examine the patient and discuss the results of the procedure and possible treatment, if appropriate. If a percutaneous closure device is used, the bedrest time has been reduced to a few hours at our institution. Several closure devices have been developed to close the arteriotomy site. These include collagen plug devices and percutaneous suture closure (142,143). The various devices to achieve rapid hemostasis require proper deployment technique to avoid complications (144,145).

Basic Angiographic Technique A detailed discussion of catheter and guidewire usage is beyond the scope of this chapter. For more information, the reader is referred to basic textbooks on the subject (61,62). Perhaps the most important aspect of angiography is the choice of an appropriate catheterization site. With the close relationship of diagnostic arteriography and interventional radiology, preparation for the former should include contingencies for the latter (83). In a similar fashion, the choice of technique for arteriography should not interfere with the planned surgical approach. In other words, a right retrograde common femoral artery approach should not be used to evaluate an occluded right superficial femoral artery, since this approach may interfere with possible thrombolytic therapy, angioplasty, or surgical treatment of this abnormality. A retrograde left common femoral artery puncture is preferred in this scenario. The most common catheterization site is the common femoral artery. Punctures may be made in the groin crease to assure the shortest penetration of subcutaneous tissue prior to vessel catheterization. This approach allows for

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ease of catheter manipulation and decreases the risk of retroperitoneal hemorrhage associated with external iliac artery puncture (69). Alternatively, punctures may be made over the femoral head, which is typically above the groin crease, thus allowing for more efficient vessel tamponade during post-procedure compression (70). Transbrachial and transaxillary catheterization sites are particularly useful when femoral pulses are weak or absent as seen in patients with severe aortoiliac disease. Both sites have complication rates that are nearly as low as the transfemoral approach (93). Once a catheterization site has been chosen and prepared, a double wall arterial puncture is generally performed using the Seldinger technique (1) which employs a puncture needle with a beveled stylet (Seldinger needle). The stylet is removed and the cannula is withdrawn until pulsatile blood flow is visualized. A guidewire is then advanced through the cannula into the vessel being catheterized and the cannula is removed, leaving the guidewire in place. Manual compression is held over the puncture site, as the guidewire by itself is insufficient for tamponade. Compression is released after a catheter or vascular sheath is successfully advanced over the guidewire into the vessel. Fluoroscopy is used to advance the catheter– guidewire combination. The catheter is never advanced without a leading floppy-tipped guidewire as this may raise an intimal flap. Similarly, mechanical contrast injection is never performed until the location of the catheter is verified fluoroscopically using a hand injection. Catheters can be exchanged over the guidewire as needed. In addition, guidewires can be exchanged as long as an indwelling catheter remains in place. The requirements of the procedure being performed will determine which catheter and guidewire combinations are optimal. Virtually all angiographic procedures require images obtained in at least two projections. This process is frequently time-consuming, as images must be evaluated before subsequent views are chosen. As a result, catheters are frequently left in the same position for minutes at a time. In order to prevent intra- and peri-catheter thrombosis and subsequent embolization, catheters have to be kept flushed with heparinized saline. In single, end hole catheters, a heparinized saline drip is sufficient. However, in those catheters with multiple end holes, a forceful injection by hand is necessary every 1 to 2 minutes. If a sheath is in place, a continuous saline drip is required by using a pressurized bag. Once the procedure is complete, the catheter and/or sheath are removed and the arterial puncture site is compressed by hand for no less than 10 minutes unless a percutaneous device is used. In obese patients, in patients with an abnormal coagulation profile, after particularly long procedures, or after large catheters or sheaths have been used, compression may have to be as held as long as 1 hour. The use of mechanical compression devices or sandbags is strongly discouraged as these prevent direct visualization and palpation of the arteriotomy site.

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Part I Imaging Techniques

Complications of Angiography Nonsystemic complications of arteriography unrelated to contrast administration are usually caused by faulty catheter and guidewire technique. These include: 1.

2. 3.

hematoma, arteriovenous (AV) fistula and/or a pseudoaneurysm (Fig. 5.2) at the arterial puncture site; intimal tear, occasionally resulting in arterial rupture, thrombosis, or pseudoaneurysm formation; distal embolization related to atheroemboli or pericatheter thrombosis.

The most common complications related to arteriography are those that occur at the arterial puncture site. These are much more common during coronary arteriography secondary to the routine use of systemic heparinization during these procedures (107,108). Hematoma and AV fistula formation (Fig. 5.3) typically occur as a result of arterial punctures below the femoral head. These punctures are frequently located in the proximal superficial femoral artery and occur as the result of the inability to compress the arterial puncture site over the femoral head at the end of the procedure. Similarly, retro-

A

peritoneal hemorrhage has been reported following external iliac artery punctures above the femoral head (93,116). Intimal tears (Fig. 5.4) typically occur as a result of forceful catheter and/or guidewire advancement. They may also occur as a result of advancing the catheter without a leading floppy-tipped guidewire. These tears usually progress in a retrograde direction and frequently require no treatment. However, if the injury is severe enough, thrombosis, pseudoaneurysm, or rupture has been known to occur. Distal embolization (Fig. 5.5) usually results secondary to one of two mechanisms. The most common and typically least serious incidents are related to inadequate catheter flushing with resultant intra- and peri-catheter thrombosis and embolization. More serious causes of distal embolization include atheroemboli as a result of mechanical injury to the vessel wall and subsequent distal embolization of vessel wall material. Multiple cholesterol emboli syndrome has also been described, which involves systemic embolization of cholesterol crystals with a subsequent mortality rate greater than 50% (117). Fortunately, this latter complication is extremely rare. If a percutaneous closure device is used, reported complications are hematoma, infection, pseudoaneurysm, embolization, and AV fistula formation (144,145).

B

FIGURE 5.2 Following coronary arteriography, a palpable right groin mass was noted. (A) Digital subtraction arteriogram demonstrates a collection of contrast material (arrow) overlying the right common femoral artery and its bifurcation. (B) Oblique view demonstrates to better advantage the pseudoaneurysm and its neck (curved arrow).

Chapter 5 Fundamentals of Angiography

A

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B

FIGURE 5.3 (A) Advanced atherosclerotic disease is demonstrated on this early arterial phase film from a digital subtraction run. (B) Two seconds later, contrast medium is still seen in the arteries but there is early and intense venous opacification on the right (arrow). Etiology is an arteriovenous fistula from a knife wound.

FIGURE 5.4 Following cardiac catheterization, diminished pulse on the right was noted. Note the intimal flap (arrow) in the right external iliac artery.

FIGURE 5.5 Embolus (arrows) in the distal popliteal artery, proximal anterior tibial and tibial peroneal trunks. Patient underwent cardiac catheterization.

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A widely quoted paper on the complications of angiography published in 1981 (95) reported the overall complication rate for transfemoral arteriography to be 1.7%; the rates for translumbar and transaxillary arteriography were 2.9% and 3.3%, respectively. These complication rates include systemic complications related to contrast administration. For further information regarding contrast-related complications, please refer to the section on Contrast Material. Since the time of that publication, angiographic techniques and the treatment and recognition of complications have improved dramatically. However, these gains have probably been more than offset by the increased use of more invasive interventional, endovascular procedures.

Angiographic Interpretation The fundamental mechanism responsible for angiographic image production is the displacement of blood by contrast media of high atomic weight, thus reducing the transmission of x-ray photons in that region. This results in differential exposure on an x-ray-sensitive film or receptor. Thus, images are obtained reflecting the flow of blood only. Differences in tissue density independent of blood flow are not evaluated. Osseous and air-filled structures visualized on conventional film-screen images are useful only as a reference for anatomic evaluation. Carbon dioxide produces a “negative” filling defect that reflects blood flow but also the effect of gravity. The patient needs to be placed in a head-down position. If improperly injected, CO2 breaks up into individual pockets of contrast. A knowledge of anatomy is crucial for proper angiographic interpretation. Once the vessel is identified, it is important to determine the location of the catheter and at what stage during the injection the image was obtained. For instance, images obtained early during contrast injection will show incomplete arterial opacification while those obtained later may only demonstrate venous filling. The pattern of vessel branching is also important. Vessels typically branch in a progressive and regular manner demonstrating normal arborization. The presence of abrupt and irregular branching, of abnormal narrowing and dilation, and of a prolonged capillary blush or stain are suggestive of neovascularity and may indicate malignancy. Malignancies may also demonstrate early draining veins due to the presence of numerous AV fistulas. After anatomical evaluation, specific vessel wall characteristics should be identified. Normal vessel walls are typically smooth and sharply marginated. The presence of linear defects or smooth undulations may be indicative of intimal tears or vascular spasm, respectively. Less subtle abnormalities such as focal stenoses or occlusions should be searched for as well. These abnormalities are typical of injury and atherosclerotic disease. The presence of large collateral vessels may be the only

indication of a hemodynamically significant stenosis or occlusion which should be searched for if this abnormality is not immediately obvious. Hemodynamic significance is generally assumed to occur when 50% of vessel diameter or 75% of vessel area is compromised (109,110). Vessels need to be observed in multiple views and the clinical and noninvasive findings explained (Fig. 5.6). The presence of hemorrhage or thrombosis should also be determined. Extraluminal, amorphous pools of contrast, which remain unchanged after the majority of contrast media has flowed out of the image, are suggestive of hemorrhage. Nonocclusive vascular filling defects or vascular occlusions with a convex inner surface are suggestive of thrombus and embolus respectively. It is also important to be aware of the numerous artifacts and technical misrepresentations, which may masquerade as real pathology. Artifacts are particularly prevalent when using digital subtraction technology (Fig. 5.6C), especially when the patient moves before mask subtraction. Numerous technical factors such as film fogging or underexposure may also affect image quality. Examples of faulty technique causing spurious findings include poor image timing or inadequate contrast injection resulting in incomplete vessel opacification. In addition, injecting contrast too rapidly, especially in a small vessel, may result in rapid venous opacification resembling an AV fistula. Finally, there should be familiarity with the angiographic appearance of vessel injury resulting from faulty catheter and guidewire technique. These complications include subintimal injection of contrast, AV fistula, pseudoaneurysm, vessel rupture, and thrombosis. These abnormalities as well as others are discussed in the section on Complications of Angiography.

Head and Neck Angiography Indications The role of arteriography in the evaluation of head and neck pathology has become much more focused as a result of the widespread acceptance of ultrasound, CT, and MRI for initial diagnostic evaluation. Magnetic resonance angiography has in particular assumed a dominant role in extracranial artery imaging. Angiography is limited to those patients for whom noninvasive imaging is inconclusive and where the information obtained will influence medical or surgical management, particularly the latter. Specific indications for arteriography include the evaluation of intra- or extracranial trauma, aneurysms, vascular malformations, neoplasms, and hemorrhage. However, the most common indication remains the assessment of cerebrovascular disease (73). Head and neck arteriography includes selective studies of the carotid, cerebral, vertebral, and spinal circulations. Carotid arteriography is performed most com-

Chapter 5 Fundamentals of Angiography

A

C

monly when evaluating extracranial cerebrovascular disease. The indications for carotid arteriography are listed in Table 5.2. Color duplex Doppler ultrasound remains the screening procedure of choice (74). Many patients then receive an MR angiogram or a CT angiogram before surgical intervention, negating the need for contrast angiography (75–77,82).

Risks Head and neck angiography is an invasive procedure and, like all such procedures, is associated with thromboembolic complications related to catheter/guidewire manipulation and contrast administration. Such events may be

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B

FIGURE 5.6 (A) 64-year-old man with bilateral lower extremity ischemic symptoms. Stenosis of right distal common iliac artery and external iliac artery is evident (arrows). No definite lesion on the left to explain symptoms and decreased pulses. Examination is with cut film. (B) Right anterior oblique view with digital subtraction filming again demonstrates the right common iliac artery stenosis (arrow) but foreshortened visualization of the left common iliac artery. (C) Left anterior oblique view demonstrates an ulcerated lesion of the left common iliac artery and a 90% stenosis of the distal left common iliac artery (arrow). Note that there is obliteration of a segment of distal left external iliac artery which appears to represent an area of occlusion. This is a subtraction artifact secondary to overlying bladder contrast media and should not be mistaken for actual pathology.

relatively well tolerated in other circulatory distributions. However, when they occur in the cerebral circulation, stroke or death may result. In order to evaluate arteriographic risks, patients without central nervous system symptoms have to be evaluated separately from those who are symptomatic for central nervous system disease (i.e., transient ischemia attack, amaurosis fugax, nondisabling stroke). In addition, permanent nonfatal central nervous system complications should be classified separately from those that are transient and/or are reversible (i.e., clearing within one week). Risk factors include high-grade stenoses, bilateral stenoses, large volume of contrast, long procedure duration, azotemia, multiple catheter and guidewire exchanges and operator inexperience (78,80–82).

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TABLE 5.2 Indications for diagnostic extracranial carotid arteriography (adapted from reference 73) I. Diagnosis and evaluation of cerebrovascular disease A. Central nervous system symptoms present 1. Angiography is indicated when hemorrhage, tumor, etc. have been excluded by other imaging modalities. Noninvasive testing is not indicated B. Central nervous system symptoms absent 1. Noninvasive testing results positive or inconclusive: angiography is indicated when confirmation is needed for medical or surgical management 2. Noninvasive testing results negative: angiography is not indicated II. Diagnosis and evaluation of head and neck tumors, carotid aneurysms, penetrating vascular trauma and blunt trauma presenting with focal neurological signs after intracranial hemorrhage or contusion has been ruled out

In asymptomatic patients undergoing selective carotid arteriography, the risk of transient/reversible central nervous system complications ranges from 2.2% to 6.0% while the permanent complication rate is about 0.3% (78,79). In symptomatic patients undergoing selective carotid arteriography, the risk of transient or reversible complications ranges from 0.7% to 5.6% while the rate for permanent central nervous system complications ranges from 0.0% to 5.7% (79–81). The generally accepted risk of symptomatic patients for transient or reversible central nervous system complications is about 4% while the risk for permanent central nervous complications in these patients is about 1% (82). The death rate for symptomatic patients undergoing selective carotid arteriography is less than 0.1% (82). For asymptomatic patients, the risks are generally half the rate observed for symptomatic patients.

The common carotid arteries are catheterized individually. Images in at least two obliquities are obtained over both the cervical and intracranial carotid circulations. We prefer the use of the digital subtraction technique as it allows for more rapid image acquisition. Stenoses are the most commonly encountered lesion in patients with cerebrovascular disease (Fig. 5.8). These typically occur at the origin of the internal carotid artery. However, they may also involve the distal common carotid artery. Plaque ulcerations (Figs. 5.9, 5.10) are an ominous finding when associated with stenotic lesions, as they are associated with an increased thromboembolic risk. Stenoses are considered hemodynamically significant when there is compromise of at least 50% of luminal diameter or 75% of luminal area (109,110). When lesions greater than 90% luminal diameter are encountered, immediate systemic heparinization is advised as these patients are at a much higher risk for stroke. Occasionally, complete occlusions of the common or internal carotid artery are encountered. When these occur, careful evaluation of the intracranial circulation is necessary in order to determine collateral flow. The findings for carotid arteriography in patients with blunt or penetrating trauma to the neck are different from those seen in patients with cerebrovascular disease. When penetrating zone II and III neck wounds are associated with focal neurological signs, active bleeding, or expanding hematoma, angiographic evaluation is deferred in favor of surgical exploration (112,113). In patients

Technique and Findings of Carotid Arteriography Carotid arteriography is typically performed following duplex Doppler ultrasound screening and as an outpatient procedure in patients referred for elective evaluation (138,139). In the absence of other significant pathology, patients are admitted for angiography only if they have rapidly progressing cerebrovascular symptoms. Angiography is performed using the femoral approach when it is available. Alternatives include the brachial or the axillary approach. Arch injections may or may not be performed prior to selective carotid artery catheterization (Fig. 5.7). Some workers believe that aortic arch arteriography increases the risk for stroke. However, we find that performing such a procedure before selective carotid artery catheterization allows for proper catheter selection for shorter procedure duration and identifies significant great vessel disease (111).

FIGURE 5.7 Thoracic aortogram performed prior to selective carotid arteriography. Minimal disease of the innominate artery. Moderate stenosis at the origin of the right vertebral artery (arrow). The left common carotid artery is normal as is the visualized portion of the right.

Chapter 5 Fundamentals of Angiography

with zone I injuries, angiography should be performed regardless of findings since vascular injury may be occult (113). In patients with zone II and III injuries but without evidence of active bleeding or focal neurological signs, angiography is performed when the penetrating injury has violated the platysma muscle (113). Angiographic findings include free extravasation of contrast, pseudoaneurysm formation, carotid artery dissection and arteriovenous fistula. In those patients who have received blunt trauma to the neck in the absence of intracranial injury, angiography is performed only when focal neurologic signs are present (115). Angiographic findings are similar to those seen with penetrating trauma but include a larger proportion of patients with isolated intimal disruption.

Pulmonary Angiography Indications

However, in the last five years, the indications have markedly contracted with the concomitant growth of CT pulmonary angiography using multislice, helical CT scanners. In our institution, patients are initially evaluated with ventilation–perfusion scans. If the study is equivocal, CTA is the next most appropriate test. Commonly, however, CTA is becoming the initial procedure of choice (146,147). Pulmonary arteriography is performed almost exclusively for the diagnosis of pulmonary embolism. Rare indications for this study include assessment of congenital heart disease and the diagnosis and possible treatment of congenital pulmonary AV malformations (Osler–Weber– Rendu syndrome). Indications for pulmonary angiography are presented in Table 5.3. In summary, this study should be performed whenever there is uncertainty regarding the diagnosis of pulmonary embolus or when the results of the ventilation–perfusion scan or CTA is at odds with the clinical picture. Pulmonary angiography should also be performed when standard treatment modalities, such as anticoagulation, are relatively contraindicated,

Unlike the other angiographic procedures discussed in this chapter, the technique of pulmonary angiography has undergone little change over the last decade.

FIGURE 5.8 Selective catheterization of the left common carotid artery demonstrates a 98% stenosis of the left internal iliac artery (arrow).

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FIGURE 5.9 Selective catheterization of the right common carotid artery demonstrates no hemodynamically significant stenosis. There is a small ulceration in the proximal internal carotid artery (arrow).

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Part I Imaging Techniques TABLE 5.3 Indications for diagnostic pulmonary arteriography (adapted from reference 73) Suspected pulmonary embolus when ventilation–perfusion scanning cannot be performed High probability ventilation–perfusion scan when there is a contraindication to anticoagulation Indeterminate or low-probability ventilation–perfusion scan in a patient with a high clinical suspicion of pulmonary embolus Diagnosis and evaluation of suspected chronic pulmonary embolus Diagnosis and evaluation of other suspected pulmonary abnormalities, such as vasculitis, congenital and acquired anomalies, tumor encasement, and vascular malformations

FIGURE 5.10 Digital subtraction arteriogram of the right carotid system demonstrating an ulcerated plaque with a hemodynamically significant stenosis at the origin of the internal carotid artery (arrow).

necessitating increased diagnostic accuracy before the institution of potentially harmful therapy.

Risk Historically, the risk of death during pulmonary arteriography was quite high. Earlier studies reported a mortality rate of 2% (84). These events occurred primarily in patients with pulmonary hypertension and a failing right ventricle. It has been hypothesized that both the volume load and the high osmolarity of contrast delivered during main pulmonary arterial injections creates an increase in

right ventricular afterload which is too high for the failing right ventricle to handle. As a result, patients develop immediate systemic hypotension, apnea, and subsequent cardiac arrest in spite of all resuscitative measures. It has been advocated that pulmonary arteriography not be performed with a right ventricular end-diastolic pressure greater than 20 mmHg (85). However, more recent reports have indicated that the death rate following pulmonary arteriography is actually 0.2% and the morbidity is 4.0% (85,86). The reduction in mortality is attributed to the use of both selective catheterization techniques and low-osmolarity contrast media. These changes have resulted in a smaller increase in right ventricular afterload during angiography. Another complication of pulmonary arteriography is perforation of the right ventricle or right ventricular outflow tract, which has been reported to be as frequent as 1% (85) but is now thought to be much more rare. This event occurs during mechanical contrast injection when a pulmonary artery catheter recoils, perforating the ventricle. Perforation may also occur during catheter manipulation in the right heart, especially when an antecubital vein approach is chosen in which a straight-tip catheter is used. This site is no longer in common use and pigtail catheters are most often used. Surprisingly, patients with right ventricular rupture usually recover without sequelae (85). Significant ventricular arrhythmias have also been known to occur during passage of the catheter through the right ventricle. This is thought to be secondary to mechanical irritation of the bundle of His located in the cephalad portion of the intraventricular septum. It is not uncommon for runs of ventricular tachycardia to be noted during this portion of the procedure. Ventricular fibrillation, right bundle branch block, complete heart block, paroxysmal atrial tachycardia, and bradycardia have also been reported. Fortunately, these arrhythmias are usually transient and terminate when the catheter is pulled out of the ventricle or advanced into the pulmonary outflow tract. Relative contraindications of pulmonary arteriography related to catheter-induced arrhythmias include a left

Chapter 5 Fundamentals of Angiography

bundle branch block, as passage of the catheter through the right ventricle may precipitate a right bundle branch block with resultant complete heart block (85). Patients with left bundle branch block should have a prophylactically placed transvenous ventricular pacer wire before pulmonary angiography.

Technique and Findings Patients referred for pulmonary arteriography are typically heparinized before the procedure by the clinical service because of suspected pulmonary embolus. However, heparinization is not a contraindication to the performance of this study. The infusion is simply turned off immediately prior to the venous puncture and restarted following procedure termination if a pulmonary embolus is identified. Bleeding sequelae in fully anticoagulated patients is extremely rare given the low hydrostatic pressure of the venous circulation. Ventilation–perfusion scans are typically ordered prior to pulmonary angiography. However, these studies are limited by their low specificity (86,87). Even patients with lowprobability scans may be referred for pulmonary arteriography, especially if there is a high index of suspicion for pulmonary embolus (73,86,88). The results of the perfusion portion of this study may be used to tailor the pulmonary arteriogram so that unnecessary vessel catheterizations are not performed. Pulmonary arteriography should be obtained within 48 hours of suspected embolization since lysis of pulmonary emboli begins to occur at this time (89). Where available, multislice helical CTA is the procedure of choice prior to routine pulmonary angiography. Pulmonary arteriography is generally performed using a femoral approach. An 8-Fr. pigtail catheter is advanced into the confluence of the inferior vena cava, and an inferior vena cavagram is obtained. This study is performed to rule out inferior vena caval thrombus. A pigtail catheter is used as it has little recoil during mechanical contrast media injection and thus maintains a stable position. The catheter is then advanced into the right atrium where right atrial pressures are obtained. Subsequently, it is passed through the tricuspid valve over the manually curved back end of a guidewire or a deflector wire. The catheter is then advanced with a twisting motion into the pulmonary outflow tract and pulmonary arterial pressures are determined. The latter is mandatory as the rate and volume of contrast administration are decreased in the presence of pulmonary hypertension. With very significant acute pulmonary hypertension, catheter pulmonary angiography may in fact be contraindicated. First- or second-level pulmonary branches are then selected and the pulmonary angiogram is performed. Images are always obtained in at least two and frequently three obliquities (91). Angiographic findings of pulmonary embolus are limited to intraluminal filling defects or pulmonary artery cutoffs or both (89,90)

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(Fig. 5.11). Occasionally contrast will be noted to flow at different rates in vessels adjacent to one another—slowed linear velocity of flow. Regional decreased blood flow (oligemia) and atelectasis may also be seen. These last three findings are suspicious for pulmonary embolus but are not diagnostic as they can be seen with other pathological conditions for which there is a large differential diagnosis (Table 5.4) (90). We film our studies using digital subtraction technique at 4 to 6 frames per second (148).

Thoracic Aortography Indications Perhaps no other area of diagnostic imaging has the immediate impact on patient management as that of angiography for the evaluation of the thoracic aorta. Thoracic aortography has long been held as the gold standard for the evaluation of life-threatening aortic dissection and traumatic injury (118–122). Emergency operative management has traditionally been based entirely on the results of such studies (120,122,123). However, this is changing, with CTA playing an ever-increasing role. Recently, efforts have been made to increase the diagnostic specificity of aortography. Less invasive screening methods have been employed with the hope of avoiding the unnecessary angiographic morbidity and mortality associated with negative studies. It has been reported that the yield of diagnostic aortography for the evaluation of traumatic aortic injury is as low as 10% because of the high true negative rate (120). CT angiography is now widely used for screening patients with suspected aortic pathology. It has both a high sensitivity and specificity (120,124,125). MRI has been found useful in the detection and assessment of aortic aneurysm but its use is strictly reserved for elective evaluation (118,126). The use of MRI for the detection of aortic dissection is currently limited by artifacts which may mimic pathology (129). Although transthoracic and transesophogeal echocardiography have been shown to be reliable diagnostic tools (127,128), their use is limited by the high degree of user dependency required for acceptable diagnostic efficacy (118). The greatest limitation, however, of all these less invasive imaging modalities is the amount of time consumed by their employment, especially in those patients whose chance of survival decreases rapidly with each passing minute. In addition to being expedient, aortography allows for delineation of the great vessel and coronary artery anatomy, which is not possible using the previously described techniques. In addition, the presence or absence of aortic regurgitation and the exact anatomy and location of the intimal tear can be clearly identified. This information is required for proper surgical planning (118). It is for these reasons that the angiographic evaluation of the thoracic aorta is still considered valuable for the evaluation of acutely ill patients.

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A

B

FIGURE 5.11 (A) Anteroposterior view of the chest for pulmonary arteriography. Catheter is placed in the right main pulmonary artery and demonstrates several small emboli. Embolus in the descending ramus is seen en face (arrow). (B) Right posterior oblique view demonstrates to better advantage the large embolus (arrow) occupying much of the descending ramus.

TABLE 5.4 Differential diagnosis for acute pulmonary embolus (adapted from reference 90) Normal Acute pneumonia Atelectasis Bronchiectasis Postinflammatory fibrosis Postsurgical changes Chronic pulmonary embolism Primary pulmonary embolism Pulmonary venous hypertension Emphysema Carcinoma

femoral approach should not be employed as this frequently leads to catheterization of the false lumen, increasing procedure length. This is particularly problematic in acutely ill patients where expediency saves lives. In trying to avoid this occurrence, we choose the right brachial approach. The false lumen is rarely catheterized using this puncture site, even with dissections extending into the innominate artery. Filming with digital subtraction angiography (DSA) is done in left anterior oblique view initially and the anteroposterior (AP) and/or lateral views.

Traumatic Aortic Injury Technique and Risk The technical approach to thoracic aortography is dependent on the pre-angiographic diagnosis. Likewise, the choice of technique is associated with risks unique to each approach. The general risks of angiography are discussed in the section entitled Complications of Angiography.

Aortic Dissection In approaching a patient with an acute aortic dissection, especially those involving the ascending aorta (Stanford type A or DeBakey type 1 and type 2) (135,136), the

For patients presenting with blunt trauma to the chest wall, aortography is performed in our medical center when the supine chest radiograph demonstrates a mediastinal width greater than 8 cm at the level of T4, when there is loss of the aortic knob contour, or upon demonstration of fractures involving any of the first three ribs (121). We do not perform aortography on the basis of injury mechanism alone, although this has been described by others as a sole indication for angiographic evaluation (133,134). If none of these radiographic findings are present, the patient is referred for thoracic CT to rule out the presence of hemomediastinum, abrupt change in aortic arch caliber, and/or abnormal aortic

Chapter 5 Fundamentals of Angiography

arch contour. Frequently, CTA is becoming the initial procedure of choice. The occurrence of any of these findings, or of a nondiagnostic study, is an indication for aortography. The femoral approach is preferred for the evaluation of traumatic aortic injury. These vessel wall disruptions rarely result in dissections so that entering the false lumen is not a consideration in evaluating patients with this pre-procedure diagnosis (121). As aortic injuries are most frequently found at the aortic isthmus, care must be taken in passing catheters and guidewires across this region, as complete disruption, with resultant death, is a possible complication (130).

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abnormalities include pseudoaneurysm formation, also most frequently seen in this region (121). Transmural laceration (rupture) of the aorta is an unusual finding as this is all but incompatible with survival. Rarely, the aorta may be occluded. Injuries to the ascending aorta are extremely rare as they usually result in death at the accident scene (137). Care must be taken to differentiate pseudoaneurysm from a ductus diverticulum, which is a normal variant (121).

Abdominal Angiography Indications

Findings Aortic Dissection The pathognomonic angiographic sign of aortic dissection is the demonstration of a double lumen separated by an intimal flap. Supporting, indirect signs include the appearance of luminal compression, aortic insufficiency and the presence of an isolated intimal flap. Additional, less important angiographic signs include displacement of an angiographic catheter more than 1 cm from the outer aortic wall shadow and the presence of a small ulcer-like collection of contrast projecting beyond the aortic wall (118). The false lumen typically originates along the outside curve of the ascending aorta traveling over the apex of the aortic arch. In DeBakey type I dissections, the lumen spirals inferiorly down the descending aorta to the posterior aspect of the abdominal aorta. The false lumen frequently reenters the true lumen at or near the aortic bifurcation. The true lumen can be differentiated from the false lumen in the ascending aorta upon visualization of the sinus of Valsalva, the coronary arteries, and the aortic valve. These three structures always fill via the true lumen (131). Demonstration of normal aortic arch vessels, and of normal flow characteristics and pressure is also further evidence of true lumen opacification. In the abdominal aorta, vessels may originate from either the true or false lumen (Fig. 5.12). Contrast extravasation into the pericardial sac and/or left pleural space is a sign of rapidly impending demise. False negative angiographic studies occur in approximately 2% of cases and are due predominantly to the presence of a completely thrombosed false lumen (132). Alternatively, both the false and the true lumen may demonstrate equal and simultaneous opacification, thereby obscuring the intimal flap (132).

Traumatic Aortic Injury The findings for traumatic aortic injury are highly variable. Abnormalities as subtle as a small intimal tear may be seen in the vicinity of the aortic isthmus. More severe

Abdominal angiography can be divided into three general areas. The first encompasses selective visceral arteriography. Visceral arteriography no longer plays the diagnostic role that it once did. This is due to the less invasive imaging modalities of ultrasound (US), CT, and MRI. Its use is limited to selected diagnostic procedures and endovascular therapy using pharmacoangiographic and embolization techniques. The most common diagnostic procedure is the evaluation of gastrointestinal (GI) bleeding. Pharmacoangiography employing pitressin to control GI hemorrhage (98) or serotonin to stimulate gastrin secretion from gastrinomas (99) is well described. Embolization techniques combined with delivery of chemotherapy are useful for treating visceral tumors, especially those of hepatic origin (100). Embolization has also been advocated for use in treating primary gastrointestinal hemorrhage or hemorrhage secondary to trauma, especially involving the spleen (101). The role of visceral angiography for the evaluation of portal hypertension is rapidly dissipating as a result of the advent of the transjugular intrahepatic portosystemic shunt (102). Abdominal aortography is used to evaluate both atherosclerotic occlusive disease and aneurysm formation. Abdominal aortic aneurysms may be atherosclerotic, mycotic, congenital, or iatrogenic in origin. US and CT are employed primarily for screening as these modalities are less invasive than aortography (103,104) (Fig. 5.14). MRI has also been employed for aneurysm evaluation (105). In fact, US, CT, and MRI have been advocated as sufficient by themselves for the preoperative workup of abdominal aneurysm (104,106). At our institution, US is used both for screening and for serial aneurysm size determination. CT is used as a screening modality in those patients whose signs and symptoms may be referable to other organ systems and for the evaluation of possible aneurysm rupture. CTA is also invaluable in preprocedure planning for abdominal aortic stent–grafting. However, despite the increasing use of US, CT, and MRI, catheter aortography for preoperative aneurysm evaluation still remains popular throughout the country. Unlike the other less invasive imaging modalities, aortography can clearly identify mesenteric and/or renal artery steno-

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Part I Imaging Techniques

A

B

FIGURE 5.12 Patient presented with severe chest and abdominal pain. Thoracic aortography demonstrated a type 3 dissection. Examination of the abdomen with digital subtraction technique. (A) Early in the run the true lumen is opacified with visualization of the superior mesenteric artery and an aberrant right main renal artery. Only a small segment of the false lumen is seen. (B) Later in the run the false lumen (arrow) is seen to better advantage.

sis, accessory renal arteries, and inferior mesenteric artery occlusion, and can determine the exact relation of the aneurysm to the major aortic branches. This modality is also particularly useful in evaluating distal runoff, especially in those patients with symptoms of claudication. It is not of value, however, in determining aneurysmal size since intramural thrombus may be present, distorting the aortic lumen (104). The third major indication for abdominal arteriography is in the evaluation of renovascular hypertension. Captopril radionuclide renography and possibly duplex color Doppler ultrasound are the imaging procedures of choice as screening techniques. MRA and CTA are also useful in this regard. Arteriography, however, is unmatched in its ability to identify, delineate, and quantify renal artery stenoses. The presence of segmental artery disease and the status of the distal vascular bed can also be assessed. Planning for angioplasty stenting or bypass grafting is also an essential benefit of the procedure.

Technique and Risk The technique and risk of abdominal aortography is discussed in the sections on Peripheral Arteriography and

Complications of Arteriography. A discussion regarding the risk and technique of visceral arteriography is beyond the scope of this chapter.

Findings The angiographic diagnosis of abdominal aneurysm is straightforward. Typically, patients with known abdominal aortic aneurysm are referred for angiographic evaluation before operation or stent–grafting. The size of the aneurysm has usually already been determined by noninvasive imaging modalities. Angiography is necessary to confirm the diagnosis and to determine the extent of aneurysmal involvement of vital structures such as the renal, mesenteric, and iliac arteries (Fig. 5.13B and C). In addition to aneurysmal involvement of these vessels, hemodynamically significant stenoses are searched for since operative ligation of potential collateral vessels may be disastrous. For example, ligation of a hypertrophied inferior mesenteric artery in the setting of superior mesenteric artery stenosis or occlusion will frequently result in bowel ischemia or infarction. Other important considerations include evaluation of the flow to the lower extremities, specifically to the iliac and femoral arteries where graft anastomoses are most commonly performed.

Chapter 5 Fundamentals of Angiography

A

C

Renal artery disease is evaluated with aortography and frequently selective renal artery catheterization (Fig. 5.14). In addition to AP views, multiple oblique views are frequently required to fully evaluate the renal artery. Stenoses can be ostial or proximal and most frequently on an atherosclerotic basis. Mid-renal arterial lesions, often with a classic “string of beads” appearance, are usually of fibromuscular dysplastic origin. The degree of luminal narrowing is assessed for determining hemodynamic significance. Modern digital subtraction angiographic systems can automatically determine degree of stenoses based on pixel densities or area measurements. Poststenotic dilation does not indicate hemodynamic significance. The presence of unopacified flow defects on selective injection may, however, be of

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B

FIGURE 5.13 (A) Computed tomography demonstrates an abdominal aortic aneurysm. The residual lumen is filled with contrast and is surrounded on the left by an eccentric thrombus. (B) Abdominal aortography demonstrates a fusiform aneurysm as manifested by its residual lumen. (C) Lateral view is utilized to better demonstrate the origins of the celiac (arrow) and superior mesenteric (arrowhead) arteries. At times the renal artery origin and, therefore, the length of the infrarenal cuff can be better seen in the lateral view.

value. Selective renal vein renins may also be useful in this regard.

Peripheral Angiography Indications and Basic Concepts Perhaps nowhere else has the role of diagnostic angiography changed so rapidly as it has for the evaluation of patients with suspected peripheral vascular disease. This has occurred primarily as a result of the increasing importance of surgical and interventional therapy for vascular disease below the knee. Refinement in noninvasive vascular testing has also changed the indications by eliminating the need for arteriography to be a screening technique.

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Part I Imaging Techniques

FIGURE 5.14 A 68-year-old woman with uncontrollable hypertension and progressive renal failure. Aortography demonstrates very advanced atherosclerotic disease of the abdominal aorta. Absent right main renal artery. High-grade stenosis of the left main renal artery near its origin (arrow).

Magnetic resonance angiography (MRA) has further redefined the indications. MRA provides excellent depiction of anatomy. Common indications for catheter angiography include incapacitating claudication, rest pain, and tissue compromise. Additional indications include threatened graft thrombosis and vascular injury. The presence of penetrating injury in proximity to a major extremity artery without signs or symptoms of a vascular injury is probably not an indication for arteriography (94,95). However, this issue is controversial and many authors still advocate elective arteriography for the evaluation of “proximity injury” (96,97). Angiographic evaluation should be limited only to those patients for whom the information obtained will have an impact in medical or surgical management. It is imperative that the angiographer possess a thorough knowledge of the patient’s medical history, presenting symptoms, physical findings, and the results of laboratory evaluation prior to angiography. Perhaps just as important is the availability of previous arteriographic studies in order to allow determination of disease progres-

sion. The angiographer is a consultant and should be able to determine the suitability of a patient for the proposed angiographic study. Essentially, two techniques are used to optimize vessel opacification and subsequent visualization (67). The first involves increasing the delivery of contrast agent to the distal vessels while the second involves methods used to increase contrast agent detection. The simplest method of increasing contrast delivery is increasing the volume and rate of contrast injection. Increases in the volume of contrast delivered result in longer injections, which take advantage of the vasodilatory effects of contrast and aid in the coordination of filming sequences (83). However, contrast will not flow faster than blood itself, so that increases in the contrast injection rate result in reflux of excess contrast agent into vessels more proximal than those being studied. Typical injection volumes and rates for programmable lower extremity arteriography are in the range 70 to 100 mL at 8 to 10 mL/s with injection at the bifurcation of the aorta. Selective unilateral catheterization necessitates appropriately lesser amounts and slower rates. Selective vessel catheterization also improves distal vessel opacification by preventing flow of contrast into contralateral vessels or into those vessels more proximal to the ones being evaluated (68). The use of inflow vessel occlusion balloons and of inflated contralateral thigh pressure cuffs has also been reported (67,69). However, we find these last two methods unnecessary for routine utilization. Peripheral vasodilation also allows for greater delivery of contrast material and multiple methods can be used to achieve the same results. The most common modality is pharmacoangiography using agents that relax smooth muscle. Those commonly employed include nitroglycerin, phentolamine, and tolazoline (62). Other methods include producing reactive hyperemia following application of a blood pressure cuff to the distal calf or following the application of local heat (67). We have found the use of nitroglycerin the most efficacious of all the methods described. Increases in contrast detection are generally achieved in two ways (67). The first involves the coordination of film sequences, allowing image acquisition only during maximum contrast opacification. At times this can be rather difficult using conventional film-screen technique since contrast flow cannot be fluoroscopically visualized during image acquisition. This problem can be solved by using stepping intra-arterial digital angiography (“bolus chose”) where direct fluoroscopic assessment of maximal contrast opacification allows for tailoring of the imaging sequence during the study injection itself. The second method employed for increasing contrast detection is the use of intra-arterial digital subtraction angiography. This method provides for a remarkable increase in contrast resolution and is invaluable for evaluating the small, low-flow vessels typically found beyond vascular occlusions. In the past, this method has been limited by the lack of technology allowing stepping

Chapter 5 Fundamentals of Angiography

sequences to be performed during digital subtraction image acquisition. Thus, a separate contrast injection was required for every subtracted image. However, stepping intra-arterial digital subtraction image acquisition is now routine available (18). With some manufacturers the tabletop is moved a precise distance, with others, the gantry is moved. With either technique, precise DSA images are obtained that can delineate vessels as small as the posterior pedal arch. Digital subtraction techniques are required for carbon dioxide studies.

Technique and Risk Peripheral arteriography is typically performed using a femoral artery approach. Alternate approaches include transbrachial/transaxillary catheterization and, rarely, translumbar entry. These approaches are useful if the patient suffers from severe aortic–iliac disease and the femoral pulses are weak or absent. The complication rates associated with these approaches are close to those of femoral catheterization (93). Please refer to the section entitled Complications of Angiography for further information. For peripheral arteriography, we use low-osmolarity contrast media exclusively since the incidence of pain and heat related to contrast injection is much lower and motion artifacts are therefore reduced. In relatively healthy patients with symptoms of aortoiliac and/or distal disease, an abdominal aortogram is obtained prior to evaluating the flow through more distal vessels (the “runoff”). This study is performed in order to evaluate the aorta itself as well as the renal and visceral arteries. Images are typically obtained in one planeunless an aortic aneurysm is present or renovascular disease is noted. In these situations, a lateral image and/or oblique views are obtained. Following evaluation of the aorta, images of the “runoff” are obtained. This study involves acquiring AP images of the pelvis and of the vessels in both lower extremities. We routinely use DSA for the evaluation of aorta and stepping DSA for the runoff. Oblique views of the iliac arteries and common femoral artery bifurcation are obtained, especially if there are symptoms of aortic–iliac disease or if inflow or outflow graft placement is planned at the common femoral artery. Additional oblique views are also frequently necessary to evaluate the below-knee runoff. We prefer lateral images of the trifurcation vessels and the major vessels of the foot in addition to standard AP views of these regions. If the patient has chronic renal failure or has symptoms only of distal disease, or if there is a vascular injury, then arteriography may be limited to the extremity or region affected.

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occlusions is important. A recent embolic occlusion is identified by its convex intravascular appearance as well as the lack of large adjacent collateral vessels (Fig. 5.15). A chronic occlusion is demonstrated by a gradual tapering of the vessel involved as well as the presence of large and numerous collateral vessels (Fig. 5.16). Patients suffering from trauma may demonstrate intimal tears, pseudoaneurysms, extravascular contrast extravasation, and AV fistulas. The hemodynamic significance of a vascular stenosis should be evaluated in patients whose symptoms appear related to decreased blood flow in that vessel. Those obstructions, which compromise greater than 50% of luminal diameter, are (75% area stenosis) considered hemodynamically significant (109,110). Slowed linear velocity of contrast flow is also noted. Hemodynamic significance can also be determined by measuring the pressure gradient across the narrowed lesion. A pressure gradient greater than 15 mm is considered hemodynamically

Findings The findings on peripheral arteriography are mostly related to the evaluation of atherosclerotic disease. Abnormalities such as stenoses and occlusions are commonly searched for. Differentiation between recent and old

FIGURE 5.15 Distal right common femoral and proximal superficial femoral arteries show the presence of several intraluminal filling defects which are emboli (arrows) in this patient with atrial fibrillation.

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Part I Imaging Techniques

B

A

FIGURE 5.16 (A) Axillary arteriography via the left axillary artery and digital subtraction filming demonstrate occlusion of the infrarenal abdominal aorta. Large collateral vessels are demonstrated. The inferior mesenteric artery is very prominent (arrows). Leriche syndrome. (B) Reconstitution of the distal most abdominal aorta just prior to the bifurcation. Small but otherwise normal iliac arteries. (C) Normal superficial femoral arteries.

C

significant. Intraluminal pressure can be determined accurately only when the stenosis is approached in a retrograde manner. When approaching a stenosis in an antegrade fashion, the catheter used to obtain the pressure measurement distal to the diseased segment will spuriously increase the pressure gradient due to the occlusive effects of the catheter within the lesion. The induction of distal vasodilation is occasionally necessary in order to simulate conditions of work or stress. This is typically done using intra-arterial nitroglycerin, although reactive hyperemia may occasionally be used (62,67).

References 1. Seldinger SI. Catheter replacement of the needle in percutaneous arteriography: a new technique. Acta Radiol (Stockh) 1953: 39: 368–376.

2. Roentgen WC. On a new kind of rays. Erste Mitt Sitzber Phys-Med Ges (Wurzburg) 1895: 137. 3. Haschek E, Lindenthal OT. A contribution to the practical use of photography according to Roentgen. Wien Klin Wochenschr 1896: 9: 63. 4. Berberich J, Hirsch S. Die roentgenographische Darstellung der Arterien und Venen am Lebenden. Munch Klin Wochenschr 1923: 2: 2226. 5. Brooks B. Intraarterial injection of sodium iodide. JAMA 1924: 82: 1016. 6. Moniz E, Diaz A, Lima A. La radioarteriographic et la topographie cranioencephalique. J Radiol Electrol Med Nucl 1928: 12: 72. 7. McPheeters HO, Rice CO. Varicose veins — the circulation and direction of the venous flow. Surg Gynecol Obstet 1929: 49: 29–33. 8. Swick N. Darstellung der Niere und Harnwege ein Röntgenbild durch intravenöse Einbringund cines neuen Konstraststoffes: des Uroselectans. J Klin Wochenschr 1929: 8: 2087–2089.

Chapter 5 Fundamentals of Angiography 9. Grainger RG. Intravascular contrast media—the past, the present and the future. Br J Radiol 1980: 55: 1. 10. Forssmann W. Die Sondierung des rechten Herzens. Klinische Wochenschrift 1929: 8: 2085–2087. 11. Moniz E, de Carvalho, Lima A. Angiopneumographic. Presse Med 1931: 53: 996. 12. Castellanos A, Pereiras R, Garcia A. La angiocardiografia radio-opaca. Arch Soc Estudios Clin (Habana) 1937: 31: 523. 13. Robb GP, Steinberg I. Visualization of the chambers of the heart, pulmonary circulation and the great blood vessels in man. AJR 1939: 41: 1–17. 14. Ziedes des Plantes BGV. Subtraction. Eine röntgenographische Method zur separaten Abbildung bestimmter Teile des Objekts. Fortschritte auf dem Gebiete der Röntgenstrahlung 1935: 52: 69–79. 15. Castellanos A, Pereiras R. Countercurrent aortography. Rev Cuba Cardiol 1939: 2: 187–205. 16. Farinas PL. A new technique for the arteriographic examination of the abdominal aorta and its branches. AJR 1941: 46: 641–645. 17. Lee KR, Templeton AW, et al. Digital venography of the lower extremity. AJR 1989: 153: 413–417. 18. Fink U, Heywang SH, et al. Peripheral DSA with automated stepping. Eur J Radiol 199l: 13: 50–54. 19. Lind CJ, Mushlin PS. Sedation, analgesia and anesthesia for radiologic procedures. Cardiovasc Intervent Radiol 1987: 10: 247–253. 20. Grainger RG. Intravascular contrast media—the past, the present and the future. 1982: 55: 1–18. 21. Speck U, Siefert HM, Klinik G. Contrast media and pain in peripheral arteriography. Invest Radiol 1980: 15: 335–339. 22. Stolberg HO, McClennan BL. Current problems in diagnostic radiology, Vol. 20. Keats TE, ed. 1991. St. Louis: Mosby Year Book. 23. Powers ER. Effects of contrast agents on platelet function and coagulation: potential importance during coronary angiographic and angioplasty procedures. J Invas Cardiol 1990: 3: 41B–46B. 24. Fureed J, Walanga JM, et al. Thrombogenic potential of nonionic contrast media. Radiology 1990: 174: 321–325. 25. Grollman JH, Lin CK, et al. Thromboembolic complications in coronary angiography associated with the use of nonionic contrast medium. Cathet Cardiovasc Diagn 1988: 14: 159–164. 26. Bull BS, Smith DC. Effects of contrast agents on blood clotting. J Invas Cardiol 1991: 3: 24B–29B. 27. McClennan BL. Ionic and non-ionic iodinated contrast media: evolution and strategies for use. AJR 1990: 155: 225–233. 28. Higgins CB, Gerber KH, et al. Evaluation of hemodynamic effects of intravenous administration of ionic and nonionic contrast materials. Radiology 1982: 142: 681–686. 29. Adams DF, Fraser D, Abrams HL. Hazards of coronary arteriography. Semin Roentgenol 1972: 7: 357. 30. Adams DF, Abrams HL. Complications of coronary arteriography: a follow-up report. Cardiovasc Intervent Radiol 1979: 2: 89. 31. Peck WW, Slutsky RA, et al. Effects of contrast media on pulmonary hemodynamics: comparison of ionic and non-ionic agents. Radiology 1983: 149: 371–374. 32. Harrington G, Michie C, et al. Blood–brain barrier changes associated with unilateral cerebral angiography. Invest Radiol 1966: 1: 431.

83

33. Gonsett RE. The neurotoxicity of water soluble contrast media: actual concepts and future. In: Contrast media in radiology, Amel M, ed. Heidelberg: Springer Verlag, 1982: 115–122. 34. Junck L, Marshall WH. Neurotoxicity of radiologic contrast agents. Ann Neurol 1982: 17: 271–275. 35. Giang DW, Kido DK. Transient global amnesia associated with cerebral angiography performed with use of iopamidol. Radiology 1989: 172: 195–196. 36. Djiandjian R. Arteriography of the spinal cord. AJR 1969: 107: 46l. 37. Berkseth RO, Kjellstrand CM. Radiologic contrastinduced nephropathy. Med Clin North Am 1984: 68: 351–370. 38. Harris KG, Smith TP, et al. Nephrotoxicity from contrast material in renal insufficiency: ionic vs non-ionic agents. Radiology 1991: 179: 849–852. 39. Lautin EM, Freeman NJ, et al. Radiocontrast-associated renal dysfunction: a comparison of lower osmolality and conventional high osmolality contrast media. AJR 1991: 157: 59–65. 40. Bush WH, Swanson DP. Acute reactions to intravascular contrast media: types, risk factors, recognition and specific treatment. AJR 1991: 157: 1153–1161. 41. Yamaguchi K, Katayama H, et al. Prediction of severe adverse reactions to ionic and non-ionic contrast media in Japan: evaluation of pretesting. Radiology 1991: 178: 363–367. 42. Harman GW, Hattery RR, et al. Mortality during excretory urography: Mayo Clinic experience. AJR 1982: 139: 919–922. 43. Katayama H, Yamaguchi K, Kozuka T. Adverse reactions to ionic and non-ionic contrast media: a report from the Japanese Committee on the Safety of Contrast Media. Radiology 1990: 175: 621–628. 44. Lasser EL, Berry CC, et al. Pretreatment with corticosteroids to alleviate reactions to intravenous contrast material. N Engl J Med 1987: 317: 845–849. 45. American College of Radiology. Manual on iodinated contrast media, 1991. 46. Weaver FA, Pentecost MJ, et al. Clinical applications of carbon dioxide/digital subtraction arteriography. J Vasc Surg 1991: 13: 266–273. 47. Hawkins IF. Carbon dioxide digital subtraction arteriography. AJR 1982: 139: 19–24. 48. Kruger RA, Mistretta CA, , et al. Computerized fluoroscopy in real time for non-invasive visualization of the cardiovascular system—preliminary studies. Radiology 1979: 130: 49–57. 49. Ergun DL, Mistretta CA, et al. A hybrid computerized fluoroscopy technique for non-invasive cardiovascular imaging. Radiology 1979: 132: 739–742. 50. Meaney TF, Weinstein MA, et al. Digital subtraction angiography of the human cardiovascular system. AJR 1980: 135: 1153–1160. 51. Crummy AB, Strother CM, et al. Digital video subtraction for evaluation of peripheral vascular disease. Radiology 1981: 141: 33–37. 52. Smith TP, Cragg AH, et al. Comparison of the efficacy of digital subtraction and film-screen angiography of the lower limb: prospective study in 50 patients. AJR 1992: 158: 431–436. 53. Picus D, Hicks ME, et al. Comparison of nonsubtracted digital angiography and conventional screen-film angio-

84

54. 55. 56.

57.

58.

59.

60.

61. 62. 63.

64. 65. 66.

67. 68.

69.

70.

71.

72.

73.

74.

75.

Part I Imaging Techniques graphy for the evaluation of patients with peripheral vascular disease. JVIR 1991: 2: 359–364. Dawson P. Digital subtraction angiography—a critical analysis. Clinical Radiology 1988: 39: 474–477. Jeans WD. The development and use of digital subtraction angiography. Br J Radiol 1990: 63: 161–168. Ball BJ, Lukin RR, et al. Complications of intravenous digital subtraction angiography. Arch of Neurology 1985: 42: 969–972. Pinto RS, Manuell M, Kricheff II. Complications of digital intravenous angiography: experience in 2488 cervicocranial examinations. AJR 1984: 143: 1295–1299. Thijssen HOM, Merx JL, et al. Comparison of brachiocephalic angiography and IVDSA in the same group of patients. Neuroradiology 1988: 30: 91–97. Cragg AH, Smith TP, et al. Randomized double blind trial of midazolam/placebo and midazolam/fentanyl for sedation and analgesia in lower extremity angiography. AJR 1990: 157: 173. Antonovich R, Rösch J, Dotter CT. The value of systemic arterial heparinization in transfemoral angiography: a prospective study. AJR 1977: 128: 737. Neiman HL, Yao JS. Angiography of vascular disease. C New York: Churchhill Livingstone, 1985. Kadir S. Diagnostic angiography. Philadelphia: W.B. Saunders, 1986. Kikuchi T, Strother CM, Boyer M. New catheter for endovascular interventional procedures. Radiology 1987: 165: 870–871. Sos TA, Cohn DJ, et al. A new open-ended guidewire catheter. Radiology 1985: 154: 817–818. Tegtmeyer CJ. Guidewire angioplasty balloon catheter: preliminary report. Radiology 1988: 169: 253–254. Grollman JH, Marcus R. Transbrachial arteriography: techniques and complications. Cardiovasc Int Radiol 1988: 11: 32–35. Darcy MD. Lower-extremity arteriography: current approach and techniques. Radiology 1991: 178: 615–621. Smith TP, Cragg AH, et al. Techniques for lower-limb angiography: a comparative study. Radiology 1990: 174: 951–955. Redman HC, Reuter SR. Percutaneous transarterial arteriography: complications and their avoidance. Angiology 1970: 21: 575–579. Rupp SB, Vogelzang RL, et al. Relationship of the linguinal ligament to pelvic radiologic landmarks: anatomic correlation and its role in femoral arteriography. JVIR 1993: 4: 409–413. Hoffman MG, Gomes AS, Pais SO. Limitations in the interpretation of intravenous digital subtraction angiography. AJR 1984: 142: 261–264. Seeger JF, Carmody RF. Digital subtraction angiography of the arteries of the head and neck. Radiol Clin North Am 1985: 23: 193–210. Standards of Practice Committee of the SCVIR: Standard for diagnostic arteriography in adults. JVIR 1993: 4: 385–395. Steinke W, Kloetzsch C, Hennerici M. Carotid artery disease assessed by color doppler flow imaging: correlation with standard doppler sonography and angiography. AJNR 1990: 11: 259–266. Mattle HP, Kent KC, et al. Evaluation of the extracranial carotid arteries: correlation of magnetic resonance an-

76.

77.

78.

79.

80.

81.

82.

83.

84. 85.

86.

87. 88.

89.

90.

91.

92.

93. 94.

95.

giography, duplex ultrasonography and conventional angiography. J Vasc Surg 1991: 13: 838–45. Litt AW, Eidelman EM, et al. Diagnosis of carotid artery stenosis: comparison of 2DFT time-of-flight MR angiography with contrast angiography in 50 patients. AJNR 1991: 12: 149–154. Gelabert HA, Moore WS. Carotid endarterectomy without angiography. Surg Clin North Am 1990: 70: 213–223. Dion JE, Gates PC, et al. Clinical events following neuroangiography: a prospective study. Stroke 1987: 18: 997–1004. Earnest, F IV, Forbes G, Sandok BA, et al. Complications of cerebral angiography: prospective assessment of risk. AJR 1984: 142: 247–253. Ball JB, Lukin RR, et al. Complications of intravenous digital subtraction angiography. Arch Neurol 1985: 42: 969–972. McIvor J, Steiner TJ, et al. Neurological morbidity of arch and carotid arteriography in cerebrovascular disease. The influence of contrast medium and radiologist. Br J Radiol 1987: 60: 117–122. Hankey GJ, Warlow CP, Sellar RJ. Cerebral angiographic risk in mild cerebrovascular disease. Stroke 1990: 21: 209–222. Murray KK, Hawkins IF. Angiography of the lower extremities in atherosclerotic vascular disease. Surg Clin No Am 1992: 72: 767–789. Hilbish TF, Herdt JRL. Complications of selective angiocardiography. Radiology 1960: 75: 197–205. Mills Sr, Jackson DC, et al. The incidence, etiologies and avoidance of complications of pulmonary angiography in a large series. Radiology 1980: 136: 295–299. The PIOPED Investigators. Value of the ventilation/ perfusion scan in acute pulmonary embolism: results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). JAMA 1990: 263: 2753–2759. Rosenow EC, Osmunndso PJ, Brown ML. Pulmonary embolism. Mayo Clin Proc 1981: 56: 161–178. Hull RD, Hirsh J, Carter CJ. Diagnostic value of ventilation–perfusion lung scanning in patients with suspected pulmonary embolism. Chest 1985: 88: 819–828. Ryu JH, Rosenow EC. Acute pulmonary embolism. In: Contemporary issues in peripheral vascular disease (cardiovascular clinics), Spittell JA, ed. Philadelphia: F.A. Davis, 1992: 22(3): 103–112. Bookstein JJ, Silver TM. The angiographic differential diagnosis in acute pulmonary embolism. Radiology 1974: 110: 25–33. Bossart PJ, Sniderman KW, et al. Pulmonary arteriography: the importance of multiple projections. Cardiovasc Int Radiol 1982: 5: 105–107. Kido DK, King PD, et al. The role of catheters and guidewires in the production of angiographic thromboembolic complications. Invest Radiol 1988: 23: S359–S364. Hessel SJ, Adams DF, Abrams HL. Complications of angiography. Radiology 1981: 138: 273–281. Schwartz MR, Weaver FA, et al. Refining the indications for arteriography in penetrating extremity trauma: a prospective analysis. J Vasc Surg 1993: 17: 116–124. Frykberg ER, Dennis JW, et al. The reliability of physical examination in the evaluation of penetrating extremity

Chapter 5 Fundamentals of Angiography

96.

97.

98.

99.

100. 101.

102.

103.

104.

105.

106.

107.

108.

109.

110. 111.

112.

113. 114.

115. 116.

trauma for vascular injury: results at one year. J Trauma 1991: 31: 502–511. Smith SH, Pond GD, et al. Proximity injuries: correlation with results of extremity arteriography. JVIR 1991: 2: 451–456. Rose SC, Moore EE. Trauma angiography of the extremity: the impact of injury mechanism on triage decisions. CVIR 1988: 11: 136–139. Rosch J, Keller FS, et al. Pharmacoangiography in the diagnosis of recurrent massive lower gastrointestinal bleeding. Radiology 1982: 145: 615–619. Doppman JL, Miller DL, et al. Gastrinomas: localization by means of selective intraarterial injection of secretin. Radiology 1990: 174: 25–29. Cho KJ, Andrews JC, et al. Hepatic arterial chemotherapy: role of angiography. Radiology 1989: 173: 783–791. Sclafani SJA, Weisberg A, et al. Blunt splenic injuries: nonsurgical treatment with CT, arteriography and transcatheter arterial embolization of the splenic artery. Radiology 1991: 181: 189–196. Richtor GM, Noeldge G, et al. The transjugular intrahepatic portosystemic stent shunt (TIPSS): results of a pilot study. Cardiovasc Intervent Radiol 1990: 13: 200–207. Vowden P, Wilkinson D, et al. A comparison of three imaging techniques in the assessment of an abdominal aortic aneurism. J Cardiovasc Surg 1989: 30: 891–896. Todd GJ, Nowygrod R, et al. The accuracy of CT scanning in the diagnosis of abdominal and thoracoabdominal aortic aneurisms. J Vasc Surg 1991: 13: 302–310. Lee JKT, Ling D, et al. Magnetic resonance imaging of abdominal aortic aneurisms. AJR 1984: 143: 1197– 1202. Ruff SJ, Watson MR. Magnetic resonance imaging versus angiography in the preoperative assessment of abdominal aortic aneurisms. Am J Surg 1988: 155: 651–654. McCann RL, Schwartz LB, Pieper KS. Vascular complications of cardiac catheterization. J Vasc Surg 1991: 14: 375–381. Kresowik TF, Khoury MD, et al. A prospective study of the incidence and natural history of femoral vascular complications after percutaneous transluminal coronary angioplasty. J Vasc Surg 1991: 13: 328–333. Mann FC, Herrick JF, et al. The effect on the blood flow of decreasing the lumen of a blood vessel. Surgery 1938: 4: 249. Moore WS, Malone JM. Effect of blood flow and vessel calibre on critical arterial stenosis. J Surg Res 1979: 26: 1. Joyce JW. Occlusive arterial disease of the upper extremity in Spittell JA (ed): Contemporary Issues in Peripheral Vascular Disease 1992: 22: 147–160. Menawat SS, Dennis JW, et al. Are arteriograms necessary in penetrating Zone II neck injuries? J Vasc Surg 1992: 16: 397–401. Hartling RP, McGahan JP, et al. Stab wounds to the neck: role of angiography. Radiology 1989: 172: 79–82. Scalfani SJA, Cavaliere G, et al. The role of angiography in penetrating neck trauma. J Trauma 1991: 31: 557–563. Fakhry SM, Jaques PF, Proctor HJ. Cervical vessel injury after blunt trauma. J Vasc Surgery 1988: 8: 501–508. Rappaport S, Sniderman KW, et al. Pseudoaneurism: a complication of faulty technique in femoral artery puncture. Radiology 1985: 154: 529–530.

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117. Rosansky SJ, Deschamps EG. Multiple cholesterol emboli syndrome after angiography. Am J Med Sci 1984: 288: 45–48. 118. Petasnick JP. Radiologic evaluation of aortic dissection. Radiology 1991: 180: 297–305. 119. DeSanctis RW, Doroghazi RM, et al. Aortic dissection. NEJM 1987: 317: 1060–1067. 120. Madayag MA, Kirshenbaum KJ, et al. Thoracic aortic trauma: role of dynamic CT. Radiology 1991: 179: 853–855. 121. Weiss JP, Feld M, et al. Traumatic rupture of the thoracic aorta. Em Med Clin N Am 1991: 9: 789–803. 122. Richardson JD, Wilson ME, Miller FB. The widened mediastinum: diagnostic and therapeutic priorities. Ann Surg 1990: 211: 731. 123. Blaisdell FW, Trunkey DD, eds. Trauma management cervicothoracic trauma. New York: Thieme, 1986: 3: 223–246. 124. Hamada S, Takamiya M, et al. Type A aortic dissection: evaluation with ultrafast CT. Radiology 1992: 183: 155–158. 125. Caputo GR, Higgins CB. Advances in cardiac imaging modalities: fast computed tomography magnetic resonance imaging and postron emission tomography. Invest Radiol 1990: 25: 838–854. 126. Dinsmore RE, Liberthson RR, et al. Magnetic resonance imaging of thoracic aortic aneurisms: comparison with other imaging modalities. AJR 1986: 146: 309–314. 127. Khandheria BK. Aortic dissection: the last frontier. Circulation 1993: 87: 1765–1768. 128. Erbel R, Oelert H, et al. The European Cooperative Study Group on Echocardiography: Effect of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography: implications for prognosis and therapy. Circulation 1993: 87: 1604– 1615. 129. Solomon SL, Brown JJ, et al. Thoracic aortic dissection: pitfalls and artifacts in MR imaging. Radiology 1990: 177: 223–228. 130. LaBerge JM, Jeffrey RB. Aortic lacerations: fatal complications of thoracic aortography. Radiology 1987: 165: 367. 131. Soto B, Harman MA, et al. Angiographic diagnose of dissection aneurysm of the aorta. AJR 1972: 116: 146– 154. 132. Eagle KA, Auertermous T, et al. Spectrum of conditions initially suggesting aortic dissection but with negative aortograms. Am J Cardiol 1986: 57: 322–326. 133. Kirsh MM, Behrendt DM, et al. The treatment of acute traumatic rupture of the aorta: a ten year experience. Ann Surg 1976: 184: 308. 134. Smith RS, Chang FC. Traumatic rupture of the aorta: still a lethal injury. Am J Surg 1986: 152: 660. 135. Daily PO, Trueblood W, et al. Management of aortic dissections. Ann Thorac Surg 1970: 60: 237–247. 136. DeBakey ME, Henly WS, et al. Surgical management of dissecting aneurisms of the aorta. J Thorac Cardiovasc Surg 1965: 49: 130–149. 137. Parmley LF, Mattingly TW, Manion WC. Nonpenetrating traumatic injury of the aorta. Circulation 1958: 17: 1086. 138. Huckman MS. Outpatient brachiocephalic angiography. Radiology 1989: 170: 317–318.

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139. Millward SF, Marsh JJ, Peterson RA. Outpatient transfemoral angiography with a two hour observation period. CVIR 1989: 12: 290–291. 140. Diaz LP, Pabon IP, et al. Assessment of CO2 arteriography in arterial occlusive disease of the lower extremities. J Vasc Interv Radiol 2000: (2Pt1): 163–169. 141. Bees NR, Beese RC, et al. Carbon dioxide angiography of the lower limbs: initial experience with an automated carbon dioxide injector. Clin Radiol. 1999: 54(12): 833–838. 142. Chamberlin JR, Lardi AB, et al. Use of vascular sealing devices (VasoSeal and Perclose) versus assisted manual compression (Femostop) in transcatheter coronary interventions requiring abciximab (ReoPro). Catheter Cardiovasc Interv 1999: 47(2): 143–147: discussion 148. 143. Carere RG, Webb JG, et al. Initial experience using Prostar: a new device for percutaneous suture-mediated closure of arterial puncture sites. Cathet Cardiovasc Diagn 1996: 37(4): 382–391.

144. Cooper CL, Miller A. Infectious complications related to use of the anagio-seal hemostatic puncture closure device. Catheter Cardiovas Interv. 1999: 48(3): 301–303. 145. Carere RG, Webb JG, et al. Groin complications associated with collagen plug closure of femoral arterial puncture sites in anticoagulated patients. Cathet Cardiovascular Diagn 1998: 43(2): 124–129. 146. Raptopoulos V, Boiselle PM. Multi-detector row spiral CT pulmonary angiography: comparison with singledetector row spiral CT. Radiology 2001 Dec: 221(3): 606–613. 147. Remy-Jardin M, Remy J, et al. Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography and scintigraphy. Radiology. 1996 Sep: 200(3): 699–706. 148. Hagspiel KD, Polak JF, et al. Pulmonary embolism: comparison of cut-film and digital pulmonary angiography. Radiology. 1998 Apr: 207(1): 139–145.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 6 Computed Tomography in Vascular Disease Frederick L. Hoff, Kyle Mueller, and William Pearce

Significant advances in computed tomography (CT) imaging technology have provided a unique view of the pathology of many vascular diseases. Prior to the 1980s, the diagnosis of many vascular diseases was based primarily on contrast angiography and venography in combination with ultrasound. While contrast arteriography and venography provide the anatomic detail for planning surgical procedures, noninvasive testing is essential to defining the physiologic importance of the anatomic lesion. Ultrasound imaging does provide both anatomic and hemodynamic detail, but its usefulness is limited to superficial structures. In the abdomen, bowel gas and solid organs interfere with the image resolution of ultrasound. In the thorax, ultrasound is limited to intracardiac pathology and the thoracic aorta. Since its advent in the 1960s, and through many advances in the modality over the following three decades, CT has become vital in the preoperative and postoperative management of many vascular diseases. The practice of medicine was transformed by computed tomography (CT). Recognizing this change, in 1979 Cormack and Hounsfield were awarded the Nobel Prize for their development of this technique (1). A key factor in the development of CT was the realization that greater advancement would be obtained not by increasing resolution but by enhancing the contrast between softtissue structures. The development of CT rested on important concepts in multiple fields including mathematics, computer science and physics. The first clinical CT unit was placed at Atkinson Morley’s Hospital in England on October 1, 1971 (1). Each

image took four minutes to acquire and two days were needed to reconstruct the series. The clinical importance of CT was immediately appreciated; by 1976, there were 22 companies manufacturing CT scanners and in 1979, there were over 1,000 scanners in use throughout the world. The procedure was initially termed “computer assisted tomographic” or “CAT” scanning; however, as images are not limited to the anatomic axial plane, this was later shortened to computed tomography (2). There has been continuous and dramatic improvement in both spatial and temporal resolution from that time due to advances in both hardware and software design. CT has had a dramatic impact on the diagnosis and treatment of vascular disease. Before the application of CT, contrast arteriography and venography were the only methods available to evaluate arterial and venous anatomy and disease. CT not only provides more information about the vessel (i.e., thrombus and wall) than these intraluminal techniques, it also provides valuable data about adjacent organs and tissues. Although 30 years old and generally considered a “mature” technology, CT continues to evolve. In the early 1990s helical CT was introduced, with significant impact on vascular applications. The ability to obtain thin, overlapping images rapidly enough to capture contrast within vessels ushered in three-dimensional techniques and “CT angiography.” The late 1990s saw the development of multidetector helical units that went far beyond the advances of helical CT. This chapter reviews both the basic principles of CT and its clinical applications.

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Image Reconstruction

Basic Principles The fundamental concept of CT is to use multiple projections of an object to reconstruct the internal structure of that object (3,4). The creation of a CT image can be divided into three steps: 1) data acquisition involves the actual exposure to radiation and scanning of the patient; 2) image reconstruction; and 3) image display. Data Acquisition A radiographic tube and an array of detectors as well as the associated electronics are mounted on a frame called a gantry (Fig. 6.1). The x-ray tube produces a fan-shaped beam of x-rays that interact with the patient via absorption or scattering; some of the x-rays pass through the patient to interact with the detector array. During data acquisition, the tube and detectors rotate around the patient and the detectors repeatedly measure the number of x-rays transmitted through the patient. The amounts of radiation transmitted to each detector and the gantry angle at the time of the measurement are recorded (Fig. 6.2). Typically, the detector array contains 500 to 1,000 detectors, each of which is sampled approximately 1,000 times per revolution (4). Each line of this information reflects the summation of the attenuation coefficients of all structures in that x-ray path. The entire dataset forms the “raw data” from which an image is reconstructed. Conventional or incremental scanning is obtained by performing a series of individual scans during suspended respiration. Following each scan the patient breathes, the patient table is advanced, and in most machines the tube and detector apparatus rewinds to begin another scan (5). Historically, most scanners operated at a rotation speed of one 360° revolution per second.

From the raw data a digital image is created. A variety of mathematical techniques can be used to accomplish this; these rely on the principles of back projection, iterative formulas, or analytic formulas, either with or without Fourier transformation (6). The result is a matrix of numbers; generally, a 512 by 512 matrix is employed in vascular CT. Each number in this matrix is called a pixel, and each pixel corresponds to a volume of tissue or voxel within the patient (Fig. 6.3). The average density of the tissue within each voxel is represented by the pixel value. The dimensions of the voxel in the scan plane are set by the field of view (FOV) and matrix; the dimensions of the pixel in these axes can be calculated by dividing the FOV by the matrix size. The third dimension, representing the voxel depth, is the image thickness, which is determined by the collimation width of the fan beam. The difference in attenuation of the contents of a voxel relative to water is defined as the CT attenuation number and expressed in Hounsfield units (HU) (7). A 12-bit number scale (212) is used which defines water as zero and air as –1000; therefore each pixel is a number from –1000 to +3095. Image Display This digital image or number matrix is converted to a visual format for interpretation. A gray scale is used, with

Data aquistion and detector assembly

X-ray generator

X-ray tube and collimator

FIGURE 6.1 Diagram demonstrating the radiographic x-ray tube and detector assembly mounted on the gantry. The patient is placed on the table and advanced through the gantry.

FIGURE 6.2 Diagram illustrating three sample positions of data measurement in obtaining a single image. Data is collected from approximately 1000 positions during each revolution. At each position, measurements are obtained from each detector in the array; while the example shows 16 detectors, in actuality between 500 and 1000 are used. The entire group of measurements forms the raw data used to reconstruct the internal structure of the scanned object.

Chapter 6 Computed Tomography in Vascular Disease

the densest materials such as bone (highest Hounsfield units) being assigned lighter shades while the least dense such as air (most negative Hounsfield units) are assigned darker shades. Any color or gray scale format can be chosen; the standard format above follows the conditions found in conventional radiographs. A problem arises in that display devices are limited to demonstrating approximately 60 shades of gray and the human eye may distinguish only 30–100 shades; the 4096 CT numbers cannot be mapped without conversion. Thus, the wide range of numbers is converted for display by window width and level controls. The window level specifies the centering of the gray scale and the choice of width specifies the numbers over which the gray scale is to extend. For example, if the window level is set to zero and the width is set to 500, every pixel a number below –250 will be black and every pixel greater than 250 will be white; if there are 50 shades of gray, each would be assigned a range of 10 numbers

Pixel

Voxel

Slice Width

FIGURE 6.3 Diagram illustrating the concepts of pixel and voxel. The average density of tissues in each volume element or voxel in the patient is represented by a single number in the computer as a pixel or picture element. The dimension of the voxel is equal to FOV/matrix in the x- and y-axes and by the slice width in the z-axis. The matrix of pixels is the digital image.

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with the middle gray used for the numbers adjacent to zero.

Electron Beam Computed Tomography Another approach to obtaining a computed tomography image is significantly different from the conventional and helical machines—electron beam scanning. This was termed “Ultrafast CT,” but now is most commonly called electron beam tomography (EBT) or electron beam computed tomography (EBCT). Developed in the early 1980s, the machine uses an electron beam that is magnetically deflected to hit tungsten targets about the patient to produce x-rays for scanning (8). The advantage is speed: initially designed for cardiac scanning, the EBT unit can obtain eight adjacent images in 50 ms. The unit was later adapted to obtain a single slice for use in body scanning (9). EBCT has not found widespread use in other vascular imaging to date.

Helical and Multidetector Helical Computed Tomography Helical or spiral CT involves a continuous rotation of the gantry as the patient is advanced at a steady rate through it, dispensing with the discrete steps of data acquisition in conventional CT (Fig. 6.4) (10,11). This creates a volume set of raw data which must then be segmented to create planar images. Although it has been argued that the term “helical” more accurately describes the concept of this new technology, both terms are found and used interchangeably in the literature (12). Introduced in 1989, there has been both rapid acceptance and distribution of the technology. The major advantages of helical scanning include rapid acquisition, unlimited ability to obtain overlapping images without increased radiation exposure, high-quality multiplanar reconstruction, and absence of respiratory misregistration (13). The slice profile and noise of images produced from a helical acquisition are frequently slightly worse than a conventionally obtained image; however, the benefits in clinical usage far outweigh these disadvantages (14–16).

FIGURE 6.4 Helical scanning involves the patient transport in a continuous fashion as the tube continuously rotates; the result can be imagined as inscribing a helix about the patient.

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Both hardware and software advances were required to develop helical scanning (17). The major hardware requirements are a slip ring gantry and increased computational power. Most previous CT scanner designs had wires that supplied the electricity to the x-ray tube and transferred the measurement data from the detectors to the computer. Thus, the gantry was only able to travel for a limited distance before it needed to reverse direction and rewind prior to obtaining the next image. The wires connecting the gantry to the base unit were eliminated by use of slip ring connectors, allowing the gantry to circle continuously in one direction. As the patient is continuously moving, the individual radiation measurements collected at each angle of the gantry are obtained at slightly different locations along the longitudinal or z-axis of the patient. Powerful interpolation algorithms are required to estimate the attenuation measurement at each angle if the patient had not been moving and the patient position had been constant. The increased computational power is needed to perform this task. Several unique new concepts that the physician must understand are introduced by helical scanning. Pitch is defined as the table feed per 360° tube revolution divided by the beam collimation. When the patient movement is equal to the beam collimation, the pitch is one. Increasing the pitch allows increased coverage in the z-direction but with some broadening of slice profile and image noise. Use of a pitch greater than one also decreases the radiation dose to the patient. The pitch does not affect the slice thickness or position of obtained images; contiguous images are still obtained with pitches greater than one. A second important concept is that of image increment and overlapping reconstructions. Once the scan has been obtained, the image thickness, which is determined by the beam collimation, cannot be changed in single-detector helical CT. However, as the data is continuous, the location of the image center along the z-axis may be altered. This has two practical applications: it allows overlapping reconstructions for use in post-processing without any increase in radiation dose to the patient and reduces volume averaging effect which may lead to improved detection of small lesions (18). The demand to scan faster continues despite the dramatic improvement provided by helical CT. Two methods are being explored to meet this need: increasing the rotational speed of the gantry and increasing the number of slices obtained with each revolution (19). Scanners have been introduced that can obtain speeds of one revolution in 0.5 seconds. The concept of multidetector CT was introduced in the early 1990s with a dual detector scanner. However, its widespread acceptance did not occur until the late 1990s with the introduction of “quad” or “four slice” machines. The principle and the advantages are easy to comprehend; however, the specifics and applications are more complex (20). Instead of collecting a single thin section or slice of data per revolution, a multidetector CT gathers radiation measurements from two to sixteen adjacent locations along the z-axis of the patient’s body

(Fig. 6.5). This gathering of more data simultaneously can be exploited in two ways (or a combination of both) (21): 1.

2.

The table can be moved faster, covering a greater distance per revolution of the gantry. This enables coverage of greater volumes in the same amount of time. The implication for vascular imaging is great: with multidetector CT the entire aortoiliac system can be scanned while there is still adequate contrast in the vessels. At the most basic, two detectors allow one to go twice as far in the same time—twice the coverage. The multidetector unit can be used to create thinner images of the same volume in the same amount of time. For example, a two-detector machine could obtain 5-mm images of the aorta in the same amount of time as a single-detector unit could do 10-mm images of the same portion of the aorta—twice the resolution.

Once again, as with helical CT technology, several new concepts are introduced. There are several technical approaches to detector design, of little importance to the clinician. However, one should become aware of the concept of detector “row” and “channel.” Most state-of-theart machines available today have between 8 and 32 detector rows. This is the number of detectors in the z-axis along the patient’s body. This does not mean that these can obtain 8 or 32 lines of data or slices per revolution. Most currently are limited to 4 to 8 channels of data per revolution—this is limited by the hard-wired ability of the electronics behind the detector to transfer the data off the gantry and into the computer for image reconstruction. The other technological advance from single to multidetector CT is the ability to change the image thickness (within limitations) after the scan is obtained.

FIGURE 6.5 Diagram illustrating acquisition with a single-detector CT and multidetector CT. The simultaneous acquisition of multiple datasets allows increased coverage in the same amount of time. Multidetector beam profile.

Chapter 6 Computed Tomography in Vascular Disease

Future Technical Innovations The history of CT has been one of obtaining high-quality, progressively thinner images increasingly quickly. The speed of scanning was recently dramatically improved with the implementation of multidetector helical techniques; however, the demand for continued improvement persists. Manufacturers are moving to meet this demand by increasing the rotational speed of the gantry and by increasing the amount of simultaneously obtained data. Increased speed and resolution will entrench time as an important fourth dimension in vascular CT imaging (22). Manufacturers are already at work on “flat panel” CT units. Using detectors used in digital mammography but attached to a CT gantry, the concept of slice thickness may become one of historical interest only. The engineering and computer processing demands posed by such a machine are great. The amount of data that can be obtained during a single revolution is so large that creating the images from the raw data can take hours or days—reminiscent of Hounsfield’s first machine. An ideal in cross-sectional imaging is approaching: the isotropic voxel. An isotropic voxel is one in which the resolution is the same in all three planes. An advantage is the ability to arbitrarily scan the patient in any position and then reconstruct the images in the plane that best demonstrates the pathology (23). Practical questions are numerous. Does the noncontrast abdominopelvic CT become the “KUB” of the twenty-first century? Is the radiation dose to the patient necessary? How are such examinations interpreted—filmed in multiple planes or on workstations? It is clear that as the acquisition capabilities improve, data display techniques will be driven toward change as well. Approaching 30 years of age, CT continues to change the way medicine is practiced.

Vascular Techniques and Protocols Like all CT studies, vascular CT examinations have specific protocols that vary with the clinical indication. In order to provide the maximum diagnostic value, several factors must be specified. For contrast enhanced studies, the most important considerations will relate to contrast delivery and distribution. Examination parameters such as slice thickness, slice interval, and pitch not only affect the resolution of the axial images but the ability to create three-dimensional images. The exact parameters depend on the capability of the specific machine and on the size of the anatomic area to be covered. Due to physical limitations of the scanner, as the area to be included increases, the overall ability to optimize the quality of the scan decreases. Intravenous Contrast Iodine-based intravenous contrast material is routinely used in computed tomography of the vasculature. When properly employed, such contrast material allows ready identification of vessels and improved lesion detection and characterization. All currently used iodine-based

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contrast agents distribute rapidly into the extracellular space. Thus, the enhancement of vessels and organs is dependent on the rate of injection and the length of time from the beginning of the injection to imaging (scan delay), as well as on intrinsic characteristics of the structure such as vascularity. Pre-contrast images are only required in specific situations and are not routinely used in survey studies of the abdomen or vasculature. With regard to the vascular tree, pre-contrast may allow more accurate depiction of wall calcification and differentiation of calcium within thrombus from enhancement (i.e. on postendograft studies). Two general classes of contrast agents are available for use: the older ionic class and the newer nonionic class. The nonionics have a decreased incidence of both minor and major side effects but are more expensive (24,25). Because there is a decreased incidence of nausea and vomiting, there is at least a theoretical advantage in body CT of obtaining fewer suboptimal studies due to the patient moving (26). The amount of contrast material required depends on equipment type and the specific vessel of interest. A 60% iodine concentration (300 mg/mL) is most commonly used; however, lower and higher concentrations are acceptable. Injection of contrast material should always be performed with a power injector. This insures that the desired injection rates and timing are achieved. The terminology used to describe the timing in helical CT has varied in the literature due to local custom and the organ of interest. Early scans (usually using a scan delay of 15 to 30 s) are often called “arterial phase” as most of the contrast remains within the arterial system. Scans through the liver following a 60-s to 70-s delay are termed “portal venous phase;” in fact, with this delay, contrast is seen throughout the parenchyma and in the hepatic veins. This delay is frequently used for routine survey imaging of the abdomen. It is important to realize that the optimal scan delay is dependent on the injection rate; when the rate is changed the delay may require adjustment as well (27,28). It is important to lengthen the scan delay when venous structures are to be examined. A CT optimized to demonstrate the abdominal aorta will provide little information about the inferior vena cava, as it will be unenhanced. As the science of contrast administration has progressed, patient-dependent factors have become more obvious. Most institutions use nearly the same technique for most adult patients. However, differences in cardiac output, weight, time from last meal, and fluid status affect the actual enhancement obtained on the images (29,30). In an effort to tailor the examination to the specific patient, automated systems are available that initiate scanning when the optimal enhancement has been reached (31,32). In general, these use a series of low-dose scans obtained at a single location within the abdomen. A region of interest cursor is placed on the aorta and a threshold density level is set. Following the beginning of the contrast administration, scans are obtained every second or so until the density measured within the region of interest reaches a threshold value. At that time, the diagnostic scan is begun.

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Acquisition Parameters Conventional CT can be used to demonstrate a great deal of vascular pathology, although not as optimally as helical CT. Dedicated vascular studies should be performed on a helical unit if one is available. When using a conventional scanner, 5-mm slice thickness, dynamic table incremention, and the minimum interscan delay should be used. Contrast is typically administered with an initial bolus of 50 mL at 2 to 4 mL/s followed by a maintenance infusion of 0.8 to 1.5 mL/s for an additional 100 to 150 mL volume. Single detector helical CT allows excellent vascular imaging. For the aorta and great vessels, slice thicknesses of 2 to 3 mm are most frequently used. As above, there is a constant trade-off between anatomic coverage and slice thickness. Once the coverage is decided, the smallest possible collimation that will allow the completion of the examination within a single breath hold (20 to 40 s depending on the patient) should be used. Pitches in the 1.5 to 2.0 range are most frequently used. As the pitch is increased the coverage increases, however there is the negative trade-off of increasing slice profile and resultant decreased resolution in the image. Approximately 150 mL of contrast should be administered at a uniphasic rate of 3 to 4 mL/s using either a timing bolus or automated bolus timing software to determine the scan delay. A 50% reconstruction overlap or increment is ideal. Multidetector helical CT allows thinner images or greater anatomic coverage than single-detector CT. For the thoracic or abdominal aorta, slice thicknesses of approximately 1 mm are used. If the scan must include the entire thoracoabdominal aorta, the aortoiliacofemoral system (CT “runoff”), or multiple post-contrast phases (such as in post-endograft studies) are needed, a 2.5-mm to 3-mm slice thickness is used. Pitches on multidetector machines have been defined in various ways by different manufacturers, leading to some confusion. However, using the “beam pitch” definition, which is most analogous to single-detector CT, pitches in the range of 1 to 2 are used. Again, a 50% reconstruction overlap is important to improve the quality of any reconstructed images. The contrast injection techniques for arterial studies using multidetector helical machines are the same as single detector. Post-processing, Three-dimensional Techniques and CT Angiography One of the important advantages of helical acquisition is that a true volume dataset is obtained. This significantly improves the ability to manipulate the data in other than the single scanned orientation. Overlapping reconstructions minimize the “stair-step” appearance in longitudinal planar and three-dimensional applications—with helical technique these can be made without increased radiation exposure. Helical scanning during a single breathhold also eliminates respiratory misregistration that can significantly interfere with these reconstructions. Postprocessing of the dataset can be performed on the scanner

itself or on an offline workstation. The availability of a workstation allows the scanner itself to remain in operation while the image manipulation is being performed. Planar reformations in sagittal, coronal, or oblique planes are the simplest of the post-processing techniques. These can be helpful in localizing masses or disease to a specific space or organ. For example, the origin of a mass located between the liver, adrenal, and right kidney may be more convincingly demonstrated on a longitudinal reformation. Clinicians particularly appreciate coronal images, which they can quickly assimilate. Curved planar reformations may be helpful in placing the entire extent of a single object with a tortuous or curving course on a single image (Fig. 6.6). The term “three-dimensional” is used to describe such techniques as surface rendering, maximum intensity profile, and volume rendering. This is a bit misleading as the images created with all these techniques are not actually three-dimensional but rather two-dimensional projections of a three-dimensional object, similar to a radiograph (33). The three are very different; each has advantages and disadvantages. Surface renderings, also known as shaded surface display (SSD), can be used to visualize selected objects such as vessels or organs from different projections. First, the object of interest is defined by setting cutoff values to define the object by including only pixels of a certain density. A mathematical model is then created of the surface of the object. At this point the size of the dataset is greatly diminished, as each pixel is either positive (defining the object surface) or negative (not on the object surface). This object is then illuminated with a virtual light source; the reflections and shadings on the image give the impression of three-dimensionality. The cutoff values chosen are critical as they can significantly change the size of the object, for example, the degree of a stenosis. This technique removes all gray-scale information: calcified plaques will be indistinguishable from adjacent luminal contrast. Maximum intensity projection (MIP) techniques are simple and particularly suited for angiographic simulation procedures (34). For each imaging direction or view, parallel rays are passed through the imaged volume (the group of axial CT images) and the maximum CT number encountered along each ray is displayed. The remainder of information along that ray is discarded, again greatly reducing the computing power needed to perform this technique. Differentiation between foreground and background is not possible on a single MIP image. To achieve a three-dimensional effect one must view a series of MIP images from different angles. Important advantages over SSD technique include lack of threshold dependency and preservation of attenuation differences (34). Volume rendering techniques add the advantages of shaded surface and MIP techniques with a variety of effects such as semitransparent views, improved surface definition and virtual endoscopic displays (35). In this technique, each voxel is assigned to one of several groups based upon its number. This allows the relationships be-

Chapter 6 Computed Tomography in Vascular Disease

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B

A FIGURE 6.6 Curved planar reformations are used to demonstrate an entire structure that does not lie in a single plane. (A) Axial image with line (arrowheads) demonstrating the path chosen for the reformatted curved coronal image hepatic artery. (B) Curved sagittal image demonstrating the common hepatic (cha) and proper hepatic (pha) arteries as well as the celiac artery (ca), superior mesenteric artery (sma), and gastroduodenal artery (gda).

tween vessels and viscera to be preserved and displayed. A histogram of voxel densities is automatically obtained with each peak representing a specific material. The probability that a single voxel belongs to a specific group is calculated based upon a Gaussian distribution of densities for each material (36,37). Inaccuracies created by the choice of threshold level in SSD and the frequent requirement of editing in MIP are avoided. Volume rendering displays the volume of data in its entirety, unlike both SSD and MIP which discard the majority of data (38). This fact indicates the greatest disadvantage of volume rendering: it requires significantly faster and more sophisticated computer technology. One of the most exciting and clinically used applications of the three-dimensional techniques is CT angiography (CTA) (39,40). Using specially tailored acquisitions and the three dimensional techniques described above, clinical questions which previously required angiography may be answered by CT with decreased cost, decreased invasiveness and decreased inconvenience to the patient. The principles involved are simple: intravenous contrast material is injected and a helix is obtained through the body part of interest while the contrast is predominately in the vessels of interest. Post-processing is then performed to view the vessels in orientations analogous to conventional angiograms (Fig. 6.7). Although all the data is available on the original axial images, the reconstructions and CTA frequently present the information in a more practical, efficient, and useful format. Meticulous technique is required to obtain highquality CTAs. The contrast material must be injected at high rates, usually 4 to 5 mL/s. A timing bolus is helpful to assure that the start of the helix is coordinated with the passage of the bolus. The length of the scan is generally

limited by either the patient’s breath-holding ability or tube heating. Therefore, planning the helix is usually a trade-off between the length of the region to be scanned and slice thickness: a thinner collimation will improve resolution but decrease the volume scanned. Most vascular applications with multidetector scanners use a slice width of 1 to 3 mm. Overlapping reconstructions reduce stair step artifact; a 50% overlap is adequate. Post-processing may use MIP, SSD, or volume-rendering techniques as described above. It is important to interpret these postprocessed images in conjunction with the original axial images, as otherwise basic advantages of CT over conventional angiography such as thrombus, wall, and adjacent organ evaluation are lost (34). Interpretation Principles The conventional approach to CT interpretation is based on “hard-copy” film. In general, a standard 14- to 17-inch film is filled with between 12 and 24 images. Images that are displayed with standard window width and level settings appropriate for differentiation of solid, fluid and aircontaining structures (“body window,” level = 40 to 70, width = 380 to 550) may not be adequate to evaluate vascular structures. With rapid bolus administration, the contrast within the arteries may be so dense that luminal irregularities including intimal flaps may be obscured. Unfortunately, owing to the wide variability of density within the vessels, no standard “vascular” window setting can be set. In general, the level should be raised (80–120) and the width increased (600–1000). A number of forces are conspiring to change interpretation from a film-based environment to “soft-copy” or monitor-based environment. The number of images obtained in multidetector vascular CT studies is frequently

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B

A FIGURE 6.7 CT Angiography. The source images (not shown) were obtained in the axial plane with a 1.25-mm collimation and 1-mm increment during the injection of intravenous contrast at 4 mL/s. (A) Shaded surface display (SSD) of the kidneys and major vessels in a patient with an occluded right common iliac artery. The celiac artery and branches, SMA and IMA are well demonstrated anterior to the aorta. (B) Maximum intensity projection (MIP) created from the same dataset. Only the portions of the SMA, IMA, and celiac branches not lying in projection with the aorta are seen on this projection; one must view MIP images from multiple angles to clarify overlapping structures. However, the calcified plaques not identified on the shaded surface display are visualized.

in the range of 250 to 500. Multiple-phase acquisitions lead to the creation of even more images. This increases both cost and inconvenience as multiple sheets of film are produced. CT interpretation is moving from image analysis to volumetric analysis; this has been defined as the treatment of data not as a stack of images but as a volume of voxels (41). Dosimetry The radiation dose calculation for CT is complex (42). Important principles include: 1. 2.

3.

the dose is administered only to a certain volume of the body, not to the entire patient; the dose can vary considerably from scanner to scanner and from image to image depending on the technical factors set; and the percentage of the dose delivered centrally compared with the skin dose is much greater with CT than with conventional radiography (3,4).

In general, the effective dose in a conventional CT of the abdomen is greater than that of conventional radiographs, generally in the range of 5 to 15 millisieverts (mSv) (43). Because of this, it is important to keep the number of sections obtained as low as possible while filling the diagnostic need (44). Dosimetry considerations are essentially the same with helical and conventional techniques (4). Multidetector CT has inherent inefficiencies, including septa between detector rows, which do not collect data, and loss of use of the radiation penumbra.

Clinical Applications Thoracic Aorta The thoracic aorta can be visualized by a number of modalities including angiography, computed tomography (CT), magnetic resonance imaging (MRI), and transesophageal echocardiography (TEE). Before the 1990s, angiography was considered the gold standard for evaluation of the thoracic aorta for dissections and aneurysms, but advances in technology have led to angiography being replaced by these noninvasive studies as the initial test of choice for evaluating the thoracic aorta. A landmark study in 1993 demonstrated that MRI, TEE, and CT have similar sensitivities for the detection of thoracic aortic dissections, at 98.3%, 97.7%, and 93.8% respectively. MRI was found to have the highest specificity at 97.8%, as compared to CT at 87.1% and TEE at 76.9% (45). A more recent study demonstrated that sensitivity for all three modalities approaches 100%, and CT is superior to both MRI and TEE in the assessment of the supra-aortic branches involved in aortic dissection (46). Despite having somewhat better sensitivity and specificity for thoracic aortic dissections, MRI is limited by its availability and slower image acquisition. The use of TEE has also been limited by its availability, as well as operator variability. It is for these reasons that spiral CT has become the test of choice for the evaluation of thoracic aortic dissection at most medical centers (47,48). The pathognomonic finding for thoracic aortic dissection on CT is two adjacent contrast-filled lumens, which represent a patent true lumen and the false lumen

Chapter 6 Computed Tomography in Vascular Disease

(Fig. 6.8). The two lumens are separated by a thin band termed the intimal flap. The intimal flap can have unusual characteristics which are detected by CT, including partial thrombosis, a circular orientation down the aorta, or multiple false channels. CT is also effective for visualizing more subtle signs of dissection such as internal displacement of intimal calcium, mural thickening, ischemia of end organs supplied by aortic branches, or a left pleural effusion (48). CT also demonstrates the course of the intimal flap in relation to the aortic arch and branch vessel ostia, which is vital for planning surgical repair (49). The major limitations of CT for thoracic aortic dissection are technical factors which can cause a false-positive reading. These include improper timing of contrast injection, aortic wall or cardiac motion, streak artifacts, and periaortic structures. In the future, continual advances in imaging technology, combined with the knowledge of an experienced radiographer, will eliminate many of these factors (50). Thoracic aortic aneurysms can be found in many varieties based on location, shape, and etiology. Approximately 75% of all thoracic aneurysms occur in the descending aorta and are fusiform in shape with an etiology of atherosclerotic disease. Previously, the gold standard for diagnosis and surgical planning of thoracic aortic aneurysms was contrast aortography. Aortography in many studies has been found to underestimate aneurysm size as a result of mural thrombus, and does not provide detail regarding mediastinal hematoma or anatomical relationship of the aneurysm to other mediastinal structures. Spiral CT has now become the primary imaging modality for the evaluation of thoracic aneurysms. The wall of the aneurysm is easily identified by intramural cal-

FIGURE 6.8 Type A or ascending aortic dissection with intimal flap seen in both the ascending and descending thoracic aorta.

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cifications allowing for accurate size measurement. CT also allows for evaluation of the extent of mural thrombus and aneurysm wall for a contained leak, as well as any associated dissection, distal embolization, or pleural effusion (51). Although arteriography remains the gold standard for evaluating traumatic disruption to the thoracic aorta, recent studies demonstrate the expanding role for CT in the diagnosis of such injuries. A prospective 1998 study found that for blunt aortic injury, helical CT had 100% sensitivity compared with 92% for aortography, and specificity for helical CT was 83% compared with 99% for aortography (52). While most centers continue to use aortography for the diagnosis of traumatic aortic injuries, many centers are expanding the role of CT to evaluate for aortic injury in patients with a normal mediastinum on chest roentgenogram but with a suggestive mechanism (53). Overall, CT has become the principal imaging modality for the evaluation of vascular disease of the thoracic aorta. CT has essentially replaced contrast arteriography in the diagnosis of thoracic aortic dissections and aneurysms, and appears to have an emerging role in the evaluation of traumatic thoracic aortic injuries.

Abdominal Aorta The role of CT in abdominal aortic aneurysm (AAA) disease emerged in the 1980s, and CT has been instrumental in the development and clinical application of endovascular repair of AAA in the 1990s. Abdominal ultrasound remains an effective screening modality for AAA disease, but CT has emerged as the primary method of measuring AAA, following rate of aneurysm expansion, and planning for both open and endovascular surgical repair. At the majority of medical centers CT is the sole imaging technique for patients with uncomplicated AAA, and aortography is reserved for the subset of patients with abnormal anatomy, juxtarenal, supraceliac, and complex aneurysms. The characteristic findings of AAA on CT are dilation of the calcified wall of the aortic wall with varying degrees of surrounding thrombus (54). CT is crucial in demonstrating characteristics of AAA requiring more emergent intervention. Evidence of disruption of calcifications with obliteration of surrounding soft tissue may denote aneurysm rupture (55). CT can also demonstrate thickening of the aortic wall and adherence to surrounding structures characteristic of inflammatory AAA (Fig. 6.9). Evidence of eccentric thickening of aortic wall with intramural air is seen in mycotic aneurysms (56). In addition, CT is the imaging method used following open repair to assess graft function as well as complications including perigraft infections and anastomotic aneurysms. The development and rapidly expanding clinical use of endovascular stent–grafts for AAA repair, in the 1990s and present, has been made possible by major advances in CT technology and computer imaging software. The selection of candidates for endograft repair and the subse-

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FIGURE 6.9 Late inflammatory abdominal aortic aneurysm. Contrast enhancement of the aortic wall is easily seen.

length measurements, within the aorta and in tortuous iliac arteries, that are crucial to proper graft sizing and success of the endovascular repair. Another novel technique, coined the “virtual graft” by Fillinger, employs advanced computer imaging to simulate a three-dimensional endograft and display that graft within a three-dimensional reconstruction of the patient’s aorta, to plan the repair and investigate possible complications (Fig. 6.11) (57). Just as CT is vital in the selection of patients and the planning of endovascular AAA repair, it is equally important for the postoperative evaluation of the endograft repair. Despite the precision in the planning of endograft repair, a significant number of life-threatening postoperative complications do occur. These complications include aneurysm enlargement, endoleak, stent deformation, and graft migration. Spiral CT combined with radiographs and Doppler ultrasound are commonly accepted as the gold standard for long-term follow-up after endograft AAA repair for the detection of late complications (58,59).

Iliac Arteries

FIGURE 6.10 With multiplanar reconstruction, accurate measurement of aortic length can be made. The transaxial image is used to determine aortic diameter for endoplacement.

quent selection of endograft sizing requires multiple precise measurements. These measurements include the length and diameter of the proximal neck of the aorta, the length and diameter of the distal cuffs, and distance from the lowest renal artery to the most distal aspect of the graft limbs (Fig. 6.10). These measurements require precision to less than 1 mm, with serious consequences for any error in graft sizing, including endoleak leading to aneurysm rupture as well as migration of the stent (Fig. 6.16). Novel techniques combining spiral CT and multiplanar reformatting have led to the development of CT angiography, allowing for precise three-dimensional reconstructions of the aorta and its branches. In addition, computer software combined with reconstructed images allows for precise

Iliac artery aneurysms are uncommon, and account for approximately 2% of all abdominal aneurysms (60). Iliac artery aneurysms have a wide range of clinical presentation, making diagnosis challenging, but with the prevalence of CT the detection of iliac aneurysms has increased in frequency (61). The high rate of rupture and associated mortality with aneurysms larger than 4 cm necessitates prompt and accurate imaging for diagnosis, as well as follow-up. The traditional approach for the diagnosis of iliac artery aneurysms has been either arteriography or duplex ultrasound. The use of CT in the diagnosis and surgical planning for iliac aneurysms is widely accepted. Studies demonstrate that there is excellent correlation between ultrasound and spiral CT in determining the size of iliac aneurysms, with ultrasound underestimating aneurysm size by 0.03 cm (62). Prior to the development of endovascular grafts, large or symptomatic iliac aneurysms were repaired using an open procedure. There has been significant experience in the treatment of isolated iliac aneurysms using endovascular grafts, and the early results have been excellent with an average decrease in the size of aneurysm of 0.516 cm per year after endograft repair (63). Just as advanced CT imaging is intrumental in the preoperative and postoperative management of endograft repair of AAA, it now has the same role in the diagnosis, operative planning, and postoperative followup for both open and endovascular repair of iliac artery aneurysms.

Peripheral Arteries Vascular pathology of the femoral and popliteal arteries can be accurately visualized by CT. Recent studies have explored the use of CT angiography for evaluating lower extremity peripheral vascular occlusive disease. One

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A

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B

FIGURE 6.11 Virtual reconstruction of the aorta (A) with proposed endograft replacement (B). (Reconstruction provided by Mark Fillinger, M.D. and Medical Media Services.)

study demonstrated CT angiography to be highly accurate in diagnosing occlusion of the femoral artery, popliteal artery, and tibial artery with sensitivities of 100%, 100%, and 94%, respectively. Overall, these studies have shown that CT angiography is not as accurate as conventional angiography in the evaluation of lower extremity vascular disease, but in the future CT angiography may become a reliable noninvasive technique for evaluating for vascular occlusive disease in the lower extremities (64,65). Spiral CT has become widely regarded as a valuable technique for the diagnosis of popliteal artery entrapment syndrome (PAES) and cystic adventitial disease of the femoral and popliteal artery (Fig. 6.12). These are important diagnoses to consider in young healthy patients presenting with claudication. In one study of 45 patients with popliteal arteriopathies, CT diagnosed 98% of the disorders while arteriography diagnosed only 70%. This study also demonstrated that CT detected popliteal artery entrapment in three patients, while arteriography failed to diagnose two of the three patients due to arterial occlusion. In addition, this study found CT effective in diagnosing three cases of adventitial cystic disease of the popliteal artery, while angiography detected disease in only one of these three patients (66). CT findings of PAES vary depending on the anatomic variant, but in the most common variant CT demonstrates that the popliteal artery and vein

FIGURE 6.12 Popliteal artery entrapment. Notice muscle band passing between the artery and vein on the left. Normal artery–vein relationship is on right.

are separated by a muscle band or the displacement of the lateral head of the gastrocnemius muscle medially. Findings of adventitial cystic disease of the femoral or popliteal artery include localized eccentric fluid-filled dilation that does not enhance with contrast. Not only does CT assist in the diagnosis of these unique vascular diseases, it defines the surrounding muscular and fascial planes to assist in planning surgical repair.

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Vena Cava and Mesenteric Venous System

Carotid Arteries

Occlusion of the inferior vena cava (IVC) can be caused by both intrinsic and extrinsic diseases. CT is sensitive for thrombosis of the IVC and tumors, but poorly visualizes the intrahepatic portion of the IVC. It is for this reason that multiple imaging modalities, including vena cavography and MRI, are required for evaluation of disease of the IVC. CT offers the advantage of identifying congenital abnormalities such as duplication of the cava, circumaortic and retroaortic renal veins, and left-sided IVC prior to operative procedures. CT accurately visualizes the portal, splenic, and superior mesenteric veins, and is the diagnostic imaging test of choice of many centers for mesenteric venous thrombosis (Fig. 6.13) (67). Pathognomonic finding of mesenteric venous thrombosis on CT includes marked edema of the mesentery with bowel wall thickening, and an enlarged mesenteric vein with a low-density center surrounded by an enhancing wall.

The imaging modalities of choice for evaluating carotid artery stenosis over the past several decades have been contrast angiography and duplex ultrasound (DU). In fact, many carotid endarterectomies are performed based solely on the results of duplex ultrasound. A recent study from Duke University investigated the accuracy of noninvasive studies of carotid artery stenosis, including MRA, DU, and CT angiography (CTA), versus contrast angiography. Due to the infrequent use of CTA at their institution they compared only DU and MRA to conventional angiography. They found that DU alone misclassified the degree of carotid stenosis in 28% of patients, while MRA alone misclassified the degree of stenosis in 18% of patients (68). Another study comparing CT angiography to conventional angiography found overall agreement between CTA and angiography for carotid stenosis in 89% of patients, and determined that using the twodimensional transverse CT with volume rendering technique provided the highest accuracy (69). A second study, using NASCET > 60% as an indicator for carotid disease, found that, compared to contrast angiography, CTA had a sensitivity of 87%, specificity of 90%, and accuracy of 89% (70). While these studies indicate that cautious decisions to proceed with surgery should be made when based solely on noninvasive imaging of the carotid artery, they also demonstrate that with continued advances in CT technology there may be an emerging role for CT angiography in the evaluation of carotid disease in the future.

Peripheral Veins Duplex ultrasound remains the gold standard for imaging of the deep veins of the leg for deep vein thrombosis, and due to cost there is little role for CT in the evaluation of the deep venous system. CT has a significant role in the identification and characterization of congenital arteriovenous malformations (AVM) of the lower extremities. Owing to the complexity of these malformations, they are best evaluated with multiple imaging modalities such as contrast angiography, CT, and MRI. While arteriography is important for defining the vessels feeding the AVM, CT is important in demonstrating muscle group involvement and fascial planes. One limitation of CT in the evaluation of AVMs is in those that are highly cellular where there is little contrast enhancement, leading to underestimation of the full extent of the malformation.

FIGURE 6.13 Mesenteric venous thrombosis is diagnosed on CT by 1) nonenhancing superior mesenteric vein with enhancing vein (arrow); 2) edema of the mesentery; and 3) bowel wall thickening.

Thoracic Outlet The thoracic outlet is a complex anatomic region. Symptoms may arise for compression of the subclavian artery and vein and brachial plexus. Because of the complex interrelationship between muscles and neurovascular structures, spiral CT is particularly helpful in the diagnosis and perioperative planning. Matsumura and colleagues demonstrated the utility of sagittal and three-dimensional reconstruction in normal individuals and in patients with thoracic outlet symptoms (71). Three-dimensional CT reconstruction provides an accurate detailed picture of cervical and abnormal first ribs. In addition, muscular hypertrophy of the scalene muscle can be seen in thin athletic patients. Sagittal reconstruction was performed before and after abduction and external rotation of the arm (Fig. 6.14). Abduction and external rotation allows the clavicle to pass upward on the first rib, producing occlusion of the subclavian vein, followed by subclavian artery occlusion. Three-dimensional CT reconstruction may also demonstrate abnormalities of the clavicle. Malunion and callous formation of the clavicle compromises the costoclavicular space, producing neurovascular compromise of the thoracic outlet (Fig. 6.15). Unfortunately, this technique is not useful in patients with neurogenic thoracic outlet. For

Chapter 6 Computed Tomography in Vascular Disease

a patient who presents with neurologic thoracic outlet, compromise of the arterial circulation during abduction and external rotation may be demonstrated on the helical CT scan.

FIGURE 6.14 CT scan for TOS is performed with a venous contrast injection with the arm at the side (A) and with the arm abducted and externally rotated (B). Note the occlusion of the subclavian vein (arrows).

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Comments The continued technical advancements made in computed tomography scanners and the computer software used for image acquisition have dramatically changed the way vascular surgeons diagnose and treat a variety of vascular diseases. Vascular surgeons and radiologists now have at their disposal the ability to rapidly and noninvasively obtain and reconstruct CT angiographic and threedimensional images of virtually the entire vascular anatomy. In combination with revolutionary technological advances in endografts, computed tomography has been essential in introducing the discipline of vascular surgery to the era of endovascular surgery. In this era of endovascular surgery, the vascular patient is able to benefit from shortened hospital stays and postoperative recovery time, as well as significant reduction in the comorbidities associated with open operative procedures. Postoperative CT surveillance is important to detect endoleaks (Fig. 6.16).

Future Directions

FIGURE 6.15 Right clavicular fracture with callus formation which compromises the costoclavicular space.

The quality of CT scans will continue to improve with faster software acquisition. However, the most important clinical development is the use of CT scanned images to calculate areas of high wall stress. Concurrent work by Fillinger and Vorpe have used finite element analysis for spiral CT scans to create models to estimate areas of high shear stress and high wall tension. Based on these studies, it is possible that in the future we shall be able to predict which small aneurysms are likely to progress to rupture. Some examples of high wall tension are illustrated in Figure 6.17. The everyday use of such tools will be invaluable. Similarly, findings of high wall tension may be helpful to better design endovascular grafts.

FIGURE 6.16 Late endoleak: notice contrast in aneurysm sac.

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FIGURE 6.17 Finite element (computational stress) analysis may be useful in determining the degree and distribution of mechanical forces or stresses acting on the wall of individual AAA. Shown here are the distributions of wall stresses on the posterior and anterior abdominal aortic walls of six different 3-D reconstructed AAAs and one nonaneurysmal control aorta. Gray-colored regions are those with artificially high stress concentrations due to edge effects. The scale provides stress magnitude. (Figure provided by David Vorp.)

Chapter 6 Computed Tomography in Vascular Disease

References 1. Friedland GW, Thurber BD.: The birth of CT. AJR 1996; 167: 1365–1370. 2. Hounsfield GN. Computed medical imaging. Nobel lecture, December 8, 1979. J Comput Assist Tomogr 1980; 4; 665–674. 3. Wiesen EJ, Miraldi F. Imaging principles in computed tomography. In Haaga JR, Lanzieri CF, Sartoris DJ (eds): Computed tomography and magnetic resonance imaging of the whole body. St. Louis: Mosby-Year Book, 1994: 3–25. 4. Barnes GT, Lakshminarayanan AV. Conventional and spiral computed tomography—physical principles and image quality considerations. In: Lee JKT, Sagel SS, Stanley RJ (eds): Computed body tomography with MRI Correlation. Philadelphia: Lippincott-Raven, 1998: 1–20. 5. Heiken JP, Brink JA, Vannier MW. Spiral (helical) CT. Radiology 1993; 189: 647–656. 6. Seeram E. Computed tomography—physical principles, clinical applications and quality control. Philadelphia: W.B. Saunders Company, 1994: 125–138. 7. Barnes JE. Characteristics and control of contrast in CT. Radiographics 1992; 12: 825–837. 8. Garrett JS, Higgins CB, Lipton MJ. Computed axial tomography of the heart. Int J Cardiac Imaging 1985; 1: 113–126. 9. Sheedy PF, Welch TJ, Breen JF. Electron beam CT: status. In Fishman EK, Federle MP, eds. Body CT categorical course syllabus. American Roentgen Ray Society 1994: 73–76. 10. Kalender WA, Seissler W. Vock P. single-breathhold spiral volumetric CT by continuous transport and continuous scanner rotation. Radiology 1989; 173(P): 414. 11. Zeman RK, Fox SH, et al. Helical (spiral) CT of the abdomen. AJR 1993; 160: 719–725. 12. Towers MJ. Spiral or helical CT? [letter]. AJR 1993; 161: 901. 13. Herts BR, Einstein DM, Paushter DM. Spiral CT of the abdomen: artifacts and potential pitfalls. AJR 1993; 161: 1185–1190. 14. Zeman RK, Zeiberg AS, et al. Routine Helical CT of the abdomen: image quality considerations. Radiology 1993; 189: 395–400. 15. Brink JA, Heiken JP, Balfe DM. Spiral CT: decreased spatial resolution in vivo due to broadening of sectionsensitivity profile. Radiology 1992; 185: 469–474. 16. Polacin A, Kalender WA, Marchal G. Evaluation of section sensitivity profiles and image noise in spiral CT. Radiology 1992; 185: 29–35. 17. Kalender WA. Technical foundations of spiral CT. Seminars in Ultrasound, CT and MRI 1994; 15: 81–89. 18. Urban BA, Fishman EK, et al. Detection of focal hepatic lesions with spiral CT: comparison of 4- and 8-mm interscan spacing. AJR 1993; 160: 783–785. 19. Foley WD. Technology/contrast: current state of the art. In Fishman EK, Federle MP (eds). Body CT categorical course syllabus. American Roentgen Ray Society 1994: 1–4. 20. Hu H, He HD, et al. Four multidetector-row helical CT: image quality and volume coverage speed. Radiology 2000; 215: 55–62.

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21. Rydberg J, Buckwalter KA, et al. Multisection CT: scanning techniques and clinical applications. Radiographics 2000; 20: 1787–1806. 22. Siegelman SS. Four-dimensional imaging. Radiology 1998; 207: 565. 23. Kalender WA. Thin-section three-dimensional spiral CT: is isotropic imaging possible? Radiology 1995; 197: 578–580. 24. Katayama H, Yamaguchi K, Kozuka T. Adverse reactions to ionic and nonionic contrast media: a report from the Japanese committee on the safety of contrast media. Radiology 1990; 175: 621–628. 25. McClennan B. Ionic and nonionic iodinated contrast media: evolution and strategies for use. AJR 1990; 155: 225–233. 26. Stockberger SM, Hicklin JA, et al. Spiral CT with ionic and nonionic contrast material: evaluation of patient motion and scan quality. Radiology 1998; 206: 631–636. 27. Oliver JH, Baron RL. Helical biphasic contrast-enhanced CT of the liver: technique, indications, and pitfalls. Radiology 1996; 201: 1–14. 28. Garcia PA, Bonaldi VM, et al. Effect of rate of contrast medium injection on hepatic enhancement at CT. Radiology 1996; 199: 185–189. 29. Sheafor DH, Keogan MT, et al. Dynamic helical CT of the abdomen: prospective comparison of pre- and postprandial contrast enhancement, Radiology 1998; 206: 359–363. 30. Bae KT, Heiken JP, Brink JA. Aortic and hepatic contrast medium enhancement at CT Part II. Effect of a reduced cardiac output in a porcine model. Radiology 1998; 207: 657–662. 31. Silverman PM, Roberts SC, et al. Assessment of a technology that permits individualized scan delays on helical hepatic CT: A technique to improve efficiency of contrast material. AJR 1996; 167: 79–84. 32. Silverman PM, Brown B, et al. Optimal contrast enhancement of the liver using helical (spiral) CT of the liver: Value of Smart Prep. AJR 1995; 164: 1169–1171. 33. Hemmy DC, Zonneveld FW, et al. A decade of clinical three-dimensional imaging: a review. Part I. Historical development. Invest Radiol 1994; 29: 489–496. 34. Prokop M, Shin HO, et al. Use of maximum intensity projections in CT angiography: a basic review. Radiographics 1997; 17: 433–451. 35. Fishman EK, Magid D, et al. Three-dimensional imaging. Radiology 1991; 181: 321–337. 36. Ney DR, Drebin RA, Fishman EK. Volumetric rendering of computed tomographic data: principles and techniques. IEEE Comput Graphic Appl 1990; 10: 24–32. 37. Johnson PT, Heath DG, et al. Three-dimensional CT: real-time interactive volume rendering. AJR 1996; 167: 581–583. 38. Kuszyk BS, Heath DG, et al. CT angiography with volume rendering: imaging findings. AJR 1995; 165: 445–448. 39. Zeman RK, Silverman PM, et al. CT angiography. AJR 1995; 165: 1079–1088. 40. Rubin GD, Dake MD, et al. Three-dimensional spiral CT Angiography of the abdomen: initial clinical experience. Radiology 1993; 186: 147–152. 41. Rubin GD, Napel S, Leung AN. Volumetric analysis of volumetric data: achieving a paradigm shift. Radiology 1996; 200: 312–317.

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42. Rothenberg LN, Pentlow KS. AAPM Tutorial: radiation dose in CT. RadioGraphics 1992; 12: 1225–1243. 43. Huda W. Radiation dosimetry in diagnostic radiology. AJR 1997; 169: 1487–1488. 44. Mini RL, Vock P, Mury R. Radiation exposure of patients who undergo CT of the trunk. Radiology 1995; 195: 557–562. 45. Nienaber CA, von Kodolitsch Y, et al. The Diagnosis of Thoracic Aortic Dissection by Noninvasive Imaging Procedures. N Engl J Med 1993; 328: 1–9. 46. Sommer T, Fehske W, et al. Aortic dissection: a comparative study of diagnosis with spiral cT, multiplanar transesophageal echocardiography, and MR imaging. Radiology 1996; 199: 347–352. 47. Torossov M, Singh A, Fein SA. Clinical presentation, diagnosis, and hospital outcome of patients with documented aortic dissection: The Albany Medical Center Experience, 1986 to 1996. Am Heart J 1999: 137: 154–161. 48. Urban BA, Bluemke DA, et al. Imaging of thoracic aortic disease. Cardiol Clin 1999; 17: 659–682. 49. Hansmann HJ, Dobert N, et al. Various spiral CT protocols and their significance in the diagnosis of aortic dissections: results of a prospective study. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb 2000; 172: 879–87. 50. Batra P, Bigoni B, et al. Pitfalls in the diagnosis of thoracic aortic dissection at CT angiography. Radiographics 2000; 20: 309–320. 51. Ledbetter S, Stuk JL, Kaufman JA. Helical CT in the evaluation of emergent thoracic aortic syndromes. Radiol Clin N Am 1999; 37: 575–589. 52. Fabian TC, Davis KA, et al. Prospective study of blunt aortic injury: Helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg 1998; 227: 666– 667. 53. Wall MJ, Hirshberg A, et al. Thoracic aortic and thoracic vascular injuries. Surg Clin N Am 2001; 81: 1375– 1393. 54. Papanicolaou N, Wittenberg J, et al. Preoperative evaluation of abdominal aortic aneurysms by computed tomography. AJR 1986; 146: 711. 55. Flinn WR, Courtney DF, et al. Contained rupture of aortic aneurysm. In Bergan JJ, Yao JST (eds). Aortic surgery. Philadelphia: WB Saunders, 1989: 341–350.

56. Wadlington VR, Nemcek AA, et al. CT and MR imaging of imflammatory abdominal aortic aneurysms. RNSA 1992; 185(P): 258. 57. Fillinger, MF. New Imaging Techniques in Endovascular Surgery. Surg Clin N Am 1999; 79: 451–475. 58. Fillinger MF. Postoperative imaging after endovascular AAA repair. Semin Vasc Surg 1999; 12: 327–338. 59. Eskandari MK, Yao JS, et al. Surveillance after endoluminal repair of abdominal aortic aneurysms. Cardiovasc Surg 9: 469–71, 2001. 60. Best IM, Vansandani G, Bumpers HL. Complications of isolated bilateral iliac artery aneurysms. Am Surg 2001; 67: 767–771. 61 Soury P, Brisset D, et al. Aneurysms of internal iliac artery: management strategy. Ann Vasc Surg 2001; 15: 321–325. 62. Santilli SM, Wernsing SE, Lee ES. Expansion rates and outcomes for iliac artery aneurysms. J Vasc Surg 2000; 31 (1 Pt 1): 114–121. 63. Sahgal A, Veith FJ, et al. Diameter changes in isolated iliac artery aneurysms 1 to 6 years after endovascular repair. J Vasc Surg 2001; 33: 289–294. 64. Rieker O, Duber C, et al. Prospective comparison of CT angiography of the legs with intraarterial digital subtraction angiography. AJR 1996; 166: 269–276. 65. Walter F, Leyder B, et al. Value of arteriography scanning in lower limb artery evaluation: a preliminary study. J Radiol 2001; 82: 473–9. 66. Rizzo RJ, Flinn WR, et al. Computed tomography for evaluation of arterial disease in the popliteal fossa. J Vasc Surg 1990; 11: 112–119. 67. Morasch MD, Ebaugh JL, Chiou AC, Matsumura JS, Pearce WH, Yao JST. Mesenteric venous thrombosis — A changing clinical entity. J Vac Surg 2001; 34: 680–684. 68. Johnston, DC, Goldstein LB. Clinical carotid endarterectomy decision making: noninvasive vascular imaging versus angiography. Neurology 2001; 56: 1109–1015. 69. Verhoek G, Costello P, et al. Bifurcation CT angiography. J Comp Assist Tomogr 1999; 23: 590–596. 70. Cinat M, Lane CT, et al. Helical CT angiography in the preoperative evaluation of carotid artery stenosis. J Vasc Surg 1998; 28: 290–300. 71. Matsumura JS, Rilling WS, et al. Helical computed tomography of the normal thoracic outlet. J Vasc Surg 1997; 26: 727–735.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 7 Magnetic Resonance Angiography Jagajan Karmacharya, Omaida C. Velazquez, Richard A. Baum, and Jeffrey P. Carpenter

Preoperative imaging using contrast angiography is the traditional standard for evaluation of vascular disease. This conventional technique is associated with an overall complication rate of 8% (1,2) including bleeding, hematoma, pseudoaneurysm, pain at the arterial puncture site, temporary or permanent renal insufficiency, contrast allergy, and death. As many as 29% of patients with peripheral vascular disease have coexisting renal insufficiency (3), placing them at increased risk of renal complications with the use of nephrotoxic contrast. Magnetic resonance angiography (MRA) represents an evolving technique that noninvasively images flowing blood without dependence upon nephrotoxic contrast agents. It is a cost-effective method of preoperative evaluation of the carotid arteries, thoracic and abdominal aorta, pelvic and peripheral circulation as well as venous anatomy (4–9). MRA accurately identifies patent runoff vessels, including angiographically occult distal circulation. MR techniques are exceedingly sensitive and can image flow velocities as low as 2 cm/s. In addition to visual information, available software can be used to measure velocities of blood flow through arterial segments, thus obtaining hemodynamic information that can be useful in grading the degree of stenosis across a lesion (10). Many centers have replaced conventional contrast angiography with MRA in the preoperative evaluation of common vascular diseases, particularly for imaging of the lower extremity distal runoff (4).

Basic Principles Magnetic resonance imaging is based on the reaction of tissues to a magnetic force field with and without presaturation by repeated bursts of radiofrequency pulses. The hydrogen nuclei or protons that are naturally found in tissues generate the signals. The spinning protons of tissues generate a magnetic field that can be expressed as magnetic vectors. In the unstimulated state, the magnetic vectors are arranged randomly. In the presence of a strong magnetic field, these vectors are aligned along the axis of the magnetic force. A burst of radiofrequency pulse perturbs the normal spin axis of protons and, as these protons return to their aligned axis, a signal (spin echo) is generated. This signal is captured by detectors on an external transmit–receive coil, thus generating an image. The signal generated is related to the proton density of the specific tissue. MRA takes advantage of the dynamic nature of blood flow signals relative to stationary tissue signals. Magnetized blood flowing into the imaging slice generates a signal that appears brighter than the background as it enters the imaging tissue slice that has been saturated by repeated bursts of radiofrequency pulses (Fig. 7.1). Nonnephrotoxic contrast agents such as gadolinium, flowing within the circulation stream, can further enhance these signals. Since it depends on flow to produce the detected image, MRA is thus a physiologic rather than anatomic method of vascular imaging. These fundamental principles are the basis of the two primary methods of MRA that are currently in use:

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Information can be generated in both twodimensional (2-D) and three-dimensional (3-D) images. Data are acquired as axial slices and projected in two or three dimensions by computer reconstruction, utilizing sophisticated software.

Clinical Application

FIGURE 7.1 Two-dimensional time-of-flight technique relies on differences of saturation of tissue protons. Magnetized blood flowing into the imaging slice generates a signal that appears brighter than background.

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time-of-flight (TOF) angiography (11); phase contrast (PC) angiography (12).

The 2-D time-of-flight technique relies on differences of saturation of tissue protons in the flowing blood and the stationary soft tissue. Rapid and repeated radiofrequency irradiation (RF) results in saturation. These protons lack sufficient time to relax, resulting in a weak echo signal or what is termed “saturation.” If, however, the slice contains a blood vessel, fresh protons from flowing blood continually flow into the slice of tissue being imaged, thereby producing a bright echo signal in response to RF pulses (13). This signal can be exceedingly sensitive in revealing blood vessel pathology, even without contrast enhancement. Phase contrast (PC) angiography takes advantage of the change in phase of proton rotation as the hydrogen nuclei move through the magnetic field. This change in the phase is proportional to the velocity of the moving protons and to the size of the magnetic field gradient. Digital subtraction technology can eliminate background by a complex method of subtraction of the applied gradient. Thus flowing blood can be detected as an image and its velocity can be calculated. Selective imaging of arterial flow vs. venous flow can be easily accomplished using magnetic resonance angiography. Saturating the tissue below the slice of interest (inferior presaturation) allows blood flowing down into the slice from the unsaturated superior region (i.e., arterial blood) to yield a strong signal with TOF techniques. The presaturated venous blood returning from the inferior to the superior tissues yields a weak (not visualized) signal. By presaturating the tissue above the imaging slice (arterial inflow), venous imaging can be accomplished (magnetic resonance venography) (14). Available software can combine, process, and project the data in greatly detailed views.

When compared with conventional angiography techniques, magnetic resonance arteriography (MRA) avoids complications of arterial puncture, eliminates risk of iatrogenic renal failure, and has a greater sensitivity for identifying patent distal vessels in patients with severe peripheral vascular disease (4). Studies comparing conventional contrast angiography and MRA demonstrate excellent concordance rates (6). MRA, when compared with conventional angiography, has a high degree of accuracy in evaluating arterial stenoses of large- and mediumsize inflow vessels and small distal vessels. Furthermore, this evolving noninvasive technique provides a superior view of the spatial relationships around the vasculature, including information on plaque morphology, anomalous vascular anatomy, and adjacent parenchymal tissue (Fig. 7.2).

Carotid Artery Although carotid angiography is accepted as the reference standard for carotid imaging, recent studies suggest that noninvasive imaging may be more sensitive, costeffective, and safer than conventional angiography (7–9). Prospective comparisons of MRA and carotid angiography demonstrate an average sensitivity and specificity for high-grade lesions of 93% and 88% respectively (Fig. 7.3) (15,16). Interestingly, when direct comparisons of carotid angiography, duplex ultrasound, and MRA were made with surgical specimens, MRA and ultrasound correlated better with endarterectomy specimens than conventional angiography (17). Duplex ultrasound and MRA are sufficient to plan carotid endarterectomy (7,18). Depending on the projection angle, standard carotid angiography may underestimate short-segment stenoses or webs that are associated with complex surrounding ulcerated lesions. It is important to realize that MRA may overestimate the percentage of stenosis. This is related to complex flow patterns in and beyond the critical lesion. One can reduce the incidence of overestimation by interpreting data from the source images, by quantitative measurements of velocity, and by using 3-D acquisitions and gadolinium enhancement (4) in multiple projection angles (19). In addition, one should be familiar with the “MR signal drop-out” effect that is characteristic of highgrade stenosis as imaged by MRA (Fig. 7.3C). The flow gap generated by the disturbed flow beyond a lesion is a reliable indication of a high degree of stenosis and gives the appearance of a short segmental occlusion of the internal carotid artery.

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FIGURE 7.2 (A) MRA is a sensitive technique that reveals not only the underlying vascular pathology but also demonstrates the surrounding tissue/organ architecture. (B) A renal allograft is seen in the right hemipelvis. A short-segment stenosis is seen at the origin of the right external iliac artery, about 3 cm proximal to the anastomosis of the transplant renal artery. (C) The findings were confirmed by an operative angiogram, at which time the lesion was successfully dilated and stented, resulting in significant improvement in allograft function.

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FIGURE 7.3 (A) Conventional angiography images of the carotids demonstrating accurate correlation with the MRA TOF images. (B) Both studies demonstrate an ulcerated plaque producing about 60% stenosis in the proximal right internal carotid artery. (C) Carotid MRA demonstrating a segment of signal dropout at the origin of the left internal carotid artery, suggestive of a high-grade stenosis of the proximal right internal carotid artery.

Since carotid arteriography is associated with a significant stroke rate (20), many vascular surgeons reserve standard angiography for discordant ultrasound and MRA results or inconclusive MRA or US imaging. However, carotid angiography may add significant information in the setting of suboptimal noninvasive imaging, which may occur with unusual postsurgical or post-traumatic anatomy, metallic objects artifact, discordant gray scale, dampened waveforms, or the patient’s lack of tolerance for the test.

Coronary Vessels While the first clinical reports using MRA for imaging coronary arteries occurred a decade ago (13), widespread

clinical application of this modality for coronary imaging has been limited. This is due to specific challenges in obtaining optimal coronary images by MR, including small vessel size, tortuosity, overlapping epicardial fat signals, and artifact from breathing and cardiac motion (15,21–23). In addition, technical challenges related to patients’ tolerance for breath-holding, relatively slow rates of data acquisition, and signal void from metal artifact from intracoronary stents lead to decreased ability of coronary MRA to accurately identify coronary stenoses. Recent developments in both MR hardware and software have led to strategies to enable the visualization of proximal epicardial vessels (15). Current protocols use ECG gating techniques to minimize motion artifacts. The general approaches that have been described include con-

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ventional spin echo, segmented gradient-echo sequences, segmented turbo-FLASH, 3-D TOF, spiral acquisitions, and echo planar imaging (13,24–26). MRA visualization of proximal coronary vessels correlates well (>95%) with that of conventional angiography (13,27). Visualization of proximal coronary vessels is far superior to distal vessel imaging and severe stenoses are more accurately identified (27). MR imaging can detect a high proportion of severe stenoses but only a low proportion of moderate stenoses. The sensitivity and specificity of coronary MRA for detecting severe stenosis are 85% and 80% respectively. A moderate decrease in blood flow results in a significant decrease of sensitivity to 38% (26). The advantages of coronary arterial imaging with MR have been mostly noted in the visualization of anomalous coronary vessels (28). Although conventional angiography can show anomalous vessels, the position of the vessel relative to the aorta and adjacent organs can be difficult to appreciate. MRA can clearly demonstrate the passage of the anomalous vessels anterior or posterior to the aorta and their spatial relationship to nerves, venous and other parenchymal structures, making it a useful preoperative imaging tool (28,29). Overall, coronary MRA for identification of coronary stenoses is not generally accepted with the currently

existing technology. Further refinement of imaging techniques is necessary before coronary MRA will achieve widespread acceptance.

Aortic Arch and Thoracic and Abdominal Aorta MRA can delineate the aortic arch and its branches with a high degree of resolution (Fig. 7.4). Aortic dissections can be reliably diagnosed and classified as either type A (involving the ascending aorta) or type B (distal to the left subclavian artery) by MRA. MRA accurately demonstrates the relationship of branch arteries to true and false lumen anatomy as well as defining the proximal and distal extents of the dissection flap (Fig. 7.5). Non-nephrotoxic contrast agents such as gadolinium (Gd) have enhanced the accuracy of imaging the aortic arch and aortic branch vessels (renal and visceral abdominal arteries). 3-D TOF MRA is used for evaluation prior to thoracoabdominal as well as infrarenal aortic, renal, and visceral reconstructions. The use of contrast enhances the resolution of the signals, improving detection of branch disease. A prospective study of 63 patients with suspected visceral aortic disease showed that using breath-hold ultrafast 3-D Gd-enhanced MRA techniques

FIGURE 7.4 Dissection and occlusion of left common carotid artery seen by arteriography (A) and MRA (B). Anomalous aortic arch (bovine) shown by contrast arteriography (C) and MRA (D). (Reproduced by permission from J Vasc Surg 1997; 25(1): 147.)

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FIGURE 7.5 Gd-enhanced MRA shows (A) an aortic dissection flap originating just distal to the left subclavian artery (type B dissection), (B) the dissection flap extending into the left common iliac artery, (C) the left renal artery origin from the false lumen, and (D) the right renal artery, celiac, and superior mesenteric arteries originating from the true lumen.

FIGURE 7.6 (A) MRA shows a left internal iliac artery aneurysm. (B) Intraoperative angiogram confirms the finding which is then successfully treated percutaneously by an endovascular approach that included coiling of the aneurysm and covering the inflow to the aneurysm using a commercially available stent graft. (C) The sizing of the stent graft was designed from the MRA images.

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combined with 2-D TOF, MR could accurately identify and grade all (n = 51) renal, celiac, superior mesenteric, and inferior mesenteric artery stenosis or occlusions. The combined MRA imaging techniques have 100% sensitivity and specificity when compared with conventional angiography (30). MRA correctly predicts cross-clamping

site in 87%, proximal anastomotic site in 95%, need for renal revascularization in 91%, and the use of bifurcated graft in 75% of abdominal aortic aneurysm patients. MRA can also be successfully used as the sole imaging modality for aortic or iliac endoprosthetic devices (Figs. 7.6 and 7.7). In a prospective study of 96 consecutive pa-

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FIGURE 7.7 (A–C) Infrarenal abdominal aneurysm treated based on preoperative MRA. (D) Intraoperative angiograms confirming the MRA findings. (E) Completion arteriogram after successful endografting.

tients, data were collected using Gd-enhanced MRA preoperatively in place of conventional imaging for patients with renal insufficiency or history of contrast allergy (31). A total of 14 patients had their endograft designed solely on Gd-enhanced MRA. The frequency of intraoperative access failure, the need for proximal or distal extensions, the rate of conversion to open procedures, as well the incidence of endoleaks were equal in both the MRA-designed and control groups.

Renal Artery Stenosis MRA has been advocated for evaluation of renal arteries for the past decade. Initial techniques were limited due to motion artifact and limited spatial resolution. Earlier TOF MRA, when compared with conventional angiography, had 91% sensitivity, with a 94% negative predictive value. Overall diagnostic accuracy of these techniques was good (81%) (32); however, the detection of accessory renal artery was poor (14). Images and diagnostic accuracy have improved greatly with the use of Gd-enhanced MRA (Fig. 7.8). Sensitivities of 50% to 70% have been reported in the identification of accessory renal arteries (33). Use of breath-hold ultra-fast 3-D Gd-enhanced techniques has increased diagnostic yield of accessory renal

arteries to between 89% and 100% (34). This is primarily due to increased spatial resolution and larger field of view with these recent techniques. Reformating the 3-D volume acquisition of the vascular anatomy can provide useful preoperative information about aberrant arteries, degree of stenosis, aneurysms, and associated aortic dissections. In contrast, conventional angiography relies on oblique imaging planes to delineate a profile of the stenosis, making ostial lesions more difficult to be accurately studied, particularly in the setting where the total amount of potentially nephrotoxic contrast volume is restricted. Contrast-enhanced MRA techniques are not associated with contrast nephropathy and can be used safely in patients with renal insufficiency.

Peripheral Circulation Lack of filling distal to serial stenoses or occlusions and the presence of bony cortex hinder the ability of conventional angiography to detect small and diseased distal runoff vessels. MRA avoids the complications of arterial puncture, eliminates the risk of contrast-induced renal failure, and has been shown to have a greater sensitivity than contrast angiography for identifying distal runoff vessels in patients with severe peripheral arterial occlusive

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FIGURE 7.8 (A) MRA demonstrating right renal stenosis. (B) Cross-sectional view confirms the renal stenosis. (C) Arrows demonstrate celiac stenosis, SMA stenosis, and an aortic ulcer visualized by MRA. (D) MRA demonstrating normal aortoiliac arterial anatomy with normal visceral and renal branches. (E) Superimposed venous, arterial and parenchymal imaging information acquired by MRI/MRA/MRV.

disease (35). Recent refinements of magnetic resonance angiography have replaced conventional angiography in some centers. In studies of the aorta, iliac, and femoral inflow, MRA is highly concordant with conventional contrast angiography. MRA has a sensitivity of 99.6%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 98.5% in detecting patent segments, occluded segments, and hemodynamically significant stenoses of aortic, pelvic, and proximal femoral inflow vessels (4). The degree of arterial stenosis is measured with high accuracy by MRA compared with conventional angiography (36). Furthermore, MRA provides better information about spatial relationship of blood flow and plaque morphology than conventional angiography (15). This is mostly the result of sophisticated software processing of MRI/MRA data, providing enhanced views that may include 3-D reconstructions in multiple longitudinal projections and rotational views in addition to the 2-D cross-sectional and axial views. MRA can be used as the sole preoperative imaging modality for successful open vascular or endovascular interventions (Figs. 7.9 to 7.11). In one such study, outpatient MRA of the juxtarenal aorta imaged 80 consecutive patients with ischemic rest pain or tissue loss through the foot

(4). Intraoperative pressure measurements of proximal vessels and post-bypass arteriography were performed. Graft patency and limb salvage was evaluated using life table analysis. All patients underwent reconstructive procedures based on MRA alone (11 aortobifemoral and 67 infrainguinal procedures). The intraoperative findings and intraoperative completion arteriography confirmed the accuracy of inflow and outflow imaging by preoperative MRA. The limb salvage rate was 84% with a 21-month patency rate of 78% for infrainguinal reconstruction based on MRA alone, and was no different from that of a control group whose operations were planned with conventional contrast angiography (37). MRA can detect angiographically occult distal runoff vessels. In studies of lower extremity ischemia patients in which MRA and conventional angiography were compared, the detection of distal runoff vessels was superior with MRA. Operative exploration and intraoperative angiograms confirmed the preoperative evaluation by MRA (4). A subsequent investigation of the adequacy of these occult runoff vessels for use in limb salvage bypass procedures showed no significant differences in primary graft patency rate between bypasses planned using conventional angiography to those done to angiographically occult runoff vessels detected only by MRA (38).

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FIGURE 7.9 (A) MRA showing normal femoral arterial segments. (B) MRA demonstrating a short-segment stenosis and a more distal segmental occlusion of right superficial femoral artery (SFA). The left SFA shows mild diffuse disease.

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FIGURE 7.10 The use of bolus chase techniques can facilitate rapid imaging of the distal runoff where the (A) popliteal, (B) infrapopliteal, and (C) foot vessels are accurately visualized.

MRA can enhance the clinical accuracy when performed in addition to conventional angiography. In a blinded prospective study in six USA hospitals, MRA was compared to contrast angiography to evaluate severe lower limb atherosclerotic occlusive disease in candidates for percutaneous or surgical intervention (39). Sensitivity in distinguishing patent segments from occluded segments was 83% with contrast angiography and 85% in MRA. However, the inclusion of MRA preoperative planning resulted in a change of treatment plan for 13% of patients and provided superior overall diagnostic accuracy (86%). The improved accuracy related mostly to the increased sensitivity of MRA in identifying patent runoff vessels (48%) when compared with conventional angio-

graphy (24%) (40). MRA is most useful in the detection of patent runoff vessels of the distal segments. The detection of patent runoff vessels by MR which are not identified by conventional angiography can lead to improved limb salvage in 13% to 22% of cases (39–40). A meta-analysis of 34 studies indicated that MRA is highly accurate for assessment of lower extremity arteries (41). Techniques using 3-D Gd-enhanced MRA appear to be superior to 2-D methods and to contrast angiography. The superiority of MR techniques over traditional imaging techniques is due to characteristics of blood flow in diseased vessels and the sensitivity of MR for detection of slow flow (2 cm/s). Images from contrast angiography may not show distal vessels owing to multiple dilutions

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FIGURE 7.11 (A) Distal runoff as visualized by conventional angiography demonstrating a diseased posterior tibial artery. (B) MRA reveals that the anterior tibial and peroneal arteries are also patent. (C) Intraoperative arteriogram after bypass performed to an angiographically occult dorsalis pedis artery visualized preoperatively by MRA, but not by preoperative contrast arteriography. (Reproduced by permission from J Vasc Surg 1996; 23: 483–489.)

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and reconstitution of the contrast material as the bolus passes distally (Fig. 7.11). MRA can also be used as a sole preoperative imaging modality prior to endovascular procedures (42). A total of 119 consecutive patients underwent MRA for symptomatic leg ischemia. Intraoperative road-map arteriography was performed in patients that underwent endovascular procedures and compared to preoperative MRA images. There were no false positive or negative studies with MRA. A reduction in cost was also noted owing to the elimination of preoperative diagnostic arteriography.

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New Developments Research in MR techniques continues to improve successful clinical applications. Bolus chase techniques involve the movement of the scanner table in a stepwise manner to allow sequential imaging of a bolus during arterial transit (43). Using conventional angiograms as a reference standard, manual bolus chase has been demonstrated to have high sensitivity (93–94%) and specificity (97–98%) (43) for stenosis >50%.

Problems There are several well-recognized limitations of the use of MRA:

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Loss of signal due to presence of metallic objects. Presence of joint prosthesis and surgical clips cause large signal dropout artifacts. Segmental occlusion may be misdiagnosed and correlation with plain films may be necessary to identify metallic clips from previous procedures. MR incompatibility—risk for device displacement. Some recent endovascular devices that use stainless steel in covered stents for aortic aneurysm treatment represent a contraindication for the use of MR imaging. MR is also contraindicated in patients with pacemakers or retinal or intracranial metallic objects. Image degradation of horizontal vasculature. Thick slices in coronal reconstructions of 2-D images (that are obtained perpendicular to the long axis of the body) result in a string of diamond appearance of horizontal vessels. Thin slices and better image resolution reduce these artifacts. Lengthy period of data acquisition: Improvements in real-time MRA and bolus chase techniques decrease the length of time required for peripheral MRA studies. Existing MRA techniques have a number of flowrelated artifacts, due to signal loss or intravoxel dephasing, resulting in overestimation of the degree and length of arterial stenosis or signal dropout artifact. Pulsatile arterial flow can also result in ghosting artifacts in peripheral arterial evaluation. Contrast agents reduce these effects.

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Conclusion The time-honored method of contrast angiography is associated with inherent risks and limitations. Developments in noninvasive modalities offer potential benefits in diagnostic accuracy and reduction of costs and morbidity. MRA represents an evolving technology that offers promise as a noninvasive adjunct for vascular imaging. Individual centers must validate their MR data and interpretation against conventional arteriography techniques. The preoperative workup and eventual therapeutic plan can in many cases be successfully accomplished with the sole or adjunctive use of MR imaging in the treatment of vascular patients.

References 1. Hessel SJ, Adams DF, Abrams HL. Complications of angiography. Radiology 1981; 138: 273. 2. Sjejado WJ, Toniolo G. Adverse reactions to contrast media: a report from the Committee on Safety of Contrast Media of the International Society of Radiology. Radiology 1980; 137: 299. 3. D’Elia JA, Gleason RE, Alday M. Nephrotoxicity form angiographic contrast material—a prospective study. Am J Med 1976; 72: 719. 4. Carpenter JP, Owen RS, et al. Magnetic resonance angiography of the aorta, iliac, and femoral arteries. Surgery 1994; 116(1): 17–23. 5. Velazquez OC, Baum RA, Carpenter, JP Magnetic resonance angiography of lower—extremity arterial disease. Surg Clin North Am 1998; 78: 519–537. 6. Yin D, Baum RA, et al. The cost-effectiveness of magnetic resonance angiography in symptomatic peripheral vascular disease. Radiology 1995; 194: 757. 7. Kent KC, Kuntz KM, et al. Perioperative imaging strategies for carotid endarterectomy: an analysis of morbidity and cost-effectiveness in symptomatic patients. JAMA 1995; 274: 888–893. 8. Turnipseed WD, Kennell TW, et al. Combined use of duplex imaging and magnetic resonance angiography for evaluation of patients with symptomatic ipsilateral high-grade carotid stenosis. J Vasc Surg 1993; 17: 832– 839; discussion 839–840. 9. Polak JF, Kalina P, et al. Carotid endarterectomy: preoperative evaluation of candidates with combined Doppler sonography and MR angiography. Radiology 1993; 186: 333–338. 10. Schiebler ML, Listerud J, et al. MR arteriography of the pelvis and lower extremities. Magnetic Resonance Quarterly 1993; 9(3): 152. 11. Keller P. Time of flight magnetic resonance angiography. Neuroimaging Clin N Am 1992; 4: 639–656. 12. Dumoulin CL. Phase Contrast MR angiography techniques. Magn Reson Imaging Clin N Am 1995; 3: 399–411. 13. Edelman RR, Mattle HP, et al. Extracranial carotid arteries: evaluation with “black blood” MR angiography. Radiology. 1990; 177: 45–50. 14. Velazquez OC, Baum RA, Carpenter JP: Magnetic resonance imaging and angiography, Chapter 15. Rutherford Vascular Surgery, 5th edn.

15. Yucel EK, Anderson CM, et al. Magnetic resonance angiography: update on applications for extracranial arteries. Circulation 1999; 100: 2284–2301. 16. Mitt RL Jr, Broderick M, et al. Blinded-reader comparison of magnetic resonance angiography and duplex ultrasonography for carotid artery bifurcation stenosis. Stroke 1994; 25(1): 4–10. 17. Pan XM, Saloner D, et al. Assessment of carotid artery stenosis by ultrasonography, conventional angiography, and magnetic resonance angiography: correlation with ex vivo measurement of plaque stenosis. J Vasc Surg 1995; 21: 82–88. 18. Kuntz KM, Skillamn JJ, et al. Carotid endarterectomy in asymptomatic patients: is contrast angiography necessary? A morbidity analysis. J Vasc Surg. 1995; 22: 706–714. 19. DeMarco JK, Nesbit GM, et al. Prospective evaluation of extracranial carotid stenosis: MR angiograph with maximum-intensity projections and multiplanar reformation compared with conventional angiography. AJR 1994; 163: 1205–1212. 20. Culebras A, Kase CS, et al. Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke: a report of the Stroke Council, American Heart Association. Stroke 1997; 28: 1480–1497. 21. Dodge JT Jr, Brown BG, et al. Lumen diameter of normal coronary arteries: influence of age, sex, anatomic variation, and left ventricular hypertrophy or dilation. Circulation 1992; 86: 232–246. 22. Wang Y, Riederer SJ, Ehman RL. Respiratory motion of the heart: kinetics and the implications for the spatial resolution in coronary imaging. Magn Reson Med 1995; 33: 713–719. 23. McDonald IG. The shape and movements of the human left ventricle during systole: a study by cineangiography and by cineradiography of epicardila markers. Am J Cardiol 1970; 26: 221–230. 24. Meyer CH, Hu BS, et al. Fast spiral coronary artery imaging. Magn Reson Med 1992; 28: 202–213. 25. Wang Y, Winchester PA, et al. Contrast-enhanced peripheral MR angiography form the abdominal aorta to the pedal arteries: combined dynamic two-dimensional and bolus-chase three-dimensional acquisitions. Investig Radiolo 2001; 36(3): 170–177. 26. Watanuki A, Yoshino H, et al. Quantitative evaluation of coronary stenosis by coronary magnetic resonance angiography. Heart Vessels 2000; 15(4): 159–166. 27. Pennell DJ, Bogren HG, et al. Assessment of coronary artery stenosis by magnetic resonance imaging. Heart 1996; 75(2): 127–133. 28. Post JC, Van Rossum AC, et al. Magnetic resonance angiography of anomalous coronary arteries: a new gold standard for delineating the proximal course? Circulation 1995; 92: 3163–3171. 29. Li D, Paschal CB, et al. Coronary arteries: threedimensional MR imaging with fat saturation and magnetization transfer contrast. Radiology 1993; 187: 401–406. 30. Siegelman ES, Gilfeather M, et al. Breath-hold ultrafast three-dimensional gadolinium-enhance MR angiography of the renovascular system. AJR 1997; 168: 1035. 31. Neschis DG, Velazquez OC, et al. The role of magnetic resonance angiography for endoprosthetic design. J Vasc Surg 2001; 33(3): 488–494.

Chapter 7 Magnetic Resonance Angiography 32. Hertz SM, Baum RA, et al. Magnetic resonance angiographic imaging of angioplasty and atherectomy sites. J Cardiovasc Surg (Torino) 1994; 35(1): 1–6. 33. Prince MR, Anzai Y, et al. MRA contrast bolus timing with ultrasound bubbles. J Magnetic Reson Imag 1999; 10: 389–394. 34. Hertz SM, Holland GA, et al. Evaluation of renal artery stenosis by magnetic resonance angiography. Am J Surg 1994; 168: 140–143. 35. Carpenter JP, Owen RS, et al. Magnetic resonance angiography of peripheral runoff vessels. J Vasc Surg 1992; 16(6): 807–813 Comment in: J Vasc Surg 1993; 17: 1136–1137. 36. Owen RS, Carpenter JP, et al. Magnetic resonance imaging of angiographically occult runoff vessels in peripheral arterial occlusive disease. N Engl J Med 1992; 326: 1577–1581. 37. Carpenter JP, Baum RA, et al. Peripheral vascular surgery with magnetic resonance angiography as the sole preoperative imaging modality. J Vasc Surg 1994; 20: 861–869.

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38. Carpenter JP, Golden MA, et al. The fate of bypass grafts to angiographically occult runoff vessels detected by magnetic resonance angiography. J Vasc Surg 1996; 23: 483–489. 39. Baum RA, Rutter CM, et al: Multicenter trial to evaluate vascular magnetic resonance angiography of the lower extremity. JAMA 1995; 274: 875–880. 40. Owen RS, Carpenter JP, et al. Magnetic resonance imaging of angiographically occult runoff vessels in peripheral arterial occlusive disease. N Engl J Med 1992; 326: 1577. 41. Koelemay, MJW, Lijmer JG, et al. Magnetic resonance angiography for the evaluation of lower extremity disease: a meta-analysis. JAMA 2001; 285: 1338–1345. 42. Levy MM, Baum RA, Carpenter JP. Endovascular surgery based solely on noninvasive preprocedural imaging J Vasc Surg 1998; 28: 995–1003. 43. Prince MR, Yucel EK, et al. Dynamic gadoliniumenhanced three-dimensional abdominal MR arteriography. J Magn Reson Imaging 1993; 3: 877–881.

PART II

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

Basic Cardiovascular Problems

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment David S. Sumner

The surgeon faced with diagnosis and treatment of vascular disease must make decisions based on an assessment of hemodynamic and rheologic factors. Fluid dynamics is exceedingly complex, even under optimally controlled conditions; therefore, no practical formulas capable of predicting outcomes have been devised. It is possible, however, to use some generally recognized principles to formulate guidelines of value to the surgeon. Although many of these principles are intuitively evident, others are less so and require some insight into the physical behavior of fluids in motion. Moreover, flow disturbances not only affect the immediate supply of blood to the peripheral tissues, but also directly interact with the wall of the conduit, playing a role—now appreciated as quite important—in the development of atherosclerotic plaques, platelet deposition, and proliferation of fibromuscular tissues, all of which may influence the outcome of any reconstructive procedure.

heat. Pressure (P)—ordinarily the largest component of total fluid energy—may be segregated into dynamic pressure, derived largely from the contraction of the left ventricle, and hydrostatic pressure (–rgh), which is equivalent to the weight of a column of blood extending from the point of measurement to the heart. In this expression, r is the density of blood (about 1.056 g/cm3); g is the acceleration due to gravity (980 cm/s2); and h is the distance in centimeters above the heart. Gravitational potential energy (+rgh) has the same dimensions as hydrostatic pressure but has the opposite sign. It represents the energy imparted to blood by virtue of its elevation relative to the surface of the earth. Since, in most circumstances, gravitational potential energy is numerically equivalent to hydrostatic pressure, the two cancel out. There are, however; situations in which the two differ—especially on the venous side of the circulation. Finally, kinetic energy, the energy imparted to blood by its motion, is proportional to the product of its density and the square of its velocity (1/2rv2).

Normal Blood Flow The fundamental principle governing blood flow is that developed by Bernoulli: P1 + 1/2rv12 + rgh1 = P2 + 1/2rv22 + rgh2 + heat

(8.1)

This equation simply states that the total fluid energy (P + 1/2rv2 + rgh) must be greater upstream than downstream if blood is to move against a resistance, the energy “lost” in the transition being dissipated in the form of

Viscous Energy “Losses” Heat is generated by the interaction of contiguous particles of fluid in motion. In a long, straight, rigid, cylindrical tube with perfectly steady laminar flow, viscosity accounts for all of the energy losses. Poiseuille’s law defines the relation between the pressure (energy) gradient and flow under these strict conditions:

117

118

Part II Basic Cardiovascular Problems P1 - P2 = v

8Lh r2

=Q

8Lh pr 4

(8.2)

where h represents the coefficient of viscosity measured in poise and r the inside radius of the vessel. This equation states that, given a constant flow, the pressure gradient is directly related to the length of the segment (L) and to the viscosity of blood but is inversely related to the fourth power of the radius. The radius, therefore, has a profound influence on energy losses. Of the many factors that determine the viscosity of blood, hematocrit is the most important, the viscosity at a hematocrit of 50% being roughly twice that at 35% (1). Thus, in situations where laminar flow predominates, the hematocrit may have a significant effect on pressure gradient or blood flow. A further complicating feature is the fact that the viscosity of blood, unlike that of water, varies with shear rate (change in velocity between adjacent laminae of blood, –dv/dr) (2). Viscosity increases markedly as shear rates drop below 10/s; above this level, the viscosity is essentially constant. Although the mean shear rate (8/3 ¥ v/r) in all blood vessels is well above this critical level, it may fall below the critical value during those phases of the pulse cycle in which the velocity decreases. These “nonNewtonian” characteristics of blood are probably not too important, producing changes of only 1% or 2% in the pressure gradient. When flow is laminar; the velocity profile across the lumen of the vessel assumes a parabolic configuration (Fig. 8.1). At the wall, blood is essentially stationary; maximal velocities are in the center of the tube; and the mean velocity is exactly half the maximum. In real life, however; profiles approaching parabolic are found only in the smaller or medium-sized blood vessels and then only during peak systole. Depending on the length, shape, and curvature of the vessel and on the phase of the pulse

cycle, the profile may be blunted or severely skewed. Since the adjacent particles of blood are flowing at nearly the same velocity when the profile is blunt, there is little viscous interaction except near the wall; consequently, Poiseuille’s law does not hold under these conditions.

Inertial Energy “Losses” Because velocity is a vector quantity, force is required to overcome inertia every time there is a change in the direction of flow. Directional changes occur in every curve, at every bifurcation or branch point, and whenever the lumen of the vessel narrows or expands. With each pulse cycle, blood accelerates during systole, decelerates and often reverses during diastole, moves toward the wall as the vessel expands, and moves toward the center of the lumen as the vessel contracts. All motion that deviates from the long axis of the vessel is inefficient in terms of moving blood toward its goal. The energy thus “lost” to friction is proportional to the product of the density of blood and the square of the change in velocity: DP = 1/2rv2

In this chapter, these losses are called inertial losses to distinguish them from those covered by Poiseuille’s equation.

Resistance As the relative contributions of viscosity and inertia vary greatly, it is impossible to characterize blood flow even under normal conditions with a simple formula; however, a general equation incorporating the foregoing concepts is as follows (3): DP = kv

FIGURE 8.1 Velocity profiles. Parabolic profiles occur only during ideal conditions. Because of entrance effects and flow disturbances, profiles are often blunted. (Reproduced by permission from Sumner DS. Hemodynamics and pathophysiology of arterial disease. In: Rutherford RB, ed. Vascular surgery, 5th edn. Philadelphia: WB Saunders, 2000.)

(8.3)

v r2

+ kiv2

(8.4)

where kv represents a constant related to viscosity and ki, a constant related to inertial losses. These constants vary with many factors, including the viscosity and density of blood, the dimensions and configuration of the vessel, reflection of pulses from the periphery, and heart rate, and are really unique to only a single situation. In all cases, the energy losses will exceed—often by a large amount— those predicted by Poiseuille’s law. The equation of continuity states that in the absence of intervening branches or tributaries, flow (Q) of an incompressible fluid (such as blood and water) is constant in all portions of a continuous vessel. Velocity, however, may differ from point to point, depending on the crosssectional area (A = pr2): Q = vA = vpr2

(8.5)

Because Q1 equals Q2: v1r12 = v2r22

or

v1 Ê r2 ˆ =Á ˜ v2 Ë r1 ¯

2

(8.5a)

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

It is interesting to note that the substitution of equation 8.5 in equation 8.4 gives: DP = kv

Q r4

+ ki

Q2 r4

(8.6)

after the constants have been appropriately modified. As the resistance (R) of a blood vessel segment is defined as the ratio of the pressure gradient across and the flow through the segment (DP/Q), it is clear that resistance is inversely proportional to the fourth power of the radius: R=

kv r4

+

kiQ r4

(8.7)

This formula also shows that resistance is not constant but increases as flow increases (3). Therefore, unlike an electrical wire, which has a rather constant resistance over a wide range of currents, the resistance of a segment of blood vessel can be defined only under precise conditions of flow, pulse rate, and other factors. Nonetheless, resistance is a very useful concept in thinking about blood flow. Analogous to electrical circuits, the resistances of blood vessels in series are roughly additive: RT = R1 + R2 + . . . + Rn

1 1 1 ... 1 = + + + RT R1 R2 Rn

Arterial Stenoses The presence of a stenotic lesion in an artery adds tremendously to the complexities of blood flow. Approaching a stenosis, the particles of blood—both microscopic and ultramicroscopic—must accelerate and change directions to squeeze through an orifice narrower than that of the uninvolved vessel upstream (Fig. 8.2). A pressure drop occurs at this point as potential energy is transformed into kinetic energy. Within the stenosis, the increase in velocity is determined by the reduction in cross-sectional area. At the exit, blood emerges at this same high velocity, forming a jet, which disintegrates into disturbed or turbulent flow as the mean velocity decreases to accommodate the larger cross-sectional area. Once again, an energy transformation occurs—this time from kinetic back to potential energy. The efficiency of these transformations determines to a large extent the energy gradient across a stenosis (Fig. 8.3). Inertial losses are greatest at the exit, where flow is most disturbed (4,5). Expressed in terms of pressure gradient, these losses are proportional to the square of the difference between the velocity of blood within the stenosis (vs) and that in the distal vessel (vd):

(8.8)

and the reciprocals of those in parallel are likewise additive: (8.9)

119

DP = k

r (vs - vd )2 2

(8.12)

The shape of the exit determines the severity of the flow disorganization, an abrupt orifice causing more disturbance than one that gradually expands (see Fig. 8.2).

where RT is the total resistance. Finally, although we can never say what the actual resistance of a blood vessel or graft is without measuring flow and pressure gradients under defined conditions, we can calculate its minimal resistance using Poiseuille’s law: Rmin

8Lh

(8.10)

pr 4

It must be emphasized that its actual resistance will always exceed this value.

Reynolds Number Fluids in motion behave similarly when they have the same Reynolds number (Re), a dimensionless number that depends on velocity, diameter (2r), and the ratio of density to viscosity (r/h): Re = v(2r )

r h

(8.11)

Laminar flow tends to break down into turbulence when Reynolds numbers exceed 2000. Although this breakdown normally occurs only during peak systole in the aortic arch, flow may become unstable in other vessels when stenoses are present—even with Reynolds numbers in the hundreds. Under these circumstances, inertial energy losses are magnified.

FIGURE 8.2 Flow patterns through axisymmetrical stenoses. Disturbances of flow are greater when the orifice is abrupt (upper panel) than they are when the orifice is smooth and tapered (lower panel). Velocities and shear rates are low in areas of flow separation where, near the wall, the direction of flow may be reversed.

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Part II Basic Cardiovascular Problems

FIGURE 8.3 Relation between percentage of diameter reduction and resistance of a 1-cm-long “abrupt” axisymmetrical stenosis in an artery with a diameter of 0.5 cm. Total resistance increases rapidly, becoming infinite at 100% stenosis (total occlusion). Resistance due to inertial factors (kinetic fraction) exceeds that due to viscosity when the diameter stenosis is between 25% and 85%, constituting over 70% of the total resistance when the diameter stenosis is between 50% and 70%. This iterative computer model is based on equations 8.2, 8.8, and 8.12.

sistance than a single lesion having a length equal to the combined lengths of the two separate lesions—assuming, of course, that the diameters are the same. The resistances of lesions in series are, however; not strictly additive (8,9). In other words, the total resistance offered by two identical lesions would be less than double their individual resistances. Although there are several reasons for this, the decrease in peak systolic flow and velocity probably accounts for most of the disparity. Since resistance is a function of velocity, any reduction in velocity would result in a decreased resistance in each of the stenoses. Pulsatile flow introduces other complexities (4,10). If flow reversal persists during a portion of the cardiac cycle, the entrance temporarily becomes the exit, and the exit, the entrance. (Usually, however, flow reversal is not maintained in the presence of significant arterial stenosis.) As in normal vessels, the periodic acceleration and deceleration augment inertial losses. Consequently, the resistance of a lesion tends to increase with increasing pulse rate. To summarize, the energy-depleting effects of a stenosis are inversely proportional to the fourth power of its radius (or the square of its cross-sectional area), are directly proportional to the velocity and to the square of the changes in velocity that occur at the entrance and exit, are more dependent on inertial than viscous effects, are usually greatest at the entrance and exit, and are influenced by the shape and symmetry of the stenotic orifices (5,11). Since resistance is a function of flow, and flow, in turn, is a function of resistance, the resistance of a stenosis may vary considerably under different physiologic conditions.

Effect on Pressure and Flow Reflecting the shape of the orifice, the constant, k, varies from about 0.2 (gradual) to 1.0 (abrupt) (6). At the entrance, a similar relation exists, but flow disturbances and inertial losses are less severe. It is also true that asymmetrical stenoses offer more resistance than axisymmetrical stenoses with the same reduction in cross-sectional area (7). In part, this may account for the surprisingly high resistance associated with iliac arteries, which do not appear to be significantly obstructed in the anteroposterior arteriographic projection but are narrowed in the lateral projection. Velocity profiles are quite blunt at the entrance to a stenosis. The distance (Le) required to regain a parabolic profile is a function of the radius of the stenosis and the Reynolds number (Le = 0.16rRe). Unless the stenosis is quite long, a fully developed parabolic profile is never established. Although there is little viscous interaction between adjacent laminae in the blunt region of the velocity profile. shear rates (dv/dr) near the wall are increased, and viscous losses actually exceed those predicted by Poiseuille’s law. Arteriosclerosis is a diffuse process, and tandem lesions occurring in the same stretch of artery are not uncommon. Because energy losses are greatest at the entrance and exit, two separate lesions will offer more re-

Arterial stenoses must always be considered as part of a larger vascular circuit, consisting not only of the vessels proximal and distal to the stenosis but also of any collateral vessels that bypass the stenotic region (12). To begin with the most simple case, the resistances distal and proximal to the stenosis are considered to be constant, and collaterals are considered to be absent. Under these conditions, advancing stenosis causes a reduction in flow and an equivalent increase in the pressure gradient (Fig. 8.4) (3). Changes in pressure and flow ordinarily become perceptible only after the cross-sectional area has been reduced by about 75%, which, in an axisymmetrically stenosed vessel, is equivalent to a 50% diameter reduction (13,14). Beyond this point, which is known as the point of “critical stenosis,” the stenosis is said to be “hemodynamically significant.” With decreasing peripheral resistance, the curves are shifted to the left, and critical stenosis occurs with less diameter reduction. Thus a lesion that does not compromise blood flow in an artery feeding a highresistance peripheral vascular bed may do so in an artery supplying a low-resistance bed (15). Gradual dilation of the peripheral arterioles is one of two mechanisms by which the body attempts to compensate for the increased resistance imposed by a stenosis (16–18). Until the arterioles become maximally dilated,

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

FIGURE 8.4 Effect of increasing diameter reduction on flow through and pressure drop across an abrupt axisymmetrical stenosis in a circuit with a fixed peripheral resistance. Same model as in Figure 8.3.

flow through the stenosis remains undiminished despite its decreasing diameter. The pressure gradient, however, will increase more precipitously (19,20). After the ability to dilate has been exhausted, further reductions in lumen area will cause a rapid fall in both pressure and flow (Fig. 8.5). The development of collaterals is the second major compensatory mechanism. Provided the collaterals are large enough, the resistance of the vascular segment containing the stenosis may remain unchanged, and peripheral pressure and flow will not be adversely affected. Under these circumstances, there will be no pressure drop across the stenosis, but flow through the stenosis will be severely curtailed. Collaterals capable of such efficiency are the exception rather than the rule; in most clinical situations, therefore, the segmental resistance is increased despite ample time for the collaterals to mature (18,21). As a result, there is usually some decrease in pressure and some drop in flow across the stenotic lesion, although one of the two may be more affected than the other. This is simply a reflection of the fact that both pressure and flow are manifestations of total fluid energy. Estimating the resistance of a lesion by measuring only pressure gradient or only flow—as some have done— is likely to provide misleading information. Both must be measured. Even then, the results pertain only to the specific conditions existing at the time.

121

FIGURE 8.5 Effect of compensatory peripheral arteriolar vasodilation on flow through and pressure drop across a stenosis. Segmental resistance refers to the combined resistances of the stenosis and the parallel collateral bed. (Reproduced by permission from Sumner DS. Correlation of lesion configuration with functional significance. In: Bond Mc, Insull W Jr., et al., eds. Clinical diagnosis of atherosclerosis: quantitative methods of evaluation. New York: Springer-Verlag, 1983.)

(vo) is determined solely by the relative radii of the stenotic (rs) and unobstructed segments (ro): rs ro =

vo v s (8.13)

or Diameter stenosis (%) = (1 - vo v s ) ¥ 100

The actual velocity of blood in the stenotic region, however, is determined not only by the relative radii but also by the flow. As a result, velocity increases with progressive narrowing of the lumen until the stenosis becomes quite severe and then drops off very rapidly as the lumen approaches total occlusion (Fig. 8.6) (22,23). Because the Doppler flow detector can measure velocity percutaneously, it has been used noninvasively to estimate the degree of stenosis. It is evident that this approach is strictly valid only if the mean velocities in the stenotic and unobstructed segments are compared. Nonetheless, when a vascular bed (such as that containing the carotid artery) is well defined and peripheral autoregulation maintains flow at normal levels, velocities above certain arbitrary values have proved to be useful in estimating the degree of stenosis, albeit within broad limits.

Effect on Velocity

Effect on Pulse Wave Contours

Unlike the pressure gradient and flow, which are functions of resistance, the ratio of the mean velocity of flow through a stenosis (vs) to that in the unobstructed vessel

A stenosis in an otherwise compliant vessel acts like a lowpass filter in an electrical circuit, attenuating the highfrequency harmonies of the flow or pressure wave (Fig.

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Part II Basic Cardiovascular Problems

8.7) (24). This tends to change the contour of the pulse distal to the stenosis, making it more rounded than that above the stenosis. The upslope becomes less steep, the peak becomes more rounded, and the downslope bows

away from the baseline (25,26). Reversed flow components are less evident and often disappear entirely (27). Fluctuations around the mean value are decreased, a fact that serves as the basis for the calculation of pulsatility indices (all of which, in one way or another, compare the total excursion of the pulse to its mean value) (28,29). Thus, decreases in the pulsatility index over an arterial segment not only predict the presence of a stenosis but also correlate with its severity (30,31). In contrast, reflections originating from the stenosis may increase the excursion of the pulse wave above a lesion and therefore increase the pulsatility index (32–34). This finding may also have diagnostic value.

Effect on Shear Rate and Atherogenesis Shear rate (D = –dv/dr) is the rate at which the velocity of flow changes between concentric laminae of blood. Although the thin layer of blood in contact with the inner wall of a vessel is static, the adjacent layers are in motion, creating a shear rate at the wall (Dw) and a corresponding shear stress (tw) on the endothelial surface. Both are directly proportional to the mean velocity of flow (v) and inversely proportional to the inner radius (r) of the vessel: FIGURE 8.6 Effect of increasing diameter reduction on velocity of flow through a stenosis. Velocity increases even though flow actually decreases until a critical point is reached. (Same model as in Figure 8.3.)

Dw = 4

v r

t w = 4h

v r

(8.14)

FIGURE 8.7 Effect of stenosis in a compliant artery on the contour of pressure and flow pulses. Faucet represents the variable resistance of the peripheral vascular bed. Mean pressure (dashed line) is reduced, but mean flow (dashed line) is unchanged (Reproduced by permission from Sumner DS. Correlation of lesion configuration with functional significance. In Bond Mc, Insull W Jr., et al., eds. Clinical diagnosis of atherosclerosis: quantitative methods of evaluation. New York: Springer-Verlag, 1983.)

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

Thus, at any instant in the pulse cycle, shear rate and shear stress increase as the mean velocity increases or the radius decreases, and they decrease as the velocity decreases or the radius increases. As the jet of blood emerges from the exit of the stenosis, it diverges, coming in contact with the wall downstream (see Fig. 8.2). This creates an area of flow separation, extending from the end of the lesion to the point of reattachment. Within the region of separation, flow is very sluggish and may even be reversed. Shear rates are therefore correspondingly low and may also be reversed. During the cardiac cycle, shear rates can alternate between forward and reversed orientations (10). The longitudinal extent of the zone of flow separation varies with Reynolds number and the shape of the orifice. When Reynolds number is low and the orifice angle is gradual, there may be little or no flow separation (7). The physiologic and pathophysiologic importance of shear rate and shear stress is now well established. Low shear rates permit the accumulation of platelets and other substances that interact with the vascular wall to foster the development of atherosclerotic plaques, intimal thickening, and fibromuscular hyperplasia (35,36). This explains the preferential location of plaques in the carotid bulb opposite the flow divider and the frequency with which atherosclerotic plaques form at the bifurcations of the terminal aorta, the common femoral artery, and popliteal artery—all areas in which geometry promotes flow separation and decreased shear rates (37,38). Once a plaque has formed, further extension may be promoted by the area of stagnant or reversed flow that develops immediately beyond the stenosis. Distal to a stenosis, altered shear stresses (39) and vibrations (40) generated in the arterial wall by disturbed or turbulent flow may be responsible for poststenotic dilation. Within the stenosis, shear rates may be quite high and may exceed values demonstrated to cause endothelial injury, but there is little evidence that this is conducive to atherogenesis (41,42). In fact, the endothelium seems to sense the increased shear and transmits this information to the muscular elements of the arterial wall; dilation occurs, and shear rates return toward prestenotic levels. This has the effect of ameliorating the severity of the stenosis and may be responsible for some of the reported arteriographic observations suggesting plaque resolution (43,44). Other investigators, however, have observed a positive correlation between shear rate and platelet and fibrin deposition on damaged endothelial surfaces and suggest that increased shear rates may be conducive to arterial thrombosis under certain circumstances (45). Thus stenoses not only affect pressure and peripheral perfusion but may also have local effects that are equally important. Research in this area promises to enhance the understanding of atherogenesis and should provide information of practical value to the surgeon involved in the management of this disease.

123

Stenosis as Part of a Larger Arterial Circuit As mentioned previously, the stenotic artery and its collaterals may be considered as a unit, an arterial segment, in other words, with its own relatively “fixed” resistance (Fig. 8.8). This segment is in series with a peripheral vascular bed, the resistance of which varies extensively in response to stress and other stimuli. Included in this peripheral bed are the arteries distal to the most distal collateral inflow site, the arterioles, capillaries, venules, and veins. Because of their small diameters, their muscular walls, and their copious innervation, most of the peripheral resistance is concentrated in the arterioles. It is the arterioles, therefore, that largely control changes in peripheral resistance. Although the actual hemodynamic features of such a complex circuit cannot be depicted by simple formulas, simple formulas analogous to Ohm’s law facilitate our understanding of the physiology (3,12). Blood flow (QT) through the peripheral vascular bed is determined not only by the pressure gradient existing between the central arteries (Pa) and the central veins (Pv) but also by the total resistance of the circuit, which is the sum of the segmental resistance (Rseg) and the peripheral resistance (Rp): QT =

Pa - Pv Rseg + Rp

(8.15)

When there is no arterial obstruction, Rseg is quite low, with most of the total resistance residing in the peripheral arterioles. With exercise or other stress that causes arteriolar dilation and a reduction in Rp, flow is markedly increased—often by as much as five to ten times baseline levels (Fig. 8.9) (20,46,47). In the presence of a proximal arterial obstruction, Rseg is almost always increased, despite the development of collaterals. As long as the autoregulatory capacity of the peripheral arterioles has not been exceeded, Rp decreases enough to compensate for the increased proximal resistance, total resistance is unchanged, and peripheral blood flow is maintained at normal levels (see Fig. 8.5). During exercise, however, further reduction in Rp is limited; consequently, the fall in total resistance is not sufficient to augment flow to the levels required to sustain the increased demands of the muscles, and claudication is experienced (Fig. 8.9) (20,46–49). In the worst situation, Rseg is so high that arteriolar dilation is unable to reduce the total resistance to normal levels, even at rest. When this situation occurs, peripheral perfusion fails to sustain normal metabolic activities, and rest pain or gangrene may ensue (50–52). The pressure gradient across a stenotic segment is determined by its resistance and the magnitude of the flow: Pa - Pd = QRseg

or

Pd = Pa - QRseg

(8.16)

where Pd is the arterial pressure distal to the stenosis but proximal to the peripheral bed. Normally, Rseg is so low

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Part II Basic Cardiovascular Problems FIGURE 8.8 (Upper panel) Components of a vascular circuit containing an arterial stenosis or occlusion. (Lower panel) An electrical analogue, in which the battery represents the left ventricle and the ground potential represents the right atrium. (Reproduced by permission from Sumner DS. Hemodynamics of abnormal blood flow. In: Wilson SE, Veith FJ, et al. eds. Vascular surgery, principles and practice. New York: McGraw-Hill, 1987.)

FIGURE 8.9 Flow (QT) segmental resistance (Rseg), peripheral resistance (Rp), and distal blood pressure (Pd) in normal limbs and limbs with single-level arterial obstruction before, during, and after exercise. (Reproduced by permission from Sumner DS. Hemodynamics of abnormal blood flow. In. Wilson SE, Veith FJ, et al., eds. Vascular surgery, principles and practice. New York: McGraw-Hill, 1987.)

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

that the gradient is only a few mmHg. [Actually, because of reflected waves, the systolic pressure in the distal artery may exceed that in the proximal artery but the mean pressure will always be somewhat less (53–55).] Even though flow is increased many-fold with exercise, the product, Q¥Rseg remains low in normal limbs, and the peripheral pressure drop is insignificant (see Fig. 8.9). If there is any concomitant rise in the arterial perfusion pressure, the distal pressure may even increase somewhat. Because compensatory peripheral arteriolar dilation maintains resting blood flow at normal levels, any increase in segmental resistance causes a similar increase in the pressure gradient across the segment and, provided that the central pressure remains constant, a decrease in peripheral arterial pressure (see Fig. 8.9). Exercise, by augmenting blood flow, causes the peripheral pressure to drop even further, not infrequently to the point where it can no longer be measured (20,54,56–58). Following the cessation of exercise, blood flow decreases as the metabolic debt incurred by the exercising muscles is repaid. In normal limbs this debt is minimal, and flow rapidly falls to pre-exercise levels, but in diseased limbs—especially those with the most severely compromised circulation—many minutes may be required before the debt is repaid and flow returns to baseline (19,54,56–60). As long as flow is increased, the peripheral pressure remains decreased, rising gradually in the postexercise period to pre-exercise levels as flow returns to normal resting values. The situation becomes more complex when there are multiple levels of obstruction (3,60,61). In such cases, the physiologic effects are not simply due to the sum of the segmental resistances but involve steal phenomena as well. Since the proximal arterial segment supplies not only the vascular bed fed by the distal segment but also a more proximal bed, exercise will cause some of the blood destined for the distal tissues to be diverted into the more proximal bed. For example, consider a series of obstructions involving the aortoiliac and superficial femoral segments. The arteries comprising the aortoiliac segment feed the tissues of the buttocks, thighs, and calf, while the superficial femoral segment mainly supplies the calf and foot. During exercise, the arterioles in all these muscles are dilated, blood flow through the iliac segment is greatly increased, and the pressure in the common femoral artery falls. Since the common femoral artery supplies the superficial femoral segment, the expected increase in flow through this segment will not develop despite a profound reduction in the resistance of the arterioles in the calf. In fact, flow may actually fall below resting values in the more peripheral tissues, such as those of the foot (47,57,62). After exercise, the flow debt to the buttock and thigh muscles is the first to be repaid. As flow through the aortoiliac segment subsides, the common femoral pressure rises, and flow through the superficial femoral segment increases, allowing repayment of the metabolic debt incurred by the calf muscles. During the postexercise period, the pressure in the distal arteries remains severely depressed until the flow through the su-

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perficial femoral segment reaches its peak and begins to fall (57,60,63). Because blood flow is difficult to measure noninvasively and because there is a wide range of normal resting values and an even wider range of normal exercise values, physiologic assessment, in clinical practice, is usually limited to the measurement of peripheral pressures (57). Unlike flow, normal values for pressure can be assumed to be close to the central arterial pressure. Moreover, pressure, which represents potential energy, reflects more accurately than flow the capacity of the circulation to accomplish its work.

Collaterals and Segmental Resistance As mentioned earlier, collateral development is rarely sufficient to maintain normal segmental resistance when the major artery of the segment is severely stenosed or occluded (18,21). Since collateral resistance parallels that of the diseased artery and since the resistance of each collateral is inversely proportional to the fourth power of its radius, it would take 16 collaterals with a diameter of 0.25 cm or 625 collaterals with a diameter of 0.1 cm to have a resistance as low as that of an unobstructed vessel with a diameter of 0.5 cm. The former would have a total crosssectional area of 3.1 cm2, and the latter, a total crosssectional area of 19.6 cm2 —4 and 25 times, respectively, that of the unobstructed vessel (0.8 cm2). Clearly, a few large collaterals are likely to be far more efficient than a large number of small collaterals. Collaterals, basically, are arteries whose primary function is to supply nutrients to the tissues through which they pass. When recruited to serve as conduits around an arterial obstruction, they dilate in response to the increased shear stress imposed by the augmented blood flow but retain their primary function (64,65). Thus their effective resistance must exceed that suggested by their lengths and diameters since only a portion of the blood they carry reenters the major arterial system (12,59). Moreover, during exercise, their effective resistance may rise as more blood is siphoned off to supply the muscular tissues through which they pass. Thus, it may be very difficult to evaluate the capacity of the collateral channels visible on an arteriogram. Segmental resistance, like that of the lesion itself, is best evaluated by physiologic tests (66).

Bypass Grafts Because increased segmental resistance is responsible for all the physiologic effects of arterial occlusive disease, the most direct treatment involves reduction of this resistance. If the lesion is well defined and short enough, reduction can be accomplished by endarterectomy or by endovascular dilation and stenting, but in the majority of cases, insertion of a bypass graft is the best approach. In essence, the bypass graft serves as another collateral chan-

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nel, acting in parallel with the diseased arteries and the existing collateral system. The resistance of the graft is determined not only by its length and diameter but also by the configuration of the proximal and distal anastomoses.

Resistance of the Graft Poiseuille’s law can be used to calculate the minimal resistance of a prosthetic graft. This calculation, ofcourse, neglects energy losses due to inertia, which occur at the entrance and exit and at each curve. These losses can be quite significant (67,68). Moreover, pulsatile flow also increases the losses over those expected for steady laminar flow. As shown in Table 8.1, a 20-cm-long aortofemoral graft with a diameter of 7 mm should be capable of sustaining flows of 3000 mL/mm with a minimal pressure drop; but a 5-mm graft would offer an appreciable resistance, even discounting inertial factors. Similarly, 40-cm-long femoropopliteal grafts with diameters of 4 mm or greater should function satisfactorily when called on to transmit flows of up to 500 mL/mm, but grafts with diameters less than 4 mm would offer an unacceptably high resistance. Long grafts (80 cm) from the femoral to tibial arteries are ordinarily used for the treatment of ischemic symptoms; resting flow rates are not high, and pressure drops of 10 mmHg may be acceptable. Still, long segments of such grafts with either distal or proximal diameters less than 3 mm are inefficient blood conduits. After implantation, prosthetic grafts develop a pseudointima that further reduces the effective internal diameter. Although a 0.5-mm layer, applied circumferentially, would have little influence on the pressure gradient

across a large graft, it might adversely affect the function of a graft with borderline dimensions. Since high velocities are conducive to the formation of a thin, tightly adherent pseudointima, graft diameters should be no larger than necessary to ensure satisfactory flow dynamics. If the diameter of the graft is too large, clots tend to form on the inner walls as the flow stream attempts to mold itself to the diameter of the recipient vessel. These clots are loosely attached and may form an embolus, causing graft failure. As indicated by equation 8.5, given the same mean flow rate, the velocity in a 7-mm graft would be double that in a 10mm graft. Because there is little difference in the functional capacity of these two grafts in the iliac region, the smaller diameter is preferred. Saphenous veins used for femoropopliteal and femorotibial bypasses contain valves that reduce the crosssectional area by about 60% (69,70). Although the length of the obstruction so created is quite short, the intact valves are capable of causing additional inertial losses. Studies have shown that resistance to flow, even in the reversed saphenous vein, is decreased by valve bisection (71,72). Autogenous vein grafts are subject to narrowing caused by intimal hyperplasia, the development of which has been shown to be associated with low shear rates (35,73). Low shear rates cause smooth muscle cells to become secretory and enhance platelet adherence (73). High shear rates, on the other hand, foster continued patency and lessen the tendency for the intima to become hyperplastic. The protective effect of high shear has been attributed to suppression of the release of endothelin-1, a peptide found in endothelial cells that acts as a vasoconstrictor and a mitogen for smooth muscle cells (74).

TABLE 8.1 Pressure gradients across grafts (mmHg) Diameter (mm)

Flow (mL/min)

Aortofemoral length = 20 cm 10 7 6 5

300 0.1 (0.1) 0.4 (0.5) 0.8 (0.9) 1.7 (2.0)

500 0.2 (0.2) 0.7 (0.9 1.4 (1.7) 2.9 (3.6)

1500 0.5 (0.9) 0.2 (3.9) 4.1 (7.2) 8.6 (15.0)

3000 1.1 (2.7) 4.5 (11.1) 8.3 (20.6) 17.1(42.8)

50 0.3 (0.3) 0.6 (0.6) 1.4 (1.4) 4.4 (4.5)

150 0.8 (0.9) 1.7 (1.8) 4.2 (4.3) 13.2 (13.7)

300 1.7 (1.8) 3.4 (3.7 8.4 (9.0) 26.4 (28.4)

500 2.8 (3.1) 5.7 (6.4) 13.9 (15.7) 44.0 (49.5)

50 1.3 (1.3) 3.5 (3.5) 13.0 (13.1)

100 2.6 (2.6) 6.9 (7.0) 26.0 (26.3)

150 3.9 (4.0) 10.4 (10.5) 39.0 (39.7)

200 5.2 (5.4) 13.8 (14.2) 52.0 (53.3)

Femoropopliteal length = 40 cm 6 5 4 3

Femorotibial length = 80 cm* 6–4 5–3 4–2

Values are viscous only, equation 8.2; or viscous + kinetic (in parentheses), equation 8.6; h = 0.035 poise; r = 1.056 g/cm3. *Evenly tapered grafts, largest diameter to smallest.

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

Distribution of Flow in Parallel Graft and Stenotic Artery Surgeons occasionally express concern over the possibility that continued patency of a stenotic artery might lead to thrombosis of a parallel graft. To allay this fear; they either avoid end-to-side anastomoses or ligate the stenotic artery. Theoretical considerations strongly suggest that such concerns are not valid, provided that the arterial segment is sufficiently diseased to merit bypass grafting. As shown in Figure 8.10, even when the preoperative pressure gradient across a stenosed artery is only 10 mmHg, over 90% of the flow will be diverted into the graft. The choice of an end-to-side anastomosis should, therefore, be based on other considerations.

Vein Grafts with Double Lumens Not uncommonly, saphenous veins bifurcate into two separate and parallel channels that rejoin after a variable distance to reconstitute a single lumen. When this situation is encountered, the surgeon must decide whether or not to include both channels in the graft. Since both of the duplicated channels will have a lumen diameter less than that of the “parent” vein, it is clear that each will offer more resistance than an equal length of undivided vein. If the channels are of the same size, their combined resistance will be greater than that of an equal length of undivided vein (unless their individual diameters exceed 84% of the diameter of the undivided vein). Thus, in most cases, the combined resistance of the two parallel channels exceeds that of the undivided vein. Obviously, the adverse hemodynamic effects are proportional to the relative lengths of the divided and undivided

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parts, in other words, at a given flow rate, the pressure gradient across a bifurcated graft increases as the length of the divided segment increases. As shown in Figure 8.11, at the same flow rate to the thigh and calf muscles, the distal (popliteal) pressure and the flow rate through a bifurcated femoropopliteal graft are higher when both channels are preserved than they are when one channel has been ligated. Although the differences are small at rest, they become appreciable during exercise. Both configurations, however, represent a marked improvement over the nonbypassed situation. The argument that preserving both channels jeopardizes the survival of the graft by decreasing flow velocity through the bifurcated segment is not valid. Even when both channels are functional, the velocity in each exceeds that in the undivided part of the vein. From this analysis, one must conclude that preservation of two equal-sized channels is desirable but certainly not mandatory. On the other hand, if one of the channels is distinctly larger than the other, there is little to be gained by preserving the smaller of the two.

Sequential Grafts In limbs with combined superficial femoral and belowknee obstructive disease, the surgeon may have the option of performing a bypass to the popliteal segment only, a femorotibial bypass, or a femoropopliteal-tibial sequential graft (75). Aside from technical and anatomic factors, which frequently dictate the choice, what are the theoretical advantages and disadvantages of each of these approaches? Limiting the reconstruction to a femoral-(blind) popliteal bypass usually secures only a modest increase in

FIGURE 8.10 Relative flow through bypass graft and stenotic artery. As the preoperative pressure drop across the artery increases (indicating increasingly severe stenosis), the percentage of flow diverted to the graft increases. Lumen of the graft is equal to that of the unobstructed artery. (Reproduced by permission from Strandness DE Jr., Sumner DS. Hemodvnamics for Surgeons. New York: Crune & Stratton, 1975.)

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Part II Basic Cardiovascular Problems FIGURE 8.11 Resting and exercise flow and flow velocity through a 40cm femoropopliteal bypass graft with a 20-cm divided segment. The diameter of the undivided graft is 5 mm and that of each of the divided segments is 3 mm. Arteries are as follows: common femoral (CF), superficial femoral (SF), profunda femoris (PF), popliteal (P), and thigh collateral (TC). Arrows indicate direction of flow. Thigh and calf resistances are autoregulated to maintain resting flows of 200 and 100 mL/mm respectively. Computer model is based on equations 8.2, 8.5, 8.8, and 8.9.

ankle and calf perfusion pressure (Fig. 8.12). If belowknee resistances are quite high, the patient may derive little benefit from this procedure. Although both femorotibial and femoropopliteal-tibial grafts yield significant and virtually equivalent increases in ankle pressure and are capable of relieving foot ischemia, the latter has the advantage of providing a greater increase in popliteal and tibial pressure. Thus sequential grafts are better equipped to cope with the demands of calf muscle exercise (Fig. 8.13). Flow rates in femorotibial grafts should theoretically be lower than those in the proximal segment of sequential grafts but higher than those in the distal segment (see Figs. 8.12 and 8.13) (76–78). The proximal segment of a sequential graft contributes blood not only to the calf but also, in a retrograde fashion, to the thigh. Having no direct communication with the popliteal artery, femorotibial grafts supply more blood in a retrograde direction to the proximal tissues of the calf than distal segments of sequential grafts do. Because flow velocities ate a function of flow rates, distal segments of sequential grafts may be

more susceptible than proximal segments to failure (79). On the other hand, a femorotibial graft may be more likely to fail than the proximal segment of a sequential graft.

Outflow Resistance Failure of infrainguinal bypass grafts has been correlated with high outflow resistance (80–82). Since outflow resistance, which is roughly analogous to Rp in equation 8.15, is in series with graft resistance, blood flow through the graft is inversely proportional to the sum of the two resistances. Although various methods for estimating outflow resistance have been described, all measure the pressure generated in the distal graft while saline is being infused into the graft at a known rate. Outflow resistance is simply the ratio of the pressure and the flow rate of saline. Measured in this way, outflow resistance reflects both the “true” resistance of the peripheral vascular bed and the resistance of the collateral arteries. At low infusion rates, the pressure developed in the graft does not exceed that at

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

129

FIGURE 8.12 Resting flow through a 40-cm femoral-(blind) popliteal bypass graft, a 60-cm femorotibial graft, and a 40-cm proximal, 20-cm distal, sequential femoropoplitealtibial graft. Diameter of the graft is 5 mm throughout. Symbols not included in Figure 8.11 are calf collateral (CC) and tibial arteries (T). Resting flows to the thigh muscle, calf muscle, and distal leg and foot are 200, 70, and 30 mL/mm, respectively.

the proximal end of the collaterals; consequently, collateral flow competes with flow from the graft to supply the peripheral vascular bed. On the other hand, at high infusion rates, the pressure developed in the graft is sufficiently high to reverse flow in the collaterals, which then become a part of the outflow system of the graft (see Fig. 8.11). It turns out, therefore, that the apparent outflow resistance varies with the rate at which saline is being infused, being deceptively high at low rates of infusion and deceptively low at high infusion rates (Table 8.2) (83). Thus, to accurately reflect outflow resistance, measurement should be made at pressures similar to those expected when the graft is functioning.

Although clamping the recipient artery proximal to the distal anastomosis decreases the size of the collateral bed and makes the measurements more reflective of the “true” peripheral resistance, it will not affect those collaterals that enter below the anastomosis. Nevertheless, this maneuver does appear to improve the ability of outflow resistance to identify those grafts destined to fail (81). The fact that saline, which has a viscosity much less than that of blood, is used as the infusate introduces another confounding variable. One would expect the resistance measured with saline to be considerably less than that actually existing when the graft is functioning.

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Part II Basic Cardiovascular Problems FIGURE 8.13 Exercise flow through femoral-(blind) popliteal, femorotibial, and sequential femoropopliteal-tibial grafts. Exercise flows to the thigh muscle, calf muscle, and distal leg and foot are 400, 140, and 30 mL/mm, respectively.

Crossover Grafts Femoral–femoral, axillary–axillary, subclavian– subclavian, axillary–femoral, and other similar grafts all depend for their proper function on the ability of the donor artery to supply an increased blood flow without sustaining an appreciably increased pressure drop. Since the drop in pressure across any arterial segment is a function of the product of its resistance and the flow rate (equation 8.16), the resistance of the donor artery must be relatively low. When the donor artery is disease free, there ordinarily is no problem; but when the donor artery contains atheroscle-

rotic plaques (as many do), a steal phenomenon may develop (Table 8.3) (84,85). Questions regarding the resistance of the donor artery are best resolved by hemodynamic measurements. Arteriography may be deceiving. For example, before performing a femoralfemoral bypass, the surgeon who is concerned about the capacity of the donor vessel should measure the common femoral artery pressure on the donor side with the flow rate at least double the resting value. This is most easily accomplished pharmacologically by the administration of papaverine. If the operation is being performed to relieve claudication, there should be relatively little pressure

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Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment TABLE 8.2 Relation of apparent outflow resistance to “true” peripheral resistance Flow Rates (mL/min) Graft Infusate

Peripheral Bed

Collateral*

Input Pressure (mmHg)

Apparent Outflow Resistance (mmHg/mL/min)

Apparent/True Resistance Ratio

109.5 118.9 128.4 137.9 156.8 175.8 213.7 251.6

+84.5 +68.9 +53.4 +37.9 +6.8 -24.2 -86.3 -148.4

65.7 71.4 77.1 82.7 94.1 105.5 128.2 150.9

2.63 1.43 1.03 0.83 0.63 0.53 0.43 0.38

4.38 2.38 1.71 1.38 1.05 0.88 0.71 0.63

25.0 50.0 75.0 100.0 150.0 200.0 300.0 400.0

Based on diagram in Figure 8.11, assuming constant resistances (mmHg/mL/min): true peripheral = 0.6, collateral = 0.35; thigh muscle = 0.475; profunda femoris = 0.017. * + indicates antegrade; – indicates retrograde collateral flow

TABLE 8.3 Theoretic effect of femoral-femoral graft (data from reference 84) No Stenosis of Donor Iliac Rest

Donor Iliac flow (mL/min) Common femoral pressure (mm Hg) Common femoral flow (mL/min) Recipient Iliac collateral flow (mL/min) Common femoral pressure (mmHg) Common femoral flow (mL/min) Cross-pubic graft flow (mL/min)

Stenotic Donor Iliac

Exercise

Rest

Exercise

Before Graft

After Graft

Before Graft

After Graft

Before Graft

After Graft

Before Graft

After Graft

250 99

476 98

1266 95

2282 91

250 80

311 75*

645 48

730 42*

250

248

1266

1211

250

235*

645

554*

250 60

18 97

426 32

84 87

250 60

157 75

426 32

369 41

250

246

426

1155

250

233

426

545

—

228

—

1071

—

76

—

176

Aortic pressure = 100 mmHg, graft resistance = 0.004 mmHg/mL/min. *Pressure and flow drops indicative of a “steal”

drop, but if the purpose is to alleviate ischemia, a somewhat larger pressure drop may be permissible. In other words, the pressure delivered to the recipient common femoral artery should be high enough to ensure adequate perfusion of the target tissues. One must also consider the effect of the reduced pressure on the donor limb. In most cases this will be minimal, but when stenoses or occlusions of the thigh or calf arteries are present, the fall in pressure may be sufficient to induce symptoms in a previously asymptomatic limb or worsen those in a previously symptomatic limb.

Anastomotic Configuration To reduce energy losses due to flow disturbances, the transition from graft to host vessel should be as smooth as possible (86,87). End-to-end anastomoses, therefore, most closely approximate the ideal. End-to-side or side-to-end anastomoses always result in alterations in flow direction

(Fig. 8.14). Tailoring the anastomosis to enter the recipient artery or leave the donor artery at an acute angle will minimize but can never eliminate flow disturbances. Although decreasing the angle will reduce flow disturbances in the antegrade limb of a recipient artery, it will accentuate those in the retrograde limb, where flow vectors are almost completely reversed (88). Other energy-depleting pitfalls to be avoided include marked disparity between the diameters of the graft and the artery to which it is connected, and slit-like configurations of the orifice between the two conduits (89). The latter occurs when the graft lumen is stretched to accommodate an excessively long incision in the artery. Despite these theoretical considerations, in practice there is usually little difference in the pressure gradients across anastomoses, regardless of their angle or configuration (provided, of course, that the anastomoses have been carefully constructed and that there are no stenoses) (90). There may, however, be important differences that

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determine the longevity of graft function (91,92). Whenever there are flow disturbances, regions of flow separation are always present (88,93). The “floor” of an end-to-side anastomosis (in the recipient vessel opposite the anastomosis), the “toe” of the anastomosis (on the near wall just beyond the suture line), and the “heel” (on the near wall proximal to the junction) appear to be prominent sites of flow separation where shear is low and shear stress fluctuates (94,95). Because low shear and oscillatory shear stresses are conducive to platelet adhesion, intimal hyperplasia, and atherosclerosis (36,88,93,96), the ultimate success of an arterial reconstruction may depend on how closely the surgeon adheres to recognized hemodynamic principles in constructing the anastomosis. Geometric considerations make it impractical to reduce the graft–host vessel angle of a conventional endto-side anastomosis much below 30% without unduly extending the length of the suture line. (Disregarding the additional few millimeters of anastomotic length associated with the change from a circular to elliptical cross-section that occurs when a larger graft is joined to a smaller artery, the minimum length of a 30% anastomosis would be twice the diameter of the graft, while that of a 10% anastomosis would be almost six times the graft

FIGURE 8.14 Flow patterns at end-to-side and side-toend anastomoses. Note areas of flow separation. Flow in some areas may reverse and travel circumferentially to reach the recipient artery or graft (Reproduced by permission from Sumner DS Hemodynamics of abnormal blood flow. In: Wilson SE, Veith FJ, et al., eds. Vascular surgery, principles and practice. New York: McGraw-Hill, 1987.)

diameter.) The Taylor patch, which uses a vein patch to extend the toe of the anastomosis, makes construction of a 10% anastomotic angle possible (97). Finite element analysis has confirmed that wall shear stress gradients at the critical toe and heel regions are significantly less with the Taylor patch than they are with the standard anastomosis, especially during exercise (98). These same computational methods have been used to design an “optimized” end-to-side anastomotic configuration that greatly reduces wall shear stress compared to the standard and Taylor patch configurations (98). The optimized anastomosis has a smooth transitional curve at the heel and toe, an anastomotic angle of 10% to 15%, and a 1.6:1 graft-to-artery diameter ratio. Because the dimensions and location of recipient arteries vary, fashioning the hoods of autogenous grafts or fabricating prosthetic cuffs that meet the ideal specifications may not be possible.

Bifurcation Grafts When Y grafts used for aortobiiliac and aortobifemoral bypasses have secondary limbs with diameters that are one-half that of the primary tube, each of the secondary limbs has 16 times the resistance of the primary tube, and, in parallel, they have eight times the resistance of the primary tube (Fig. 8.15). Flow velocity is doubled, and

FIGURE 8.15 Hemodynamic attributes of bifurcation grafts. (r1, radius of primary tube; r2, radius of secondary limbs; A1, cross-sectional area of primary tube; and A2, cross-sectional area of secondary tube.) (Reproduced by permission from Strandness DE Jr. Sumner DS. Hemodynamics for surgeons. New York. Grune and Stratton, 1975.)

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment

almost 50% of the incident pulsatile energy is reflected. The reflected energy may contribute to weakening of the proximal suture line in a severely diseased friable aorta, leading to the development of false aneurysms and aortoenteric fistulas (99). Clearly, this is not the optimum configuration (100). No geometric configuration will satisfy all requirements (12). For example, to maintain a constant flow velocity across the bifurcation, the ratio of the diameter of the secondary tube to that of the primary tube must be 0.71; to maintain the same pressure gradient, the diameter ratio must be 0.84; and to achieve minimal pulse reflection, the diameter ratio must be 0.76 (see Fig. 8.15). In animals and in human infants, the ratio is about 0.74 to 0.76, suggesting that the body attempts to minimize reflections at bifurcations. The 16 ¥ 9 mm, 14 ¥ 8 mm, and 12 ¥ 7 mm grafts that are now commercially available have diameter ratios of 0.56, 0.57, and 0.58 respectively. While these ratios represent some improvement over the 0.5 ratio of the older grafts, they still result in increased flow velocity, an increased pressure gradient, and relatively little decrease in the amount of energy reflected (30% vs. 50%). Thus the hemodynamically optimum bifurcation graft has yet to be manufactured. The angle between the limbs of a bifurcation graft is also of hemodynamic importance. Flow disturbances are minimized when the angle is narrow and are exaggerated when the limbs are widely separated (Fig. 8.16). The latter configuration generates regions of flow separation along the walls opposite the flow divider, encouraging the deposition of thrombus. By keeping the primary limb short and using longer secondary limbs, the surgeon can reduce the angle.

FIGURE 8.16 Effect of angle between limbs of bifurcation graft on flow disturbances. When the limbs are widely separated, areas of flow separation (indicated by shading) develop. (Reproduced by permission from MaIan E, Longo T. Principles of qualitative hemodynamics in vascular surgery. In: Haimovici H, ed. Vascular surgery, principles and techniques, 2nd ed. East Norwalk, CT: AppletonCentury-Crofts, 1984.)

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Conclusion Understanding the symptoms of arterial occlusive disease, interpreting the results of physiologic tests, and planning effective surgical therapy are all facilitated by a basic knowledge of hemodynamic and rheologic principles. When predicting the effects of a stenosis, a graft, or other changes in the vascular circuit, one must consider all aspects of the circuit, including collateral input, peripheral resistance, autoregulation, direction of flow, steal phenomena, and inertial factors; otherwise, “armchair” conclusions are apt to be erroneous. This chapter has concentrated on “generic solutions” to various problems commonly encountered in vascular surgery and has based these solutions primarily on models; consequently, the absolute values may differ somewhat from those encountered in real life. Each situation is different and requires careful physiologic assessment, by either noninvasive or invasive measurement of both pressure and flow. It is hoped that this chapter will stimulate others to make these measurements and that the information presented will aid in their interpretation.

References 1. Johnson G Jr, Keagy BA, et al. Viscous factors in peripheral tissue perfusion. J Vasc Surg 1985; 2: 530. 2. Litwin MS, Chapman K. Physical factors affecting human blood viscosity. J Surg Res 1970; 10: 433. 3. Sumner DS. Essential hemodynamic principles. In: Rutherford RB, ed. Vascular surgery. 5th edn. Philadelphia: WB Saunders, 2000. 4. Young DF, Tsai FY. Flow characteristics of models of arterial stenosis. II. Unsteady flow. J Biomech 1973; 6: 547. 5. Berguer R, Hwang NHC. Critical arterial stenosis: a theoretical and experimental solution. Ann Surg 1974; 1 80: 39. 6. Daugherty HI, Franzini JE. Steady flow of incompressible fluids in pipes. In: Fluid mechanics with engineering applications, 4th edn. New York: McGraw-Hill, 1965: 191. 7. Young DF, Tsai FY. Flow characteristics in models of arterial stenoses. I. Steady flow. J Biomech 1973; 6: 395. 8. Flanigan DP, Tullis JP, et al. Multiple subcritical arterial stenoses: effect on poststenotic pressure and flow. Ann Surg 1977; 186: 663. 9. Karayannaeos PE, Talukder N, et al. The role of multiple noncritical arterial stenoses in the pathogenesis of ischemia. J Thorac Cardiovasc Surg 1977, 73: 458. 10. Cheng LC, Clark ME, Robertson JM. Numerical calculations of oscillating flow in the vicinity of square wall obstacles in plane conduits. J Biomech 1972; 5: 467. 11. Byar D, Fiddian RV, et al. The fallacy of applying Poiseuille equation to segmented arterial stenosis. Am Heart J 1965; 70: 216. 12. Strandness DE Jr. Sumner DS. Hemodynamics for surgeons. New York: Grune & Stratton, 1975. 13. May AG, Van deBerg L, et al. Critical arterial stenosis. Surgery 1963; 54: 250.

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14. Moore WS, Malone JM. Effect of flow rate and vessel calibre on critical arterial stenosis. J Surg Res 1979: 26: 1 15. Moore WS, Hall AD. Unrecognized aorto-iliac stenosis. A physiologic approach to the diagnosis. Arch Surg 1971: 103: 633. 16. Jones RD, Berne RM. Intrinsic regulation of skeletal muscle blood flow. Circ Res 1964; 14: 126. 17. Kjellmer I. On the competition between metabolic vasodilation and neurogenic vasoconstruction in skeletal muscle. Acta Physiol Scand 1965; 63: 450. 18. Ludbrook J. Collateral artery resistance in the human lower limb. J Surg Res 1966; 6: 423. 19. Shepherd Jr. Physiology of the circulation in human limbs in health and disease. Philadelphia: WB Saunders, 1963. 20. Wolf EA Jr. Sumner DS, Strandness DE Jr. Correlation between nutritive blood flow and pressure in limbs of patients with intermittent claudication. Surg Forum 1972; 23: 238. 21. Edwards EA. Scope and limitations of collateral circulation. Arch Surg 1984; 119: 761. 22. Spencer MP, Reid JM. Quantitation of carotid stenosis with continuous-wave (c-w) Doppler ultrasound. Stroke 1979: 10: 326. 23. Russell JB, Miles RD, et al. Effect of arterial stenosis on Doppler frequency spectrum. Proc 32nd Annu Conf Eng Med Biol 1979; 21: 45. 24. Keitzer WF Fry WJ, et al. Hemodynamic mechanism for pulse changes seen in occlusive vascular disease. Surgery 1965; 57: 163. 25. Strandness DE Jr., Bell JW. Peripheral vascular disease. Diagnosis and objective evaluation using a mercury strain gauge. Ann Surg 1965; 161 (Suppl): 1. 26. Darling RC, Raines JK, et al. Quantitative segmental pulse and volume recorder: a clinical tool. Surgery 1973; 72: 873. 27. Jager KA, Phillips DJ, et al. Noninvasive mapping of lower limb arterial lesions. Ultrasound Med Biol 1985; 1 1: 515. 28. Woodcock JE, Gosling RG, Fitzgerald DE. A new noninvasive technique for assessment of superficial femoral artery obstruction. Br J Surg 1972: 59: 226. 29. Johnston KW, Matuzzo BC, Cobbold RSC. Doppler methods for quantitative measurement and localization of peripheral arterial occlusive disease by analysis of the blood velocity waveform. Ultrasound Med Biol 1978; 4: 209. 30. Evans DH, Barrie WW, et al. The relationship between ultrasonic pulsatility index and proximal arterial stenoses in a canine model. Circ Res 1980; 46: 470. 31. Baird RN, Bird DR, et al. Upstream stenosis, its diagnosis by Doppler signals from the femoral artery. Arch Surg 1980; 115: 1316. 32. Rittenhouse EA, Maxiner W, et al. Directional arterial flow velocity: a sensitive index of changes in peripheral vascular resistance. Surgery 1976; 79: 359. 33. Farrar DJ, Malindzak GS Jr., Johnson G Jr. Large vessel impedance in peripheral atherosclerosis. Circulation 1977; 56 (Suppl 2}: 171 34. Skidmore R, Woodcock JP. Physiological interpretation of Doppler-shift waveforms. II. Validation of the Laplace transform method for characterization of the common femoral blood-velocity/time waveform. Ultrasound Med Biol 1980: 6: 219.

35. Berguer R, Higgins RF, Reddy DJ. Intimal hyperplasia. An experimental study. Arch Surg 1980; 1 15: 332. 36. Zarins CK, Giddens DP, et al. Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res 1983: 53: 502. 37. Ku DN, Giddens DP, et al. Pulsatile flow and atherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low and oscillating shear stress. Arteriosclerosis 1985; 5: 293. 38. Sharp WV, Donovan DL, et al. Arterial occlusive disease: a function of vessel bifurcation angle. Surgery 1982; 91 : 680. 39. Ojha M, Johnston KW, Cobbold RSC. Evidence of a possible link between poststenotic dilation and wall shear stress. J Vasc Surg 1990; 1 1: 127. 40. Boughner DR, Roach MR. Effect of low frequency vibration on the arterial wall. Circ Res 1971; 29: 136. 41. Zarins CK, Bomberger RA, Glagov S. Local effects of stenoses: increased flow velocity in hi bits atherogenesis. Circulation 1981; 64 (Suppl 2): 221. 42. Vaishnav RM, Patel DJ, et al. Determination of the local erosion stress of the canine endothelium using a let impingement method. ASME J Biomech Eng 1983; 105: 77. 43. Zarins CK, Zatina MA, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg 1987; 5: 413. 44. Glagov S, Weisenberg F, et al. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987; 316: 1371. 45. Ouriel K, Donayre C, et al. The hemodynamics of thrombus formation in arteries. J Vasc Surg 1991; 14: 757. 46. Pentecost BL. The effect of exercise on the external iliac vein blood flow and local oxygen consumption in normal subjects, and in those with occlusive arterial disease. Clin Sci 1964: 27: 437. 47. Lassen NA, Kampp M. Calf muscle blood flow during walking studied by the Xe133 method in normals and in patients with intermittent claudication. Scand J Clin Lab Invest 1965; 17: 447. 48. Folse R. Alterations in femoral blood flow and resistance during rhythmic exercise and sustained muscular contractions in patients with arteriosclerosis. Surg Gynecol Obstet 1965; 121: 767. 49. Hauser CJ, Shoemaker WC. Use of transcutaneous Po2 regional perfusion index to quantifv tissue perfusion in peripheral vascular disease. Ann Surg 1983; 197: 337. 50. Clyne CAC, Ryan J, et al. Oxygen tension on the skin of ischemic legs. Am J Surg 1982; 143.315. 51. Tonnesen KH, Noer I, et al. Classification of peripheral occlusive arterial disease based on symptoms, signs, and distal blood pressure measurements. Acta Chir Scand 1980; 146: l01. 52. Ramsey DE, Manke DA, Sumner DS. Toe blood pressure—a valuable adjunct to ankle pressure measurement for assessing peripheral arterial disease. J Cardiovasc Surg 1983; 24: 43. 53. Remington JW, Wood EH. Formation of peripheral pulse contour in man. J Appl Physiol 1956; 9: 433. 54. Yao ST. Haemodynamic studies in peripheral arterial disease. Br J Surg 1970; 57: 761. 55. Westerhof N, Sipkema P et al. Forward and backward waves in the arterial system. Cardiovasc Res 1972; 6: 648.

Chapter 8 Hemodynamics of Vascular Disease: Applications to Diagnosis and Treatment 56. Strandness DE Jr, Bell JW. An evaluation of the hemodynamic response of the claudicating extremity to exercise. Surg Gynecol Obstet 1964; 119: 1237. 57. Sumner DS, Strandness DE Jr. The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 1969; 65: 763. 58. Lewis JD, Papathanaiou C, et al. Simultaneous flow and pressure measurements in intermittent claudication. Br J Surg 1972; 59: 418. 59. Sumner DS, Strandness PE Jr. The effect of exercise on resistance to blood flow in limbs with an occluded superfidal femoral artery. Vasc Surg 1970; 4: 229. 60. Angelides NS, Nicolaides AN, et al. The mechanism of calf claudication: studies of simultaneous clearance of 99mTc from the calf and thigh. Br J Surg 1978; 65: 204. 61. Angelides NS, Nicolaides AN. Simultaneous isotope clearance from the muscles of the calf and thigh. Br J Surg 1980; 67: 220. 62. Allwood MJ. Redistribution of blood flow in limbs with obstruction of a main artery. Clin Sci 1962; 22: 279. 63. Sumner DS. Hemodynamics of abnormal blood flow. In: Wilson SE, Veith FJ, et al., eds. Vascular surgery, principles and practice. New York: McGraw-Hill, 1987. 64. Rosenthal SL, Guyton AC. Hemodynamics of collateral vasodilation following femoral artery occlusion in anesthetized dogs. Circ Res 1968: 23: 239. 65. Conrad MC, Anderson JL Ill, Garrett JB Jr. Chronic collateral growth after femoral artery occlusion in the dog. J Appl Physiol 1971; 31: 550. 66. Flanigan DP, Ryan TJ, et al. Aortofemoral or femoropopliteal revascularization? A prospective evaluation of the papaverine test. J Vasc Surg 1984; 1 : 215. 67. Schultz RD, Hokanson DE, Strandness DE Jr. Pressure–flow relations of the end-side anastomosis. Surgery 1967; 62: 319. 68. Sanders RJ, Kempczinski RF, et al. The significance of graft diameter Surgery 1980; 88: 856. 69. Whitney DG, Kuhn EM, Estes JW. Valvular occlusion of the arterialized saphenous vein. Am Surg 1976; 42: 879. 70. McCaughan JJ, Walsh DB, et al. In vitro observations of greater saphenous vein valves during pulsatile and nonpulsatile flow and following lysis. J Vasc Surg 1984: 1: 356. 71. Walsh DB, Downing S, et al. Valvular obstruction of blood flow through saphenous veins.J Surg Res 1987; 42: 39. 72. Ku DN, Klafta JM, et al. The contributions of valves to saphenous vein graft resistance.J Vasc Surg 1987; 6: 2 74. 73. Okadone K, Yukizane T, et al. Ultrastructural evidence of the effects of shear stress variation on intimal thickening in dogs with arterially transplanted autotogous grafts. J Cardiovasc Surg 1990; 31: 719. 74. Sharefkin JB, Diamond SL, et al. Fluid flow decreases preproendothel in mRNA levels and suppresses endothelin-1 peptide release in cultured human endothelial cells. J Vasc Surg 1991; 14: 1. 75. Brewster DC, Charlesworth PM, et al. Isolated popliteal segment v. tibial bypass. Comparison of hemodynamic and clinical results. Arch Surg 1984: 119: 775.

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76. Jarrett F, Perca A, et al. Hemodynamics of sequential bypass grafts in peripheral arterial occlusions. Surg Gynecol Obstet 1980; 150: 377. 77. Jarrett F, Berkoff HA, et al. Femorotibial bypass grafts with sequential techniques. Arch Surg 1983; 116: 709. 78. Hadcock MM, Ubatuba J, et al. Hemodynamics of sequential grafts. Am J Surg 1983; 146: 170. 79. Flinn WR, Flanigan DP, et al. Sequential femotal-tibial bypass for severe limb ischemia. Surgery 1980; 88: 357. 80. Ascer E, Veith FJ, et al. Components of outflow resistance and their correlation with graft patency in lower extremity arterial reconstructions. J Vasc Surg 1984: 1: 817 81. LaMorte WW, Menzoian JO, et al. A new method for the prediction of peripheral vascular resistance from the preoperative angiogram. J Vasc Surg 1985; 2: 703. 82. Ascer E, Veith FJ, et at. lntraoperative outflow resistance as a predictor of late patency of femoropopliteal and infrapopliteat arterial bypasses. J Vasc Surg 1987; 5: 820. 83. Bliss BP. Peripheral resistance in the leg in arterial occlusive disease Cardiovasc Res 1971; 5: 337. 84. Sumner DS, Strandness DE Jr. The hemodynamics of the femorofemoral shunt. Surg Gynecol Obstet 1972; 134: 629. 85. Shin CS, Chaudhry AG. Hemodvnamics of extraanatomical bypass following restriction of inflow’ and outflow in the donor artery in dogs. World J Surg 1980; 4: 71 7. 86. Malan E, Noseda G, Longt T. Approach to fluid dynamic problems in reconstructive vascular surgery. Surgery 1969; 66: 994. 87. Malan E, Longo T. Principles of qualitative hemodynamics in vascular surgery. In: Haimovici H. Vascular surgery, 2nd edn. Norwalk, CT: Appleton-CenturyCrofts, 1984. 88. Crawshaw HM, Quist WC, et al. Flow disturbance at the distal end-to-side anastomosis. Effect of patency of the proximal outflow segment and angle of anastomosis. Arch Surg 1980; 115: 1280. 89. Klimach 0, Chapman BLW, et al. An investigation into how the geometry of an end-to-side arterial anastoinosis affects its function. Br J Surg 1984; 71: 43. 90. Lye CR, Sumner DS, Strandness DE Jr. The hemodynamics of the retrograde crosspubic anastoniosis. Surg Forum 1975; 26: 298. 91. Bond MG, Hostetler JR, et al. Intimal changes in arteriovenous bypass grafts. Effect of varying the angle of implantation at the proximal anastomosis and of producing stenosis in the distal runoff artery. J Thorac Cardiovasc Surg 1976; 71: 907. 92. LoGerfo FW, Quist WC, et al. Downstream anastomotic hyperplasia. A mechanism of failure in Dacron arterial grafts. Ann Surg 1983; 197: 479. 93. LoGerfo FW, Soncrant T, et al. Boundary layer separation in models of side-to-end arterial anastomoses. Arch Surg 1979; 114: 1369. 94. Bassiouny HS, White S, et al. Anastomotic intimal hyperplasia: mechanical injury or flow induced. J Vasc Surg 1992; 15: 708. 95. Ojha M, Ethier CR, et al. Steady and pulsatile flow fields in an end-to-side arterial anastomosis model. J Vasc Surg 1990; 12: 747.

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96. McMillan DE. Blood flow and the location of atherosclerotic plaques. Stroke 1985; 16: 582. 97. Taylor RS, Loh A, McFarland RJ, Cox M, Chester JF. Inproved techniques for PTFE bypass grafting: long-term results using anastomotic vein patches. Br J Surg 1991; 79: 348. 98. Lei M, Archie JP, Kleinstreuer C. Computational design of a bypass graft that minimizes wall shear stress gradients in the region of the distal anastomosis. J Vasc Surg 1997; 25: 637. 99. Newman DL, Gosling RG, et al. Pressure amplitude increase on unmatching the aorto-iliac unction of the dog. Cardiovasc Res 1973; 7: 6. 100. Buxton BF, Wukasch DC, et al. Practical considerations in fabric vascular grafts. Introduction of a new bifurcated graft. Am J Surg 1973; 125: 288.

Bibliography Archie JP Jr. Presidential address: A brief history of arterial blood flow—from Harvey and Newton to computational analysis. J Vasc Surg 2001; 34: 398. Nichols WW, O’Rourke MF. McDonald’s blood flow in arteries. Philadelphia: Lea & Febiger, 1990. Milnor WR. Hemodynamics, 2nd edn. Baltimore: Williams & Wilkins, 1989. Strandness DE Jr., Sumner DS. Hemodynamics for surgeons. New York: Grune & Stratton, 1975. Patel DJ, Vaishnav RN. Basic hemodynamics and its role in disease processes. Baltimore: University Park Press, 1980. Sumner DS. Essential hemodynamic principles. In Rutherford RB, ed. Vascular surgery, 5th edn. Philadelphia: WB Saunders, 2000.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 9 Atherosclerosis: Biological and Surgical Considerations Bauer E. Sumpio

Historical Perspective The word atherosclerosis is derived from the Greek— meaning both softening (athere) and hardening (skleros)— and refers to a complex disease process affecting the major blood vessels of the body. It is a disease that has plagued humans for centuries. There is evidence that ancient Egyptians suffered from atherosclerosis much the same way as we do now. Paleopathologists have used sophisticated histological techniques to study the blood vessels of Egyptian mummies dating to 1400 BC. Peripheral arteries were harvested from limbs that had escaped the mutilation that usually accompanied embalming. Patches of atheromatous plaques lined along the length of the aorta, the common carotid, and the iliac vessels. The smaller tributaries of the vessels of the lower limbs were like calcified tubes. Histologically, these ancient diseased vessels demonstrated endothelial and muscular degeneration with focal areas of increased fibrosis and calcification (Fig. 9.1) (1,2). The study of atherosclerosis spans centuries, but the most significant findings have been made only within the last 150 years (Table 9.1). Although the ancient Greek physician Galen reported many vascular anomalies such as aortic and peripheral arterial aneurysms, there is no evidence that he described atherosclerotic lesions (3). Even as late as the sixteenth century, when the infamous anatomist Andreas Vesalius carefully characterized aneurysms, there was still no concept of the atherosclerotic lesion and its significance (4). Despite the contribution of William Harvey and Daniel Sennet to the understanding of the anatomy and physiology of the circulatory sys-

tem, there was still no recognition of the atherosclerotic disease process (5). It was not until the mid-seventeenth century that a process that resulted in degeneration of the arteries with advancing age was recognized. In 1755, the Swiss physiologist Albrecht von Haller reported on progressive atherosclerotic changes in the blood vessels of the elderly (6). Later, in 1761, the Italian physician and pathologist Giovanni Battista Morgagni heralded the idea of using microscopic evaluation of tissues to correlate disease with histology. His work, and that of his pupil Antonio Scarpa, correlated a lesion they described as similar to an ulcerated plaque to aneurysm formation (7). Thus, atheromatous lesions became the focus of study—first, as a precursor to aneurysm formation, and then, as a separate pathologic entity. The earliest evidence of understanding atherosclerosis comes from the research of a surgeon, Joseph Hodgson, in London. He proposed that inflammation was the underlying cause of these plaque formations and hypothesized that the process was linked to the intimal layer of blood vessels. In his monograph (1852), the Viennese pathologist Carl Rokitansky included accurate descriptions of atherosclerotic lesions. Rokitansky was one of the first to observe and document that there were both thrombogenic and calcific components to atherosclerotic lesions (8). Eventually, the proposals of Hodgson and Rokitansky were clarified by the pioneering observations and studies done by Rudolf Virchow (Fig. 9.2). Virchow concluded that atherosclerotic lesions were located in the intimal layer and described the process of plaque formation that was initiated by the formation of a coagulum which he called thrombus. By studying microscopic sections of

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diseased vessels, Virchow generated a theory of atherosclerosis that involved connective tissue proliferation stimulated by intimal deposits, resulting in further vessel wall degeneration (9,10). The studies of Alexander Ignatovski and Nikolai Anitschkov in the early 1900s demonstrated that atherosclerotic changes could be induced in animals by a diet rich in cholesterol (11). This led to the important discovery in 1910 by German chemist Adolf Windaus that human atherosclerotic lesions contained cholesterol. Further research has focused not only on understanding the atherosclerotic process but also on trying to intervene to retard and reverse the clinical manifestations of this disease.

to generalized hardening and thickening of arteries whereas atherosclerosis is more specific to the process resulting in lipid accumulation within the intimal layer of blood vessels. In arteriosclerosis, the increase in vessel wall thickness is due to an increased amount of basement material and plasma protein deposition (12). Although often associated with hypertension, arteriosclerosis is not necessarily pathologic and may simply represent benign changes that occur as a result of the aging process. Interestingly, however, arteriosclerosis is pronounced in patients with hypertension and diabetes mellitus—

Epidemiology The word atherosclerosis should not be used interchangeably with arteriosclerosis, a word introduced by French pathologist Jean Lobstein in 1829. Arteriosclerosis refers

FIGURE 9.1 Frozen section of tibial artery from Egyptian mummy. Lipid deposition can be seen in an atheromatous lesion.

FIGURE 9.2 Rudolf Virchow (1821–1902). He made significant contributions to the understanding of atherosclerosis and vascular disease.

TABLE 9.1 Historical evolution of the understanding of vascular disease Name Andreas Vesalius and Gabriel Fallappio Willam Harvey Daniel Sennet Albrecht von Haller Giovanni Batista Morgagni Antonio Scarpa Joseph Hodgson Jean Lobstein Carl Rokitanski Rudolf Virchow Alexander Ignatovski Adolf Windaus Nikolai Anitschkov and Ludwig Aschoff

Year 1500s 1628 1628 1755 1761 1804 1815 1829 1852 1854 1908 1910 1933

Contribution Described aortic and peripheral aneurysms Described cardiovascular system as a circuit Described arteries as comprised of two concentric layers Described progressive changes within arterial walls Described microscopic changes occurring within atheromas Correlated ulcerated atheromatous lesions with aneurysmal development Proposed inflammation as a cause of atherosclerosis Coined the term arteriosclerosis Detailed descriptions of early and mature atheromatous plaques Described the process of thrombosis and embolism Experimentally induced atherosclerosis in rabbits Discovered cholesterol within atherosclerotic lesions Provided summaries of early experimentation and reults regarding the research of atherosclerosis

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

Incidence/1,000 men at risk (%)

diseases that are both also associated with a higher risk of atherosclerosis. Atherosclerosis-related cardiovascular disease is the most common cause of morbidity and mortality in the United States. Atherosclerosis resulting in myocardial infarction, stroke, and gangrene of the extremities is responsible for approximately 50% of all mortality. As will be discussed later, atherosclerosis has a predilection for specific anatomic sites at the ostia and bifurcations of the aorta, iliac, and femoral arteries. Atherosclerosis remains the leading disorder affecting lower limb circulation. Infrapopliteal arteries are commonly affected, contributing to end-organ disease (i.e., ischemia and gangrene). Patients with comparable degrees of atherosclerotic disease, anatomically, may, nonetheless, present with varying degrees of clinical symptoms. Symptomatology depends on several different factors other than the presence or absence of atherosclerosis (13). For example, the rate of disease progression, the severity of the decrease in blood flow, the presence or absence of collateral circulation, and the presence of thrombus or embolism causing acute vasospasm or occlusion are all factors affecting presentation. The majority of patients with peripheral arterial disease tend to exhibit a stable course over a 5-year period. However, 15–20% of these patients will eventually develop tissue loss or rest pain requiring vascular surgery. Moreover, amputation will ultimately be required in 1% of patients per year. The Framingham study allowed close evaluation of a defined cohort over the span of 30 years. A comparison of incidences in angina, TIA, and calf claudication is shown (Fig. 9.3). In comparison to angina, peripheral artery disease increases in prevalence throughout life and even exceeds anginal symptoms if the patients live over the age of 75 (14,15). In addition to heart and peripheral vascular disease, cerebrovascular disease is also a major consequence of the atherosclerotic process. Stroke, with an incidence of 500,000 cases yearly, is the third leading cause of death in the US. In one study, the annual stroke rate was determined to be 1.3% per year in patients with up to 75% carotid stenosis. The rate of stroke is nearly tripled in patients with higher-grade lesions (Table 9.2) (16). Thus, the results of untreated or poorly treated atherosclerotic disease has significant medical consequences.

10 8

Angina Claudication TIA

6

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Normal Anatomy The vascular system is derived from the mesoderm and originates as aortic arches which bridge to connect the embryonic dorsal aorta to the aortic sac. Some branches of the dorsal aorta remain as either intercostal arteries or lumbar intersegmental arteries. The fifth pair of lumbar intersegmental arteries become the common iliac arteries. By the fourth week of development, the aortic arches transform and develop into their adult derivatives. Of note, the third pair of arches becomes the common carotid arteries and the pulmonary arteries arise from the sxth pair. The earliest vascular primordia are endothelial cell clusters called blood islands. These rests of cells arise on the yolk sac between the splancnic mesoderm and endoderm. The blood island cells differentiate and separate into peripherally located endothelial cells and central blood cells. Mesenchymal cells then migrate into the subendothelial space and differentiate into smooth muscle cells. Development of the extracellular matrix then progresses as smooth muscle cells and fibroblasts secrete angiogenic factors such as fibroblast growth factor (FGF) and vascular endothelial cell growth factor (VEGF). These signaling substances promote the generation of new branches that extend from the preexisting main vessels (Fig. 9.4) (17). Arteries are made up of three distinct concentric layers (Fig. 9.5). The innermost layer, the intima, is composed of endothelial cells. The media, the next layer, contains smooth muscle cells in various configurations and is separated from the intima by the internal elastic lamina, a network of alveolar and elastic tissue. The outermost layer, the adventitia, is a meshwork of collagen, elastic, and fibrous tissue that, along with the media, provides a strong physical support. The media and adventitia are separated by the external elastic lamina. The intima and inner portion of the media receive blood supply directly from luminal blood. In contrast, there is a complex network of small vessels called the vasa vasorum that supply the adventitia and outer media (18). The proximal vessels are subjected to a high-pressure system and this is reflected in the structure and composition of these vessels as represented in Figure 9.6. These proximal, large elastic arteries serve to smooth the flow of blood through systole and diastole. The media of these arteries have thick, highly organized layers of elastic fibers arranged circumferentially that expand and recoil TABLE 9.2 The risk of transient ischemic attacks (TIAs) and stroke in patients with asymptomatic carotid stenosis

4 2 0 35–44

45–54

55–64 65–74 Age (years)

75–84

FIGURE 9.3 Symptoms of atherosclerotic disease in the Framingham study.

Degree of Stenosis <50% (mild) 50–75% (moderate) >75% (severe)

TIA (%)

Stroke (%)

1.0 3.0 7.2

1.3 1.3 3.3

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2.

as elastin, collagen, and proteoglycans. The endothelial cell layer serves to protect against thrombosis by providing a selective barrier between circulating blood and interstitial fluid. Smooth muscle cells are contained deeper within the arterial wall, constituting 40% to 50% of the medial volume in large elastic arteries and 80% to 85% in smaller muscular arteries. Smooth muscle cells maintain vascular tone of the arterial wall and secrete extracellular matrix proteins such as elastin, collagen, and glycosaminoglycans. In addition, smooth muscle cells have been found to contain receptors for lipoproteins and growth factors and synthesize prostaglandins to mechanically regulate blood flow.

In vivo, endothelial cells and smooth muscle cells usually exist in a quiescent state. The endothelium, via contact inhibition, exists as an obligate monolayer. Smooth muscle cells, however, have been shown to have a turnover rate of 0.06% per day. These two cell types exist together with a complex network of signals between them modulating each other’s function. For example, endothelial cells secrete products which influence smooth muscle cell function (19). Vasodilating substances such as prostacyclin, prostaglandin E2, and endothelialdependent relaxing factor (EDRF) are secreted by functional endothelium in response to local thrombotic events (20). This may explain the observation that coronary vessels with intimal lesions causing less than 40% luminal stenosis become dilated in response to changes in blood flow. Only after the intimal lesion occupies greater than 40% of the lumen does the blood flow decrease (Fig. 9.6) (21). The increase in vessel wall size is dependent not on endothelial cell proliferation, but on accumulation of smooth muscle cells and associated matrix proteins within the intima. Several stimulators have been elucidated and, as will be discussed in a later section, platelet-derived growth factor (PDGF) has been found to be one of the most potent.

FIGURE 9.4 Differentiation of vessels in the embryo. The process proceeds from endothelium differentiation to full development of veins and arteries.

through each cardiac cycle. In contrast, distal blood vessels tend to be more muscular in structure. The media of these arteries are comprised mainly of smooth muscle cells with few intermixed unorganized elastic fiber layers. Muscular arteries are highly contractile and under the direct control of the autonomic nervous system. Arteries consist of two major cell types: 1.

Endothelial cells line the luminal surface serve to control vascular tone and secrete matrix substances such

Theories of Atherosclerosis Monoclonal Hypothesis This theory is borne from the observation by Benditt and Benditt that individual cells from plaques of heterozygote females for the X-linked glucose-6-phosphate dehydrogenase (G-6PD) gene usually only exhibit one G-6PD isotype (Fig. 9.7) (22). This suggests that the cells of a particular plaque are derived from a single progenitor smooth muscle cell, and, although, some smooth muscle cells may infiltrate the intima, the bulk of the cells found within a plaque are likely a result of monoclonal proliferation of modified smooth muscle cells. Another study has corroborated the monoclonal behavior of human plaque cells using LDH as a marker. LDH isoenzyme analysis

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

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Adventitia

Media

Intima

A

Endothelium Internal elastic lamina

Intima

Intima

Media External elastic lamina

Lamellar unit

Media

Adventita

B

Adventita

C FIGURE 9.5 (A) Cross-section of an arterial wall. (B) Normal muscular artery. (C) Normal elastic artery.

FIGURE 9.6 Diagrammatic representation of the possible sequence of changes occurring in an atherosclerotic artery leading, eventually, to lumen narrowing.

carried out on the blood vessel and plaque separately revealed a shift in isoenzyme pattern (Fig. 9.8). This shift represents an alteration of smooth muscle type, distinguishing plaque smooth muscle cells from intimal smooth muscle cells (23). This finding adds support to the monoclonal hypothesis, but does not explain other aspects of the atherosclerotic process.

FIGURE 9.7 Zymogram of samples from: (1) blood, (2) normal tissue, and (3–6) atheromatous plaques. Samples from the different plaques demonstrate expression of the Type A or Type B forms of the enzyme, both of which are found in the blood and normal tissue.

Intimal Cell Mass Hypothesis This hypothesis comes from the observation that small accumulations of smooth muscle cells can be found in children where atherosclerosis later develops. It is uncertain how these rests develop, but they may be primordial rests of stem cells that are susceptible to atherogenesis. These accumulations of smooth muscle cells within the vessels of

FIGURE 9.8 Representative LDH isoenzyme blot staining for: (A) media and (B) plaque.

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children can be found worldwide regardless of the prevalence of atherosclerosis. This suggests that the eventual development of atherosclerosis is determined by extrinsic factors such as increased cholesterol levels, cigarette smoking, etc. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) research group examined this phenomenon. Coronary arteries, aortas, and other pertinent tissues from persons 15 to 34 years of age were collected and studied. The researchers reported that aortic fatty streak lesions were prevalent in almost all individuals by the age of 15 and that raised, fibrous plaques were present in some by the age of 20. Consistent with clinical observations, the coronary arteries of young males were found to have a significantly increased number of raised plaques as compared to their female counterparts (24).

smooth muscle cells, increased death of proliferating smooth muscle cells, impaired endothelium healing, and monocyte proliferation via upregulation of monocyte chemoattractant protein-1 (MCP-1) secretion from endothelial cells (27).

Reaction-to-Injury Hypothesis The process of atherosclerosis is a chronic and insidious one usually occurring over several decades. Several theo-

Encrustation Hypothesis The encrustation hypothesis proposes that repeated cycles of thrombosis and healing serve as the source of plaque progression. As thrombosis is known to be a late component of the atherosclerotic lesion, this theory does not explain the initiation of plaque formation (25).

Lipid Hypothesis An alternative hypothesis postulates that increased levels of LDL results in abnormal lipid accumulation in smooth muscle cells and macrophages as it passes through the vessel wall (26,27). As LDL is oxidized, endothelial cells become damaged and the atherogenic events mentioned previously proceed to form plaque. Oxidized lipoproteins have been found to cause cell injury regardless of how the oxidation occurs (28–31). Lipoprotein oxidation results in the development of several toxic products that include 7-b-hydroperoxycholesterol, 7-ketocholesterol, lysoPC, oxidized fatty acids, and epoxysterols (32,33). The exact mechanism by which cell death occurs is not yet known. One theory for the development of atherosclerosis caused by oxidized LDL is illustrated (Fig. 9.9) (34). VLDL and LDL accumulate in the intima. Increased lipoprotein levels and binding to connective tissue elements increases the residence time of the lipoproteins in the intima, thereby increasing the probability of undergoing oxidation (35,36). Once oxidized, the modified lipoproteins stimulate the entry of monocytes and lymphocytes into the intima. Oxidized LDL also promotes migration and proliferation of smooth muscle cells, contributing to the genesis of an atherosclerotic plaque. Evidence supporting this hypothesis has recently emerged. Specifically, it has been shown that the lipid found in plaques comes directly from the blood and there is substantial evidence that links hypercholesterolemia with an increased propensity to develop atherosclerotic lesions (37,38). Increased serum levels of LDL lead to increased interstitial levels of LDL which bind to proteoglycans. This accumulation of LDL increases the propensity for lipoprotein oxidation to occur which has been shown to cause increased PDGF expression by

FIGURE 9.9 Schematic of a hypothetical sequence in which lipoprotein oxidation causes atherosclerosis.

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

ries have been postulated to explain how the process begins. One such theory arises from research that has found that endothelial cell dysfunction leads to atherosclerosis. Endothelial cell dysfunction results in increased vascular permeability, increased leukocyte adherence, and functional imbalances in pro- and antithrombotic factors, growth modulators, and vasoactive substances (Fig. 9.10). This initial dysfunction of endothelial cells

also triggers progression of atherosclerosis. Leukocytes which accumulate at the site of injury release more growth factors which induce migration of vascular smooth muscle cells into the intima. This reaction-to-injury hypothesis also postulates that platelets which are present in areas of denuded endothelium secrete potent mitogenic factors, thereby stimulating smooth muscle proliferation. This hypothesis incorporates three important processes that are involved in atherogenesis: 1.

2. 3.

FIGURE 9.10 Endothelial dysfunction in response to injury.

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focal intimal migration, proliferation, and accumulation of various cells such as macrophages and smooth muscle cells; increased production of extracellular matrix; and lipid aggregation.

These processes are set into motion when the vessel endothelium is exposed to some sort of injury. Continuous exposure to endothelial injury elicits a chronic focal inflammatory response that results in the development of an atherosclerotic plaque (Fig. 9.11). Indeed, all of the theories mentioned attempt to explain atherosclerosis, but, at best, help only to explain particular aspects of a very complex process (39–41).

FIGURE 9.11 Reaction-to-injury hypothesis. Of note, each of the stages is potentially reversible if the injurious agent(s) are removed.

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Morphology and Hemodynamics It should be reiterated that arterial blood vessels are subjected to major hemodynamic forces which impact on the endothelial cell lining. The endothelial cell monolayer is an active participant in the complex interactions that occur between the luminal blood and vessel wall. In fact, it is the biologic response of the endothelium to hemodynamic forces that is pivotal in the process of atherosclerosis. The arterial blood vessel is subjected primarily to two major hemodynamic forces: shear stress and cyclic strain (Fig. 9.12). As blood moves along the endothelium, a tangential drag force is produced called shear stress (42,43). The magnitude of the shear stress is directly proportional to blood viscosity and inversely proportional to the radius of the blood vessel cubed. Research has shown that high shear stress is inversely proportional to the distribution of early intimal lesions. That is, areas affected by increased shear stress were protected and had fewer intimal lesions compared with areas of low or oscillatory levels of shear stress (Fig. 9.13) (44–46). This finding has led to a vast amount of investigation trying to characterize the effects of hemodynamics on vascular biology. Results of these studies demonstrate that endothelial cells respond to shear stress in several different ways (Table 9.3). For example, endothelial cells have been found to change alignment in the direction of flow when subjected to shear stress. Additionally, reorganization of endothelial cell Factin contained within the cytoskeleton allows morphologic changes to occur under the influence of shear stress (Fig. 9.14) (47–50). As illustrated in this figure, prominent actin microfilament bundles are localized and aligned in areas of high shear stress. In areas where the shear stress is low and flow is nonlaminar, the actin monofilament bundles remain dense and nonaligned. It has been shown that

shear stress inhibits endothelial cell migration and proliferation (51). Lastly, shear stress affects the biologic function of endothelial cells, providing evidence of its role in protecting vessels from atherosclerosis. Shear stress increases prostacyclin secretion, which acts as a potent vasodilating and anti-platelet-aggregating substance (52,53). Similarly, secretion of tissue plasminogen activator, a potent thrombolytic, and nitric oxide, a potent mediator of vasomotor tone and smooth muscle proliferation, is enhanced with higher levels of shear stress (54,55). These findings imply a possible mechanism that may explain the finding of increased atherogenicity in areas of low shear stress. Cyclic strain refers to the repetitive, circumferential pulsatile pressure distention conferred to the vessel wall. As with shear stress, endothelial cells react in specific ways to cyclic strain. Cultured endothelial cells have been shown to proliferate and exhibit morphologic changes in response to cyclic strain (Table 9.3). The morphologic changes occur secondary to actin rearrangement within the cytoskeleton resulting in an organized cellular alignment perpendicular to the force vector (56,57). Several macromolecules have been found to be stimulated by cyclic strain. As with cells that are subjected to shear stress, endothelial cells undergoing cyclic strain exhibit increased levels of prostacyclin and tPA. In addition, endothelial nitric oxide synthase and, subsequently, nitric oxide levels are also increased (58–60). Moreover, cyclic strain has been shown to stimulate expression of cellular adhesion molecules such as ICAM-1 (61). Studies have also shown that second messenger systems such as the adenylate cyclase-cAMP and diacylglycerol-IP3 pathways become activated by cyclic strain (62). Al-

High-shear region

Low-shear region

Cross-section of carotid sinus

FIGURE 9.12 Schematic of hemodynamic forces generated during systole. The shear stress force vector is parallel to blood flow and is unidirectional. In contrast, cyclic strain force vectors are multiplanar and multidirectional.

FIGURE 9.13 Diagrammatic representation of the flow field in the area of the carotid bifurcation.

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TABLE 9.3 Hemodynamic effects on cell function Cell Function

Exposure to Shear Stress

Exposure to Cyclic Strain

Proliferation

Inhibition of endothelial and smooth muscle cell proliferation Endothelial cells elongate and align themselves in the direction of flow Stimulation of nitric oxide, PGI2 and tPA secretion Activation of DAG/IP3 pathways, integrins, and MAP kinases

Stimulation of smooth muscle cell proliferation

Orientation Secretion Signal transduction

Endothelial cells align themselves perpendicular to the force vector Stimulation of nitric oxide, PGI2 and tPA secretion Activation of DAG/IP3 pathways, MAP kinases and TGF-b

FIGURE 9.14 Morphologic changes in actin microfilaments of rabbit aorta under the effects of shear stress. (A) Thoracic aorta. (B) Low shear stress. (C) High shear stress. (D) Electron photomicrograph of endothelial cells subjected to high stress. Note the prominent actin microfilament bundle.

A

C

B

D

though not clearly defined as yet, these findings may provide clues to the mechanism or mechanisms by which endothelial cell responses are mediated when affected by atherosclerosis. In the support of the critical role of hemodynamic forces, it should be noted that atherosclerotic lesions do not occur randomly within the vasculature (63). Michael DeBakey and co-workers (64) divided arterial plaque distribution into five categories. They noted that the coronary arteries, the major branches of the aortic arch, the abdominal aorta, and the major visceral and lower extremity branches were particularly susceptible to atherosclerosis. Plaque localization at these sites accounts for the majority of clinical manifestations associated with this disease (Fig. 9.15) (65). 1.

Category 1 includes the coronary arteries which contain many branch points that are subjected to me-

2.

3.

4.

chanical torsions during each heartbeat. Atherosclerotic lesions are commonly found at the bifurcations of major vessels such as where the left main coronary artery splits into the left anterior descending and left circumflex arteries. Category 2 includes major branches of the aortic arch. The carotid arteries are especially prone to atherosclerotic disease. The third category consists of the visceral branches of the abdominal aorta. Susceptible category 3 arteries include the celiac axis, the superior and inferior mesenteric arteries, and the renal arteries. Category 4 vessels include the distal abdominal aorta and its ileofemoral branches. Most patients with atherosclerotic disease fall into this category. Additionally, patients with symptomatic plaques in the terminal aorta and lower extremities had the highest probability of having atherosclerotic disease elsewhere (64).

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The last category (category 5) consists of patients having disease diagnosed in two or more of the aforementioned regions at the same time.

Of note, the superficial femoral artery at the level of the adductor canal is another vessel that has a propensity to develop stenosis even though no major branch points exist. Patients may become symptomatic from stenosis of this vessel due to its lack of compensatory ability (66). As mentioned earlier, luminal lesions usually need to occupy more than 40% of the cross-sectional area before becoming symptomatic because of the compensatory dilation that occurs in order to maintain blood flow. Because of anatomical restrictions, the SFA is not able to compensate and patients may experience symptoms with smaller lesions. Blood flow within human arteries is generally laminar. In straight, unbranching segments of vessels, flow is parabolic as well as laminar. Velocity is greatest at the center of the vessel and is the least at the blood–endothelium interface because of friction. Bifurcations and other geometric changes affect local flow characteristics, resulting in turbulent flow. Turbulent flow results in random and erratic flow profiles and is dependent on fluid viscosity, mean velocity, and blood vessel diameter (67).

There is an elevation in shear stress and turbulence at areas of branching in the vascular tree (46). The velocity vector of blood flow in these areas becomes nonlinear. It may be that these changes in hemodynamic factors that occur at bifurcations account for the topographical distribution of atherosclerosis. Research has demonstrated that mitotic division of endothelial cells was 50% more frequent in areas of turbulent flow than in contiguous areas (68). Moreover, hypercholesterolemia may decrease the malleability of endothelial cells, making them more susceptible to hemodynamic forces especially at arterial branch points (69).

Stages of Atherosclerosis Initiation Once the process of atherosclerosis has been initiated, a series of events follow that result in the formation of a fatty streak, considered the earliest atherosclerotic lesion (Fig. 9.16). Increased vascular permeability leads to increased intimal lipid accumulation, resulting in the development of a fibrofatty plaque (Fig. 9.17) (70). It has also been suggested, based on rabbit models, that prolonged blood residence time in areas of low shear stress may contribute to increased migration of lipoproteins into the inti-

FIGURE 9.16 Fatty streak lesions of the thoracic aorta.

FIGURE 9.15 Predominant sites for the localization of atherosclerotic lesions.

FIGURE 9.17 Fibrofatty plaque in human aorta. A, Adventitia; M, media; LC, lipid core; PS, plaque shoulder; E, endothelium; FC, fibrous cap.

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

ma (37,38). These lipoproteins, now residing within the blood vessel, associate with proteoglycan molecules located within the arterial extracellular matrix and become oxidized. Both moieties of the lipoproteins undergo modification into products that promote atherogenesis. Lipids are oxidized into hydroperoxides, oxyesterols, and other aldhydic products (33). Proteins are similarly modified and broken down into compounds that are still being characterized. Oxidative stress is thought to be carried out by NAD, NADP, and lipooxygenases found in the area of atheroma formation (71,72). Other factors such as hypercholesterolemia, homocysteinemia, and cigarette smoking also contribute to increased lipoprotein oxidation (73–76). Of note, lipoproteins in patients with diabetes also undergo nonenzymatic glycosylation which results in a promoter product of atherosclerosis (Fig. 9.18) (77,78). Once the endothelium has sustained injury, there is increased expression of cell adhesion molecules such as VCAM-1, ICAM-1, and E-selectin. The cell adhesion molecules are of two main categories: those that are members of the immunoglobulin superfamily (ICAM, VCAM) and others that are membrane-associated glycoproteins (selectins). VCAM-1 has been found to interact with verylate forming antigen-4 (VLA-4), a specific integrin found on leukocytes, monocytes, and T-lymphocytes that are commonly found within atheromatous plaques. ICAM-1, another cell adhesion molecule thought to play a role in atheroma formation, serves as a receptor for the LAF-1 and Mac-1 integrins found on various different kinds of leukocytes. Endothelial cell selectin, or E-selectin, is a membrane-associated glycoprotein that also seems to play a significant role in leukocyte adherence. E-selectin mediates the adhesion of neutrophils to endothelial cells. These cell adhesion molecules along with other selectins, such as P-selectin (platelet) and L-selectin (leukocyte), promote saltatory movement of leukocytes against the endothelium (Fig. 9.19) (79). The time-course expression of each of these cell adhesion molecules is distinctly different and provides insight into understanding their specific roles in leukocyte adhesion (Fig. 9.20) (80). E-selectin appears within 1 to 2 hours (h) of cytokine activation and peaks expression at 4 to 6 h. VCAM-1 appears 4 to 6 h after activation and peaks at 12 to 18 h. ICAM-1 expression appears to be intermediate with peak expression at 4 to 6 h. It should be noted that, whereas E-selectin degrades quickly after about 6 h even in

Aggregation Glycation?

Immune complex LDL

Oxidation

Proteoglycan complex

FIGURE 9.18 Possible fates of LDL leading to the initiation of atherosclerosis.

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the presence of cytokines, ICAM-1 expression persists as long as cytokine is present and VCAM-1 expression degrades over a period of days. This differing time-course of peak expression and degradation may indicate a progression of endothelial cell adhesiveness. E-selectins may initially begin the process of leukocyte rolling, giving way to ICAM-1 and, eventually, VCAM-1, signifying a change to a more permanent leukocyte adhesion (79). These stronger interactions between endothelium and leukocyte may herald the initiation of leukocyte infiltration into the intima, beginning the atherosclerotic process. Recent studies have reported that constituents of oxidized lipoproteins such as lysophosphatidylcholine can augment the expression of these cell adhesion molecules (81). In addition, in areas where laminar shear flow is disrupted and, therefore, decreased, VCAM expression has been found to be enhanced (82). These cellular adhesion molecules increase vascular adherence at the site of injury and monocyte and Tlymphocyte aggregation. The lymphocytes migrate into the vessel wall and accumulate within the intima. Oxidized LDL and monocyte chemoattractant protein-1 (MCP-1), both products of endothelial cells in oxidative conditions, act as cellular chemoattractants for interleukins and other cytokines (83,84). This inflammatory state results in higher levels of tumor necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1), which are known promoters of leukocyte adherence and augment the atherosclerotic process. Although the mechanism by which the cytokines work is still being refined, some associations have been elucidated. IL-1 and TNF-a have been shown to increase VCAM-1 and ICAM-1 expression. These cytokines along with growth factors secreted from macrophages are also involved in smooth muscle cell migration and proliferation (Fig. 9.21) (41,85). However, this process does not continue unregulated. There is evidence that nitric oxide released from the endothelium serves to limit VCAM-1 expression even at low levels (86). L-arginine is metabolized to nitric oxide and the byproduct L-citrulline. This occurs via the inducible synthase endothelial nitric oxide synthase (eNOS) which is a membrane-bound calcium-calmodulin dependent enzyme (87–89). eNOS can be upregulated by local hormonal activity such as by bradykinin, ATP, and histamine. Moreover, there is data suggesting that hemodynamic forces such as shear stress and cyclic strain increase eNOS amounts (59). Therefore, at areas of denuded endothelium, nitric oxide may mediate vasomotor control and smooth muscle cell proliferation. Within the intima, monocytes differentiate into macrophages and accumulate lipid which, in turn, become foam cells as their lipid content increases. These cellular scavengers endocytose modified lipoproteins via a non-LDL-specific receptor mediated pathway and attempt to remove them from the intima. However, because of an imbalance between lipid accumulation and foam cell clearance, there is a net accumulation within the intima (18). The process of “scavenging” lipoproteins by

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Part II Basic Cardiovascular Problems Flowing * Chemoattractant

P-Selectin

7

Adherent

LFA-1

L

7

L

7

7

L-Selectin

ICAM-1,2

ICAM-1,2 L-Selectin ligand L

LFA-1

L

7

Mac-1

7

Mac-1 L-Selectin

7 7

7

A

P,E-Selectin ligand

L

C 7

7

* Histamine, Thrombin

* Cytokines P-Selectin

Roiling

LFA-1 7

7

7

ICAM-1,2

ICAM-1,2

L-Selectin ligand

7 7

L-Selectin ligand Mac-1 7

Mac-1 L-Selectin

D

7

L-Selectin 7

7

B

7 7

P,E-Selectin ligand

E-Selectin

Adherent

LFA-1 7

7

7

P,E-Selectin ligand

P,E-Selectin ligand 7

FIGURE 9.19 The sequence of events in granulocyte adhesion. (A) Without inflammation, the granulocyte does not interact with the endothelium. (B) In the presence of inflammation, the endothelial cells rapidly express selectins and granulocytes begin to roll. (C) Chemoattractants cause the granulocyte to convert to a more adhesive conformation resulting in binding with ICAMs. (D) The granulocyte becomes adherent.

E-selectin

VCAM-1

ICAM-1

TNF-a 50 U/mL 0h

6h

24 h

These lesions regress in early life and return later in childhood (90). Interestingly, females tend to have a greater number of fatty streak lesions in the aorta than males earlier in life. This contrasts, however, with the finding that men tend to develop more advanced lesions later in life (91,92). These contrasts make the association between fatty streak presence and progression to atherosclerosis difficult and confusing. However, it may be that the events that follow fatty streak development involving vascular smooth muscle cells herald the development of clinically significant atheromatous lesions.

Progression FIGURE 9.20 Time course of cell adhesion molecules on human umbilical vein endothelial cells (HUVEC) stimulated by TNF-a.

macrophages leads to the release of cytokines which stimulate smooth muscle migration and proliferation (Fig. 9.22) (41). The fatty streak precedes the development of a more advanced atheromatous plaque. Microscopically, fatty streaks are highly cellular, monocyte- and Tlymphocyte-rich lesions. Grossly, they may be visible to the naked eye as yellow streaks or dots on the blood vessel wall (70). However not all fatty streaks mature into problematic lesions. Recent investigations have shown that fatty streaks are present in the vessels of human fetuses.

Whereas endothelial cell dysfunction is central to the formation of atherosclerotic lesions, smooth muscle cell proliferation becomes an important factor of plaque evolution (Fig. 9.23). Chemoattractants such as PDGF induce vascular smooth muscle cell migration from the media into the intima (94–96). Once these smooth muscle cells have migrated from the media, growth factors stimulate their proliferation and growth. These include fibroblast growth factor (FGF), heparin-binding epidermal growth factor (HB-EGF), and PDGF and TGF-b in addition to PDGF (97–101). Vascular endothelial cell growth factor (VEGF) is another substance found to be a potent mitogen for endothelial cells. Produced by endothelial cells and macrophages, VEGF induces endothelial cells to produce collegenase, urokinase plasminogen activator (uPA), tPA, and plasminogen activator inhibitor 1 (PAI1) —factors that are important in promoting vascular repair (102). Other potent mitogens that have been

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FIGURE 9.21 A schematic depicting neutrophil adhesion and transmigration.

FIGURE 9.22 The potential roles of the macrophage in atherogenesis.

FIGURE 9.23 Smooth muscle proliferation.

found include IL-1, thrombin, and TNF-a. These work indirectly by stimulating PDGF activity (103–105). In addition to growth factors and cytokines, coagulation factors contribute to the maturation of atherosclerotic lesions. At areas where the endothelium has been

denuded, platelet-rich microthrombi form. The activated platelets contained within these lesions release several factors promoting a fibrotic response (92,106,107). As the plaque matures, small vessels develop and extend from the vasa vasorum surrounding the artery. This microcirculation serves to provide a portal of delivery of substances that progress the evolution of the atheroma. Additionally, focal hemorrhages may occur, releasing thrombin into the area of the plaque. Thrombin, in addition to blood coagulation, modulates smooth muscle cell activity via PDGF activity, thereby, fueling the cycle of intimal cellular accumulation in response to injury (108). The smooth muscle cells that occupy the intima proliferate slowly over decades with punctuated spurts of increased cell division brought on by intermittent plaque disruption (109). This proliferation is regulated, however, by local cytostatic mediators such as TGF-b and IFN-g, which inhibit smooth muscle cell division (110,111). Additionally, there is data to support that apoptosis of smooth muscle cells also plays a role in inhibiting prolifer-

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ation (112,113). This may explain why more mature plaques are characterized by increased fibrous and less cellular architecture. It should be emphasized that the smooth muscle cells that migrate to the intima are morphologically different from the native smooth muscle cells found in the media (Fig. 9.24). The smooth muscle cells of the atheromatous plaque tend to be less mature histologically and highly secretory in function. These cells produce the connective tissue and cellular constituents that make up the surrounding arterial extracellular matrix (ECM). The matrix includes type I and type III collagen, elastin, and proteoglycans (41). Investigations have shown that under the influence of cyclic strain, smooth muscle cells increase production of collagen. This accumulation of connective tissue increases as the plaque matures (114). In addition, as neovascularization occurs within the lesion, microthrombi form serving as a nidus for platelet aggregation and, subsequently, amplification of the atherosclerotic process via PDGF. As with each of the previous steps in plaque formation, there is a regulatory process that controls ECM formation. This is achieved by matrix metalloproteinases (MMPs), which enzymatically break down the various ECM macromolecules (115).

Plaque Stability If the plaques persist and continue to mature, they may rupture and cause more acute symptoms. Vulnerable plaques are more prone to disruption and subsequent thrombus formation. The plaques which are more lipidrich are more likely to rupture than those which are collagen rich. Studies have revealed that high lipid content, intense inflammatory activity, and lack of smooth muscle cell-mediated healing are some of the factors that determine plaque vulnerability (Table 9.4). The central core of

an atheromatous lesion is devoid of connective tissue and consists mainly of lipid and apoptotic nuclear fragments (116–120). Moreover, the plaques which tend to rupture contain high concentrations of cholesterol esters rather than free cholesterol (121,122). Areas of the plaque where the fibrous cap is the thinnest and most heavily infiltrated by foam cells are most vulnerable to the physical forces that cause their disruption. As the size of the core increases so too does its propensity to rupture (123). Recent investigations have also shown that foam cells reside at the site of disrupted fibrous caps in high concentrations (124). These immune-activated macrophages are capable of secreting MMPs, cysteine proteinases, and serine proteinases that can degrade the ECM and fibrous cap, further destabilizing the plaque. Collagen secreted by smooth muscle cells serves to stabilize plaques. However, studies show that at areas of plaque rupture, collagen and intact smooth muscle cells are present in small quantities (125–129). It may be that smooth muscle cell proliferation becomes impaired or retarded in rupture-vulnerable areas or it may be that apoptosis of these cells plays a role. Along with the intrinsic factors mentioned above, there are also extrinsic factors that contribute to plaque stability and their propensity to become disrupted. Extrinsic factors that trigger plaque disruption are listed in Table 9.4. Blood pressure exerts circumferential tension on the blood vessel wall. Compressive stress is pressure exerted onto the lumen due to vasospasm, vasa vasorum bleeding, or plaque edema. Circumferential bending stress refers to the bending of soft plaques by cyclic blood pressure changes. This causes eccentric plaques to bend at the edges, which may weaken the plaque. Hemodynamic forces (as mentioned earlier) can promote plaque complications by accelerating the atherosclerotic process by exposing the endothelium to low or oscillatory shear stress (130). Atheromatous plaques may become calcified with time (131). This calcification alters the elastic properties and has significant hemodynamic consequences. Large atheromatous plaques have an increased tendency and capacity for calcium binding than does normal arterial wall. Whereas calcium tends to bind elastin on normal vessel walls, in plaques, calcium binds with collagen. Large deposits of calcium found on atheromatous plaques can TABLE 9.4 Factors affecting plaque stabilization Intrinsic factors 1. Atheromatous core lipid content 2. Fibrous cap thickness 3. Presence of cap inflammation 4. Fatigue

FIGURE 9.24 The two different phenotypic states of smooth muscle cells in atherosclerosis.

Extrinsic factors 1. Circumferential stress 2. Compressive stress 3. Circumferential bending stress 4. Hemodynamic forces

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thereby be directly mediated by this interaction with collagen. However, there may also be increased deposits of calcium that arise from hemorrhages within plaques that result in ischemic necrosis (Fig. 9.25) (132).

in smaller caliber vessels. The results of plaque embolization is a spectrum of symptoms ranging from transient ischemic attacks and gangrene of toes to massive strokes and acute arterial occlusion.

Plaque Complications

Classification of Atherosclerotic Plaques

Complicated plaques refer to advanced lesions that usually lead to acutely critical symptomatic conditions. It is important to note that most atherosclerotic lesions do not produce symptoms. One reason for this is that blood vessels undergo compensatory enlargement. As mentioned earlier, the endothelium interacts with hemodynamic forces and attempts to maintain smooth blood flow. To accomplish this, the blood vessel grows in an abluminal direction, effectively keeping luminal diameter constant. This compensation in vessel size remains effective only as long as the atherosclerotic lesion occupies less than 40% of the lumen. Above this level, stenosis of the lumen occurs and blood flow is compromised (133,134). Another reason stable lesions may not progress to acute symptoms has to do with the body’s ability to respond to multiple bouts of hypoxic injury. When this occurs, usually on a chronic basis, the body responds by developing collateral circulation to supply those areas where blood supply is compromised under demand situations. Lesions that cause limitations to blood flow under demand situations present as angina pectoris or intermittent lower extremity claudication (Fig. 9.26). When disrupted, the plaques become ulcerated and tissue factor within the plaques is exposed. The clotting cascade is initiated and thrombus formation occurs. This process is dynamic with thrombosis and thrombolysis occurring simultaneously. Most disrupted plaques develop a small mural thrombus and only occasionally does a major near-occlusive or occlusive thrombus form (135). Another complication that may occur is embolization of a disrupted plaque causing arterial occlusion downstream

In studying the formation and progression of atherosclerotic plaques, five distinct phases can be identified by which to classify the plaques (Fig. 9.27). Phase I lesions are early changes found in arteries that will progress in a stable fashion for several years. Phase II lesions are lipidrich plaques that are prone to disruption. Phase III and phase IV lesions refer to acutely complicated plaques that lead to either a nonocclusive (phase III) or occlusive (phase IV) thrombus. Either of these lesions can then evolve into a phase V lesion which is a more organized and fibrotic thrombus. Atherosclerotic plaques can also be categorized histologically as they progress through the various clinically significant phases. Type I, II, and III lesions are Phase II lesions that differ in cell number and lipid quantity. As the lesions become more lipid-rich, two histologically different types of lesions predominate. Type IV describes a lesion with intermixed lipids and fibrous tissue whereas type Va is a lesion with an increased lipid core covered by a thin fibrous cap. Types Vb and Vc represent lesions which are progressively more and more fibrotic. The designation of type VI lesion is reserved for those lesions found in phase III and IV causing acute syndromes (136–138).

FIGURE 9.25 Atherosclerotic plaque demonstrating focal hemorrhage. M, Media; MD, media degradation; LC, lipid core; PH, plaque hemorrhage; PS, plaque shoulder; FC, fibrous cap.

Risk Factors Hyperlipidemia There are ample data from animal, epidemiological, and interventional studies that implicate a role for high cholesterol in the atherosclerotic process. Cholesterol transport mediated by lipoproteins has a primary role in the genesis of atherosclerosis. Lipoproteins are high-molecularweight complexes of circulating lipid and protein that function in the transport of fatty acids and lipids to cells. Lipoproteins are also metabolic precursors to prostaglandins, thromboxanes, and leukotrienes. There are three classes of lipoproteins: VLDL, LDL, and HDL. Of the group, LDL contains the highest concentration of cholesterol (60–70% of total serum cholesterol). Lipoproteins are composed of lipids and proteins held together by covalent bonds (Fig. 9.28). Proteins associated with lipoproteins are called apoproteins. These amphipathic molecules interact with the lipid-soluble portion of lipoproteins and serve to stabilize their structure. Dietary fats are digested into triglycerol-rich molecules that are absorbed into the bloodstream through the intestinal mucosa in the form of a mixed micelle called the chylomicron. Lipoprotein lipase, an enzyme found in the

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Part II Basic Cardiovascular Problems Stage I Asymptomatic

Stage II Symptomatic

Stage III Complications

FIGURE 9.26 Diagram of the natural history of atherosclerosis. First, fatty streaks develop. These lesions progress to fibrous plaque and thrombus formation. Clinically, these lesions will manifest as myocardial infarction, stroke, gangrene, or aneurysm.

Cholesterol ester Core Triglyceride A-I, A-II B-100,B-48 C-I, C-II, C-III Apolipoproteins E (E2/E3/E4) Coat Unesterified cholesterol Phospholipids

FIGURE 9.28 Structure of lipoproteins.

FIGURE 9.27 Classification of atherosclerotic plaques.

bloodstream, further digests the triglycerides within the chylomicron into free fatty acids and glycerol. Surface apoproteins and lipids detach from the chylomicron to become HDLs. The chylomicron is taken up by the liver and cleared from the bloodstream (Fig. 9.29). Endogenously produced lipoproteins, i.e., VLDL is similarly catabolized into intermediate-density lipoproteins (IDLs) and surface fragments that get incorporated into HDLs. VLDL is produced in the liver and 20% to 60% of VLDL is eventually converted to LDL. The catabolism process renders the LDL particle triglyceride-deficient but cholesterol-rich (Fig. 9.30). HDL is similar to LDL, but does not contain apoprotein B (ApoB). HDL functions to transport cholesterol into and out of peripheral tissues. However, LDL is the major cholesterol-carrying lipoprotein and accumulates in plasma if there is increased dietary intake or decreased removal by the liver (139–144).

Elevated levels of LDL affect the atherosclerotic process by both increasing the influx of cholesterol into the intima as well as inhibiting its efflux. In addition, LDLs also promote thrombosis (145,146). HDL, on the other hand, promotes cholesterol efflux and inhibits the accumulation of LDL cholesterol, protecting vessels from atherosclerosis. Consequently, diets high in saturated fats and cholesterol are associated with increased atherosclerosis and thrombogenesis (147–149). The atherogenic contribution of lipoproteins is related mainly to their size. VLDLs and chylomicrons are too large to penetrate the vessel wall and are nonatherogenic. HDLs are small molecules that can easily enter and leave the vessel wall and are, therefore, also nonatherogenic. It has been speculated that HDLs serve a protective effect by transporting cholesterol out of vessel walls. Increased HDL levels are associated with a decreased atherosclerotic risk; however, the exact mechanism is unknown (150–152). Lipoprotein(a) is another lipoprotein which is a triglyceride-rich particle that has been associated with increased rates of atherosclerosis. Lipoprotein(a) is a particle consisting of an apoprotein A molecule bound to the apolipoprotein b moiety of LDL-cholesterol. Lipopro-

Chapter 9 Atherosclerosis: Biological and Surgical Considerations Dietary cholesterol and triglycerides

FIGURE 9.29 Chylomicron metabolism.

B-48 E

E es

lycerid Trig CE

153

Small intestine

CIII

CIII CII

E

CII

CIII AI E CE

CE

AII

AII

CII

AI

B-48

E

E

Remnant receptor (LRP)

Lipoprotein lipase

CIII

Capillaries

E Free fatty acids

es

lycerid Trig CE

LDL receptor

CIII

Liver

CIII Muscle

E Chylomicron remnant

apo E apo C-III apo C-II

apo A-I apo A-II apo B-48

Hypertension

Antioxidant Beta-carotene Vitamin E Ubiquinol

Lipoprotein core

Unesterified cholesterol

Cholesterol ester

H2N Triglyceride

Apo B-100 HOOC

Fat tissue

225–275A

Phospholipid

FIGURE 9.30 The structure of LDL. Its surface comprises cholesterol, phospholipids, and apoprotein B-100.

tein(a) levels have been found to be elevated in particular populations, e.g., 15% of the African-American population have elevated levels. Lipoprotein(a) localizes in atherosclerotic plaques, where it likely acts to promote plaque complications (153,154). This may occur via the ApoA portion of lipoprotein(a) which behaves like plasminogen, thereby inhibiting fibrinolysis.

Hypertension, defined as systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg, is associated with a twofold increase in death secondary to coronary heart disease (155). It should be emphasized that hypertension, per se, is not atherogenic. In studies using laboratory animals with normal cholesterol levels, hypertension in these animals did not induce atherosclerosis (156). However, it has been shown that hypertension or relative hypertension may accelerate the atherosclerotic process. For example, veins do not usually undergo atherosclerotic changes unless subjected to higher than normal pressures, as is the case when using vein graft for CABG or distal revascularization. Similarly, pulmonary vessels which normally operate under a lowpressure, low-resistance environment rarely exhibit atherosclerotic changes. This finding changes, however, in the presence of pulmonary hypertension (157–160). Hypertension may promote atherogenesis by a direct effect on the vascular architecture. Arteries exposed to hypertension have increased vascular permeability, which results in an increased ability of macromolecules including lipoproteins to migrate into the intima. Numerous investigations have demonstrated that the transduction of mechanical forces directly to smooth muscle cells alters their function, thereby contributing to the progression of atherosclerosis (161–165). Smooth muscle cells, unlike endothelial cells, reside in the arterial subendothelium

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and are not exposed to shear stress due to their medial location within the arterial wall. However, smooth muscle cells are affected by cyclic strain caused by the pulsatile stretching of the vessel wall by blood pressure. The transferred pressure increases as blood pressure increases. This increased pressure induces changes in smooth muscle cell shape, orientation, proliferation, and secretion of extracellular matrix substances that contribute to the development of atherosclerotic lesions. There is new evidence that suggests hypertension affects vessel wall remodeling by altering the balance between cellular proliferation and apoptosis (166,167).

Diabetes Mellitus Diabetes mellitus can also promote atherogenesis, as evidenced by the fact that over 75% of hospitalizations of diabetics are related to cardiovascular complications (Fig. 9.31) (168). There is evidence that atherosclerosis is more accelerated and diffuse in patients with diabetes. Diabetic patients demonstrate a disease pattern of accelerated atherosclerosis that affects sites that are otherwise not commonly involved in atherosclerosis, such as the deep femoral and distal tibial and peroneal arteries (169,170). The effects of atherosclerosis on a diabetic patient are serious and debilitating. Diabetic patients have a twoto three-fold increased risk of developing claudication (171). In addition, there is an increased risk of amputation in these patients (172). The underlying mechanism, however, may be multifactorial. For instance, there is an increased atherosclerotic risk with diabetes because of its association with dyslipidemias and hypertension (171). Patients with diabetes mellitus exhibit significant alterations in their lipid profiles (Table 9.5) (173). These changes include increased triglyceride levels, decreased HDL levels, and increased amounts of chylomicron fragments. LDL levels may be mildly elevated. Hypertension is also two times more prevalent in patients with diabetes mellitus that in the general population (174). However, more recent data seems to suggest that other factors such as smoking, elevated cholesterol levels, and increased blood pressure may confound these associations (175). One interesting obser-

vation is that patients with elevated glucose levels, but not in the diabetic range, still maintain an increased risk of developing atherosclerosis (176,177). Nonenzymatic glycosylation of LDL is enhanced in patients with diabetes mellitus. This nonenzymatic glycosylation has been shown to impair LDL binding to its receptor, thereby resulting in hyperlipidemia (Fig. 9.32) (178). In addition, glycosylated LDL has been shown to increase the formation of foam cells typically found in early atherosclerotic lesions (175). Some data reports that immune mechanisms also play a role in the development of atherosclerosis in the diabetic patient. Modified lipoproteins may trigger the formation of autoantibodies that interact with oxidized LDL. These complexes, once taken up by macrophages, may then stimulate the release of cytokines and growth factors that lead to the progression of plaque formation (179,180). In chronic hyperglycemia, for example, increased levels of circulating immune complexes may signal the release of insulinrelated growth factors (e.g., IGF-1), which, in turn, stimulate the formation and growth of mature plaques (181,182). In addition to affecting smooth muscle cells, hyperglycemia also affects the components of the extracellular matrix. In patients with diabetes mellitus, the basement membrane, normally an amorphous structure composed of type VI collagen, glycoproteins, and proteoglycans, is thickened. The composition of the basement membrane changes during chronic hyperglycemia and displays increased amounts of hydroxylysine, glucose disaccharides, and type IV collagen. In contrast, the amounts of proteoglycans, heparin sulfate, and the glycoprotein laminin are decreased (183–187). This thickened basement membrane may play a role in changing the stability of the vessel wall and may help explain the increased vascular permeTABLE 9.5 Quantitative changes of serum lipoproteins in patients with diabetes mellitus Lipid or Lipoprotein

IDDM

NIDDM

≠ ≠ ≠ ≠ Ø

≠ ≠≠ ≠≠ ≠ ≠

Serum cholesterol Serum triglyceride VLDL LDL HDL

Cardiovascular (77%) N

Other (4%)

Liver

LDl receptor

Apo B C LDL

Ophthalmic (4%) Neurologic (6%)

Glucose

Small dense LDL

Peripheral tissues Renal (9%)

FIGURE 9.31 Major causes of hospitalization in patients with diabetes mellitus.

Abnormalities in diabetes mellitus

FIGURE 9.32 LDL metabolism in diabetes mellitus.

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

ability often seen in the vasculature of multiple organs in patients with diabetes mellitus. In patients with poorly controlled diabetes mellitus, there may be an additional effect on the progression of atherosclerosis. These patients tend to have increased triglyceride levels with decreased HDL levels. This results in protein modification to a more dense LDL that is more atherogenic than that of patients with diabetes mellitus (109,188). Additionally, lipoprotein(a) abnormalities are found to be more common in patients with poorly controlled diabetes mellitus. Thrombotic events are enhanced in these patients, thereby increasing the risk of atherosclerosis-related complications. Increased platelet activity, levels of fibrinogen, and levels of PAI-1 have been demonstrated in patients with diabetes mellitus (189,190). These may additionally contribute to the endothelial dysfunction and erosion commonly seen in diabetic atherosclerotic lesions.

Obesity/Physical Inactivity Obesity, by itself, is not directly associated with increased risk of atherosclerosis. However, obesity and physical inactivity predispose patients to hypertension, diabetes mellitus and hyperlipidemia. Moreover, increased physical activity has been associated with an increased HDL and decreased LDL, thereby favoring an antithrombogenic lipid profile (191).

Cigarette Smoking Cigarette smoking and its effects on various disease processes have been studied extensively. With regards to its effects on the cardiovascular system, cigarette smoking has been associated with an increased risk of acute myocardial infarction, sudden death, and stroke. In addition, smoking has been demonstrated to aggravate stable angina pectoris, intermittent claudication, and vasospastic angina (192–194). The Framingham study has established smoking as one of five important predictors of atherosclerosis. Moreover, smoking history has been found to be the most predictive of the development of intermittent claudication (195). Cigarette smoke contains more than 4000 compounds. Of these, nicotine, aromatic hydrocarbons, sterols, aldehydes, nitriles, cyclic ethers, and sulfur compounds are the most important (196,197). Cigarette smoking has been shown to increase cardiac output via nicotine-mediated effects on heart rate and contractility (198–200). In addition, nicotine promotes hyperlipidemia by stimulating lipolysis. Nicotine increases LDL and decreases HDL (201). Moreover, the oxidant gases contained within cigarette smoke result in higher levels of oxidized LDL which may confer the increased risk of atherosclerosis seen in patients that smoke. Endothelial cell damage secondary to smoking has been documented (202,203). Studies have shown endothelial cell swelling, luminal surface projections, and nuclear folding with

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basal fibroblasts in smokers. In addition, smooth muscle cells are affected by nicotine. They are converted from a contractile to a synthetic phenotype (204,205). Other effects of cigarette smoking that may enhance atherosclerosis include increased levels of fibrinogen, increased platelet activity, and increased blood viscosity (206). Additionally, nicotine appears to decrease prostacyclin levels. This alteration promotes increased vascular tone, perhaps subjecting the vessel to increased levels of cyclic strain (Fig. 9.33) (207).

Homocysteine Homocysteinemia is an autosomal recessive disease that results in a deficiency of the enzyme cystathionine bsynthase. Deficiency of this enzyme leads to a decreased conversion of homocysteine derived from dietary methionine to cystathionine. Elevated levels of homocysteine have been correlated with an increased risk of coronary heart disease, stroke, and peripheral vascular disease (208–212). One study has reported that a 12% increase of homocysteine levels above normal increases the risk of myocardial infarction more than three times. Investigations have shown homocysteine to cause endothelial cell dysfunction, smooth muscle cell proliferation, and collagen production. These effects are thought to be mediated by increased LDL oxidation and inhibition of endogenous anticoagulant activity (213–217). Recent studies indicate that homocysteine may potentiate the latter effect by blocking the activation of Protein C and thrombomodulin expression on endothelial cells (218).

Estrogen Although the major risk factors for atherosclerosis development are similar for both sexes, men tend to manifest clinical complications 10 to 15 years earlier than women. Women have a low incidence of heart disease before menopause, after which it rises to levels similar to those found in men. Moreover, women who receive hormone replacement therapy are at a lower risk for heart disease than women who do not receive such treatment (219,220). The idea of estrogen serving a protective function against atherosclerosis has been put forward based on these observations. In premenopausal women, higher levels of estrogen promotes increased levels of HDL and decreased levels of serum total cholesterol, LDL, and lipoprotein(a) (219,221). Interestingly, with the onset of menopause, LDL levels have been found to rise while HDL levels fall, changing the previously antiatherogenic lipid profile to one more equivalent to that seen in men. Estrogen alters serum lipoprotein levels via estrogen receptor-mediated effects on hepatic expression of apoproteins. There is a net increase in apoprotein production that results in a 10% to 15% rise in HDL. Concomitantly, estrogen causes an upregulation of hepatic LDL receptors which results in increased LDL catabolism by the liver. Although this unfavorable lipid profile can be

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VSMC Modulation ? Matrix metalloproteinase expression VSMC Migration Alterations in lipid metabolism

Endothelial injury NICOTINE (+)TXA-2 (–)PGI2 Platelet Aggregation

Sympathetic stimulation

Increase heart rate Increase cardiac contractility

Coronary vasoconstriction

Intimal hyperplasia

Increased catecholamines

ATHEROSCLEROSIS

Cardiac arrhythmias

FIGURE 9.33 Role of nicotine in atherosclerosis.

altered with the use of estrogen replacement, the effects of the atherosclerotic process are not completely reversed (222). There are data to suggest that estrogen may have antioxidant, eNOS-mediated cytoprotective, and antithrombogenic effects as well. Estrogen may, therefore, have direct atheroprotective properties that retard the atherosclerotic process.

Therapeutic Implications The goals of treatment for patients with peripheral vascular disease are to relieve symptoms, improve function, improve wound healing, prevent limb loss, and improve quality of life. For the purposes of therapy, a surgeon must understand the pathobiologic and biochemical mechanisms of atherosclerosis. With this understanding, preventive and therapeutic strategies, both operative and nonoperative, can be employed to efficiently and effectively combat atherosclerosis early in its course. There are a variety of major risk factors for the development of atherosclerosis, and, in turn, peripheral vascular disease (Table 9.6). Because of the presence of these risk factors and the systemic nature of atherosclerosis, patients with PVD should be considered as candidates for behavior modification and drug therapies. Lipid lowering drugs should be a part of any treatment regimen. Several studies have shown a decrease in LDL and lipoprotein(a) levels with the use of HMG-CoA reductase inhibitors (223–225). A goal of LDL cholesterol less than 100 mg/dL and triglyceride levels less than 150 mg/dL should be pursued. The use of statins may be augmented with the use of niacin, which helps to increase HDL levels (226).

TABLE 9.6 Major cardiovascular risk factors Modifiable

Fixed

Lipids and lipoproteins Cholesterol Triglycerides LDL HDL Remnant lipoproteins Postprandial lipoproteins Lp(a) Blood pressure Diabetes mellitus Cigarette smoking Central obesity/insulin resistance

Age Gender Family history

Although no particular antihypertensive medication has been shown to impact the progression of PVD, appropriate control of heart rate and blood pressure should be done to minimize cardiac events (227). There is some evidence to suggest that the use of ACE inhibitors may reduce ischemic events in patients with PVD (228). Diabetic patients should be aggressively treated and monitored. Fasting blood sugars should be less than 120 mg/dL, postprandial glucose should be less than 180 mg/dL, and hemoglobin A1c should be less than 7% (226). Patients should be encouraged to seriously curb and discontinue cigarette use by attending smoking cessation programs, using nicotine replacement therapy, or using the antidepressant bupropion (229,230). Dietary supplementation of vitamin B12 and folic acid should be pre-

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

scribed, especially to patients with homocysteinemia (231). All patients should be advised to maintain a regular exercise regimen and to minimize dietary fat intake (226,232). Lastly, the use of anti-platelet drugs has been shown to reduce the risk of fatal and nonfatal ischemic events in patients with vascular disease. There are several drugs that are available; however, aspirin and clopidogrel have been found to be quite effective. Understanding the biology of atherosclerosis and realizing why lesions occur where they do has an impact on how patients with PVD are approached surgically. For example, plaque formation occurs at the origin of the proximal internal carotid artery, whereas the common and distal internal carotid are not prone to atherosclerosis. The area of the carotid sinus opposite the flow divider exhibits low shear stress, and plaque formation there is increased. Correlative studies done with glass models of the carotid bifurcation revealed that maximal intimal thickness occurred on the side opposite the flow divider. As illustrated in Figure 9.13, this region is subject to changes in hemodynamic forces that promote atherosclerosis. In contrast, the flow remained laminar and intimal thickening was minimal on the inner wall of the flow divider (46). These observations have led to the widespread abandonment of arteriography as a diagnostic tool in evaluating patients with carotid artery stenosis. Armed with this information, efficient and effective surgical treatment can be implemented by the vascular surgeon. For patients with carotid disease, a good quality Doppler study gives the surgeon ample information prior to surgery. In coronary arteries, atherosclerotic plaques tend to form at branch points distal to the bifurcation of the left main and at branch points along the left anterior descending and left circumflex arteries. The coronary vessels are subject to low blood velocity and oscillating shear stress contributing to the increased rate of atherosclerotic lesion encountered in this vascular tree (233,234). Studies have also showed that heart rate, in addition to shear stress changes, increases the propensity of atherosclerotic lesions to form. As heart rate increases, the coronary system is exposed to diastole for a shorter period of time. Whereas oscillatory shear stress predominates during systole, during diastole steady laminar flow predominates (235). In animal studies, plaque formation was retarded by a 20% decrease in resting heart rate (236). Within the aorta the infrarenal aorta is preferentially affected by atherosclerosis. This is a result of the lower blood flow that reaches the infrarenal aorta. About 25% of the cardiac output is diverted to the renal arteries and a significant amount is also diverted to the celiac and superior mesenteric tributaries. Similar to the carotid bifurcation, the aortic bifurcation is exposed to the same hemodynamic changes of altered shear stress and flow characteristics. At the aortic bifurcation, atherosclerosis is preferentially localized to the lateral walls opposite the flow divider. Again, as in the case of carotid disease, these observations have resulted in newer treatment strategies. For example, percutaneous transluminal an-

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gioplasty (PTA) has been found to be a viable treatment option in patients with ostial lesions and aortoiliac disease (237,238). Research on the process of atherosclerosis is ongoing. Our understanding of the disease and its clinical effects has increased almost exponentially since the beginning of the twentieth century. Although many advances have been made, both in medical and surgical treatment, atherosclerosis remains a worthy adversary, impacting the lives of many. With the development of techniques making it possible to alter and modify genes, a new modality may be on the horizon of vascular disease therapy. Gene therapy may allow treatment directed at the initiation and progression steps of atherogenesis. It may be possible, someday, to reverse the already initiated process. However, achieving these goals will require more intensive investigation and a better understanding of a very complex process.

References 1. Brothwell D, Sandison AT, eds. Diseases in antiquity: a survey of the diseases, injuries and surgery of early populations. Springfield, IL: Charles C Thomas; 1967: 474–488. 2. Moodie RL. Paleopathology: an introduction to the study of ancient evidences of disease. Urbana, IL: University of Illinois Press; 1923. 3. Harris CRS. The heart and vascular system in Ancient Greek medicine from Alcmaeon to Galen. Oxford: Clarendon Press; 1973. 4. Bing RJ, ed. Cardiology: the evolution of the science and the art. Philadelphia, PA: Harwood Academic Publishers; 1992: 127–143. 5. Harvey W. Leake C, translator. Exercitatio anatomica. De motu cordis et sanguinis in animalibus. Springfield, IL: Charles C Thomas; 1928. 6. Haimovici H, DePalma RG, et al., eds.. Vascular surgery principles and techniques, 3rd edn. Norwalk, CT: Appleton and Lange; 1989: 161–187. 7. Long ER. A history of pathology. New York: Dover Publications; 1965. 8. Fuster V, Ross R, Topol EJ, eds. Atherosclerosis and coronary artery diseases. Philadelphia, PA: LippincottRaven Publishers; 1996: 1–12. 9. Virchow R, Vogel J, Stiebel SFS, eds. Handbuch der Speciellen Pathologie und Therapie, Vol. 1. Erlangen, Germany: Ferdinand Enke; 1854: 95–270. 10. Rather LJ. A Commentary on the Medical Writings of Rudolf Virchow. San Francisco: Norman Publishing; 1990. 11. Cowdry EV, ed. Anitschokov N. Arteroscerosis: A Survey of the Problem. New York: Macmillan; 1933: 271–322. 12. Rubin E, Farber JL, eds. Pathology, 3rd edn. Philadelphia: Lippincott-Raven Publishers; 1999: 512–513. 13. Braunwald E, Creager MA, eds. Hirsch AT. Atlas of heart disease: vascular disease. Vol. 7. St. Louis: Mosby-Year Book, Inc.; 1996: 3.1–3.30. 14. Kannel WB, Wolf PA, Garrison RJ, eds. The Framingham Study: An Epidemiologic Investigaation of Cardiovascular Disease. NIH Publication No. 87–2703; 1987.

158

Part II Basic Cardiovascular Problems

15. Gordon T, Kannel WB. Predisposition to atherosclerosis in the head, heart, and legs: the Framingham study. JAMA 1974; 221: 661–666. 16. Norris JW, Zhu CZ, et al. Vascular risks of asymptomatic carotid stenosis. Stroke 1991; 22: 1485–1490. 17. Moore KL, Persaud TVN. The developing human: clinically oriented embryology, 5th edn. Philadelphia: WB Saunders, 1993: 332–353. 18. Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001: 995–1008. 19. Sidawy AN, Sumpio BE, eds. DePalma RG, Gallagher GL. The Basic science of vascular disease. Armonk, NY: Futura Publishing, 1997: 151–186. 20. Greenfield LJ, Mulholland M, et al., eds. Clowes AW. Surgery: scientific principles and practice, 2nd edn. Philadelphia: Lippincott-Raven Publishers; 1997: 1585–1595. 21. Glagov S, Weisenberg E, Zarins CK. Compensatory enlargement of human atherosclerotic coronary arteries. NEJM 1987; 316: 1371–1375. 22. Benditt EP, Benditt JM. Evidence for a monoclonal origin of human atherosclerotic plaques. Proc Natl Acad Sci 1973; 70: 1753–1756. 23. Gown AM, Benditt EP. Lactate dehydrogenase (LDH) isoenzymes of human atherosclerotic plaques. Am J Pathol 1982; 107: 316–321. 24. Strong JP. Natural history of aortic and cornary atherosclerotic lesions in youth: findings from the PDAY study. Arterio Thromb 1993; 13: 1291–1298. 25. Dugid JB. Thrombosis as a factor in the pathogenesis of aortic atherosclerosis. J Path Bact 1948; 60: 57. 26. Page JH. Atherosclerosis: an introduction. Circulation 1954; 10: 1. 27. Steinberg D, Parthasarathy S, et al. Modification of lowdensity lipoprotein that increases its atherogenecity. N Engl J Med 1989; 320: 915. 28. Morel DW, DiCorleto PE, Chisolm GM. Endothelial and smooth muscle cells alter low-density lipoprotein in vivo by free radical oxidation. Arteriosclerosis 1984; 4: 357–364. 29. Steinbrecher UP, Parthasarathy S, Leake DS, Witztum LJ, Steinberg D. Modification of low-density lipoprotein by endothelial cells involves lipid peroxidation and degradation of LDL phospholipids. Proc Natl Acad Sci USA 1984; 81: 3883–3887. 30. Heinecke JW, Rosen H, Chait A. Iron and copper promote modification of LDL by human arterial smooth muscle cells in culture. J Clin Invest 1984; 74: 1890–1894. 31. Cathcart MK, Morel DW, Chisolm GM. Monocytes and neutrophils oxidize low-density lipoprotein making it cytotoxic. J Leukocyte Biol 1985; 38: 341–350. 32. Zhang H, Basra HJK, Steinbrecher UP. Effects of oxidatively modified LDL on cholesterol esterification in cultured macrophages. J Lipid Res 1990; 31: 1361–1369. 33. Chisolm GM, Ma G, et al. 7b-Hydroperoxycholest-5en3b-ol, a component of human atherosclerotic lesions, is the primary cytotoxin of oxidized human low-density lipoprotein. Proc Natl Acad Sci USA 1994; 91: 11452–11456. 34. Fuster V, Ross R, Topol EJ, eds. Chisolm GM, Penn MS. Atherosclerosis and Coronary Artery Diseases. Philadelphia: Lippincott-Raven Publishers; 1996: 140–142.

35. Camejo G, Hurt-Camejo E, et al. Association of Apo B lipoproteins with arterial proteoglycans: pathological significance and molecular basis. Atherosclerosis 1998; 139: 205–222. 36. Williams KJ, Tabas I. The Response-to-retention hypothesis of atherogenesis reinforced. Curr Opin Lipidol, 1998; 9: 471–474. 37. Schwenke DC, Carew TE. Initiation of atherosclerotic lesions in cholesterol-fed rabbits. I. Focal increases in arterial LDL concentration precede development of fatty streak lesions. Arteriosclerosis 1989: 9: 908–918. 38. Schwenke DC, Carew TE. Initiation of atherosclerotic lesions in cholesterol-fed rabbits. II. Selective retention of LDL vs. selective increases in LDL permeability in susceptible sites of arteries. Arteriosclerosis 1989: 9: 908–918. 39. Ross R, Glomset JA. The pathogenesis of atherosclerosis. N Engl J Med 1976; 295: 369. 40. Ross R. The pathogenesis of atherosclerosis: an update. N Engl J Med 1986; 314: 488. 41. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993; 362: 801. 42. Sumpio BE, ed. Hemodynamic forces and vascular cell biology. Austin, TX: RG Landes Publishers; 1993. 43. Sumpio BE. Mechanical stress and cell growth. J Vasc Surg 1989; 10: 570–571. 44. Zarins CK, Giddens DP, et al. Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res 1983; 53: 502–514. 45. Friedman MH, Hutchins GM, Bageron CB. Correlation between intimal thickness and fluid shear in human arteries. Atherosclerosis 1981; 39: 425–436. 46. Ku DN, Giddens DP, et al. Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque localization and low and oscillatory shear stress. Arteriosclerosis 1985; 5: 293–302. 47. Gotlieb AI, Langille BL, et al. The structure and function of the endothelial cytoskeleton. Lab Invest 1991; 66: 123–127. 48. White GE, Gimbrone MA, Fujiwara K. Factors influencing the expression of stress fibers in vascular endothelial cells in situ. J Cell Biol 1983; 97: 416–424. 49. Wong AJ, Pollard TD, Herman IM. Actin filament stress fibers in vascular endothelial cells in vivo. Science 1983; 219: 867–869. 50. Kim DW, Langille BL, et al. Patterns of endothelial microfilament distribution in the rabbit aorta in situ. Circ Res 1989; 64: 21–31. 51. Sumpio BE, ed. Hemodynamic forces and vascular cell biology. Austin, TX: RG Landes Co; 1993: 47–65. 52. Frangos J, Eskin S, McIntire L. Flow effects on prostacyclin production by cultured human endothelial cells. Science 1985; 227: 1477–1479. 53. Okahara K, Kambayahi J. Upregulation of prostacyclin synthesis related gene expression by shear stress in vascular endothelial cells. Arterio Thromb Vasc Biol 1998; 18: 1922–1926. 54. Diamond SL, Eskin S, McIntire L. Fluid flow stimulates tissue plasminogen activator secretion by cultured human endothelial cells. Science 1989; 246: 1483–1485.

Chapter 9 Atherosclerosis: Biological and Surgical Considerations 55. Ziegler T, Silacci P, et al. Nitric oxide synthase expression in endothelial cells exposed to mechanical forces. Hypertension 1998; 32: 351–355. 56. Sumpio BE, Banes AJ, et al. Alterations in aortic endothelial cell morphology and cytoskeletal protein synthesis during cyclic tensional deformation. J Vasc Surg 1988; 7: 130–138. 57. Sumpio BE, ed. Hemodynamic forces and vascular cell biology. Austin, TX: RG Landes Co; 1993: 66–89. 58. Awolesi MA, Sessa WC, Sumpio BE. Cyclic strain upregulates nitric oxide synthase gene. FASEB J 1993; 7: A755. 59. Awolesi MA, Widmann MD, et al. Cyclic strain increases nitric oxide synthase activity. Surgery 1994; 116: 439–445. 60. Iba T, Sumpio BE. tPA expression in human endothelial cells exposed to cyclic strain in vitro. Cell Transplant 1992; 1: 43–50. 61. Cheng JJ, Wung BS, et al. Cyclic strain enhances adhesion of monocytes to endothelial cells by increasing intercellular adhesion molecule-1 expression. Hypertension 1996; 28: 386–391. 62. Evans L, Frenkel L, et al. Activation of diacylglycerol in cultured endothelial cells exposed to cyclic strain. Am J Physiol 1997; 272: c650-c656. 63. Frangos SG, Gahtan V, Sumpio BE. Localization of atherosclerosis: role of hemodynamics. Arch Surg 1999; 134: 1142–1149. 64. DeBakey ME, Lawrie GM, Glaser DG. Patterns of atherosclerosis and their surgical significance. Ann Surg 1985; 201: 115–131. 65. Rutherford RB, ed. Zarins CK, Glagov S. Vascular surgery, 4th edn. Philadelphia: WB Saunders, 1995: 204–221. 66. Blair JM, Glagov S, Zarins CK. Mechanism of superficial femoral artery adductor canal stenosis. Surg Forum 1990; 41: 359–360. 67. Sidawy AN, Sumpio BE, DePalma RG, eds. Tropea BI, Glagov S, Zarins CK. The basic science of vascular disease. Armonk, NY; Futura Publishing, 1987: 107–126. 68. Ziegler T, Nerem RM. Effect of flow on the process of endothelial cell division. Arterio Thromb 1994; 14: 636–43. 69. Smilde TJ, van den Berkmortel FW, et al. The effect of cholesterol lowering on carotid and femoral artery wall stiffness and thickness in patients with familial hypercholesterolemia. Eur J Clin Invest 2000; 30: 473–80. 70. Stary HC, Chandler AB, Glagov S. A definition of initial fatty streak and intermediate lesions of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Atherosclerosis, American Heart Association. Arterio Thromb 1994; 14: 840. 71. Reuckschloss U, Galle J, et al. Induction of NAD(P)H oxidase by oxidized low-density lipoprotein in human endothelial cells: antioxidative potential of hydroxymethylglutaryl coenzyme A reductase inhibitor therapy. Circulation 2001; 104: 1767–72. 72. Matsushita H, Lee KH, Tsao PS. Cyclic strain induces reactive oxygen species production via an endothelial NAD(P)H oxidase. J Cell Biochem 2001; 36 (Suppl.): 99–106. 73. Hermann RA, Malinauskas RA, Truskey GA. Characterization of sites with elevated LDL permeability at intercostal, celiac, and iliac branches of the normal rabbit aorta. Arterio Thromb 1994; 14: 313–323.

159

74. Kritchevsky D. Atherosclerosis and nutrition. Nutr Int 1986; 2: 290. 75. Kannel WB. Update on the role of cigarette smoke in coronary artery disease. Am Heart J 1981; 101: 319. 76. Malinow MR. Hyperhomocysteinemia: a common and easily reversible risk factor for occlusive atherosclerosis. Circulation 1990; 81: 2004–2006. 77. Ginsberg HN. Lipoprotein physiology in non-diabetic and diabetic states: relationship to atherosclerosis. Diabetes Care 1991; 14: 839–855. 78. Vlassara H, Bucala R, Striker L. Pathogenesis effect of advanced glycosylation: biochemical and biologic implication for diabetes and aging. Lab Invest 1994; 70: 138–151. 79. Sumpio BE, ed. Hemodynamic forces and vascular cell biology. Austin, TX: RG Landes Co; 1993: 151–186. 80. Erl W, Weber C, et al. Adhesion properties of Mono Mac 6, a monocyte cell line with characteristics of mature human monocytes. Atherosclerosis 1995; 113: 99– 107. 81. Witztum JL, Berliner JA. Oxidized phospholipids and isoprostanes in atherosclerosis. Curr Opin Lipidol 1998; 9: 441. 82. Walpola PL, Gotlieb AI, et al. VCAM-1 expression and monocyte adherence in arteries exposed to altering shear stress. Arterio Thromb Vasc Biol 1995; 15: 2–10. 83. Rollins BJ, Yoshimura T, Leonard EJ. Cytokine-activated human endothelial cells synthesize and secrete a monocyte chemoattractant, MCP-1/JE. Am J Pathol 1990; 136: 1229–1233. 84. Nelken N, Coughlin S, Gordon D. Monocyte chemoatttractant protein-1 in human atheromatous plaques. J Clin Invest 1991; 88: 1121–1127. 85. Reape TJ, Groot PHE. Chemokines and atherosclerosis. Atherosclerosis 1999; 147: 213–225. 86. Spiecker M, Darius H, et al. Differential regulation of endothelial cell adhesion molecule expression by nitric oxide donors and antioxidants. J Leukoc Biol 1998; 63: 732–9. 87. Palmer RM, Moncada S. A novel citrulline-forming enzyme implicated in the formation of nitric oxide by vascular endothelial cells. Biochem Biophys Res Commun 1989; 158: 348–352. 88. Palmer RM, Rees DD, et al. L-arginine is the physiological precursor for the formation of nitric oxide in endothelium-dependent relaxation. Biochem Biophys Res Commun 1988; 153: 1251–1256. 89. Schmidt HHH, Nau H, Wittfoht W. Arginine is a physiological precursor of endothelium-derived nitric oxide. Eur J Pharm 1988; 154: 213–216. 90. Napoli C, Glass CK, Witztum JL. Influence of maternal hypercholesterolemia during pregnancy on progression of early atherosclerotic lesions in childhood: Fate of Early Lesions in Children (FELIC) study. Lancet 1999; 354: 1234–1241. 91. McGill HC, McMahan CA, Malcom GT. Effects of serum lipoproteins and smoking on atherosclerosis in young men and women. The PDAY Research Group. Arterio Thromb 1997; 17: 95–106. 92. Davies MJ, Woolf N. Atherosclerosis: what is it and why does it occur? Br Heart J 1993; 69 (Suppl.): S3–S11. 93. Stary HC, Chandler AB, et al. A definition of advanced types of atherosclerotic lesions and a histological classifi-

160

94.

95.

96.

97.

98.

99.

100.

101.

102.

103.

104.

105. 106.

107.

108.

109.

110.

111.

112.

Part II Basic Cardiovascular Problems cation of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995; 92: 1355–1374. Ross R, Raines EW, Bowen-Pope DF. The biology of platelet-derived growth factor. Cell 1986; 46: 155–169. Hart CE, Forstrom JW, et al. Two classes of PDGF receptor recognize different isoforms of PDGF. Science 1988; 240: 1529–1531. Heldin CH, Westermark B. Platelet-derived growth factor: mechanism of action and possible in vivo function. Cell Regul 1990; 1: 555–566. Burgess WH, Maciag T. The heparin-binding (fibroblast) growth factor family of proteins. Ann Rev Biochem 1989; 58: 575–606. Klagsbrun M, Edelman ER. Biological and biochemical properties of fibroblast growth factors: implications for the pathogenesis of atherosclerosis. Arteriosclerosis 1989; 9: 269–278. Folkman J, Klagsbrun M, et al. A heparin-binding angiogenic protein—basic fibroblast growth factor—is stored within basement membrane. Am J Pathol 1988; 130: 393–400. Higashiyama S, Abraham JA, et al. A heparin-binding growth factor secreted by macrophage-like cells that is related to EGF. Science 1991; 251: 936–939. Sporn MB, Roberts AB, et al. Some recent advances in the chemistry and biology of transforming growth factorbeta. J Cell Biol 1987; 105: 1039–1048. Ferrara N, Houck KA, et al. Vascular endothelial growth factor family of polypeptides. J Cell Biochem 1991; 47: 211. Raines EW, Dower SK, Ross R. Interleukin-1 mitogenic activity for fibroblasts and smooth muscle cells is due to PDGF-AA. Science 1989; 243: 393–396. Libby P, Friedman GB, Salomon RN. Cytokines as modulators of cell proliferation in fibrotic diseases. Am Rev Respir Dis 1989; 140: 1114–1117. Old LJ. Tumor necrosis factor (TNF). Science 1985; 230: 630–632. Rauch U, Osende JI, et al. Thrombus formation on atherosclerotic plaques: pathogenesis and clinical consequence. Ann Intern Med 2001; 134: 224–238. Burrig KF. The endothelium of advanced arteriosclerotic plaques in humans. Arterio Thromb 1991; 11: 1678–1689. Braunwald E, Fauci A, et al. eds. Libby P. Harrison’s principles of internal medicine, 15th edn. New York: McGraw-Hill Co., Inc.; 2001: 1337–1382. Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders, 2001: 1000. Moses HL, Yang EY, Pietenpol JA. TGF-beta stimulation and inhibition of cell proliferation: new mechanistic insights. Cell 1990; 63: 245–247. Ray-Chaudhury A, D’Amore PA. Endothelial cell regulation by transforming growth factor-beta. J Cell Biochem 1991: 47: 224–229. Amento EP, Ehsani N, et al. Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells. Arterio Thromb 1991; 11: 1223–1230.

113. Geng YJ, Libby P. Evidence for apoptosis in advanced human atheroma. Am J Pathol, 1995; 147: 251–266. 114. Bjorkerud S, Bjorkerud B. Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T-cells), and may contribute to the accumulation of gruel and plaque instability. Am J Pathol 1996; 149: 367–380. 115. Sumpio BE, Banes AJ, et al. Enhanced collagen production by smooth muscle cells during repetitive mechanical stretching. Arch Surg 1988; 123: 1233–1236. 116. Fuster V, Alexander RW, et al. eds. Hurst’s the Heart, Arteries, and Veins. 10th ed. New York, NY: McGrawHill; 2000: 1072. 117. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1995; 92: 657–671. 118. Toschi V, Gallo R, et al. Tissue factor modulates the thrombgenicity of human atherosclerotic plaque. Circulation 1997; 95: 594–599. 119. Fuster V, Alexander RW, et al., eds. Hurst’s the heart, arteries, and veins, 10th edn. New York: McGraw-Hill; 2000: 1073. 120. Libby P. Molecular bases of the acute coronary syndromes. Circulation 1995; 91: 2844–2850. 121. Ball RY, Stowers EC, et al. Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma. Atherosclerosis 1995; 114: 45–54. 122. Small DM. Progression and regression of atherosclerotic lesions: insights from lipid physical biochemistry. Arterioslcerosis 1988; 8: 103–129. 123. Lundberg B. Chemical composition and physical state of lipid deposits in atherosclerosis. Atherosclerosis 1985; 56: 93–110. 124. Richardson PD, Davies MJ, Born GV. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet, 1989; 2: 941–944. 125. Van der Wal AC, Becker AE, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaque is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994; 89: 36–44. 126. Matrisian LM. The matrix-degrading metalloproteinases. BioEssays 1992; 14: 455–463. 127. Shah PK, Falk E, et al. Human monocyte-derived macrophages express collagenase and induce collagen breakdown in atherosclerotic fibrous caps: implications for plaque rupture. Circulation 1993; 88 (Suppl. I): 254. 128. Galis ZS, Sukhova GK, et al. Increased expression of matrix-metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994; 94: 2493–2503. 129. Rennick RE, Ling KLE, et al. Effect of acetyl-LDL on monocyte-macrophage expression of matrix metalloproteinases. Atherosclerosis 1994; 109 (Suppl.): 192. 130. Fuster V, Alexander RW, et al. eds. Hurst’s the heart, arteries, and veins, 10th edn. New York: McGraw-Hill; 2000: 1072–1074 131. Fuster V, Ross R, Topol EJ, eds. Chisolm GM, Penn MS. Atherosclerosis and Coronary Artery Diseases. Philadelphia: Lippincott-Raven; 1996: 493–496. 132. Tse J, Martin-McNaulty B, et al. Accelerated atherosclerosis and premature calcified cartilaginous metaplasia in the aorta of diabetic male ApoE knockout mice can be

Chapter 9 Atherosclerosis: Biological and Surgical Considerations

133.

134.

135.

136.

137. 138.

139. 140. 141.

142.

143.

144.

145.

146.

147. 148.

149.

150.

151.

152.

prevented by chronic treatment with 17-b-estradiol. Atherosclerosis 1999; 144: 303–313. Braunwald E, Brown WV, eds. Gravanis MB. Atlas of heart disease: vascular disease, Vol. 10. St. Louis: MosbyYear Book, 1996: 1.10. Zarins CK, Weisenberg E, et al. Differential enlargement of artery segments in response to enlarging atherosclerotic plaques. J Vasc Surg 1988; 7: 386–394. Glagov S, Weisenberg E, et al. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987; 316: 1371–1375. Fuster V, Ross R, Topol EJ, eds. Chisolm GM, Penn MS. Atherosclerosis and Coronary Artery Diseases. Philadelphia: Lippincott-Raven, 1996: 497–498. Fuster V, Fayad ZA, Badimon JJ. Acute coronary syndrome: biology. Lancet 1999; 353 (Suppl. II): SII5–9. Fuster V, Gotto AM, et al. 27th Bethesda Conference: matching the intensity of risk factor management with the hazard for coronary disease events. Task Force 1. Pathogenesis of coronary disease: the biologic role of risk factors. J Am Coll Cardiol 1996; 27: 964–76. Scanu AM, Landsberger FR, eds. Lipoprotein structure. Ann NY Acad Sci 1980; 348. Gotto AM, Pownall HJ, Havel RJ. Introduction to the plasma lipoproteins. Methods Enzymol 1986; 128: 3–41. Segrest JP, Jackson RL, et al. A molecular theory of lipidprotein interaction in the plasma liporoteins. FEBS Lett 1974; 38: 247–253. Fredrickson DS, Levy RI, Lees RS. Fat transport in lipoproteins-an integrated approach to mechanisms and disorders. NEJM 1967; 276: 148–156. Lindgren FT. The plasma lipoproteins: historical developments and nomenclature. Ann NY Acad Sci 1980; 348: 1–15. Steiner G, Shafrir E, eds. Brewer HB, Santamarina-Fojo S, Hoeg JM. Primary hyperlipoproteinemias. New York: McGraw-Hill, 1990: 43–47. Parthasarathy S, Steinberg D, Witztum JL. The role of oxidized low-density lipoprotein in the pathogenesis of atherosclerosis. Annu Rev Med 1992; 43: 219–255. Cushing SD, Berliner JA, et al. Minimally modified low-density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells. Proc Natl Acad Sci USA 1990; 87: 5134–5138. Keys A. Coronary heart disease in seven countries. Circulation 1970; 41 (Suppl. I): I-1-I-211. Keys A, Menotti A, et al. The diet and 15-year death rate in the Seven Countries study. Am J Epidemiol 1986; 124: 903–915. Grundy SM, Denke MA. Dietary influences on serum lipids and lipoproteins. J Lipid Res 1990; 31: 1149–1172. Miller GJ, Miller NE. Plasma high-density lipoprotein concentration and development of ischemic heart disease. Lancet 1975; 1: 16–19. Gordon T, Castelli WP, et al. High-density lipoprotein as a protective factor against coronary heart disease: the Framingham study. Am J Med 1977; 62: 707–714. Kriesberg RA, Segrest JP (eds.), Scanu AM. Plasma, Lipoproteins, and Coronary Artery Disease. Cambridge, MA. Blackwell Scientific; 1992: 175–199.

161

153. Scanu AM, Fless GM. Lipoprotein(a): its inheritance and molecular basis of its atherothrombotic role. Mol Cell Biochem 1992; 113: 127–131. 154. Widmann MD, Sumpio BE. Lipoprotein(a): a risk factor for peripheral vascular disease. Ann of Vasc Surg 1993; 7: 446–451. 155. Kannel WB. Blood pressure as a cardiovascular risk factor: prevention and treatment. JAMA 1996; 275: 1571–1576. 156. Fuster V, Alexander RW, et al., eds. Hurst’s the Heart, Arteries, and Veins, 10th edn. New York, NY: McGrawHill; 2000: 1078–1079. 157. Hollander W. Role of hypertension in atherosclerosis and cardiovascular disease. Am J Cardiol 1976; 38: 786–800. 158. Roberts WC. Frequency of systemic hypertension in various cardiovascular diseases. Am J Cadiol 1987; 60: 1E-8E. 159. Falk E. Cardiac causes of death in hypertension. Scand J Clin Lab Invest 1989; 49 (Suppl. 196): 33–41. 160. Glagov S, Ozoa AK. Significance of the relatively low incidence of atherosclerosis in the pulmonary, renal, and mesenteric arteries. Ann NY Acad Sci 1968; 149: 940–955. 161. Williams PT, Haskell WL, et al. Associations of resting heart rate with concentrations of lipoprotein subfractions in sedentary men. Circulation 1985; 71: 441–449. 162. Bomberger RA, Zarins CK, et al. Effect of hypotension on atherogenesis and aortic wall composition. J Surg Res 1980; 28: 402–409. 163. Bretherton KN, Day AJ, Skinner SL. Hypertension-accelerated atherogenesis in cholesterol-fed rabbits. Atherosclerosis 1977; 27: 79–87. 164. Chobanian AV. The influence of hypertension and other hemodynamic factors in atherogenesis. Cardiovasc Dis 1983; 26: 177–196. 165. Hollander W, Prusty S, et al. Role of hypertension in ischemic heart disease and cerebral vascular disease in the Cynomolgus monkey with coarctation of the aorta. Circ Res 1977; 40 (Suppl. I): 70–83. 166. Fleischmann D, Hastie TJ, et al. Quantitative determination of age-related geometric changes in the normal abdominal aorta. J Vasc Surg 2001; 33: 97–105. 167. Xu C, Lee S, et al. Molecular mechanisms of aortic wall remodeling in response to hypertension. J Vasc Surg 2001; 33: 570–578. 168. American Diabetes Association. Managing Diabetes in the 1990s. Alexandria, VA: American Diabetes Association, 1989. 169. Marshall SM, Home PD, eds. Lopes-Virella MF. Diabetes annual. Amsterdam: Elsevier Science, 1994: 365–387. 170. Frykberg RG, ed. Gibbons GW. The high risk foot in diabetes mellitus. New York: Churchill Livingstone; 1991: 273–296. 171. Brand FN, Abbott W, Kannel WB. Diabetes, intermittent claudication and risk of cardiovascular events: the Framingham study. Diabetes 1989; 38: 504–509. 172. US Department of Health and Human Services. The treatment and control of diabetes: a national plan to reduce mortality and morbidity: a report of the National Diabetes Advisory Board. Washington, DC: US Government Printing Office: NIH Publication 81–2284; 1980. 173. Rudermann N, Williamson J, Brownlee M, eds. Wilson PWE, Kannel WB. Hyperglycemia, diabetes, and vascular disease. New York: Oxford Press; 1992: 21–29.

162

Part II Basic Cardiovascular Problems

174. Chriestlieb AR, Warram JM, et al. Hypertension, the major risk factor in juvenile-onset insulin dependent diabetes. Diabetes 1981; 30: 90–96. 175. Kamal K, Powell RJ, Sumpio BE. The pathobiolgy of diabetes mellitus: implications for surgeons. J Am Coll Surg 1996; 183: 271–289. 176. Kissebah AH. Low-density lipoprotein metabolism in non-insulin-depedent diabetes mellitus. Diabetes Metab Rev 1987; 3: 619–651. 177. Sosenko JM, Breslow JL, et al. Hyperglycemia and plasma lipid levels: a prospective study of young insulin-dependent diabetes patients. N Engl J Med 1980; 302: 650–654. 178. Ginsberg HN. Lipoprotein metabolism and its relationship to atherosclerosis. Med Clin N Am 1994; 78: 1–20. 179. Witztum JL, Steinbrecher UP, et al. Autoantibody to glycosylated protein in the plasma of patients with diabetes mellitus. Proc Natl Acad Sci USA 1984; 81: 3204–3208. 180. Lopes-Virella M, Virella G. Immune mechanisms of atherosclerosis in diabetes mellitus. Diabetes 1992; 41: 86–91. 181. Pfeifle B, Ditschuneit H. Two separate receptors of insulin and insulin-like growth factors on arterial smooth muscle cells. Exp Clin Endocrinol 1983; 81: 280–286. 182. Bornfeldt KE, Arnqvist JH, Capron L. In vivo proliferation of rat vascular smooth muscle in relation to diabetes mellitus, insulin-like growth factor 1 and insulin. Diabetologia 1992; 35: 104–108. 183. Sages H. Collagens of basement membranes. J Invest Dermatol 1982; 79: 51S-59S. 184. William JR, Tilton RG, et al. Membrane abnormalities in diabetes mellitus: relationship to clinical microangiopathy. Diabet Metab Rev 1988; 4: 339–370. 185. Boyd RB, Burke JP, et al. Significance of capillary basement membrane changes in diabetes mellitus. J Am Podiatr Med Assoc 1990; 80: 307–313. 186. Shimomura H, Spiro RG. Studies on macromolecular component of human glomerular basement membrane and alteration in diabetes: decreased levels of heparan sulfate proteoglycan and laminin. Diabetes 1987; 36: 374–381. 187. Ziaydeh FN. Renal tubular basement membrane and collagen type IV in diabetes mellitus. Kidney Int 1993; 43: 114–120. 188. Barakat HA, Carpenter JW, et al. Influence of obesity, impaired glucose toleratnce and NIDDM on LDL structure and composition: possible link between hyperinsulinemia and atherosclerosis. Diabetes 1990; 39: 1527–1533. 189. Gough SCL, Grant PJ. The fibrinolytic system in diabetes mellitus. Diabet Med 1991; 8: 898–905. 190. Stiko-Rahm A, Wiman B, et al. Secretion of plasminogen activator inhibitor I from cultured umbilical vein endothelial cells is induced by very low density lipoprotein. Arteriosclerosis 1990; 10: 1067–1073. 191. Berlin JA, Colditz GA. A meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol 1990; 132: 612–628. 192. Hammond EC, Horn D. The relationship between human smoking habits and death rates. JAMA 1954; 155: 1316–1328.

193. McBride PE. The health consequences of smoking: cardiovascular diseases. Med Clin N Am 1992; 76: 333–353. 194. Department of Health and Human Services. The health consequences of smoking: nicotine addiction. A report of the Surgeon General. Washington DC: Government Priniting Office: DHSS CDC Publication No. 88–8406; 1988. 195. Kannel WB, McGee D, Gordon T. A general cardiovascular risk profile: the Framingham study. Am J Cardiol 1976; 38: 4–51. 196. Villablanca AC, McDonald JM, Rutledge JC. Smoking and cardiovascular disease. Clin Chest Med 2000; 21: 159–172. 197. Stedman RL. The chemical composition of tobacco and tobacco smoke. Chemical Rev 1968; 68: 153–207. 198. Tachmes L, Fernandez RJ, Sadmer MA. Hemodynamic effects of smoking cigarettes of high and low nicotine content. Chest 1978; 74: 243. 199. Aronowy WS, Dendinger J, Rokaw SN. Heart rate and carbon monoxide levels after smoking high, low, and non-nicotine cigarettes. Ann Int Med 1971; 74: 697. 200. Ball K, Turner R. Smoking and the heart: the basis for action. Lancet 1974; ii: 822. 201. Diana JN, ed. Olsson AG, Molgaard J. Tobacco smoking and atherosclerosis. New York: Plenum Press; 1990. 202. Bylork A, Bondjers G, et al. Surface ultrastructure of human arteries with special referance to the effects of smoking. Acta Path Microbiol Scand 1979; 87 (section A): 201. 203. Boayse FM, Osikowicz G, Quargoot AJ. Effects of chronic oral consumption of nicotine on the rabbit aortic endothelium. Am J Pathol 1981; 102: 229. 204. Kilaru S, Frangos SG, et al. Nicotine: a review of its role in atherosclerosis. J Am Coll Surg 2001; 193: 538–544. 205. Thyberg J. Effects of nicotine on phenotypic modulation and initiation of DNA synthesis in cultured arterial smooth muscle cells. Virchows Arch B Cell Pathol Incl Mol Pathol 1986; 52: 25–32. 206. Hawkins RI. Smoking, platelets, and thrombosis. Nature 1972; 236: 450. 207. Pittilo RM, Mackie IJ, et al. Effects of cigarette smoking on the ultrastructure of rat thoracic aorta and its ability to produce prostacyclin. Thromb Haemostas 1982; 48: 173. 208. Stampfer MJ, Malinow MR, et al. A prospective study of plasma homocysteine and risk of myocardial infarction in US physicians. JAMA 1992; 268: 887–881. 209. Arensen E, Refsum H, et al. Serum total homocysteine and coronary artery disease. Int J Epidemiol 1995; 24: 704–709. 210. Boushey CJ, Beresford SAA, et al. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid intakes. JAMA 1995; 274: 1049–1057. 211. Verhoef P, Hennekens CH, et al. A prospective study of homocysteine and risk of ischemic stroke. Stroke 1994; 25: 1924–1930. 212. Den Heijer M, Koster T, et al. Hyperhomocysteinemia as a risk factor for deep vein thrombosis. N Engl J Med 1996; 334: 759–762.

Chapter 9 Atherosclerosis: Biological and Surgical Considerations 213. Wall RT, Harlan JM, et al. Homocysteine-induced endothelial cell injury in vitro: a model for the study of vascular injury. Thromb Res 1980; 18: 112–121. 214. Upchurch GR, Welch GN, et al. Homocysteine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase. J Biol Chem 1997; 272: 17012–17017. 215. Woo DK, Dudrick SJ, Sumpio BE. Homocysteine stimulates MAP kinase in bovine aortic smooth muscle cells. Surgery 2000; 128: 59–66. 216. Tsai JC, Perrella MA, et al. Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc Natl Acad Sci USA 1994; 91: 6369–6373. 217. Majors A, Ehrhart LA, Pezack EH. Homocysteine as a risk factor for vascular disease: enhanced collagen production and accumulation by smooth muscle cells. Arterio Thromb Vasc Biol 1997; 17: 2074–2081. 218. Rodgers GM, Conn MT. Homocysteine, an atherogenic stimulus, reduces protein C activation by arterial and venous endothelial cells. Blood 1990; 75: 895–901. 219. Walsh BW, Schiff I, et al. Effects of postmenopausal estrogen replacement on the concentrations and metabolism of plasma lipoproteins. N Engl J Med 1991; 325: 1196–1204. 220. Bush DE, Jones CE, et al. Estrogen replacement reverses endothelial dysfunction in postmenopausal women. Am J Med 1998; 104: 552–558. 221. Knopp RH. The effects of postmenopausal estrogen therapy on the incidence of arteriosclerotic vascular disease. Obstet Gynecol 1988; 72 (Suppl. 5): S23-S30. 222. iting Group for the PEPI Trial. Effects of estrogen or estrogen/progestin regimens on the heart disease risk factors in postmenopausal women. The Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial. JAMA 1995; 273: 199–208. 223. Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention Trial Results: I. Reduction in incidence of coronary heart disease and II: The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA 1984; 251: 351–374. 224. Hunnninghake DB. HMG-CoA reductase inhibitors. Curr Opin Lipidol 1992; 3: 22–28. 225. Wood AJJ, ed. Hiatt WR. Medical treatment of peripher-

226.

227.

228.

229.

230.

231.

232.

233.

234.

235.

236.

237. 238.

163

al arterial disease and claudication. N Engl J Med 2001; 344: 1608–1622. Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). J Vasc Surg 200; 31 (Suppl.): S1–S296. Hiatt WR, Stoll S, Nies AS. Effect of b-adrenergic blockers on the peripheral circulation in patients with peripheral vascular disease. Circulation 1985; 72: 1226–1231. The Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high risk patients. N Engl J Med 2000; 342: 748. Quick CRG, Cotton LT. The measured effect of stopping smoking on intermittent claudication. Br J Surg 1982; 69 (Suppl.): S24-S26. Jorenby DE, Leischow SJ, et al. A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 1999; 340: 685–691. Jacques PF, Selhub J, et al. The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 1999; 340: 1449–1454. Hiatt WR, Regensteiner JG, et al. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation 1990; 81: 602–609. Svindland A. The localization of sudanophilic and fibrous plaques in the main left coronary arteries. Atherosclerosis 1983; 48: 139–145. Sabbah HN, Khaja F, et al. Blood velocity in the right coronary artery: relation to the distribution of atherosclerotic lesions. Am J Cardiol 1984; 53: 1008–1012. Boudoulas H, Rittgers SE, et al. Changes in diastolic time with various pharmacologic agents: implication for myocardial perfusion. Circulation 1979; 60: 164–169. Beere PA, Glagov S, Zarins CK. Retarding effect of lowered heart rate on coronary atherosclerosis. Science 1984; 226: 180–182. Cikrit DF, Dalsing MC. Lower-extremity arterial endovascular stenting. Surg Clin N Am 1998; 78: 617–629. Wilson SE, Wolf GL, Cross AP. Percutaneous transluminal angioplasty versus operation for peripheral arteriosclerosis. Report of a prospective randomized trial in a selected group of patients. J Vasc Surg 1989; 9: 1–9.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 10 Intimal Hyperplasia Christopher K. Zarins, Chengpei Xu, Hisham S. Bassiouny, and Seymour Glagov

Intimal thickening is a feature of the normal adaptive response of arteries to hemodynamic stresses as well as a characteristic of the healing of arterial injuries. Intimal hyperplasia in the region of endarterectomy, balloon angioplasty, and vascular bypass graft anastomoses is a major feature of long-term failure of vascular reconstruction (1–3). Despite extensive investigation, the mechanisms underlying the control of intimal thickening and the factors that lead to uncontrolled intimal hyperplasia are poorly understood.

Hypotheses Most investigators have been focused on the “response to injury” hypothesis of intimal hyperplasia, which emphasizes the role of endothelial injury, platelet adherence and activation, elaboration of mitogenic factors, and smooth muscle cell proliferation and migration (4–6). Experimental animal models have centered on the artery wall response to a variety of injurious agents such as mechanical, cytotoxic, immunologic, and thermal. Balloon catheter injury of the endothelium and subjacent media has been widely used. Such injury induces an intimal smooth muscle proliferative response that is usually self-limiting and usually does not proceed to occlusion (7,8). The balloon injury experiments have produced important new knowledge regarding artery wall biology and mediators of smooth muscle cell proliferation and migration (9), but application of this knowledge has not yet resulted in successful strategies to control intimal hyperplasia in humans.

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Pharmacologic efforts to control anastomotic intimal hyperplasia in humans based on control of the healing response to injury in animals and the control of cell proliferation in culture have been largely unsuccessful (10,11), and restenosis continues to complicate 30% to 50% of angioplasty procedures (12). A second line of investigation is based on the reactive–adaptive remodeling responses of arteries to biomechanical and metabolic factors including compensatory responses to enlarging atherosclerotic plaques (13–15). This line of investigation includes consideration of the effects of local and systemic alterations in blood pressure and blood flow on artery wall structure, composition, and function. Alterations induced by plaques, endarterectomy, angioplasty, or bypass grafts create new geometric configurations and induce major alterations in the conditions of the blood flow field with changes in wall shear stress, tensile stress, tissue vibration, and artery wall compliance (13). These forces may stimulate intimal thickening, smooth muscle cell proliferation, and migration. In vitro endothelial cells respond to changes in shear stress by alterations in orientation, morphology and cytoskeletal structure (16), prostacyclin (17) and mitogen secretion (18), tissue plasminogen activator transcription (19,20), and potassium channel activation (21). Mechanical forces such as cyclic stretching stimulate smooth muscle cells to increase collagen production (22) and play an important role in artery wall biologic responses. Evidence suggests that all intimal thickenings are not the same and that mechanisms regulating adaptive intimal thickening and pathologic intimal hyperplasia may vary (23). It is not clear why control mechanisms of adaptive intimal thick-

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ening may fail and why an intimal hyperplasic response develops with progression to an uncontrolled lesion resulting in arterial or anastomotic stenosis and occlusion. In this chapter we will examine normal adaptive and healing responses of the arterial intima and consider how this type of intimal thickening may differ from intimal hyperplasia. We will consider how hemodynamic and biomechanical forces may influence intimal thickening of vascular grafts.

Adaptive Responses of Arteries Arteries adapt to changes in blood flow or blood pressure by alterations in the dimensions, structure, and composition of the lumen and artery wall (13). Blood flow is the primary determinant of lumen diameter and blood pressure and lumen radius are the primary determinants of wall thickness and composition.

Wall Shear Stress The column of flowing blood in an artery exerts a shearing stress at the blood-endothelial surface that is directly related to blood flow and inversely related to the third power of the lumen radius. This relation is expressed by the formula: TW =

4mQ pr3

where TW is wall shear stress, m is viscosity coefficient, Q is flow, and r is radius. Thus a small change in lumen radius can produce a large change in wall shear stress. Endothelial release of nitric oxide in response to acute increases in shear stress results in an increase in lumen radius. Chronic alterations in lumen diameter in response to changes in wall shear stress also appear to be endothelium dependent (24). Arteries respond to chronic increases in blood flow and shear stress by increasing lumen diameter until wall shear stress returns to a normal mean level of approximately 15 dyne/cm2 (25,26). Experimentally produced arteriovenous fistulas produce an immediate 10fold increase in blood flow and a three-fold increase in wall shear stress. Within 24 hours, artery enlargement begins, and at the end of 4 weeks lumen radius enlarges twofold and wall shear stress returns to normal (27). Conversely, chronic reduction in wall shear stress and blood flow results in a reduction in lumen diameter and normalization of wall shear (28). Evidence from both human arteries and experimental models indicates that in adults, reduction in lumen radius in response to chronic changes in blood flow is achieved at least in part by intimal thickening. In straight vessels the reduction in lumen caliber is achieved by concentric intimal thickening (Fig. 10.1). Such thickening can be seen in arteries with no lumen stenosis or distal to flow-limiting stenoses. Experimental observations in monkey aortic coarctations with induced

FIGURE 10.1 Concentric intimal thickening due to fibrocellular hypertrophy in human coronary artery. Lumen caliber is normal with no coronary stenosis and no coronary atherosclerosis. Intimal thickness exceeds the thickness of the media.

changes in shear stress reveal that the degree of intimal thickening is inversely related to the level of wall shear stress with low wall shear stress promoting intimal thickening, and high wall shear stress inhibiting intimal thickening (29). Special geometric configurations in the arterial tree, such as at bifurcations, bends, and anastomoses, can produce focal regions of reduced wall shear stress and stimulate intimal thickening. Thus the concave aspects of tortuous arteries are exposed to reduced wall shear stress, and a thickened intima develops in this region. A wellcharacterized example of a localized, significant reduction in wall shear stress occurs at the carotid bifurcation (30). The human carotid bifurcation is characterized by a sinus formation on the first portion of the internal carotid artery. This localized lumen enlargement together with the branching and different outflow resistances of the internal and external carotid arteries results in a highly complex flow field. Flow separation occurs along the outer wall of the internal carotid sinus opposite the flow divider with skewing of the laminar flow velocity profile toward the inner wall of the internal carotid artery. These flow characteristics result in a large area along the outer wall of the carotid sinus that is chronically exposed to low wall shear stress and periods of flow reversals with each pulse cycle. This region of the carotid bifurcation is selectively prone to intimal thickening (30,31) (Fig. 10.2). Conversely, the inner wall of the carotid bifurcation is characteristically exposed to high wall shear stress and unidirectional flow and rarely develops intimal thickening. Thus intimal thickening tends to occur focally where geometric features alter the flow profile effectively to reduce wall shear stress. Other local flow field factors, usually associated with low wall shear stress, have been identified that promote intimal thickening. These factors include flow separation and stasis, which tends to result in increased particle residence time and would favor time-dependent

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Wall Tensile Stress Changes in blood pressure or lumen radius stimulate adaptive changes in artery wall thickness as approximated by the equation S=

FIGURE 10.2 Cross-section of human carotid bifurcation. External carotid is above, internal carotid is below. Localized intimal fibrocellular hypertrophy occurs along the outer wall of the internal carotid sinus (bottom) opposite the bifurcation flow divider. This is an area exposed to flow separation, low wall shear stress, increased particle residence time, and oscillation of shear stress direction. The inner wall is exposed to high shear stress and has no intimal thickening.

blood–endothelium interactions (13). In addition, the location of intimal thickening is related to localized complex flow patterns and oscillation of shear stress direction (31). Because the number of oscillations or reversals of flow direction in the lateral wall of the sinus over time is related to the intimal thickness, the long-term effect of oscillation in flow direction would be expected to be directly related to heart rate. Indeed, reduction in heart rate prevents carotid and coronary atherosclerotic intimal thickening in experimental animals (32,33). Thus, both local blood flow velocity patterns related to geometry and more general systemic factors such as heart rate are mutually potentiating factors for the development of intimal thickening. In summary, the hemodynamic factors favoring intimal hypertrophy are: 1. 2. 3. 4.

flow separation; low wall shear stress; increased particle residence time; and oscillation in shear stress vector.

Pr d

where S is wall tensile stress, P is pressure, r is radius, and d is wall thickness. Increased intraluminal pressure such as occurs in hypertension increases wall tensile stress and stimulates an increase in wall thickness and changes in structure or composition to reduce tensile stress to normal. The influence of blood pressure is apparent in the differentiation of the ascending aorta and pulmonary trunk in the postpartum period. In utero, the ascending aorta and pulmonary artery have similar blood pressure and blood flow and are equivalent in lumen diameter and wall thickness. Immediately after birth, with closure of the ductus arteriosus and expansion of the lungs, blood pressure falls in the pulmonary artery and rises in the aorta with blood flow remaining equivalent. This results in a rapid increase in thickness of the aorta with an increased accumulation of collagen and elastin and an increase in the number of medial lamellae compared with the pulmonary trunk. The lumen diameters of the two vessels remain equivalent (34). In adult life increased wall thickness in response to the increased pressure may be achieved by intimal thickening as is apparent in arteries from patients with longstanding hypertension. Increases in lumen radius also induce modifications of wall thickness, structure, and composition. Increased lumen radius can result from changes induced by flow, as noted above, or from the atherosclerotic process itself, with compensatory enlargement in response to increasing intimal plaques (15,35). Changes in geometry induced by anastomoses, endarterectomy, or angioplasty result in often complex localized changes in effective lumen radius. Increases in radius induce compensatory responses of intimal thickening, which tend to augment total wall thickness and normalize wall tensile stress (36). As noted above, the inside or concave side of a vessel bend and the region opposite the flow divider at a bifurcation are exposed to higher mural tensile stress and have a thicker wall than the outer or convex wall of a curve and the flow divider of a branch, which have a lower tensile stress and thinner wall (Fig. 10.2). At the carotid bifurcation, wall thickness is variable and is directly related to mural tensile stress (37). The biomechanical conditions are particularly complex in bypass grafts. When a vein is used as an arterial bypass, it is frequently larger than the bypassed artery. The thin-walled vein is exposed to increased wall tension owing to the sudden exposure to arterial pressure and responds by increasing wall thickness to normalize wall tensile stress. The greater radius of the vein compared with the associated artery may also result in a level of wall

Chapter 10 Intimal Hyperplasia

shear stress well below the normal level for arteries of 15 dyne/cm2. Thus both elevated tensile stress and low wall shear stress may stimulate intimal thickening in the same vessel (38), and both factors act to increase wall thickness and reduce lumen caliber in vein grafts. The cells of the vessel wall respond by proliferating and elaborating matrix fibers, thereby thickening and restructuring the wall and intima to maintain mural stability (36). This response may be uniform in straight segments of arteries or bypass grafts and asymmetric at branches, curves, or anastomoses where effective radius differs with circumferential position (39,40).

Adaptive Remodeling of Arteries The adaptive responses of arteries to blood flow, blood pressure, and vessel radius are, of necessity, closely linked. For example, increased blood flow induces an increase in lumen radius, which in turn induces an increase in wall thickness in response to the increase in wall tensile stress. Conversely, reduction in wall shear stress below baseline values results in a reduction of radius and a corresponding adjustment in vessel composition in response to the reduced tensile stress (41,42). Thus adaptive remodeling of arteries can be summarized as follows: 䊏

䊏

Shear stress regulation of lumen caliber Increased shear Æ arterial enlargement Reduced shear Æ intimal thickening Tensile stress regulation of wall thickness Increased pressure Æ intimal thickening Increased lumen radius Æ intimal thickening

Intimal thickening, therefore, may be a response to reduced flow, increased radius, or increased blood pressure or a combination of these factors. The complex altered geometries created by vascular anastomoses, angioplasties, and endarterectomies produce large local variations in tensile and wall shear stress and may stimulate different local responses and wall thickening.

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of atherosclerosis. Thrombus may be deposited on the vessel intimal surface, become organized, and be incorporated into the underlying artery wall. Such organized thrombus may appear as nonatherosclerotic intimal thickening. Marked intimal fibrocellular hypertrophy may be present without evidence of plaque development, and relatively small plaques and fatty streaks may occur with little or no evidence of intimal fibrocellular hypertrophy. Both forms of nonatherosclerotic intimal thickening occur in regions of reduced wall shear stress and increased tangential tension, including the proximal inflow edges opposite flow dividers at branch sites and bifurcations. Both may be seen in coronary intimal thickenings retrieved by directional atherectomy after balloon angioplasty, but both also may be found in atherectomy specimens from arteries without previous intervention (43).

Intimal Fibrocellular Hypertrophy Intimal fibrocellular hypertrophy is an orderly, uniformly layered, intimal thickening that includes both smooth muscle cells and collagen and elastin matrix fibers. It is similar to, but not identical with, the architecture of the media and is usually separated from the media by the internal elastic lamina (Fig. 10.3). The intima may be thicker than the underlying media and may occupy the entire circumference of straight vessels (Fig. 10.1). In regions of intimal fibrocellular hypertrophy, computations of mural tensile stress that take into account only the width of the media yield values that are abnormally elevated. If, however, the media and intima are taken as total wall thickness, mural tensile stress approaches normal values (37). The pattern and geometric configuration of intimal fibrocellular hypertrophy suggest an association with

Intimal Fibrocellular Hypertrophy and Hyperplasia Intimal thickening occurs in two principal morphologic forms: 1. 2.

intimal fibrocellular hypertrophy; and intimal hyperplasia.

Both are characterized by intimal smooth muscle and matrix fiber accumulation and differ from atherosclerotic plaque formation. Intimal fibrocellular hypertrophy and hyperplasia lack macrophages, foam cells, lipid cores, necrosis, or calcifications, all of which are characteristics

FIGURE 10.3 Intimal fibromuscular hypertrophy in a section of human coronary artery. The intimal thickening consists of an orderly layered intimal structure including both smooth muscle cells and matrix fibers and separated from the media by the internal elastic lamina.

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local distribution of flow and mural tension (36). Thus on both microarchitectural and functional grounds, it is reasonable to presume that intimal hypertrophy is an adaptive reaction to mechanical stresses related to local features of flow and wall tension. At both venous and prosthetic bypass graft anastomoses, well-organized and differentiated intimal fibrocellular layers usually form and result in remodeling and smoothing of the luminal surface to restore baseline values of wall shear stress or tensile stress or both (39).

Intimal Hyperplasia Intimal hyperplasia by contrast is a poorly organized and structured intimal proliferative reaction. It consists of a fairly uniform accumulation of cells with smooth muscle or myofibroblast features, often in an abundant stroma but with few formed fibers, and usually without a welldefined, oriented, or layered architectural organization (Fig. 10.4). The overlying endothelium is intact. As with intimal fibrocellular hypertrophy, intimal hyperplasia tends to localize either at anastomoses or in regions where flow is obstructed or distorted (Fig. 10.5). Areas of stenoses, irregular disrupted plaques, and anastomotic sites where vessel walls and vascular prostheses differ greatly in compliance, composition and dimensions are vulnerable to both intimal fibrocellular hypertrophy and intimal hyperplasia (39). These observations suggest that the normal self-limiting organized reaction characteristic of intimal fibrocellular hypertrophy may be delayed or prevented in intimal hyperplasia. Persistence of abnormal geometric configurations and flow velocities in such regions may prevent stabilization and differentiation of the intimal proliferative healing response into intimal fibrocellular hypertrophy. In addition, normal signal and control mechanisms responding to wall shear and tensile stress may be distorted in relation to risk factors and indi-

FIGURE 10.4 Artery cross-section with intimal hyperplasia and lumen stenosis. Widely spaced cells are surrounded with abundant matrix with few distinct collagen or elastin fibers and little geometric orientation.

vidual differences in tissue responses, and differentiation into the layered fibrocellular organization characteristic of intimal fibrocellular hypertrophy may be prevented. The continuation of the hyperplasic reaction thus may be a “runaway” proliferative response. The stimuli to intimal thickening persist, but physical constraints prevent the establishment of a stable remodeling outcome. Low cardiac output, inflow obstruction, and poor distal runoff, which produce overall low-flow states, combined with local complex flow field changes that engender persistent focal low-shear regions would accentuate this situation. Intimal hyperplasia may therefore be considered to be a dysplastic-hyperplastic response. Like other dysplasias it appears to reflect the lack of formation of a structure consistent with the establishment of an equilibrium state (39). In addition to the local underlying biomechanical stimuli that may influence intimal thickening, there most likely are individual differences in tissue reactivity and metabolic influences. Experimental evidence suggests that the intimal hyperplastic response induced by balloon injury may be modulated by increase arterial flow (43). It has also been suggested that failure of compensatory enlargement, rather than intimal hyperplasia itself, accounts for lumen narrowing following experimental angioplasty (44). Thus both local and systemic risk factors and complicating, pathologic conditions are likely to be important variables in the development of intimal hyperplasia. The development of atherosclerosis in the afferent artery, altered cardiac output, and the degree of shunting and turbulence may also modify local conditions and healing responses. Intimal fibrocellular hypertrophy and intimal hyperplasia may readily be found in isolated “pure” forms of the reaction or as a combination (45). Composite forms probably indicate that changes in flow conditions

FIGURE 10.5 Microscopic section of intimal hyperplasia producing lumen stenosis at distal end-to-side tibial bypass graft anastomosis. Cells in a fairly uniform accumulation with smooth muscle or myofibroblast features are surrounded by a myxoid stroma with few formed fibers and without a definite orientation or layered architectural organization. The endothelial surface is intact.

Chapter 10 Intimal Hyperplasia

favoring one or the other of the reactions occurred. Whether the intimal responses lead to stabilized intimal fibrocellular hypertrophy or progressive hyperplasia may be largely determined by the individual localized physical and metabolic environment.

Anastomotic Intimal Hyperplasia Anastomotic intimal hyperplasia is a proliferative nonatherosclerotic form of intimal thickening and is a major cause of anastomotic stenosis and bypass graft failure (1–3). Factors that differentiate healing at anastomoses and nonocclusive intimal thickening from occlusive hyperplasia have not been defined. Considerable attention has been focused on endothelial injury and compliance mismatch as determinants of anastomotic intimal hyperplasia. Endothelial injury and surgical trauma exist at all anastomoses at the time of their construction, yet only some develop intimal hyperplasia. As the intimal proliferative response to acute injury is likely to be selflimiting as soon as the proliferation necessary for healing is complete (8), factors other than acute injury must play a role. Vascular anastomoses create major alterations in vessel geometry, lumen radius, and wall tensile stresses, and hemodynamic and biomechanical factors have been implicated in intimal hyperplasic responses (39) (Fig. 10.6). Because anastomotic intimal hyperplasia is more prominent in prosthetic graft anastomoses than autogenous vein anastomoses, it has been suggested that differences in the mechanical properties of graft and artery wall may promote anastomotic intimal hyperplasia (46,47). Regions of hypercompliance have been demonstrated in arterial anastomoses, suggesting that the mere presence of a suture line can induce biomechanical stresses, promoting hyperplasia (48). Although hypercompliance may result

FIGURE 10.6 Anastomotic intimal hyperplasia in a PTFE anterior tibial bypass anastomosis with distal outflow obstruction. Note intimal thickening at toe of anastomosis as well as along the floor of the anastomosis to the anterior tibial artery. The floor of the anterior tibial artery is exposed to flow separation, flow stasis, low shear, and shear stress oscillation.

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in increased smooth muscle cyclical stretch and collagen synthesis (22), evidence for this mechanism in the production of intimal hyperplasia is lacking. Conversely, reduction of artery wall motion has been shown to reduce artery wall metabolism and biosynthesis of matrix components (49). We have conducted parallel in vivo animal experiments and model flow studies to study the relation between hemodynamic and biomechanical factors in distal end-to-side anastomoses and anastomotic intimal thickening. In a canine model, autogenous vein and polytetrafluoroethylene (PTFE) iliofemoral bypass grafts were constructed for the study of intimal thickening (50). Analogous flow models were created from vascular casts, and the anastomotic flow field was characterized using quantitative and qualitative techniques (51). Flow behavior in models of end-to-side vascular graft anastomoses was studied under steady and pulsatile flow conditions. Reynolds numbers, division of flow in the outflow tracts, and the pulsatile waveform used were taken from measurements obtained from the canine anastomoses. Flows in the model were visualized with white, neurally buoyant particles that demonstrated particle pathlines, streamlines, and streaklines (Fig. 10.7). Strong threedimensional helical patterns formed in the anastomotic junction and were prominent features of the flow fields. Flow tended to be skewed toward the hood; consequently, only a fraction of the lumen actually participated in flow delivery to the host vessel. This is due to the sudden expansion in cross-sectional area in the anastomosis that does not aid in flow delivery, but rather tends to produce flow separation and flow disturbance. Flow separation occurred along the lateral walls of the anastomotic sinus, and particles accumulated in these zones under both steady and pulsatile flow conditions. Particle stasis in this separated region was virtually eliminated by imposition of a high flow rate which simulated exercise (52).

FIGURE 10.7 Model flow visualization in end-to-side vascular anastomosis. Flow streaminess occur along the hood of the anastomosis. Flow separation, stasis, and oscillation of shear stress direction occur along the floor of the anastomosis in the recipient artery.

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Flow separation also occurred along the distal segment of the anastomotic hood, and a stagnation point with oscillation of shear stress direction developed along the floor of the recipient artery. The stagnation and oscillation zone appeared to be similar to the threedimensional separation region observed along the outer wall along the sinus of the human internal carotid artery, which is prone to intimal thickening (30). Indeed, experiments have demonstrated that intimal hyperplasia developed along the floor of the recipient artery in end-to-side anastomosis (50) (Fig. 10.8). Intimal thickening in canine vein and PTFE anastomoses occurred in two distinct and separate sites: at the suture line and along the floor of the anastomosis in the recipient artery opposite the anastomotic hood (Fig. 10.8). Suture line intimal thickening appeared to represent vascular healing and remodeling in response to mechanical injury or compliance mismatch, and appeared to be modulated by flow characteristics across the suture line. Suture line intimal thickening was increased in PTFE anastomoses compared with vein anastomoses, suggesting a possible role for compliance mismatch in this response (50) (Fig. 10.9). The thickening along the floor of the anastomosis in the recipient artery was the same in both vein and PTFE anastomoses, suggesting that hemodynamic forces played a primary role in its development. Intimal thickness was absent along the graft hood, where flow was laminar and shear stress was high and short particle residence times were observed. Arterial floor intimal thickening developed in a region corresponding to the stagnation zone where low and oscillatory shear prevailed. Flow patterns consistent with separation, relatively low shear, and long particle residence time also formed along the heel and lateral wall of the sinus, where suture lone intimal thickness was also present. These findings suggest that hemodynamic factors may play a significant role in the development of anastomotic intimal thickening. However, all anastomotic intimal thickenings are not the same, and multiple and differing variables may govern the degree of intimal thickness of various sites in the anastomosis.

Effects of Flow Augmentation on Anastomotic Intimal Thickening Anastomotic model flow studies in which flow rates and pulsatile frequency were increased to simulate exercise flow conditions demonstrated that the regions of flow stasis in anastomoses were virtually eliminated (52). Exercise in humans has the effect of transiently increasing flow and wall shear stress and reducing particle residence time in arteries. The influence that exercise flow conditions may have on limiting intimal hyperplasia in vascular graft anastomoses has yet to be determined. Experimental augmentation of flow in anastomoses by creation of a distal arteriovenous fistula, however, resulted in a significant reduction in intimal thickening in experimental canine prosthetic graft anastomoses (53). Arteriovenous fistulas were constructed 15 cm downstream from iliofemoral bypass grafts in canines with opposite PTFE iliofemoral bypasses serving as controls. A continuous twofold increase in blood flow and shear stress at the distal anastomosis was produced by the distal arteriovenous fistula. Anastomotic intimal thickening was markedly reduced on the side with the arteriovenous fistula. Whether similar benefit can be achieved in human PTFE anastomoses is unclear. PTFE bypasses used in humans as arteriovenous shunts for dialysis are particularly prone to developing intimal hyperplasia at the distal graftto-vein anastomosis (39). However, this high-flow junction is complicated by a marked pressure reduction and turbulence at the venous anastomosis and is not comparable to a distal arterial anastomosis. The potential benefit of more physiologic methods of increasing flow and

FIGURE 10.8 Illustration of sagittal section of end-toside anastomosis demonstrating the site of localization of anastomotic intimal thickening (IT) at the suture line and along the artery floor. (Reproduced by

FIGURE 10.9 Anastomotic suture line intimal thickening at experimental PTFE-to-artery anastomosis. Pannus of intimal fibrocellular hypertrophy extends from the artery at the left to the PTFE graft surface at the right. The triangular deformity is filled in and remodeled to form a smooth flow surface. Intimal thickening was greater in PTFE than in vein anastomoses, suggesting a possible role for compliance mismatch in the pathogenesis. (Reproduced by permission from

permission from Bassiouny HS, White S, et al. Anastomotic intimal hyperplasia: mechanical injury or flow induced? J Vasc Surg 1992,15:708–717.)

Bassiouny HS, White S, et al. Anastomotic intimal hyperplasia: mechanical injury or flow induced? J Vasc Surg 1992;15:707–717.)

Chapter 10 Intimal Hyperplasia

shear stress at anastomoses, such as can be achieved by exercise, deserves investigation. Regular, intermittent increases in flow and shear stress may prevent the development of occlusive intimal hyperplasia and improve long-term graft patency (Fig. 10.10).

Restenosis and Intimal Hyperplasia Restenosis after endarterectomy, atherectomy, or vascular bypass is usually due to uncontrolled intimal hyperplasia. Despite great advances in our knowledge of vascular biology and the reactions of arteries and veins to injury and biomechanical forces, prevention and control of intimal hyperplasia have thus far been largely unsuccessful. The factors that differentiate normal healing and remodeling mechanisms that are self-limited from uncontrolled intimal thickening that results in lumen stenosis are unclear. Complex remodeling and healing reactions that occur in arteries in the presence of atherosclerosis account for some of the features of plaque structure that tend to

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sequester the lesion, stabilize flow, preserve lumen caliber, and prevent plaque rupture (54). These same reactions occur in response to vascular interventions such as angioplasty, endarterectomy, and vascular bypass procedures. The intimal proliferative response that occurs after intervention is a part of the healing response, which is usually self-limited and modulated by conditions of flow and vascular geometry. Uncontrolled intimal hyperplasia and restenosis are likely the result of failure to reestablish a satisfactory and stable baseline wall shear stress and wall tensile stress following intervention. Thus the manipulation of mediators of smooth muscle proliferation including genetic targeting at the time of angioplasty is unlikely to reduce the incidence of restenosis if the mechanicalhemodynamic conditions do not permit a favorable selflimiting remodeling outcome (55). Further refinements in our understanding of the control mechanisms of intimal proliferation may permit local or systemic pharmacologic control which, together with improved control of systemic and local hemodynamic environments, may prevent or control intimal hyperplasia.

Intimal Thickening Resulting from Subnormal Wall Shear Stress

FIGURE 10.10 Sagittal section of floor of artery in experimental end-to-side anastomosis. Intimal hyperplasia developed in a region of flow separation and stasis where shear stress was low and oscillated in direction. This form of intimal thickening may be hemodynamically modulated. (Reproduced by permission from Bassiouny HS, White S, et al. Anastomotic intimal hyperplasia: mechanical injury or flow induced? J Vasc Surg 1992,15:708–717.)

Chronic reduction in blood flow volume and blood flow velocity exposes the endothelium to reduced levels of shear stress, resulting in intimal thickening. Experimental studies in which rabbit carotid arteries were subjected to chronic, repetitive increases and decreases in blood flow demonstrated that progressive intimal thickening occurs during the period of time that the artery is exposed to low wall shear stress (56,57). In these experiments, the left carotid artery of rabbit was first subjected to increased blood flow for 4 weeks by creation of an arterial venous fistula (AVF) between the left common carotid artery and corresponding external jugular vein. The left common carotid artery enlarged in response to the increased blood flow and increased wall shear stress. No intimal thickening occurred during this time. After 4 weeks of high flow, the AVF was closed, resulting in an immediate blood flow reduction to normal and reduction of wall

FIGURE 10.11 Histologic changes in left common carotid artery proximal to AVF after cycles of increases and decreases in blood flow induced by opening and closing AVF. (A) There was one layer of intimal thickening (I1) after cycle 1. (B) Two layers of intimal thickening (I1 and I2) appeared after cycle 2. (C) There were three layers of intimal thickening (I1, I2, and I3) after cycle 3. EC, endothelial cells; IEL, internal elastic lamina; M, media; Ad, adventitia.

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shear stress to subnormal levels. After 6 weeks of normal flow and low shear stress, significant intimal thickening developed. Second and third exposures to periods of high flow and normal flow by opening and closing the fistula revealed that intimal thickening developed only during periods of decreased blood flow and low wall shear stress (Fig. 10.11). This demonstrated that intimal thickening can develop in response to hemodynamic forces of subnormal wall shear stress and does not require endothelial or artery wall injury. The subnormal level of shear stress was directly associated with the intimal thickening, suggesting that intimal thickening may be an adaptive response to hemodynamic inferences on an artery. Intimal thickening under these conditions appears to be both fibrocellular hypertrophy and hyperplasia, with medial

SMCs being the predominant cell source in subnormal wall shear stress-induced intimal thickening (58).

Intimal Hyperplasia in Stents Endoluminal stents and stent grafts have been widely used in recent years to treat vascular disease (59,60). Intimal hyperplasia has been found to be the major cause of instent restenosis in coronary artery and peripheral stents (61,62). The pathology of intrastent restenosis parallels wound healing responses. These events include early thrombus deposition and acute inflammation, granulation tissue development, and ultimately smooth muscle cell proliferation and extracellular matrix synthesis (64).

uPA

A Syndecan

Type IV collagen MMP 9

MMP 2

Laminin MMP 2 ADAM a1b1Integrin a2b1Integrin

Inhibitory signals

Prostaglandin

cAMP cGMP

Smooth muscle cell

B

Nitric oxide

?

TGF-b

Heparanasedegraded syndecan Fibronectin MMP 3

MMP 1

a3b4a2b3Integrin

Positive signals

a3b1Integrin

Multiple transduction pathways

Monomeric Type I, II collagen

PDGF, FGF-2 thrombin, etc.

FIGURE 10.12 A working hypothesis for intimal hyperplasia. (A) The quiescent state. Quiescent smooth muscle cells are surrounded with a basement membrane of type IV collagen and laminin that is rich in heparan sulfate proteoglycans including syndecans. Binding to b1 integrins, together with the action of cyclic nucleotides (cAMP, cGMP) and unknown mediators of transforming growth factor-b action, generates signals that maintain quiescence. Release from quiescence requires turnover of matrix components, which is initiated by extracellular proteases including metalloproteinases (MMP), urokinase plasminogen activator (uPA), and a disintegrin and metalloproteinase containing proteins (ADAMs). (B) The activated state. Synthetic smooth muscle cells have degraded their basement membrane and come into contact with interstitial matrix components including monomeric types I and II collagen and fibronectin. These also bind to integrin, including importantly a5b1 and avb3 integrins, which may provide the signals for migration and proliferation, and fibronectin can provide pathways for migration. Activation of smooth muscle cells is associated with upregulation of MMP-1 and MMP-3, which can promote turnover of the intertitial matrix. (Reproduced with permission from Newby AC, Zaltsman AB. Molecular mechanisms in intimal hyperplasia. J Pathol 2000;190(3):300–9.)

Chapter 10 Intimal Hyperplasia

Interventions have been tried to prevent in-stent restenosis, including brachytherapy (61) and drug-eluting stents. Drug-coated stents, for example, significantly reduced in-stent restenosis without eliciting inflammation (65). Radioactive stents have been shown to reduce in-stent restenosis (66–68). However, in other studies, plaque growth is not reduced but inverted into an outward direction from the stent (69). Modification of stents and stent graft materials have provided an increased understanding of pathologic process. For example, a comparison study on biocompatibility and performance of various stent-grafts to those of a bare stent in an ovine model revealed that all stent-grafts studied induced an inflammatory vessel wall reaction with neointimal hyperplasia. Polyester-covered endoprostheses induced a marked tissue reaction with induction of 50% luminal stenosis. Endothelialization was retarded with reduced lumen stenosis with ePTFE-covered stentgraft. The bare stent performed best in regard to neointimal formation and caused the least inflammatory response (70). Future studies are needed to improve stent graft biocompatibility and performance.

Molecular Mechanisms in Intimal Hyperplasia Intimal hyperplasia is characterized by migration and proliferation of vascular smooth muscle cells (VSMCs) which are induced by injury, inflammation, and alterations in hemodynamic forces. A working hypothesis on molecular mechanisms has been postulated (71). Fully differentiated VSMCs are maintained in a contractile state by interactions of basement membrane components with specific integrin subtypes (Fig. 10.12A). Heparan sulfate proteoglycans, and cAMP- or cGMP-elevating vasodilator agents, reinforce quiescence. Injury, inflammatory infiltration or mechanical stretch may activate heparanases and a cascade of proteases, which in turn may modulate the interactions between extracellular matrix and VSMCs. Outside-in signal transduction via integrins may trigger a phenotypic shift from a contractile to a secretary state. This may involve the rapid induction of genes, which regulate responses to growth factors and chemoattractants and the expression of new cell surface integrins and extracellular matrix molecules (Fig. 10.12B). Other peptide agents such as thrombin, endothelin-1 and angiotensin-II, and inflammatory cytokines may also act cooperatively to trigger proliferation and migration, provided that there are correct extracellular matrix cues, such as fibronectin binding to integrins. Fibronectin polymerizes into fibers, providing pathways for migration. Osteopontin also has a migratory effect on VSMCs, which is mediated by complexing with the avb3 integrin. Vitronectin is also known to promote migration (71). Recently, activation of big mitogen-activated protein kinase-1 has been shown to regulate smooth muscle cell replication (72). Future investigations in the regulatory

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pathways of VSMC proliferation and migration will further clarify the mechanisms which control intimal hyperplasia.

References 1. Mills JL, Fujitani RM, Taylor SM. The characteristics and anatomic distribution of lesions that cause reversed vein graft failure: a five-year prospective study. J Vasc Surg 1993;17:195–206. 2. Garratt KN, Edwards WD, et al. Differential histopathology of primary atherosclerotic and restenotic lesions in coronary arteries and saphenous vein bypass grafts: analysis of tissue obtained from 73 patients by directional atherectomy. J Am Coll Cardiol, 1991;17:442–448. 3. Thatte HS, Khuri SF. The coronary artery bypass conduit: I. Intraoperative endothelial injury and its implication on graft patency. Ann Thorac Surg 2001;72(6):S2245–52; discussion S2267–70. 4. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990’s. Nature 1993;362:801–809. 5. Jackson CL, Reidy MA. Basic fibroblast growth factor: its role in the control of smooth muscle cell migration. Am J Pathol 1993;143:1024–1031. 6. Zubilewicz T, Wronski J, et al. Injury in vascular surgery—the intimal hyperplastic response. Med Sci Monit 2001;7(2):316–24. 7. Kalmes A, Daum G, Clowes AW. EGFR transactivation in the regulation of SMC function. Ann N Y Acad Sci 2001;947:42–54; discussion 54–5. 8. Reidy MA, Fingerle J, Lindner V. Factors controlling the development of arterial lesions after injury. Circulation 1992;86 (Suppl III):III-43-III-46. 9. Ferns GA, Raines EW, et al. Inhibition of neointimal smooth muscle accumulation after angioplasty by antibody to PDGE Science 1991;253:1129–1132. 10. Clowes AW, Reidy MA. Prevention of stenosis after vascular reconstruction: pharmacologic control of intimal hyperplasia-a review. J Vasc Surg 1991;13:885–891. 11. McCready R, Price M, et al. Failure of antiplatelet therapy with ibuprofen (Motrin) to prevent neointimal fibrous hyperplasia. J Vasc Surg 1985;2(1):205–213. 12. Franklin SM, Faxon DP. Phamacological prevention of restenosis after coronary angioplasty: review of randomized clinical trials. Coron Artery Dis 1993;4:232–242. 13. Glagov S, Zarins CK. et al. Hemodynamics and atherosclerosis: insights and perspectives gained from studies of human arteries. Arch Pathol Lab Med 1988;112:1018– 1031. 14. Zarins CK. Adaptive responses of arteries. J Vasc Surg 1989;9:382. 15. Glagov S, Weisenberg E, et al. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316:1371–1375. 16. Davies PF, Dewey CF, et al. Influence of hemodynamic forces on vascular endothelial function: in vitro studies of shear stress and pinocytosis in bovine aortic cells. J Clin invest 1984;73:1121–1129. 17. McAllister TN, Du T, Frangos JA. Fluid shear stress stimulates prostaglandin and nitric oxide release in bone mar-

174

18.

19.

20.

21.

22.

23.

24. 25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

Part II Basic Cardiovascular Problems row-derived preosteoclast-like cells. Biochem Biophys Res Commun 2000 Apr 13;270(2):643–8. Palumbo R, Gaetano C, et al. Different effects of high and low shear stress on platelet-derived growth factor isoform release by endothelial cells: consequences for smooth muscle cell migration. Arterioscler Thromb Vasc Biol 2002;22(3):405–11. Redmond EM, Cullen JP, et al. Endothelial cells inhibit flow-induced smooth muscle cell migration: role of plasminogen activator inhibitor-1. Circulation 2001; 103(4):597–603. Ward MR, Tsao PS, et al. Low blood flow after angioplasty augments mechanisms of restenosis: inward vessel remodeling, cell migration, and activity of genes regulating migration. Arterioscler Thromb Vasc Biol 2001;21(2):208–13. Olesen SR, Clapham DE, Davies PE. Hemodynamic shear stress activates a K current in vascular endothelial cells. Nature 1988;331:168–170. Leung DYM, Glagov S, Mathews MB. Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. Science 1976;191:475. Glagov S, Zarins CK. Intimal hyperplasia: an adaptive response or a pathologic process? J Vasc Surg 1989;10:571–573. Raitakari OT, Celermajer DS. Flow-mediated dilatation. Br J Clin Pharmacol 2000;50(5):397–404. Zarins CK, Zatina MA, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg 1987;5:413–420. Kamiya A, Togawa T. Adaptive regulation of wall shear stress to flow change in the canine carotid artery. Am J Physiol 1980;239:H14–H21. Masuda H, Bassiouny H, et al. Artery wall restructuring in response to increased flow. Surg Forum 1989;40:285–286. Langille BL, O’Donnell F. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science 1986;231:405–407. Bassiouny HF, Lieber BB, et al. Quantitative inverse correlation of wall shear stress with experimental intimal thickening. Surg Forum 1988;39:328–330. Zarins CK, Giddens D, et al. Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res 1983;53:502–514. Ku DN, Giddens DR, et al. Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque location and low and oscillation shear stress. Arteriosclerosis 1985;5:293–302. Beere PA, Glagov S, Zarins CK. Experimental atherosclerosis at the carotid bifurcation of the cynomolgus monkey: localization, compensatory enlargement and the sparing effect of lowered heart rate. Arterioscler Thromb 1992;12:1245–1253. Beere PA, Glagov S, Zarins CK. Retarding effect of lowered heart rate on coronary atherosclerosis. Science 1984;226:180–182. Leung DYM, Glagov S, Mathews MB. Flastin and collagen accumulation in rabbit ascending aorta and pulmonary trunk during postnatal growth: correlation of cellular synthetic response with medial tension. Circ Res 1977;41:316–323.

35. Zarins CK, Weisenberg F, et al. Differential enlargement of artery segments in response to enlarging atherosclerotic plaques. J Vasc Surg 1988;7:386–394. 36. Glagov S, Zarins CK, et al. Mechanical functional role of non-atherosclerotic intimal thickening. Front Med Biol Eng 1993;5:37–43. 37. Masawa N, Glagov S, et al. Intimal thickness normalizes mural tensile stress in regions of increased intimal area and artery size at the carotid bifurcation. Arteriosclerosis 1988;8:612a. 38. Dobrin PB, Littooy FN, Endean ED. Mechanical factors predisposing to intimal hyperplasia and medial thickening in autogenous vein grafts. Surgery 1989:105:393–400. 39. Glagov S, Giddens DP, et al. Hemodynamic effects and tissue reactions at graft to vein anastomosis for vascular access. In: Sommer BC, Henry ML, eds. Vascular access for hemodialysis. Precept Press, 1991:320. 40. Kleinstreuer C, Hyun S, et al. Hemodynamic parameters and early intimal thickening in branching blood vessels. Crit Rev Biomed Eng 2001;29(1):1–64. 41. Langille BL, Bendeck MP, Keeley FW. Adaptations of carotid arteries of young and mature rabbits to reduce carotid blood flow. Am J Physiol 1989;256:H931– R939. 42. Vyalov S, Langille BL, Gotlieb AI. Decreased blood flow rate disrupts endothelial repair in vivo. Am J Pathol 1996;149(6):2107–18. 43. Mattsson EJ, Kohler TR, et al. Increased blood flow induces regression of intimal hyperplasia. Arterioscler Thromb Vasc Biol 1997;17(10)2245–9. 44. Coats WD Jr, Currier JW, Faxon DP. Remodelling and restenosis: insights from animal studies. Semin Interv Cardiol 1997;2(3):153–8. 45. Miller MJ, Kuntz RE, et al. Frequency and consequences of intimal hyperplasia in specimens retrieved by directional atherectomy of native primary coronary artery stenoses and subsequent restenosis. Am J Cardiol 1993;71:652–658. 46. Megerman J, Hamilton G, et al. Compliance of vascular anastomoses with polybutester and polypropylene sutures. J Vasc Surg 1993;18(5):827–34. 47. Megeman J, Abbott WM. Compliance in vascular grafts. In: Wright C, ed. Vascular grafting. Boston: John WrightPSB, 1983:344–364. 48. Hasson J, Megerman J, Abbott WM. Increased compliance near vascular anastomoses. J Vasc Surg 1985;2:419–423. 49. Lyon R, Runyon-Hass A, et al. Protection from atherosclerotic lesion formation by reduction of artery wall motion. J Vasc Surg 1987;5(1):59–67. 50. Bassiouny HS, White S, et al. Anastomotic intimal hyperplasia: mechanical injury or flow induced? J Vasc Surg 1992;15:708–717. 51. White SS, Zarini CK, et al. Hemodynamic patterns in two models of end-to-side vascular graft anastomoses: effects of pulsatility, flow division, Reynolds number and hood length. J Biomech Eng 1993;115:104–111. 52. Giddens EM, Giddens DP, et al. Exercise flow conditions eliminate stasis at vascular graft anastomoses. In: Schneck DJ, Lucas CL, eds. Biofluid dynamics, 3rd ed. Biomedical engineering monograph series. New York: New York University Press, 1991;255–267.

Chapter 10 Intimal Hyperplasia 53. Bassiouny HS, Krievins D, et al. Distal arteriovenous fistula inhibits experimental anastomotic intimal thickening. Surg Forum 1993;44:345–346. 54. Stary HC, Blankenhorn DH, et al. A definition of the intima of human arteries and of its atherosclerosis-prone regions: a report from the committee on vascular lesions of the Council on Arteriosclerosis, American Heat Association. Circulation 1992;85:391–405. 55. Glagov S. Intimal hyperplasia, vascular modeling and the restenosis problem. Circulation 1994;89:2888–2891. 56. Singh TM, Zhuang YJ, et al. Intimal hyperplasia in response to reduction of wall shear stress. American College of Surgeons, 83rd Annual Clinical Congress, Surgical Forum 1997;444–446. 57. Zhuang YJ, Singh TM, et al. Sequential increases and decreases in blood flow stimulates progressive intimal thickening. Eur J Vasc Endovasc Surg 1998;16(4):301–10. 58. Sho M, Sho E, et al. Subnormal shear stress-induced intimal thickening requires medial smooth muscle cell proliferation and migration. Exp Mol Pathol 2002 Apr;72(2):150–60. 59. Al Suwaidi J, Berger PB, Holmes DR Jr. Coronary artery stents. JAMA 2000;284(14):1828–36. 60. Zarins CK, White RA, et al. The AneuRx stent graft: four-year results and worldwide experience 2000. J Vasc Surg 2001;33(2 Suppl):S135–45. 61. Ajani AE, Kim HS, Waksman R. Clinical trials of vascular brachytherapy for in-stent restenosis: update. Cardiovasc Radiat Med 2001;2(2):107–13. 62. Lowe HC, Oesterle SN, Khachigian LM. Coronary instent restenosis: current status and future strategies. J Am Coll Cardiol 2002;39(2):183–93.

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63. Eton D, Warner DL, et al. Histological response to stent graft therapy. Circulation 1996;94(9 Suppl):II182–7. 64. Virmani R, Farb A. Pathology of in-stent restenosis. Curr Opin Lipidol 1999;10(6):499–506. 65. Hong MK, Kornowski R, et al. Paclitaxel-coated Gianturco-Roubin II (GR II) stents reduce neointimal hyperplasia in a porcine coronary in-stent restenosis model. Coron Artery Dis 2001;12(6):513–5. 66. Waksman R, Bhargava B, et al. Intracoronary radiation with gamma wire inhibits recurrent in-stent restenosis. Cardiovasc Radiat Med 2001;2(2):63–8. 67. Chan AW, Moliterno DJ. In-stent restenosis: update on intracoronary radiotherapy. Cleve Clin J Med 2001;68(9):796–803. 68. Gurberg L, Waksman R. Intravasscular radiation for the prevention of recurrence of restenosis in coronary arteries. Expert Opin Investig Drugs 2001;10(5):891– 907. 69. Wexberg P, Kirisits C, et al. Vascular morphometric changes after radioactive stent implantation: a doseresponse analysis. J Am Coll Cardiol 2002;39(3): 400–7. 70. Cejna M, Virmani R, et al. Biocompatibility and performance of the Wallstent and several covered stents in a sheep iliac artery model. J Vasc Interv Radiol 2001;12(3):351–8. 71. Newby AC, Zaltsman AB. Molecular mechanisms in intimal hyperplasia. J Pathol 2000;190(3):300–9. 72. Luo H, Reidy MA. Activation of big mitogen-activated protein kinase-1 regulates smooth muscle cell replication. Arterioscler Thromb Vasc Biol 2002;22(3): 394–9.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 11 Therapeutic Angiogenesis K. Craig Kent

More than 200,000 people in the United States develop symptoms of lower extremity ischemia each year. Atherosclerosis is the most common cause. Patients can present with claudication or limb-threatening ischemia. Whenever possible, treatment of lower extremity arterial disease should be offered to those individuals in whom amputation is imminent. Moreover, selected individuals whose lifestyles are significantly limited by symptoms of claudication may also benefit from revascularization. Although numerous medical treatments have been explored, the mainstay of therapy for lower extremity ischemia is revascularization, either by catheter-based or open surgical techniques. Both approaches have been extremely effective in reducing the morbidity associated with this disease process. However, not all patients with peripheral arterial ischemia are candidates for intervention. In some patients, particularly those with diabetes, renal insufficiency, or Buerger’s disease, reconstruction is not technically possible owing to the absence of viable runoff vessels. In still other patients, multiple comorbidities associated with diffuse atherosclerosis preclude the use of invasive treatments. Moreover, there is a large cohort of elderly patients disabled with claudication, who are currently not treated because the risks of invasive therapy outweigh the benefits. Consequently, a less invasive strategy would be a welcome adjunct to the current therapeutic alternatives for patients with lower extremity occlusive disease. Patients with atherosclerotic lesions often develop collateral circulation. However, collateral networks are never sufficient to completely restore the deficiency in circulation produced by a major arterial occlusion. Thera-

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peutic angiogenesis is a novel strategy now being explored whereby collateral blood vessel formation in ischemic tissues is enhanced by the administration of angiogenic proteins. Reestablishing blood flow to an ischemic extremity through angiogenesis has the potential to provide a biological “bypass” for patients with atherosclerotic occlusive disease. Studies in animals have suggested that the exogenous provision of angiogenic factors, particularly fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF), may augment blood flow in regions of arterial ischemia, thereby improving tissue perfusion. Although a number of methods are available by which these proteins can be introduced, the most efficient and least invasive is through a simple intramuscular injection. The successful development of therapeutic angiogenesis as a minimally invasive approach to vascular insufficiency could tremendously expand our ability to treat patients with limb-threatening ischemia and limiting claudication.

Angiogenesis and Arteriogenesis Three different processes (vasculogenesis, arteriogenesis, and angiogenesis) contribute to the growth of blood vessels. 1.

Vasculogenesis is the primary process responsible for growth of new vasculature during embryonic development and may play a yet undefined role in mature adult tissues. This process is characterized by the differentiation of pluripotent endothelial cell precursors

Chapter 11 Therapeutic Angiogenesis

2.

3.

into endothelial cells that subsequently form primitive blood vessels (1). Arteriogenesis occurs in adult vessels and refers to the development of new “large” arteries that possess a fully developed tunica media. Examples include the formation of angiographically visible collaterals in patients with advanced peripheral vascular and coronary disease. All vascular cells types, including smooth muscle cells and pericytes, are involved in the formation of these vessels. Angiogenesis is a process that also occurs in adult tissues whereby new capillaries develop from preexisting vasculature. There are many existing examples of angiogenesis. Physiological angiogenesis accompanies wound healing and endometrial expansion whereas retinal neovascularization and rheumatoid arthritis are examples of pathological angiogenesis. Angiogenesis is also required for the development of neoplasms and their metastases (2).

The two processes that have been most extensively investigated are angiogenesis and arteriogenesis. Angiogenesis requires extensive interaction of a variety of cells and is controlled by various peptides and other modulating factors. Hypoxia is one of the main stimuli driving angiogenesis (3). This process begins with proteolytic degradation of the existing basement membrane of a blood vessel wall and the surrounding extracellular matrix. This is followed by migration of endothelial cells and pericytes or smooth muscle cells out of the vessel into the region of ischemia. These cells then proliferate, produce new matrix proteins and basement membrane, and form capillary networks. Matrix degradation and endothelial and smooth muscle cell/pericyte migration are modulated by the interplay of numerous factors, including plasminogen activators, matrix metalloproteinases, and their inhibitors. There are multiple additional regulators of endothelial and smooth muscle cell proliferation that are also important components of the angiogenic process. The two growth factors that appear to be capable of initiating angiogenesis are fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF), although multiple intermediate factors such as hypoxia-inducible factor (HIF-1), transforming growth factor-alpha (TGFa), platelet-derived growth factor (PDGF), angiopoietin, and epidermal growth factor (EGF) are required to complete this process (Table 11.1). Arteriogenesis refers to the development of collateral arteries. One hypothesis is that these collaterals develop from preexisting arterioles that are recruited following occlusion of a large feeding artery. A newly formed pressure gradient results in an increase in flow and velocity within these arterioles and hence an increase in shear stress. Increased shear stress produces marked activation of the endothelium with corresponding increased expression of monocyte chemoattractant protein (MCP-1) and the endothelial surface receptors that are involved in monocyte recruitment and migration (4–6). Recruited monocytes transform into macrophages,

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TABLE 11.1 List of known angiogenic growth factors Angiogenin Angiopoietin-1 Epidermal growth factor (EGF) Fibroblast growth factors: acidic (aFGF) and basic (bFGF) Follistatin Granulocyte colony-stimulating factor (G-CSF) Hepatocyte growth factor (HGF) Hypoxia-inducible factor-1 (HIF-1) Interleukin 8 (IL-8) Leptin Midkine Placental growth factor Platelet-derived endothelial cell growth factor (PD-ECGF) Platelet-derived growth factor-BB (PDGF-BB) Pleiotrophin (PTN) Proliferin Transforming growth factor-alpha (TGF-a) Transforming growth factor-beta (TGF-b) Tumor necrosis factor-alpha (TNF-a) Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF)

which produce numerous cytokines and growth factors (including tumor necrosis factor-alpha (TNF-a), and basic fibroblast growth factor (bFGF) involved in arteriogenesis (7). These proteins stimulate remodeling and dilatation of arterioles, leading to the development of functional collaterals (Fig. 11.1).

Angiogenic Protein Vascular Endothelial Growth Factor VEGF (or VEGF-A) is a family of 34- to 46-Da dimeric glycoproteins discovered first in 1983. These proteins were initially characterized as vascular permeability factors, although in 1989, VEGF, isolated from pituitary folliculostellate cells was characterized and cloned as an angiogenic factor (8). Five isoforms, distinguished according to their number of amino acid residues (VEGF121, VEGF145, VEGF165, VEGF189, VEGF206) are produced from a single gene by alternative mRNA splicing (9). Most cell types produce several VEGF isoforms; however, the most commonly expressed proteins are VEGF121 and VEGF165. VEGF has a signaling sequence that permits its secretion by intact cells. Thus, VEGF produced in transfected cells has the ability to be secreted and become biologically active. All five isoforms have similar biological activity but differ in their ability to bind to the cell surface and to extracellular matrix proteins. VEGF121 and VEGF165 bind weakly to cells and matrix and thus are theoretically more biologically available. The larger iso-

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Part II Basic Cardiovascular Problems Monocytes

SHEAR STRESS

Adhesion Molecules MCP-1 NOS NO

Cytokines

MCP-1

Endothelial Cell

NO

GMCSF

Macrophages Cytokines

VEGF

SMC

FGF

FIGURE 11.1 Cellular mechanisms involved in arteriogenesis. Increased shear stress induces expression of numerous gene products such as MCP-1 and cell adhesion molecules that are involved in monocyte recruitment and migration. These changes cause monocytes to migrate into the subintimal space where they phenotypically differentiate into macrophages, which then express cytokines and growth factors that predispose to vascular remodeling (arteriogenesis). GMCSF prolongs the life span of monocytes/macrophages via inhibition of apoptosis of these cells. MCP-1, monocyte chemoattractant protein; NOS, nitric oxide synthase; NO, nitric oxide; GMCSF, granulocyte–macrophage colony-stimulating factor; VEGF, vascular endothelial growth factor; FGF, fibroblast growth factor; SMC, smooth muscle cell.

forms (VEGF189 and VEGF206) are less efficiently secreted, and are sequestered by heparan sulfate proteoglycans to the cell surface and to extracellular matrix. VEGF appears to be the most potent regulator of angiogenesis. Although VEGF is synthesized by a variety of cell types in and around the vessel wall, this protein specifically affects the endothelial cell. VEGF stimulates endothelial cell proliferation by binding to two transmembrane tyrosine kinase receptors: flt-1 (VEGFR-1) and KDR/flk-1 (VEGFR-2) (10). Moreover, VEGF enhances endothelial cell survival, an event that complements its mitogenic effect. Although VEGF does not have a direct effect on smooth muscle cells or pericytes, indirectly, through factors released by the endothelial cell, VEGF can stimulate SMC migration and proliferation. Hypoxia is a potent stimulus for VEGF expression (11). Transcription of VEGF mRNA is mediated in part by the binding of hypoxia-inducible factor-1 to a binding site located on the VEGF promoter (12). Furthermore, VEGF mRNA is intrinsically labile; however, in response to hypoxia, there is stabilization of its mRNA (13,14). Moreover, the expression of VEGF receptors is upregulated by hypoxia (15). Thus, hypoxia in vivo appears to be a potent stimulus for angiogenesis by increasing transcription of VEGF as well as its receptor.

Fibroblast Growth Factor Fibroblast growth factor (FGF) is a family of structurally homologous 16- to 24-kDa proteins that enhance the pro-

liferation of endothelial cells, fibroblasts, and smooth muscle cells. At present, the FGF family is known to contain at least 20 factors, which have 30% to 70% homology (16). Unlike VEGF, the classical FGFs, FGF-1, FGF-2 (also known as acidic and basic fibroblast growth factors, respectively), lack the signal sequence that allows direct cellular secretion of the protein. Thus, techniques to overexpress FGF must be accompanied by a mechanism that promotes protein secretion. FGF has no effect on vascular permeability. The biological effects of FGFs are mediated by four structurally related tyrosine kinase receptors, which are broadly expressed (17,18). Like VEGF, FGF stimulates angiogenesis and collateral vessel formation. However, FGF also directly stimulates smooth muscle cell proliferation, which can lead to intimal thickening and blood vessel occlusion. Thus, administration of FGF can have both beneficial and adverse effects on the vascular system. Moreover, systemic treatment with FGF has been associated with renal and hematologic toxicity, both of which may affect the potential therapeutic use of this protein (19).

Hepatocyte Growth Factor Recent studies have identified the protein, hepatocyte growth factor (HGF), as a member of the family of angiogenic growth factors. HGF is a mesenchyme-derived pleiotropic factor, which regulates growth, motility, and morphogenesis of various cell types (20,21). Moreover, HGF is similar to VEGF in that it is contains a sequence that allows secretion of the protein from cells and it also is an endothelium-specific growth factor.

Hypoxia-inducible Factor Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric transcription factor that regulates the expression of a number of oxygen-dependent genes. VEGF has been shown to be a bona fide HIF-1 target gene, as the VEGF gene contains a hypoxia response element (HRE) within its promoter that is responsive to this factor (3). A novel approach to promote angiogenesis in hypoxic muscle might be the gene transfer of HIF-1, which may mimic the physiological angiogenic response that occurs after ischemia.

Mechanisms of Drug Delivery One of the primary mechanisms through which angiogenic proteins can be introduced is via gene therapy. The goal of gene therapy is to introduce recombinant DNA into a host cell/tissue, which initiates or accentuates expression of a protein that may alter the course of a disease. In the case of therapeutic angiogenesis, gene therapy is designed to increase the production of a protein that stimulates the formation of capillary or collateral blood vessels. This same effect can also be achieved by administering exogenous angiogenic proteins directly into tissues. There

Chapter 11 Therapeutic Angiogenesis

are, however, distinct advantages of gene therapy over direct protein delivery. Proteins generally have short halflives and therefore sustained biological activity requires frequent or continuous protein administration. Alternatively, with gene transfer, the “turned-on” gene can lead to the release of high concentrations of the therapeutic protein over a sustained period of time. Moreover, with gene therapy, the genetic material to be introduced can be constructed so that it is only turned on in specific “target” cells. This allows the selective expression of proteins by specific cells within a tissue. This specificity cannot be achieved by exogenous administration of protein. For gene transfer to be successful, the foreign gene must cross the outer membrane of the host cell and be transported to the nucleus. To accomplish this, the gene is first inserted into a plasmid, a naturally occurring circular DNA molecule. The delivery of the plasmid into the host cell and the subsequent expression of the gene is a process known as transfection. Direct gene transfer (or transfection with naked DNA) is a process whereby cells are exposed to high concentrations of plasmid DNA. Uptake of the DNA under this circumstance is by endocytosis. Because of the hydrophilic nature of DNA, host cell uptake and thus expression of naked DNA is limited. Alternatively, a carrier, referred to as a vector, can be used to deliver recombinant DNA into the host cell. Viruses are commonly used vectors. Viruses, through a receptor-mediated mechanism, are extremely efficient at transporting genetic material across the cell membrane. Currently, the most efficient vector for in vivo vascular gene transfer is the adenovirus. Transfection efficiencies can be achieved with the adenovirus that are many-fold greater than what can be achieved by exposing cells to naked DNA (22). Unfortunately, when an adenovirus is used to infect a target cell, a host immune response to the adenovirus is incited. Neutralizing antibodies to the adenovirus then form, and these antibodies eliminate the possibility of using an adenoviral vector on subsequent occasions, and also limit the duration of expression of the DNA (23,24). Naked DNA has been used in several models of therapeutic angiogenesis (25–27). In other models, tissues have been transfected using an adenoviral vector. The advantage of naked DNA is its simplicity and the fact that there is no immune response; thus, the foreign DNA can be reinjected on multiple successive occasions. The obvious disadvantage is that high transfection efficiencies cannot be achieved, and protein production may be low. Alternatively, adenoviral vectors can produce high levels of gene expression and protein production; however, the immune response eliminates the possibility of subsequent injections. Regardless of whether naked DNA or an adenoviral vector is used, the gene encoding for the angiogenic protein can be introduced into the ischemic tissue via two different techniques. Genes can be injected directly into the arterial circulation proximal to the occlusion. This approach allows the genetic material to be dispersed into collaterals and presumably carried distally to the point where neovascularization might be optimally needed.

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Systemic toxicity is a potential side effect of this approach. Local delivery can be achieved by direct injection of the angiogenic protein into the muscles through which collaterals pass. Local injection markedly diminishes the potential for systemic toxicity and confines the expression of the protein to the tissues into which the gene has been injected (28,29).

Potential Side Effects Systemic exposure of the angiogenic protein carries the risk of stimulating neovascularization in non-target tissues such as the eyes or joints. Because tumor growth is dependent upon angiogenesis, there is a risk with systemic administration of angiogenic factors of accelerating the progression of latent tumors. The actual risk of any of these untoward events is unknown. Fortunately, most normal tissues do not express measurable levels of the receptors for these proteins. Therefore, it may be that aberrant neovascularization will not occur unless tissues are exposed for prolonged periods to high doses of exogenously administered angiogenic agent (30). However, it is necessary that there be an awareness of the potential side effects of therapeutic angiogenesis and the occurrence of these events must be clearly monitored in clinical trials.

Clinical Trials Innumerable preclinical studies in animals have established that angiogenic growth factors can promote collateral artery and capillary development in models of peripheral and myocardial ischemia. Moreover, human clinical experience with therapeutic angiogenesis for the treatment of myocardial and lower extremity ischemia is gradually accumulating, with several trials under way. Outlined below are results from completed or ongoing clinical trials that pertain to the lower extremity circulation.

VEGF Trials Baumgartner et al. in 1997 reported the results of a phase I clinical trial of intramuscular (IM) injection of VEGF165 in nine patients with critical limb ischemia (31). The majority of these patients had either rest pain or nonhealing ulcers and all were not considered to be candidates for surgical or percutaneous revascularization. Gene transfer was performed by IM injection into ischemic limbs of 2000 mg of naked plasmid DNA encoding VEGF165. These injections were performed on two occasions separated by a 4-week interval. Successful gene expression in patients was documented by an increase in serum VEGF levels. Angiography and MRA were performed before and 4 weeks after these treatments, and patients were followed for an average of 6 months. The investigators noted an improvement in the average ankle–brachial index (ABI) at 12 weeks from 0.33 ± 0.05 to 0.48 ± 0.03

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(p = 0.02). Contrast angiography demonstrated new collateral vessels in seven limbs and magnetic resonance angiography revealed improved distal flow in eight. Rest pain resolved in all three patients who presented with rest pain alone. Ischemic ulcers either healed or improved in four of seven limbs. Three patients subsequently required below-knee amputation. Subsequently, six patients with Buerger’s disease and critical limb ischemia were treated by the same investigators (28). The patients were treated twice, 4 weeks apart, with 2 mg or 4 mg of intramuscular VEGF165, which was administered at four arbitrarily selected sites in the ischemic limb. Newly visible collaterals were visible in all seven limbs, as demonstrated by magnetic resonance (MRA) and serial contrast angiography. Healing of gangrenous ulcers or toes occurred in three limbs. Two limbs with preestablished necrotic lesions of the forefoot eventually required amputation. Nocturnal rest pain was relieved in the remaining two patients. The same group of investigators recently completed a similar dose escalation, placebo-controlled trial using naked DNA encoding VEGF-2 (32). VEGF-2 is a member of the VEGF family that is present primarily in the lymphatic endothelium and has a high affinity for the VEGFR3 receptor. A total of 48 patients, including 12 treated with placebo, were enrolled. In an initial report of 13 patients (six with rest pain alone and seven with ischemic ulcers and rest pain) there was improvement in five patients with rest pain and three patients with ischemic ulcers. Enrollment has since been completed and data analysis is under way. A placebo-controlled, randomized and double-blind phase II study is in progress at the University of Kuopio in Finland (33), comparing administration of VEGF165 or placebo in patients with lower extremity arterial occlusive disease after angioplasty or stent placement. Adenovirus or plasmid liposomes containing the VEGF gene were administered intra-arterially. Analysis of 45 enrolled patients (15 plasmid, 15 adenovirus and 15 placebo) revealed at 3 months a statistically significant increase in vascularity distal to the gene transfer site in the VEGF (plasmid/virus) group compared to placebo as measured by digital subtraction angiography. However, as of yet there has been no significant difference in clinical outcome in these patients. A phase II, double blind, randomized, placebocontrolled, multicenter trial (Parke-Davis) is under way using intra-arterial delivery of VEGF121 for patients with severe intermittent claudication. The results of this trial should be forthcoming over the next year.

FGF Trials A phase I, randomized, double-blind, placebo-controlled, dose escalation trial was conducted by Lazarous et al. (Scios Corporation) using the bFGF protein for the treatment of patients with claudication (34). The outcomes measured were drug safety and calf blood flow using strain gauge plethysmography. A group of 19 patients

were enrolled and randomized to four groups (placebo, bFGF 10 mg/kg, bFGF 30 mg/kg, and bFGF 30 mg/kg on two consecutive days). The route of administration was via the femoral artery. Inclusion criteria for the study were claudication >6 months and ABI < 0.8 at rest. Results of this phase I study showed that intra-arterial bFGF was well tolerated. A dose–response relationship between bFGF and calf blood flow was found and a subjective improvement in symptoms was noted in the majority of the patients treated. Following these encouraging results, a randomized, double blind, placebo-controlled phase II trial was designed using bFGF. In this trial, however, a different dosage regime (2 mg/kg weekly for 6 weeks) and an alternate different route of delivery (intravenous) were used. Outcome measures evaluated included change in peak walking time and functional status. A total of 24 patients were treated with either placebo or bFGF. Inclusion criteria were a resting ABI < 0.90 and a decrease in ABI by 20% following exercise. This study was terminated prematurely because of the development of severe proteinuria in five of 16 subjects who received intravenous bFGF. Moreover, analysis of efficacy was performed in those patients who were able to tolerate therapy and no difference between treatment and control groups was evident for any of the measures tested. In a recently completed phase II, multicenter, randomized, double blind, placebo-controlled trial (Traffic, Chiron Corporation), patients with intermittent claudication were randomized to placebo or one or two doses of recombinant FGF provided intra-arterially on day 1 or days 1 and 30. A total of 192 patients were enrolled. Inclusion criteria were symptomatic claudication with a resting ABI < 0.8. Outcome measures included change in peak walking time (PWT) and quality of life at 90 and 180 days. A clinically relevant increase in peak walking time was noted at 90 days in the single-dose cohort but not the double-dose group. At 180 days, treatment with FGF did not alter PWT, claudication severity, stair climbing, walking speed, or walking distance. Although a positive effect was observed at an early time point in one treatment arm, the findings of this study in general were discouraging. In a recently completed phase I multicenter trial (Aventis Corporation) the safety and tolerability of an increasing single dose of plasmid-linked DNA (NV1FGF) was tested in patients with limb-threatening peripheral occlusive disease (35). A total of 51 patients were enrolled and doses ranging from 500 mg to 4000 mg of NV1FGF were injected intramuscularly into the thigh and calf of ischemic extremities. Inclusion criteria were rest pain or trophic lesions related to ischemia present for more than 14 days, an ABI < 0.4 and an angiogram that demonstrated occlusion of either the superficial femoral, popliteal, or infrapopliteal arteries. No serious adverse events were noted during the course of the study. Fifteen patients were available for follow-up (mean 6 months). A significant decrease in rest pain was noted and the ABI increased in all patients. Moreover, healing was observed in all nine pa-

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tients who presented with ulcers. These encouraging results have resulted in the initiation of a phase II placebo controlled trial, which is currently under way.

invasive strategy for the treatment of lower extremity ischemia.

New Horizons

References

The mixed outcomes of current human trials involving angiogenesis may be related to a variety of factors. There has been slow progress in the arena of gene transfer. Improvements are needed in efficacy, specificity, and regulation of gene expression. The emergence of novel, safe, and more effective vectors will improve the feasibility of skeletal muscle gene therapy. It is now widely recognized that both angiogenesis and arteriogenesis require the cooperative action of multiple cytokines and growth factors. Thus, gene therapy using combinations of vectors/plasmids (gene cocktails) may offer another strategy that might increase its efficacy. In has recently been discovered that production of nitric oxide (NO) is critical to the success of angiogenic therapy. NO also appears to be important in arteriogenesis leading to early dilatation of small collateral vessels. Thus, strategies to stimulate the production of NO may be yet another method of enhancing circulation to ischemic tissues. Recently, Asahara et al. have shown that endothelial progenitor cells (EPCs) circulate in adult peripheral blood (36). Differentiated EPCs in embryonic tissues are the precursors to new blood vessels (37). It has been demonstrated that transplantation in humans of either culture-expanded EPCs or adult stem cells isolated from bone marrow effectively enhances angiogenesis in ischemic tissues (38). Biologically modified EPCs may be a potent therapeutic alternative for enhancing angiogenesis.

Summary Clinical studies of therapeutic angiogenesis in humans are at a very early stage and the preliminary results are inconclusive. Clinicians familiar with patients afflicted with peripheral vascular disease realize that, with proper treatment, wounds can heal and rest pain can resolve even in severely ischemic limbs. Thus, positive findings in nonrandomized trials do not demonstrate efficacy. Patients with lower extremity occlusive disease manifesting as claudication or limb-threatening ischemia are a heterogenous group. Experience with other treatment modalities has demonstrated that, in this patient population, efficacy can only be proven through large randomized trials. There is still much to learn about the complex processes of angiogenesis and arteriogenesis. Phase I trials using new agents and combination therapy are under development at many institutions, including our own. The promise of this technique is great. It is our anticipation that advances over the next several years will allow therapeutic angiogenesis to become a practical, minimally

1. Bussolino F, Mantovani A, Persico G. Molecular mechanisms of blood vessel formation. trends Biochem Sci 1997;22:251–256. 2. Hanahan D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell 1996;86:353–364. 3. Semenza GL. Hypoxia inducible factor 1: master regulator of oxygen homeostasis. Curr Opin Genet Dev 1999;8:588–594. 4. Shyy JY, Hsieh HJ, et al. Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 expression in vascular endothelium. Proc Natl Acad Sci 1994;91:4678–4682. 5. Chappell DC, Varner SE, et al. Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ Res 1998;82:532–539. 6. Ito WD, Arras M, et al. Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res 1997;80:829–837. 7. Wolf C, Cai WJ, et al. Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol 1998;30:2291–2305. 8. Ferrara N, Henzel WJ. Pituitary follicular cells secrete a novel heparin-binding growth factor specific for vascular endothelial cells. Biochem Biophys Res Commun 1989;161(2):851–858. 9. Ferrara N. Vascular endothelial growth factor: molecular and biological aspects. Curr Top Microbiol Immunol 1999;237:1–30. 10. Shibuya M, Ito N, Claesson-Welsh L. Structure and function of vascular endothelial growth factor receptor-1 and -2. Curr Top Microbiol Immunol 1999;237:59– 83. 11. Levy AP, Levy NS, et al. Transcriptional regulation of the rat vascular endothelial growth factor gene by hypoxia. J Biol Chem 1995;270(22):13333–13340. 12. Semenza GL. HIF-1, O(2), and the 3 PHDs: how animal cells signal hypoxia to the nucleus. Cell 2001;107(1): 1–3. 13. Ross J. mRNA stability in mammalian cells. Microbiol Rev 1995;59(3):423–450. 14. Paulding WR, Czyzyk-Krzeska MF. Hypoxia-induced regulation of mRNA stability. Adv Exp Med Biol 2000;475:111–121. 15. Brogi E, Schatteman G, et al. Hypoxia-induced paracrine regulation of vascular endothelial growth factor receptor expression. J Clin Invest 1996;97(2): 469–476. 16. Cross MJ, Claesson-Welsh L. FGF and VEGF function in angiogenesis: signalling pathways, biological responses and therapeutic inhibition. Trends Pharmacol Sci 2001; 22(4):201–207. 17. Jaye M, Schlessinger J, Dionne CA. Fibroblast growth factor receptor tyrosine kinases: molecular analysis and signal transduction. Biochim Biophy Acta 1992;1135: 185–199.

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Part II Basic Cardiovascular Problems

18. Szebenyi G, Fallon JF. Fibroblast growth factors as multifunctional signaling factors. Int Rev Cytol 1999;185: 45–106. 19. Unger EF GL, Epstein SE, et al. Effects of a single intracoronary injection of basic fibroblast growth factor in stable angina pectoris. Am J Cardiol 2000;85(12): 1414–1419. 20. Matsumoto K, Nakamura T. Emerging multipotent aspects of hepatocyte growth factor. J Biochem (Tokyo) 1996;119:591–600. 21. Matsumoto K, Nakamura T. Hepatocyte growth factor (HGF) as tissue organizer for organogenesis and regeneration. Biochem Biophys Res Commun 1997;239: 639–644. 22. Nabel EG, Nabel GJ. Complex models for the study of gene function in cardiovascular biology. Annu Rev Physiol 1994;56:741–761. 23. Wilson JM. Adenoviruses as gene-delivery vehicles. N Engl J Med 1996;334(18):1185–1187. 24. Zabner J, Petersen DM, et al. Safety and efficacy of repetitive adenovirus-mediated transfer of CFTR cDNA to airway epithelia of primates and cotton rats. Nat Genet 1994;6:75–83. 25. Wolff JA, Malone RW, et al. Direct gene transfer into mouse muscle in vivo. Science 1990;247:1465–1468. 26. Lin H, Parmacek MS, et al. Expression of recombinant genes in myocardium in vivo after direct injection of DNA. Circulation 1990;82:2217–2221. 27. Hedin U, Wahlberg E. Gene therapy and vascular disease: Potential applications in vascular surgery. Eur J Vasc Endovasc Surg 1997;13:101–111. 28. Isner JM, Baumgartner I, et al. Treatment of thromboangiitis obliterans (Buerger’s disease) by intramuscular gene transfer of vascular endothelial growth factor: Preliminary clinical results. J Vasc Surg 1998;28:964–973. 29. Tsurumi Y, Takeshita S, et al. Direct intramucular gene transfer of naked DNA encoding vascular endothelial

30.

31.

32.

33.

34.

35.

36.

37.

38.

growth factor augments collateral development and tissue perfusion. Circulation 1996;94:3281–3290. Banai S, Jaklitsch MT, et al. Effects of acidic fibroblast growth factor on normal and ischemic myocardium. Circ Res 1991;69(1):76–85. Baumgartner I, Pieczek A, et al. Constitutive expression of phVEGF165 after intramuscular gene transfer promotes collateral vessel development in patients with critical limb ischemia. Circulation 1998;97(12):1114–1123. Rauh G, Gravereaux E, et al. Asessment of safety and efficacy of intramuscular gene therapy VEGF-2 in patients with critical limb ischemia (abstract). Circulation 1999;100:1–770. Makinen K, Manninen H, et al. VEGF gene transfer to human lower limb artery: a placebo-controlled, randomized, double-blinded phase II study (abstract). Circulation 2001;104:253. Lazarous DF, Unger EF, et al. Basic fibroblast growth factor in patients with intermittent claudication: results of a phase I trial. J Am Coll Cardiol 2000;36(4):1239– 1244. Comerota AJ, Throm RC, et al. Plasmid-linked naked DNA (NV1FGF) for the treatment of end-stage unreconstructible lower extremity ischemia: preliminary results of a phase. 49th Scientific Program, Am Assoc Vasc Surg. Baltimore, MD; 2001. Asahara T, Murohara T, et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997; 275:964–967. Asahara T, Masuda H, et al. Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization. Circ Res 1999;85:221–228. Iwaguro H, Yamaguchi J, et al. Endothelial progenitor cell vascular endothelial growth factor gene transfer for vascular regeneration. Circulation 2002;105: 732–738.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 12 Thrombogenesis and Thrombolysis Donald Silver, Leila Mureebe, and Thomas A. Shuster

Surgeons who operate on the cardiovascular system have an added challenge to those who perform other types of surgery. The cardiovascular surgeon must render blood noncoagulable during times of total or local circulatory arrest and later must achieve sufficient hemostasis to prevent wound complications and exsanguinating hemorrhage. In addition, the ability to lyse unwanted thromboemboli should be part of the cardiovascular surgeon’s armamentarium. Thus, the cardiovascular surgeon must be intimately familiar with the physiology and the methods for ensuring and inhibiting thrombogenesis and thrombolysis.

Thrombogenesis Hemostasis The complex reactions that lead to hemostasis have been divided into two stages: vasoconstriction and platelet plug formation (i.e., primary hemostasis); and thrombus formation and stabilization (i.e., secondary hemostasis). Vasoconstriction, occurring within seconds, is the earliest event following vessel injury, with the muscular elements contracting in response to neurogenic and myogenic influences. Platelets subsequently adhere to the injured vessel and secrete epinephrine, serotonin, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and thromboxane, which contribute to the vasoconstriction (1). These substances released by the platelet, in addition to aiding vasoconstriction, contribute to further

platelet aggregation and the development of the platelet plug. Secondary hemostasis, the formation of a fibrin network, maintains the hemostasis begun by the initial events. The fibrin monomers polymerize into insoluble strands of fibrin. The stable thrombus provides long-term hemostasis.

Platelets Platelets are small (1–4 μm), anuclear fragments of megakaryocytes that have a circulating life of 8–12 days. The normal count in peripheral blood is 150,000–450,000/mm3. Younger platelets are more functional; senescent platelets are removed from the circulation by the spleen. Small numbers of platelets are constantly consumed in the maintenance of vascular integrity. Platelets adhere to exposed subintimal collagen, von Willebrand factor (vWF), and tissue factor (TF, tissue thromboplastin) at sites of intimal disruption. Adhesion requires the participation of several glycoprotein receptors on the platelet membrane (2). The complex of glycoproteins Ib–V–IX is the receptor for vWF, and the Ia–IIa complex is the receptor for collagen. Many additional substances cause platelet activation, including epinephrine, ADP, and thrombin. Activation of platelets results in transforming of platelets from a resting discoid shape to a rounded appearance with cytoplasmic extensions that facilitate adhesion (platelet–substrate interaction) (3). Adhesion is followed by platelet secretion (degranulation).

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Platelets contain three types of granules: a-granules contain platelet factor 4, b-thromboglobulin, mitogenic factor, fibronectin, factor VIII-related antigen (factor VIII:RAg), plasminogen activator inhibitor 1 (PAI-1), a2antiplasmin, factors V and XI, protein S, platelet-derived growth factor, high-molecular-weight kininogen (HMWK), and fibrinogen; dense granules contain calcium, serotonin, ADP, and ATP; and the lysosome-like granules contain numerous acidic hydrolases. Alphagranules are 8 to 50 times more prevalent than dense granules (4). Platelets usually do not adhere to each other or to normal vascular endothelium. However, within seconds after vascular injury, platelets adhere to the injured vessel, especially to exposed basement membrane and collagen. Adhesions are also promoted by the presence of vWF, which is present in the subendothelial matrix and binds to a platelet surface receptor, glycoprotein Ib. The release of ADP activates the platelet–glycoprotein receptor complex GpIIb–IIIa, which binds to fibrin and other adhesive molecules, thus promoting platelet aggregation. Adhesion and aggregation contribute to the formation of the platelet plug. The platelets supply procoagulant activity as platelet factor III and release coagulation factors in the early stages of aggregation. The release of these substances helps activate the coagulation system. The platelet surface is a lipoprotein membrane upon which coagulation factors interact to promote and regulate the coagulation cascade. Activated factors V and X (Va and Xa) combine with calcium on the platelet membrane to form the prothrombinase complex, which cleaves prothrombin to thrombin. Thrombin, in addition to cleaving fibrinogen to fibrin, is a strong platelet aggregator and also causes granule release and increased production of thromboxane A2. The thrombin that is produced promotes more platelet aggregation and also the establishment of the fibrin network that stabilizes the platelet hemostatic plug. Platelet Disorders Platelet disorders may be quantitative or qualitative and congenital or acquired. Quantitative platelet disorders include thrombocytopenia and thrombocytosis. Thrombocytopenia is defined as a platelet count below 100,000/mm3. When the count drops below 20,000 to 30,000/mm3, increased vascular fragility, permeability, and petechiae may occur. Spontaneous bleeding may occur with a count of less than 30,000/mm3, and is rare with platelet counts greater than 50,000/mm3. Thrombocytopenia may be drug induced, or caused by portal hypertension, disseminated intravascular coagulation, sepsis, viral illness, or may be idiopathic. Drug-induced thrombocytopenia results from platelet destruction by drug-dependent antibodies. In a recent review of drug-induced thrombocytopenia, George et al. cited 152 drugs in 515 patients. The most commonly implicated drug was quinidine, followed by quinine. Quinidine was also the drug associated with the most bleeding complications (14 major and minor, out of 91

total events). Some other drugs associated with thrombocytopenia include rifampin, TMP-SMX, methyldopa, acetaminophen, digoxin and gold (5). Of patients who receive heparin, 2% to 3% develop heparin-associated antiplatelet antibodies (HAAb). Antibody formation is independent of heparin type, dose, route or duration of therapy. The antibodies (most commonly IgG, but also IgM and IgA) form against a heparin–platelet factor 4 complex. These antibodies, in the presence of heparin and platelet factor 4, cause platelet activation and aggregation. Patients with the heparininduced thrombocytopenia syndrome (HIT) may present with a low or falling platelet count, resistance to anticoagulation with heparin, and/or heparin-induced arterial or venous thromboses. Qualitative platelet disorders should be suspected when bleeding occurs in the presence of normal coagulation test results and normal platelet count results. Qualitative platelet disorders contribute to spontaneous bleeding less frequently than do the quantitative ones. Abnormal platelet function is rarely the cause of bleeding but may exacerbate existing bleeding such as that occurring with trauma or surgery. Acquired qualitative abnormalities are commonly related to the ingestion of drugs such as aspirin, dipyridamole, indomethacin, and ibuprofen. Other acquired causes of platelet malfunction include cirrhosis, uremia, and macroglobulinemias. Patients with acquired qualitative platelet function abnormalities usually have normal platelet counts but prolonged bleeding times secondary to defects in aggregation. Congenital qualitative platelet disorders include von Willebrand disease (vWD), “storage pool disease,” and other thrombocytopathies. These patients have normal platelet counts, may have large platelets or abnormally shaped platelets, and always have abnormal platelet function. Perhaps the most common hereditary abnormality of hemostasis, vWD is associated with a deficiency of VIII:RAg. Patients with vWD have prolonged bleeding times owing to poor platelet adhesion and aggregation. A qualitative disorder of platelets that is recognized with increased frequency is the sticky platelet syndrome. The syndrome, first described in 1983, is marked by augmented platelet reactivity to stimulation by agonists. Patients are at increased risk for venous and arterial thromboses. Patients are effectively managed with lowdose (81 mg per day) aspirin (6). Platelet Function Inhibition The most widely used platelet function inhibitor remains acetylsalicylic acid (aspirin). Aspirin irreversibly acetylates platelet prostaglandin G/H synthase, leading to permanent inactivation of platelet cyclo-oxygenase, which is responsible for generation of thromboxane A2 (7). However, only the platelets produced during the circulating time of the drug (half-life of 30 to 45 minutes) are affected. ADP, a weak agonist of platelet stimulation, binds to specific receptors on the platelet membrane (P2 receptors). ADP induces platelet shape change and aggregation.

Chapter 12 Thrombogenesis and Thrombolysis

Both ticlopidine and clopidogrel are selective and irreversible antagonists of the ADP platelet receptor P2YT. The active substances are assumed to be hepatic metabolites (8). Both drugs require administration for 3 to 5 days before full physiologic activity, and the effects persist for up to 10 days after withdrawal of drugs. Although it is a potent inhibitor of ADP-induced platelet aggregation, ticlopidine is infrequently used clinically due to its toxicities (granulocytopenia in 2%, diarrhea in 20%) and overall lack of increased efficacy over aspirin. Clopidogrel, on the other hand, is associated with a lower stroke rate compared with aspirin and has a low occurrence of side effects (4). Phosphodiesterase catalyzes the hydrolysis of the second-messenger cyclic adenosine monophosphate (cAMP) into the low-energy adenosine monophosphate (AMP). Dipyridamole and cilostazol interfere with phosphodiesterase activity. Dipyridamole has a low phosphodiesterase activity after oral dosing, and minimal intrinsic anti-platelet activity (4). Cilostazol (Pletal, Otsuka American Pharmaceutical) is a novel phosphodiesterase inhibitor that inhibits phosphodiesterase E3 (9). It inhibits platelet aggregation and produces arterial vasodilation. Its vasodilatory action is most likely due to its effect on cAMP levels (10). In addition to its effect on platelets, it also has been shown to reduce intimal hyperplasia (11). There are three randomized trials demonstrating the efficacy of cilostazol in the treatment of claudication (4), as well as studies documenting the beneficial effects of this drug on platelet aggregation (12), and lipid profile (13). The major contraindication to the use of cilostazol is the presence of congestive heart failure. The glycoprotein IIb–IIIa complex is an attractive target for pharmacologic inhibition of platelet functions. The initial glycoprotein IIb–IIIa complex inhibitor is abciximab, a monoclonal antibody that binds not only to the glycoprotein IIb–IIIa but also to the receptor for vitronectin and a neutrophil-associated receptor (14). Abciximab improves outcomes after percutaneous coronary intervention (4). However, its dissociation time is up to 4 hours, creating a long therapeutic window for inhibition of both platelet and leukocyte adhesion. Two lowmolecular-weight (500–700 Da) parenteral inhibitors, tirofiban and eptifibatide, are selective for the glycoprotein IIb–IIIa complex. The dissociation time for these low-molecular-weight agents is less than 1 minute. These low-molecular-weight platelet function inhibitors have demonstrated short-term benefit in both unstable angina and in non-Q-wave myocardial infarction (14).

Coagulation The activated platelet membrane phospholipid serves as a scaffold for reactions catalyzed by a series of serine proteases (Table 12.1). Tissue factor (TF), a transmembrane protein expressed by epithelial cells, macrophages, and other cells not normally in contact with flowing blood

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(15), is exposed by vessel injury. TF and activated factor VII (VIIa) forms a complex which activates both factors X and IX. Activated factor X (Xa) and activated factor V (Va) enter the prothrombinase complex (Xa, Va, calcium, and phospholipid), which converts prothrombin to thrombin. Amplification of the cascade by factors VIIIa and IXa is required for sustained hemostasis (16,17). Thrombin activates factors VII and V, as well as platelets (18), and cleaves fibrinogen to fibrin monomers, which are polymerized and subsequently cross-linked through the action of factor XIIIa. This series of reactions was initially called the extrinsic pathway (Fig. 12.1). The intrinsic pathway begins with the activation of factor XII by its exposure to a negatively charged surface (19). XIIa and thrombin activate XI which leads to the activation of IX. Activated IX and VIIIa form the tenase complex, which also activates X, leading to the additional conversion of prothrombin to thrombin. The reactions of the coagulation cascade are tightly regulated. The generation of thrombin via the extrinsic pathway is inhibited through the activity of tissue factor pathway inhibitor (TFPI). TFPI binds to and inactivates the TF–VIIa complex and thus inhibits activation of factor X. TFPI also directly inactivates Xa. Both activities lead to a reduction of the activation of prothrombin to thrombin (17). TFPI is synthesized by endothelial cells and is one of the many antithrombotic properties of the endothelium. It is also present in smooth muscle cells, platelets and macrophages. TFPI is often present in decreased concentrations during septicemia and disseminated intravascular coagulation (DIC). The serum concentration of TFPI is increased two- to fourfold by heparin administration (20). The activity of TFPI is enhanced by heparin and calcium (21). Thrombin, thrombomodulin and protein C also regulate thrombosis. Thrombin activates platelets, catalyzes fibrinogen to fibrin and activates plasma factors V, VIII, XI and XIII. Thrombomodulin is an endothelial cell transmembrane glycoprotein, which neutralizes the procoagulant and platelet-activating ability of thrombin. After binding to thrombomodulin, thrombin functions as a weak anticoagulant by activation of protein C. Protein C is a serine protease that inactivates factors Va and VIIIa. The binding of thrombomodulin to thrombin also allows thrombin to be degraded within cells. Increases in plasma levels of thrombomodulin have been shown to correlate with a decreased incidence of coronary artery disease (22). Antithrombin (AT), synthesized in the liver and the endothelium, is the major inhibitor of thrombin and Xa. It inhibits all of the serine proteases except factor C. Antithrombin binds to heparin, and undergoes a conformational change, greatly enhancing antithrombin’s ability to complex with the serine proteases. Heparin then dissociates and acts as a catalyst for the formation of other antithrombin–serine enzyme complexes. Heparin cofactor II directly inactivates the thrombin conversion of fibrinogen to fibrin monomers (23). Protein

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TABLE 12.1 Coagulation proteins. Names, concentrations and additional characteristics of the proteins engaged in the coagulation pathways are summarized. Concentration of many proteins have been previously published [Kalafatis, 1997 #30]. Factor

Synonym

Plasma Concentration

Time1/2 (h)

Vitamin K?

I

Fibrinogen

300 mg/dL

90

No

II

Prothrombin

1,400 nmol/L

60

Yes

III IV V

Tissue thromboplastin Calcium Proaccelerin

8.5–10.5 mg/dL 20 nmol/L

VII

Proconvertin

VIII

IX X XI XII

Manifestation of Deficiency

Inheritance

Serious neonatal and early bleeding Serious neonatal and early bleeding

AR

Mild, excessive bleeding early in life Mild to moderate bleeding or purpura Bleeding during infancy; excessive bleeding after minor trauma, dental procedures and minor surgery Excessive bleeding after trauma or surgery Mild bleeding in later life Excessive bleeding after trauma or surgery, may be delayed Rarely associated with significant bleeding. Thrombosis possible Neonatal bleeding is common, with cord hemorrhage, ecchymoses, and hematomas Spontaneous gastrointestinal bleeding and easily bruised

AR (high penetrance) AR

AR

No 15

No No

10 nmol/L

6

Yes

Antihemophilic factor A

0.7 nmol/L

12

No

Antihemophilic factor B Stuart–Prower Plasma thromboplastin antecedent Hageman

90 nmol/L

25

Yes

170 nmol/L 30 nmol/L

40 45

Yes No

50

No

XIII

Fibrin-stabilizing factor

120

No

vWF

Von Willebrand factor

12

No

SR

SR AR AR AR AR

AD and AR

AR, autosomal recessive; AD, autosomal dominant; SR, sex-linked recessive.

Tissue Factor

Circulating VIIa Antithrombin

TF•VIIa complex

XI Remote from cell IX

On cell

X

IIa XIa +HMWK +Zn++

TFPI

Xa

Prothrombinase complex (Xa, Va, PL, Ca++)

IXa

Va Xa II

Tenase VIIIa complex (IXa, VIIIa) X

IIa Antithrombin

Platelet activation Activation of V, VIII, IX Fibrinogen

Fibrin

Activation Inhibition

FIGURE 12.1 Coagulation pathways. Tissue factor and activated factor VII (VIIa) initiate the extrinsic pathway, which culminates in the production of thrombin (IIa). Activation of factor XI leads to additional thrombin production via separate intermediary reactions. Thrombin is responible for activation of coagulation factors, platelets as well as the conversion of fibrinogen to fibrin.

C is a vitamin-K-dependent serine protease. Once activated by thrombin, it acts as an anticoagulant by inactivating factors Va and VIIIa. Activated protein C (APC) activity occurs on phospholipid surfaces, with factor S as a cofactor. a2-Macroglobulin acts in a similar manner to the heparin–AT complex. It complexes with the serine proteases of the coagulation cascade, preventing their function. Dysfibrinogenemia is a family of disorders, which usually presents with mild to moderate hemorrhage. There are over 100 congenital variants. However, 10% of patients with dysfibrinogenemias will present with either venous or arterial thromboses. The pathophysiology is most often abnormal polymerization of fibrin, or impaired fibrinolysis. Patients who present with thromboses require anticoagulation with heparin followed by warfarin (23).

Hypercoagulable Syndromes Hypercoagulable syndromes are a major concern to vascular surgeons. Venous thromboembolism is a common manifestation of hypercoagulable states. Between 10% and 30% of patients undergoing vascular reconstruction

Chapter 12 Thrombogenesis and Thrombolysis

may have a hypercoagulable state (24,25), which may contribute to an early failure of the reconstruction. Characteristic features of hypercoagulable syndromes include a family history of thrombotic disorders, thrombosis at a young age, thrombosis with absence of risk factors, thromboses in unusual locations, and recurrent thromboses. The hypercoagulable states are conveniently categorized into congenital and acquired conditions. Congenital Hypercoagulable Syndromes Antithrombin (AT) deficiency, the first defined hypercoagulable syndrome, was reported in 1965 (24). It has an incidence of 1 in 2000 (25), and is transmitted as an autosomal dominant trait. There are three types of AT deficiency (28). Type I is most common and is marked by decreased levels of the AT protein but normal function. Type II is marked by production of an abnormal protein, resulting in a diminished activity although the serum concentration is normal, and type III consists of impaired binding of AT to heparin. AT deficiency is associated with an up to 20-fold increase in risk of venous thromboembolism. AT deficiency manifests most often as venous thrombosis after the age of 15. There is an identifiable precipitating event for many thromboses. The inciting event may be surgery, trauma, pregnancy, oral contraceptive use, infection, or others. However, spontaneous thromboses are not uncommon. Diagnosis is confirmed by a low serum level of AT, which is assayed when the patient has not taken warfarin and after the acute thrombotic event, as warfarin increases AT concentration and AT is consumed during active thrombosis. Heparin is the mainstay for managing thromboses in patients with antithrombin deficiencies. Larger amounts of heparin may be required and concentrates of AT may also be necessary (23). Heparin cofactor II (HCII) is a glycoprotein that complexes with thrombin, but not with Xa. HCII deficiency is transmitted as an autosomal dominant trait. HCII deficiency (less than 60% normal levels) is associated with arterial or venous thromboses. Heparin and other sulfated polysaccharides increase the anticoagulant effect of HCII. HCII deficiency is associated with a 0.7% to 1% risk of unexplained venous thrombosis. The management of acute thromboses is anticoagulation with heparin (23). Warfarin is offered to those patients with recurrent thromboses or persistent risk factors for venous thromboembolism. Protein C deficiency accounts for 6% to 10% of cases of venous thromboses or pulmonary embolism (27). Heterozygotic individuals often manifest protein C deficiency with thromboses (usually venous) before the age of 30. Protein C deficiency has also been associated with warfarin-induced skin necrosis. Purpura fulminans neonatalis, a condition involving thrombosis of cutaneous capillaries and veins, may be seen in some neonates with homozygous protein C deficiency (30). Acquired protein C deficiencies may occur in DIC, sepsis, malignancy, liver disease, and in patients receiving warfarin.

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Patients with protein C deficiency who have had recurrent or life- or limb-threatening thromboses are offered long-term anticoagulation to prevent recurrent episodes. Warfarin is the preferred long-term anticoagulant, but heparin must be administered with the warfarin for the first few days to avoid increasing the hypercoagulable state. Protein S deficiency manifests in a manner similar to that of protein C deficiency. The trait is inherited in an autosomal dominant manner, and presentation is often of a venous thrombosis prior to the age of 30. Arterial thrombosis is less common than with protein C deficiency. Patients with protein S deficiencies who develop thromboses are managed with long-term anticoagulation with warfarin, after initial anticoagulation with heparin. Resistance to activated protein C may be the most common congenital hypercoagulable state. The factor V Leiden mutation is the most common cause of activated protein C resistance, affecting up to 5% of all caucasians, and 20% to 50% of patients presenting with a deep vein thrombosis (DVT) (23). A single-point mutation in the gene coding for factor V is most often responsible for failure of factor V to be inactivated by APC. Factor V Cambridge, a similar point mutation in factor V, also results in APC resistance. APC resistance can be acquired through oral contraceptive and estrogen use. A single-point mutation in the gene coding for prothrombin (PT) results in a defective protein, leading to a hypercoagulable state. The PT20210 abnormality is present in 5.7% of patients with arterial disease (history of myocardial infarction, cerebral occlusive disease, and peripheral arterial disease), as compared to 0.33% in a control population (23). Patients with the PT20210 abnormality are at a three-fold risk for DVT when compared with the general public. Thrombotic episodes are managed with heparin anticoagulation followed by warfarin. However, due to the high rate of concomitant hypocoagulable states (40% of patients also have factor V Leiden), the patient should be tested for additional thrombophilic disorders. Acquired Hypercoagulable Syndrome The lupus anticoagulant is an IgG or, less commonly, an IgM antibody, which causes prolongation of the prothrombin time, partial thromboplastin time, the bleeding time, and all tests that use phospholipid. It inhibits thrombomodulin, antithrombin, and the endothelial synthesis of prostacyclin I2. The lupus anticoagulant also decreases plasminogen activation and increases platelet adhesiveness (30). About 10% of patients with systemic lupus have the lupus anticoagulant. The anticoagulant may occur as a primary development or as part of a drug-related lupus syndrome and may be responsible for thromboses in up to 10% of individuals without lupus. Despite the term “lupus anticoagulant,” the most common presentation is thrombosis. Patients frequently have thrombocytopenia, recurrent DVT, and spontaneous pregnancy loss. In patients with lupus anticoagu-

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lant who require vascular reconstruction, there is a 50% risk of thrombotic events (31). Patients with thromboses and the lupus anticoagulant should be treated with longterm anticoagulation. The anticoagulation should be continued until the anticoagulant and/or antiphospholipid antibodies can no longer be detected. Hyperhomocystinemia is defined as a plasma level of homocysteine of greater than 10 mmol/L. It can be caused by a genetic trait (autosomal recessive), or acquired via dietary causes (deficiencies of vitamin B12, B6 or folate), or systemic conditions (renal insufficiency, hypothyroidism, breast or pancreatic carcinoma). Hyperhomocystinemia is present in 5% to 7% of the population. The most common genetic defect is decreased activity of cystathionine b-synthase. Hyperhomocystinemia may also result from inadequate substrate for cystathionine b-synthase. Folate, and vitamins B12 and B6 are important cofactors for this enzyme, and inversely affect the serum level of homocysteine. Patients with hyperhomocystinemia present with severe accelerated atherosclerosis, arterial and venous thromboses, including mesenteric arterial thrombosis, ischemic stroke, and pregnancy loss (32,33). Treatment is by supplementation with folate (3–5 mg/day), and B6 and B12 if needed. The hypercoagulable state associated with malignancy was first described by Trousseau in 1865. About 10% of cancer patients have thromboembolic disorders (34). Patients with carcinomas of the lung, pancreas, stomach, colon, prostate, ovary, and uterus, certain leukemias, and myeloproliferative disorders have the highest risks. The hypercoagulability associated with malignancy has been related to elevated levels of factors II, V, VIII, IX, and X, and decreases of antithrombin. Platelet aggregation is increased in some patients with malignancy (35). Patients with malignancy are frequently relatively resistant to anticoagulation. Treatment of the malignancy improves the hypercoagulable state (34). Pregnancy confers an increased risk for venous thrombosis and has been described as a state of compensated disseminated intravascular coagulation. There is an increase of platelet aggregability, decreases in AT and protein S, and increases in plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2). There are also increases in factor I, VII, VIII, IX, XI, and XII. Oral contraceptives (OCPs) are associated with an elevated risk of venous thrombosis (36). OCP administration is associated with increases in prothrombin, factors VII, VIII, X, fibrinogen, and prothrombin fragments 1+2. In the absence other risk factors, current dosage of OCPs (low estrogen content) is associated with a three- to sixfold increase in the risk of venous thrombosis. The risk of venous thrombosis is increased from 1 to 4 per 100,000 person-years with the use of OCPs (37). Diabetes mellitus (DM) is being recognized more often as an independent hypercoagulable state. There are abnormalities of both the vascular endothelium and platelets. Platelets from patients with DM have a heightened aggregation response to epinephrine. Platelets of

diabetics also generate increased amounts of thromboxane while their endothelial cells produce decreased amounts of prostacyclin. Laboratory markers of active thrombosis, such as prothrombin fragments 1+2 are elevated, as are serum levels of many of the serine proteases (38). Other coagulation abnormalities found in diabetics include increased levels of factor VIII:RAg, impaired fibrinolysis, increased blood viscosity, and increased adhesion of red blood cells to endothelium. Smoking creates a hypercoagulable state by causing endothelial damage with increased platelet adhesion and increased endothelial permeability to low-density lipoprotein. Smoking increases the serum concentration of fibrinogen, thrombin, and the expression of TF. The deleterious effects of smoking are reversible with cessation of smoking (39–42). Other Acquired Hypercoagulable States Heparin-induced thrombocytopenia causes thromboembolic complications in up to 69% of affected patients (43). Vasculitis causes decreased fibrinolytic activity and increased thrombin activity by the endothelium. These defects are found in Behçet’s disease (44). Hyperviscosity may be a cause of thrombosis in patients with polycythemia vera and other myeloproliferative syndromes, leukemia, and sickle-cell anemia.

Anticoagulation Thrombin Inhibition Thrombin catalyzes the conversion of fibrinogen to fibrin and also activates protein C and cleaves plasminogen to plasmin. Two platelet thrombin receptors have been identified on human platelets. Thrombin’s activity can be controlled by increasing its binding by AT (indirect inhibition) or by rendering it incapable of activating the receptors (direct inhibition). The most commonly used antithrombin is the indirect inhibitor, heparin. Unfractionated heparin (UH) is a mixture of polysulfated glycosaminoglycan chains of varying lengths. It is derived from beef lung or pork intestinal mucosa. Low-molecular-weight heparins (LMWH) are produced by fractionation of UH. Both UH and LMWH accelerate the action of AT on thrombin and factor Xa. As compared to UH, LMWH has increased anti-Xa activity and decreased anti-IIa activity. Bleeding risk correlates with IIa levels, and anticoagulation correlates with inactivation of Xa. LMWH has a longer half-life than UH. UH’s half-life is approximately 90 minutes, and is not altered by hepatic or renal insufficiency. Heparin neither crosses the placenta nor is excreted in breast milk. Heparin may be administered subcutaneously two or three times daily. Large doses of heparin are needed for anticoagulation during cardiopulmonary bypass and vascular reconstructions. Lower doses are administered for treatment of venous thromboembolism, prevention of in-

Chapter 12 Thrombogenesis and Thrombolysis

travascular thrombosis, and prophylaxis for DVT. The effect of heparin is usually monitored by measuring the prolongation of the aPTT. A therapeutic level of anticoagulation is achieved when the aPTT is two to three times the control. Heparinoids are glycosaminoglycans with heparinlike properties. As with LMWH, heparinoids have a lower antithrombin/anti-Xa ratio than does UH. However, this has not translated into a significant decrease in hemorrhagic complications. Because heparinoids and LMWH are less likely to prolong the aPTT, anti-Xa levels are used to monitor their effects. There are several commercially available direct thrombin inhibitors, including argatroban and lepirudin. Argatroban (Glaxo SmithKline Pharmaceuticals) is a small (527 da), synthetic direct thrombin inhibitor derived from L-arginine. Its action does not require AT. It binds reversibly to the catalytic domain of thrombin. There is activity against both free and clot-bound thrombin, with no activity against factor Xa or plasmin. In a study using historical controls (HIT patients treated with heparin), argatroban resulted in improved clinical outcomes and no increase in hemorrhagic complications (45). Standard dosage is 2 mg/kg/min i.v., and the drug is titrated to achieve an aPTT of 1.5 to 3 times the control. Argatroban undergoes hepatic metabolism and excretion. The half-life is between 40 and 50 minutes. The most common complication of argatroban is hemorrhage, followed by dyspnea, hypotension, fever, diarrhea, and sepsis, among others. Lepirudin (Refludan, Schering AG) is a recombinant hirudin (6980 da), derived from yeast cells. It is a highly specific, direct inhibitor of thrombin. The drug has been safely utilized as alternative therapy for patients with HIT (46). As many as 40% to 50% of patients develop drugspecific antibodies without clinical sequelae. Lepirudin is renally cleared, and its anticoagulant effect is monitored by the aPTT. The dose for patients with normal renal function is a bolus of 0.4 mg/kg followed by continuous infusion at 0.15 mg/kg/h. Warfarin blocks the vitamin-K-dependent carboxylation of factors II, VII, IX, and X (Table 12.1) and protein C. Warfarin is rapidly absorbed from the intestinal tract, reaching peak levels in about 6 hours. It may also be administered intravenously with same dose schedule. Levels of factor VII (half-life 6 hours) decrease rapidly and may thus cause an early prolongation of the PT. However, full anticoagulation is not achieved for 4 to 6 days, at which time the levels of factors II, IX, and X reach therapeutic levels. Doses of warfarin adequate to increase the PT to 1.5 to 2.0 times the control value are effective in the prevention of new and recurrent thromboemboli. Because of international differences in the thromboplastin reagents used in determining the PT, the World Health Organization has urged that the PT ratio be reported as the international normalized ratio (INR). The range of therapeutic INRs in patients on stable doses of warfarin, comparable

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to the PT ratios noted above, is 2.0 to 3.0. Many drugs, variation in dietary vitamin K intake, malabsorption, hypermetabolic states, alcohol use, diet, and age alter the anticoagulant effect of warfarin. For this reason, the PT should be determined daily until the desired level is achieved and every 2 to 3 weeks thereafter. Warfarin’s effect can be reversed by the administration of vitamin K or fresh-frozen plasma if rapid (<24 h) correction of the prothrombin time is required. The most frequent complication of warfarin therapy is hemorrhage. The frequency of clinically significant hemorrhage in patients on well-controlled warfarin therapy has been reported to be 4.3% per treatment year (47). The risk of major bleeding during warfarin therapy is increased with patient age greater than 65 years, history of gastrointestinal bleeding, history of intracerebral hemorrhage, or multiple (more than four) comorbid conditions (48). Other complications of warfarin therapy include dermatitis, alopecia, hypersensitivity reactions, nausea, emesis, and diarrhea. Warfarin is not used during pregnancy because it crosses the placenta and has teratogenic effects. Skin necrosis is a rare but dramatic complication of warfarin therapy. Warfarin-induced skin necrosis is manifest by cutaneous microvascular thrombosis and necrosis. It occurs most commonly in women and within the first few days after starting warfarin. Low levels of protein C have been associated with warfarin-induced skin necrosis, but they are neither necessary nor predictive for its development. The use of heparin until anticoagulation with warfarin is achieved is recommended to avoid this complication. Avoidance of “loading doses” of warfarin may also decrease the risk of warfarin-induced skin necrosis (23). Inhibition of the tissue factor pathway is an attractive antithrombotic target due to its central location in the coagulation cascade. TFPI is a naturally occurring inhibitor of VIIa, Xa, and the TF–VIIa complex. It has a short halflife after intravenous administration. It has shown initial clinical utility in reducing venous thromboembolism in patients with sepsis, and is undergoing phase III trials. The extrinsic pathway may also be inhibited through modification of factor VII. A recombinant factor VIIa has been created with the active site inactivated. This molecule has a higher affinity for tissue factor than native VIIa, and results in a VIIa–TF complex that has no catalytic activity. This drug has been used in trials as an adjunct to thrombolytic therapy. Doses in the range 50 to 400 mg/kg were found to decrease the number of ischemic events associated with coronary thrombolysis. The amount of heparin required during thrombolysis was likewise reduced (18). IXa is necessary for the amplification of the coagulation cascade and sustained thrombosis. There are experimental inhibitors of two types: molecules directed against the active site of the IXa protein, or directed against the entire molecule. Either type of inhibition results in competitive (with noninhibited IXa molecules) inhibition for entry into the tenase complex with resultant decrease in

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activity of the tenase complex. There are currently no IXa inhibitors in human trials.

Developing Anticoagulants Inhibition of Xa may reduce thrombin production without increasing hemorrhagic risk (49). Inhibition of factor Xa has been demonstrated by several naturally occurring compounds (tick anticoagulant peptide (TAP), antistatin, lefaxin) and several synthetic compounds (DX-9065a, YM-60828). TAP was isolated from the soft tick and is a specific peptide inhibitor of Xa. TAP (50 mg/kg/min continuous infusion) has been shown to either delay or prevent thrombosis (in comparison to heparin) in an animal model after coronary fibrinolysis or electrical injury (50). Synthetic direct inhibition has been demonstrated by several low-molecular-weight reversibly bound nonpeptides (DX-9065a, YM-60828, SF303, SK549). Of these, only DX-9065a has reached clinical trials. However, YM60828 and SK549 have demonstrated oral bioavailability in animals. Synthetic pentasaccharide is an indirect inhibitor of factor Xa which functions by increasing the inactivation of Xa by AT (51). The efficacy of the synthetic pentasaccharide Org31540/SR90107A in prevention of DVT following total hip replacement has been evaluated in phase III trials. Daily subcutaneous administration (between 2.0 and 8.0 mg) was found to decrease the rate of DVT (82% risk reduction) following total hip replacement as compared to enoxaparin (30 mg subcutaneously administered each 12 hours) (52).

Thrombolysis The fibrinolytic system reduces intravascular fibrin deposits, thereby helping to maintain vascular patency. Fibrinolytic activity is determined by the action of plasminogen activators on available plasminogen, the effect of fibrinolytic inhibitors, and the affinity of these substances for fibrin.

Physiology Fibrinolysis depends upon the conversion of a proenzyme, plasminogen, to the active fibrinolytic enzyme, plasmin, by plasminogen activators. Plasminogen is a 90,000-Da glycoprotein synthesized in the liver. It has a plasma half-life of approximately 20 hours and a plasma concentration of approximately 2.4 mmol/L, which is about twice the concentration of a2-antiplasmin. It is composed of five domains that mediate binding to fibrin and to endothelial cells. Plasminogen activators are widely distributed, being found in vascular epithelial cells, urine, seminal fluid, and other tissues. There are two major categories of activators: one with a high affinity for fibrin-bound plasminogen, and one with a low affinity for the fibrin-bound plasminogen. Blood plasminogen activator comes predominately from the endothelium.

Plasmin, a serine protease with a high affinity for fibrin, is primarily responsible for fibrinolysis. Plasmin digests fibrin into fragments D and E. Fragment D is released in its dimeric form D-dimer, and is a marker for ongoing fibrinolysis. Plasmin also digests several other plasma proteins including fibrinogen, factors V, VII, and VIII, and components of the complement system. Plasmin is usually formed in immediate contact with clot-bound fibrin and is thus protected to a large extent from inhibition by a2antiplasmin. Free plasmin is rapidly and strongly bound to fast-acting plasmin inhibitors such as a2-antiplasmin. Other inhibitors, a2-macroglobulin, and a1-protease have lesser roles in inhibiting the action of plasmin. These inhibitors neutralize free plasmin but are not as effective as fibrin-bound plasmin (Fig. 12.2).

Activators Several activators are available to convert plasminogen into plasmin. Activators with a high affinity for fibrinbound plasminogen, as opposed to a high affinity for circulating plasminogen, have become the preferred activators for clinical use (53) (Table 12.2). Streptokinase, produced by beta-hemolytic streptococci, is an indirect activator of plasminogen. It binds to plasminogen, producing a streptokinase–plasminogen activator complex which then activates other plasmino-

Fibrin-Bound Plasminogen

Free Plasminogen

t-PA, rt-PA scu-PA Staphylokinase

Streptokinase tcu-PA APSAC PAI-1

PAI-1

Plasmin Fibrin-Plasmin

} {

a2-Antiplasmin a1-Protease Antithrombin a2-Macroglobulin C1-Inhibitor Fibrin Degradation Products

Fibrin Fibrinogen, Factor V, VIII, XII, vWF

Degradation Products

FIGURE 12.2 Non-fibrin-specific plasminogen activators (including streptokinase, APSAC and tcu-PA) convert circulating plasminogen to plasmin. Plasmin produced in the circulation is quickly neutralized by antiplasmins (a2-antiplasmin, a1-protease, a2macroglobulin). Some of this circulating plasmin is able to bind to free proteins and produce degradation products. Fibrin-specific thrombolytic agents (t-PA, rt-PA, scu-PA, staphylokinase) activate plasminogen at the fibrin surface, resulting in preferential fibrinolysis at the clot surface with sparing of circulating plasminogen. Fibrin-bound plasmin is stoichiometrically protected from inhibition by a2antiplasmin and thus efficiently degrades clot-bound fibrin only. t-PA, Tissue-type plasminogen activator; rt-PA, recombinant tissue type plasminogen activator; APSAC, acylated streptokinase–plasminogen complex; scu-PA, single-chain urokinase; tcu-PA, twochain urokinase; PAI-1, plasminogen activator inhibitor. Dashed line represents inhibition.

Chapter 12 Thrombogenesis and Thrombolysis TABLE 12.2 Thrombolytic agents for peripheral vascular occlusive disease Culture-derived agents Streptokinase (SK) Anistreplase (APSAC) Urokinase (UK) Recombinant technology Recombinant t-PA (rt-PA) Reteplase Lanoteplase Monteplase Tenecteplase (TNK-t-PA) Pamiteplase Staphylokinase Pro-urokinase (scu-PA, surplase)

gen to plasmin. Since streptokinase is of bacterial origin, its administration may be associated with allergic reactions, sensitization and production of antibodies. Streptokinase, the first thrombolytic activator, is rarely used at present because it is less effective than other agents, is antigenic, and is associated with substantial rates of bleeding. Urokinase is a direct plasminogen activator. It is derived from neonatal kidney cells by tissue culture techniques. It is neutralized in the circulation by PAI-2. It is considered a mid-fibrin affinity plasmin activator with a circulating half-life of approximately 15 minutes. Urokinase is not currently available in the United States secondary to viral contamination during its production. Acylated streptokinase–plasminogen complex (APSAC, Anistreplase) is a complex of streptokinase and acylated plasminogen. It has a plasma half-life of 70 minutes. It was designed to increase the activation of plasminogen bound to fibrin. However, its fibrin binding and fibrin activity is similar to that of streptokinase. It also elicits an antigenic response similar to streptokinase; therefore, it has limited use (54). The lack of fibrin specificity, the production of antibodies by streptokinase, the systemic lytic state, and the high bleed rates of the first generation of plasminogen activators (i.e., streptokinase, urokinase, and acylated streptokinase) led to the development of a second generation of plasminogen activators [i.e., tissue plasminogen activator (t-PA or alteplase), single-chain urokinase-type plasmin activator (scu-PA), and pro-urokinase], which are more fibrin-specific plasminogen activators but are also associated with induction of systemic thrombolytic states with the depletion of circulating fibrinogen and plasminogen. Tissue plasminogen activator (alteplase) is a tissue plasminogen activator produced by recombinant DNA technology. It has received broad clinical application, including use in management of patients with acute myocardial infarctions, acute ischemic strokes, pulmonary embolism, venous or arterial thrombosis, thrombotic graft occlusions, etc. It has been administered as a

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bolus, constant infusion and by intra-thrombus catheter injection. It has a circulating half-life of 4 to 6 minutes and its clearance is primarily by the liver. t-PA is currently our preferred thrombolytic agent. The search for better thrombolytic agents has continued with the development of third-generation thrombolytic agents. These agents are “. . . conjugates of plasminogen activators with monoclonal antibodies against fibrin, platelets, or thrombomodulin; mutants, variants, and hybrids of alteplase and pro-urokinase (amediplase); or new molecules of animal (vampire bat) or bacterial (staphylococcus aureus) origin” (55). The third generation agents were derived to overcome the problems encountered with the current thrombolytic agents, specifically PAI inhibition, fibrin selectivity, short half-life and incidence of intercranial hemorrhage. The “. . . third generation thrombolytic agents such as monteplase, tenecteplase, reteplase, lanoteplase, pamiteplase, and staphylokinase . . .” are undergoing clinical evaluation and thus far have been found to be good fibrinolytic agents with mortality rates similar to other lytic agents. The “. . . bleeding risks, however, may be greater” (55).

Inhibitors Fibrinolysis is modulated through the control of the activation of plasminogen and/or by inhibiting the activity of plasmin. The five plasma proteases that inhibit plasmin are a1-protease inhibitor, antithrombin, a2-microglobulin, C1 inhibitor, and a2-antiplasmin, which is the most important inhibitor of plasmin-induced fibrinolysis (Fig. 12.2). a2-Plasmin inhibitor interferes with the absorption of plasminogen to fibrin and rapidly inhibits plasmin’s activity. It also inhibits plasmin activators such as urokinase and t-PA. Plasminogen activators are rapidly inactivated by several specific inhibitors. PAI-1 secreted from endothelial cells is the main inhibitor of t-PA. PAI-2, formed by the placenta, is active against both t-PA and urokinase. PAI-3, found in urine, inhibits only urokinase. Synthetic fibrinolytic inhibitors, e-amino caproic acid (EACA) and tranexamic acid, are potent antifibrinolytic agents. They inhibit the activity of plasmin and of plasminogen activators. They also inhibit the binding of plasminogen to fibrin, thus further contributing to the inhibition of fibrinolysis. EACA is the inhibitor most often used clinically to control excessive fibrinolysis. The usual dose for an adult is 5 g, intravenously or orally, followed by 1 g per hour until the excessive lysis is controlled. If EACA is administrated intravenously, it should be given slowly because hypotension, bradycardia, and arrhythmias have been associated with rapid infusions.

Hyperfibrinolysis Excessive fibrinolytic activity is frequently associated with bleeding and, unless controlled, may lead to exsanguinating hemorrhage. Increased fibrinolytic activity usually falls into one of three categories: primary fibrinolysis,

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secondary fibrinolysis, or induced fibrinolysis. The extent of the lytic state can be monitored by specific laboratory tests (euglobulin clot lysis time or whole blood lysis time), which are usually not available for clinical use. There is no known test that predicts the likelihood of bleeding during thrombolytic therapy. Patients undergoing lytic therapy should have a baseline blood count, platelet count, prothrombin time, activated partial thromboplastin time, and fibrinogen level. These tests are repeated at intervals of 6 to 8 hours during thrombolytic therapy and can be used in guiding therapy if bleeding occurs. Primary fibrinolysis is not associated with intravascular coagulation, nor is it induced by infusion of activators or plasmin. Primary fibrinolysis results from excessive plasminogen activation during a variety of pathologic conditions (e.g., electric shock, extracorporeal circulation, profound hypotension, leukemia, hepatic failure, ulcerative colitis, etc.). Management of primary fibrinolysis is directed toward eliminating or controlling the underlying cause and, if indicated, using EACA to control the lytic state. Secondary fibrinolysis refers to the fibrinolysis that accompanies clotting. Most often the lysis is limited to the thrombus being lysed and is usually of no consequence. However, during times of extensive intravascular coagulation (DIC), the release of large amounts of activators may result in the excessive activation of circulating plasminogen. When this occurs, the inhibitors may be overwhelmed, and an intense lytic state may occur. The fibrinolysis often contributes to bleeding by lysing thromboses and digesting the coagulation proteins, further lowering the concentrations of the clotting factors, which are also being consumed by the clotting. The platelet count helps differentiate between primary and secondary fibrinolysis. The platelet count is normal during primary fibrinolysis and is low, secondary to the intravascular coagulation, during secondary fibrinolysis. The hyperfibrinolysis that accompanies DIC must be treated cautiously because the lytic state is important in maintaining patency of the microcirculation. Consequently, the DIC must be controlled first, then, if the excessive lytic state persists, it is controlled with EACA.

Clinical Thrombolysis Clinical thrombolysis began with the intravenous injection of streptokinase into patients with induced thromboses in 1959 (56). Since then, there has been constant evolution of indications, protocols, and agents for inducing thrombolysis. Successful thrombolysis is affected by the age and texture of the thrombus. Crosslinked fibrin is less susceptible to lysis than noncrosslinked fibrin, so older clots are relatively resistant to lysis. The binding of a2-antiplasmin to fibrin by XIIIa adversely inhibits thrombolysis. The thrombolytic state is directly dependent on the concentrations and interactions of plasminogen, plasminogen activators, plasminogen activator inhibitors, plasmin, and plasmin inhibitors.

Thrombolytic therapy has an important role in the management of lower extremity venous and arterial thromboembolic occlusions, acute myocardial infarction and stroke. Urokinase was the most frequently employed thrombolytic agent, but is no longer approved in the United States. t-PA, or those activators generated with recombinant technology, are currently the preferred activators. The STILE (surgery versus thrombolysis for ischemia of the lower extremity) trial was a prospective, randomized trial comparing surgery and thrombolysis (urokinase or rt-PA). There was no difference in mortality, amputation rate, or major morbidity between the two treatment groups based on the intent to treat (57). Patients with acute (<14 days) limb ischemia treated with lytic therapy had better amputation-free survival rates (85%) at 6 months than did those treated with surgery (62%). The thrombolysis or peripheral arterial surgery (TOPAS) I and II studies evaluated the use of recombinantly derived urokinase and surgery in treating acute limb ischemia. There were no differences in mortality or amputation rates, but the magnitude of surgery was reduced in the thrombolysis group (58). Thrombolytic therapy is frequently used to restore arterial patency and establish reperfusion. Arteriograms at the completion of thrombolysis demonstrate the underlying arterial pathology, which can be corrected by either operative or endovascular techniques. Thrombolytic therapy also restores the patency of runoff vessels that are not easily cleared by conventional techniques. Clotted hemodialysis access grafts are excellent candidates for thrombolytic therapy; many of the grafts will have no anatomic defect when patency is restored. Several methods are available for delivering thrombolytic agents in the management of peripheral arterial and venous thromboses. These include intravenous infusions, intra-arterial continuous infusions, bolus infusions, pulse-spray techniques and combinations of these. Intravenous and intra-arterial infusions of thrombolytic agents in the treatment of peripheral thromboses are not widely utilized because the length and volume of the thrombus make it unlikely that circulating thrombolytic agents would induce adequate clot lysis. Continuous infusion of the thrombolytic agent through an endhole catheter is an effective technique for inducing thrombolysis. The catheter tip is periodically repositioned from the proximal to distal regions of the thrombus. A dose of thrombolytic agent (which is usually 0.5 to 1 unit of t-PA per hour over 5 to 24 hours) is given through the endhole catheter, using a continuous infusion pump. Periodically (at 4- to 6-hour intervals), arteriography is used to determine when sufficient lysis in one area has been accomplished and advancement of the catheter tip is warranted (59). Intra-thrombus bolusing or “lacing” is a technique that involves placement of guidewire and multi-holed catheter within a thrombus and infusing the thrombolytic agent. This method of saturating the thrombus with a plasminogen activator increases the rate of thrombolysis,

Chapter 12 Thrombogenesis and Thrombolysis

and frequently reduces the time to reperfusion. Pulse spray thrombolysis (usually 2 to 5 units in 50 mL as an initial bolus, followed by 0.5 units t-PA per hour infusion) (PST) refers to the technique of forcefully injecting the thrombolytic agent into the thrombus. The intent is to fragment the thrombus, increasing the surface area available for enzymatic action by the plasminogen activator and shorten the lysis time. In a pilot study, thrombolysis achieved within 2 hours with PST compared well with thrombolysis induced in 25 hours in historical controls with continuous infusions (60). Though rapid recanalization has been achieved with PST, not all patients will be successfully treated using PST alone; many will require additional continuous infusions to ensure more complete thrombolysis. In a study of 28 patients with occluded arteries treated with PST (using rtPA), reperfusion was established in a mean time of 110 minutes, but complete lysis required an additional infusion of rt-PA in 89% of patients (thus, extending the overall lytic procedure to an average of 17 hours) (61). Systemic anticoagulation with heparin is commonly used during and after successful thrombolysis and during subsequent interventions to prevent rethrombosis (62). Platelet glycoprotein receptor IIb/IIIa antagonists in combination with lytic agents are the focus of current clinical trials. Long-term anticoagulation therapy is required for patients with persistent uncontrolled risk factors for recurrent thrombosis (61). Although thrombolytic therapy for pulmonary embolism restores pulmonary arterial patency and improves hemodynamics more often and more rapidly than heparin, patient survival is the same with the two forms of therapy (63). Thrombolytic therapy for DVT restores early venous patency more often than heparin: 45% vs. 4% (64), but only three studies have shown an advantage to thrombolytic therapy when long-term hemodynamic improvement was evaluated. Thrombolytic therapy has an important initial role in the management of subclavian vein thrombosis, which is often associated with thoracic outlet compression (65,66). Reports have established the role of recombinant t-PA in restoring patency in thrombosed hemodialysis grafts. The use of the pulse-spray technique employing rtPA with a dose of 2 to 5 units followed by an infusion of 0.5 u/h has led to successful graft lysis with an average lytic infusion time of 32 minutes. This method of thrombolysis often unmasks the underlying pathology, which can be corrected with additional intervention (59).

References 1. Vanhoutte PM. Platelets, endothelium and blood vessel wall. Experientia 1988; 44(2): 105–109. 2. Ruggeri ZM, Dent JA, Saldivar E. Contribution of distinct adhesive interactions to platelet aggregation in flowing blood. Blood 1999; 94: 172–178. 3. George JN. Platelets. Lancet 2000; 355: 1531–1539.

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4. Bennett JS. Novel platelet inhibitors. Annu Rev Med 2001; 52: 161–184. 5. George JN, Raskob GE, Shah SR, et al. Drug-induced thrombocytopenia: a systematic review of published case reports. Ann Int Med 1998; 129(11): 886–890. 6. Mammen EF. Stickey platelet syndrome. Semin Thromb Hemost 1999; 25: 361–365. 7. Patrono C. Aspirin as an antiplatelet drug. N Eng J Med 1994; 330: 1287–1294. 8. Gachet C. Platelet activation by ADP: the role of ADP antagonists. Ann Med 2000; 1 (Suppl 1): 15–20. 9. Ikeda Y. Antiplatelet therapy using cilostazol, a specific PDE3 inhibitor. Thromb Hemost 1998; 82: 435–438. 10. Tanaka T, Ishikawa T, et al. Effects of cilostazol, a selective cAMP phosphodiesterase inhibitor on the contraction of vascular smooth muscle. Pharmacology 1988; 36: 313–320. 11. Kubota Y, Kichikawa K, et al. Pharmacologic treatment of intimal hyperplasia after metallic stent placement in the peripheral arteries. An experimental study. Investig Radiology 1995; 30: 532–537. 12. Sudo T, Tachibana K, et al. Potent effects of novel antiplatelet aggregatory cilostamide analogues on recombinant cyclic nucleotide phosphodiesterase isozyme activity. Biochem Pharmac 2000; 59: 347–356. 13. Tani T, Uehara K, et al. Cilostazol, a selective type III phosphodiesterase inhibitor, decreased triglyceride and increases HDL cholesterol levels by increasing lipoprotein lipase activity in rats. Atherosclerosis 2000; 152: 299–305. 14. Scarborough RM, Kleiman NS, Phillips DR. Platelet glycoprotein IIb/IIIa antagonists. What are the relevant issues concerning their pharmacology and clinical use? Circulation 1999; 100: 437–444. 15. Coughlin SR. Thrombin signalling and proteaseactivated receptors. Nature 2000; 407: 258–264. 16. Bajaj SP, Joist JH. New insights into how blood clots: implications for the use of APTT and PT as coagulation screening tests and in monitoring of anticoagulant therapy. Semin Thromb Hemosta 1999; 25: 407–418. 17. Broze GJ. Tissue factor pathway inhibitor and the revised theory of coagulation. Annu Rev Med 1995; 46: 103–112. 18. Hedner U, Erhardtsen E. Future possibilities in the regulation of the extrinsic pathway: rFVIIa and TFPI. Ann Med 2000; 32 (Suppl 1): 68–72. 19. Minnema MC, Ten Cate H, Hack CE. The role of factor XI in coagulation: a matter of revision. Semin Thromb Hemosta 1999; 25: 419–428. 20. Sandset PM, Abildgaard U, Larsen ML. Heparin induces release of extrinsic coagulation pathway inhibitor (EPI). Thromb Res 1988; 50: 803–813. 21. Wesselschmidt R, Likert K, et al. Structural requirements for tissue factor pathway inhibitor interactions with factor Xa and heparin. Blood Coagul Fibrinoly 1993; 4: 661–669. 22. Wu KK, Matijevic-Aleksic N. Thrombomodulin: a linker of coagulation and fibrinolysis and predictor of risk of arterial thrombosis. Ann Med 2000; 32 (Suppl 1): 73–77. 23. Baker WF Jr, Bick RL. Treatment of hereditary and acquired thrombophilic disorders. Semin Thromb Hemost 1999; 25: 387–406.

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24. Eldrup-Jorgensen J, Flanigan DP, et al. Hypercoagulable states and lower limb ischemia in young adults. J Vasc Surg 1989; 9: 334–341. 25. Donaldson MC, Weinberg DS, et al. Screening for hypercoagulable states in vascular surgical practice: a preliminary study. [see comments] J Vasc Surg 1990; 11: 825–831. 26. Kearon C, Crowther M, Hirsh J. Management of patients with hereditary hypercoagulable disorders. Ann Rev Med 2000; 51: 169–185. 27. Rosenberg RD. Actions and interactions of antithrombin and heparin. N Engl J Med 1975; 292: 146–151. 28. Tollefsen DM. Laboratory diagnosis of antithrombin and heparin cofactor II deficiency. Semin Thrombo Hemosta 1990; 16(2): 162–168. 29. Bick RL, Ucar K. Hypercoagulability and thrombosis. Hematol Oncol Clin North Am 1992; 6: 1421–1431. 30. Comp PC. Hereditary disorders predisposing to thrombosis. Prog Hemost Thromb 1986; 8: 71–102. 31. Ahn SS, Kalunian K, et al. Postoperative thrombotic complications in patients with lupus anticoagulant: increased risk after vascular procedures. J Vasc Surg 1988; 7: 749–756. 32. Gradman WS, Daniel J, et al. Homocysteine-associated acute mesenteric artery occlusion treated with thrombectomy and bowel resection. Ann Vasc Surg 2001; 15: 247–250. 33. Sarkar PK, Lambert LA. Aetiology and treatment of hyperhomocysteinanemia causing ischaemic stroke. Int J Clin Pract 2001; 55: 262–268. 34. Rickles FR, Edwards RL. Activation of blood coagulation in cancer: Trousseau’s syndrome revisited. Blood 1983; 62: 14–31. 35. Rickles FR, Edwards RL, et al. Abnormalities of blood coagulation in patients with cancer. Fibrinopeptide a generation and tumor growth. Cancer 1983; 51(2): 301–307. 36. Stadel BV. Oral contraceptives and cardiovascular disease (first of two parts). N Engl J Med 1981; 305: 612–618. 37. Vandenbroucke JP, Rosing J, et al. Oral contraceptives and the risk of venous thrombosis. N Engl J Med 2001; 344: 1527–1535. 38. Carr ME. Diabetes mellitus: a hypercoagulable state. J Diabet Complicat 2001; 15(1): 44–54. 39. Tuut M, Hense HW. Smoking, other risk factors and fibrinogen levels. Evidence of effect modification. Ann Epidemiol 2001; 11: 232–238. 40. Hioki H, Aoki N, et al. Acute effects of cigarette smoking on platelet-dependent thrombin generation. Eur Heart J 2001; 22: 56–61. 41. Matetzky S, Tani S, et al. Smoking increases tissue factor expression in atherosclerotic plaques: implications for plaque thrombogenicity. Circulation 2000; 102(6): 602–604. 42. McGill HC Jr. The cardiovascular pathology of smoking. Am Heart J 1988; 115( 1 Pt 2): 250–257. 43. Laster J, Cikrit D, et al. The heparin-induced thrombocytopenia syndrome: an update. Surgery 1987; 102: 763–770. 44. Schafer AI. The hypercoagulable states. Ann Int Med 1985; 102: 814–828.

45. Lewis BE, Wallis DE, et al. Argatroban anticoagulant therapy in patients with heparin-induced thrombocytopenia. Circulation 2001; 103: 1838–1843. 46. Mudaliar JM, Liem TK, et al. Lepirudin is a safe and effective anticoagulant for patients with heparinassociated antiplatelet antibodies. J Vasc Surg 2001; 34(1): 17–20. 47. Forfar JC. A 7-year analysis of haemorrhage in patients on long-term anticoagulant treatment. Br Heart J 1979; 42: 128–132. 48. Levine MN, Raskob G, et al. Hemorrhagic complications of anticoagulant treatment. Chest 2001; 119 (1 Suppl): 108S-121S. 49. Wong PC, Crain EJ, et al. Nonpeptide factor Xa inhibitors II. Antithrombotic evaluation in a rabbit model of electrically induced carotid artery thrombosis. J Pharmacol Exp Ther 2000; 295: 212–218. 50. Lynch JJ, Sitko GR, et al. Primary prevention of coronary arterial thrombosis with the factor Xa inhibitor rTAP in a canine electrolytic injury model. Thromb Haemost 1995; 74: 640–645. 51. Weitz JI, Hirsh J. New anticoagulant drugs. Chest 2001; 119 (1 Suppl); 95S-107S. 52. Turpie AG, Gallus AS, Hoek JA. Pentasaccharide Investigators. A synthetic pentasaccharide for the prevention of deep-vein thrombosis after total hip replacement. N Engl J Med 2001; 344: 619–625. 53. Duckert F. Thrombolytic therapy. Semin Thromb Hemost 1984; 10: 87–103. 54. Walker ID, Davidson JF, et al. Acylated streptokinase–plasminogen complex in patients with acute myocardial infarction. Thromb Haemost 1984; 51: 204–206. 55. Verstraete M. Third generation thrombolytic agents. Am J Med 2000; 109: 52–58. 56. Johnson AJ, McCarty WR. The lysis of artificially induced intravascular clots in man by intravenous infusions of streptokinase. J Clin Invest 1959; 38: 1627–1643. 57. Anonymous. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: STITLE trial. Ann Surg 1994; 220: 251–268. 58. Ouriel K, Veith FJ, Sasahara AA. Thrombosis or peripheral arterial surgery (TOPAS): Phase I results. J Vasc Surg 1996; 23: 64–75. 59. Valji K. Evolving strategies for thrombolytic therapy of peripheral vascular occlusions. J Vasc Intervent Radiol 2000; 11: 411–420. 60. Vorchheimer DA. Current state of thrombolytic therapy. Curr Cardiol Rep 1999; 1: 212–220. 61. Ouriel K, Katzen B, et al. Reteplase in the treatment of peripheral arterial and venous occlusions: a pilot study. J Vasc Interven Radiol 2000; 11: 849–854. 62. Davidian MM, Powell A, et al. Initial results of reteplase in the treatment of acute lower extremity arterial occlusions. J Vasc Interven Radiol 2000; 11: 289–294. 63. Goldhaber SZ. Thrombolytic therapy for pulmonary embolism. Semin Vasc Surg 1992; 5: 69–75. 64. Comerota AJ, Aldridge SC. Thrombolytic therapy for deep vein thrombosis. Semin Vasc Surg 1992; 5: 76–81.

Chapter 12 Thrombogenesis and Thrombolysis 65. Berridge DC, Gregson RH, et al. Randomized trial of intra-arterial recombinant tissue plasminogen activator, intravenous recombinant tissue plasminogen activator and intra-arterial streptokinase in peripheral arterial thrombolysis. Br J Surg 1991; 78: 988–995.

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66. Machleder HI. Evaluation of a new treatment strategy for Paget–Schroetter syndrome: spontaneous thrombosis of the axillary–subclavian vein. J Vasc Surg 1993; 17: 305–317.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 13 Etiology of the Abdominal Aortic Aneurysm Ahmad F. Bhatti, Tonya P. Jordan, and M. David Tilson

Over the past two decades there have been several changes in our understanding of the pathogenesis of the abdominal aortic aneurysm (AAA). As recently as 1990, a major textbook of pathology stated that “atherosclerosis is the most common cause of aortic aneurysms in the Western World” (1). The following year a surgical textbook claimed that “more than 95% of abdominal aortic aneurysms are due to atherosclerosis” (2). However, at the time of this writing, the authors believe most investigators in the AAA field would agree that the causes are multifactorial. There appear to be environmental, genetic, autoimmune, inflammatory, and structural factors. The notion that atherosclerosis is etiologic in AAA pathogenesis has been questioned (3–9).

Definitions The term “atherosclerotic AAA” is misleading because it suggests that atherosclerosis is a necessary cause of AAA disease, in the same sense that Treponema pallidum is a necessary cause of syphilitic aneurysm disease. A “necessary” cause is one that must be present for a disease to occur (7). While some patients with AAA have atherosclerotic occlusive peripheral vascular disease, others have minimal atherosclerotic disease (9). For this reason, the Joint Committee of the Society for Vascular Surgery and the North American Chapter of the International Society of Cardiovascular Surgery proposed a set of reporting standards for AAA disease, recommending that the term “non-specific AAA” be used (10,11). In the context of the

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rapid growth of new knowledge in the field of AAA pathobiology over the past decade, perhaps this terminology may be revisited with more precise nomenclature in the future. The definition of AAA has varied in the literature over the years, but all definitions have in common a specification of the degree of aortic dilation. This specification may be either absolute (e.g., >3 cm) or relative (e.g., diameter increase of > 50%). The consensus definition published by the above-mentioned joint committee was “a permanent localized dilation of an artery having at least a 50% increase in diameter compared with the expected normal diameter of the artery or of the diameter of the segment proximal to the dilation” (10,11). According to this definition, an infrarenal AAA could then be defined as 3.0 cm if 2.0 cm is the expected maximal diameter of the infrarenal aorta in an individual of a specified body scale (usually based on height). Others have sought to deal with this imprecision by considering other references of scale, such as the transverse area of a lumbar vertebra (12). Thus, there is no universally accepted definition of AAA. Accordingly, the data reported in various screening, population, and autopsy studies may not always be strictly comparable.

Epidemiology—Prevalence and Mortality The prevalence of small AAAs ranges from 2.9% to 7.9% if the criterion of diameter greater than 29 mm is used

Chapter 13 Etiology of the Abdominal Aortic Aneurysm

(13). Men are affected more than women by a ratio of about 4:1, varying between 2:1 and 8:1 depending on the methods of measurement and populations involved in various studies. The incidence of AAA is three times higher in the white male population than in the general black population (14). Necropsy studies have shown the frequency of AAA to be low in men before the age of 55, with this value rapidly increasing and reaching a peak of 5.9% at 80 to 85 years old. In women, aneurysms start to appear at age 70, and the frequency increases to 4.5% at age 90 and older (15,16). AAA is ranked as the 13th leading cause of death in the United States, making it responsible for 0.8% of all deaths (10,13,17). Rupture of AAAs cause 1% to 2% of all male deaths over the age of 65 years in western countries (10). In men, peak proportional mortality rate owing to AAA rupture occurs between 65 and 85 years. However, the peak proportional rate in women continues to increase with age after age 70 (13). The mortality rate due to AAA has increased more than threefold from 2.8 per 100,000 white males in the population to 10.8 per 100,000 between 1951 and 1981 (17–19). Other population groups have followed similar trends. This increase does not reflect an increase in atherosclerotic disease, because mortality rates secondary to coronary artery disease and cerebrovascular accidents have been decreasing in the same time period (17).

Risk Factors The aneurysm detection and management (ADAM) study was a screening program of the Department of Veteran Affairs, which used ultrasound to screen two cohorts of veterans (20). The first cohort consisted of 73,451 veterans and the second 52,943. The study defined AAA as an infrarenal diameter greater than 3.0 cm. The final results from the combined groups showed the strongest positive associations with age, male sex, smoking, and a family history of AAA. An association is also seen with atherosclerotic disease, but not with hypertension. Several studies have shown that negative risk factors for AAA are female sex, diabetes, and black race. The ADAM study also showed these negative associations. It is not clear why these factors are protective in terms of developing AAA. The ADAM study showed that the strongest association is with smoking. This association increased with the number of years of smoking and decreased with the number of years of abstinence from smoking. Tobacco smoking is a risk factor for both aorto-occulsive disease (AOD) and AAA; the relative risk for AAA is as high as 25-fold in patients who roll their own cigarettes (17). However, it is possible that the two diseases (AOD and AAA) are different observable effects of a single cause (7). There may be mitogens in smoke that trigger proliferation and migration of smooth muscle cells into the subendothelium to promote atherosclerosis. Paik et al. have suggested the mechanism of tobacco injury in AAA may be related to the matrix-destructive effects of the high levels of inhaled ni-

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tric oxide and nitrogen dioxide in smoke (21,22). Paik et al. have also reported that deleterious effects of nitrite may operate through a different mechanism in the case of collagen versus elastin (21,22). Shapiro et al. showed that smoking induces an inflammatory condition in which macrophages produce elastase. This is consistent with the proposed theory of an inflammatory cascade playing a role in the breakdown of matrix proteins in the aortic wall (20,23).

Family History The genetic predisposition for AAAs has been investigated in several studies (24–27). A recent study suggests an autosomal dominant mode of inheritance. Verloes and his group studied 313 AAA patients and their families (28). Although the etiology of AAA is probably multifactorial, their data suggested that there may be an inheritable defect that behaves as an autosomal dominant trait with low age penetrance. Verloes et al. showed, as other studies have, that familial cases of AAA may have an earlier onset and a higher rate of rupture; but these observations may be a consequence of a higher level of AAA awareness in the families studied (28). Most studies agree that individuals who have a firstdegree relative with an AAA exhibit an increased risk for developing an AAA. This risk has been reported variably, ranging from a twofold to 12-fold relative risk over the general population. Bengtsson reported on a compilation of studies that showed an AAA frequency of 8.6% in brothers and 3.6% in sisters of patients with AAA compared with 5.5% and 1%, respectively, in normal population controls (15,29,30). Another study showed that 6% to 20% of patients with nonspecific AAAs, and 8% to 17% of patients with inflammatory AAAs, have firstdegree relatives with an AAA, compared with 2.4% in the population controls (17,31). One study used ultrasound on 87 asymptomatic siblings of AAA patients and showed that 29% of the brothers and 6% of the sisters had AAA (17,32).

Molecular Genetics The HLA class II genes located on chromosome 6 are related to the immune response (33). Members of certain families may be at higher risk for AAA because the genes associated with modulating which antigens cause an immune response may predispose them to generating an inflammatory reaction against their own aortic selfproteins. Separate studies have identified certain HLA class II alleles as genetic determinants of both nonspecific and inflammatory AAA. Rasmussen showed that B1*02, which include B1*15, B1*16, and B1*04, were risk determinants for development of nonspecific and inflammatory AAA (33). Our laboratory has also reported on the significance of HLA-DR-2 in relationship to AAA disease,

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specifically the B1*15 allele (34,35). We have also found that HLA-DQ3 may be a negative risk factor (36). Our laboratory has also investigated a black family with several members who have exhibited aneurysmal dilation of different arterial beds, including aortic, iliac, and cerebral. Genetic testing has shown the affected family members are HLA DR B1*15 (37). Types I and III collagen are the major load-bearing components in the arterial wall. Although AAA formation is multifactorial, elastin and collagen failure are common components. It has been hypothesized that genetic defects in elastin or collagen could lead to these structural failures. Kontusaari et al. have described a family with four members who died of aortic rupture. The common mutation found in these family members was in the alpha1 chain of type III pro-collagen. The codon for glycine at position 619 was changed to a codon for arginine. This change decreased the temperature for thermal unfolding as compared to control type III pro-collagen (38). However, a follow-up study by the co-authors showed that mutations in type III pro-collagen are the cause of only about 2% of all AAAs (39). This conclusion was drawn after cDNA sequencing determined that 50 unrelated patients who had a family history of AAA did not share a common mutation in collagen III. Other heritable conditions that can cause a predisposition to AAA formation are known. One example of this is Ehlers–Danlos syndrome (EDS), type IV—“vascular type.” The disease causes a deficiency of collagen III due to mutations of the pro-alpha chains of collagen III (40). It is associated with spontaneous aortic rupture, often with little or no dilation. In one retrospective study of EDS type IV, the most common cause of death was arterial rupture (41). While some have expressed reservations about the occurrence of AAA disease in EDS, it seems likely that there are variants of EDS in which fusiform aneursymal disease may occur (42–45). Another example of a heritable condition leading to aneurysm formation is Marfan syndrome. In Marfan syndrome there is a mutation in the gene for fibrillin-1, which is thought to be a scaffolding protein for developing elastin (46–49). This deficiency may leave elastin susceptible to either mechanical or proteolytic degradation. It is not obvious how mutation in a gene that is intimately associated biochemically with elastin leads to structural failure of the load-bearing collagen of the aorta; but one recent study has suggested colocalization immunohistochemically of antibody against fibrillin with collagenassociated aortic microfibrillar proteins (50).

Atherosclerosis and AAA Aneurysmal degeneration of vessels has been attributed to atherosclerosis for many years. One of the first historical attributions of the disease to atherosclerosis is traceable to the translation into English of a book by the Italian surgeon, Scarpa, in the early nineteenth century (51). Halsted

was among the first to perform experimental studies of poststenotic aneurysms, followed some years later by Holman (52,53). Halsted noted intimal and medial architecture disruption, while the role of the adventitia was not carefully considered (52). His views reinforced the notion that atherosclerosis, which causes similar disruptions of the intima and media, was the cause of aneurysms. In consideration of more recent biomechanical studies, it is now believed that the adventitia is the “strength” layer (54). An example of adventitial strength is seen in carotid endarterectomies, where the intima and media are stripped, and the adventitia remains—yet no aneurysmal degeneration occurs. The aneurysmal aorta has features that are different from AOD: specifically, the presence of inflammation within the adventitia and the weakening of adventitial collagen. Atherosclerosis, on the other hand, is primarily a disease of the subendothelium, associated with the migration and proliferation of cells that may lead to rigidity of the vessel and stenosis of the lumen (55,56). Nevertheless, there are associations between atherosclerosis and AAA. As mentioned, patients with AAA have more atherosclerotic lesions in all their major arterial beds, except cerebral. The incidence of lower extremity ischemia in AAA patients is three times that of agematched control subjects. Ischemic heart disease is also more common in AAA patients (17). Although hypertension is seen in 40% of patients with AAA, elevated blood pressure is more positively associated with atherosclerotic aorto-occlusive disease (17). Diabetes mellitus and hyperlipidemia are established positive risk factors for AOD and peripheral vascular disease, but diabetes is a negative risk factor for AAA. Also, the male sex is a risk factor in AAA, but not for AOD (5,17). More research is required to determine the role of atherosclerosis in AAAs. Our research group has reported that there are boundary layer separations, turbulence, and reversal of flow on the surface of a glass model aneurysm of the human aorta (5). These conditions at the flow surface have been shown by many workers to stimulate the development of atherosclerotic lesions. In other words, biomechanical failure of the load-bearing collagen in the adventitia may have predictable consequences for the flow surface of the endothelium. Accordingly, the finding of Reed and coworkers, that a large portion of the flow surface of an aneurysm is atherosclerotic, is an expected result (57).

Structural Physiology The three gross layers of the aorta compose its dynamic architecture. The intima is the innermost layer of the artery wall. It forms the lumen with the endothelial cells resting on its basal lamina. The media in elastic arteries is made up of lamellae or concentric fibromuscular layers where the spaces between elastin are filled in with circumferentially oriented smooth muscle. There is some crosslinking between the lamellae via the elastin. The ad-

Chapter 13 Etiology of the Abdominal Aortic Aneurysm

ventitia is the outermost layer, composed of fibrous tissue such as collagen (58). Vasa vasorum, which nourish the media in large vessels like the aorta, are also present in this layer. Elastin, found mainly in the media, is responsible for the elasticity of a vessel. This protein is made up two major components. The amorphous elastin is placed upon a “scaffolding” of microfibrillar proteins. Elastin is crosslinked with the microfibrillar proteins via fenestrations forming cylindrical sheets. Elastin can be stretched up to twice its length and still rapidly rebound to its original dimensions (17,58). At small aortic diameters, elastin bears the oscillating load generated by the beating heart and circulating blood. It bears stress longitudinally, circumferentially, and radially (59). Each lamella bears 2500 dynes/cm2, and the number of lamellae found in a vessel is generally proportional to the load it bears (60). Elastin has a half-life of 60 to 70 years. Elastin is produced by smooth muscle cells and fibroblasts; the turnover of elastin is low. Elastin, which is similar in mechanical properties to rubber, is felt to deteriorate with time because of the number of oscillations it experiences. Rubber is known to fatigue, fracture, and suffer structural damage when subjected to approximately 109 oscillations—which correlates to 25 to 30 years in a human with an average heart rate of 60 to 70 (61–64). Many new types of collagen have been discovered in recent years, but type I collagen predominates in the aortic adventitia and bears most of the circumferential stress (65). Collagen types I, III (in a ratio of 3:1), and, to a lesser degree, V are found in the media of the aorta (56). Smooth muscle cells secrete the collagen in the media and fibroblasts secrete collagen in the adventitia. Collagen has a significant turnover, unlike elastin; it is continuously made throughout life. Collagen is a protein consisting of repeating amino acid units: glycine-X-Y, where X is frequently proline and Y is frequently hydroxyproline. These repeating units form left-handed helices or alpha chains forming three-stranded right-handed helices that are tightly crosslinked, limiting their extensibility. Collagen only can stretch about 2–4%, which is significantly less than elastin. However, collagen’s tensile strength is 10,000 times that of elastin. Medial collagen is load-bearing at high physiologic pressures. At normal physiologic pressures, only 1% of adventitial collagen is load-bearing. At larger diameters, more adventitial collagen is recruited to bear the load (56). The laboratory of the authors has recently shown the presence of collagen type XI alpha-1, in the normal aorta and in AAA (66). It is abnormally abundant in aneursymal aortic tissue. Its presence and significance are presently being investigated in our laboratory. The abdominal aorta handles stress and pressure variations in a nonlinear fashion. Under normal physiologic conditions, the elastin-rich media is load-bearing. This flexible, yet strong, elastic layer bears most of the pressure wave generated with each cardiac cycle. At higher pressures, with the elastin maximally bearing load, further stress is dissipated to the outer collagen-rich

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adventitial layer. While the adventitia is primarily collagen-rich, the inner third of the adventitia has elastin alternating with collagen. The stiffer collagen (100–1000 times stiffer than elastin) allows for much higher loadbearing without significantly increasing the diameter of the aorta (54,67,68). This leads to a nonlinear pressure–diameter curve. Smooth muscle cells are believed to have little impact on these pressure–diameter relationships in the aorta (69). It is elastin and collagen, in the media and adventitia respectively, that bear the cyclical stresses.

Structural Pathophysiology The abdominal aorta is subject to more oscillations than other smaller and stiffer arteries. In addition to systemic pressures, it is also subject to pressure waves reflecting off branches and bifurcations. There is a significant drop in the elastin content as the aorta crosses the diaphragm. The abdominal aorta, although more elastic than smaller vessels, is still stiffer than the thoracic aorta due to a higher collagen-to-elastin ratio. These factors expose this portion of the aorta to higher pressures and stresses which lead to a variety of sequelae. Thus, the infrarenal aorta may be more prone to structural deterioration (68,70–72). Some have offered the hypothesis that aneurysmal formation may be an adaptive change. Dobrin et al. have calculated and shown, theoretically, certain advantages in remodeling from a cylinder to a sphere (56). The spherical transformation allows a 50% reduction in stress forces. Laminar thrombus in the AAA has little role in changing the stresses. Dobrin et al. feel that the evolution of the aneurysm centers around an adaptive compensation for increased stresses. This compensation occurs by increased collagen recruitment, increased collagen production, and spherical transformation (56). In AAAs, collagen and elastin are both increased, disproportionately. The collagen-to-elastin ratio increases from 1.9:1 in normal human aortas to 7.9:1 in human AAAs (56). The tortuosity of AAAs may be attributed to a “buckling” of the vessel between fixed points (e.g., major branches) and a decrease in longitudinal retractive forces (elastin failure) (56). Elastin and collagen both fail in the sequence of events leading to the development of an AAA. Dobrin et al. conducted in vitro studies on human internal iliac arteries (IIAs), which support this assertion (73). The human arteries in their experiments were treated with elastase and/or collagenase, to observe the biometric response of these treated vessels under increasing intraluminal pressures. The study showed the IIAs treated with just elastase dilated and became stiffer. This stiffness resulted from elastin being maximally loaded and stretched. Collagen was then recruited to help bear the load. There was no rupture of the elastase-treated vessels. The IIAs treated with only collagenase dilated less than seen with the elastase treatment. The collagenase-treated vessels became

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more compliant; each vessel ruptured with only a small increase in diameter. The IIAs treated with elastase and then collagenase dilated markedly to aneurysmal proportions and ruptured. These findings led to a notion which became widespread that elastase caused aneurysms and collagenase caused rupture. However, it was pointed out that vessels treated with elastase only did not dilate to dimensions that could accurately be described as “aneurismal” (74). After additional experimentation, Dobrin and coworkers came to the conclusion that collagen failure was an essential feature of aneurysm formation (75).

Changes Related to Normal Aging As a person ages, changes also occur on a micro- and macroscopic scale to elastin and collagen layers. The collagen-to-elastin ratio increases. This is not merely a decrease in elastin from fraying, splitting, fragmenting, and calcifying (76). This is also from an increase in collagen (77). This increase in collagen leads to a thickened adventitial layer and arterial wall thickness. There is also increased crosslinking of collagen with time (69). A vessel which already has less than the expected elasticity becomes stiffer as more of the load is shifted to collagen (68). Paik et al. suggest that nonenzymatic nitration of the collagen leads to tyrosine depletion and increased crosslinking of collagen. This leads to a less distensible or stiffer aorta with age (21).

Enzymatic Degradation When considering the structural and mechanical etiologies of AAAs, any process that jeopardizes the structural proteins could cause aneurysmal degeneration. More specifically, collagenase and/or elastase have been implicated in the etiology of aneurysms. Animal models have reproduced these findings on many levels, although their consistency and results vary. Elastin and collagen are both degraded by specific proteinases. Both proteins can be lysed by specific matrix metalloproteinases (MMPs) which require metals as cofactors. MMPs and other proteases can be produced by the native aorta smooth muscle cells (SMCs) and/or fibroblasts. Immunohistochemical studies have identified broad, low level production of MMP-1 (interstitial collagenase) by adventitial vascular SMCs. Cultured AAA SMCs have increased elastin degradation activity compared with normal SMCs secondary to increased MMP-2 and MMP-9 activity (78). Elastin can also be degraded by serine proteinases (17). However, most studies point to MMPs causing the degradation of the aortic matrix (17,78,79). Other nonspecific proteinases have also been implicated in AAA. Nonmatrix protein enzymes have also been identified, such as plasminogen activators (e.g., tissue plasminogen activator) have also been found elevated in the adventitia of AAAs (78). In vitro macrophages exhibit increased elastinolytic

activity when exposed to activated plasmin. A combination of immunohistochemical and in situ hybridization studies have localized the expression of MMP-9, MMP-2, and MMP-3 to inflammatory cells within the periadventitial tissue. These enzymes are felt to be produced as a result of the recruitment of various immune cells (macrophages, plasma cells, etc.) in the adventitia. The initiating stimuli in the recruitment of these immune cells is unclear, but inflammation is a well-documented component of AAAs and atherosclerotic disease of the aorta. The primary source of MMP-9 has been shown to be macrophages that are conspicuously abundant in AAAs (79). It has been postulated that inhibition of these proteases may halt or perhaps even regress aneurysmal pathology. The recent finding by Thompson and coworkers that MMP-9 null/null knockout mice are resistant to the development of experimental aneurysms underscores the significance of the role of MMP-9 in AAA formation (80). These proteinases have inhibitors such as tissue inhibitor of MMP (TIMP) and a1-antitrypsin. The increased protease activity may be associated with decreased protease inhibitors within the AAA wall. Leukocyte elastase inhibits TIMP. In almost a circular fashion, macrophage elastase inactivates alpha-1-antitrypsin, the major inhibitor of serine elastases (17,81). There is a question of a genetic defect, which upsets the balance between the proteinases and their inhibitors, liberating elastin degradation products. Elastin degradation products possess chemotactic activity for very many cell types, including inflammatory cells and fibroblasts (81). Their liberation causes the influx of inflammatory cells, further upsetting the balance by liberating more proteases. These decreases in protease inhibitors have been the subject of many other investigations. Herron et al. localized MMP-9 and TIMP-1 to the vasa vasorum of the aorta—and suggested that an imbalance between the two might be the cause of the profound neovascularization that is commonly seen in AAAs (82). We have reported that elastin degradation products alone stimulate intense neovascularization of the aortic segment exposed to the Anidjar/Dobrin model of experimental aneurysm formation induced by intraluminal elastase (83). Doxycycline and its derivatives have been shown to exhibit MMP-inhibitory effects (84,85). This inhibition by doxycycline has been postulated to suppress AAA expansion. A small pilot study by Mosorin et al. suggested that “doxycycline may favorably alter the outcome of patients with small AAA” (86). These findings may have implications for AAA prevention or treatment. Further studies are required to assess the viability of such options.

Inflammation The normal aorta has few inflammatory cells within in its wall. An influx of CD3+ cells and lymphocytes is seen in AAA tissues Although 66% of all lymphocytes in AAAs are in the adventitia, polyclonal B-lymphocytes are abun-

Chapter 13 Etiology of the Abdominal Aortic Aneurysm

dant in the media. IgG is elevated in AAA specimens. Beckman showed an inflammatory infiltrate in the adventitia in 68% of 156 AAA resection specimens examined retrospectively (87). Macrophages are found throughout the wall of AAA specimens (81). The macrophage Fc receptors regulate the secretion of proteinases by receptor specific mechanisms. Phagocytes produce proteinases such as elastase and collagenase (17). Newman et al. implicated collagenase, stromelysin, and gelatinase-B (MMP-1,3,9) in the destruction of the aorta matrix (79). Cytokines are released by inflammatory cells and smooth muscle cells in the aorta. They are predominantly: interleukin 1 (IL-1), IL-6, IL-8, monocyte chemoattractant protein (MCP-1), tumor necrosis factor (TNF), and interferon (IFN) (88). These cytokines, to varying degrees, cause MMP expression, TIMP reduction, induction of prostaglandin synthesis, lymphocyte proliferation, and chemotaxis. An autoimmune or inflammatory cascade, as proposed in some etiologies of AAAs, is perpetuated via the use of cytokines.

Aortic Autoantigens/ Autoimmunity Autoimmunity may precipitate the inflammatory cascade. Several studies in our laboratory have attempted to identify possible autoantigens. Aneurysm aortic extract was studied and noted to contain large quantities of IgG. Further studies revealed that the IgG from AAA patients was present and reactive against various proteins present in the aneurysmal aorta. One of the initial putative autoantigen extracts was an 80-kDa dimer, designated aortic aneurysm associated protein-40 (AAAP-40). AAAP-40 was reactive with 79% (11 of 14) of AAA IgG preparations, and 11% (1 of 9) of controls (p = 0.002) (89). Other autoantigens have subsequently been found, and are currently under investigation in our laboratory. Evidence continues to accumulate to support the notion that autoimmunity may play an important role in aneurysmal degeneration of the aorta. Some of these autoantigens are absent in the external iliac artery, perhaps explaining why this artery rarely becomes aneurysmal (90,91). Various groups within Tilson’s laboratory have studied other matrix cell adhesion molecules or MatCAMs: MatCAM 1 (clone 1) and MatCAM 5 (clone 5). These are closely associated with the collagen microfibrils in the adventitia. Fibroblasts from AAA have been shown to make these putative autoantigens (92). They show a high degree of similarity to light chains in the IgK family. Antibodies made against unique amino acid sequences in these proteins show conspicuous immunoreactivity in the adventitia of AAA patients. Clone 1 is present in the aorta, common iliac artery, and internal iliac artery. However, it is not present in the external iliac artery, popliteal artery, or carotid artery. AAAP-40 is in all vessels except the external iliac artery which, as mentioned, rarely develops

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aneurysms. Clone 5 is present in most vessels, as well as the external iliac artery. Antibodies against a peptide based on a unique sequence within clone 5 are immunoreactive against peritoneal structures as well as the lung. The unexpected distribution of clone 5 might explain why inflammatory AAAs exhibit more retroperitoneal inflammation (93).

Molecular Mimics Triggering of autoimmunity can be brought about by autoantigens or molecular mimics. For example, molecular mimicry may occur with cytomegalovirus and clone 1 (94). Also, rabbit antibody against Treponema pallidum and herpes simplex have been shown to bind to the adventitial elastin-associated microfibrils. The putative autoantigen AAAP-40 has homologies with Treponema pallidum and herpes (95). The hypothesis is that there are epitopes in the microbial proteins that are similar to the AAAP-40, thereby triggering an autoimmune response. Tanaka et al. detected herpes simplex viral DNA in 12 of 44 AAA specimens, compared with 1 of 10 normal subjects (96). Molecular mimicry may have also occurred when Capuchin monkeys were experimentally treated with herpes at the National Institute of Health. Several years later, some monkeys developed ruptured AAAs (97).

Chlamydia AAA is often associated with an inflammatory infiltrate. It is thought that nonspecific and inflammatory AAAs are different points on the spectrum of the same disease process (33). Could AAA be caused by a direct low-grade infection? Chlamydia pneumoniae has been found to be associated with atherosclerotic disease and acute myocardial infarction. This obligate intracellular organism can reproduce in vascular endothelium as well as monocytes and alveolar macrophages. C. pneumoniae has been found in the macrophages located in AAA lesions and in the smooth muscle cells beneath the plaques. Juvonen et al. took tissue specimens from 12 AAA patients. All of the tissue specimens were positive for C. pnemoniae by immunohistochemistry. Some of the specimens were positive for the microbe on PCR. Electon transmission microscopy demonstrated pear-shaped C. pneumoniae-like organisms. This observation suggests recent or present infection (98). Lindholt showed serological signs of recent or present C. pneumoniae infection in his study of 100 AAA patients. He demonstrated elevated titers of IgA or IgG which were associated with aneurysm expansion. However, the Viborg study did not show a positive correlation between antibody titers and AAA expansion (99). It has been shown that having chronic obstructive pulmonary disease (COPD) may be a risk factor for developing and rupturing an AAA. COPD has been associated with chronic C. pneumoniae infection, as well. Smoking,

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which is a risk factor for both COPD and AAA, has also been associated with chronic C. pneumoniae infection (98). It might be hypothesized that smoking, COPD, and AAA could all be linked by one common factor: C. pnemoniae. However, Lederle et al. studied two large cohorts that included smokers and no association was shown between COPD and AAA (20).

Vitamin E Deficiency Recent studies have pointed to an inverse relationship between vitamin E (a-tocopherol) levels and the incidence of arterial disease. Vitamin E is an important lipid-soluble antioxidant that localizes to the hydrophobic area of biologic membranes (100). In terms of AAA, it is hypothesized that activated polymorphonuclear cells (PMNs) release proteinases which degrade the aortic wall matrix. These same PMNs would also release oxidative enzymes, generating toxic oxygen species such as hydrogen peroxide which would lead to lipid peroxidation. Vitamin E is considered a specific, though indirect, index of in vivo peroxidation (101). Sakalihasan et al. showed that a small group of AAA patients had decreased vitamin E levels but not decreased vitamin E/total lipid ratios compared with controls (coronary artery disease and normal patients) (100). Accordingly, the AAA patients may be under increased oxidative stress (e.g., increased inflammation or PMN activation) but do not have decreased concentrations of plasma vitamin E carriers. More clinical studies are necessary to determine the significance of these findings.

Conclusion Long gone are the days when a simplistic approach to the question of the “etiology” of the nonspecific AAA could be taken. AAA appears to be caused by an interplay of structural, biochemical, environmental, and genetic factors, each of which may modify the expression of the other. The four principal positive risk factors for AAA are smoking, age, male sex, and family history. While smoking clearly seems to be an environmental factor, issues related to addiction and dose–effect responses are doubtless modified by genetic influences. The three principal negative risk factors for AAA are diabetes, female sex, and African-American descent, all of which are genetically determined. Clearly our understanding of the etiology of AAAs is in its infancy, and further research is necessary to elucidate the causes of AAAs and their interactions with one another. Many studies have attempted to elucidate the various etiologies of AAAs. At the time of this writing, the gene most widely implicated as a positive cause of AAA in both the Japanese and American populations is HLA class II DR-B1–15 (33–35). No doubt the interplay of genetic influences, some of which have been discovered only in the past decade, will occupy investigators with an interest in

AAA etiology for many years to come. As a dynamic structure, the abdominal aorta is subject to the laws of physics, including flow dynamics. Collagen fragmentation, elastin degradation, stress distribution, and flow changes all have implications in the pathogenesis of AAA. The etiology of these structural changes is multifactorial. Whether this structural degeneration is the primary or secondary process may vary from patient to patient. The presence of various inflammatory mediators within the aortic wall have been shown in aneurysmal degeneration. There are various proposed inciting events, such as autoimmunity or molecular mimicry, leading to the inflammation cascade. While advances in treatment of AAAs have been made, progress in prevention and screening has lagged behind. Slowing the progression of AAAs with pharmaceuticals remains underinvestigated and public awareness remains poor. This chronic, often asymptomatic, disease carries significant risk for high morbidity and mortality. Understanding the basic science behind AAAs, their multifactorial etiology, may help us one day to screen patients, define high-risk patients, halt aneursymal progression, or even prevent AAAs.

References 1. Titus JL, Kim H-S. Blood vessels and lymphatics. In : Anderson’s pathology, 9th edn, ed. JM Kissane. C.V.Mosby Company, St. Louis, 1990, p 778. 2. Sabiston DC, Jr. Aortic abdominal aneurysms. In: Textbook of surgery, 14th end. ed. DC Sabiston, Jr. W. B. Saunders Company, Philadelphia, 1991, p. 1566. 3. Blanchard JF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: results of a case-control study. Am J Epidemiol 2000; 15: 575–83. 4. Blanchard JF. Epidemiology of abdominal aortic aneurysms. Epidemiol Rev 1999; 21: 207–21. 5. Tilson MD, Sumpio B. Do aneurysms cause atherosclerosis? Ann NY Acad Sci 1996; 800: 268–9. 6. Tilson MD. Editorial: Atherosclerosis and aneurysm disease. J Vasc Surg 1990; 12: 371–2. 7. Tilson MD. On causality and the problem of aneurysms. Chronic Diseases in Canada 1994; 15 (Suppl): S18–20. 8. Tilson MD. Aortic aneurysms and atherosclerosis (editorial). Circulation 1992; 85: 378–379. 9. Tilson MD, Stansel HC. Differences in results for aneurysms vs. occlusive disease after bifurcation grafts: results of 100 elective grafts. Arch Surg 1980; 115: 1173–1175. 10. van der Vliet JA, Boll APM. Seminar: Abdominal Aortic Aneurysm. Lancet 1997; 349: 863–66. 11. Johnston KW, Rutherford RB, et al. Suggested standards for reporting on arterial aneurysms. J Vasc Surg 1991; 12: 444–450. 12. Ouriel K, Green RM, et al. An evaluation of new methods of expressing aortic aneurysm size: relationship to rupture. J Vasc Surg 1992, 15: 12–18. 13. Wilmink ABM, Quick CRG. Epidemiology and potential for prevention of abdominal aortic aneurysm. Br J Surg 1998; 85: 155–162.

Chapter 13 Etiology of the Abdominal Aortic Aneurysm 14. Johnson G, Avery A, et al. Aneurysms of the abdominal aorta: incidence in blacks and whites in North Carolina. Arch Surg 1985; 120: 1138–40. 15. Keen RR, Dobrin PB, eds. Medical Intelligence Unit 17: Development of aneurysms. Landes Bioscience, Texas 2000. Chapter 1: Epidemiology of abdominal aortic aneurysm. Bengtsson H; 1–8. 16. Bengtsson H, Bergqvist D, Sternby NH. Increasing prevalence of abdominal aortic aneurysms, a necropsy study. Eur J Surg 1992; 158: 19–23. 17. Patel MI, Hardman DTA, et al. Current views on the pathogenesis of abdominal aortic aneurysms. J Am Coll Surg 1995; 181: 371–82. 18. Bickerstaff LK, Hollier LH, et al. Abdominal aortic aneurysms: the changing natural history. J Vasc Surg 1984; 1: 6–12. 19. Lillienfeld DE, Gunderson PD, et al. The epidemiology of abdominal aortic aneurysms: Mortality trends in the United States 1951–1980. Arteriosclerosis 1987; 7: 637–643. 20. Lederle FA, Johnson GR, et al. The Aneurysm Detection and Management study Screening Program: Validation Cohort and Final Results. Arch Intern Med; 160: 1425–30. 21. Paik DC, Dillon J, et al. The Nitrite/Collagen reaction: Non-Enzymatic Nitration as a Model System for Connective Tissue Damage. Connect Tiss Res 2001; 42: 111–22. 22. Paik DC, Ramey WG, et al. The nitrite/elastin reaction: implications for in vivo degenerative effects. Connect Tiss Res 1997; 36: 241–251. 23. Shapiro SD. Diverse roles of macrophage matrix metalloproteinases in tissue destruction and tumor growth. Thromb Haemost 1999 Aug; 82(2): 846–9. Review. 24. Rammusen TE, Hallett Jr. JW, et al. Genetic risk factors in inflammatory abdominal aortic aneurysms: Polymorphic residue 70 in the HLA-DR B1 gene as a key genetic element. J Vasc Surg 1997; 25: 351–64. 25. Tilson MD, Seashore MR. Fifty families with abdominal aortic aneurysms in two or more first-order relatives. Am J Surg 1984; 147: 551–553. 26. Tilson MD, Seashore MR. Human genetics of abdominal aortic aneurysm. Surg Gynecol Obstet 1984; 15: 129. 27. Norrgard O, Rais O, Angquist KA. Familial occurrence of abdominal aortic aneurysms. Surgery 1984; 95: 650–656. 28. Verloes A, Sakalihasan N, et al. Aneurysms of the abdominal aorta: familial and genetic aspects in three hundred thirteen pedigrees. J Vasc Surg 1995; 21: 646–55. 29. Bengtsson H, Bergqvist D, et al. A population based screening of abdominal aortic aneurysms (AAA). Eur J Vasc Surg 1991; 5: 53–57. 30. Bengtsson H, Norrgard O, et al. Ultrasonographic screening of the abdominal aorta among siblings of patients with abdominal aortic aneurysms. Br J Surg 1989; 76: 589–591. 32. Rasmussen TE, Hallett JW Jr. Inflammatory Aortic Aneurysm: A Clinical Review with New Perspectives in Pathogenesis. Annals of surgery 1997; 225: 155–66. 32. Webster MW, St. Jane PL, Steed DL, et al. Abdominal aortic aneurysm, result of a family study. J Vasc Surg. 1991; 13: 366–372.

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33. Rasmussen TE, Hallett JW Jr., et al. Genetic similarity in inflammatory and degenerative abdominal aortic aneurysms: a study of human leukocyte antigen class II disease risk genes. 34. Hirose H, Takagi M, et al. Genetic risk factor for abdominal aortic aneurysm: HLA-DR2(15), a Japanese study. J Vasc Surg 1998; 27: 500–503. 35. Tilson MD, Ozsvath KJ, et al. A genetic basis for autoimmune manifestations in the abdominal aortic aneurysm resides in the MHC Class II Locus DR-beta-1. Ann N Y Acad Sci (1996) 800: 208–215. 36. Hirose H, Tilson MD. Negative genetic risk factor for abdominal aortic aneurysm: HLA-DQ3, a Japanese study. J Vasc Surg 1999; 30: 959–60. 37. Jordan TP, Bhatti AF, et al. Aneurysmal diseases cosegregate in an African-American kindred with HLA Class II DR-B1–15. [Unpublished.] 38. Kontussari S, Tromp G, et al. A mutation in the gene for type iii procollagen (COL3A1) in a family with aortic aneurysms. J Clin Invest 1990; 86: 1465–73. 39. Tromp G, Wu Y, et al. Sequencing of cDNA from 50 unrelated patients reveals that mutation in the triple Helical domain of type III procollagen are an infrequent cause of aortic aneurysms. J Clin Invest 1993; 91: 2539–45. 40. Superti-Furga A, Steinmann B, et al. Molecular defects of type III procollagen in Ehlers–Danlos syndrome type IV. Hum Genet 1989; 82: 104–108. 41. Pepin M, Schwarze U, et al. Clinical and genetic features of Ehlers–Danlos syndrome type IV, the vascular TYPE. N Engl J Med 2000; 342: 673–680. 42. Barabas AP. Ehlers-Danlos Syndrome. The cause and management of aneurysms. eds: RM Greenhalgh, JA Mannick, JT Powell. London: W. Saunders, 1990; 57–67. 43. Barabas AP. Heterogeneity of the Ehlers–Danlos syndrome. Br Med J 1967; 2: 612. 44. Kontusaari S, Tromp G, et al. Inheritance of an RNA splicing mutation (G+1 IVS200 in the type III procollagen gene (COL3AI) in a family having aortic aneurysms and easy bruisability: phenotypic overlap between familial arterial aneurysms and Ehlers–Danlos syndrome Type IV. Am J Hum Genet 1990; 47: 112–120. 45. Tilson, M.D. Commentary on “Multiple aneurysms in a young man,” by A Nemes and C Dzsinich. Postgraduate Vasc Surg 2: 14–16, 1991. 46. Dietz HC, Cutting GR, et al. Marfan syndrome caused by a recurrent de novo missense mutation in the fibrillin gene. Nature 1991; 352: 337–339. 47. Dietz HC, Pyeritz RE, et al. The Marfan syndrome locus: confirmation of assignment to chromosome 15 and identification of tightly linked markers at 15q-q21.3. Genomics 1991; 9: 355–361. 48. Dietz HC, Cutting GR, et al. Marfan syndrome caused by a recurrent de novo missense mutation in the fibrillin gene. Nature 1991; 352: 337–339. 49. Dietz HC, Saraiva JM, et al. Clustering of fibrillin (FBN1) missense mutations in Marfan syndrome patients at cysteine residues in EGF-like domains. Hum Mutati 1992; 1: 366–374. 50. Schutzer R, Gabriel Y, et al. Localization of fibrillin in aortic adventitia may explain the development of aneurysm in patients with marfan syndrome. Cardiovasc Surg 1999; 7: 87.

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Part II Basic Cardiovascular Problems

51. Tilson MD, Gregory AK, Hingorani AP. Aneurysmal disease of the abdominal aorta. In: The basic science of vascular disease, eds Sidawy AN, Sumpio BE, DePalma RG. Armonk, NY: Futura Publishing, 1997: 641–662. 52. Halsted WS. An experimental study of circumscribed dilation of the subclavian artery observed in certain cases of cervical rib. J Exp Med 1916; 24: 271–285. 53. Holman E. On circumscribed dilation of an artery immediately distal to a partially occluding band: poststenotic dilation. Surgery 1954 36: 3–24. 54. Sonesson B, Vernersson E, et al. Sex difference in the mechanical properties of the abdominal aorta in the in human beings. J Vasc Surg 1994; 20: 959–69. 55. Stehbens WE. The pathogenesis of atherosclerosis: a critical evaluation of the evidence. Cardiovasc Pathol 1997; 6: 123–153. 56. Stehbens WE. Atherosclerosis and degenerative diseases of blood vessels. In: Stehbens WE, Lie JT, eds. Vascular pathology. London: Chapman & Hall, 1995: 175–269. 57. Reed D, Reed C, et al. Are aortic aneurysms caused by atherosclerosis? Circulation 1992; 85: 205–211. 58. Keen RR, Dobrin PB, eds. Medical Intelligence Unit 17: Development of Aneurysms. Landes Bioscience, Texas 2000. Chapter 4: Elastin, collagen, and the pathophysiology of arterial aneurysms. Dobrin PB; 4: 42–63. 59. Dobrin PB, Canfield TR. Elastase, collagenase, and the radical elastic properties of arteries. Experientia 1985; 41: 1040–1042. 60. Wolinsky H, Glagov S. Lamellar unit of aortic medial structure and function in mammals. Circ Res 1967; 20: 99–111. 61. Hass GM. Elastic tissue III. Relations between the structure of the aging aorta and the properties of isolated aortic tissue. Arch Pathol 1943; 35: 29–45. 62. Caldwell SM, Merrill RA, Sloman CM, Yost FL. Dynamic fatigue life of rubber. Industr Eng Chem 194; 12: 19–23. 63. Larson EW, Edwards WP. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1984; 53: 849–855. 64. Glagov S, Vito R, et al. Microarchitecture and composition of arterial walls: relationships to location, diameter, and distribution of medial stress. J Hypertens 1992; 10: S101–S104. 65. Dobrin PB, Gley WC. Elastase, collagenase, and the radial elastic properties of arteries. Experientia 1985; 41: 1040–1042. 66. Ewing DR, Bhatti AF, et al. The role of collagen type XI in the pathogenesis of the abdominal aortic aneurysm [Unpublished]. 67. Roach MR, Burton AC. The reason for the shape of the distensibility curves of arteries. Can J Biochem Physiol 1957; 35: 681–90. 68. Burton AC. Relationship of structure to function of the tissues of the wall of blood vessels. Physiol Rev 1954; 34: 619–42. 69. Keen RR, Dobrin PB, eds. Medical Intelligence Unit 17: Development of aneurysms. Landes Bioscience, Texas 2000. Chapter 3: The mechanical properties of the normal and aneuysmal abdominal aorta in vivo. Sonesson B, Lanne T; 3: 24–41. 70. Dobrin PB. Pathophysiology and pathogenesis of aortic aneurysms. Surg Clin N Am 1989; 69: 687–703.

71. Newman DL, Gosling RG, Bowden NLR. Pressure amplitude increase and matching the aortic iliac junction of the dog. Cardiovasc Res 1973; 7: 6–13. 72. Gosling RG, Newman DL, Bowden L. The area ratio of normal aortic junctions. Br J Radiol 1971; 44: 850–3. 73. Dobrin PB, Baker WH, Gley WC: Elastolytic and collagenolytic studies of arteries: Implications for the mechanical properties of arteries. Arch Surg 1984; 119: 405–409. 74. Tilson MD, Elefteriades J, Brophy CM. Tensile strength and collagen in abdominal aortic aneurysm disease. In: The cause and management of aneurysms, ed. RM Greenhalgh, JA Mannick, JT Powell. London: WB Saunders, 1990; 97–104. 75. Dobrin PB, Mrkvicka R. Failure of elastin or collagen as possible critical connective tissue alterations underlying aneurysmal dilation. Cardiovasc Surg 1994; 2: 484–488. 76. Hornbeck W, Adnett JJ, Robert L. Age dependent variations of elastin and elastase in aorta and human breast cancers. Exp Gerontol 1978; 13: 293–298. 77. Faber M, Moeller-Hou G. The human aorta. Acta Pathol Microbiol Scand 1952; 31: 377–82. 78. Keen RR, Dobrin PB, eds. Medical Intelligence Unit 17: Development of Aneurysms. Landes Biosecience, Texas 2000. Chapter 12: A perspective on the etiology of abdominal aortic aneurysms. Chew DKW, Knoetgen III J, Tilson III MD; 206–13. 79. Newman KM, Jean-Claude J, et al. Cellular localization of matrix metalloproteinases in the abdominal aortic aneurysm wall. J Vasc Surg, 1994; 20: 814–20. 80. Pyo R, Lee JK, et al. Targeted gene disruption of matrix metalloproteinase-9 (gelatinase B) suppresses development of experimental abdominal aortic aneurysms. J Clin Invest 2000; 105: 1641–49. 81. Brophy CM, Reilly JM, et al. The role of inflammation in nonspecific abdominal aortic aneurysm disease. Ann Vasc Surg 1991; 5: 229–33. 82. Herron GS, Unemori E, et al. Connective tissue proteinases and inhibitors in abdominal aortic aneurysms. Arterioscler Throm 1991; 11: 1667. 83. Nackman GB, Karkowski FJ, et al. Elastin degradation products induce adventitial angiogenesis in the Anidjar/Dobrin rat aneurysm model. Ann NY Acad Sci 1996; 800: 260–262. 84. Thompson RW, Baxter BT. MMP inhibition in abdominal aortic aneurysms. Rationale for a prospective randomized clinical trial. Ann NY Acad Sci 1999 Jun 30; 878: 159–78. 85. Curci JA, Petrinec D, et al. Preoperative treatment with doxycycline reduces aortic wall expression and activation of matrix metalloproteinases in patients with abdominal aortic aneurysms. J Vasc Surg 2000 Feb; 31(2): 325–42. 86. Mosorin M, Juvonen J, et al. Use of doxycycline to decrease the growth rate of abdominal aortic aneurysms: a randomized, double-blind, placebo-controlled pilot study. J Vasc Surg 2001; 34: 606–10. 87. Beckman EN. Plasma cell infiltrates in atherosclerotic in abdominal aortic aneurysms. Am J Clin Pathol 1986; 85: 21–24. 88. Hingorani A, Newman K, et al. A soluble extract from abdominal aortic aneurysm wall stimulates protein secre-

Chapter 13 Etiology of the Abdominal Aortic Aneurysm

89.

90.

91.

92.

93.

94.

tion and gelatainase expression in cultured macrophage like cells (U937). Surgical Forum 1994; 45: 375–377. Gregory AK, Yin NX, et al. Feature of autoimmunity in the abdominal aortic aneurysm. Arch Surg 1996; 13: 85–88. Chew DKW, Knoetgen J III, et al. Regional distribution in human of a novel aortic collagen-associated microfibrillar protein. Exp Mol Pathol 1999; 66: 59–65. Borreomeo RJ, Koshy N, et al. Regional distribution in the mouse of protein homologous to artery-specific antigenic proteins (ASAPs). J Surg Res 1999; 85: 217–24. Gefen JY, Ewing DR, Tilson MD. Differential expression of microfibrillar glycoproteins in cultured aorta and skin fibroblast. Presented at Society for Vascular Surgeons/American Society of Vascular Surgeons Combined Annual Spring Meeting June 2001. Syn D, Hardy K, et al. A molecular hypothesis for the phenomenon of generalized arteriomegaly and/or peritoneal inflammation in some patients with abdominal aortic aneurysms. Presentation at Meeting of the association for Academic Surgery Nov 2000. Ozsvath KJ, Hirose H, et al. Expression of two novel recombinant proteins from aortic adventitia (kappafibs) sharing amino acid sequences with cytomegalovirus. J Surg Res 1997; 69; 277–282.

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95. Ozsvath KJ, Hirose SX, Tilson MD. Molecular mimicry in human aortic aneurysmal Disease. Ann NY Acad Sci 1996; 16: 1–6. 96. Tanaka S, Komori K, et al. Detection of active cytomegalovirus infection n inflammatory aortic aneurysms with RNA polymerase chain reaction. J Vasc Surg 1994; 20: 235–243. 97. DePalma RG. In: The cause and management of aneurysms. Greenhalgh, RM, Mannick JA, Powell JT, eds. London: WB Sanders,1990: 97–104. 98. Juvonen J, Juvonen T, et al. Demonstration of Chlamydia pneumoniae in the walls of abdominal aortic aneurysms. J Vasc Surg 1997; 25: 499–505. 99. Lindholt JS, Ashton HA, Scott AP. Indicators of infection with the Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysms. J Vasc Surg 2001; 34: 212–15. 100. Sakalihasan N, Pincemail J, et al. Decrease of plasma vitamin E (alpha-Tocopherol) levels in patients with abdominal aortic aneurysm. Ann NY Acad Sci 1996; 800: 278–82. 101. Betrand Y, Pincemail B, et al. Differences in tocopherol–lipid ratio in ARDS and non-ARDS patients. Intens Care Med 1989; 15: 87–93.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures John D. Bisognano, Thomas W. Wakefield, and James C. Stanley

Careful preoperative assessment of cardiopulmonary function is essential in the planning of major arterial reconstructive surgery. In fact, recognition and treatment of underlying cardiac or pulmonary disease may be of greater importance in some patients than the performance of the vascular surgical procedure itself. Additionally, the preoperative evaluation affords an opportunity for the physician to institute risk factor modification that may be of particular benefit in this high-risk patient pool. Coronary artery disease causes many, if not the majority, of immediate and late postoperative deaths following peripheral vascular surgical procedures. Although the role of impaired pulmonary function in contributing to operative mortality with peripheral vascular procedures is not as well defined as is cardiac disease, postoperative morbidity attributed to severe pulmonary disease is well recognized. Coronary artery disease is clearly an important factor in determining the eventual outcome of vascular reconstructions in many patients. For example, cardiac complications after carotid endarterectomy, abdominal aortic aneurysm resection, and lower extremity revascularization at the Cleveland Clinic were responsible for 43% of early deaths, and fatal myocardial infarctions occurred in 20% of the survivors during an 8-year period of follow-up (1). In this later experience, 5- and 10-year actuarial sur-

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vivals were 82% and 49%, respectively, among patients without antecedent indications of coronary artery disease, compared with 67% and 31% at these same time points among those suspected of having coronary artery disease. Myocardial infarction at this same institution accounted for 37% of early postoperative deaths among 343 patients undergoing operations for abdominal aortic aneurysm and 52% of early postoperative deaths among 273 undergoing operations for lower extremity ischemia (2,3). Others have encountered similar mortality and morbidity rates, a clear reflection that patients with peripheral vascular disease often have coexistent lifethreatening coronary artery disease (4), and the risk of cardiac events appears to be as great during vascular reconstructions for severe infrainguinal vascular disease as for aortic disease (5).

Preoperative Cardiac Assessment The value of screening for coronary artery disease depends, in part, on the incidence of confirmed disease among patients undergoing peripheral vascular surgical reconstructions. Among 1000 patients subjected to mandatory coronary arteriography before undergoing aortic reconstruction, lower extremity revascularization,

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

or carotid artery surgery between 1978 and 1982 at the Cleveland Clinic, only 8% had normal coronary arteries (6). In this same series, coronary artery disease was considered mild to moderate in 32%, advanced but compensated in 29%, severe but surgically correctable in 25%, and inoperable in 6%. Severe coronary artery disease was present in 36% of patients being treated for abdominal aortic aneurysms, 32% of those being treated for cerebrovascular disease, and 28% of those undergoing operation for lower extremity ischemia. Surgically correctable severe coronary artery disease affected 34% of patients having a positive cardiac history or abnormal electrocardiogram (ECG), and a surprising 14% of those with a negative cardiac history and normal ECG. Thus, neither the specificity nor sensitivity of the patient’s history and routine ECG appears adequate for screening purposes. Cardiac risk in surgery patients was assessed by Goldman and his colleagues, who evaluated 1001 patients undergoing noncardiac procedures in a classic study published more than 20 years ago (7). Nine independent factors were found to represent significant cardiac risks, including: 1. 2. 3. 4. 5. 6. 7. 8. 9.

an S3 gallop or jugulovenous distension; myocardial infarction during the 6 months before surgery; rhythm other than sinus or premature atrial contractions; more than five premature ventricular contractions per minute; intraperitoneal, intrathoracic, or aortic operations; age greater than 70 years; significant aortic stenosis; emergency operative procedures; and poor general health evidenced by hypoxemia, hypercarbia, hypokalemia, chronic liver disease, or impaired renal function.

Using multivariate analysis, these risk factors correctly predicted and classified 81% of subsequent cardiac outcomes and became known as the Goldman index. Unfortunately, this index was not particularly useful in early assessments of patients undergoing vascular surgery (8,9) and has not been found useful in more recent times (10,11). Similarly, other clinical scoring systems, such as the Detsky modified risk index, the Dripps-ASA classification, and the Cooperman probability equation have not proved useful for the accurate prediction of postoperative outcome in patients undergoing peripheral vascular surgery (11). On the other hand, certain clinical information gained from a scoring system is relevant to the patient facing vascular surgery. Classification of cardiac risks by Evans in 566 patients subjected to peripheral vascular procedures revealed six variables having significant individual associations with cardiovascular complications (12), including:

1. 2. 3. 4. 5. 6.

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presence of congestive heart failure; prior myocardial infarction; prior stroke; arrhythmia; abnormal ECG; and angina.

Applying these factors in an equation defining risk, postoperative cardiac complications occurred in a predictable fashion, affecting 1.3% of low-risk patients as opposed to 23.2% of high-risk patients. The role of prior myocardial infarction is well established as a dominant risk factor for perioperative myocardial events in all surgical patients. In a Mayo Clinic study, patients undergoing operation within 3 months of a transmural myocardial infarction experienced a 27% reinfarction rate (13). This decreased to 11% within 6 months, and the reinfarction rate for longer periods was 4% to 5%. The recommendation that at least 6 months pass between a previous myocardial infarction and subsequent elective surgery was advanced by these data. Although in a study between 1973 to 1976, perioperative reinfarction occurred in 36% and 26% of those from 0 to 3 months and from 4 to 6 months after myocardial infarction, from 1977 to 1982 only 5.7% and 2.3% experienced reinfarction during the same times following their initial infarction (14). This suggests that contemporary perioperative monitoring and cardiac support have caused a decrease in reinfarction rates. A number of basic tests are available for preoperative cardiac assessment (Table 14.1), and their use in practice deserves individualized discussion.

Stress Electrocardiography Stress electrocardiography was one of the first screening tests for cardiac disease (15–18). Findings initially reported to correlate with physiologically important coronary artery stenoses included typical angina pectoris and a positive exercise test with more than 1.0 mm of ST-segment depression in three or more leads; a positive exercise test and an abnormal thallium scan; and a positive exercise test with 2.0 mm of ST-segment depression in three or more leads (19). However, a study of 100 patients requiring arterial reconstructive surgery employing either treadmill testing or arm ergometry revealed that the degree of ST-segment depression was not a good predictor of cardiac complications unless the patient also failed to achieve 85% of the predicted maximum heart rate (20). Those with ST-segment depression of more than 1.0 mm and less than 85% predicted maximum heart rate had a 33% myocardial complication rate, whereas those patients with a positive stress test who were able to achieve greater than 85% of their predicted maximum heart rate had no complications (p < 0.05). Unfortunately, many vascular surgical patients cannot adequately participate in exercise-related stress testing. Gage and his colleagues reported that only 76% of

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TABLE 14.1 Preoperative cardiac assessment Low Risk

Moderate Risk

High Risk

Normal ECG, >85% predicted maximum heart rate Ejection fraction >55%

Abnormal ECG, 75–85% predicted maximum heart rate

Abnormal ECG, < 75% predicted maximum heart rate

Ejection fraction 36–55%

Ejection fraction < 35%

No defect or redistribution

Fixed defect without redistribution (scar from prior infarction)

Dobutamine stress echocardiography

No wall motion abnormality

Coronary angiography

No disease, mild compensated disease, or corrected disease

Resting wall motion abnormality; worsening of pre-existing wall motion abnormality Advanced but compensated disease

Thallium redistribution, especially with congestive heart failure, angina, prior infarction, or diabetes mellitus New wall motion abnormality

Stress ECG Radionuclide angiocardiography Dipyridamole– thallium scan

patients were able to undergo adequate stress for testing purposes (15). Among 38 of 50 cases in their experience in whom the stress studies were complete, 25 were abnormal, but only 15 were confirmed by coronary arteriography to be truly positive. Just as important was the fact that a third of patients without cardiac symptoms and a normal ECG exhibited an abnormal stress test, indicating once again that silent coronary artery disease among vascular surgery patients is common. Further concern regarding screening with exercise-stress electrocardiograms has been expressed by Weiner, who noted that 65% of men and 33% of women with angina and significant coronary artery disease had negative exercise studies (18). The actual predictive value of these tests depends on the disease prevalence, which is relatively low, a factor that further lessens their screening value. An attempt to better quantitate exercise stress testing evolved from an evaluation of 2842 patients undergoing exercise electrocardiography within 6 weeks of cardiac catheterization (21). This study described a treadmill score, defined as exercise time—(5 ¥ ST deviation)— (4 ¥ treadmill angina index). Patients with three-vessel disease and a score of –11 or less had a 5-year survival of 67% versus a 5-year survival of 93% with a score of +7 or more. The value of such a system to predict operative complications in patients undergoing peripheral vascular surgical procedures remains to be determined.

Radionuclide Ventriculography Radionuclide ventriculography also serves as a screening test for coronary artery disease (22). This test is relatively precise at measuring the cardiac ejection, with correlations between dye dilution and 99Tcm pertechnetate determined cardiac output measurements being 0.94 in healthy individuals and 0.89 in patients with a history of coronary artery disease. Nuclide scanning defines the volumes of the heart during end-diastole and end-systole. Analvsis of 300 to 400 cardiac cycles allows accurate quantitation of the ventricular ejection fraction. Such gated-pool ra-

Severe uncorrected or inoperable disease

dionuclide ventriculograms (MUGA scans) provide quantitative data regarding cardiac function. Among patients at the New York University Medical Center undergoing major abdominal aortic reconstructions who had preoperative radionuclide ventriculography, perioperative myocardial infarction was 0%, with a MUGA-determined ejection fraction between 56% and 85%, 20% with an ejection fraction between 36% and 55%, and 80% if the ejection fraction was less than 35% (23). In a British study of patients undergoing aortic surgery, ejection fractions greater and less than 30% were associated with cardiac-related deaths in 2.7% and 75% respectively (24). Similar experiences have been reported in patients undergoing extremity revascularizations (25). The importance of ejection fraction defining overall survival has also been noted for patients undergoing carotid endarterectomy (26), abdominal aortic aneurysm repair (27), and lower extremity revascularization (28,29). Finally, the effect of exercise on the ejection fraction provides further prognostic information regarding the severity of the underlying coronary artery disease (30).

Radionuclide Myocardial Imaging Thallium-201 chloride provides a marker of myocardial blood flow, and allows recognition of decreased or redistributed flow during increased cardiac activity, a finding suggesting that the cardiac muscle is at risk (Fig. 14. 1). In this regard, a fixed defect on both stress and rest thallium scanning, such as would occur in the region of previous myocardial infarction and fibrosis, represents a less hazardous situation than would occur with redistribution. Such fixed defects represent nonreactive ventricular scar. Thallium studies using maximal coronary vasodilation with intravenous administration of dipyridamole were an outgrowth of difficulties in achieving adequate stress using treadmill exercise with both electrocardiographic as well as radionuclide studies (31–36). These testing methods have overcome difficulties in testing pa-

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

FIGURE 14.1 Radionuclide myocardial imaging with thallium-201 chloride. Perfusion defect during stress (S) in the inferolateral left ventricle (arrows) that is not present 3 hours later during recovery (R). Such redistribution of myocardial blood flow establishes the existence of tissue that is vulnerable to further ischemic injury. (Reproduced by permission from Haimovici H, Callow AD, et al. eds. Vascular surgery principles and techniques, 3rd edn. East Norwalk, CT: Appleton & Lange, 1989: 197.)

tients with extremity vascular disease who cannot adequately exercise, as well as those receiving beta-blockers who are unable to increase their heart rate and generate an acceptable rate-pressure product. An early evaluation of thallium–dipyridamole studies was performed by Brewster and his colleagues at Massachusetts General Hospital on 54 patients, nearly equally divided between aortic and peripheral arterial reconstructive procedures (34). In this experience, 22 patients, including five who had evidence of an old myocardial infarction on ECG, exhibited a normal test, and none developed postoperative cardiac ischemic events. Among the remaining 15 patients who demonstrated thallium redistribution, seven patients experienced definite myocardial ischemia postoperatively, including one fatal myocardial infarction, three nonfatal transmural myocardial infarctions, and four instances in which unstable angina developed. In this study, perioperative myocardial ischemia did not correlate with age greater than 70 years, a history of angina pectoris, the type of operation performed, or with anginal discomfort and ST-segment changes accompanying administration of dipyridamole. Most importantly, a previous myocardial infarction in this study was not predictive of perioperative ischemic events unless accompanied by thallium redistribution. Cutler reported on 116 patients undergoing dipyridamole stress–thallium studies. Among these patients, 60

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had normal preoperative scans with no myocardial infarctions after abdominal aortic aneurysm surgery, and 31 had abnormal preoperative scans, with eight suffering myocardial infarctions (35). The risks of developing a myocardial infarction were 12 times greater in a patient having an abnormal scan. Such positive scans occurred with similar frequencies with clinically asymptomatic as well as symptomatic coronary artery disease. A second published study on dipyridamole stress– thallium testing from the Massachusetts General Hospital involved a total of 111 patients (36). In the first 61 patients studied, myocardial events occurred in 8 of 18 patients with preoperative thallium redistribution compared with no events in 43 patients without thallium redistribution. In a subsequent portion of this study, patients were categorized as those without evidence of congestive heart failure, angina pectoris, previous myocardial infarction, or diabetes mellitus, as opposed to those with one or more of these factors. None of the 23 patients in whom these clinical conditions were absent had adverse outcomes, despite the fact that six exhibited thallium redistribution. On the other hand, 27 patients had more than one of these clinical risk factors, and of 18 patients with redistribution, eight experienced postoperative ischemic events, compared with only two events among the nine patients without redistribution. Thus, dipyridamole–thallium scanning may be useful in stratifying patients at risk of myocardial ischemia when one or more clinical markers of cardiac disease or diabetes exist. The overall incidence of perioperative ischemic events in this series was 45% with thallium redistribution, compared with 7% without redistribution. Overall, combining five studies from the literature, the incidence of perioperative cardiac events in aortic surgery patients was 22% with a positive scan and 0.5% in those with a negative scan, including fatal myocardial infarction in 8.1% of those with a positive scan compared with 0% in those with a negative scan (33,35–38). The thallium scan has been quantitated so as to increase its predictive value, by determining the number of myocardial segments with redistribution, the maximal severity of the reversible defect, and the amount of myocardial tissue at risk (11). Likewise, delayed imaging has been advocated by some who observed that fixed defects initially on thallium scanning may show late redistribution and indicate a high risk of myocardial infarction (10), and by others who suggest that fixed defects correlate in a significant fashion with long-term cardiac morbidity and deaths (39). Thallium reinjection 4 hours after the first injection is a means of improving detection of ischemic cardiac muscle that initially appeared as a fixed defect on the primary image, with up to 49% of initial fixed defects demonstrating improved or normal thallium uptake after a second injection (40). Finally, two studies suggest that select patients undergoing aortic surgery may undergo thallium testing, and not all patients need to undergo such preoperative evaluations. In one study, patients undergoing abdominal aortic

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aneurysm repair had critical coronary artery disease predicted by a history of myocardial infarction, stable angina, or an abnormal echocardiogram (36% vs. 0% without such a history) (41). This study suggested that thallium scanning was not necessary in the absence of such findings. In a second study (42), vascular surgery patients were stratified on admission by analysis of five key risk factors: 1. 2. 3. 4. 5.

age greater than 70 years; diabetes; Q-wave on ECG; history of ventricular arrhythmia requiring therapy; history of active angina.

Among the 151 patients with abdominal aortic aneurysms and 51 patients with aortoiliac occlusive disease, preoperative thallium scans were found necessary in 29%, coronary arteriograms were performed in 11%, and preoperative cardiac intervention (percutaneous transluminal coronary angioplasty or surgery) was undertaken in 9% of patients. The overall operative mortality was excellent at 2%, with major cardiac morbidity occurring in 4%. Only 20% of those with zero or one risk factor underwent thallium scans while 50% of those patients with two or more factors underwent testing. Although this was not a prospective randomized study, the authors suggest that patients with zero to one risk factors need not undergo preoperative testing, while those with two or more risk factors should undergo testing. Importantly, no single clinical marker of coronary artery disease predicted the adverse cardiac events in this series. A cautionary note regarding thallium-stress imaging is warranted in hypertensive patients with a low likelihood of coronary artery disease who have had diastolic pressures exceeding 90 mmHg for at least 2 years. These patients are more likely to have abnormal scans than normotensive patients, perhaps as a reflection of limited coronary reserve due to hypertension-related myocardial hypertrophy (43). Such findings may lessen the specificity of these tests. A second word of caution relates to the potential of dipyridamole-induced myocardial ischemia, allegedly caused by coronary “steal” in the presence of epicardial coronary collateral vessels (44). This potential hazard has received little attention given the large number of useful studies performed without occurrence of this complication. Finally, not all groups have concluded that dipyridamole–thallium scintigraphy is useful. In a study of 60 patients undergoing vascular reconstruction in which the investigators were unaware of the scan results, the sensitivity of the test was only 40% to 54%, the specificity only 65–71%, the positive predictive value only 27% to 47%, and the negative predictive value only 61% to 82% (45). Furthermore, although thallium scans are most often used in the preoperative evaluation of the aortic surgery patient, the cost and time required to perform this test have been questioned by some authors. Thus, controversy remains as to the precise effec-

tiveness of thallium scanning as a preoperative screening procedure.

Dobutamine Stress Echocardiography Stress echocardiography has evolved as a means of assessing the adequacy of the coronary artery circulation. In 60 patients undergoing aortic surgery (27 with aneurysms and 33 with occlusive disease), a 4.6% cardiac event rate (1/22) was found in those with a negative study, while a 29% cardiac event rate affected patients with an abnormal test (46). In fact, patients with a new wall motion abnormality suffered a 39.1% cardiac event rate. In a second report, 51 patients undergoing resection of abdominal aortic aneurysms, 46 aortofemoral bypasses, and 39 infrainguinal arterial reconstructions were studied (47). The dobutamine echocardiogram was positive in 35 of the patients in this study, including five who died of myocardial infarction, nine who had unstable angina, and one who developed pulmonary edema. By multivariate analysis, only age greater than 70 years and new wall motion abnormalities were significant as to their predictive value. In a third study, dobutamine stress echocardiography in 98 consecutive patients undergoing vascular surgery resulted in 70 normal studies, 23 studies with new or worsening wall motion abnormalities, and five equivocal studies (48). All negative studies were associated with uneventful surgical procedures. Of the 23 patients with positive studies, 19 underwent cardiac catheterization, all revealing greater than 50% lumen narrowings in one or more major coronary distributions, and 13 underwent preoperative coronary artery bypass; four of ten positive patients without preoperative coronary revascularizations suffered a perioperative cardiac event. The safety of dobutamine stress echocardiography has been addressed in an experience involving 1118 patients (49). An aggressive dobutamine dosing regimen was used, and atropine was employed in 420 (37%) of these patients. There were no deaths, episodes of myocardial infarction, or sustained ventricular tachycardia, and noncardiac side effects were infrequent. Approximately 20% of patients developed angina that was well treated with sublingual nitroglycerin or short-acting beta-blockers. The above studies and others from the cardiology literature suggest that dobutamine stress echocardiography may eventually replace thallium studies in the preoperative evaluation of the vascular surgery patient as a more cost-effective study. Perioperative Holter monitoring has been advocated as a means of revealing occult coronary artery disease. The presence of 1 hour or more of ischemia appears to be the cutoff point predicting overall cardiac morbidity and mortality (50). Likewise, myocardial ischemia noted with the use of a two-channel Holter recorder, for 2 days before surgery, during surgery, and 2 days after surgery, was associated with a 2.8-fold increase in the odds of an adverse cardiac outcome (51). The exact role for this technology is

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

not clear in relation to thallium scanning and stress echocardiography.

Arteriography The most accurate means of identifying anatomic and surgically correctable coronary artery disease in patients who are candidates for peripheral vascular surgery is arteriography. However, arteriography cannot identify functionally important disease. Its use as a screening test has been questioned by many, including surgeons from the Mayo Clinic where routine coronary artery bypass plus aortic aneurysmectomy in certain subgroups carries a risk exceeding that of aneurysm resection alone (52,53). Mortality among patients at the Mayo Clinic who have not had prior coronary artery bypass before aortic aneurysm resection in the age group of 50 to 69 was due to a cardiac cause 70% of the time, compared with 50% for patients 70 to 79 years old, and 33% for patients older than 80 years. In 1996, the American College of Cardiology and the American Heart Association published guidelines for perioperative cardiovascular evaluation for noncardiac surgery (54) (Table 14.2). These guidelines indicate that asymptomatic patients with a history of coronary revascularization within 5 years need no further coronary evaluation preoperatively. Other patients are risk stratified based on clinical predictors and cardiac risk for the planned surgical procedure. All vascular procedures are considered “high-risk,” including peripheral vascular procedures. Patients with high-risk predictors such as unstable coronary syndromes, decompensated CHF, significant arrhythmias, or severe vascular disease may benefit from coronary angiography before vascular surgery. With that in mind, the only patients who may proceed to vascular surgery without coronary evaluation are those who can perform > 4 METS of physical activity and have no intermediate clinical predictors such as angina, prior myocardial infarction, compensated or prior CHF, or diabetes. All other patients require stress evaluation for

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risk stratification, including all patients whose physical activity is generally below 4 METS. Activities associated with 4 METS of activity include baking, slow ballroom dancing, golfing with a cart, playing a musical instrument, or walking at 2–3 mph. Most patients with claudication cannot achieve a workload of 4 METS. Naturally, the risk of stress testing and the potential of subsequent coronary arteriography and intervention must be weighed in the individual patient. Some evidence is emerging that, patients undergoing carotid endarterectomy under local anesthesia suffer fewer cardiac complications than with general anesthesia (55). But this is the result of a meta-analysis of nonrandomized data, and will require additional data for confirmation. Most patients undergoing any vascular procedure, irrespective of their stress test results, will also benefit from perioperative beta blockade and aggressive postoperative lipid treatment.

Empiric Beta Blockade Preoperative cardiac evaluation and intervention comes with risks, particularly in patients with atheromatous vessels and renal insufficiency, conditions common in patients requiring vascular surgery. A multicenter study involving 173 patients with abnormal dobutamine echocardiograms tested standard therapy against empiric perioperative treatment with the b1-selective antagonist bisoprolol (56). In this study, 173 patients with planned vascular surgery who had abnormal dobutamine stress echocardiograms were evaluated. Of these, 53 were excluded because they were already taken beta-blocking drugs, and eight were excluded because of extensive wall motion abnormalities during the stress or rest portion of the test. Patients were treated with bisoprolol 5 mg daily for at least 1 week preoperatively, and for 30 days postoperatively. In patients whose heart rate remained above 60 beats per minute, the dose was increased to 10 mg daily. Control patients received standard peroperative care without beta blockade.

TABLE 14.2 Preoperative risk stratification for patients undergoing vascular surgery Presentation

Preoperative Approach

Emergent surgery

Proceed to operating room Consider beta blockade Postoperative risk stratification and risk factor management Proceed to operating room Consider beta blockade Postoperative risk factor management Consider coronary angiography and subsequent care dictated by the findings Consider delay or cancellation of noncardiac surgery Noninvasive testing with subsequent care dictated by the findings

Coronary revascularization within 5 years or recent coronary evaluation in patient with no recurrent signs or symptoms Patients with major clinical predictors (unstable coronary syndromes, decompensated CHF, significant arrhythmias, or severe valvular disease) Patients with intermediate clinical predictors (mild angina, prior MI, compensated or prior CHF, diabetes) Patients with minor or no clinical predictors (advanced age, abnormal ECG, rhythm other than sinus, low functional capacity, history of stroke, uncontrolled systemic hypertension)

If functional capacity exceeds 4 METS: proceed to operating room and consider beta blockade If functional capacity is 4 METS or less, perform noninvasive testing

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The results of this study showed a statistically significant decrease in death due to cardiac causes and in nonfatal myocardial infarction in patients treated with bisoprolol. While the patients at highest risk were excluded from randomization, this study shows a clear beneficial effect of perioperative beta blockade in patients undergoing vascular surgery, and who have evidence of coronary insufficiency. Additionally, perioperative beta-blocker use has also been associated with decreased occurrence of atrial fibrillation, which can occur in many patients 2 to 4 days postoperatively (57). With this information, it may be reasonable to treat all patients undergoing vascular surgery with beta blockade to achieve a heart rate of about 60 and/or to use intravenous metoprolol to achieve a heart rate of < 80 in patients who are unable to take oral medication.

Intraoperative Cardiac Management Intraoperative risk analysis based on anesthetic classification has allowed definition of overall operative mortality rates. For example, the mortality in class I ASA risk patients is 0.1%, while the mortality in class V ASA patients is 9.4% (58). However, this classification does not distinguish treatable factors contributing to myocardial infarction, which may affect 50% to 60% of patients undergoing certain major vascular procedures. Surgeons should be familiar with those intraoperative maneuvers that decrease the cardiac risks of peripheral vascular reconstructions. Swan–Ganz catheter placement has allowed for more optimal fluid administration during performance of vascular procedures. Such monitoring is of particular use in patients with decreased systolic function in whom seemingly minor variations in preload and afterload can cause considerable variation in cardiac output and renal function. It is important to minimize the time that a Swan–Ganz catheter remains in place. Once fluid status and cardiac output can be adequately (albeit not optimally) monitored by noninvasive means (blood pressure, urine output, renal function), the catheter should be removed to decrease the chance of infection. The Brigham group has reported on Swan–Ganz catheter monitoring preoperatively to determine Starling responses to incremental infusions of salt-poor albumin and lactated Ringer’s solution, with subsequent pulmonary capillary wedge pressures maintained intraoperatively and postoperatively at levels consistent with optimal left ventricular performance as predicted by the preoperative studies (59). They reported 110 consecutive patients undergoing elective or urgent repair of abdominal aortic aneurysms, with no 30-day mortality, a 0.9% in-hospital mortality, and a 5-year cumulative survival of 84%. Increased arterial pressures were treated with sodium nitroprusside as a vasodilator, but monitoring of the cardiac index and pul-

monary capillary wedge pressures suggested that this was seldom necessary and at times hazardous. In fact, the Brigham group does not now use vasodilators during aortic cross-clamping. Others have had similar experiences, and have reported that optimal fluid management with aortic reconstruction included administration of balanced salt solutions rather than hypotonic solutions (60). Maintenance of pulmonary capillary wedge pressures with volume expansion is often supplemented with both inotropic drugs and afterload-reducing agents (61). These drugs become important because the diastolic compliance or the relation between the wedge pressure and the end-diastolic volume index may decrease after aortic declamping (62). This is probably a reflection of early myocardial ischemia, and under such circumstances the wedge pressure may need to be restored to a higher level to return the cardiac index to acceptable levels. Others have also suggested that careful titration of the pulmonary artery catheter wedge pressure may lower the frequency of adverse intraoperative cardiac events, cardiac morbidity, and early graft thromboses in patients undergoing peripheral vascular surgical procedures (63). Other types of intraoperative monitoring contribute to improved myocardial performance and detection of early myocardial ischemia. One such technique includes online computerized monitoring of systolic time intervals, left ventricular pre-ejection times, left ventricular ejection times, and ratios of left ventricular pre-ejection time to election time (64). Experience with this type of monitoring revealed systolic time intervals to be sensitive indices for dosing anesthetic and vasoactive drugs, while pulmonary artery diastolic pressures appeared more specific for administering blood and fluids. Perhaps a more direct approach to assess intraoperative cardiac function and myocardial ischemia is twodimensional transesophageal echocardiography (65,66). In a study of 24 ASA class III and IV patients, half underwent supraceliac clamping and half underwent suprarenal-infraceliac or infrarenal aortic crossclamping, with a special 3.5-MHz two-dimensional electrocardiographic transducer placed in the esophagus to provide a cross-sectional view of the left ventricle through the base of the papillary muscle (65). Supraceliac aortic occlusion caused major increases in left ventricular end-systolic and end-diastolic areas, decreases in ejection fraction, and frequent wall motion abnormalities. Suprarenal clamping caused similar but less pronounced effects, while infrarenal clamping caused minimal changes. Wedge pressures changes often did not correlate with findings of two-dimensional electrocardiography. For example, with supraceliac aortic cross-clamping, wedge pressures and systemic pressures were normal in 10 of 12 patients, whereas 11 of 12 developed wall motion abnormalities indicative of myocardial ischemia. Twodimensional echocardiography in another study of 50 patients revealed 24 individuals who developed segmental wall motion abnormalities, of whom only six had exhibited concomitant ST-segment changes on ECG (66).

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

Thus intraoperative two-dimensional transesophageal echocardiography appears to be a sensitive means of identifying segmental wall motion abnormalities indicative of early myocardial ischemia that occur before either ST-segment changes or abnormal wedge pressures develop. In addition, transesophageal Doppler monitoring has been found to correlate with thermodilution cardiac output measurements taken at end-expiration, with r values of 0.94 (preclamp), 0.70 (during clamping), and 0.85 (after clamping) (67). Vasodilators administered during aortic cross-clamping decrease the systemic arterial blood pressure and afterload that the heart must pump against. Nitroglycerin and nitroprusside are the most common agents used to achieve this effect. Nitroglycerin is a potent venous vasodilator and a mild arterial vasodilator. It decreases myocardial oxygen demand, lessens myocardial ischemia by reducing diastolic volume, and may increase oxygen delivery to ischemic myocardium by dilating coronary arteries and collateral vessels. Nitroprusside, on the other hand, is a relatively balanced arterial and venous vasodilator. It has greater relaxing effects on coronary resistance vessels and less influence on coronary collateral vessels. In this regard, nitroprusside decreases blood flow in the ischemic myocardium of patients with stable angina and increases ST-segment elevations in those with acute myocardial infarction, supporting the suggestion by Fremes and his colleagues that it may cause myocardial oxygen supply to be reduced in patients with significant cardiac disease (68). In a related study by this later group, 33 hypertensive patients undergoing coronary bypass procedures had their arterial pressure decreased to 85 mmHg with both nitroglycerin and nitroprusside, but only the nitroglycerin resulted in improved myocardial metabolism, as assessed by myocardial lactate flux (69). Volume loading may be an important adjunct to the use of vasodilators. The Brigham group reported on 50 patients undergoing abdominal aortic aneurysm resection, of whom 10 received customary preoperative maintenance fluids, 23 received 1500 mL of balanced salt solution in the 12 hours before the operative procedure in order to keep the pulmonary capillary wedge pressure at 10 to 13 mmHg, and 17 received the same fluid regimen with the addition of vasodilators (70). Fourteen of the latter patients received nitroprusside at a rate of 1.5 to 6.0 mg/kg/min, and three received nitroglycerin at a rate of 0.5 to 3.5 mg/kg/min. Both vasodilators were given after aortic cross-clamping to control afterload, and additional volume expansion was used to maintain a constant preload. However, the mean arterial blood pressure and cardiac index fell, and furthermore the cardiac index remained depressed after aortic declamping. These events occurred with increased pulmonary capillary wedge pressures without corresponding increases in cardiac index, suggesting myocardial depression. In this setting vasodilators did not appear useful. The combined administration of inotropic and vasodilator agents in patients after coronary artery bypass

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grafting has been advocated by the Stanford group (71). Volume loading with the addition of vasodilators and dopamine increased the cardiac index 45%, increased the left ventricular stroke work index 30%, decreased systemic vascular resistance 41%, and decreased mean arterial pressure only 10%. In comparison with dopamine alone, addition of vasodilators and volume infusion increased the cardiac index 14% and decreased systemic vascular resistance 24%, without a significant change in the left ventricular stroke work index. This form of combined therapy appears to facilitate beneficial responses from both drugs, while minimizing their individual disadvantages. In this regard, the usefulness of dopamine is limited if the preload is decreased, when its enhanced inotropic activity may actually increase myocardial oxygen demand and consumption. Similarly, nitroprusside alone is contraindicated when left ventricular failure is complicated by hypotension, when it may also decrease cardiac output if the preload is inadequate. The usefulness of vasodilators in cardiac surgery procedures may relate to the severe vasoconstriction known to occur after coronary artery grafting and cardiopulmonary bypass (71). In addition, cardiac output with ventricular failure is more sensitive to afterload than preload, and patients with severe ventricular failure would more likely benefit from nitroprusside afterload reduction. Another important issue regarding vasodilators is their effect on regional blood flow in ischemic tissue. For example, it is in patients requiring high thoracic-aortic cross-clamping that vasodilator therapy should be most useful. However; as noted in canine experiments, thoracic aortic cross-clamping and infusion of nitroprusside causes the mean arterial blood pressure below the occlusion to decrease, causing further reductions in renal and spinal cord blood flow, events that may negate any cardiac protection afforded by the vasodilator (72,73). On the other hand, during infrarenal aortic cross-clamping in similar laboratory studies, nitroprusside caused a 30% decrease in arterial pressure, brought cardiac output back down to baseline, and appeared to normalize hepatic and intrarenal blood flow (74). Thus, with infrarenal aortic occlusion, renal and splanchnic blood flow do not appear to be adversely affected by the administration of nitroprusside. In summary, vasodilator and inotropic drug use during aortic cross-clamping is controversial. Those with the poorest myocardial function, most dependent on afterload reduction, would appear to benefit the greatest from use of vasodilators, but perfusion pressures below the level of high aortic cross-clamping in such settings must be closely monitored to ensure adequate regional blood flow to vital organs. Finally, there is the issue of intraoperative thoracic epidural anesthesia combined with light general anesthesia versus standard balanced general anesthesia for patients undergoing aortic surgery. In a study of 173 patients equally divided between these two techniques undergoing operations for abdominal aortic aneurysms and aortoiliac

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occlusive disease, thoracic epidural offered no advantage over general anesthesia (75). A similar conclusion was reached comparing epidural versus general anesthesia in patients undergoing infrainguinal arterial reconstruction (76).

Preoperative Pulmonary Assessment Adequate pulmonary assessment is dependent on acquisition of a detailed history, the presence or absence of specific physical findings, measurement of arterial blood gases, and performance of certain pulmonary function tests using spirometric techniques. Historically, the number of pack-years of smoking becomes important, with 20 pack-years appearing to be the level at which significant pulmonary risks become apparent (77). The presence or extent of shortness of breath with activity, prior episodes of respiratory failure, existence of asthma, and exposure to noxious environmental agents are all relevant in assessing the pulmonary status. The quantity and nature of sputum production is particularly important in patients with long-standing lung disease, because this may allow one to distinguish chronic bronchitis from emphysema. The physical examination easily detects hypoventilation in weak or debilitated patients, and hyperinflation in patients with chronic obstructive pulmonary disease. The ability to climb one or two flights of stairs at a steady pace without dyspnea is a practical test, and if such cannot be done, further tests may be needed to define the pulmonary status. Chest radiographs augment the findings of routine physical examination. Arterial blood gases should be measured preoperatively on all patients identified as being at high risk by history, physical examination, or spirometric testing. Oxygenation is assessed by measuring PaO2 during roomair breathing, and is dependent on the appropriate matching of alveolar gas to pulmonary blood flow. Ventilation is assessed by measuring PaCO2, inasmuch as CO2 removal is dependent entirely on alveolar ventilation. Arterial blood gases define both alveolar hypoventilation (PaCO2 >45 mmHg) and significant right-to-left shunting, diffusion block and ventilation–perfusion mismatch (PaO2 <70 mmHg). Definitions of normal pulmonary function tests (Table 12.3) are useful in assessing the preoperative status of vascular surgery patients. Tidal volume (VT) is the amount of air exchanged during a normal resting ventilatory cycle. Vital capacity (VC), also known as forced expiratory volume (FEV) or forced vital capacity (FVC), is the volume of air expelled with maximal exhalation after a maximal inspiration. Functional residual capacity (FRC) is the volume of air remaining in the lungs after VT exhalation. Typical normal values for these volumes are VT of 7 to 8 mL/kg of body weight, VC of 30 to 50 mL/kg of body

TABLE 14.3 Preoperative pulmonary assessment Normal Vital capacity (VC) Forced expiratory volume in 1 second (FEV1) Maximal midexpiratory flow (FEF25–75) Maximal ventilatory volume (MVV) PaO2 room air PaCO2 room air

High Risk

30–55 mL/kg; < 30–50% > 80% predicted > 80% predicted < 40–50% 150–200 L/min; > 80% predicted 150–500 L/min; > 80% predicted 85 ± 5 mmHg 40 ± 4 mmHg

< 35–50% < 35–50% < 50–55 mmHg > 45–55 mmHg

weight, and FRC of 15 to 30 mL/kg of body weight. Volume measurements are reported as the percentage of predicted value, with 80% to 120% being considered within the normal range. Expiratory flow rates are commonly expressed as volume/time, such as FEV0.5, which defines the volume of forced expiration over 0.5 second. This measure is dependent on patient effort and reveals the existence or absence of obstructive airway disease. Flow measurements are also expressed as a percentage of the expected value for the individual patient being studied. FEV1 is a similar measure except that it assesses volume exhaled over 1 second. The FEF25–75 (maximal mid-expiratory flow rate, MMFR) is most sensitive to disease in smaller airways and is considered normal when greater than 80% predicted or 150 to 200 L/min. The maximal ventilatory volume (MVV) an individual can generate is highly dependent on patient effort, the ratio of dead space to tidal volume, and lung compliance. MVV usually ranges between 150 and 500 L/min. MVV is one of the more sensitive tests for predicting pulmonary complications because an abnormal value (< 80% predicted) may be caused by general patient weakness as well as pulmonary disease. Static compliance is defined as the VT divided by the peak inspiratory pressure and is normally 100 to 200 mL/cmH2O. An esophageal balloon is required to measure compliance. Effective compliance is the VT/plateau pressure on a ventilator, with normal being greater than 50 mL/cmH2O. Inspiratory force (IF) is defined as the maximal subatmospheric pressure that can be exerted on a closed airway. A normal IF is –100 cmH2O, with –20 cmH2O being the lower limit of acceptability. Patients with obstructive defects have an essentially normal VC but abnormal expiratory air flows such as FEV1, FLV0.5, and FEF25–75, whereas patients with restrictive defects have a low VC but normal expiratory air flows. Some have suggested that the MVV, as measured directly or approximated by the FEV1 ¥ 30, is the best test to predict postoperative pulmonary complications. With a MVV less than 50% of predicted, respiratory complications developed in a high proportion of patients undergoing thoracotomy, and in the majority, multiple

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

complications ensued (78). Other more detailed tests such as measurement of functional residual capacity using helium dilution or nitrogen washout, diffusing capacity, or response of arterial PaO2 to breathing 100% oxygen are rarely necessary in these preoperative assessments. Variations in pulmonary function studies over a 24-h period for patients with normal lungs were 500 for FEV1, 5% for FVC, and 13% for FEF25–75. Similar variations in patients with chrome obstructive pulmonary disease were 130, 0, 11%, and 23% respectively (79). Thus, with interventions such as use of bronchodilators, these percentages represent the minimal changes necessary to assume that a significant therapeutic effect has occurred. The importance of blood gas analysis and spirometrically derived pulmonary function tests is evidenced in a pulmonary complication rate of 3% in patients with chronic obstructive pulmonary disease with normal preoperative tests, compared with pulmonary complications in 70% of those with abnormal tests, the most important predictor being a PaCO2 greater than 45 mmHg and a PaO2 less than 60 mmHg (80). Even patients at increased risk with seemingly prohibitive function, such as MVV less than 50 L/min and FEF25–75 less than 50 L/min, can undergo major operative procedures with a low mortality and an acceptable pulmonary complication rate (81). Some have questioned the value of preoperative spirometry to detect surgically important occult disease with a beneficial effect on patient outcome (82). Poor performance on spirometric testing is not a contraindication to a major vascular procedure, but rather a means of identifying those patients who will require special preoperative preparation and attention to postoperative mechanical ventilation. Patients with chronic obstructive pulmonary disease, asthma, or chronic bronchitis should undergo respiratory flow measurements before and after administration of bronchodilators. Intensive preoperative preparation using these agents and respirator exercises until pulmonary function is optimized, as documented by spirometry, has reduced by half the pulmonary complication rate associated with chronic obstructive pulmonary disease (83). Postoperative respiratory complications in these patients are best prevented by discontinuation of smoking and vigorous preoperative and postoperative pulmonary toilet (84). In a small series of patients at Duke University undergoing abdominal aortic aneurysm resection with very severe preoperative pulmonary compromise, there was no mortality, and only 20% required prolonged ventilatory support (85). Preoperatively all patients stopped smoking for at least 1 month, pulmonary infection was treated with antibiotics, nebulized bronchodilators and humidified air were administered, and exercises were instituted that stressed improved inspiratory effort. Intraoperatively, blood filters were used for all blood transfusions, minimization of anesthetic time was emphasized, blood use was lessened, and the pulmonary capillary wedge pressure was used as a guide for fluid administration. Postopera-

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tively, these patients were mechanically ventilated, but extubated as soon as possible. They were reintubated early if such became necessary. The amount of narcotics usually given was reduced, and patients were ambulated early. All of these factors lessened operative mortality and morbidity in vascular surgery patients whose preoperative pulmonary function was marginal. Another issue regarding patients at high risk of pulmonary complications during aortic reconstruction has been the use of the left flank retroperitoneal incision rather than the more standard transperitoneal approach (86,87). This incision may decrease pulmonary complications, although not all groups have found this to be the case (88).

Conclusion The objectives of perioperative cardiopulmonary assessment and intervention in patients who are candidates for vascular surgery are twofold. First is performance of the surgical procedure with minimal morbidity and mortality. Second is an improved long-term survival of the patient, in particular by reducing late cardiac mortality. Patients undergoing preoperative coronary artery bypass prior to peripheral vascular reconstructions have been found to have excellent outcomes, with operative mortality reported as low as 0.2% in one large study (89). Even severely ill patients have been able to undergo abdominal aortic aneurysm resection with a mortality rate under 6%, despite such factors as the use of home oxygen, a PaO2 less than 50 mmHg, FEF25–75 less than 25%, New York Heart Association classification III or IV, active angina pectoris, an ejection fraction less than 30%, recent congestive heart failure, complex ventricular ectopy, large left ventricular aneurysms, severe valvular heart disease, or unreconstructable coronary artery disease (90). The late 43% mortality from heart disease reported by Crawford and his colleagues among 949 patients undergoing treatment for aortoiliac occlusive disease should be lessened in contemporary practice (91). For instance, 5-year survival rates of more than 90% may be expected following coronary artery reconstruction, even in patients with multiplevessel disease (92–94). One of the first long-term studies on an aggressive preoperative cardiac assessment and management in patients undergoing peripheral vascular surgery involved 246 patients with infrarenal abdominal aortic aneurysms treated at the Cleveland Clinic (95). Severe coronary artery disease was documented in 39%, of whom 28% underwent myocardial revascularization with a mortality rate of 5.7%. A total of 56 patients in this subset underwent staged aneurysm repair with an accompanying 1.8% mortality rate. Over the follow-up interval, 25% of the patients in this group died, leaving a 5-year survival rate of 75%, but there was only a 5% cardiac mortality rate. This survival was nearly identical to that for patients having both trivial coronary lesions and severe coronary

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involvement without an aneurysm who had undergone coronary revascularization, and was much better than the reported 5-year survival rate of only 29% for patients with uncorrectable or inoperable coronary artery disease. Although some might contend that expensive and invasive coronary screening programs are unnecessary in the majority of patients undergoing vascular surgery including elective aortic surgery and carotid surgery (96–98), considerable evidence supports more aggressive treatment of correctable coronary artery disease in vascular surgery patients, either in the preoperative/perioperative period or in the postoperative period. The challenge for vascular surgeons is to better define those situations that will allow for improved specificity of noninvasive cardiac testing while maintaining excellent sensitivity for detecting important coronary artery disease.

References 1. Hertzer NR. Clinical experience with preoperative coronary angiography. J Vasc Surg 1985; 2: 510. 2. Hertzer NR. Fatal myocardial infarction following abdominal aortic aneurysm resection. Three hundred forty-three patients followed 6–11 years postoperatively. Ann Surg 1980; 192: 667. 3. Hertzer NR. Fatal myocardial infarction following lower extremity revascularization. Two hundred seventy-three patients followed six to eleven postoperative years. Ann Surg 1981; 193: 492. 4. Nicolaides AN. The diagnosis and assessment of coronary artery disease in vascular patients. J Vasc Surg 1985; 2: 501. 5. Krupski WC, Layug EL, et al. Comparison of cardiac morbidity between aortic and infrainguinal operations. J Vasc Surg 1992; 15: 354. 6. Beven EG. Routine coronary angiography in patients undergoing surgery for abdominal aortic aneurysm and lower extremity occlusive disease. J Vasc Surg 1986; 3: 682. 7. Goldman L, Caldera DL, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977; 297: 845. 8. Calvin JE, Kieser TM, et al. Cardiac mortality and morbidity after vascular surgery. Can J Surg 1986; 29: 93. 9. Jeffrey CC, Kunsman J, et al. A prospective evaluation of cardiac risk index Anesthesiology 1983; 58: 462. 10. McEnroe CS, O’Donnell TF, et al. Comparison of ejection fraction and Goldman risk factor analysis to dipyridamole–thallium 201 studies in the evaluation of cardiac morbidity after aortic aneurysm surgery. J Vasc Surg 1990; 11: 497. 11. Lette J, Waters D, et al. Multivariate clinical models and quantitative dipyridani–thallium imaging to predict cardiac morbidity and death after vascular reconstruction. J Vasc Surg 1991; 14: 160. 12. Cooperman M, Pflug B, et al. Cardiovascular risk factors in patients with peripheral vascular disease. Surgery 1978; 84: 505. 13. Steen PA, Tinker JH, Tarhan S. Myocardial reinfarction after anesthesia and surgery. JAMA 1978; 239: 2566.

14. Rao TLK, Jacobs KR. Reinfarction following anesthesia in patients with myocardial infarction, Anesthesiology 1983; 59: 449. 15. Gage AA, Bhayana JN, et al. Assessment of cardiac risk in surgical patients. Arch Surg 1977; 112: 1488. 16. Cutler BS, Wheeler HB, et al. Assessment of operative risk with electrocardiographic exercise testing in patients with peripheral vascular disease. Am J Surg 1979; 1 37: 484. 17. Cutler BS, Wheeler RB, et al. Applicability and interpretation of electrocardiographic stress testing in patients with peripheral vascular disease. Am J Surg 1981; 141: 501. 18. Weiner DA, Ryan TJ, et al. Exercise stress testing. Correlations among history of angina, ST-segment response and relevance of coronary-artery disease in the coronary artery surgery study (CASS). N EngI J Med 1979; 301: 230. 19. Selwyn AR. The value of Holter monitoring in managing patients with coronary artery disease. Circulation 1987; 75 (Suppl 11): 11–31. 20. McPhail N, Calvin JE, et al. The use of preoperative exercise testing to predict cardiac complications after arterial reconstruction.J Vasc Surg 1988; 7: 60. 21. Mark DB, Hlatky MA, et al. Exercise treadmill score for predicting prognosis in coronary artery disease. Ann Intern Med 1987; 106: 793. 22. Jones RH, Douglas JM, et al. Noninvasive radionuclide assessment of cardiac function in patients with peripheral vascular disease. Surgery 1979; 85: 59. 23. Pasternack PF, Imparato AM, et al. The value of radionuclide angiography as a predictor of perioperative myocardial infarction in patients undergoing abdominal aortic aneurysm resection. J Vasc Surg 1984; 1: 320. 24. Mosley JG, Clarke JMF, et al. Assessment of myocardial function before aortic surgery by radionuclide angiocardiography. Br J Surg 1985; 72: 886. 25. Pasternack PF, Imparato AM, et al. The value of the radionuclide angiogram in the prediction of parioperative myocardial infarction in patients undergoing lower extremity revascularization procedures. Circulation 1985; 72 (Suppl): Il-213. 26. Kazmers A, Cerqueira MD. Zierler E. The role of preoperative radionuclide left ventricular ejection fraction for risk assessment in carotid surgery Arch Surg 1988; 123: 416. 27. Kazmers A, Cerqueira MD, Zierler RE. The role of preoperative radionuclide ejection fraction in direct abdominal aortic aneurysm repair. J Vasc Surg 1988; 8: 128. 28. Kazmers A, Cerqueira MD, Zierler RE. Perioperative and late outcome in patients with left ventricular ejection fraction of 35% or less who require major vascular surgery. J Vasc Surg 1988; 8: 307. 29. Kazmers A, Moneta GL., et al. The role of preoperative radionuclide ventriculography in defining outcome after revascularizarion of the extremity. Surg Gynecol Obstet 1990; 171: 481. 30. Bonow RD. Exercise testing and radionuclide procedures in high-risk populations. Circulation 1987; 75 (Suppl): 11–18. 31. Albro PC, Gould KL, et al. Noninvasive assessment of coronary stenoses by myocardial imaging during phar-

Chapter 14 Cardiopulmonary Assessment for Major Vascular Reconstructive Procedures

32.

33.

34.

35.

36.

37.

38.

39.

40

41.

42.

43.

44. 45.

46.

47.

48.

macologic coronary vasodilation: III. Clinical trials. Am J Cardiol 1978; 42: 751. Leppo J, Boucher CA, et al. Serial thallium-201 myocardial imaging after dipyridamole infusion: diagnostic utility in detecting coronary stenoses and relationship to regional wall motion. Circulation 1982; 66: 649. Boucher CA, Brewster DC, et al. Determination of cardiac risk by dipyridamole–thallium imaging before peripheral vascular surgery. N Engl J Med 1985; 312: 398. Brewster DC, Okada RD, et al. Selection of patients for preoperative coronary angiography: use of dipvridamole-stress-thallium myocardial imaging. J Vasc Surg 1985; 2: 504. Cutler BS, Leppo JA. Dipyridamole thallium 201 scintigraphy to detect coronary artery disease before abdominal aortic surgery. J Vasc Surg 1987; 5: 91. Eagle KA, Singer DE, et al. Dipyridamole–thallium scanning in patients undergoing vascular surgery: optimizing preoperative evaluation of cardiac risk. JAMA 1987; 257: 2185. Sachs RN, Tellier P, et al. Assessment by dipyridamole thallium-201 myocardial scintigraphy of coronary risk before peripheral vascular surgery. Surgery 1988; 103: 584. Fletcher JP, Antico VF, et al. Dipyridamole–thallium scan for screening of coronary artery disease prior to vascular surgery. J Cardio Vasc Surg 1988; 29: 666. Cutler BS, Hendel RC, Leppo JA. Dipyridamole– thallium scintigraphy predicts periopcrative and longterm survival after major vascular surgery. J Vasc Surg 1992; 15: 972. Dilsizian V, Rocco TP, et al. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med 1990; 323: 141. Strawn DJ, Guernsey JM. Dipyridamole thallium scanning in the evaluation of coronary artery disease in elective abdominal aortic surgery. Arch Surg 1991; 126: 880. Cambria RP, Brewster DC, et al. The impact on selective use of dipyridamole–thallium scans and surgical factors on the current morbidity of aortic surgery. J Vasc Surg 1992; 15: 43. Schulman DS, Francis CK, et al. Thallium-201 stress imaging in hypertensive patients. Hypertension 1987; 10: 16. Keltz TN, Innerfield M, et al. Dipyridamole-induced myocardial ischemia. JAMA 1987; 257: 1515. Mangano DT; London MJ, et al. Dipyridamole thallium201 scintigraphy as a preoperative screening test: a reexamination of its predictive potential. Circulation 1991; 84: 492. Lalka SG, Sawada SG, et al. Dobutamine stress echocardiography as a predictor of cardiac events associated with aortic surgery. J Vasc Surg 1992; 15: 831. Poldermans D, Fioretti PM, et al. Dobutamine stress echocardiography for assessment of perioperative cardiac risk in patients undergoing major vascular surgery. Circulation 1993; 87: 1506. Davila-Roman VG, Waggoner AD, et al. Dobutamine stress echocardiography predicts surgical outcome in patients with an aortic aneurysm and peripheral vascular disease. J Am Coll Cardiol 1993; 21: 957.

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49. Mertes H, Sawada SG, et al. Symptoms, adverse effects, and complications associated with dobutamine stress echocardiography. Experience in 1,118 patients. Circulation 1993; 88: 15. 50. Pasternack PF, Grossi EA, et al. Silent myocardial ischemia monitoring predicts late as well as perioperative cardiac events in patients undergoing vascular surgery. J Vasc Surg 1992; 16: 171 51. Mangano DT, Browner WS, et al. Association of penrioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery. N Engl J Med 1990; 323: 1781. 52. Brown OW, Hollier LH, et al. Abdominal aortic aneurysm and coronary artery disease. A reassessment. Arch Surg 1981; 116: 1484. 53. Reigel MM, Hollier LH, et al. Late survival in abdominal aortic aneurysm patients: the role of selected myocardial revascularization on the basis of clinical symptoms. J Vasc Surg 1987; 5: 222. 54. Eagle KA. Brundage BH, et al. Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). J Am Coll Cardiol 1996; 27(4): 910–48. 55. McCleary AJ, Maritati G, Gough MJ. Carotid endarterectomy; local or general anaesthesia? Eur J Vasc Endovasc Surg 2001; 22(1): 1–12. 56. Poldermans D, Boersma E, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N Engl J Med 341: 1789–94, 1999. 57. Blackshear JL, Kopecky SL, et al. Management of atrial fibrillation in adults: prevention of thromboembolism and symptomatic treatment. Mayo Clin Proc 1996; 71: 150–60. 58. Vacanti CJ, VanHouten RJ, Hill RC. A statistical analysis of the relationship of physical status to postoperative mortality in 68, 388 cases. Anesth Analg 1970; 49: 564. 59. Whittemore AD, Clowes AW, et al. Aortic aneurysm repair: reduced operative mortality associated with maintenance of optimal cardiac performance. Ann Surg 1980; 192: 4 14. 60. Romberger RA, McGregor B, DePalma RG. Optimal fluid management after aortic reconstruction: a prospective study of two crystalloid solutions. J Vasc Surg 1986; 4: 164. 61. Babu SC, Sharma PVP, et al. Monitor-guided responses. Operability with safety is increased in patients with peripheral vascular disease. Arch Surg 1980; 115: 1384. 62. Kalman PG, Wellwood MR, et al. Cardiac dysfunction during abdominal aortic operation: the limitations of pulmonary wedge pressures. J Vasc Surg 1986, 3: 773. 63. Berlauk JF, Abrams JH, et al. Preoperative optimization of cardiovascular hemodynamics improves outcome in peripheral vascular surgery: a prospective, randomized clinical trial. Ann Surg 1991; 214: 289. 64. Dauchot PJ, DePalma R, et al. Detection and prevention of cardiac dysfunction during aortic surgery. J Surg Res 1979; 26: 574.

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65. Roizen MF, Beaupre PN, et al. Monitoring with twodimensional transesophageal echocardiography. Comparison of myocardial function in patients undergoing supraceliac, suprarenal–infraceliac, or infrarenal aortic occlusion. J Vasc Surg 1984; 1: 300. 66. Smith JS, Cahalan MK, et al. lntraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two-dimensional transesophageal echocardiography. Circulation 1985; 72: 1015. 67. Perrino AC Jr, Fleming J, LaMantia KR. Transesophageal doppler cardiac output monitoring: performance during aortic reconstructive surgery. Anesth Analg 1991; 73: 705. 68. Fremes SE, Weisel RD, et al. A comparison of nitroglycerin and nitroprusside. II. The effects of volume loading. Ann Thorac Surg 1985; 39: 61. 69. Fremes SE, Weisel RD, et al. A comparison of nitroglycerin and nitroprusside. I. Treatment of postoperative hypertension. Ann Thorac Surg 1985; 39: 53. 70. Grindlinger GA, Vegas AM, et al. Volume loading and vasodilators in abdominal aortic aneurysmectomy. Am J Surg 1980; 139: 480. 71. Miller DC, Stinson EB, et al. Postoperative enhancement of left ventricular performance by combined inotropic vasodilator therapy with preload control. Surgery 1980; 88: 108. 72. Gelman S, Reves JG, et al. Regional blood flow during cross-clamping of the thoracic aorta and infusion of sodium nitroprusside. J Thorac Cardiovasc Surg 1983; 85: 287. 73. Lasehinger JC, Owen J, et al. Detrimental effects of sodium nitroprusside on spinal cord motor tract perfusion during thoracic aortic cross-clamping. Surg Forum 1987; 38: 195. 74. Gelman S, Petel K, et al. Renal and splanchnic circulation during infrarenal aortic cross-clamping. Arch Surg 1984; 119: 1394. 75. Baton J-F, Bertrand M, et al. Combined epidural and general anesthesia versus general anesthesia for abdominal aortic surgery. Anesthesiology 1991; 75: 611. 76. Rivets SP, Scher LA, et al. Epidural versus general anesthesia for infrainguinal arterial reconstruction. J Vasc Surg 1991; 14: 764. 77. Auchincloss JH. Preoperative evaluation of pulmonary function. Surg Clin N Am 1974; 54: 1015. 78. Boysen PG, Block AJ, Moulder PV. Relationship between preoperative pulmonary function tests and complications after thoracotomy. Surg Gynecol Obstet 1981; 153: 813. 79. Pennock BE, Rogers RM, McCaffree DR. Changes in measured spirometric indices. What is significant? Chest 1981; 80: 97. 80. Gaensler ES, Weisel RD. The risks in abdominal and thoracic surgery in COPD. Postgrad Med 1973; 54: 183. 81. Williams CD, Brenowitz JB. “Prohibitive” lung function and major surgical procedures. Am J Surg 1976; 132: 763.

82 Lawrence VA, Page CP, Harris GD. Preoperative spirometry before abdominal operations. A critical appraisal of its predictive value. Arch Intern Med 1989; 149: 280. 83. Gracey DR, Divertie MB, Didier EP. Preoperative pulmonary preparation of patients with chronic obstructive pulmonary disease. A prospective study. Chest 1979; 76: 123. 84. Jackson CV. Preoperative pulmonary evaluation. Arch Intern Med 1988; 148: 2120. 85. Smith PK, Fuchs JCA, Sabiston DC. Surgical management of aortic abdominal aneurysms in patients with severe pulmonary insufficiency. Surg Gynecol Obstet 1980; 151: 407. 86. Sicard GA, Freeman MB, et al. Comparison between the transabdominal and retroperitoneal approach for reconstruction of the infrarenal abdominal aorta. J Vasc Surg 1987; 5: 19. 87. Shephard AD, Tollefson DJF, at al. Left flank retroperitoneal exposure: a technical aid to complex aortic reconstruction. J Vasc Surg 1991; 14: 283. 88. Cambria RP, Brewster DC, at al. Transperitoneal versus retroperitoneal approach for aortic reconstruction: a randomized prospective study. J Vasc Surg 1990; 11: 314 89. Reul GJ Jr, Cooley DA, et al. Thc effect of coronary bypass on the outcome of peripheral vascular operations in 1093 patients. J Vasc Surg 1986; 3: 788. 90. Rollier LH, Reigel MM, et al. Conventional repair of abdominal aortic aneurysm in the high-risk patient: a plea for abandonment of nonresective treatment. J Vasc Surg 1986; 3: 712. 91. Crawford ES, Bomberger RA, et al. Aortoiliac occlusive disease: factors influencing survival and function following reconstructive operation over a twenty-five year period. Surgery 1981; 90: 1055. 92. Crawford ES, Morris GC Jr, et al. Operative risk in patients with previous coronary artery bypass. Ann Thorac Surg 1978; 26: 215. 93. Loop FD, Cosgrove DM, et al. An 11 year evolution of coronary arterial surgery (1967–1978). Ann Surg 1979; 190: 444. 94. Mahar LJ, Steen PA, et al. Perioperative myocardial infarction in patients with coronary artery disease with and without aorta-coronary bypass grafts. J Thorac Cardiovasc Surg 1978; 76: 533 95. Hertzer NR, Young JR, et al. Late results of coronary bypass in patients with infrarenal aortic aneurysms. The Cleveland Clinic Study. Ann Surg 1987; 205: 360. 96. Golden MA, Whittemore AD, et al. Selective evaluation and management of coronary artery disease in patients undergoing repair of abdominal aortic aneurysms. Ann Surg 1990; 212: 415. 97. Taylor LM, Yeager RA, et al. The incidence of perioperative myocardial infarction in general vascular surgery. J Vasc Surg 1991; 15: 52. 98. Yeager RA, Moneta GL, et al. Analysis of risk factors for myocardial infarction following carotid endarterectomy. Arch Surg 1989; 124: 1142.

PART III

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

Basic Vascular and Endovascular Techniques

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 15 Vascular Sutures and Anastomoses Henry Haimovici

The history of vascular sutures and anastomoses is that of the beginning of blood vessel surgery itself (Chapter 1). It was not until 1889 that a successful repair of arteries was achieved by Jassinowsky (1). He used fine curved needles and fine silk and made interrupted stitches placed close together but avoided penetrating the intima. In 1899, Dörfler published the essential features of his method, which consisted of continuous sutures embracing all the coats of the vessel (2). He was the first to point out that the penetration of the intima did not lead to any changes in, or interfere with, the patency of the lumen. In 1901, Clermont successfully reunited the ends of a divided inferior vena cava by means of a continuous fine silk suture (3). In 1900, Carrel began his pioneering studies of vascular anastomoses (4). In the beginning, his method differed from Dörfler’s in that he avoided penetrating the intima. Later, together with Guthrie, he discontinued avoiding the intima and instead included it in suturing the vessel. Carrel and Guthrie added other modifications to this technique until it was well adapted for arterioarterial, venovenous, or arteriovenous anastomoses (5). The list of surgeons who contributed before and after the basic principles of vascular anastomoses were evolved by Carrel is a long one. It is enough to mention only that, since the advent of the contemporary vascular era, a number of further improvements were made to meet the needs of newer and more complex vascular techniques.

Exposure and Mobilization of Arteries After the various anatomic layers covering the vessels have been divided and the involved vascular bundle has been exposed, attention is directed to the actual dissection and mobilization of the artery or vein or both. If the vessels are surrounded by a vascular sheath, as most are, the latter can be lifted off and opened. A vascular sheath is a tubular structure investing both the artery and its adjacent vein. Its structural characteristics are variable and depend on the location and the specific segment of the vessel. Usually a thin layer of cellular tissue separates the sheath from the vascular wall. The ease of exposing and mobilizing an artery or vein depends largely on whether the vessel is normal or diseased. A normal artery can be easily mobilized by identifying and opening its sheath (Fig. 15.1A and B). Often this procedure can be facilitated by ligating and dividing small crossing veins that course between larger accompanying veins, particularly those which parallel arteries peripheral to the groin. After incision of the sheath along its axis, the artery is freed on each side by means of the blunt tip of curved scissors (Fig. 15.1C). In dissecting its posterior wall, great care is necessary to avoid injuring a possible invisible branch. This is achieved by using the tip of a Mixter clamp, which facilitates the dissection from one side of the artery to the other until the clamp passes behind the artery without difficulty. Then an umbilical or silicone rubber tape is passed around the artery (Fig. 15.1D). By

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lifting the artery with the tape, the dissection can proceed proximally and distally under direct vision. Exposure of a major artery with a significant branch is made by first mobilizing the main trunk above and below the branch, and then freeing the latter (Fig. 15.2A and B). A similar procedure is used in mobilizing a bifurcation (Fig. 15.2C). In doing so, care must be taken to avoid

injuring the collateral vessels as well as the adjacent vein and its tributaries (Fig. 15.2D). A diseased artery is often more difficult to mobilize because of loss of identity of its sheath as a result of perivascular fibrosis. Injection of a few milliliters of saline solution or procaine under the superficial layer of the sheath may help in lifting it from the underlying artery. After a cleavage plane is developed with the tip of blunt scissors or a fine clamp, the sheath is opened longitudinally. Mobilization of the diseased artery, however, may be more laborious and difficult than for a normal one because of extensive and dense perivascular fibrosis and hypervascularization of the sheath. Because the same process extends to the collateral branches from the main trunk, great care must be exercised in freeing not only the main trunk but its branches as well.

Clamping of an Artery

FIGURE 15.1 An artery and its sheath. (Redrawn from Cormier JM. Techniques générales de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris: Masson et Cie, 1970.)

Temporary control of arteries can be achieved either by occluding tapes or by cross- or lateral clamping (Fig. 15.3). The latter results in only a partial occlusion of the lumen, usually useful in operations, particularly in procedures involving the thoracic aorta. Before clamping is done, digital palpation of the arterial wall may disclose the extent of calcified plaques and soft areas. The best way to assess the degree of mural involvement is to compress the artery between the index finger and the thumb, after temporary occlusion is obtained with tapes placed tightly around the vessel. Arterial clamps are of several designs. They are devised to prevent damage to the vessel, notably to the intima and its atherosclerotic plaques. Unfortunately, few of the current arterial clamps are entirely atraumatic, and they must be used with extreme care and minimal force if

FIGURE 15.2 Freeing an artery from its sheath and mobilizing the artery with a major collateral vessel or its bifurcation. (Redrawn from Cormier JM. Techniques générales de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris: Masson et Cie, 1970.)

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FIGURE 15.3 Clamping of an artery. (A and B) Cross-clamping. (C) Lateral clamping. (Redrawn from Cormier JM. Techniques générales de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris: Masson et Cie, 1970.)

injury is to be minimized. For a medium-sized artery, such as the femoral, popliteal, axillary, or brachial, it is best to use double-looped silicone rubber vessel loops. For the aorta or iliac, arterial clamps are most suitable. Although cross-clamping is most commonly used for temporary control, lateral clamping may be indicated in some cases, except in the ascending or descending thoracic aorta. One of the possible complications of lateral clamping, especially of the abdominal aorta, is fracture of a calcific plaque, usually located on its posterior wall. If the latter is noted beforehand, it may contraindicate lateral clamping for fear of intimal damage with subsequent thrombosis. Tolerance of tissues to temporary arterial clamping varies with the area involved. The brain and the kidney, as is well known, are extremely sensitive to anoxia due to clamping of the respective artery. Similarly, crossclamping of the thoracic aorta cannot usually be tolerated for more than 30 to 45 minutes because of the ensuing paraplegia unless preexisting collaterals are present. Prolonged cross-clamping of the infrarenal abdominal aorta is another such example, albeit of lesser intolerance. If prolonged, striated muscle ischemia may induce a serious metabolic syndrome, which may lead to myoglobinuria, renal shutdown, and possible gangrene of the extremities. It behooves the surgeon, therefore, to minimize the duration of clamping of a major artery or to use methods to minimize ischemia.

Arterial Ligation Arterial ligations are rarely indicated, except as a temporary measure for hemorrhage control or in cases in which

the vessels cannot be repaired because of the extent of the lesions, presence of infection, or poor general condition of the injured individual. Although arterial ligations were practiced mostly for battle casualties, they may also be indicated in civilian injuries, but to a lesser extent. Since the Korean War, the introduction of arterial repairs has superseded arterial ligation whenever possible. Unlike the practice in the past, ligations are rarely used today as a definitive treatment for arterial aneurysms or arteriovenous fistulas.

Technique of Ligation In the presence of vascular injury, the first step is control of hemorrhage. Indeed, preliminary hemostasis is absolutely necessary before a formal ligation of the traumatized vessel can be achieved. This may be accomplished by the use of a tourniquet around the root of the extremity proximal to the traumatized vessel. An alternative method is digital compression or application of vascular clamps on the injured vessels, both proximal and distal to the injury whenever possible. Wide exposure of the vessels is essential for good access to an adequate segment both above and below the laceration of the vessels. In doing so, every effort must be made to preserve the collaterals, especially the muscular branches. Once hemostasis and exposure have been achieved, mobilization of the involved artery is carried out according to the principles described above. The material used for ligation of the arteries depends on the size of the vessel. For small vessels, a simple or double ligature of fine catgut or silk or synthetic fibers may suffice. For arteries of medium-sized diameter, the vessel

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FIGURE 15.4 Types of arterial ligations. (Redrawn from Cormier JM. Techniques générales de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris: Masson et Cie, 1970.)

FIGURE 15.5 Division and suturing of arterial ends. (Redrawn from Cormier JM. Techniques générales de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris: Masson et Cie, 1970.)

may have to be divided and double ligatures placed on each end (Fig. 15.4). The first ligature is a simple one. The second is a suture ligature placed distal to the previous one. For larger arteries, in addition to ligation of the vessel, oversewing of the stump with one or two rows of a continuous suture is a safety measure, and it is particularly important if the available length of vessel is limited or the artery is diseased (Fig. 15.5). Release of the clamp after completion of the ligation should be slow and progressive. Ligation of a medium-sized artery should be done by dividing the vessel, double-ligating the distal end, and closing its origin with a lateral over-and-over suture (Fig. 15.6A), care being taken to avoid narrowing the main artery. The alternative to a lateral suture is ligating the divided stump close to its origin. The pitfall of this maneuver may be a blowout of the stump or, if the stump is too long, subsequent thrombus formation and potential embolization. It should therefore be avoided (Fig. 15.6B). Results of arterial ligations for injuries or any other cause depend on the arterial segment involved. If the liga-

FIGURE 15.6 Division of a major collateral and lateral closure of its origin on the parent vessel. (A) Correct procedure. (B) Incorrect ligation of collateral. (Redrawn from Cormier JM. Techniques généraIes de chirurgie artérielle. In: Nouveau traité de technique chirurgicale. Paris-:Masson et Cie, 1970.)

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tion is below a major branch that may assume the role of collateral supply, the effects of the ligation may be minimal. Certain arterial segments are more vulnerable than others. The common iliac, common femoral, and, particularly, popliteal arteries are critical anatomic locations. Their ligation may lead to a high rate of gangrene. By contrast, the external iliac, superficial femoral, and tibial arteries are less critical and usually tolerate ligations with few ischemic changes.

Arteriotomy The chosen segment for arteriotomy is exposed, mobilized, and isolated. Occlusion of the vessels is not carried out until everything is ready for the arteriotomy, thus minimizing the occlusion time. The arteriotomv for most purposes should be longitudinal. The opening of the artery is done with the cutting-blade edge of the scalpel, not with its point. The longitudinal arteriotomy is initiated first with a short opening of the lumen, which is signaled by the extrusion of a few drops of blood. The arteriotomy is then completed by introducing a Potts-angled scissors in the lumen. Alternatively, the incision can be lengthened by inserting a fine clamp and continuing with a sharp new scalpel blade. This method is particularly useful when one is opening a diseased artery in preparation for anastomosis with a bypass graft. The length of the arteriotomy depends on the type of procedure contemplated. For an embolectomy or a thrombectomy, it should not exceed 0.75 to 1 cm; if it is intended for an anastomotic area, it may be somewhat longer. A transverse arteriotomy is usually semicircular and is carried out in the same technical fashion as the longitudinal one. Care should be taken to avoid using the point of the scalpel blade and thus possibly entering too far into the artery and injuring its posterior wall. Control of large (aorta, iliac) vessels may be gained occasionally, by either cross- or lateral clamping. The latter is carried out by means of a Satinsky clamp of suitable size, thus obviating complete arrest of arterial flow. In this instance, the arteriotomy is longitudinal and is used for anastomosing a graft. In contrast to the type of arteriotomy that is easy to make in a soft, normal arterial wall, this procedure in an arteriosclerotic artery may result in dissection of an atherosclerotic plaque from the outer layer of the arterial wall. Calcification of an artery may render the arteriotomy and subsequent procedure more difficult. If the linear incision of the artery is changed into an elliptical opening, excision of the edges with ordinary scissors most often results in a jagged arteriotomy with loose intima. The factors responsible for these technical difficulties are accounted for by the arteriosclerotic changes of the arterial tissue. Indeed, the increased thickness of the artery, the existence of a cleavage plane between the intima and media, and the presence of uneven calcific plaques make it

FIGURE 15.7 Arteriotomy scissors.

FIGURE 15.8 Arteriotomy: three steps using the arteriotomy scissors. (Reproduced by permission from Haimovici H. Arteriotomy scissors. Surgery 1963;54:745.)

difficult to obtain clean-cut arteriotomy edges. Scissors with a powerful shearing action and the capability of providing sharply delineated edges (Fig. 15.7) were specifically designed for this purpose by the author (6). Another technique has been described that consists of an intraoperative fracture used to overcome the rigidity of the arterial wall in calcified arteries. This technique, described by Ascer et al., did not prevent the implantation of the grafts, which resulted in patency and limb salvage (7). The steps are simple and consist, first, of a longitudinal linear arteriotomy and then, with the arteriotomy scissors, excision of its edges one at a time. This results in a minor ellipsisshaped arteriotomy (Fig. 15.8). These scissors (manufactured by J. Sklar Manufacturing Co.) are available in two sizes, a large one for the aorta and iliac and a smaller one for the femoral and popliteal vessels. The resulting cleancut arteriotomy greatly facilitates an end-to-side graft

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anastomosis in arteries with marked arteriosclerotic and calcific changes. Closure of a longitudinal linear arteriotomy may be done with a continuous over-and-over suture or

interrupted stitches (Fig. 15.9). One of the pitfalls of closing a longitudinal arteriotomy, especially in a medium-sized or small artery, may be its narrowing by the suture. In such cases, use of a patch graft is indicated (see Chapter 16). Closure of a transverse arteriotomy is best carried out by interrupted stitches. One should start with the placement of stay stitches at each angle and then proceed with the others between these two points taking care to include the entire thickness of the arterial wall and to have intimato-intima coaptation.

Vascular Anastomoses End-to-End Anastomosis Various types of techniques are available for anastomoses of blood vessels. They can be accomplished by an over-

FIGURE 15.9 Closure of a longitudinal arteriotomy with a continuous over-and-over suture.

FIGURE 15.10 (A, B) End-to-end anastomosis by means of two stay stitches. (C) Anterior wall anastomosis. (D) Posterior wall anastomosis after 180° rotation of the two vessels.

FIGURE 15.11 End-to-end anastomosis performed by means of intraluminal anastomosis of the posterior wall (B).

A

B

C

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FIGURE 15.12 End-to-side anastomosis with four guy sutures and a continuous over-and-over stitch.

B

A

C

D

E

FIGURE 15.13 End-to-side anastomosis with the four-stay suture technique. (Reproduced by permission from Haimovici H. A four-stay suture technique for end-to-side arterial anastomoses. Surgery 1960;47:266.)

and-over suture or by a continuous everting mattress suture. Approximation of the two ends of the divided vessels can be accomplished by several methods: 1. 2.

two stitches placed on the posterior wall close to each other; equidistant stitches placed at each angle;

3. 4.

three stitches placed at equal distance [triangulation of Carrel (4)]; or placement of four equidistant stitches [quadrangulation of Frouin (8)].

Figure 15.10 depicts the anastomosis of two vessels by means of two stay stitches and a continuous over-and-

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Part III Basic Vascular and Endovascular Techniques FIGURE 15.14 End-to-side anastomosis in which the posterior wall of the vessels is anastomosed by the intraluminal technique.

A

C

B

D

E

over stitch. First, the anterior wall is approximated by this suture technique. The vessels are then rotated by 180°, and the anastomosis is completed on the posterior wall, in an anterior position. Figure 15.11 shows an end-to-end anastomosis performed by suturing the posterior wall through the lumen of the vessel. After intraluminal closure on the posterior wall, the anterior row is completed in the usual fashion, by the extraluminal technique.

End-to-side Anastomosis Figure 15.12 depicts an end-to-end anastomosis, which is applicable to both large and small vessels. The arteriotomy indicated in Figure 15.12A and B can be used as an ellipsis-shaped opening for medium-sized arteries or as a rectangular-shaped opening for small vessels, although we have found that, even with tiny arteries in the foot, anastomoses can be fashioned effectively to an elliptical anastomosis (Veith). Figure 15.12C demonstrates the direction of the sutures, starting from one end and proceeding by a continuous over-and-over stitch. The graft is then flipped over to provide direct vision for the anastomosis of the opposite edges, as indicated in Figure 15.12D and E. Alternatives to this are a four-stay suture technique for the end-to-side anastomosis, as described previously (9) (Fig. 15.13), or a technique with heel-and-toe sutures

run down each side and tied at the midpoints of the anastomosis. Figure 15.14 depicts an end-to-side anastomosis, similar to the previous one, except that the posterior wall of the vessels is anastomosed by the intraluminal technique. The anterior row is sutured by the usual extraluminal method.

Side-to-side Anastomosis Figure 15.15 depicts a side-to-side anastomosis of two vessels. Two stay sutures are placed at each angle, and the anterior edges of the vessels are retracted by means of stay sutures placed in their center. The needle of the upper angle is passed back through the vessel into the lumen, and the anastomosis of the posterior wall is carried out by an intraluminal technique as indicated in Figure 15.15C. After the intraluminal anastomosis is completed, the two sutures are tied together, and the distal needle is then used for the anastomosis of the anterior wall by an extraluminal technique, as indicated in Figure 15.15D and E.

Everting Suture Technique Use of the everting technique for intraluminal vascular suturing was introduced by Blalock and Taussig for

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FIGURE 15.15 Side-to-side anastomosis.

the shunt procedure in the treatment of the tetralogy of Fallot (10). The technique consisted of placing a continuous everting mattress suture along the posterior half of the circumference of the anastomosis before approximating the vessels and drawing the suture taut. This procedure has proved useful in areas where there are short cuffs or other limitations of exposure, necessitating suturing of the back walls from within the lumina (11). Use of

this type of vascular suturing is applicable to end-to-end anastomoses as well as to end-to-side anastomoses, as depicted in Figures 15.16 and 15.17. The parachute technique can be used with continuous and everting techniques and is facilitated by monofilament polypropylene sutures. Specific techniques for some graft implantations will be found in subsequent chapters.

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A A

B

B

C C

D

D

FIGURE 15.17 End-to-side anastomosis with an eversion technique and intraluminal vascular suturing.

FIGURE 15.16 End-to-end anastomosis with an eversion technique and intraluminal vascular suturing.

References 1. Jassinowsky A. Die Arreriennaht: Eine experimentelle Studie. Inaug Diss Dorpat, 1889. 2. Dörfler J. Über Arteriennaht. Beitr Klin Chir 1899;25:781. 3. Clermont G. Suture latérale et circulaire des veines. Presse Med 1901;1:229. 4. Carrel A. La technique opératoire des anastomoses vasculaires et la transplantation des viscéres. Lyon Med 1902;98:859. 5. Carrel A, Guthrie CC. Uniterminal and biterminal venous transplantation. Surg Gynecol Obstet 1906,2:266. 6. Haimovici H. Arteriotomy scissors. Surgery 1963;54:745.

7. Ascer E, Veith FJ, Flores SAW. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986;152:220. 8. Frouin A. Sur la suture des vaisseaux. Presse Med 1908;16:233. 9. Haimovici H. A four-stay suture technique for end-toside arterial anastomoses. Surgery 1960;47:266. 10. Blalock A, Taussig HR. Surgical treatment of malformations of the heart in which there is pulmonary stenosis or atresia. JAMA 1945;128:189. 11. Shumacker HB Jr, Muhm HY. Arterial suture techniques and grafts: past, present, and future. Surgery 1969;66:419.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 16 Patch Graft Angioplasty Henry Haimovici

One of the important limiting factors in the reconstruction of vessels, especially of medium and small arteries, is the constriction of the lumen resulting from closure of a longitudinal arteriotomy. This luminal constriction can easily be prevented by use of a patch graft. This principle of arterial repair, widely used today, was demonstrated experimentally by Carrel and Guthrie as early as 1906 (1,2). They defined this procedure as follows: “The patching consists of closing an opening in the wall of a vessel by fitting and sewing to its edges a flap taken from another vessel or from some other structure such as the peritoneum.” In describing anastomosis of blood vessels by the patching method and transplantation of the kidney, they further stated: “The anastomosis by the patching method consists of extirpating a vessel together with an area or patch from the vessel of origin, the patch being so cut that the mouth of the extirpated vessel is situated in the center of the patch. The edges of the patch are then fixed to the edges of a suitable opening made in the wall of another vessel” (Fig. 16.1). Although Carrel and Guthrie long ago demonstrated the feasibility of this surgical technique (1,2), it is only since the advent of the current reconstructive arterial surgical era that this procedure has assumed a significant place among corrective vascular methods. In 1959, Crawford et al. (3) and Senning (4) used autogenous vein patch grafts for closure of an arteriotomy in small arteries. These experiments confirmed the concept that they widen the lumen and prevent annular constriction from a longitudinal arteriotomy or even a circular suture line. In 1962, DeBakey et al. reported extensive clinical use of patch graft angioplasty in the treatment of all types of occlusive arterial diseases and aneurysms (5). Subsequently, several

investigators evaluated different types of patch material for the closure of arteriotomy of small arteries, (6–12). Reinforced by these laboratory and clinical experiences, patch graft arterial repair is now a well-established procedure.

Indications Indications for patch graft angioplasty are determined by three main factors: 1. 2. 3.

size of arteries; longitudinal arteriotomy; and nature and extent of the mural lesion necessitating partial excision of the wall.

In brief, any closure of an arteriotomy of a longitudinal wound that consumes the arterial circumference represents a major indication for this procedure. Its principal aim is to prevent stenosis and thrombosis at the site of the arteriotomy (Fig. 16.2).

Patch Graft Material Carrel and Guthrie, in their original experiments, used autogenous arterial, venous, and peritoneal patches (1, 2). Clinically, both tissue and prosthetic materials are used for that purpose. Autogenous vein patches, favored by most surgeons, are indicated mostly for medium-sized and small arteries. Synthetic material is more suitable for larger vessels, such as the aorta and iliac arteries.

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A

B

C

D

FlGURE 16.2 Arteriotomy closure by direct method and patch graft. (A) Artery containing a mural lesion. (B) Longitudinal arteriotomy over the lesion. (C) Direct closure of arteriotomy, resulting in constriction of lumen. (D) Patch graft closure illustrating the prevention of constriction.

FIGURE 16.1 Transplantation of a renal artery, together with a segment of the aortic wall implanted as a patch graft. (Reproduced by permission from Carrel A, Guthrie CC. Anastomosis of blood vessels by the patching method and transplantation of the kidney. JAMA 1906,47:1648.)

The histologic changes that take place in different patch graft materials over long periods have been the subject of several investigations (6–12). Grafts in the large vessels heal almost uniformly, irrespective of the type of patch material. The critical test, however, is in the smaller arteries. There is general agreement that both autogenous vein patches and autogenous arterial patches are usually less susceptible to local complications than are the synthetic grafts.

Vein Patch Grafts The autogenous vein patch graft is soon incorporated into the host artery. Arteriographic studies and gross examination cannot readily identify them unless there is some stricture at the suture line. In such cases, the arteriogram displays a slight narrowing at that level. Localized dilation may be present if the patch graft is too large. Macroscopically, most of these grafts display a smooth intimal lining. Histologic studies of vein patches have shown progressive alterations within a few weeks after implanta-

tion. Although in some of the grafts there is a partial preservation of normal venous architecture, consisting of elastic fibers with recognizable layers of the vein wall, smooth muscle disappears and is replaced by extensive fibrosis. The endothelial surface appears to remain intact without any accumulation of fibrin. Although the histologic vein structure is lost completely in many instances and replaced by fibrous tissue, it still functions properly without evidence of dilation or narrowing of the host artery (7,10).

Arterial Patch Grafts Autogenous arterial patches have significantly fewer degenerative changes and seem to be preferred over vein patches whenever possible (6,8). Although the arterial patch retains some of its histologic characteristics, unlike the veins, arteries are not readily available or expandable and are therefore rarely used as patch grafts.

Prosthetic Patch Grafts The healing patterns of Dacron patch grafts are similar to those reported by investigators of synthetic tubular grafts. Within 2 or 3 weeks, the patch acquires an inner lining, which in the beginning is loosely attached. A marked fibrotic reaction is usually found surrounding the graft (9,10). This increases gradually and forms a thick layer by the end of 6 weeks.

Chapter 16 Patch Graft Angioplasty

233

FIGURE 16.3 Method for attaching a patch graft with rectangular ends to a longitudinal oval arteriotomy. (A) Rectangular piece of graft and arteriotomy. (B) Placement of the stay sutures in the four angles and anchoring of the patch to the edges of the arteriotomy. (C) Continuous everting stitch, resulting in a rectangular patch with prevention of narrowing of the lumen.

Dacron velour displays less thrombosis and fibrotic reaction than the conventional Dacron material (12). The histologic appearance indicates a good incorporation of this fabric into the host artery, with only minimal thickening of the neointima. Polytetrafluoroethylene (PTFE or Goretex) vascular patch material, available in sheet form, almost immediately develops a layer of proteinaceous material on the luminal surface, while the outer wall is surrounded by wound tissue and blood clot. Within 2 weeks, the clot is absorbed, a healed connective tissue capsule is being formed, and collagen penetration into the wall is noted. The healing reaction is more an incorporation than a simple encapsulation.

Methods and Technique of Patching Patch graft angioplasty is most suitable for short arteriotomy closures, rather than for long segments. Its use for the latter, especially if they exceed 8 cm, may lead to poor long-term results. This procedure may be used as an isolated modality, but more often it is combined with other reconstructive surgical techniques, such as thromboendarterectomy, excision with graft replacement, or bypass graft. Need for a patch graft may be anticipated from the arteriographic findings, or it may become necessary in the course of a surgical reconstructive procedure.

If one anticipates the use of a vein graft, preoperative preparation of the area supplying the vein should be carried out. If it is in the area of the femoral or popliteal artery, the saphenous vein is easily accessible. Otherwise, one should prepare the skin if the patch is to be secured from another area. The segment of the saphenous vein is opened longitudinally. Its length is tailored to the arteriotomy to be closed. The resulting patch is rectangular in shape. Two methods may be used for its implantation. In one, the rectangular shape is maintained, and the graft is attached to the edges of the arteriotomy by four-stay stitches placed through the four corners (Fig. 16.3). The alternative is to excise the corners of the rectangle so as to obtain an oval shape at each end of the patch graft (Fig. 16.4). The graft is attached at each end of the arteriotomy with double-arm No. 5–0 fine synthetic suture material. Silk, because of its eventual loss of tensile strength, is to be avoided. A continuous everting stitch is used between the stay sutures. The patch must be under tension to allow good approximation between the graft and the edges of the host artery. Aneurysmal dilation is avoided by limiting the width of the patch graft. To achieve a patch without redundancy, the surgeon must use stay sutures at each end and at the midpoint of each edge of the arteriotomy (Fig. 16.4). The direction of the stitch, as in any other implant, goes from the graft to the host artery. Before the patch is completed, it is essential to check the proximal and distal arterial tree for possible thrombo-

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FIGURE 16.4 Oval patch grafts. (A) Longitudinal arteriotomy. (B) Excision of the angles of the arteriotomy. (C) Rectangular arteriotomy. (D) Tailoring of a patch graft to match the arteriotomy. (E) Use of the four-stay suture technique for graft implantation. (F) Prosthetic patch graft completed. (G) Vein patch graft completed.

sis. Once the patency has been checked, the suturing of the graft is completed.

Patching at Different Arterial Sites Although the technique of patching varies somewhat with the location and extent of the arterial lesion, the principle is essentially the same for all areas. The best results obtained are in short segmental occlusions. Localized segmental lesions occurring in the common iliac, common femoral, internal carotid, vertebral, renal, popliteal, and axillary arteries are the most suitable indications for patch graft angioplasty. The incision in the artery extends from the uninvolved proximal segment through the region of the obstruction into the uninvolved distal segment. After the endarterectomy is completed, the patch is attached in the manner described above. In the arteries below the inguinal ligament or those in the neck, vein patch grafts are most suitable, whereas in the aorta or the iliac artery Dacron or another synthetic material can be used to advantage. When a patch graft is used at the level of a relatively

large vessel that divides into two branches, such as the common femoral, which bifurcates into a superficial and a profunda vessel, the patch graft can be placed in three different manners. The following modalities are applicable to all arteries of similar anatomic configurations (e.g., carotid, iliac, aorta): 1.

2.

3.

Patch attached to the common and superficial femoral. It is exceptional to stop the patch graft in the common femoral, since the superficial, at least at its initial segment, is also involved by the atherosclerotic process. Therefore, the patch should always extend beyond the origin of the superficial femoral artery by about 3 to 5 cm (Fig. 16.5A). Patch attached to the common femoral and to the profunda. The patch is tailored in such a way as to extend from the common to the profunda beyond its origin, usually to the level of the bifurcation of the latter vessel (Fig. 16.5B). Patch attached to the common femoral and both branches. In some instances in which both the superficial and profunda femoral vessels are involved by

Chapter 16 Patch Graft Angioplasty

A

A

235

B

B C FIGURE 16.6 Patch grafts combined with tubular grafts. (A) Tubular graft attached to a patch. (B) Tubular graft attached proximal to a patch. (C) Long bevel of a tubular graft with an additional patch for closing an extensive arteriotomy.

C FIGURE 16.5 Patch graft at a femoral arterial bifurcation. (A) Patch to the common and superficial femoral arteries. (B) Patch to the common femoral and profunda. (C) Y-shaped patch to the common femoral and its two branches.

the arteriosclerotic process, a Y-shaped patch is necessary for closing of the arteriotomy of these three vessels (Fig. 16.5C).

3.

A combination of tubular graft with extended patch may be used in certain cases if the distal end of a graft has to be attached to an area of extensive involvement of the arterial wall. Then the beveling of the graft is fashioned with a long flap that offers this combination (Fig. 16.6C).

A number of other combinations of these various techniques may be necessitated by pathologic findings involving both occlusive and aneurysmal disease.

Combination Graft Procedures Patch graft angioplasty may be associated with bypass grafts. Three main combination procedures may be used: 1.

2.

A patch graft attached to the main artery may provide an area for the anastomosis of a tubular graft. The necessity for this modality is the presence of a small, narrowed artery or the loss of the anterior wall because of severe arteriosclerotic changes with calcification (Fig. 16.6A). At a bifurcation of a major artery, a patch graft may be combined with a tubular graft implanted proximal to the patch (Fig. 16.6B).

Complications and Pitfalls Complications of patching of arteries may result from technical errors or from the type of patch graft material. Early thrombosis or hemorrhage may occur as a result of a technical error. Late thrombosis or hemorrhage may be due to the disruption of the anastomosis or to the progression of the degenerative changes of the arterial wall. Local infection is a potential hazard to which one should always be alert. Pitfalls to be avoided are excessive length or width of the graft, which may lead to aneurysmal formation at the site of the graft.

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Conclusion Patch graft angioplasty has proved to be useful in performing the various reconstructive surgical procedures. The main advantage is prevention of stenosis at the site of the closure of an arteriotomy, especially in a small vessel. The long-term results obtained with this procedure are gratifying.

References 1. Carrel A, Guthrie CC. Résultats du patching des artères. C R Soc Biol (Paris) 1906;60:1009. 2. Carrel A, Guthrie CC. Anastomosis of blood vessels by the patching method and transplantation of the kidney. JAMA 1906;47:1648. 3. Crawford ES, Beall AC, et al. A technic permitting operation upon small arteries. Surg Forum 1959; 10:671. 4. Senning A. Strip-graft technique. Acta Chir Scand 1959;118:81.

5. DeBakey ME, Crawford ES, et al. Patch graft angloplasty in vascular surgery. J Cardiovasc Surg 1962;3:106. 6. Chatarjee KN, Warren R, Gore I. Long-term functional and histologic fate of arteriotomy patches of autogenous arterial and venous tissue: observations on arterialization. J Surg Res 1964;4:106. 7. Norton LW, Spencer FC. Long-term comparison of vein patch with direct suture: technique of anastomosis of small arteries. Arch Surg 1964;89:1083. 8. Rossi NP, Koepke JA, Spencer FC. Histologic changes in long-term arterial patch grafts in coronary arteries. Surgery 1965;57:335. 9. Dale WA, Lewis MR. Experimental arterial patch grafts. J Cardiovasc Surg 1965;6:24. 10. Pena LI, Husni EA. A comparative study of autogenous vein and Dacron patch grafts in the dog. Arch Surg 1968;96:369. 11. Wagner M, Ruel G, et al. The use of Spandex as a vascular patch graft material. Surg Gynecol Obstet 1968;127:805. 12. Menon SMR, Talwar JR. et al. Comparison of Dacron velour and venous patch grafts for arterial reconstruction. Surgery 1973:73:423.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 17 Endarterectomy Henry Haimovici

Endarterectomy, first performed by J. Cid dos Santos in 1946, was originally designed for simple removal of thrombi but turned out to be more than a simple thrombectomy (1,2). Attempts at disobstruction of occluded arteries by simple thrombectomy were not new. Severeanu in 1880 (2), Jianu in 1909 (3), and Delbet in 1906 and again in 1911 (4) are credited with attempting arterial thrombectomy. These early trials were all unsuccessful. The procedure was thus relegated to oblivion until 1946, when dos Santos decided to do this operation with the patient under the cover of heparin. The first patient on whom he tested this concept was a 66-year-old man with a left ischemic limb due to an iliofemoral occlusion. The procedure resulted in patency of the vessels lasting 3 days, at which time the patient died of advanced uremia. The arteriograms taken after the procedure and at postmortem confirmed the patency of the iliofemoral vessels. Histopathologic examination of the removed specimen showed not only the thrombus but also the whole intima and part of the media. In spite of this histopathologic finding, there was no rethrombosis. Encouraged by these findings, dos Santos next used this procedure on a 35-year-old woman with a subclavian–axillary arterial thrombosis associated with a cervical rib. The histopathologic findings were similar to those in the first case. The clinical recovery with patency of the subclavian–axillary artery persisted for 29 years, as of the date of his publication in 1976 (5). The data provided by these two cases were quite revealing, and dos Santos stated: “I really had performed a different operation from the one I originally intended to do; and I could conclude that, under heparin action, blood could flow against muscle without giving place to throm-

bosis” (2). He thus felt that the integrity of the intima is no longer always mandatory for a successful surgical procedure. This new procedure, later called thromboendarterectomy, represented a wholly new concept in arterial surgery. It appeared as a revolutionary idea because it seemed to negate the prevailing concept, according to which an injured intima leads inevitably to vascular thrombosis. Indeed, unlike embolectomy, in which only the thrombus is removed, in thromboendarterectomy both the thrombus and the endartery (intima and part of the inner media) are excised. The accidental finding that arterial thrombosis does not necessarily occur after removal of the intimal lining and a portion of the media is a typical example of serendipity. As a result of these findings, a new chapter emerged in the field of vascular surgery. Dos Santos’s pioneering efforts were soon confirmed and expanded by Bazy et al. (6), Leriche and Kunlin (7), Wylie et al. (8,9), Cannon and Barker (10), and a few others. Although sporadic reports started to appear shortly thereafter, greater acceptance of this new operation had to await further technical refinements and improvements in instrumentation, since, as stated by dos Santos, “At the beginning failure was the usual, success the occasional.” This procedure, even after 37 years, is still not entirely without some controversies. Endovascular techniques have recently offered an alternative to the classic procedure of endarterectomy. Mechanical atherectomy devices have become available to replace the surgical method for dealing with arterial atheromatous lesions. The basic concepts of the two modalities are quite different. The dos Santos principle will be dealt with in this chapter on classic endarterecto-

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my, while mechanical atherectomy will be presented in Chapters 66 and 67. The readers will find in these two concepts the old and the new, which offer similar scopes but different approaches of how to deal with arterial mural lesions of atherosclerosis.

Subintimal The subintimal cleavage plane is located between the intima and the media along the outside of the internal elastic membrane. Transmedial

Terminology Originally dos Santos named this operation “arterial disobstruction” or “disobliteration.” Later Bazy and Reboul coined the term endarterectomy (11), but Leriche preferred the more comprehensive term thromboendarterectomy (7). These two terms, often used interchangeably, are designed to indicate removal not only of the intima and thrombus but also of the media. Consequently, since “endartery” and “intima” are used as synonyms, the term endarterectomy appears to convey an incomplete meaning of the procedure. Sanctioned by long-time usage, however, these terms are widely accepted, notwithstanding the above semantic limitations.

The transmedial plane lies between the involved and intact layer of the media, usually between the inner threequarters and the outer one-quarter. Subadventitial The subadventitial plane is situated between the media and the adventitia along the inner surface of the external elastic membrane. As it is not possible to know preoperatively which cleavage plane is available, great care should be exercised to determine its exact location in each case. As a rule, the best planes to use are either subadventitial or transmedial. Use of the subintimal plane may lead to thrombosis and should be avoided.

Principles of Endarterectomy Early arteriosclerotic lesions involve mostly the intima and, to a lesser extent, the media. At a later stage, the internal elastic membrane is usually fragmented, and the atheromatous changes invade the medial coat. When the lumen is partially or completely occluded, a fibrosclerotic core is present with or without an organized thrombus.

Cleavage Plane A cleavage plane, usually present in the outer portion of the arterial wall, represents the mural pathologic component that is the key to the performance of an endarterectomy. The cleavage plane varies with the size, location, and pathology of the particular artery. In arteries of the muscular type, such as the superficial femoral, the media includes circular fibers in its inner three-quarters and longitudinal ones in its external onequarter. The latter layer also has elastic fibers, which increase in number and thickness in the vicinity of the external elastic membrane. As a consequence of this anatomic characteristic, the cleavage plane in such an artery is situated between the inner three-quarters and the outer one-quarter of the media, as determined by the different orientation of the two layers of muscular fibers (Fig. 17.1). The cleavage planes are not all situated at the same level (12). As a rule, normal planes of cleavage are close to either the internal or external elastic membrane. Based on the extent and location of the mural lesions, the following three cleavage planes are found most commonly: subintimal, transmedial, and subadventitial (Fig. 17.1B).

Pathology of Lesions Endarterectomized Specimen Such a specimen has the appearance of an irregular, flattened plaque of grayish white tissue, speckled with yellow streaks (Fig. 17.2). Often, segments of throm-botic material are encrusted in the folds of the intima. Some of the plaques are ulcerated and are covered with thrombi. Histologically, the endothelial layer is difficult or impossible to identify, the internal elastic membrane is usually fragmented or absent, and lipid infiltration with cholesterol crystal clefts and fibrotic lesions are present in the subintimal region and media, with frequent calcific degenerative changes in the latter (Fig. 17.3). Thromboendarterectomized Specimen This specimen consists of a tubular structure resembling the arterial wall on the outside, with the lumen totally occluded by a thrombus that is firmly attached to the wall (Fig. 17.4). Histologically, the arterial wall shows thickening, hyalinization, cholesterol deposition, and calcification, with a well-organized thrombus. In some areas, the organization is represented by early fibroblastic infiltration and minimal iron pigment deposition.

Residual Arterial Wall The residual arterial wall is usually glistening without any evidence of atheromatous tissue. If the cleavage plane is close to the external elastic membrane, all the circular fibers should have been removed. If shreds of this layer are

Chapter 17 Endarterectomy

239

FIGURE 17.1 Principles of endarterectomy. (A) Longitudinal arteriotomy extending beyond the occluding core and three cross-sections at different levels of the arterial lesions. (B) Planes of cleavage: (1) subintimal, (2) transmedial, (3) subadventitial. Note the two muscular fiber layers of the media, the circular (internal) and longitudinal (external). (C) Dissection and mobilization of an atherothrombotic occluding core. (D) Excision of the core. (E) Distal intimal edge reattached to the arterial wall with interrupted stitches.

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Common femoral artery

Inguinal ligament

Superficial femoral artery

Profunda femoris artery

B

A

C FIGURE 17.2 (A) Femoral arteriogram indicating marked stenosis of the common femoral proximal to its bifurcation. (B) Artist’s reproduction of the arteriogram. (C) Endarterectomy specimen.

still present, they should be carefully stripped away. Microscopically, the residual arterial wall includes in variable amounts medial fibers, the external elastic membrane, and the adventitia. Within minutes after completion of the surgical procedure, the inner surface of the residual wall becomes covered with a fibrin layer. Subsequently, an inner fibrous coat is formed, which may lead occasion-

ally to reduction of the arterial lumen. For this reason, as mentioned previously, the most external cleavage plane should be used to avoid possible subsequent stenosis. The existence of a neointima in the endarterectomized artery is still a moot question. Neointimal hyperplasia, especially in anastomotic areas, is a frequent complication. Periarterial fibrotic reaction to the en-

Chapter 17 Endarterectomy

241

The conventional technique of endarterectomy c an be performed through the semiclosed or the open method.

Semiclosed Endarterectomv Exposure and Mobilization of the Vessel Wide exposure is essential for proximal and distal control of not only the main artery but all collaterals. Exposure of the artery is usually made by means of two or three skin incisions, not exceeding 8 to 10 cm, along the involved vessel (Fig. 17.5A). A longitudinal arteriotomy is carried out at each end of the involved vessel. After the cleavage plane is developed, a lateral dissector separates the lesion circumferentially. Then the distal end of the lesion is transected sharply. Dissection of the lesion (Fig. 17.5B) is carried out by using a combination of lateral and ring dissectors. The entire occluding core is mobilized and then extruded through either the lower or upper incision (Fig. 17.5C). Great care must be exercised in handling the distal intimal flap, reattaching it, if necessary, to the rest of the arterial wall with interrupted stitches across its edge (Fig. 17.5E). FIGURE 17.3 Intimal lesion from an endarterectomized specimen.

Closure The arteriotomies are closed by a simple arteriography or by a patch graft angioplasty.

darterectomy is often noted, although its degree varies from case to case.

Hemodynamic Factors Endarterectomy is designed to reconstruct the arterial lumen with at least part of its original characteristics, namely, with a diameter that allows near-adequate capacity and a geometrical shape that ensures normal flow. This ideal aim, however, cannot always be achieved, as it is nearly impossible to restore the arterial wall once it has lost its original tissue characteristics and its normal physical properties. Nevertheless, it may be feasible to obtain a reasonably uniform cross-section of the lumen in all its involved segments. This may be achieved either by direct suturing of the arterial wall or by means of a patch graft angioplasty, which is particularly advisable in the vicinity of bifurcations (13). Arteries after endarterectomy become obviously thin-walled and soft. In spite of these morphologic changes, the endarterectomized vessel is able to withstand arterial pressures and to maintain the suture line. The endarterectomized segments appear to contain less smooth muscle but more nonprotein material compared with normal arteries, and owe their high elastic stiffness primarily to the collagen fibers concentrated in the outer layers of the wall (14).

Overpass Dos Santos in 1963 described this technical detail, not only for securing the distal edge of the artery better but also for allowing direct visualization of the outflow area (Fig. 17.5F). A vein patch is implanted at this level for additional safety (15).

Pitfalls Pitfalls of the semiclosed method, especially for long segments, may be quite serious and consist of: 1. 2. 3.

incomplete removal of the lesion, leaving residual strands of media that could lead to rethrombosis; rupture of the arterial wall with subsequent troublesome hemorrhage; and retrograde bleeding during the procedure due to inadequate control of collaterals.

Open Endarterectomy Open endarterectomy is unquestionably more adequate and safer than the semiclosed method.

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Part III Basic Vascular and Endovascular Techniques FIGURE 17.4 Cross-section of a thromboendarterectomy specimen at two different levels. (A) Lumen is filled by recent thrombosis. (B) Lumen is filled by fibrosclerotic mass. (C) Enlargement of the calcified area as seen in the medial coat of A.

A

B

C

Exposure

Reattachment

The vessel is exposed along its entire length and is mobilized from end to end together with all its collaterals. A longitudinal arteriotomy is carried out slightly proximal from the uninvolved area through the lesion and distally beyond the obliterating core.

It is not mandatory to reattach the proximal end of the intimal flap, although in some instances it may be necessary to do so. The distal end is treated in a fashion similar to the semiclosed method. A patch may be attached to this area, especially if the artery is of small caliber. In such a case, it may be necessary to consider changing the acute angle of the distal arteriotomy into a broader end. This can be accomplished in two ways, as described in Chapter 16, (see Figs. 17.5F and 17.6C).

Cleavage Plane The dissection of the lesion is started by a limited arteriotomy through the adventitia and the external layer of the media, for the purpose of developing a cleavage plane. The initial limited arteriotomy is then extended both proximally and distally along the cleavage plane. Once the core is mobilized, the two ends are transected sharply. Sometimes the hypertrophied intima tapers off at the distal end. The occluding mass is then removed.

Dissection Whenever possible, an extraluminal dissection of the occluding core is desirable. This may offer a twofold advantage: it facilitates the dissection of the lesion and it may shorten the period of total arterial occlusion. This may be

Chapter 17 Endarterectomy

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FIGURE 17.5 Semiclosed endarterectomy. (A) Two small separate arteriotomies carried through the subadventitial cleavage plane. (B) Dissection and mobilization of an atherothrombotic core with a lateral dissector. (C) Removal of the occluding core after sharp transection at both ends. (D) Proximal intimal edge fixed to the arterial wall with interrupted stitches. (E) Distal intimal edge fixed in a similar fashion. (F) Overpass (see text).

of great value in visceral arterial endarterectomy (Figs. 17.7 and 17.8). The indication for open versus semiclosed endarterectomy may be determined by the extent of the lesion or by the preference of the individual surgeon. The author prefers the open technique.

Heparin A combination of systemic and local heparinization offers the best method for preventing thrombosis during these usually long procedures. Postoperative heparinization has been abandoned because the possible troublesome

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A

B C

FIGURE 17.6 Endarterectomy of femoral bifurcation. (A) Line of incision of the femoral artery. (B) Mobilization of the occluding core. (C) Closure of the arteriotomy with a patch graft.

A

B

C

FIGURE 17.7 Extraluminal endarterectomy. (A) Dissection of an occluding core after arteriotomy performed through a subadventitial cleavage plane. The arteries proximal and distal to the procedure remain intact at this phase. (B) Excision of the occluding core. Occlusion of proximal and distal segments is necessary at this phase. (C) Closure of arteriotomy.

complications outweigh its effectiveness in preventing thrombosis at this stage.

Combined Procedures Endarterectomy is often necessary prior to the distal implantation of a graft because of severe stenosis or occlusion at that level. Such cases may be encountered in any

arterial segments but are more common in aortofemoral or femoropopliteal bypass procedures. In arterial embolism, it is not uncommon to find the embolus impacted into a bifurcation involved with severe atherosclerotic changes. It is then essential to perform, in conjunction with the balloon catheterization, a meticulous endarterectomy before completing the embolectomy.

Chapter 17 Endarterectomy

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FIGURE 17.8 Specimen removed from the right common femoral artery by extraluminal dissection of the occluded core.

Comments: Endarterectomy Versus Percutaneous Balloon Catheterization With the advent of the percutaneous balloon catheter or laser angioplasty for management of arterial stenosis or occlusion, the indications for endarterectomy have been reassessed. The interventional radiologic procedures are often helpful either as a definitive treatment or as an adjunct to arterial surgery. Endarterectomy is still the most widely used operation for well-defined arterial lesions for which the radiologic interventions appear unsuitable. Of these, carotid endarterectomy, as mentioned above, is widely used. In order of decreasing incidence, other uses are for atherosclerotic lesions, for stenosis or occlusion of the abdominal aorta, and as an adjunct in grafting limb arteries in which the balloon catheter is unsuitable anatomically (16). Knowledge of the basic principles of endarterectomy, of the anatomopathology of the lesions, and of the healing of the arterial wall is essential for understanding the scope and extent of the surgical procedure. This knowledge also provides a better comparison with the results of the mural response following the angioplasty techniques. Notwithstanding the fact that nonsurgical methods have superseded endarterectomy in some cases, the usefulness of the latter nevertheless remains widely applicable in well-defined arterial lesions.

References 1. Dos Santos JC. Sur la désobstruction des thromboses artérielles anciennes. Mem Acad Chir 1947;73: 409.

2. Dos Santos JC. Introduction to a round table on endarterectomy. J Cardiovasc Surg (Special Issue for the 15th International Congress of the European Society of Cardiovascular Surgery), 1966:223. 3. Jianu I. Thrombectomia arteriala pentru un caz de gangrene uscata a piciorului. Soc Chir (Bucarest) 1912;27:11. 4. Delbet P. Chirurgie arterielle et veineuse. In: Les modernes acquisitions. Paris: Bailliere, 1906:104. 5. Dos Santos JC. From embolectomy to endarterectomy, or the fall of a myth. J Cardiovasc Surg 1976;17: 113. 6. Bazy L, Huguier J, et al. Désobliteration d’une thrombose ancienne segmentaire. de 17 cm long, dans une artère fémorale superficielle, atteinte d’arténte pariétale calcifée. Mem Acad Chir 1947;73:602. 7. Leriche R, Kunlin J. Essais de désobstruction des artères thrombosés suivant la technique de Jean Cid Dos Santos. Lyon Chir 1947;42:475. 8. Wylie EJ, Kerr E, Davis O. Experimental and clinical experiences with the use of fascia lata applied as a graft about major arteries after thromboendarterectomy and aneurysmorrhaphy. Surg Gynecol Obstet 1951;92:257. 9. Wylie EJ. Thromboendarterectomy for arteriosclerotic thrombosis of major arteries. Surgery 1952; 23:275. 10. Cannon J, Barker W. Successful management of obstructive femoral arteriosclerosis by endarterectomy. Surgery 1955;38:48. 11. Bazy L, Reboul H. Technique de l’endartériectomie désobliterante. J Int Chir 1950;65:196. 12. Malan E, Botta JC. Normal and pathologic planes of cleavage. J Cardiovasc Surg (Special Issue for the 15th International Congress of the European Society of Cardiovascular Surgery), 1966;261. 13. Malan E, Longo T. Hemodynamic factors in endarterectomy. J Cardiovasc Surg (Special Issue for the 15th International Congress of the European Society of Cardiovascular Surgery), 1966;265.

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14. Sumner DS, Hokanson DE, Strandness DE. Arterial walls before and after endarterectomy: stress-strain characteristics and collagen-elastin content. Arch Surg 1969;99:606. 15. Dos Santos JC. Late results of reconstructive arterial surgery (restoration, disobliteration, replacement with

the establishment of some operative principles). J Cardiovasc Surg 1964;5:445. 16. Inahara T. Endarterectomy for segmental occlusive disease of the superficial femoral artery. Arch Surg 1981;116:1547.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 18 Balloon Angioplasty of Peripheral Arteries and Veins Juan Ayerdi, Maurice M. Solis, and Kim J. Hodgson

Advances in endoluminal technology have led to an exponential rise in the number of percutaneous endovascular procedures performed over the past two decades. In patients afflicted with peripheral arterial and venous obstruction, percutaneous transluminal angioplasty (PTA) is the most commonly performed endovascular procedure, often supplemented with endoluminal stents (to be reviewed in Chapter 19). The ideal PTA technique would be inexpensive, easily performed, associated with low morbidity and mortality, and have reasonable shortand long-term rates of restenosis. Largely achieving these goals, PTA has become a standard technique in the armamentarium of vascular surgeons. Frequently the impetus for performance of PTA is to replace a complicated high-risk surgical procedure with a minimally invasive intervention having an acceptable rate of patency and clinical success. Though not always as durable as the corresponding surgical revascularization, the low risk to benefit ratio of PTA and its typical repeatability often make it the procedure of choice, particularly in patients with significant or prohibitive medical comorbidities. While PTA is considered “low risk,” failures and complications are not innocuous and can result in adverse clinical outcomes, most often involving either the vascular distribution of the target vessel or that of the site of vascular access. Systemic complications related to catheter manipulation, radiographic contrast, or physiologic stress may include stroke, myocardial infarction, renal failure,

limb loss, or even death. Required conversion to open procedures for salvage of an early post-procedure complication carries all the risks of an emergency procedure in a high-risk patient. For these reasons it is critical that the vascular surgeon has thorough knowledge and understanding of the pathophysiology of the condition being treated, the indications and potential complications of the therapeutic alternatives, and the training and experience in the catheter and guidewire skills necessary to perform PTA with good results.

History One of the most important developments in the evolution of endovascular surgery was the invention of the embolectomy balloon catheter by Thomas J. Fogarty (1). Charles T. Dotter, inspired by the work of Fogarty, performed the first PTA on January 16, 1964 (2,3). The patient, an 83year-old woman, was admitted for dry gangrene of three left toes. She had refused amputation, and revascularization was considered contraindicated due to her poor medical condition and limited runoff. Under local anesthesia, 8 Fr. and then 12 Fr. Teflon catheters were sequentially passed over a guidewire to dilate a proximal popliteal artery stenosis. Soon after dilation she became ambulatory and her foot promptly healed (4). Ten months later, Dotter and Judkins reported on 11 patients treated for

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iliac occlusive disease by transluminal dilation with sequentially larger rigid polytetrafluoroethylene catheters introduced from the ipsilateral common femoral artery (2). Despite acceptable results, concern over atheroembolization during passage of the catheters resulted in significant skepticism of the technique. The following year, Dotter used latex Fogarty balloons wrapped over one another for extra thickness and performed the first iliac balloon angioplasty as we know it today. Fourteen years later this first balloon angioplasty was still patent (4). Dotter went on to conceive that this transluminal approach would work in most arterial systems, stating in 1969: “We have long awaited to treat renal artery stenosis percutaneously. The coronary arteries will someday be effectively treated transluminally — perhaps on an outpatient basis . . . ” (5). A fundamental improvement to the Dotter technique was reported in 1974 by Gruntzing and Hopff, who changed the balloon material from latex to polyvinyl chloride, a less elastic material which produced a more effective disruption of the arteriosclerotic plaque (6). Since then, PTA catheters have undergone many improvements in design including reduced-friction hydrophilic coatings, lower catheter and balloon profiles, stronger and more puncture-resistant balloons, monorail “fast-track” catheters, and plaque-cutting balloons. These design improvements have made PTA easier to perform and expanded its applicability, but the pathophysiology, indications, technique, results, and complications of balloon angioplasty alone have remained fairly constant.

Pathophysiology The success of PTA was initially attributed to compression and redistribution of the arteriosclerotic plaque (2). However, subsequent histologic studies have shown that plaque compaction accounts for very little of PTA’s effectiveness (7,8). Current evidence suggests that PTA produces a controlled plaque fracture, plaque separation, intimal dissection, and stretching of the media and adventitia, often with accompanying rupture of the media (7,9). The overstretched media does not return to its original size and carries with it the attached plaque fragments (7,10). Vascular remodeling follows, enlarging the vessel lumen in most circumstances (11). The ability to achieve immediate technical success with PTA is reduced in arteries with eccentric plaques or hyperplastic recurrent stenoses, and in veins or vein grafts. Balloon dilation of eccentric plaque may fail to achieve plaque fracture as the radial dilation force of the balloon simply stretches the arterial wall opposite the plaque. Balloon dilation of the nonatherosclerotic lesions typically present in venous and recurrent arterial stenoses may fail due to recoil of an inelastic fibrous medial layer. In the long term, patency following PTA is frequently limited by continued vascular smooth muscle cell proliferation, which may progress to

myointimal hyperplasia and the development of a recurrent stenosis 912).

Indications In most sites affected by vascular occlusive disease, the clinical indications for PTA are similar to those for surgical interventions, although the minimally invasive nature of PTA may lower the symptom threshold for treatment of favorable lesions. PTA is more successful and thus more clearly indicated as an alternative to surgical reconstruction for short-segment lesions (<5 cm) and in arteries with a large diameter and high flow (e.g., iliac arteries), as opposed to long-segment lesions in arteries of smaller diameter and low flow (e.g., tibial arteries). In addition, PTA fares better in treating stenoses than occlusions, single rather than multiple lesions, and in nonostial (>5 mm from the origin) rather than ostial lesions. Asymptomatic lesions of the lower extremity circulation are not generally treated, unless they are placing a lower extremity bypass graft at risk of thrombosis. Symptomatic aortoiliac occlusive disease is currently the most common indication for peripheral PTA, as the results of iliac artery PTA have been excellent and the complication rates low (13–15). Even though the risk–benefit ratio for PTA in the treatment of femoropopliteal segment occlusive disease is not as commending as for the iliac arteries, the indications have expanded to include lifestyle limiting claudication, rest pain, or tissue loss in patients with favorable lesions proximal to reasonable outflow, significant risk factors for operative reconstruction, or as an adjunct to surgical revascularization. Because of relatively high rates of restenosis in the femoral and popliteal arteries, the risk–benefit ratio favors PTA for only short concentric lesions (<10 cm), stenoses with good runoff, or for high-risk patients who do not have autogenous tissue for reconstructive surgery (16,17). A recent cost-effectiveness analysis suggested that PTA should be the preferred initial treatment in patients with femoropopliteal stenosis and disabling claudication. Patients with femoropopliteal occlusions and/or tibial artery disease suffering from critical lower extremity ischemia are best managed with bypass grafting, as limb salvage results for PTA in this setting have been poor (18). Although tibial PTA for limb salvage may be warranted in patients with good inflow and focal tibial disease, especially in patients lacking autologous bypass graft material or at prohibitive risk for vascular reconstruction, such patients are a rarity in most practices. The most common indication for renal artery PTA is renovascular hypertension and/or renal dysfunction in patients with renal artery stenosis (ischemic nephropathy) (19). More controversial is the recommendation by some authors for PTA of hemodynamically significant renal artery stenoses in the absence of uncontrolled hypertension to prevent progression of the stenosis and subsequent

Chapter 18 Balloon Angioplasty of Peripheral Arteries and Veins

loss of renal function (20). Evaluations of the renal resistance index using Doppler ultrasound or captopril scintigraphy are effective methods by which to classify patients as responders or nonresponders to intervention (21,22). Other indications for renal artery PTA include fibromuscular dysplasia, Takayasu arteritis, and post-transplantation stenosis. Patients with classic symptoms of chronic mesenteric ischemia and a favorable lesion have good results after PTA. Patients with less than optimal mesenteric lesions may also be approached with PTA when considered poor candidates for revascularization. Most ostial renal and mesenteric lesions may be approached with primary PTA, though most of them will require stenting. Carotid angioplasty for arteriosclerotic occlusive disease is presently undergoing extensive study, with no clear indications for its performance outside ongoing clinical trials (23–25). Carotid angioplasty for the management of symptomatic fibromuscular dysplasia of the carotid arteries on the other hand has produced excellent results and become an accepted standard of care (26,27). PTA of the brachiocephalic, subclavian, and axillary artery may be considered for the treatment of exertional upper extremity ischemia, ulcerative lesions, “subclavian steal” syndrome, “coronary steal” syndrome, and in anticipation for coronary or axillofemoral bypasses. The results of subclavian artery PTA for upper extremity ischemia or subclavian steal syndrome compare favorably with those of carotid–subclavian bypass (28). The role of PTA in the treatment of chronic venous occlusions has been significantly expanded by the introduction of vascular stents. The results of PTA alone in patients with symptomatic superior vena cava/brachiocephalic or inferior vena cava/iliac vein stenosis or occlusion have been universally inferior to those seen on the arterial side of the circulation (29).

Access

Technique

Guidewire Crossing

Preparation PTA is well tolerated under local anesthesia with 1% lidocaine, and liberal use of intravenous sedation will avert patient anxiety and discomfort. Using these measures, even major vascular, endovascular, or hybrid interventions can be performed (30,31). All patients should have electrocardiographic and blood pressure monitoring. A urinary catheter may be considered, depending on the anticipated length of the intervention. All patients undergoing PTA should be on antiplatelet therapy, which should be continued for at least 3 months after the procedure. After confirming intra-arterial access and before wire and catheter manipulation, systemic anticoagulation is obtained with heparin 50–100 units/kg. Although there is no strong evidence to support the prophylactic use of antibiotics in endovascular cases, if stent placement is anticipated, antibiotic prophylaxis with a first-generation cephalosporin is recommended (32–34).

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Obtaining vascular access is fundamental to the performance of PTA. The percutaneous approach is preferred when it can be performed safely. A cutdown technique should be considered when the access vessel is small or recently surgically dissected (less than 4 to 6 weeks) to minimize access site complications (35). The preferred site of vascular access is that which is closest to the lesion to be dilated but which allows adequate working room to complete the procedure. This optimizes catheter tracking (“pushability”), the lack of which can be a problem when working over acutely angled aortic bifurcations or through tortuous iliac arteries. Proximal iliac lesions are therefore best treated from an ipsilateral, retrograde, common femoral access, whereas lesions of the very distal external iliac artery, common femoral artery, or proximal SFA can only be treated from the contralateral femoral or axillary approach, since an ipsilateral puncture would not provide adequate working room for the balloon, even without a sheath. Lesions distal to the proximal third of the SFA are best approached through an ipsilateral, antegrade, common femoral puncture. Renal arteries can be approached from either a femoral or left axillary site of access, while mesenteric arteries are best approached from the axillary artery. A 5 or 6 Fr. introducer sheath can accommodate most angioplasty catheters, but if the use of a guiding catheter or stent is anticipated, a larger diameter (7 to 10 Fr.) sheath may be needed. For renal, subclavian, or contralateral iliac arteries, guiding catheters or long guiding sheaths are invaluable for wire/catheter stabilization and contrast injection for angiographic monitoring of the procedure. They are also required for the safe delivery of balloondeployed stents.

Successful crossing of the intended lesion with a guidewire is the next and often most difficult step in PTA. While a Jtipped guidewire has the lowest potential for vessel injury, the large profile nondirectional leading element will not allow wire advancement across most severely stenotic lesions. Alternatively, a straight or angled floppy-tipped wire such as a Wholey (Mallinckrodt Inc., St Louis, MO), Terumo Glidewire (Boston Scientific Co., Natick, MA), or Bentson (Cook Inc., Bloomington, IN) can be used with careful fluoroscopic guidance. The Glidewire has a hydrophilic coating that renders it so slippery that extreme care must be taken not to advance the wire in a dissection plane behind the offending lesion as subsequent dilation within the wrong plane may result in a hemodynamically significant dissection and vessel occlusion. At times, performance of a floppy-tipped guidewire benefits from the additional support afforded by advancing a diagnostic catheter to within a centimeter or two of the end of the wire. Altering the position of the stiffening catheter relative to the tip of the guidewire can provide a variable de-

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gree of floppiness to the guidewire tip. The coaxial use of angle-tipped catheters adds steerability to a straighttipped wire that can aid in directing the wire through tortuous vessel segments or angulated lesions. This may be particularly helpful when dilating renal, subclavian, or other branch vessels, and specific catheter shapes are available for all commonly encountered anatomic configurations to direct the guidewire towards the origin of the vessel of interest. Once the lesion is crossed, great care must be taken during subsequent catheter exchanges to insure that the guidewire position across the lesion is maintained without advancing the wire far beyond the lesion, where it might cause damage to branch vessels. Crossing arterial occlusions poses additional challenges. An occlusion with a soft thrombotic core may easily allow guidewire passage. This generally mandates use of an angled or floppy-tipped Glidewire. Resistant occlusions may require extra support for the guidewire, which can be provided by a straight catheter positioned within a centimeter or two of the tip of the guidewire. This allows the flexible tip to probe the lesion while preventing the wire from buckling under the stress of firm forward pressure. Guidewire passage through occlusions often occurs, not surprisingly, in a subintimal plane. Therefore, it is imperative that reentry of the guidewire into the lumen of the vessel be confirmed to insure that dilation will reestablish continuity of the flow channel rather than extend the occlusion. Spinning the wire and observing free rotation of the angled tip, careful inspection of the course of the wire in several projections, or advancing a small catheter over the guidewire into the reentered vessel and injection of contrast are all measures that can be employed to confirm that reentry has occurred. Following traversal of an occlusion, a trial of thrombolytic therapy may be warranted, since a significant component of the occlusion may be thrombotic in nature and, therefore, amenable to dissolution. Not only can this reduce the overall length of the vessel requiring subsequent dilation but also minimizes the chance of embolization of unstable thrombus during the dilation. While the chances of successful clot lysis are significantly enhanced if the thrombus is less than 2 weeks old (36–38), even substantially older thrombus can be successfully lysed, though less predictably so (38). The inherent instability of acute thrombus mandates a trial of lysis prior to dilation in patients suspected of having unstable thrombus, while the need to attempt lysis in clinical situations suggestive of more chronic occlusions remains a subject of debate.

Angioplasty Selection of an angioplasty balloon requires judgment and, at times, calibration and measurement of angiographic images. Once selected, the angioplasty balloon is prepared by placing it under negative pressure by a syringe containing half-strength contrast. Upon release of the suction the balloon inflation channel fills with the contrast,

allowing visualization of the balloon inflation and minimizing the risk of air embolization were the balloon to rupture. Balloon angioplasty catheters are generally not test inflated prior to use since this would enlarge the profile of the balloon, possibly complicating its passage across a lesion. The guidewire channel is simply irrigated with saline. Correct positioning of the balloon across the lesion to be dilated can be achieved by fluoroscopic reference to anatomic structures or radiopaque external markers placed at the time of the scout angiogram. Care must be taken to insure that the marker system not be moved and that alignment of the scout and positioning images are identical. “Road-mapping” fluoroscopy, whereby a contrast-enhanced vessel image is overlaid onto a live fluoroscopic image, may be helpful for accurate positioning. Contrast injections through an adequately positioned and oversized guiding catheter or sheath can be used to effectively monitor the position of the balloon. It is generally preferable to inflate angioplasty balloon catheters with dilute contrast delivered by a pressure monitoring device to insure that safe inflation pressure limits are not exceeded. Balloon inflation is monitored fluoroscopically, and, as the pressure within the balloon increases, any waist in the balloon profile disappears as the lesion dilates. The optimal number and duration of inflations is not currently known. Experimental data would suggest that inflation periods of 30 to 60 seconds are sufficient to allow for a desirable plastic deformation of the cellular components of the media (10,39). After fluoroscopic confirmation of a complete deflation, the angioplasty balloon is withdrawn from the region and out of the guiding catheter or introducer sheath. The appreciation of pain by the patient upon dilation is common and generally resolves with deflation of the balloon. Pain during PTA may be related to stretching of the adventitial nerve fibers and failure to experience pain may indicate insufficient dilation. Persistent pain after deflation of the balloon should prompt reevaluation of the situation by contrast injection since it may indicate arterial rupture with extravasation. This further reinforces the need to maintain guidewire crossing of all lesions until their final assessment has been performed since treatment of any vessel rupture or severe dissection endoluminally requires maintained access to the true vascular channel. Atherosclerotic plaques occurring at bifurcations are essentially single plaques with extensions into both vessels and require special consideration because of this. Dilation of only one branch vessel can result in fracture of the plaque in the other branch, with the potential for dissection, stenosis, or occlusion. The aortic bifurcation is a common location for this situation, with atherosclerotic plaque involving the origins of both of the common iliac arteries. In such situations dilation is best accomplished with the “kissing balloon” technique, whereby both proximal common iliac arteries are dilated simultaneously

Chapter 18 Balloon Angioplasty of Peripheral Arteries and Veins

from bilateral femoral artery punctures with the balloons “kissing” in the distal aorta. This approach supports both sides during dilation and is recommended for proximal common iliac lesions, even if only one of them is severe enough to warrant therapeutic dilation. At the very least, placing a guidewire across the “contralateral” vessel will preserve access to that pathway should a dissection or occlusion require treatment (13). Similarly, when the lesion to be treated is in close proximity to a branch vessel, such as in a mid-renal artery stenosis, passage of two guidewires, one into each branch, will insure access to both branches should a dissection or occlusion occur after treatment of the proximal lesion. Dilation across branch vessel origins must be approached with caution since it may result in occlusion of the branch vessel. While this may be of little consequence for some vessels, such as the hypogastric artery, loss of a vertebral artery during dilation of a subclavian lesion may have more severe consequences and good clinical judgment is warranted.

Assessment of Results Anatomically, PTA is considered a technical success if there is less than a 30% residual stenosis and no flowlimiting dissection present upon completion of the procedure as determined by multiplane arteriograms or intravascular ultrasound. A greater than 30% residual stenosis, though not necessarily hemodynamically significant, correlates with early recurrence. Assuming dilation has been performed with an appropriately sized balloon, treatment of a >30% residual stenosis, a persistent pressure gradient, or a severe dissection is generally by placement of a stent. Hemodynamic assessment when possible is considered a more reliable measure of PTA success than the angiographic appearance alone. Simultaneous pressure determinations, proximal and distal to the treated lesion, are the most accurate method of assessing hemodynamics (Fig. 18.1). However, this requires two sites of arterial access, which may not otherwise be needed, rendering this method an impracticable standard. More commonly, the “pull-through” pressure measuring technique is utilized, in which pressures are measured by an end-hole catheter as it is withdrawn across the treated area. A resting pressure difference across the lesion of >5 mmHg indicates an inadequate dilation. Disadvantages of pull-through pressures include having to lose wire crossing in order to monitor pressure, and potentially inaccurate measurements if the catheter originates from the upstream side of the lesion due to partial obturation of the vessel lumen by the catheter. Pharmacologic vasodilation produced by the direct injection of vasodilators into the downstream vascular system can be used to detect borderline hemodynamically significant lesions, which are mani-

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fested by a drop in pressure downstream of the lesion of >20 mmHg (Table 18.1).

Complications Complications of PTA may occur at the access site, in the trajectory course, at the PTA site, in the runoff vascular bed, and systemically, as summarized in Table 18.2. Arterial puncture is the most uncontrolled part of the PTA procedure and not surprisingly hematoma at the entry site is the most common complication of arteriography and PTA. Risk factors for this complication include hypertension, the use of large sheaths, and/or thrombolytic therapy. For common femoral artery access, vessel punctures cephalad to the inguinal ligament or caudal to the femoral head are associated with an increased risk of bleeding complications because of the inability to effectively apply compression after removal of the catheter or sheath (35). Hematomas typically occur soon after the catheter and sheaths are removed. In patients given heparin, removal of the sheath is usually delayed until the activated coagulation time (ACT) is less than 200 or, alternatively, the anticoagulation has been reversed with protamine. Occasionally, hematomas may occur during the procedure from bleeding around the sheath, which may be lessened by upgrading to a larger sheath. Upper extremity access carries a higher risk of complications due to the smaller caliber of the brachial or axillary arteries and the close proximity of the brachial plexus. Axillary artery hematomas producing neurological symptoms must be recognized early and drained surgically to prevent permanent neurological deficits. Performing a high brachial puncture just lateral to pectoralis major muscle, where the nerves are less approximated to the brachial artery and arterial compression is most effectively applied, can mitigate most of these complications (40). Other access site complications include arteriovenous fistulas, pseudoaneurysm, dissection, and thrombosis. Ultrasound-guided compression or thrombin injection is an effective treatment for most puncture site pseudoaneurysms (41). Larger arteriovenous fistulas and pseudoaneurysms, or those in patients requiring continuous anticoagulation, are more effectively treated by embolization techniques, implantation of covered stents, and, rarely, surgical repair (41,42). A puncture site dissection recognized prior to advancement of the sheath is usually effectively treated by simply withdrawing the needle or wire. If a sheath has been advanced into a dissection, an intervention to seal the dissection after removal of the sheath may be required. Major complications related to the actual balloon angioplasty include embolization, dissection, spasm, and perforation. Embolization is most likely to result from wire/catheter manipulation or balloon dilation of irregular or ulcerated lesions or fresh thrombus. Treatments for

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Part III Basic Vascular and Endovascular Techniques

A

I

B

1 mV

Gain: 100

1 mV

II

1 mV

Gain: 100

1 mV

200

s s

s

s

s

s

s

s s

100

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FIGURE 18.1 (A) Initial contrast AP aortogram via a right femoral artery access demonstrates a left common iliac artery stenosis of unclear hemodynamic consequences in a patient with symptoms of left lower extremity claudication. (B) Catheterization of left iliac via a second access site in the ipsilateral left femoral artery. The graduated guidewire across the lesion allows for precise vessel measurements for accurate sizing of PTA balloon catheters. (C) Arterial pressure waveforms from the right and left femoral sheaths reveal a 30 mmHg systolic gradient. (D) Post-PTA aortogram demonstrated an excellent anatomic result with no residual stenosis.

Chapter 18 Balloon Angioplasty of Peripheral Arteries and Veins

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TABLE 18.1 Periprocedural criteria for determining technical success of percutaneous transluminal angioplasty Parameters

Criteria

Anatomic Angiographic residual stenosis Intravascular ultrasound

<30% stenosis <30% stenosis

Hemodynamic Symmetrical pressures determinations Pull-through pressures Pharmacologic stress

<5 mmHg gradient <5 mmHg gradient <20 mmHg gradient

TABLE 18.2 Complications from percutaneous transluminal angioplasty Access site Hematoma Hemorrhage Nerve laceration by entry needle Nerve ischemia from neurovascular sheath hematoma Arteriovenous fistula Intimal dissection Arterial thrombosis Pseudoaneurysm

A

Catheter related Inadvertent bleeding from open end or side-ports Air embolism Accidental displacement of coils or stents PTA site Dissection Thrombosis Failure of balloon deflation Arteriovenous fistula Arterial rupture Accelerated arteriosclerosis Runoff site Embolization Spasm Thrombosis Systemic Allergic reactions Fluid overload Nephrotoxicity Vasovagal response Arrhythmias

B clinically significant embolization include catheterdirected thrombolysis or surgical thrombectomy. Consideration should be given to primary stenting without predilation of lesions thought to be at high risk for embolization. In this scenario, the stent helps to trap atherosclerotic debris and, therefore, reduce the risk of embolization. Dissection following angioplasty may occur from the manipulation of wires and catheters through atherosclerotic lesions or bifurcation points, or from the therapeutic dilation by the balloon angioplasty catheter, and may pre-

FIGURE 18.2 (A) Severe left common iliac artery dissection following PTA. (B) Successful treatment of iliac artery dissection by post-PTA stent deployment.

sent as a small flap of little clinical significance or as a complete arterial occlusion. Localized intimal dissection following PTA is a normal occurrence and should not be considered a complication of the procedure (10). On the other hand, angiographically prominent or hemodynamically significant dissections should be treated by stent deployment (Fig. 18.2).

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Spasm is a common condition following PTA in certain anatomic locations, such as renal and tibial vessels. This condition must be rapidly differentiated from acute thrombosis and treated with vasodilators or thrombolytic agents as appropriate. Arterial rupture following PTA is an unusual event, usually caused by overdilation of a highly calcified artery or sclerotic vein. Arterial rupture may result in hemorrhage, hematoma, arterial occlusion, or the formation of an arteriovenous fistula (Fig. 18.3) (43–50). Management options include observation, deployment of a stent or stent-graft, or emergency surgical intervention, depending on the clinical circumstance.

Surveillance and Recommended Follow-up

A

Close monitoring following PTA is as important to good long-term results as in open vascular reconstructions (51,52). Treatment of a recurrent stenosis with a second endovascular procedure is more likely to be successful and durable than an attempt to restore patency of an occlusion that might result from inadequate follow-up. A variety of modalities are used to monitor the status of endovascular interventions, applying clinical, hemodynamic, and anatomic criteria. Duplex ultrasound is most frequently used for postangioplasty follow-up. Because there are currently no well-defined criteria to determine a 30% degree of stenosis with this modality, a clinically significant restenosis is usually defined by duplex criteria that identify a >50% stenosis of the treated lesion. Evaluation intervals for all sites of PTA are somewhat arbitrary. In general we recommend clinical evaluation and duplex scanning at the time of discharge and at 1, 3, and 6 months, with follow-up every 6 months thereafter. Suspected restenotic lesions should be confirmed with arteriography, and addressed promptly.

B

Conclusion

C FIGURE 18.3 (A) Right femoral angiogram demonstrates a focal high-grade superficial femoral artery stenosis in a patient with claudication. (B) Post-PTA angiogram demonstrates an AV fistula with early opacification of the superficial femoral vein. (C) Successful treatment of superficial femoral AV fistula by post-PTA stent deployment.

The technologies related to PTA continue to rapidly evolve, driven by high demand from patient and physician for more effective minimally invasive techniques for treating vascular disease. Continued development of new technologies and adjuvant techniques, such as subintimal angioplasty, microwave thermal balloon angioplasty, cutting-balloon angioplasty, remote endarterectomy, drug-eluting or irradiating stents, and endovascular grafting, in combination with new pharmacologic agents, insures that PTA will play an ever-increasing role in the treatment of arterial occlusive disease.

References 1. Fogarty T, Cranley J, et al. A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstetrics 1963; 116:241–244.

Chapter 18 Balloon Angioplasty of Peripheral Arteries and Veins 2. Dotter CT, Judkins M. Transluminal treatment of arteriosclerotic obstruction: description of a new technique and preliminary report of its application. Circulation 1964; (30):654–670. 3. Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction. Description of a new technic and a preliminary report of its application. 1964. Radiology 1989; 172(3 Pt 2):904–920. 4. Dotter CT. Transluminal angioplasty: a long view. Radiology 1980; 135(3):561–564. 5. Dotter CT, Judkins MP, Rosch J. Transluminal angioplasty in arteriosclerotic obstruction of the lower extremities. Med Times 1969; 97(7):95–108. 6. Gruntzig A, Hopff H. [Percutaneous recanalization after chronic arterial occlusion with a new dilator-catheter (modification of the Dotter technique) (author’s transl)]. Dtsch Med Wochenschr 1974; 99(49):2502–2511. 7. Castaneda-Zuniga WR, Formanek A, et al. The mechanism of balloon angioplasty. Radiology 1980; 135(3):565–571. 8. Castaneda-Zuniga WR, Sibley R, Amplatz K. The pathologic basis of angioplasty. Angiology 1984; 35(4):195–205. 9. Zarins CK, Lu CT, et al. Arterial disruption and remodeling following balloon dilation. Surgery 1982; 92(6):1086–1095. 10. Castaneda-Zuniga WR, Tadavarthy SM, et al. ‘Pseudo’ intramural injection following percutaneous transluminal angioplasty. Cardiovasc Intervent Radiol 1984; 7(2):104–108. 11. Guzman LA, Mick MJ, et al. Role of intimal hyperplasia and arterial remodeling after balloon angioplasty: an experimental study in the atherosclerotic rabbit model. Arterioscler Thromb Vasc Biol 1996; 16(3):479–487. 12. Fanelli C, Aronoff R. Restenosis following coronary angioplasty. Am Heart J 1990; 119(2 Pt 1):357–368. 13. Hood DB, Hodgson KJ. Percutaneous transluminal angioplasty and stenting for iliac artery occlusive disease. Surg Clin North Am 1999; 79(3):575–596. 14. Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology 1997; 204(1):87–96. 15. Zdanowski Z, Albrechtsson U, et al. Percutaneous transluminal angioplasty with or without stenting for femoropopliteal occlusions? A randomized controlled study. Int Angiol 1999; 18(4):251–255. 16. Johnston KW. Aortoiliac disease treatment. A surgical comment. Circulation 1991; 83(2 Suppl):I61–I62. 17. Johnston KW. Factors that influence the outcome of aortoiliac and femoropopliteal percutaneous transluminal angioplasty. Surg Clin North Am 1992; 72(4):843–850. 18. Hunink MG, Wong JB, et al. Revascularization for femoropopliteal disease. A decision and costeffectiveness analysis. JAMA 1995; 274(2):165–171. 19. Leertouwer TC, Gussenhoven EJ, et al. Stent placement for renal arterial stenosis: where do we stand? A metaanalysis. Radiology 2000; 216(1):78–85. 20. Hood DB, Hodgson KF. Renovascular Disease. In Ahn WSMaSS, ed. Endovascular Surgery. Philadelphi, PA: W.B. Saunders, 2001. pp. 233–241. 21. Radermacher J, Weinkove R, Haller H. Techniques for predicting a favourable response to renal angioplasty in

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36. 37.

38.

255

patients with renovascular disease. Curr Opin Nephrol Hypertens 2001; 10(6):799–805. Radermacher J, Chavan A, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renalartery stenosis. N Engl J Med 2001; 344(6):410–417. Clagett GP, Barnett HJ, Easton JD. The carotid artery stenting versus endarterectomy trial (CASET). Cardiovasc Surg 1997; 5(5):454–456. Hobson RW, 2nd. Carotid angioplasty-stent: clinical experience and role for clinical trials. J Vasc Surg 2001; 33(2 Suppl):S117–123. Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): a randomised trial. Lancet 2001; 357(9270):1729–1737. Ballard JL, Guinn JE, et al. Open operative balloon angioplasty of the internal carotid artery: a technique in evolution. Ann Vasc Surg 1995; 9(4):390–393. Wilms GE, Smits J, et al. Percutaneous transluminal angioplasty in fibromuscular dysplasia of the internal carotid artery: one year clinical and morphological follow-up. Cardiovasc Intervent Radiol 1985; 8(1):20–23. Motarjeme A, Gordon GI. Percutaneous transluminal angioplasty of the brachiocephalic vessels: guidelines for therapy. Int Angiol 1993; 12(3):260–269. Sanders RJ, Haug C. Subclavian vein obstruction and thoracic outlet syndrome: a review of etiology and management. Ann Vasc Surg 1990; 4(4):397–410. Barkmeier LD, Hood DB, et al. Local anesthesia for infrainguinal arterial reconstruction. Am J Surg 1997; 174(2):202–204. Henretta JP, Hodgson KJ, et al. Feasibility of endovascular repair of abdominal aortic aneurysms with local anesthesia with intravenous sedation [see comments]. J Vasc Surg 1999; 29(5):793–798. Paget DS, Bukhari RH, et al. Infectibility of endovascular stents following antibiotic prophylaxis or after arterial wall incorporation. Am J Surg 1999; 178(3):219–224. Deitch JS, Hansen KJ, et al. Infected renal artery pseudoaneurysm and mycotic aortic aneurysm after percutaneous transluminal renal artery angioplasty and stent placement in a patient with a solitary kidney. J Vasc Surg 1998; 28(2):340–344. Dravid VS, Gupta A, et al. Investigation of antibiotic prophylaxis usage for vascular and nonvascular interventional procedures. J Vasc Interv Radiol 1998; 9(3):401–406. Hodgson KJ, Mattos MA, Sumner DS. Access to the vascular system for endovascular procedures: techniques and indications for percutaneous and open arteriotomy approaches. Semin Vasc Surg 1997; 10(4):206–221. Ouriel K. Thrombolysis or operation for peripheral arterial occlusion. Vasc Med 1996; 1(2):159–161. Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS) Investigators. N Engl J Med 1998; 338(16):1105–1111. Wholey MH, Maynar MA, et al. Comparison of thrombolytic therapy of lower-extremity acute, subacute, and chronic arterial occlusions. Cathet Cardiovasc Diagn 1998; 44(2):159–169.

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39. Consigny PM, LeVeen RF. Effects of angioplasty balloon inflation time on arterial contractions and mechanics. Invest Radiol 1988; 23(4):271–276. 40. Lipchik EO, Sugimoto H. Percutaneous brachial artery catheterization. Radiology 1986; 160(3):842–843. 41. Hood DB, Mattos MA, et al. Determinants of success of color-flow duplex-guided compression repair of femoral pseudoaneurysms. Surgery 1996; 120(4):585–588; discussion 588–590. 42. Waigand J, Uhlich F, et al. Percutaneous treatment of pseudoaneurysms and arteriovenous fistulas after invasive vascular procedures. Catheter Cardiovasc Interv 1999; 47(2):157–164. 43. Korogi Y, Takahashi M, et al. Percutaneous transluminal angioplasty: pain during balloon inflation. Br J Radiol 1992; 65(770):140–142. 44. Kelly AJ. Case report: iliac artery rupture — percutaneous treatment by stent insertion. Clin Radiol 1995; 50(12):876–877. 45. Alfonso F, Goicolea J, et al. Arterial perforation during optimization of coronary stents using high-pressure balloon inflations. Am J Cardiol 1996; 78(10):1169– 1172. 46. Formichi M, Raybaud G, Benichou H, Ciosi G. Rupture of the external iliac artery during balloon angioplasty:

47.

48.

49.

50.

51.

52.

endovascular treatment using a covered stent. J Endovasc Surg 1998; 5(1):37–41. Cooper SG, Sofocleous CT. Percutaneous management of angioplasty-related iliac artery rupture with preservation of luminal patency by prolonged balloon tamponade. J Vasc Interv Radiol 1998; 9(1 Pt 1):81–83. Matsi PJ, Manninen HI. Complications of lowerlimb percutaneous transluminal angioplasty: a prospective analysis of 410 procedures on 295 consecutive patients. Cardiovasc Intervent Radiol 1998; 21(5):361–366. Scheinert D, Ludwig J, et al. Treatment of catheterinduced iliac artery injuries with self-expanding endografts. J Endovasc Ther 2000; 7(3):213–220. Redman A, Cope L, Uberoi R. Iliac artery injury following placement of the memotherm arterial stent. Cardiovasc Intervent Radiol 2001; 24(2):113–116. Sampson L, Ayerdi J, Gupta S. Intraprocedural monitoring. In White R, Fogarty T, eds. Peripheral endovascular interventions. New York, NY: Springer, 1998. pp. 93–102. Henretta JP, Hodgson KJ. Postintervention survillance of endovascular procedures. In White R, Fogarty T, eds. Peripheral endovascular interventions. New York, NY: Springer, 1998. pp. 103–118.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 19 Stents for Peripheral Arteries and Veins Carber C. Huang and Samuel S. Ahn

Vascular stents are devices that can be placed intraluminally to maintain the patency of the artery against either compressive forces or compromise by residual plaque after angioplasty. The concept of vascular stents was first described in 1912 by Alexis Carrel (1). Dotter and Judkins, in 1964, performed the first transluminal angioplasty in a patient with ischemic extremities (2). Dotter, at that time, predicted the need for an endoluminal “splint” following angioplasty, to prevent early failure due to recoil and dissection (2). Five years later, Dotter reported his experience with stainless-steel, coil-spring endarterial tube grafts in canine popliteal arteries (3). In 1983, Dotter et al. and Cragg et al. separately reported the first application of transluminal nitinol coil stents (4,5). Enthusiasm for vascular stents did not begin to blossom until the advent of rigid angioplasty balloons composed of polyvinyl chloride or polyethylene in the late 1970s (6). These rigid, low-compliance balloons achieved a much higher radial force in fully inflated state than previous balloons made of latex materials, thus producing better clinical results of transluminal balloon angioplasty. Despite improved clinical success rate, however, transluminal balloon angioplasty has complications and limitations. Early restenosis due to elastic recoil of the arterial wall or occlusion caused by intimal dissection may occur after angioplasty. Mural thrombus formation produced by residual luminal irregularities after angioplasty may cause thrombotic occlusion of the artery. Heavily calcified vessels are not amenable to balloon angioplasty. Late restenosis due to intimal hyperplasia or progression of atherosclerosis may occur after angioplasty. The need to deal with these complications and limitations of translu-

minal angioplasty fueled the development of modern vascular stents and led to their widespread clinical application today.

General Principles of Vascular Stents Vascular stents provide an intraluminal mechanical scaffold to oppose elastic recoil and to seal dissection planes created by angioplasty. Therefore, certain characteristics are desirable in a vascular stent. The stent should possess high radial force yet maintain longitudinal flexibility. It should have a low-profile delivery catheter system with a simple deployment mechanism. The stent should allow precise delivery to the target vessel with minimal foreshortening. It should be biologically inert yet promote a thin layer of endothelialization without causing intimal hyperplasia. The stent should be thromboresistant, isocompliant with the vessel at the leading and trailing stent edges, highly radiopaque, and retrievable in the event of suboptimal placement. The stent should be durable and provide long-term patency. It should be inexpensive and available in different lengths and diameters. Becker described these characteristics of an ideal metallic stent in 1991 (Table 19.1) (7). Unfortunately, the ideal stent does not exist. All of the available stents today have some advantages and disadvantages. Vascular stents can be categorized by their methods of deployment into three broad categories: balloonexpandable, self-expanding, and thermal-expanding.

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Balloon-expandable Stents Balloon-expandable stents (7–12) are designed to be preloaded and compressed on an angioplasty balloon catheter before insertion and deployment in the vessel. Once the stent is positioned intraluminally, it is deployed by inflating the balloon to expand the stent. Balloonexpandable stents can be reinflated beyond their predetermined diameter with a larger balloon if needed in order to embed the struts of the stent well into the vessel wall. Balloon-expandable stents possess high radial strength, making them very rigid once deployed. The rigidity of these stents is advantageous against elastic recoil of the vessel wall after angioplasty and in stenotic vessels with calcified plaques. They also resist external compression

TABLE 19.1 Ideal characteristics of metallic stent (modified from reference 7) Strong radial force to oppose elastic recoil Good longitudinal flexibility Minimal foreshortening to allow precise placement Resistant to external compression Biologically inert Thromboresistant Isocompliant with the vessel Allows endothelization without neointimal hyperplasia Highly radiopaque Low-profile delivery catheter system Simple mechanism of deployment Retrievable after deployment Durable with good long-term patency rate Available in various sizes and lengths Inexpensive

A

B

C

once placed inside the vessels. Owing to their inflexibility, balloon-expandable stents have relatively minimal foreshortening, permitting precise placement to cover the target lesion. The stable, non-shifting surface of the struts also facilitates early endothelialization (13). The main disadvantage of balloon-expandable stents is the lack of longitudinal flexibility, which may cause difficulty in treating lesions in tortuous vessels. In addition, the lack of longitudinal flexibility does not permit deployment across areas of flexion, such as behind the inguinal ligament, behind the knee, or in thoracic outlet areas due to the risk of stent collapse (14). Common examples of balloonexpandable stents are the Palmaz stent (Cordis, Miami, FL), the Strecker stent (Boston Scientific, Quincy, MA), the Gianturco–Roubin stent (Wilson-Cook, WinstonSalem, NC), and the Wiktor stent (Medtronic, Minneapolis, MN). Palmaz Stent The Palmaz stent is the most widely used balloonexpandable stent in the United States. Although available in assorted sizes, only the P308 is approved by Food and Drug Administration (FDA) for use in the common and external iliac arteries. The P indicates Palmaz, the 30 denotes the length (in mm) of the stent in its nonexpanded state, and the 8 corresponds to the minimal expansion diameter (in mm) of the stent. The Palmaz stent is constructed from medical grade 316L stainless-steel tube bearing staggered rows of rectangular slots that have been etched into the wall (Fig. 19.1). The rows encompass the circumference of the tube. Upon balloon expansion, the rectangular slots enlarge to produce diamond-shaped openings within the stent. Unlike self-expanding or thermal-expanding stents, the final diameter of the expanded Palmaz stent can be adjusted by the size of the balloon used. For example, the P308 stent can achieve a maximal

FIGURE 19.1 Palmaz balloon-expandable stent. (A) Unmounted stent. (B) Stent loaded and crimped onto an angioplasty balloon. (C) Fully expanded stent. (Adapted from Song M, Rodino W, Wisselink W, Panetta TF: Vascular Stents. In Moore WS, Ahn SS, eds. Endovascular Surgery, 3rd edn. Philadelphia: WB Saunders, 2001, p. 72.)

Chapter 19 Stents for Peripheral Arteries and Veins

259

TABLE 19.2 Comparison of Palmaz stent’s expanded length to its expanded diameter (from reference 12) Length at Expanded Diameter (mm) Stent

Length (mm)

P104 P154 P204 P294 P394

10 15 20 29 39

P128 P188 P308

12 18 30

A

4

5

6

7

8

9

9.9 14.7 19.6 29.2 38.9

9.7 14.5 19.2 28.7 38.2

9.4 14.0 18.6 27.8 37.0

9.0 13.5 17.8 26.6 35.5

8.5 12.7 16.8 25.1 33.4

7.8 11.6 15.4 23.0 30.6

11.8 17.6 28.9

11.6 17.3 28.4

B

C

D

E

10

11

12

11.4 17.0 27.8

11.1 16.5 NA

10.8 16.0 26.2

F

FIGURE 19.2 Primary stenting with predilation. (A) Guidewire is placed across the lesion. (B) Distensibility of the lesion is demonstrated by balloon inflation. (C) The sheath/dilator combination is advanced across the lesion. (D) The dilator is replaced by the balloon/stent combination. (E) Balloon inflation follows retraction of the sheath. (F) Fully expanded stent is in place. (Adapted from Song M, Rodino W, Wisselink W, Panetta TF: Vascular Stents. In Moore WS, Ahn SS, eds. Endovascular Surgery, 3rd edn. Philadelphia: WB Saunders, 2001, p. 73.)

expansion diameter of 12 mm using a 12-mm balloon. However, a certain degree of stent shortening will occur as a result of overdilation (Table 19.2). Depending upon the balloon catheter diameter, these stents will require a 6- to 12-Fr. introducer sheath system. The Palmaz stent comes either premounted on an angioplasty balloon or unmounted from the manufacturer. The Palmaz stent is usually deployed in conjunction with an introducer sheath which is used to cross the lesion to be stented. With the introducer sheath in place, the stentballoon assembly is advanced within the sheath to the level of the stenotic lesion (Fig. 19.2). The sheath is then retracted, uncovering the mounted stent. Deployment of the stent is achieved by inflating the balloon. Repeated

balloon dilation is often necessary to make sure the stent is properly embedded in the vessel wall and not protruding into the lumen. The balloon is deflated and withdrawn, and then a completion angiogram is performed (14,15). Strecker Stent The Strecker stent is a balloon-expandable stent made of interwoven tantalum wire mesh. This mesh composition provides greater flexibility and elasticity than the Palmaz stent. The high density of the tantalum makes the stent radiopaque and therefore extremely visible during deployment. The stent comes premounted by the manufacturer on an angioplasty balloon catheter with its ends covered

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by retractable Silastic sheaths. When the balloon is inflated, the Silastic sheaths shorten, exposing the stent to the arterial lumen. Because no introducer sheath is required, the stent-balloon assembly has a low-profile configuration and can be placed through a relatively small 8-Fr. delivery system. For stents greater than 7 mm, a 9-Fr. delivery system is required. Strecker stents are available in 4 to 12 mm diameters and a maximum length of 8 cm (16,17). Gianturco–Roubin Stent The Gianturco–Roubin stent is a balloon-expandable, flexible stent made of stainless-steel wire wrapped cylindrically with bends adopting alternating U and inverted U configurations every 360°. This stent is also called the “book binder” stent because it resembles the binding of a spiral notebook. When expanded, it covers 10% of the surface area within the stented region. The stent comes preloaded on a balloon catheter. It is very low profile, thus allowing introduction through a 6-Fr. introducer with no protective sheath required. Because of its low expansion ratio, stenting a large vessel would require an excessively large catheter and an even larger delivery sheath. Therefore, peripheral vascular applications are limited to small vessels like the tibial arteries and renal branch vessels. Currently, it is FDA approved for coronary artery stenting. Gianturco–Roubin stents are available in 2 to 4 mm diameters and maximum length of 20 mm.

A

Wiktor Stent The Wiktor stent is a balloon-expandable, sinusoidal stent composed of tantalum wire wound into an open helix. The stent can be delivered without the use of a protective sheath via an 8-Fr. introducer. Its use is limited to small vessels because of its low expansion to compression ratio.

Self-expanding Stents Self-expanding stents (7–12), composed of stainless steel, are compressed within a delivery catheter and deployed at the target vessel by withdrawing the catheter while the stent is maintained in position with a plunger. Selfexpanding stents rely on a mechanical springlike design to expand to their predetermined diameter. They have a higher degree of longitudinal flexibility, are relatively easier to deploy, and require smaller-diameter delivery systems than balloon-expandable stents. The flexibility of self-expanding stents allows them to be placed in tortuous vessels and permits stent deployment across the aortic bifurcation into the contralateral iliac vessels. The trade-off, however, is less resistance to radial compressive force, or so-called hoop strength. The length of the self-expanding stent after deployment varies considerably with different degrees of expansion because the stent shortens as its diameter increases. To account for this foreshortening characteristic of the self-expandable stent, it is recommended to select a stent diameter approximately 1 mm greater

B

FIGURE 19.3 Wallstent (Schneider). (A) Partially deployed. (B) Fully deployed.

than the desired vessel diameter for deployment. Although the stent self-expands upon release from its delivery system, postdeployment balloon angioplasty should be carried out to ensure that the stent is fully expanded and impacted into the plaque. Unlike the balloonexpandable stents, dilation of the self-expanding stent with a larger balloon is not possible once the predetermined diameter of the stent has been reached. Common examples of self-expanding stents are the Wallstent (Schneider USA/Boston Scientific, Plymouth, MA), and the Gianturco Z-stent (Wilson-Cook Medical, WinstonSalem, NC). Wallstent The Wallstent is the most commonly used self-expanding stent in the United States. It was approved by the FDA in 1996 for use in the common and external iliac arteries. The Wallstent is constructed of thin Elgiloy (cobalt-based) stainless-steel filaments woven into a flexible, tubular braid configuration (Fig. 19.3A and B). It expands by an intrinsic spring action. The filament crossing points are free to pivot, resulting in a very flexible tubular structure

Chapter 19 Stents for Peripheral Arteries and Veins

261

and allowing the stent to be placed through a relatively small introducer system. Additionally, the thickness of the stainless-steel filaments and the braiding angle of the Wallstent determine the stent’s flexibility, degree of foreshortening, and column strength. Wallstents are available in a range of sizes from 2.5 to 15 mm in diameter and length up to 150 mm. The smaller stents are made of stainless-steel filaments from 0.075 to 0.100 mm in diameter and can be delivered on a 5-Fr. catheter system with a 0.014-in. guidewire. The larger stents are constructed from 0.12 to 0.17 mm stainless-steel filaments and require a 7-Fr. delivery system using a 0.035 in. guidewire. The main disadvantage of the Wallstent, owning to its design, is marked shortening upon expansion. As packaged by the manufacturer, the Wallstent is stretched to its lowest profile under a constraining exterior catheter sheath. Due to the low radiopacity of the Wallstent, radiopaque markers are placed near the leading and the trailing ends of the stent to facilitate visualization during deployment. To deploy, the stent delivery system is first advanced across the lesion so the leading end of the stent is slightly beyond its desired final position. The exterior catheter sheath is then retracted, exposing the stent to allow it to expand while the inner plunger holds the stent in place. This unique mechanism of deployment, combined with the Wallstent’s springloaded design, permits the partially deployed stent to be retracted back into the delivery system for redeployment if the position of the stent is unsatisfactory.

of strength and superelasticity (4,19). Superelasticity allows the nitinol alloy to have a high degree of flexibility and resistance to kinks or external compression (20). The nitinol’s predetermined configuration is achieved by heating the nitinol alloy at very high temperatures (5000–10,000°F; 2760–5500°C). Minor variations in alloy composition and processing can alter the transition temperature over a wide range. For medical applications, however, the transition temperature of nitinol is usually set at around 900°F (480°C). The advantage of shape memory allows nitinol stents to be packaged in a compact delivery system. Nitinol stents, similar to Wallstents, should always be slightly oversized to the diameter of the target vessel to ensure good wall apposition, because an undersized stent could not be balloon-expanded further. They are fairly flexible, both during and after deployment, and have relatively minimal foreshortening upon expansion, making stent placement more precise than the Wallstents. The deployment mechanism is similar to that of the self-expanding stents, but nitinol stents are not reconstrainable once deployment has commenced. Nitinol stents are currently only approved by the FDA for stenting in the biliary tree. They are, however, being used in the arterial tree in “offlabel” fashion. Some examples of thermal-expanding stents are the Symphony stent (Boston Scientific, Quincy, MA), the Memotherm stent (C.R. Bard, Murray Hill, NJ), the SMART stent (Cordis, Miami, FL), and the Cragg stent (MinTech, La Ciotat, France).

Gianturco Z Stent

Symphony Stent

The Gianturco Z stent, another type of self-expanding stent, is made of medical grade 304 stainless-steel wire bent into a zigzag pattern. Its ends are connected to form a cylinder. The design of the Gianturco Z stent allows for a high expansion-to-compression ratio, making it suitable for placement in large vessels. The stent is compressed radially and loaded into a delivery system catheter. The deployment mechanism is similar to that of the Wallstent system described above.

The Symphony stent is constructed from a single piece of 0.008 in. nitinol wire bent into large hexagonal cells. The parallel portions of the hexagonal cells are welded together to form a cylindrical tube. The ends of the stent are looped and smooth with gold markers embedded to enhance the radiopacity of the stent (21). Its low profile allows deployment via a 7-Fr. sheath. Depending on the sizes, there is 4.6% to 11.7% of stent shortening upon expansion. Symphony stents are available in sizes from 6 to 14 mm in diameter and length up to 60 mm.

Thermal-expanding Stents

Memotherm Stent

Thermal-expanding stents (7–12) are made of nitinol, an alloy of titanium and nickel. The term nitinol is derived from (Ni)ckel, (Ti)tanium, and (N)aval (O)rdinance (L)aboratories of the United States government, where nitinol was first developed during the 1960s. The unique feature of nitinol is that it possesses the property of shape memory (4,5,18). This refers to the ability of nitinol to reform to its predetermined shape when heated above a preset transition temperature. At temperatures below the transition temperature, the nitinol alloy assumes a malleable configuration which is more suitable for handling and delivery into the vessels. Metallurgically, this thermally induced reversion reflects a crystalline transition from the martensitic phase, the malleable state, to an austenitic phase, in which the alloy exhibits a high degree

The Memotherm nitinol stent is made by cutting rhomboid-shaped patterns out of a plate of nickel–titanium alloy with a laser. The resulting wire mesh is then formed into a pipe shape with no wire crossings (22,23). The Memotherm nitinol stent is less flexible than the Wallstent but more flexible than the Palmaz stent. The transition temperature is between 790 and 950°F. It is low profile and can be deployed via a 7-Fr. sheath. SMART Stent The shape memory alloy recoverable technology nitinol stent, the so-called SMART stent, is composed of short segments of zigzag hoops. This segmented geometry provides the stent greater longitudinal flexibility and conformability than the self-expanding stent. The ability to

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conform, or to adapt, to the contour of the vessel is particularly advantageous in tortuous arteries, as in the internal carotid arteries with redundancies and bends, where the stented vessel ends could be subjected to kinking (24). The transition temperature of the SMART stent is set at 790 to 900°F (420 to 480°C). Cragg Stent The Cragg stent is made of nitinol wire bent in a zigzag configuration and tied together with unresorbable 7–0 polypropylene ligatures in a spiral to form a tube (25). When constrained in the delivery system, the stent has an outer diameter of 2.5 mm and a length of 31 or 62 mm. At body temperature, the stent expands to 8 or 10 mm in diameter and shortens to 29 or 58 mm, respectively, giving it 7% shortening (25). The Cragg stent has good longitudinal flexibility and its radial stiffness is equal to that of the Wallstent. Deployment requires an 8.5-Fr. introducer sheath.

Biologic Response to Intravascular Stent Placement The immediate and long-term patency rates of an implanted stent are intimately related to the biologic tissue responses generated at the tissue–stent interface. The tissue–stent interaction is a dynamic process and is influenced by the surface composition, the size, and the design of the stent. The reactivity of a metal surface placed in contact with circulating blood depends on the physical characteristics of the surface (26). A smooth surface elicits less tissue–stent reaction, making the stent more thromboresistant. This is important because thrombogenicity of the stent surface can be altered by the manufacturing process. Electropolishing, a common finishing process for 300-series stainless steels, removes most of the elements from the metal surface resulting in a very thin, smooth layer of chromium oxide. This stabilizes the surface of the stainless-steel stent by preventing further oxidation and reduces the thrombogenic property of the stent (13,27). Most metals and alloys used for intravascular devices are electropositive in electrolytic solutions, whereas all biological intravascular surfaces are negatively charged (13,27). The positive electrical potential of metallic struts attracts the negatively charged plasma proteins within a few seconds of stent implantation. This proteinaceous layer of fibrinogens, only 5–20 nm thick, inactivates the metal surface, decreasing its thrombogenicity before the arrival of platelets and white blood cells (13). Another property of the stent that imparts metal reactivity with blood is its critical surface tension. For a solid surface to be relatively thromboresistant, the critical surface tension must be between 20 and 30 dynes/cm (13).

Most metals have higher critical surface tensions and are therefore thrombogenic. However, the proteinaceous layer of fibrinogens developed within seconds of stent implantation reduces the critical surface tension to within the thromboresistant range (13,27). The relationship between the diameters of the implanted stent and the vessel also influences tissue–stent interactions. Ideally, stents should be well embedded into the vessel wall upon deployment, creating areas of intimal projection in between the embedded struts. These areas of intimal projection allow reendothelialization of the stent to occur whereas troughs produced by the embedded struts are covered with thrombus formation. If the struts are not properly embedded, thrombus deposition can occur along the entire stented surface, thus severely limiting early reendothelialization through the meshwork of the stent. With continued thrombus deposition and proliferation of fibromyocytes, the luminal diameter decreases further, leading to early restenosis and premature thrombosis of the stent (13,28). Typically, sizing the stent diameter 10% to 15% larger than the diameter of the vessel adjacent to the target area will embed the struts well into the vessel wall. The design of the stent can also influence the biologic response of the tissue to the stent. The characteristic of longitudinal flexibility in a stent is desirable because it permits stent placement in tortuous vessels and contralateral stent deployment across aortic bifurcation. However, longitudinal flexibility can negatively affect the long-term patency of the stent. Dimensional changes imposed by flexion, extension, and radial expansion of the stent create an unstable platform for the endothelial cells to grow, and make them susceptible to sloughing. Consequently, endothelial cells covering the stent are less mature and the underlying neointimal layer is thicker, resulting in a poorer long-term patency rate (13). Within a few minutes after stent implantation, scanning electron microscopy shows amorphous clot irregularly covering the stent surface. At 24 hours after exposure, this cellular layer is replaced by fibrin strands oriented in the direction of flow, providing a favorable substrate for the lateral growth of endothelial cells (13,28). In a few days to weeks, fibromuscular tissues predominantly cover the stent struts and expand eccentrically into the lumen (13). By the end of the 4th week, proliferation of smooth muscle cells, along with the deposition of extracellular matrix, can produce a neointimal layer of approximately 1 mm in thickness (28). In canine arteries, extracellular matrix reaches maximal thickness by the end of the eighth week and is then replaced by collagen (29). Reduction of stent diameter due to this layer of neointimal growth can affect the long-term patency of the stent, particularly in small vessels where there is a greater percentage of luminal narrowing compared to the larger vessels. Neointimal hyperplasia, perhaps, is one of the reasons why it is difficult to achieve long-term patency in stenting small vessels (8).

Chapter 19 Stents for Peripheral Arteries and Veins

Indications for Stent Placement The US FDA has approved stent placement in the iliac artery for the treatment of 1) stenotic or occlusive atherosclerotic lesions and 2) failed or inadequate balloon angioplasty. Initial technical success after balloon angioplasty is generally defined as less than 30% residual diameter stenosis and no significant pressure gradient across the treated lesion at rest and after pharmacologic vasodilation. Pharmacologic vasodilation that simulates exercise can be achieved by injecting a vasodilator, such as nitroglycerin (100–200 mg) or papaverine (10–20 mg), directly into the artery. This provocative test is valuable because up to 75% of patients with a normal resting pressure gradient were found to have an elevated pressure gradient after pharmacologic vasodilation (30). A resting pressure differential exceeding 5–10 mmHg or a vasodilated differential of 10–20 mmHg downstream of the treated lesion indicates the persistence of a hemodynamically significant stenosis (11,31). The presence of a hemodynamically significant stenosis despite repeated attempts at balloon angioplasty is an indication for stent placement. Angiographic residual stenosis of 30% or greater, unstable intimal flap, and acute dissection along the subintimal or the medial layers of the vessel wall are considered inadequate balloon angioplasty results. Stent placement in these situations is also justified to improve initial technical success rate. In addition to FDA-approved indications, there are other conditions for which stent placement is relatively indicated. Although there is no proof, stent placement in areas of restenosis after balloon angioplasty is generally accepted in order to delay the restenotic process due to neointimal hyperplasia or progression of atherosclerosis (32). However, repeat angioplasty and possibly additional stenting may be needed to maintain long-term patency (32–35). In patients with multilevel occlusive disease, balloon angioplasty alone or with stent placement to improve the inflow artery can be used as an adjunctive procedure to a distal, open bypass operation (36–39). This combination of procedures can be performed in a staged or simultaneous fashion. The staging method, endovascular procedure followed at an interval by distal bypass operation, allows the assessment of the hemodynamic results after balloon angioplasty and/or stent placement. The advantages of simultaneous intraoperative balloon angioplasty and/ or stenting with a distal bypass operation are lower rate of complications and shorter length of hospital stay. Both approaches are safe and effective (39,40). Atherosclerotic lesions with complex morphology, such as calcified lesions, eccentric stenoses, and plaques with ulceration or focal aneurysm, are prone to develop complications when treated by balloon angioplasty alone. In addition, they are less amenable to balloon angioplasty, resulting in unsatisfactory long-term patency rates (41–43). Primary stenting, stent placement without prior

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balloon angioplasty, is more effective in treating these lesions (15,44–46). Vessels with calcification are most susceptible to injury by balloon angioplasty, thus primary stenting is preferred. In eccentric stenoses, balloon angioplasty causes uneven stretching of the eccentric plaques. Primary stenting, on the other hand, can dilate the plaques concentrically by applying the dilating force equally around the entire circumference (45). Plaques with ulceration or focal aneurysm are potential sources of distal embolization during balloon angioplasty. In these situations, primary stenting can be employed to seal the ulcerated plaque or focal aneurysm immediately or soon after stent placement, thus avoiding embolization (46). In dealing with occluded arteries, the initial technical success rate of balloon angioplasty alone is unsatisfactory (6,41,47–49,76,85). Postangioplasty stent placement has been used to improve the initial technical success and the long-term patency rates of the occluded iliac arteries (15,25,31,33,50–52). A major concern of postangioplasty stent placement, however, is the risk of distal embolization caused by balloon dilation during recanalization. To minimize this complication, primary stenting has been advocated as the method of choice for the treatment of occluded iliac vessels (53–58). The stent prevents embolization by compressing the atherosclerotic plaque and thrombus against the vessel wall. As in the occluded iliac arteries, stent placement in femoropopliteal artery obstructions has improved initial technical success. However, it fails to achieve better long-term patency rate compared to balloon angioplasty alone (17,50,51,59–63). Furthermore, stent placement in femoropopliteal artery obstructions is associated with increased complications and cost. Therefore, stent placement in the femoropopliteal arteries should be reserved for postangioplasty complications such as extensive or flow-limiting dissections. Stent placement has been utilized to treat symptomatic chronic venous obstructions from various causes that are resistant to balloon dilation. However, the longterm patency rate of venous stenting is rather unsatisfactory (64–66). In addition, the application of endovascular stent-grafts, stents covered with either autologous or synthetic graft materials, has provided an alternative to the surgical treatment of peripheral aneurysms and traumatic vascular injuries (67–69). Table 19.3 summarizes the indications for vascular stent placement.

Contraindications to Stent Placement Arterial perforation due to balloon angioplasty is a contraindication to placement of a vascular stent. Stent placement may lead to severe bleeding or development of a pseudoaneurysm (10). Severely calcified vessels may not be amenable to stent placement and are prone to develop

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TABLE 19.3 Indications for vascular stent placement Inadequate angioplasty Hemodynamically significant stenosis Angiographically significant stenosis, >30% Complicated angioplasty Unstable intimal flap Acute dissection Restenosis post-PTA Adjunctive procedure to distal bypass surgery Symptomatic venous stenosis or obstruction refractory to PTA Complex plaque morphology (primary stenting) Calcified lesions Eccentric stenoses Ulcerated plaques Focal aneurysms Occluded iliac arteries (primary stenting)

complications. Stent placement in a markedly tortuous vessel, particularly with the rigid balloon-expandable stents, is contraindicated. Self-expanding and thermalexpanding stents, with their greater longitudinal flexibility, are more appropriate to treat lesions in tortuous vessels. Stent placement in areas across flexion, such as inguinal ligament, knee, and shoulder, is not desirable due to the risk of stent collapse. Thermal-expanding stents, possessing both radial strength to resist external compression and longitudinal flexibility to allow bending, have been used in areas across flexion, but the long-term durability is not clear (21). Peripheral aneurysms, traumatic arteriovenous fistulas, and pseudoaneurysms should not be treated by bare stents. Covered stents are more suitable for these types of lesions. Stent placement should be avoided in areas of the arteries that may be involved in the proximal or distal site of a bypass graft. Clamping a stented artery may injure the artery and crush the stent in the process. (10). Patients with hypercoagulable disorders should not have a stent placed because it may trigger the coagulation cascade, leading to stent thrombosis (10,50,70). Table 19.4 summarizes the contraindications to vascular stent placement.

Complications The incidence of complications related to stent placement ranges from 1.6% to 19.4% (15,21,33,44,45,50,59–61, 70–74). Most of the complications can be attributed to balloon angioplasty and the puncture site. These complications include arterial spasm, hematoma, pseudoaneurysm, arteriovenous fistula, intimal dissection, vessel perforation, side branch occlusion, and plaque embolism. Other complications are related to the stent and the deployment process. An improperly mounted stent, a Palmaz stent in particular, could become dislodged in the delivery system prior to deployment. Furthermore, stents

TABLE 19.4 Contraindications to vascular stent placement Perforated vessels Severely calcified vessels Marked tortuous vessels (for Palmaz stent) Lesions across areas of flexion Hypercoagulable disorder Lesions in target vessels where clamping may be required for bypass grafting

ABLE 19.5 Complications associated with vascular stent placement Stent related Stent dislodgement in the delivery system Stent migration or embolization Stent misplacement Acute stent thrombosis Stent infection Procedure related Arterial spasm Hematoma Pseudoaneurysm Arteriovenous fistula Intimal dissection Vessel perforation Side branch occlusion Plaque embolism Others Contrast agent allergic reaction Contrast-induced transient renal failure

mounted on certain types of balloon angioplasty catheters with slippery coating may slip during deployment. Such balloon angioplasty catheters should be identified and then abraded with a dry gauze to remove the lubrication so that the stent will not “watermelon seed” off the balloon during inflation and deployment. One should check with the balloon manufacturer to ascertain whether the angioplasty catheter is coated with such slippery lubricants. Inadequately deployed or undersized stents could migrate or embolize from the original site of deployment. A complication specific to self-expanding stents is stent misplacement due to foreshortening upon expansion. Acute stent thrombosis has been observed in stent placement and is usually associated with stenting of occluded vessels, multiple stent placement, and hypercoagulopathy (33,50,75). Lastly, prophylactic antibiotic administration before stent placement is recommended to minimize the risk of stent infection and its devastating consequences (74). As with all radiographic procedures, transient contrast-induced renal failure has been reported after stent placement (15,50,72). The 30-day mortality rate of vascular stent placement is less than 1.5%, with myocardial infarction as the leading cause of death (50,72). Table 19.5 summarizes the complications associated with stent placement.

Chapter 19 Stents for Peripheral Arteries and Veins

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TTABLE 19.6 Results of selective stent placement for iliac occlusive disease* Primary Patency (%)/Secondary Patency (%) Author

Year

Patients

Palmaz stent Palmaz et al. (72) Cikrit et al. (33) Henry et al. (50)

1992 1995 1995

486 38 184

Wallstent Vorwerk et al. (44) Martin et al. (78) Murphy et al. (79)†

1996 1995 1996

109 140 66

Strecker stent Long et al. (70)‡ Strecker et al. (80)

1995 1996

61 289

Complication Rate (%)

Initial Success (%)

1 year

2 years

3 years

4 years

5 years

99 97 99

91/NA 87/91 94/98

84/NA 74/91 91/96

69 (43 months) 74/91 86/94

67/91 86/94

63/86 NA

97 97 91

95/96 81/91 78/86

88/93 71/86 53/NA

86/91 NA 53/82 (32 months)

82/91 NA

72/83 NA

98 99

84/90 NA

69/81 NA

NA 85/NA

NA 84/NA

NA 79/NA

10 18 4 6.8 8 9 12 17

*Each series contained less than 10% iliac occlusion unless otherwise indicated. †Forty-one percent of treated limbs were chronically occluded iliac arteries. ‡Forty-four percent of treated lesions were occluded iliac arteries.

Stents in Iliac Arteries The effectiveness of percutaneous transluminal angioplasty (PTA) in the treatment of iliac occlusive disease is well established, particularly in the common iliac arteries. Johnston reported the success rates of common iliac PTA at 1 year, 3 years, and 5 years to be 81%, 71%, and 65% respectively (76). For external iliac PTA, the success rates are 74% at 1 year, 51% at 3 years, and 48% at 4 years (76). Numerous factors, including indication (claudication vs. ischemia), site of lesion (common vs. external iliac), type of lesion (focal stenosis vs. diffuse stenosis or occlusion), and runoff status (good vs. poor) have been identified as predictors of successful PTA (41,48,77). Judicious selection of target lesions with favorable factors has yielded reasonable long-term success rates for iliac PTA. Neointimal hyperplasia and progression of the atherosclerotic process are the major factors affecting the long-term failure rate of PTA (33,41,48,76). Vascular stents have generated considerable interest as the possible solution to overcoming the long-term failure rate of PTA, especially in unfavorable lesions, in the treatment of iliac occlusive disease. In addition, the use of vascular stents to treat inadequate or complicated angioplasty has improved the initial technical success rate of PTA. Many series have reported excellent clinical success of stent placement in the treatment of iliac occlusive disease (33,44,50,70,72,78–80). The results of these series are summarized in Table 19.6. Most of the series utilized the indications for selective stenting to place stents. However, the indications for endovascular intervention, such as claudication vs. ischemia and stenosis vs. occlusion, were not separated, making the results difficult to compare. Regardless, several general trends can be concluded from these series. Stent placement has improved the initial technical success rate (91–99%) and the mid-term primary patency rate of iliac PTA (3-year primary patency rates

ranged from 53% to 86%). Secondary patency rates, ranging from 82% at 32 months to 94% at 3 years, are attainable. However, surveillance at regular intervals and multiple reinterventions performing repeat PTA and/or stent placement may be needed to achieve these favorable outcomes. Several risk factors, including lesion type (stenosis vs. occlusion), lesion location (common vs. external iliac), length of lesion (greater or less than 4 cm), and runoff status (good vs. poor), are associated with early stent failure, mainly stent thrombosis (80). As in iliac PTA, neointimal hyperplasia and progression of atherosclerosis are the major causes affecting the long-term success of vascular stents. Some investigators have advocated primary stent placement in the treatment of iliac occlusive disease (81–83). The rationale behind this approach is that stent placement can exclude the postangioplasty subendothelial layer, producing a smoother endoluminal surface for blood flow which may decrease the incidence of restenosis from intimal hyperplasia (11,50). However, stents themselves also induce intimal hyperplasia, thus affecting longterm patency. Tetteroo et al., in a prospective, randomized trial, compared the effectiveness of primary stent placement to selective stent placement in the treatment of iliac occlusive disease (83). A total of 279 patients with intermittent claudication were randomized into the study. In the selective stent placement group, 43% of patients required stent placement due to inadequate PTA. At 2-year follow-up, no significant difference was found between the two treatment strategies based on clinical and hemodynamic assessments. The 2-year clinical success rate was 78% in the primary stenting group compared with 77% in the selective stenting group. Cumulative patency and reintervention rates were also similar: 71% vs. 70%, and 7% vs. 4% respectively. As summarized in Table 19.7, the results of primary stent placement, in these series, have demonstrated no improved patency as compared to the

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TABLE 19.7 Results of primary stent placement for iliac occlusive disease Patency (%) Author

Year

Patients

Complication Rate (%)

Murphy et al. (81) Sullivan et al. (82) Tetteroo et al. (83)

1995 1997 1998

83 288 143

9.7 14 4

Initial Success (%)

1 year

2 years

3 years

4 years

99 90 81

89 81 78

NA 73 71

NA NA NA

86 NA NA

TABLE 19.8 Results of PTA versus primary stent placement in occluded iliac vessels Primary patency (%)/Secondary patency (%) Author

Year

Patients

Complication Rate (%)

Embolization Rate (%)

Initial Success (%)

1 year

2 years

3 years

4 years

5 years

6 years

PTA Johnston (76) Gupta et al. (85)

1993 1993

82 50

13 12

1.2 8

76 82

60 79/90

53 76/81

48 76/81

NA 76/81

NA 76/81

76/81

Primary stenting Vorwerk et al. (55) Reyes et al. (56) Dyet et al. (57) Henry et al. (58)

1995 1997 1997 1998

103 59 72 105

12 13 13 11

4.8 6.8 5.6 4.8

96 92 93 88

87/94 78/– 88/– 75/79

83/90 73/88 NA 67/73

81/88 72/– NA 62/71

78/88 NA NA 59/71

54/75 NA NA 56/71

52/66

approach of selective stent placement. When the added expense of the stent and the potential risks associated with stent implantation are included in the analysis, primary stent placement to treat iliac occlusive disease is not a costeffective treatment strategy and should not be recommended (84). The ability to achieve recanalization and the danger of embolization are the two major drawbacks in the percutaneous treatment of iliac artery occlusion. The age of the occlusion, instead of the occluded length, is the determining factor in achieving recanalization. Henry et al. reported that chronic occlusions >3 months were more difficult to recanalize and prone to subintimal wire passage (58). Many occluded iliac arteries can be recanalized percutaneously through various techniques. Passage of a hydrophilic wire through the occluded artery is the simplest method (57,58,85). The wire can be passed from the ipsilateral femoral artery in a retrograde manner or from the contralateral femoral or brachial artery in an antegrade fashion. Fibrinolytic therapy has been employed to lyse the occluded lesion in order to facilitate wire passage (47,52,58,76). If the combination of lytic therapy and wire passage is not successful, the technique of traversing the occluded segment blindly with a catheter has been utilized (47). This approach, however, risks inadvertent subintimal passage, predisposing to iliac artery rupture. Mechanical thrombectomy devices, such as the Hydrolyser (Cordis, Miami, FL) and AngioJet (Possis Medical, Minneapolis, MN), can also be used with or without lytic therapy to achieve recanalization (58). Once the occluded segment is recanalized, some investigators advocate primary stenting without precedent balloon angioplasty to

minimize periprocedural embolic events (53–58). The results of PTA alone and primary stent placement for iliac artery occlusion are summarized in Table 19.8 (55–58,76,85). In general, the initial technical success rates of endovascular treatment of occluded iliac arteries are not as favorable as those obtained for iliac stenosis, mainly due to the technical difficulties and complications of recanalization. Stent placement in recanalized arteries has been demonstrated to have better initial success rates than PTA alone. Interestingly, the reported embolization rates of the two treatment modalities, at least in these series, are similar (1.2% to 8% in PTA vs. 4.8% to 6.8% in primary stenting) suggesting that the perceived benefit of primary stenting in minimizing distal embolization may not exist. Long-term patency between the two approaches is less clear. Three-year primary patency rates of PTA alone range from 48% to 76% whereas the primary patency rates of the stented group range from 62% to 81%. Between the two series with the longest follow-up, PTA alone appears to have better patency rate than primary stenting, 76% vs. 52%. It should be cautioned that the number of patients at the 6-year follow-up in the PTA group was one (2% of the study group) compared with 13 patients in the primary stenting group (12.4% of the study group). In subgroup analysis, the age of the patient and the presence of hypertension have been identified as risk factors significantly affecting the long-term patency rate in the PTA group (85). In the primary stenting group, the duration of occlusion (less than 3 months) and the length of the occluded segment (less than 6 cm) are factors associated with higher patency rate, whereas other factors, including the location of the occluded segment, vessel

Chapter 19 Stents for Peripheral Arteries and Veins

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TABLE 19.9 Estimated pooled primary patency rates after PTA and stent implantation in patients with claudication (modified from reference 87) PTA Lesion Type and Year after Treatment

Stent Implantation

Patency (%)

Range (%)

Patency (%)

Range (%)

100 77 66 61 57 55

98–100 78–80 63–71 55–68 54–63 52–62

100 75 67 66 NA NA

99–100 73–790 65–710 64–700 NA NA

88 65 54 48 44 42

81–94 55–71 45–61 40–55 36–53 33–51

99 73 66 64 NA NA

92–100 69–750 61–680 59–670 NA NA

Stenosis 0 1 2 3 4 5 Occlusion 0 1 2 3 4 5

diameter, gender, and runoff status, have no influence on long-term patency (58).

Stents in Femoropopliteal Arteries Occlusive disease of the femoropopliteal arteries is less responsive to endovascular interventions than the iliac arteries. As reported by Johnston, the initial technical success rate was 89% out of 254 femoropopliteal PTAs (41,49). Patency rates were 62.5% at 1-year follow-up, 52.6% at 2-year, 50.7% at 3-year, 44.1% at 4-year, 38.1% at 5-year, and 35.7% at 6-year follow-up (49). The length of the lesion, the type of lesion, and the status of the runoff vessels are variables affecting the long-term patency of the femoropopliteal arteries after angioplasty. Category 1 lesions, short stenotic lesions < 2 cm with good runoff, are the femoropopliteal lesions most responsive to PTA. Longer, multiple, and calcified lesions with or without occlusion are more difficult to treat by angioplasty, and are subject to early failure postangioplasty. As in the iliac vessels, stents have been used to improve the initial technical success rate of femoropopliteal PTA by preventing elastic recoil of the vessel wall and by covering intramural dissection and intimal flaps (50,59). Restenosis, however, is not prevented by stent placement. The presence of the stent actually increases intimal hyperplasia around the stent, leading to early restenosis particularly in the smaller femoropopliteal arteries as compared to the iliac arteries (13,28,50,59,86). Numerous studies have reported the long-term results of PTA versus stent placement in the treatment of

femoropopliteal occlusive disease. However, most of these data were not obtained in a randomized prospective manner. Muradin et al. recently performed a meta-analysis of the long-term results of PTA and stent implantation in the treatment of femoropopliteal arterial disease (Tables 19.9 and 19.10) (87). Nineteen studies, including only one randomized prospective study, representing a total of 923 balloon dilations and 473 stent implantations, were analyzed using a weighted multiple linear regression model. The data were tabulated according to clinical indication (claudication vs. ischemia) and lesion type (stenosis vs. occlusion). For less severe femoropopliteal disease, as in claudication with stenosis, the 3-year patency rates of PTA and stent implantation were similar, 61% vs. 66% respectively. For more severe disease, stent implantation appeared to provide better long-term patency rates. These results, however, may have been affected by publication bias and the nonuniformity of different study designs, reporting methods, and patient populations. Table 19.11 summarizes two recently published randomized prospective trials of PTA versus stent placement in the treatment of femoropopliteal disease (59,88). Both study groups included patients with moderate to severe lesions. At up to 39 months of follow-up, stent placement does not produce better results than PTA alone. The benefit of stent placement lies in its ability to rescue PTA failure, thus yielding a higher initial success rate than PTA alone, 99% vs. 84%. However, this advantage is lost over time due to late luminal loss in the stented lesions (59). In conclusion, stent placement should be deployed selectively after PTA against residual hemodynamic or angiographic stenosis, elastic recoil, obstructing intimal flaps, and dissections.

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TABLE 19.10 Estimated pooled primary patency rates after PTA and stent implantation in patients with critical ischemia (modified from reference 87) PTA Lesion Type and Year after Treatment

Stent Implantation

Patency (%)

Range (%)

Patency (%)

Range (%)

Stenosis 0 1 2 3 4 5

83 60 49 43 40 38

69–88 46–63 35–54 30–51 26–46 24–44

100 74 66 65 NA NA

94–100 68–800 59–720 58–710 NA NA

Occlusion 0 1 2 3 4 5

70 47 36 30 27 25

62–75 41–51 28–41 20–37 16–34 13–32

98 73 65 63 NA NA

94–100 68–750 60–680 58–680 NA NA

TABLE 19.11 Results of PTA vs. Palmaz stent placement in femoropopliteal lesions Primary Patency (%)/ Secondary Patiency (%) Author Cejna et al. 2001 (59)* Grimm et al. 2001 (88)†

Intervention

Limbs

Complication Rate (%)

Initial Success (%)

1 year

2 years

3 years

PTA Palmaz PTA Palmaz

77 77 30 23

5.2 2.6 0 0

84 99 100 100

72/860 77/790 84/100 75/900

65/74 65/73 77/91 72/90

NA NA 70/91 (39 months) 73/93 (39 months)

*A total of 141 patients with 154 limbs: 108 limbs with claudication, 46 ischemic limbs; lesion length < 5 cm and at least one runoff vessel; mean followup 12 months. †All patients had occluded or severely stenotic SFA; lesion length < 5 cm with at least two runoff vessels; mean follow-up 25 months.

Stents in Peripheral Veins The most frequent application of stent placement in the vein is to salvage a failing hemodialysis graft by stenting the stenotic venous drainage refractory to balloon angioplasty. Polytetrafluoroethylene dialysis grafts placed in the extremity of patients requiring hemodialysis are prone to venous stenosis, thrombosis, and eventual failure. Dialysis access stenosis is thought to result from intimal hyperplasia that consists of smooth muscle cell proliferation and extracellular matrix deposition. Angioplasty is usually successful in dilating venous stenosis, but occasionally results may be suboptimal because of elastic stretch and recoil. Stent placement helps to maintain luminal diameter in these situations where angioplasty is unsuccessful. The most commonly used stents for hemodialysis access salvage are the Palmaz stent and the Wallstent. However, stents themselves are prone to develop intimal hyperplasia once placed inside veins (65,89). Periodic maintenance redilation is required in nearly all

stents placed for hemodialysis-related venous stenosis. Eventually, the stent becomes well incorporated with the intimal hyperplasia matrix and the resulting restenosis may be very difficult to dilate and may eventually cause the graft to fail. Surgical removal of the stent or patch angioplasty revision of the anastomosis may be impossible. Some investigators have observed that the vein segments adjacent to the stented veins can develop similar strictures that may require additional stent placement to relieve the obstruction (90). Another concern with the use of stents is that they may be thrombogenic, causing clots to form at the sites of the stents. Quinn et al. have demonstrated that routine stent deployment provided no benefit compared with balloon angioplasty in a randomized prospective study (91). Both have similar primary patency rate at 12 months, 10% for PTA and 11% for stenting. Furthermore, given the potential problems associated with the use of a stent in the vein, stent placement should be reserved only for venous stenosis refractory to balloon angioplasty. Finally, stents should not be placed in the

Chapter 19 Stents for Peripheral Arteries and Veins

axillosubclavian vein for patients with thoracic outlet syndrome. Stents placed in this location will almost invariably develop thrombosis, intimal hyperplasia, and stent fracture secondary to external compression and repetitive movement.

Summary Over the past two decades the vascular stent has played an increasingly vital role in the percutaneous treatment of arterial and venous diseases. Clinical application of stents in iliac occlusive disease, combined with balloon angioplasty, has provided surgeons with a reliable alternative to open surgical repair. The benefits and the long-term success of balloon angioplasty and stent placement can only be fully realized by our judicious use of these technologies, employing them in selective, favorable lesions that will yield the most durable clinical outcomes. We have made significant progress in treating occluded iliac arteries with stents. However, further work need to be continued, perhaps with the use of covered stent grafts or new stent materials and designs, before stent placement for occluded iliac vessels can be considered as an alternative to surgery. For the time being, this approach should be reserved for patients who present prohibitively high surgical risks. In dealing with infrainguinal arteries, stent placement is appropriate when the results of balloon angioplasty are unsatisfactory or for complications arising from angioplasty. Similarly, the application of vascular stents in veins should be reserved as the last measure in hemodialysis graft salvage, principally because of the eventual stent stenosis and scarring caused by intimal hyperplasia. Intimal hyperplasia is the Achilles’ heel of vascular surgery. Development of new coating materials, either pharmacologic or biologic, to enable the stent surface to resist intimal hyperplasia may be the answer.

References 1. Carrel A. Results of the permanent intubation of the thoracic aorta. Surg Gynecol Obstet 1912, 15: 245– 248. 2. Dotter CT, Judkins MP: Transluminal treatment of arteriosclerotic obstruction: description of a new technique and a preliminary report of its application. Circulation 1964, 30: 654–670. 3. Dotter CT. Transluminally placed coil-spring endarterial tube grafts: long-term patency in canine popliteal artery. Invest Radiol 1969, 4: 329–332. 4. Dotter CT, Buschmann RW, et al. Transluminally expandable nitinol coil stent grafting: Preliminary report. Radiology 1983, 147: 259–260. 5. Cragg A, Lund G, et al. Nonsurgical placement of arterial endoprosthesis: A new technique using nitinol wire. Radiology 1983, 147: 261–263. 6. Gruntzig A, Kumpe DA. Technique of percutaneous transluminal angioplasty with the Gruntzig balloon catheter. Am J Roentgenol 1979, 132: 547–552.

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7. Becker GJ. Intravascular stents: general principles and status of lower extremity arterial applications. Circulation 1991, 83(suppl I): 122–136. 8. Song M, Rodino W, et al. Vascular stents. In Moore WS, Ahn SS (eds): Endovascular Surgery, 3rd ed. Philadelphia, WB Saunders, 2001, pp. 70–74. 9. Wisselink W, Panetta TF. Endoluminal treatment of vascular occlusive disease. Surg Clin North Am 1998, 78: 863–878. 10. Lin PH, Weiss VF, Lumsden AB. Stented balloon angioplasty in aortoiliac arterial occlusive disease. In Moore WS, Ahn SS (eds). Endovascular Surgery, 3rd ed. Philadelphia, WB Saunders, 2001, pp. 233–241. 11. Hood DB, Hodgson KJ. Percutaneus transluminal angioplasty and stenting for iliac artery occlusive disease. Surg Clin North Am 1999, 79: 575–596. 12. Ahn SS, Obrand DI. Stents. In: Ahn SS, Obrand DI. Handbook of Endovascular Surgery. Basel, Switzerland, Karger Landes Systems, 1997, pp. 85–104. 13. Palmaz JC. Intravascular stents: tissue-stent interactions and design considerations. Am J Roentgenol 1993, 160: 613–618. 14. Ahn SS, Concepcion B. Indications and results of arterial stents for occlusive disease. World J Surg 1996, 20: 644–648. 15. Palmaz JC, Garcia O, et al. Placement of balloon expandable intraluminal stents in iliac arteries: first 171 procedures. Radiology 1990, 174: 969–75. 16. Strecker EP, Hagen B, et al. Current status of the strecker stent. Cardiology Clinics 1994, 12(4): 673– 687. 17. Strecker EP, Hagen B, et al. Iliac and femoropopliteal vascular occlusive disease treated with flexible tantalum stents. Cardiovasc Intervent Radiol 1993, 16(3): 158–164. 18. Sutton CS, Oku T, et al. Titanium-nickel intravascular endoprosthesis: A 2-year study in dogs. Am J Roentgenol 1988, 151: 597–601. 19. Duerig TW, Pelton AR, Stockel D. The utility of superelasticity in medicine. Biomed Mater Eng 1996, 6: 255–266. 20. Rabkin DJ, Lang EV, Brophy DP. Nitinol properties affecting uses in interventional radiology. J Vasc Interv Radiol 2000, 11: 343–350. 21. Lugmayr HF, Holzer H, et al. Treatment of complex arteriosclerotic lesions with nitinol stents in the superficial femoral and popliteal arteries: A midterm follow up. Radiology 2002, 222(1). 22. Schrumann K, Vorwerk D, et al. Neointimal hyperplasia in low-profile nitinol stent, Palmaz stents, and Wallstents: A comparative experimental study. Cardiovasc Intervent Radiol 1996, 19: 248–254. 23. Raza Z, Shaw JW, et al. Management of iliac occlusions with a new self-expanding endovascular stent. Eur J Vasc Endovasc Surg 1998, 5: 439–443. 24. Phatouros CC, Higashida RT, et al. Endovascular stenting for carotid artery stenosis: Preliminary experience using the shape-memory-alloy-recoverable-technology (SMART) stent. Am J Neuroradiol 2000, 21: 732– 738. 25. Hausegger KA, Cragg AH, et al. Iliac artery stent placement: Clinical experience with a nitinol stent. Radiology 1994, 190: 199–202.

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26. DePalma VA, Baier RE, et al. Investigation of threesurface properties of several metals and their relationship to blood compatibility. J Biomed Mater Res 1972, 3: 37–75. 27. Baier RE, Dutton RC: Initial events in interaction of blood with a foreign surface. J Biomed Mater Res 1969, 3: 191–206. 28. Palmaz JC, Tio FO, et al. Early endothelization of balloon-expandable stents: experimental observations. J Intervent Radiol 1988, 3: 119–124. 29. Schatz RA, Palmaz JC, et al. Balloon-expandable intracoronary stents in the adult dog. Circulation 1987, 76: 450–457. 30. Tetteroo E, Haaring C, et al. Intraarterial pressure gradients after randomized angioplasty or stenting of iliac artery lesions. Dutch Iliac Stent Trial Study Group. Cardiovasc Intervet Radiol 1996, 19: 411–417. 31. Vorwerk D, Gunther RW: Percutaneous interventions for treatment of iliac artery stenoses and occlusions. World J Surg 2001, 25: 319–326. 32. Powell RJ, Fillinger M, et al. Predicting outcome of angioplasty and selective stenting of multisegment iliac artery occlusive disease. J Vasc Surg 2000, 32: 564–569. 33. Cikrit DF, Gustafson PA, et al. Long-term follow-up of the Palmaz stent for iliac occlusive disease. Surgery 1995, 118: 608–614. 34. Cikrit DF, Dalsing MC. Lower-extremity arterial endovascular stenting. Surg Clin North Am 1998, 78: 617–629. 35. Vorwerk D, Guenther RW, et al. Late reobstruction in iliac arterial stents: percutaneous treatment. Radiology 1995, 197: 479–483. 36. Aburahma AF, Robinson PA, et al. Selecting patients for combined femorofemoral bypass grafting and iliac balloon angioplasty and stenting for bilateral iliac disease. J Vasc Surg 2001, 33(Suppl 2): S93–99. 37. Perler BA, Williams GM: Does donor iliac artery percutaneous transluminal angioplasty or stent placement influence the results of femorofemoral bypass? Analysis of 70 consecutive cases with long-term follow-up. J Vasc Surg 1996, 24: 363–369. 38. Lau H, Cheng SW. Intraoperative endovascular angioplasty and stenting of iliac artery: an adjunct to femoropopliteal bypass. J Am Coll Surg 1998, 186: 408–414. 39. Schneider PA, Caps MT, et al. Intraoperative superficial femoral artery balloon angioplasty and popliteal to distal bypass graft: an option for combined open and endovascular treatment of diabetic gangrene. J Vasc Surg 2001, 33: 955–962. 40. Schneider PA, Abcarian PW, et al. Should balloon angioplasty and stents have any role in operative intervention for lower extremity ischemia? Ann Vasc Surg 1997, 11: 574–580. 41. Johnston KW, Rae M, et al. Five-year results of a prospective study of percutaneous transluminal angioplasty. Ann Surg 1987, 206: 403–413. 42. Becker GJ, Katzen BT, Dake MD. Noncoronary angioplasty. Radiology 1989, 170: 921–940. 43. Onal B, Ilgit ET, et al. Primary stenting for complex atherosclerotic plaques in aortic and iliac stenoses. Cardiovasc Intervent Radiol 1998, 21: 386–392. 44. Vorwerk D, Guenther RW, et al. Aortic and iliac stenoses: follow-up results of stent placement after insufficient

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

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balloon angioplasty in 118 cases. Radiology 1996, 198: 45–48. Bonn J, Gardiner GA Jr, et al. Palmaz vascular stent: initial clinical experience. Radiology 1990, 174: 741– 745. Vorwerk D, Guenther RW, et al. Ulcerated plaques and focal aneurysms of iliac arteries: treatment with noncovered, self-expanding stents. Am J Roentgenol 1994, 162: 1421–1424. Colapinto RF, Stronell RD, Johnston WK. Transluminal angioplasty of complete iliac obstructions. Am J Roentgenol 1986, 146: 859–862. Cambria RP, Faust G, et al. Percutaneous angioplasty for peripheral arterial occlusive disease. Correlates of clinical success. Arch Surg 1987, 122: 283– 287. Johnston KW. Femoral and popliteal arteries: reanalysis of results of balloon angioplasty. Radiology 1992, 183: 767–771. Henry M, Amor M, et al. Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2–4 year follow-up. Radiology 1995, 197: 167–174. Zollikofer CL, Antonucci F, et al. Arterial stent placement with use of the Wallstent: midterm results of clinical experience. Radiology 1991, 179: 449–456. Blum U, Gabelmann A, et al. Percutaneous recanalization of iliac artery occlusions: results of a prospective study. Radiology 1993, 189: 536–540. Sapoval MR, Chatellier G, et al. Self-expandable stents for the treatment of iliac artery obstructive lesions: longterm success and prognostic factors. Am J Roentgenol 1996, 166: 1173–1179. Yedlicka JW Jr, Ferral H, et al. Chronic iliac artery occlusions: primary recanalization with endovascular stents. J Vasc Interv Radiol 1994, 5: 843–847. Vorwerk D, Guenther RW, et al. Primary stent placement for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995, 194: 745–749. Reyes R, Maynar M, et al. Treatment of chronic iliac artery occlusions wire guide wire recanalization and primary stent placement. J Vasc Interv Radiol 1997, 8: 1049–1055. Dyet JF, Gaines PA, et al. Treatment of chronic iliac artery occlusions by means of percutaneous endovascular stent placement. J Vasc Interv Radiol 1997, 8: 349–353. Henry M, Amor M, et al. Percutaneous endoluminal treatment of iliac occlusions: long-term follow-up in 105 patients. J Endovasc Surg 1998, 5: 228–235. Cejna M, Thurnher S, et al. PTA versus Palmaz stent placement in femoropopliteal artery obstructions: a multicenter prospective randomized study. J Vasc Interv Radiol 2001, 12: 23–31. Vroegindeweij D, Vos LD, et al. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997, 20: 420–425. Cheng SW, Ting AC, Wong J. Endovascular stenting of superficial femoral artery stenosis and occlusions: results and risk factor analysis. Cardiovasc Surg 2001, 9: 133–140.

Chapter 19 Stents for Peripheral Arteries and Veins 62. Strecker EP, Boos IB, Gottmann D. Femoropopliteal artery stent placement: evaluation of long-term success. Radiology 1997, 205: 375–383. 63. Liermann D, Strecker EP, Peters J. The Strecker stent: indications and results in iliac and femoropopliteal arteries. Cardiovasc Intervent Radiol 1992, 15: 298–305. 64. Oderich GS, Treiman GS, et al. Stent placement for treatment of central and peripheral venous obstruction: a long-term multi-institutional experience. J Vasc Surg 2000, 32: 760–769. 65. Hood DB, Yellin AE, et al. Hemodialysis graft salvage with endoluminal stents. Am Surg 1994, 60: 733–737. 66. Hurst DR, Forauer AR, et al. Diagnosis and endovascular treatment of iliocaval compression syndrome. J Vasc Surg 2001, 34: 106–113. 67. Henry M, Amor M, et al. Percutaneous endovascular treatment of peripheral aneurysms. J Cardiovasc Surg 2000, 41: 871–883. 68. Van Sambeek MR, Gussenhoven EJ, et al. Endovascular stent-grafts for aneurysms of the femoral and popliteal arteries. Ann Vasc Surg 1999, 13: 247–253. 69. Parodi JC, Schonholz C, et al. Endovascular stent-graft treatment of traumatic arterial lesions. Ann Vasc Surg 1999, 13: 121–129. 70. Long AL, Sapoval MR, et al. Strecker stent implantation in iliac arteries: patency and predictive factors for longterm success. Radiology 1995, 194: 739–744. 71. Vorwerk D, Gunther RW. Stent placement in iliac arterial lesions: three years of clinical experience with the Wallstent. Cardiovasc Intervent Radiol 1992, 15: 285–290. 72. Palmaz JC, Laborde JC, et al. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992, 15: 291–297. 73. Ballard JL, Sparks SR, et al. Complications of iliac artery stent deployment. J Vasc Surg 1996, 24: 545–555. 74. Deiparine MK, Ballard JL, et al. Endovascular stent infection. J Vasc Surg 1996, 23: 529–533. 75. Long AL, Page PE, et al. Percutaneous iliac artery stent: angiographic long-term follow-up. Radiology 1991, 180: 771–778. 76. Johnston KW. Iliac arteries: reanalysis of results of balloon angioplasty. Radiology 1993, 186: 207–212. 77. Parsons RE, Suggs WD, et al. Percutaneous transluminal angioplasty for the treatment of limb threatening ischemia: Do the results justify an attempt before bypass grafting? J Vasc Surg 1998, 28: 1066–1071. 78. Martin EC, Katzen BT, et al. Multicenter trial of the Wallstent in the iliac and femoral arteries. J Vasc Interv Radiol 1995, 6: 843–849.

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79. Murphy TP, Webb MS, et al. Percutaneous revascularization of complex iliac artery stenoses and occlusions with use of Wallstents: three-year experience. J Vasc Interv Radiol 1996, 7: 21–27. 80. Strecker EP, Boos IB, Hagen B. Flexible tantalum stents for the treatment of iliac artery lesions: long-term patency, complications, and risk factors. Radiology 1996, 199: 641–647. 81. Murphy KD, Encarnacion CE, et al. Iliac artery stent placement with the Palmaz stent: follow-up study. J Vasc Interv Radiol 1995, 6: 321–329. 82. Sullivan TM, Childs MB, et al. Percutaneous transluminal angioplasty and primary stenting of the iliac arteries in 288 patients. J Vasc Surg 1997, 25: 829–838. 83. Tetteroo E, van der Graaf Y, et al. Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Dutch Iliac Stent Trial Study Group. Lancet 1998, 351: 1153–1159. 84. Bosch JL, Tetteroo E, et al. Iliac arterial occlusive disease: cost-effectiveness analysis of stent placement versus percutaneous transluminal angioplasty. Dutch Iliac Stent Trial Study Group. Radiology 1998, 208: 641–648. 85. Gupta AK, Ravimandalam K, et al. Total occlusion of the iliac arteries: results of balloon angioplasty. Cardiovasc Intervent Radiol 1993, 16: 165–177. 86. White GH, Liew SC, et al. Early outcome and intermediate follow-up of vascular stents in the femoral and popliteal arteries without long-term anticoagulation. J Vasc Surg 1995, 21: 270–281. 87. Muradin GS, Bosch JL, et al. Balloon dilation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 2001, 221: 137–145. 88. Grimm J, Muller-Hulsbeck S, et al. Randomized study to compare PTA alone versus PTA with Palmaz stent placement for femoropopliteal lesions. J Vasc Interv Radiol 2001, 12: 935–941. 89. Vesely TM, Hovsepian DM, et al. Upper extremity central venous obstruction in hemodialysis patients: treatment with Wallstents. Radiology 1997, 204: 343–348. 90. Funaki B, Szymski GX, et al. Treatment of venous outflow stenosis in thigh grafts with Wallstents. Am J Roentgenol 1999, 172: 1591–1596. 91. Quinn SF, Schumann ES, et al: Percutaneous transluminal angioplasty versus endovascular stent placement in the treatment of venous stenosis in patients undergoing hemodialysis: intermediate results. J Vasc Interv Radiol 1995, 6: 851–855.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 20 Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis W. Todd Bohannon and Michael B. Silva, Jr

Thrombolytic therapy for arterial and venous occlusions has become an important tool for vascular surgeons and vascular interventionalists. A wide variety of thrombotic disorders can be treated with either local or systemic administration of fibrinolytic agents. Although the systemic administration of fibrinolytic agents is still used in some clinical situations, such as acute coronary artery occlusions, pulmonary emboli and strokes, the contemporary vascular interventionalist uses catheter-based techniques to deliver these agents directly in to the affected arterial or venous segments. Local and regional infusions of thrombolytic agents are effective in the treatment of acute arterial thrombosis, including embolic, graft, and native artery occlusions, and acute venous thrombosis in both the upper and lower extremities.

Plasmin and the Fibrinolytic System With arterial or venous thrombosis, the balance between the formation and degradation of fibrin has been lost (1). The fibrin network, critical in formation of clot, contains plasminogen in addition to other coagulation factors. Endothelial cells produce plasminogen activators that convert plasminogen to plasmin (2). Plasmin is a serine protease that degrades fibrin and other coagulation factors. The fibrinolytic agent’s action on plasminogen allows for clot dissolution. The currently available

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thrombolytic agents are plasminogen activators, which produce fibrinolysis by activating the body’s natural fibrinolytic system. They convert plasminogen to plasmin, which in turn cleaves and dissipates fibrin. The most effective thrombolysis is achieved when the fibrin-bound plasminogen is converted to plasmin rather than free plasmin (3,4). This is why directly delivered fibrinolytic agents into the area of clot formation are more effective (3,4).

Thrombolytic Agents In clinical practice, variants of streptokinase, urokinase, and tissue plasminogen activator are used to treat arterial and venous thrombosis. While they all ultimately convert plasminogen to plasmin, each has unique molecular and biologic properties to consider when selecting a thrombolytic agent. These factors include source or origin of the agent, fibrin specificity and affinity, plasma half-life, and antigenicity.

Streptokinase Streptokinase is derived from streptococci and is a foreign protein, which is antigenic. It has a low fibrin specificity and affinity. Antibodies to streptococcus neutralize streptokinase; the major clinical limitation is related to antigenicity. Following the administration of streptokinase, two half-lives can be noted. The first is approximately 16

Chapter 20 Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis

minutes and is related to the neutralization by the antibodies. The second is 90 minutes long and is the actual biologic half-life. Clinically significant allergic reactions occurs in approximately 2% of patients treated with streptokinase (5).

Urokinase Urokinase (UK) is an autogenous plasminogen activator which is obtained from human neonatal kidney cells. It is a non-antigenic serine protease with a direct activation of plasminogen to form plasmin. As UK is non-antigenic, the systemic reactions seen with streptokinase are rarely observed. Urokinase (Abbokinase, Abbott Laboratories, Abbot Park, IL) was approved for use in the systemic treatment of acute massive pulmonary emboli. At the time of this writing, the FDA had suspended the use of UK due to the theoretical risk for biotransmissions. It is expected to return to clinical use, as these theoretical risks do not appear to be seen clinically.

Tissue Plasminogen Activator Endothelial cells produce tissue plasminogen activator (t-PA). This is produced in a recombinant form (rt-PA), alteplase (Activase, Genentech, San Francisco, CA), and is FDA approved for systemic administration for the treatment of massive pulmonary emboli in myocardial infarctions. Tissue plasminogen activator has a higher fibrin specificity and affinity than streptokinase and urokinase. It is a direct plasminogen activator, and in the presence of fibrinogen the efficiency and activation of plasminogen is increased. Variants of t-PA have been bioengineered. TNK-t-PA is a modification of t-PA with a longer half-life and fibrin specificity (6). Reteplase (Retavase, Centocor, Alvernon, PA) is a recombinant plasminogen activator (r-PA) and variant of t-PA with a longer half-life and a reduced fibrin affinity (7). The reduced fibrin affinity is thought to reduce potential bleeding complications. Tissue plasminogen activators are non-antigenic.

Arterial Thrombolysis The ultimate goal of thrombolytic and surgical therapy for arterial occlusion is resolution of the occlusive thrombus or embolus and restoration of blood flow to the ischemic limb. Thrombolytic therapy can be employed as a primary treatment modality for acute arterial occlusions secondary to emboli, bypass graft thrombosis, or progression of native atherosclerotic disease. Prompt recognition of limb ischemia and proper selection of patients will allow for clinical success. While arterial thrombolysis is most commonly thought of for use in acute occlusions, it may be used as an adjunctive procedure in identifying the origin of a chronic arterial occlusion.

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Trials Addressing Arterial Thrombolysis Ouriel and colleagues compared thrombolytic therapy with operative revascularization. Patients with acute ischemia of less than 7 days were randomized to either thrombolysis with UK or surgery (8). The 1-year survival was significantly higher for the thrombolysis group than for the surgical group (75% vs. 52%). The limb salvage rate at 12 months was not significantly different. Major bleeding complications occurred in 11%, with one mortality from an intracerebral hemorrhage. The surgery versus thrombolysis for ischemia of the lower extremity (STILE) trial was a randomized prospective multicenter trial that treated arterial ischemia with surgery or thrombolysis (t-PA or urokinase) (9). Limbs with acute and chronic ischemia were included in the trial. However, acute embolic occlusions were excluded from the study. A composite clinical outcome (death, ongoing or recurrent ischemia, major amputation, and major morbidity) was chosen as the primary end point. The composite of end points and a higher occurrence of persistent ischemia in the thrombolysis group resulted in the early termination of the study. The majority of the patients had chronic ischemia, and only 30% of patients had acute symptoms. Patients with acute symptoms (less than 14 days) and treatment with thrombolysis had a lower amputation rate at 6 months compared with similar patients treated with surgery (11% vs. 30%). When symptoms were present for longer than 14 days, surgical therapy resulted in a significantly lower amputation rate (3% vs. 12%). The overall bleeding complication rate was 5.6%. The investigators concluded that there was no difference in safety or efficacy between rt-PA and UK. The thrombolysis or peripheral arterial surgery trial (TOPAS) compared thrombolysis with UK with open vascular surgery in the treatment of acute (less than 14 days) lower extremity ischemia (10). The primary end point was amputation-free survival, with additional end points to include need for additional surgery and major hemorrhagic complications. The amputation-free survival at 1 year was not significantly different between the lysis and surgical groups (65% vs. 70%). The bleeding complications were greater in the lysis group than the surgical group (12.5% vs. 5.5%), with all four intracerebral hemorrhagic complications occurring in patients receiving thrombolytic therapy.

Thrombolytic Therapy of Arterial Occlusions An intercontinental panel of vascular interventionalists presented a consensus document on the use of thrombolysis in the management of lower extremity arterial occlusions. This working party on thrombolysis in the management of limb ischemia made 37 recommendations regarding lower extremity thrombolysis (11), including a consensus on the definitions and end points of treatment, thrombolytic agents, indications for thrombolysis, contraindi-

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cations, adjunctive treatments, monitoring, and complications. The primary end point in reporting results should be amputation-free survival and the secondary end point should include individual patency of the vessel being treated (11). A patient presenting with an acute arterial occlusion should be first assessed as to what degree of limb ischemia is present. The severity of the limb ischemia needs to be well documented: 1. 2. 3. 4.

Category I limbs are viable and not immediately threatened. Category IIa limbs are threatened but salvageable if treated. Category IIb limbs are salvageable if treated as an emergency. Category III limbs have irreversible ischemia and are not salvageable (11).

Therefore, patients whose limbs are viable and do not appear immediately threatened (category I), as well as those threatened but salvageable without paralysis but with mild sensory changes (category IIa), are potential candidates for thrombolytic therapy (11). Patients with threatened limbs with more significant neurologic changes (category IIb) require a more urgent intervention, and may best be served with an operative intervention (11). Patients with irreversible ischemia and non-salvageable limb usually require primary amputation. Those patients with viable or minimally threatened limbs are candidates for thrombolytic therapy. They must have no contraindication to thrombolysis (Table 20.1), which would include an active bleeding diathesis, recent gastrointestinal bleeding (less than 10 days), intracranial or spinal surgery, or intracranial trauma within the previous 3 months. Also, patients with a recent cerebral vascular accident within 2 months represent an absolute

A

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contraindication to thrombolysis. Relative major contraindications include major nonvascular surgery or trauma within the previous 10 days, uncontrolled hypertension, and puncture of noncompressible vessels, intracranial tumors, or recent eye surgery. Minor contraindications to thrombolysis include hepatic failure, bacterial endocarditis, pregnancy, and diabetic hemorrhagic retinopathy (11). Acute native artery ischemia has many different etiologies; however, almost all can be treated with lytic therapy. Upper and lower extremity emboli can be successfully lysed (12–15). Acute thrombosis due to native atherosclerotic disease (Fig. 20.1) can be treated with thrombolytics to reveal the underlying lesion (8–10,16–19). Limb salvage is improved with preoperative thrombolytic therapy of thrombosed popliteal aneurysms (20–24). Venous (Fig. 20.2) and prosthetic (Fig. 20.3) bypass graft occlusions can be treated with thrombolysis (9,19,25,26). The STILE trial demonstrated that 61% of graft occlusions were successfully accessed (9). Of these

TABLE 20.1 Contraindications to thrombolysis Absolute contraindication to thrombolysis Active bleeding diathesis Recent gastrointestinal bleeding Intracranial or spinal surgery Intracranial trauma within the previous 3 months Recent cerebral vascular accident within 2 months Relative contraindications Major nonvascular surgery or trauma within the previous 10 days Uncontrolled hypertension Puncture of noncompressible vessels Intracranial tumors Recent eye surgery

C

D

FIGURE 20.1 Native arterial occlusion. Upon presentation for acute right lower extremity pain a 60-year-old man with a history of diabetes and renal failure was found to have an acute occlusion of the right external iliac, common femoral, and superficial femoral arteries (A and B). A guidewire was passed, via a sheath in the contralateral femoral artery, through the occlusion into a patent popliteal artery and a continuous infusion of t-PA was used to recanalize the occlusion (C). A complex common femoral plaque was also discovered and this was later treated with open surgery (D).

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G

FIGURE 20.2 Lower extremity vein graft bypass occlusion. A patient with a history of a left above-knee popliteal to posterior tibial artery bypass placed eight years ago following a gunshot wound to the knee presents with acute left leg pain. The graft was occluded but a guidewire passed through the proximal anastomosis (A). A continous infusion of rt-PA revealed a proximal graft stenosis (B). The stenosis was treated with balloon angioplasty (C) which resolved the lesion (D). Completion angiogram demonstrated a widely patent graft with good outflow (E–G).

grafts, patency was restored in 82% of vein grafts and 85% of prosthetic grafts. An underlying lesion was revealed in 81%, and the 30-day amputation rate for all grafts was 17%. An analysis of patients in this study with acute graft occlusions (less than 14 days) did better with thrombolysis. Chronic graft occlusions (greater than 14 days) had a better outcome with surgery (9). Thrombolytic therapy can also be used as an adjunct in the treatment of chronic arterial occlusions (27). As with the acute arterial occlusions, the likelihood of success is increased with successful traversal of the lesion with the guidewire. An infusion of thrombolytic therapy across an apparent chronic occlusion can often decrease the length of occlusion and identify a more focal area of disease (Fig. 20.4).

Technique of Arterial Thrombolysis In patients without an immediately threatened limb, an angiogram is usually performed for a complete assess-

ment of arterial anatomy. Once the site of arterial occlusion is identified, a guidewire traversal test is performed. If the guidewire passes through the occlusion, there is a good possibility that thrombolysis will be successful (28). Other angiographic factors which may indicate a favorable outcome in peripheral arterial thrombolysis include a short occlusion and visualization of the distal runoff vessels. As one would expect, if the guidewire cannot cross the occlusion, the occlusion is extensive; if the distal runoff cannot be visualized, the chance of thrombolytic success is reduced. Generally, once the patient is identified as having an acute arterial occlusion, systemic anticoagulation with intravenous heparin is commenced. As previously mentioned, the thrombolytic agents are most effective when introduced into the occluding thrombus (28). If the guidewire does not cross the occlusion, a trial of regional thrombolysis in the vicinity of the clot may be tried for a brief period. Once the occlusion is crossed, a variety of infusion catheters can be used for delivery of the

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B

A

D

C

FIGURE 20.3 Femoropopliteal bypass graft occlusion. Three months following a femoral to above-knee popliteal bypass with PTFE, a patient presented with left lower extremity rest pain. Initial angiography (A) confirmed the graft occlusion with reconstitution of the above-knee popliteal artery near the distal anastomosis (arrow: clips in proximity of distal anastomosis). An infusion of t-PA cleared the thrombus within the graft and demonstrated a stenosis at the distal anastomosis (B). Angioplasty (C) was successful in resolving the stenosis (D).

A

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C

FIGURE 20.4 Chronic iliac artery occlusion. A patient with a right common iliac and external iliac occlusion was accessed via the left common femoral artery (A). A guidewire was directed over the aortic bifurcation and through the occluded iliac arteries. A continuous infusion of rt-PA resolved the majority of thrombus and identified chronic disease at the proximal right external artery (B). Completion angiogram following angioplasty and stent placement (C).

thrombolytic agents. These catheters can either be endhole catheters or catheters with multiple side holes for a more even distribution of agent throughout the thrombus. In addition to infusion catheters, there are infusion guidewires, which are passed through the catheter and placed in a more distal location. This allows for tandem infusion of thrombolytics within the proximal and distal vascular tree of the affected extremity. The thrombolytic agent, whether it is t-PA or UK, can be administered as a

continuous infusion with or without an initial bolus. An initial bolus of thrombolytic agent may shorten the duration of lytic therapy required for peripheral arterial occlusions (29,30). This may be important in certain situations in which a longer infusion time may not be tolerated. Acute renal or mesenteric ischemia from an embolus or native arterial thrombosis requires prompt resolution of the occlusive thrombus before irreversible end organ damage occurs (Fig. 20.5). High-dose administration of

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D

FIGURE 20.5 Acute occlusion of mesenteric arterial bypass. A patient with a history of a right common iliac to superior mesenteric artery (SMA) bypass with a reversed saphenous vein graft presented with acute abdominal pain. The graft is occluded with only visualization of the vein graft hood of the proximal anastomosis (A). Following guidewire traversal through the occluded graft into the SMA, a Mewissen infusion catheter is positioned across the graft (B) and a pulse-spray infusion of t-PA begins to clear away the thrombus (C). A proximal graft stenosis was revealed and successfully treated with balloon angioplasty (D).

TABLE 20.2 Thrombolytic technique of lower extremity arterial thrombosis Common femoral access via micropuncture set Diagnostic angiogram to define arterial anatomy and site of occlusion Guidewire traversal test Positive: Lysis likely successful Negative: Consider brief infusion in proximity of occlusion Consider mechanical or rheolytic catheter to reduce the thrombus load Infusion of thrombolytic agent (t-PA) Pulse spray (usually 0.5 to 2 mg rt-TPA) Continuous infusion (infusion catheter and wire) Heparin infusion via sheath (300 to 500 units/h) Monitor extremity pulses and Doppler signals Return in 8 to 12 hours for follow-up angiogram

thrombolytic agents, however, may increase the bleeding complications and must be rated against the clinical severity of the ischemia. Once the thrombolytic therapy is initiated, the heparin infusion is reduced. The patient is monitored closely in the intensive care unit, and then returned to the endovascular suite at intervals of 6–12 hours to follow the lysis progression and to adjust the catheter position as needed (Table 20.2).

Localization of Gastrointestinal Bleeding Catheter-directed delivery of thrombolytic therapy is most often used to treat unwanted arterial thrombosis in critical locations and restore blood flow to ischemic tissues. Another application that exploits the actions of

these lytic agents is that of localization of gastrointestinal bleeding (31–34). The thrombus that is temporarily halting the bleeding source in patients with recurrent gastrointestinal bleeding is acute and should be amenable to thrombolysis. Thus, patients with gastrointestinal hemorrhage unable to be localized by traditional means can be helped by provoking bleeding at the time of mesenteric angiography (Fig. 20.6). Heparin, t-PA or UK, and a vasodilator given in combination via the superior mesenteric artery have been used to stimulate bleeding in order to localize the source and to further guide therapy (33–34).

Venous Thrombolysis Venous thrombosis is a serious clinical entity with a potential to cause death or major morbidity. Pulmonary embolus and venous hypertension are common complications of venous thrombosis. The standard initial treatment for venous thrombosis, regardless of the vascular bed, has been systemic anticoagulation. Theoretically, it is supposed to prevent further thrombosis and thrombus propagation. However, thrombus propagation can still occur despite apparent therapeutic anticoagulation with heparin (35,36). Caps and associates reported a 26% incidence of contiguous and non-contiguous DVT extension during a 3-week observational period while on traditional anticoagulation with heparin and/or coumadin (36). Thrombolytic therapy with active clot dissolution may be more effective than traditional treatment of DVT with anticoagulation and clot stabilization. The preservation of venous valvular function appears to be related to timely thrombus clearance. Meissner and

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FIGURE 20.6 Localization of gastrointestinal bleeding. A 56-year-old man with recurrent gastrointestinal bleeding that was not localized after upper and lower endoscopy and tagged red blood cell scan. Mesenteric angiography was performed and no active bleeding or obvious arterial malformation was identified (A). Provocation of bleeding (arrow) was accomplished with heparin, papaverine, and t-PA (B). Active bleeding in the cecum was stopped with a single embolization coil (C). The patient underwent a right hemicolectomy.

colleagues demonstrated a relationship between early recanalization of deep venous thrombosis and the preservation of venous valve integrity (37). Patients who were treated with anticoagulation alone were followed over time with serial duplex ultrasonography (37). Those patients with early deep venous recanalization had less deep venous valvular insufficiency (37). The systemic administration of streptokinase in the treatment of acute DVT has been shown to have a reduction in the long-term development of the post-thrombotic syndrome when compared with anticoagulation alone (38,39). Therefore, a more rapid resolution of the venous thrombus with thrombolytic therapy can potentially salvage deep venous valvular function. Systemic anticoagulation, even when given at therapeutic levels, does not demonstrate reliable thrombus removal, and the phlebographic clearance of DVT is significantly better in those patients who receive systemic lytic therapy compared with heparin alone (40). Comerota pooled data from 13 studies and compared the outcome of thrombus lysis of limbs with acute DVT treated with anticoagulation alone and thrombolytic therapy (40); 4% of limbs treated with anticoagulation versus 45% of limbs treated with thrombolytic therapy had significant or complete phlebographic clearance of thrombus. No detectable evidence of lysis was seen in 82% of patients receiving anticoagulation, compared with 37% following thrombolysis. While there was significant improvement over anticoagulation alone, the systemic administration of lytic therapy resulted in significant or complete thrombus clearance in less than one half of patients (40).

As an alternative to systemic therapy, local or regional administration of thrombolytics via catheter-directed techniques are performed in order to enhance the clearance of thrombus and reduce the systemic effect of the lytic agent.

Thrombolytic Therapy of Lower Extremity Deep Venous Thrombosis Traditional therapy for acute DVT of the lower extremity with systemic anticoagulation has been generally effective in reducing the incidence of pulmonary embolus. However, it does not prevent the post-thrombotic syndrome. The clinical symptoms range from pain and leg swelling to chronic skin changes and venous stasis ulceration. This late manifestation of DVT can occur from months to years following the initial episode of venous thrombosis (41). Thrombolytic therapy has the potential to restore venous outflow and preserve the valve function of the affected limb. Early treatment of venous thrombosis can be safely and effectively treated with thrombolytic therapy and there is growing evidence for improved quality of life (42), preservation of valve function, and a reduction in the post-thrombotic syndrome. Therefore we consider all patients with DVT for thrombolytic therapy, and offer this option to those patients with acute thrombosis (less than 10 days) within the iliofemoral venous segments and no contraindication to lytic therapy. Thrombolytic therapy is not withheld from patients with chronic thrombosis (greater than 10 days). Older DVT

Chapter 20 Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis

can still be cleared with thrombolytic therapy and these patients may also benefit from a reduction in the postthrombotic syndrome. Patients with a large thrombus burden or progression of thrombus despite adequate traditional anticoagulation are offered thrombolytics. Catheter-directed thrombolysis of symptomatic lower extremity deep venous thrombosis (LE DVT) is both safe and effective (43–46). Mewissen et al. reported the findings of a large multicenter series of patients with symptomatic LE DVT (46). A total of 221 patients with iliofemoral and 79 with femoropopliteal DVT underwent a continuous UK infusion for a mean time of 53.4 hours. In all, 31% of patients had complete (grade III) clearance of DVT, and 52% had a 50% to 99% (grade II) reduction in DVT. Only 17% had less than half (grade I) of the DVT removed. Following thrombolysis, 99 iliac and five femoral vein stenoses were treated with percutaneous transluminal angioplasty and stenting. The grade of lysis was a predictor of patency, with 79% of limbs with completed lysis remaining patent at 1 year. The improved grade III limb patency was statistically significant compared with the other grades, with only 58% of grade II and 32% of grade I limbs patent at 1 year. Patency was also better at 1 year in the limbs with iliofemoral DVT (64%) compared with femoropopliteal DVT (47%). Significant improvement in patency was demonstrated at 1 year with limbs that received adjunctive iliac vein stents (74%) compared with no stent (53%). This multicenter registry reported an 11% major bleeding complication rate. Of the bleeding complications, 39% occurred at the venous access site. The major neurologic complication rate was 0.4% and this consisted of one fatal intracranial bleed and one nonfatal subdural hematoma. Six patients (1%) had pulmonary emboli during treatment. One patient died as a result of their pulmonary embolus. The overall mortality for LE DVT thrombolysis was 0.4% (46). While early descriptions indicate that successful LE DVT thrombolysis was achieved through an internal jugular or contralateral common femoral vein approach (43,44), we prefer popliteal venous access using ultrasound guidance while the patient is in the prone position (Fig. 20.7). Systemic antiocoagulation with heparin is begun at the time of DVT diagnosis and continued during the procedure. Once a sheath is positioned in the popliteal vein, a venogram is performed to delineate the thrombosis. An angled guidewire is then used to traverse the occlusion, then an infusion catheter (Mewissen Infusion Catheter, Boston Scientific, Quincy, MA) is used to administer t-PA (3–5 mg) as a pulse-spray bolus over 15–30 min. A continuous infusion of t-PA at a rate of 0.5 to 2 mg/h follows the bolus and the patient is monitored in the intensive care unit. The heparin infusion is given via the sheath and reduced to approximately 400 to 500 u/h. The patient returns to the angiography suite at 8-h to 12-h intervals over the next 24 to 48 hours to assess thrombus clearance. Venous angioplasty is performed as needed, with stent placement usually being reserved for proximal iliac vein lesions resistant to balloon dilation (Table 20.3).

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Upper Extremity Deep Venous Thrombosis Upper extremity deep venous thrombosis (UE DVT) was once believed to have a relatively low incidence and benign consequences (47–49). UE DVT now comprises up to 4% of DVT (49). Primary UE DVT occurs spontaneously and is usually found in the younger patient population (49). The causes are usually idiopathic or related to effort thrombosis (Paget-Schroetter syndrome) (49,50). The frequency of primary UE DVT is less than secondary UE DVT (49). Secondary UE DVT occurs in patients with either acquired or inherited risk factors. These factors include central venous catheters, pacemaker wires, malignancy, trauma, hypercoagulable states, and extrinsic compression from tumors (49–51). These patients are usually older and chronically ill. Often, there is an associated malignancy or long-term intravenous catheters (49). The complications of UE DVT are significant and include pulmonary embolus and post-thrombotic syndrome (47,49,52,53). Prompt diagnosis and treatment are recommended for patients with UE DVT (47,49,50). Traditional treatment, as with LE DVT, is systemic anticoagulation with heparin and coumadin. Catheter-directed thrombolysis is the treatment of choice in patients with acute axillosubclavian deep venous thrombosis. Venous access is usually via the basilic vein of the involved limb, but femoral access may sometimes be successful (Fig. 20.8). Ultrasound guidance may be useful in localizing the basilic vein for percutaneous access. A venogram is performed once sheath access is secured. This will delineate the venous anatomy prior to guidewire crossing of the occlusion. An infusion catheter is placed across the occluded venous segment. A variety of strategies for lytic agent administration can be used. A pulse-spray technique alone can be an effective treatment with the dose depending on the thrombus load (54). Usually, a continuous infusion of t-PA is delivered into the thrombus via a Mewissen catheter, and heparin is given at a low rate through the sheath. The patient is observed closely in the intensive care unit, and returned to the endovascular suite for followup venography after 12 to 24 hours. Serial venography is performed at regular intervals in order to monitor clot lysis and reposition the catheter as needed. The infusion may last as long as 48 to 72 hours. Angioplasty of axillosubclavian venous stenoses may be required, but stents are generally avoided prior to thoracic outlet decompression.

Mesenteric Venous Thrombosis Mesenteric venous thrombosis (MVT) is an uncommon condition accounting for 5% to 15% of cases of acute mesenteric ischemia (55). The diagnosis of MVT can be difficult as it often presents with nonspecific abdominal symptoms (56–58). While a wide variety of noninvasive

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tests are effective in identifying MVT, computed tomography is the diagnostic study of choice with a sensitivity reported as high as 100% (57). MVT can usually be treated initially with systemic anticoagulation (55,59). If this is

F

FIGURE 20.7 Thrombolysis of lower extremity deep venous thrombosis. A 21-year-old woman with extensive acute left lower extremity deep venous thrombosis from the popliteal to the common iliac veins underwent catheter-directed thrombolysis. The patient was placed in the prone position (A) and using ultrasound guidance a sheath was placed in the popliteal vein (B). Initial venogram demonstrated popliteal and superficial femoral venous thrombosis (C and D). Mechanical thrombolysis was initially used to reduce the thrombus load (E). Residual femoral and iliac venous thrombosis (arrows, F) cleared with an infusion of t-PA (G). A proximal left common iliac vein stenosis (arrow) was discovered following thrombolysis (H). Note the retrievable inferior vena caval filter that was placed before lytic therapy (arrowhead).

not successful, bowel infarction may occur, requiring surgical intervention (55,57,59). The addition of thrombolytic therapy to the treatment of patients with MVT may enhance clearance of

Chapter 20 Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis TABLE 20.3 Thrombolytic technique of lower extremity deep venous thrombosis Prone position Popliteal access via ultrasound guidance (5-Fr. sheath) Venogram to delineate venous occlusion Guidewire across occlusion Consider mechanical or rheolytic catheter to reduce the thrombus load Infusion of thrombolytic agent (t-PA) Pulse spray Continuous infusion (infusion catheter and wire) 24 to 48 hours Angioplasty if needed Stenting of treatable proximal lesions (e.g., iliac)

thrombus and hasten improvements in clinical symptoms. There have been several case reports and small series studies of patients with MVT treated with systemic infusions of SK, UK or t-PA (60–62). In order to deliver the thrombolytic agents directly to the thrombus, others have reported successful resolution of MVT with a transhepatic (63–65) or transjugular intrahepatic (66–68) approach to the portal and mesenteric veins. Also, transarterial infusion of t-PA or UK infused via the SMA (Fig. 20.9) has been reported (69–73). More directed administration of t-PA or UK reduce potential systemic complications of thrombolytic therapy. There are several additional potential advantages to transarterial infusion of thrombolytics (69). The venous thrombosis may have originated in the small venules of the mesentery and then propagated to the larger venous branches. A concentrated lytic infusion

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FIGURE 20.8 Axillosubclavian venous thrombosis. Upper extremity venography in a young woman with acute right arm swelling demonstrates a right subclavian vein occlusion (A). Minimal improvement was seen after initial pulse-spray of t-PA with an infusion catheter (B). A continuous infusion for 24 hours cleared the majority of acute thrombus (C). Careful balloon angioplasty (D) provided further improvement in the proximal subclavian vein stenosis (E). The patient underwent first rib resection at a later date.

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FIGURE 20.9 Portal venous thrombosis. A 35-year-old man presented with increasing abdominal pain, and a computed tomographic scan demonstrated portal (arrow) and superior mesenteric vein thrombosis (A). A catheter was positioned in the proximal SMA beyond the origin or the replaced common hepatic artery (arrow, B). Selective digital subtraction mesenteric angiography with delayed venous phase images confirmed the venous thrombosis and a bolus of t-PA was given followed by a continuous infusion (C). The patient clinically improved and was monitored in the intensive care unit until he returned for a follow-up angiogram at 24 hours. This demonstrated an improvement in the visualization of the portal vein (D) and the mesenteric venous arcades. The t-PA infusion was continued for an additional 24 hours, and the completion angiogram showed a widely patent portal vein (E). Computed tomography following thrombolysis showed complete dissolution of the portal venous thrombosis (F).

into the mesenteric arterial tree may be more effective at thrombus clearance in these smaller thrombosed veins. The transjugular or transhepatic approach may treat the larger venous branches effectively but not deliver the lytic agent to the venules. This route also avoids the likely added complexity and potential complications of transjugular or transhepatic access to the portal and mesenteric veins. The transjugular route has been used to introduce mechanical thrombectomy catheters to clear the MVT (74).

Conclusion Local and regional catheter-directed thrombolytic therapy is an effective tool in the treatment of a variety of arterial and venous thrombotic disorders. With direct delivery of thrombolytics into the clot, systemic hemorrhagic complications are reduced and thrombus clearance

is improved. Careful physical assessment of limb ischemia is essential for proper selection of patients for thrombolysis, and patients with native arterial and graft occlusions whose ischemia is not prohibitive can be successfully treated. The long-term consequences of deep venous thrombosis are significant, and venous thrombolysis offers a promising treatment option for reducing the thrombus burden and preserving valvular function.

References 1. Flier JS, Underhill LH. Molecular and cellular biology of blood coagulation. N Engl J Med 1992; 326: 800–806. 2. Chang R, Powell RJ, Sumpio BE. Tissue plasminogen activator-biologic perspectives for surgeons. J Am Coll Surg 1997; 184: 529–39. 3. Blinc A, Francis CW. Transport processes in fibrinolysis and fibrinolytic therapy. Thromb Haemost 1996; 76: 481–91.

Chapter 20 Thrombolytic Therapy for Peripheral Arterial and Venous Thrombosis 4. Alkjaersig N, Fletcher AP, Sherry S. The mechanism of clot dissolution by plasmin. J Clin Invest 1959; 38: 1086–95. 5. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17, 187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988 Aug 13; 2(8607): 349–60. 6. Keyt BA, Paoni NF, et al. A faster-acting and more potent form of tissue plasminogen activator. Proc Natl Acad Sci 1994, 91: 3670–4. 7. Meierhenrich R, Carlsson J, et al. Effect of reteplase on hemostasis variables: analysis of fibrin specificity, relation to bleeding complications and coronary patency. Int J Cardiol 1998, 65: 57–63. 8. Ouriel K, Shortell CK, et al. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 1994, 19: 1021–30. 9. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE Trial. Ann Surg 1994; 220: 251–68. 10. Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinate urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS) Investigators. N Engl J Med 1998; 338: 1105–11. 11. Thrombolysis in the management of lower limb peripheral arterial occlusion: a consensus document. Working party on thrombolysis in the management of limb ischemia. Am J Cardiol 1998; 81: 207–18. 12. Coulon M, Goffette P, Dondelinger RF. Local thrombolytic infusion in arterial ischemia of the upper limb: mid-term results. Cardiovasc Intervent Radiol 1994; 17(2): 81–6. 13. Widlus DM, Venbrux AC, et al. Fibrinolytic therapy for upper-extremity arterial occlusions. Radiology 1990; 175(2): 393–9. 14. Cejna M, Salomonowitz E, et al. rt-PA thrombolysis in acute thromboembolic upper-extremity arterial occlusion. Cardiovasc Intervent Radiol 2001 Jul-Aug; 24(4): 218–23. 15. Sylvester PA, Davies AH, et al. The role of thrombolysis in the management of thromboembolic disorders: a fouryear review. Eur J Vasc Endovasc Surg 1995; 9(4): 459–62. 16. Ouriel K, Kandarpa K, et al. Prourokinase versus urokinase for recanalization of peripheral occlusions, safety and efficacy: The PURPOSE Trial. JVIR 1999; 10: 1083–91. 17. Matas Docampo M, Gomez Palones F, et al. Intraarterial urokinase for acute native arterial occlusion of the limbs. Ann Vasc Surg 1997; 11(6): 565–72. 18. Swischuk JL, Fox PF, et al. Transcatheter intraarterial infusion of rt-PA for acute lower limb ischemia: results and complications. J Vasc Interv Radiol 2001; 12(4): 423–30. 19. Schilling JD, Pond GD, et al. Catheter-directed urokinase thrombolysis: an adjunct to PTA/surgery for management of lower extremity thromboembolic disease. Angiology 1994: 45; 851–866. 20. Steinmetz E, Bouchot O, et al. Preoperative intraarterial thrombolysis before surgical revascularization for popliteal artery aneurysm with acute ischemia. Ann Vasc Surg 2000; 14(4): 360–4.

283

21. Hoelting T, Paetz B, et al. The value of preoperative lytic therapy in limb-threatening acute ischemia femoropopliteal artery aneurysm. Am J Surg 1994; 168(3): 227–31. 22. Greenberg R, Wellander E, et al. Aggressive treatment of acute limb ischemia due to thrombosed popliteal aneurysms. Eur J Radiol 1998; 28(3): 211–8. 23. Garramone RR Jr, Gallagher JJ Jr, Drezner AD. Intraarterial thrombolytic therapy in the initial management of thrombosed popliteal artery aneurysms. Ann Vasc Surg. 1994; 8(4): 363–6. 24. Marty B, Wicky S, et al. Success of thrombolysis as a predictor of outcome in acute thrombosis of popliteal aneurysms. J Vasc Surg 2002 Mar; 35(3): 487–93. 25. Nackman GB, Walsh DB, et al. Thrombolysis of occluded infrainguinal vein grafts: Predictors of outcome. J Vasc Surgery 1997; 25: 1023–32. 26. Graor RA, Risius B, et al. Thrombolysis of peripheral arterial bypass grafts: Surgical thrombecomy compared with thrombolysis. J Vasc Surg 1988; 7: 347–55. 27. Flinn WR, McCarthy WJ, et al. Thrombolytic therapy in the management of chronic arterial occlusions. In: Comerota AJ (ed). Thrombolytic therapy for peripheral vascular disease. Lippincott Co., Philadelphia, PA, 1995: 269–277. 28. Ouriel K, Shortell CK, et al. Acute peripheral arterial occlusion: Predictors of success in catheter-directed thrombolytic therapy. Radiology 1994; 193: 561–6. 29. Sullivan KL, Gardiner GA, et al. Acceleration of thrombolysis with a high-dose transthrombus bolus technique. Radiology 1989; 173: 805–808. 30. Braithwaite BD, Buckenham TM, et al. A prospective randomized trial of high dose verses low dose tissue plasminogen activator infusion in the management of acute limb ischemia. Br J Surg 1997; 84: 646–650. 31. Glickerman DJ, Kowdley KV, Rosch J. Urokinase in gastrointestinal tract bleeding. Radiology 1988; 168(2): 375–6. 32. Malden ES, Hicks ME, et al. Recurrent gastrointestinal bleeding: use of thrombolysis with anticoagulation in diagnosis. Radiology 1998; 207(1): 147–51. 33. Bloomfeld RS, Smith TP, et al. Provocative angiography in patients with gastrointestinal hemorrhage of obscure origin. Am J Gastroenterol 2000; 95(10): 2807–12. 34. Ryan JM, Key SM, et al. Nonlocalized lower gastrointestinal bleeding: provocative bleeding studies with intraarterial tPA, heparin, and tolazoline. J Vasc Interv Radiol 2001; 12(11): 1273–7. 35. Strandness DE Jr. Thrombus propagation and level of anticoagulation. J Vasc Surg 1990; 12(4): 497–8. 36. Caps MT, Meissner MH, et al. Venous thrombus stability during acute phase of therapy. Vasc Med 1999; 4(1): 9–14. 37. Meissner MH, Manzo RA, et al. Deep venous insufficiency: The relationship between lysis and subsequent reflux. J Vasc Surg 1993; 18: 596–608. 38. Arnesen H, Hoiseth A, Ly B. Streptokinase or heparin in the treatment of deep venous thrombosis: follow-up results of a prospective study. Acta Med Scand 1982; 211: 65–71. 39. Jeffery P, Immelman E, Ammore J. Treatment of deep venous thrombosis with heparin or streptokinase: long-

284

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

Part III Basic Vascular and Endovascular Techniques term versus function assessment. Proceedings of the Second International Vascular Symposium, London, 1986. Comerota AJ, Aldridge SC. Thrombolytic therapy for deep venous thrombosis: a clinical review. Can J Surg 1993; 36(4): 359–64. Johnson BF, Manzo RA, et al. Relationship between changes in the deep venous system and the development of the postthrombotic syndrome after an acute episode of lower limb deep vein thrombosis: A one- to six-year follow-up. J Vasc Surg 1995; 21: 307–13. Camerota AJ, Throm RC, et al. Catheter-directed thrombolysis for iliofemoral deep venous thrombosis improves health-related quality of life. J Vasc Surg 2000; 32: 130–7. Semba CP, Dake MD. Iliofemoral deep venous thrombosis: Aggressive therapy with catheter-directed thrombolysis. Radiology 1994; 191: 487–94. Comerota AJ, Aldridge SC, et al. A strategy of aggressive regional therapy for acute iliofemoral venous thrombosis with contemporary venous thrombectomy or catheterdirected thrombolysis. J Vasc Surg 1994; 20(2): 244–54. Bjarnason H, Kruse JR, et al. Iliofemoral deep venous thrombosis: safety and efficacy outcome during 5 years of catheter-directed thrombolytic therapy. J Vasc Interv Radiol 1997; 8(3): 405–18. Mewissen MW, Seabrook GR, et al. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: Report of a national multicenter registry. Radiology 1999; 211: 39–49. Hingorani A, Ascher E, et al. Upper extremity deep venous thrombosis and its impact on morbidity and mortality rates in a hospital-based population. J Vasc Surg 1997; 26: 853–60. Kerr TM, Lutter KS, et al. Upper extremity venous thrombosis diagnosed by duplex scanning. Am J Surg 1990; 160: 202–206. Prandoni P, Bernardi E. Upper-extremity deep vein thrombosis. Current opinions in pulmonary medicine 1999; 5: 222–226. Carman TL, Fernandez BB. Issues and controversies in venous thromboembolism. Cleve Clin J Med 1999; 66: 113–23. Horattas MC, Wright DJ, et al. Changing concepts of deep venous thrombosis of the upper extremity: report of a series and review of the literature. Surgery 1988; 104: 561–7. Hingorani A, Ascher E, et al. Upper extremity verses lower extremity deep venous thrombosis. Am J Surg 1997; 174: 214–217. Prandoni P, Polistena P, et al. Upper-extremity deep vein thrombosis: risk factors, diagnosis, and complications. Arch Intern Med 1997; 157: 57–62. Chang R, Horne MK, et al. Pulse-spray treatment of subclavian and jugular venous thrombi with recombinant tissue plasminogen activator. JVIR 1996; 7: 845–851. Morasch MD, Ebaugh JL, et al. Mesenteric venous thrombosis: a changing clinical entity. J Vasc Surg 2001; 34(4): 680–4. Rhee RY, Gloviczki P, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994; 20(5): 688–97.

57. Rhee RY, Gloviczki P. Mesenteric venous thrombosis. Surg Clin North Am 1997; 77(2): 327–38. 58. Hassan HA, Raufman JP. Mesenteric venous thrombosis. South Med J 1999; 92(6): 558–62. 59. Brunaud L, Antunes L, et al. Acute mesenteric venous thrombosis: case for nonoperative management. J Vasc Surg 2001; 34(4): 673–9. 60. Schafer C, Zundler J, Bode JC. Thrombolytic therapy in patients with portal vein thrombosis: case report and review of the literature. Eur J Gastroenterol Hepatol 2000; 12(10): 1141–5. 61. Suzuki S, Nakamura S, et al. Portal vein thrombosis after splenectomy successfully treated by an enormous dosage of fibrinolytic agent in a short period: report of two cases. Surg Today 1992; 22(5): 464–9. 62. Guckelberger O, Bechstein WO, et al. Successful recanalization of late portal vein thrombosis after liver transplantation using systemic low-dose recombinant tissue plasminogen activator. Transpl Int 1999; 12(4): 273–7. 63. Yankes JR, Uglietta JP, et al. Percutaneous transhepatic recanalization and thrombolysis of the superior mesenteric vein. Am J Roentgenol 1988; 151289–90. 64. Bilbao JI, Rodriguez-Cabello J, et al. Portal thrombosis: percutaneous transhepatic treatment with urokinase: a case report. Gastrointest Radiol 1989; 14(4): 326– 8. 65. Bizollon T, Bissuel F, et al. Fibrinolytic therapy for portal vein thrombosis. Lancet 1991; 337(8754): 1416. 66. Rivitz SM, Geller SC, et al. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Interv Radiol 1995; 6(2): 219–23. 67. Sehgal M, Haskal ZJ. Use of transjugular intrahepatic portosystemic shunts during lytic therapy of extensive portal splenic and mesenteric venous thrombosis: longterm follow-up. J Vasc Interv Radiol 2000; 11(1): 61–5. 68. Aytekin C, Boyvat F, et al. Catheter-directed thrombolysis with transjugular access in portal vein thrombosis secondary to pancreatitis. Eur J Radiol 2001; 39(2): 80–2. 69. Poplausky MR, Kaufman JA, et al. Mesenteric venous thrombosis treated with urokinase via the superior mesenteric artery. Gastroenterology 1996; 110(5): 1633–5. 70. Train JS, Ross H, et al. Mesenteric venous thrombosis: successful treatment by intraarterial lytic therapy. J Vasc Interv Radiol 1998; 9(3): 461–4. 71. Ludwig DJ, Hauptmann E, et al. Mesenteric and portal vein thrombosis in a young patient with protein S deficiency treated with urokinase via the superior mesenteric artery. J Vasc Surg 1999; 30(3): 551–4. 72. Rundback JH. Mesenteric venous thrombosis: successful treatment by intraarterial lytic therapy. J Vasc Interv Radiol 1999; 10(1): 98–9. 73. Antoch G, Taleb N, et al. Transarterial thrombolysis of portal and mesenteric vein thrombosis: a promising alternative to common therapy. Eur J Vasc Endovasc Surg 2001; 21(5): 471–2. 74. Sze DY, O’Sullivan GJ, et al. Mesenteric and portal venous thrombosis treated by transjugular mechanical thrombolysis. Am J Roentgenol 2000; 175(3): 732–4.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 21 Role of Angioscopy in Vascular Surgery Arnold Miller and Charles P. Panisyn

Since the introduction of angioscopy to the practice of modern vascular surgery more than a decade ago, it has become an integral part of the vascular surgeon’s armamentarium. Its utilization still depends to some degree on the perspective and interest of the individual surgeon, and its exact role in the practice of vascular surgery continues to be refined. Endoluminal visualization in areas of the vasculature remote from open surgical sites provides unique detailed endoluminal information in threedimensional real-life colors, unavailable by other imaging techniques. This unique information continues to contribute to patient care as well as promoting understanding of the basic mechanisms of vascular disease. The clinical role of angioscopy remains mostly diagnostic. The main obstacles to the easy implementation of any therapeutic application are the well-known limitations of the technique, namely the requirement of a visual field clear of any blood cells and the forward viewing lens systems of current angioscopes. In addition, the inability to accurately measure and size the intraluminal image reduces the reproducibility of the study and complicates image interpretation. In this chapter, a review of the instrumentation, techniques and role of angioscopy in the practice of modern vascular surgery is presented.

Instrumentation Flexible angioscopes in clinical use range in external diameters from 0.5 to 3.0 mm. They consist of bundles of flexible glass fibers (3000 to as many as 30,000 or more) of various types and refractive indices (clear glass or quartz)

coherently arranged and covered by an outer coating or “cladding” which ensures undistorted light and image transmission (Fig. 21.1). The number of fiber bundles (“pixels”) and the lensing systems are responsible for the resolution of the angioscopic image: the more fibers the more “pixels” and the higher the resolution. The fiber bundles are organized into those for imaging and those conducting light. At the distal end of the angioscope a convex lens is fitted to capture the light emitted from the viewed intraluminal object and refocus the “image” onto the mosaic of fibers of the optical bundle. Because the fiber bundles are coherently arranged, this image is faithfully reproduced at the opposite end of the optical bundle, which is attached to a CCD chip video camera and viewed as an image on a monitor. To inject sufficient light for transmission through the small volume of fiber bundles available in the angioscope for satisfactory intraluminal viewing, a very intense and focused light source, most usually derived from quartz-halogen or xenon-arc lamps, is used. The definitive clinical angioscope may consist of only the flexible light fibers, or include hollow channels allowing irrigation at the distal tip of the angioscope or for use as a working channel for special intraluminal instrumentation. Steering of the distal tip of the angioscope is possible. This is usually mechanical and is facilitated by thin cables which extend along the surface of the angioscope sheath. Such specialized features, hollow channels or steering mechanisms increase the external diameter of the angioscope as well the overall rigidity of the instrument. Inclusion of these special features into a particular angioscope is always a compromise between the resolution and

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light intensity (total number of fiberoptic bundles) and the external diameter of the angioscope. Standard video and audio equipment is used for the intraoperative recording the angioscopic procedure.

Angioscopic Technique

FIGURE 21.1 The anatomy of an angioscope. (Reproduced with permission from Miller A, Jepsen S. Technique of intraoperative angioscopy in lower extremity revascularization. In Yao JST, Bergan JJ, ed. Techniques in Arterial Surgery. Philadelphia, PA: WB Saunders, 1989.)

A

To achieve consistent high-quality angioscopic studies requires familiarity with the equipment, and frequent use (1) (Fig. 21.2A and B). Angioscopes no larger than 50% of the endoluminal diameter of the vessels to be viewed should always be selected. Larger-diameter angioscopes can injure the vessels or induce severe spasm. The most useful angioscopes are in the 1 to 2 mm range. For a small vein, an angioscope as small as 0.8 mm will be used. In veins of larger diameters, steerable angioscopes improve visualization and intraluminal manipulation. Although angioscopes with a built-in irrigation channel are convenient, in general, angioscopes without an irrigation channel are preferable, especially for the smaller-diameter angioscopes (<2 mm OD) where the built-in irrigation channel may be too narrow to achieve the necessary flow rates for successful angioscopy. The built-in irrigation channel increases the diameter as well as the rigidity of the

B

FIGURE 21.2 (A) Standard technique for completion angioscopy for infrainguinal in situ saphenous vein bypass graft. (Reproduced with permission from Miller A, Jepsen S. Technique of intraoperative angioscopy in lower extremity revascularization. In Yao JST, Bergan JJ, ed. Techniques in Arterial Surgery. Philadelphia, PA: WB Saunders, 1989.) (B) Technique to ensure complete endoluminal visualization. (Reproduced with permission from Miller A, Jepsen S. Technique of intraoperative angioscopy in lower extremity revascularization. In Yao JST, Bergan JJ, ed. Techniques in Arterial Surgery. Philadelphia, PA: WB Saunders, 1989.)

Chapter 21 Role of Angioscopy in Vascular Surgery

angioscope, increasing the chances of vessel injury such as dissection or even perforation, unless great care is utilized. Angioscopes without the built-in irrigation channel are more flexible and carry more optical and light fibers per unit size. Irrigation is provided by a dedicated angioscopy pump, either coaxially through a standard irrigation sheath with a hemostatic valve, or collaterally, with an angiocath or blunt needle. Understanding the principles of irrigation is critical (2). The use of proximal occlusion, high flow rates (250 to 400 mL/min) to establish a clear fluid column and then maintain this clear column of fluid with a low flow rate (50 to 70 mL/min) minimizes the volume of fluid delivered. With skill and practice most angioscopic studies can be performed with less than 500 mL of fluid, a volume of IV fluid easily tolerated. This volume of IV fluid must be counted as part of the total fluid volume given the patient during the operative procedure. Cooperation with the anesthesiologist is essential (3). Other technical aids in reducing the irrigation fluid load during angioscopy include simple maneuvers to reduce the backbleeding and collateral flow. Prevention of infusion of blood into the clear irrigation fluid column can be achieved by the appropriate use of simple digital pressure, a torniquet, vessel loop or arterial clamp. In general, viewing on withdrawing the angioscope rather than on insertion also reduces the total volume of irrigation fluid for any procedure (Fig. 21.2A).

Interpretation The value and reliability of the angioscopic examination is enhanced with the development of interpretative skills and experience of the endoscopist. These skills may be acquired from review of previous studies but are refined with the continued and critical review and evaluation of the angioscopic findings after each study. It is especially important to appreciate that the angioscope in its current form is a qualitative instrument. The accurate assessment of size on the video monitor remains problematic. Magnification of the image changes with the distance between the angioscope lens and the object: the closer the lens to the object the larger the image. This makes much of the interpretation of the angioscopic images subjective and the significance of many of the more subtle endoluminal findings difficult to assess even with a large amount of experience. Methods to quantitate the angioscopic image would substantially enhance the value of angioscopy (4).

Indications The current indications for angioscopy are summarized in Table 21.1. Vein preparation during bypass or vascular access surgery, and completion angioscopy, especially after thrombectomy or other intraluminal manipulations, are the most commonly used angioscopic applications.

287

TABLE 21.1 Indications for angioscopy Diagnostic Monitoring of surgical/interventional procedures Bypass, endarterectomy, thrombectomy or embolectomy Angioplasty or atherectomy Clinicopathological correlation Endoscopic findings and graft failure Therapeutic Surgical Endoluminal vein graft preparation (valvulotomy and tributary occlusion) Catheter-directed thrombectomy or embolectomy Percutaneous Thrombolysis Assisted interventions (angioplasty/atherectomy/stenting)

Bypass Surgery Vein Conduit Preparation Routine angioscopy during vein bypass surgery is of particular value in the evaluation of conduit quality, the key factor in graft durability (5–7). Angioscopy is a simple and effective technique to evaluate quality of the vein as a conduit intraoperatively prior to establishment of the bypass. This is a significant advantage over the other commonly used monitoring techniques, intraoperative Duplex ultrasound and angiography, which are feasible only after blood flow is reestablished after completion of the bypass graft. Of these three monitoring techniques, angioscopy is the most sensitive in diagnosing intraluminal venous pathology, most commonly areas of thrombosis and recanalization, seen angioscopically as webs, bands or strands (8) (Fig. 21.3). These areas of recanalization may be dense or sparse, involving short or long vein segments. The incidence of the various intraluminal pathologies varies both in the patient population and the particular vein harvested. In those patients undergoing bypass, this intraluminal pathology is most frequently seen in the arm vein harvested for conduit, where the incidence is as high as 60% to 70% (9). In the harvested greater saphenous vein, the incidence is only 10–20%. In renal failure patients undergoing upper extremity vascular access procedures for hemodialysis, the incidence is only 20% to 30% (10). The occurrence of this venous pathology in the various upper extremity veins is shown in Fig. 21.4A. The difference in frequency of this finding reflects the accessibility of the vein and suggests the most likely cause of this pathology to be associated with previous phlebotomy or intravenous infusion. Thrombophlebitis, either spontaneous or traumatic, is the other common etiology. Appropriate interventions done with angioscopic guidance such as lysis of the finer bands or strands, vein patch angioplasty for short stenotic areas or the exclusion of the more severely diseased segments from the final graft conduit, significantly improve patency (9,11). The bene-

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A

B

FIGURE 21.3 (A) Angioscopic appearance of recanalized segment of cephalic arm vein showing typical webs and strands. (B) Low-power photomicrograph of vein cross-section demonstrating residual webs from recanalization of vessel indicative of organized thrombus (hematoxylin–eosin, ¥20). (Modified from Miller A, Jepsen S, et al. New angioscopic findings in graft failure during infrainguinal bypass grafting. Arch Surg 1990; 125: 749–755.)

45

100

34 20

37

31

Patency (%)

80

22

60

12

12 8

40 20 0

4

4

Normal vs. Inferior Upgraded vs. Inferior months p-value months p-value 1 0.04 1 0.02 3 0.002 3 0.0002 6 0.0001 6 0.0003 12 0.001 12 0.01

0

A

14

2

4

6 Months

(n = 42) Normal Upgraded (n = 47) (n = 20) Inferior

8

10

12

B

FIGURE 21.4 (A) The incidence and distribution of the segmental pathology detected with angioscopic preparation and monitoring of 113 arm veins harvested for infrainguinal bypass conduits. (Reproduced with permission from Marcaccio E, Miller A, et al. Angioscopically directed interventions improve arm vein bypass grafts. J Vasc Surg 1993; 17: 994–1004.) (B) Comparison of primary graft patency for the 109 infrainguinal arm vein bypass grafts as determined by life tables with comparisons of “normal” vs. “upgraded” vs. “inferior” quality arm vein grafts. (Reproduced with permission from Marcaccio E, Miller A, et al. Angioscopically directed interventions improve arm vein bypass grafts. J Vasc Surg 1993; 17: 994–1004.)

fits of “upgrading” arm vein conduit on graft patency is shown in Fig. 21.4B. Angioscopically directed valve lysis for nonreversed and in-situ veins minimizes early failure due to technical problems and results in improved early and late postoperative graft patency (12,13). Direct visualization ensures completeness of valvulotomy and minimizes inadvertent vein injury during valve lysis. On initiation of vein harvest, if there is suspicion that the vein may be diseased a retrograde examination of the entire vein may be performed to avoid harvest of the vein which later could be found to be unusable. This approach may save significant operative time, minimizing unnecessary surgical expenses with a reduction in patient morbidity (Fig. 21.5).

Our technique for valvulotomy is shown in Figs. 21.6 and 21.7. For ex-vivo valvulotomy, a simple modified Mills valvulotome suffices. For the in-situ bypass, use of the long retrograde valvulotome with the detachable head simplifies the procedure. Although complete exposure of the vein may be used for vein preparation, we now routinely use a semiclosed technique with small interrupted incisions to ligate the main venous tributaries and cut the valves under angioscopic direction. This has significantly reduced the patient morbidity related to wound healing complications. A variety of incision-sparing approaches, both closed and semiclosed techniques, have been described (14–16). The addition of tributary occlusion to angioscopically directed valvulotomy allows complete

Chapter 21 Role of Angioscopy in Vascular Surgery

289

FIGURE 21.5 Technique of in-situ retrograde arm vein inspection. A small incison exposes the distal forearm cephalic vein. The angioscope is introduced through an irrigation sheath and systematic inspection of the cephalic and basilic arm vein is performed. All intraluminal disease is noted and vein harvest planned accordingly. (Reproduced with permission from Marcaccio E, Miller A, et al. Angioscopically directed interventions improve arm vein bypass grafts. J Vasc Surg 1993; 17: 994–1004.)

FIGURE 21.6 Technique of angioscopy-directed valvulotomy in harvested non-reversed vein grafts. (Reproduced with permission from Stonebridge P, Miller A, et al. Angioscopy of arm vein infrainguinal bypass grafts. Ann Vasc Surg 1991; 5: 171–175.)

endovascular vein conduit preparation. Review of this developing experience confirms the advantages of this approach with significantly decreased morbidity due to wound complications and reduction in overall hospitalization (17). Whether there are any inherent benefits in terms of long-term graft patency when performing the procedure by the endovascular approach over conven-

tional techniques with complete or limited graft exposure still remains to be determined. The main limitations to the general application of this elegant surgical technique are technical, with difficulties experienced mostly with the small vein conduit (<4 mm) due to the size of the instrumentation and expense of the instrumentation and occlusion coils (17).

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Part III Basic Vascular and Endovascular Techniques FIGURE 21.7 Technique for valvulotomy in the in-situ bypass. (A) The saphenous vein is completely exposed and the tributaries ligated (currently we use the semiclosed method — see text). The patient is heparinized and the vein transected at both ends. The vein is gently distended with papaverine–saline solution, and the first proximal valve excised with scissors. (B) The valvulotome with the introducer in place is passed through the vein from the distal end to protrude through the proximal end of the vein. The introducer is replaced with the appropriately sized valvulotome. (C) The valvulotome is withdrawn under constant angioscopic direction, steering past the tributary orifices and accurately cutting each valve leaflet. (D) Long flexible valvulotome with detachable head allowing insertion with an introducer and attachment of different size valvulotomy heads.

A Proximal end

Threads Introducer

Valvulotome

B

(Reproduced with permission from Miller A, Stonebridge P, et al. Angioscopically directed valvulotomy: a new valvulotome and technique. J Vasc Surg 1991; 13: 813–21.)

C Index

Blade

D

Rigid shaft With 3° bend

Flexible shaft

Monitoring Bypass Grafts In a prospective randomized study, we attempted to determine whether using the angioscope to routinely monitor infrainguinal bypass grafting rather than the “gold standard” intraoperative angiogram could improve early (30day) graft patency (18). Our study was limited to primary bypass grafts using only autogenous saphenous vein. All revision bypasses and use of other vein, such as arm vein, where we had already shown a significant improvement in early graft patency using the angioscope, were excluded from enrollment into this study.

Grip

The prospective randomization of the 293 patients for the study resulted in well-balanced groups for each of the monitoring modalities, but two significant unforeseen “biases” evolved during the study. The first bias was the preference of all the participating surgeons to prepare the vein conduit with the angioscope whenever they felt the quality of the vein was in question. Of the 43 exclusions from the study after initial randomization, 12 “clinically” assessed poor-quality veins were excluded from the completion angiography group. In the angioscopy group, such veins were not excluded but prepared with the aid of the angioscope and included in the study. The sec-

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A

B

C

FIGURE 21.8 Life-table analysis to 1 month comparing primary graft failure. (A) The entire angioscopy (n = 128) and angiography (n = 122) groups. The difference at 1 month is not statistically significant (p = 0.2). (B) The 11 bypasses to the plantar arteries and the remaining 239 bypasses in the study. At 1 month the difference in statistically significant (p = 0.04). (C) The angioscopy and angiography groups with the 11 plantar arteries excluded. The difference at 1 month is statistically significant (p = 0.03). (Reproduced with permission from Miller A, Marcaccio E, et al. Comparison of angioscopy and angiography for monitoring infrainguinal bypass grafts: results of a prospective randomized trial. J Vasc Surg 1993; 17: 382–98.)

ond bias was the inclusion of a small group of 11 bypass grafts to the plantar arteries of the foot. The 30-day patency for these 11 bypasses to the plantar arteries was only 65% compared with 95.4% for the remaining 239 bypass grafts, reflecting a poor “runoff” situation rather than a failure of either of the monitoring techniques to detect technical errors. By chance, more failures of this group occurred in the angioscopy group. Thus, although our study did not demonstrate a statistically significant difference between the completion monitoring techniques in the early patency in this selected group of patients, with optimal quality vein conduit, it did show a clear-cut trend favoring the angioscope as the preferable intraoperative monitoring method to detect “correctable” problems that could affect early graft patency (Fig. 21.8). Perhaps the most important and least expected finding of this study was the paucity of findings in the completion angiography group that led to subsequent surgical interventions, only seven in the 122 bypasses randomized to this group. Of the seven findings, two were false-positives resulting in unnecessary explorations of the distal anastomoses. In contrast, in the angioscopy group, there

TABLE 21.2 Relevant findings resulting in 39 interventions in 36 bypass grafts during the completion monitoring of 250 infrainguinal bypass grafts (reproduced with permission from reference 38) Angioscopy

Angiograpphy

Vein conduit Residual competent valves Vein preparation/selection Tributary ligation Anastomosis Distal artery

28 9 6 13 3 1

1 1 0 0 5* 1

Total

32

7

*Two of these five findings were false-positive.

were 32 findings in the 128 bypass grafts that led to interventions, with no false-positive interventions. The majority of angioscopic findings were in the vein conduit. This difference was statistically significant (p < 0.0001) (Table 21.2).

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These findings were confirmed by Thörne et al. (13) in a prospective study using the angioscope to monitor in-situ saphenous vein bypass grafts after completion of valvulotomy but prior to performing the distal anastomosis. They showed an improved 12-month primary patency rate and confirmed that the use of angioscopic monitoring minimized residual arteriovenous fistula, uncut or incompletely cut valve leaflets and detected other intraluminal defects. They also showed that this reduced the need for later postoperative reintervention (13). Review of the literature (19,20) reveals a progressive improvement in the patency rates for infrainguinal bypass grafts despite operating in the most severely threatened limbs and ill and elderly patients and extending the grafts more distally in the leg and foot. It appears that, provided the conduit is of good quality and the surgeon proficient in the surgical techniques, excellent results are possible. In those bypasses where the vein conduit is of good quality, the “runoff” vasculature adequate, and the technique proficient, monitoring the bypass surgery for technical or correctable errors by any means does not appear to significantly alter the early graft patency. However, with a conduit of less than optimal quality, or a borderline “runoff”, the role of monitoring of the bypass surgery assumes a new significance. These studies clearly show that intraoperative angioscopy is a most efficient way to monitor the autogenous vein graft, the anastomosis, and distal artery for correctable intrinsic abnormalities or technical defects. It clearly is the most effective way to ensure an optimally prepared graft conduit with best early and late patency.

Arterial and Graft Thrombectomy and the Role of Angioscopy in the Failing or Failed Bypass Grafts The role of angioscopy for thrombectomy of native vessels and failing and failed bypass grafts is not fully appreciated (21–23). Angioscopy is different from the angiogram. It provides clear visualization of the surface of the vessel as well as the luminal contents. The angiogram reflects inverse shadows of the intraluminal pathology, often obscuring non-occlusive and surface lesions. The angioscope easily differentiates intraluminal clot from unsuspected occlusive arterial wall plaque or organized thrombus and is most sensitive in determining any residual thrombus in the main vessel. In synthetic grafts, residual thrombus, fresh and organized, or flaps of pseudointima are easily detected, allowing the appropriate interventions (22). Angioscopy does not delineate the distal or runoff circulation. Where this is necessary, intraoperative angiography should be performed as well. With minimal surgical exposure, the angioscope allows evaluation of the entire graft conduit, both proximal and distal anastomoses and the inflow and runoff arteries as well (Fig. 21.9). Thus, it is not only effective in monitoring the

adequacy of thrombectomy or intraoperative thrombolysis but often elucidates the underlying cause of the graft failure (Table 21.3). In a review of 79 consecutive failing or failed vein bypass grafts (21), we showed that the angiogram consistently underestimates the amount of residual thrombus in the graft or native vessel. Our results showed that the more residual thrombus within the graft conduit, anastomosis, and runoff artery, after all the necessary reoperative procedures, the poorer the early and long-term graft patency (Fig. 21.10). This may explain the finding that despite an initial high “success” rate of 48% to 86% for preoperative thrombolysis or graft thrombectomy, where even with correction of underlying lesion thought to be responsible for the graft occlusion, the long-term patency remains disappointingly low, being only 20% to 50% at 1 year. The fate of graft endothelium and intimal surfaces following thrombosis is unknown, but it has been suggested that ischemic or inflammatory changes occur during the period of graft thrombosis until resumption of arterial blood flow can be achieved, revitalizing the endothelium. The angioscopic appearance of the graft endoluminal surface following thrombolysis and thrombectomy provides a clue to the “health” of the vascular endothelium. In those vein graft conduits with shiny clean intimal surfaces and no residual adherent thrombus, patency is similar to that of failing grafts, provided the underlying cause of the failure is corrected. Grafts with significant residual adherent mural thrombus despite technically adequate thrombectomy or thrombolysis probably contain large areas of dead or dysfunctional endothelium and are inherently thrombogenic with poor patency. The angioscope is a simple method to select viable from nonviable graft conduit or graft conduit segments so that decisions to preserve or abandon a graft can be made in an objective fashion.

Vascular Access Surgery Indications and Techniques Vascular access surgery is useful for the establishment of the access as well as in the evaluation of the failing or failed access (10,24). Unsuspected recanalization in the runoff vein is one of the more frequent reasons why the autogenous fistula fails to mature or the synthetic graft fistula unexpectedly fails. Detection of this pathology intraoperatively, at the time of access surgery, allows immediate remedial surgery to be done. If minimal, this may be endoluminal lysis of the bands or strands with a standard retrograde valvulotome; if more dense, a vein patch angioplasty may be required. If the involved segment is long, the entire vein or vein segment may be abandoned and a different site chosen for the access procedure. For surgical revision of the failed or failing access, angioscopy allows assessment of the venous and arterial

Chapter 21 Role of Angioscopy in Vascular Surgery

293

FIGURE 21.9 Technique of angioscopy to evaluate a failed or failing graft. The angioscope is inserted through a small skin incision and a small opening in the graft. The angioscope is directed proximally and distally to evaluate the graft, both anastomoses and native vessels. If additional sites of pathology are localized, limited exposure is facilitated by the light of the angioscope shining through the skin marking the site of the pathology. (Reproduced with permission from Hölzenbein T, Miller A, et al. Role of angisocopy in reoperation for the failing or failed infrainguinal vein bypass graft. Ann Vasc Surg 1994; 8: 74–91.)

TABLE 21.3 Endovascular findings associated with graft failure (reproduced with permission from reference 39) Vein graft Residual competent valve leaflets (uncut/partially cut) Unligated tributaries (AV fistula) Valvulotome-induced injury Thrombosis and recanalization (webs, bands, strands) Thrombus (organized, platelet, fresh) Intimal hyperplasia Mural sclerosis Atherosclerotic degeneration Anastomosis Intimal flaps/residual valve leaflet on hood Distorted or small apex or outflow tract Irregular suture line Thrombus (organized, platelet, fresh) on suture line/hood/floor Arterial/vein wall pathology Artery Intimal flap/dissection Clamp injury Thrombus (organized, platelet, fresh) Atherosclerotic disease (? plaque characteristics)

anastomoses for the presence of stenosis or other technical abnormalities. Our technique for revision of the occluded synthetic bridge graft is illustrated in Fig. 21.11. A small incision is made, usually at the apex of the loop graft or in the midsection of the straight graft. A few centimeters of synthetic graft are freed up to allow placement of fine occluding clamps for control after reestablishing flow. Rummel tourniquets are placed to prevent leakage of irrigation fluid around the angioscope once inserted. A transverse opening is made in the anterior wall of the graft. Balloon thrombectomy of the venous limb is performed first to take advantage of the lack of bleeding from the occluded arterial limb. The arterial limb is approached only after completion of all manipulations on the venous limb. The angioscope is then introduced through an irrigation sheath and passed through the graft, anastomosis and into the runoff vein. The extent and location of any endoluminal pathology, completeness of the thrombectomy, or result of endoluminal intervention is observed. Repeat angioscopic examination may be performed after each manipulation. On occasion, the light of the angioscope shining through the skin may serve as a guide to direct further exposure of the graft or runoff vein at the site of a particular abnormality. This allows much of the revision procedure to be performed through separate small skin

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A

B

C

and graft incisions, limiting surgical exposure of the graft and the extent of the surgery. Thus most procedures can be performed under local anesthesia. To minimize the volume of irrigation fluid used during angioscopy various techniques are used. A standard tourniquet may be applied to the upper arm preoperatively and inflated to occluding pressures during the angioscopy. This is particularly useful for the more prolonged procedures in which repeated angioscopically directed interventions such as curetting the lining of the graft or repeated thrombectomy is performed. Simple digital pressure of the upper arm to compress the veins, pressure directly on inflow artery to control arterial bleeding, or intraluminal balloon occlusion is a useful adjunct and frequently applied. We have previously shown that angioscopy for vascular access procedures is technically feasible and can be performed safely, with high-quality studies, even in the anuric patient (10). With careful planning and technique, we were able to limit the total irrigation fluid volume to less than 300 mL in primary access surgery and approximately 500 mL during revision surgery. Angioscopy provides the surgeon with additional information to the intraoperative findings in unexposed areas of the hemodialysis fistula, otherwise inaccessible without surgical exploration. The angioscope is a most

FIGURE 21.10 Graft patency analysis by life-table analysis within subgroups defined by the amount of residual thrombus noted within the failed graft at completion of thrombectomy and revision surgery. Patency was calculated for this reoperation only and did not include additional interventions or operations. (A) Grafts which had failed early (<30 days of original bypass) (p < 0.001, log-rank analysis). (B) grafts which had failed late (>30 days of original bypass) (p = 0.0016). (C) Failing grafts (>30 days from original bypass) (p = 0.0194). (Reproduced with permission from Hölzenbein T, Miller A, et al. Role of angisocopy in reoperation for the failing or failed infrainguinal vein bypass graft. Ann Vasc Surg 1994; 8: 74–91.)

effective and valuable tool with which to monitor and assess the amount and localization of residual thrombus, intimal hyperplasia or other pathological changes within the autogenous vein, anastomosis, or synthetic graft. This is particularly important in the revision surgical procedure where routine angioscopy may detect the underlying cause of graft failure and ensure the completeness of thrombectomy. Although intimal hyperplasia at the venous anastomosis is generally considered the commonest cause of failure of synthetic bridge graft fistula, we have shown that stenosis in the midgraft at the needle puncture site of the venous or arterial limb is another important cause of access failure. We have observed the various stages of this phenomenon endoluminally: the initial defect in the graft caused by the needle stick, the subsequent ingrowth of a tissue “plug”, and finally, the confluence and calcification of this tissue which goes on to form a midgraft stenosis. These findings are similar to those reported on the pathology of explanted PTFE vascular access grafts showing the disrupted graft at the needle puncture sites sealed by ingrowth of fibrous tissue (25). In the autogenous vein, we have noted loss of wall, thinning, and aneurysmal dilation. In the synthetic bridge graft fistula, the high occurrence of midgraft stenosis also leads us to suspect that pseudointimal dissection and disruption

Chapter 21 Role of Angioscopy in Vascular Surgery Dense wehbing

Intimal hyperplasia at venous anastomosis

Puncture site stenosis

Cephalic vern

Angioscope

Radial artery

Brachial artery

Thrombus at arterial anastomosis

295

FIGURE 21.11 Technique of angioscopy to evaluate a failed vascular access graft. The angioscope is inserted through a small skin incision and a transverse opening in the graft and directed towards the venous and arterial anastomosis to evaluate the graft, both anastomoses and native vessels. If additional sites of pathology are localized, exposure at the site of pathology is facilitated by the location of the light of the angioscope shining through the skin. Occlusive lesions are removed under direct vision with a Kevorkian–Young curette. (Reproduced with permission from Hölzenbein T, Miller A, et al. The role of routine angioscopy in vascular access surgery. J Endovasc Surg 1995; 2: 10–25.)

Angioscopically-directed graft curettage

Irrigation Sheath

following needle puncture at the time of dialysis may be a more common cause of acute occlusion than is generally appreciated. Unlike routine blind curettage of the midgraft as described by Puckett and Lindsay (26), angioscopy allows selective curettage only when midgraft stenosis is present, avoiding excessive removal of the pseudointima with bleeding or graft disruption or leaving large intraluminal flaps which may result in early reocclusion.

Miscellaneous Applications Carotid Endarterectomy Angioscopy may be performed following both standard (27,28) and eversion (29) endarterectomy. A larger angioscope, 2 to 3 mm, with a built-in irrigation channel, is preferable. In standard endarterectomy, after closure of the arteriotomy, except for the last few sutures, and with the clamps still in place, the angioscope is introduced, allowing systematic examination the internal, external, and common carotid with visualization of the “end point” of the endarterectomy. In eversion endarterectomy, the “end point” is monitored immediately after the endarterecto-

my, prior to reattachment of the internal carotid artery. In our own experience, with standard carotid endarterectomy this occurs in less than 1% of endarterectomies (unpublished data). Thus, we perform angioscopy selectively basis, i.e., only if there is any concern of completeness of the end point.

Venous Surgery Angioscopy has been used successfully in venous surgery for monitoring venous thrombectomy (30) and for repair of valvular incompetence (31,32) for chronic venous insufficiency, with some success. The key to successful angioscopy is the isolation of the venous segment minimizing the total irrigation fluid volume used. In transfemoral venous thrombectomy, the common iliac vein is isolated by the use of proximal occlusion catheters, and control of the larger tributaries allows antegrade angioscopy. Retrograde angioscopy to examine the proximal femoral vein can also be performed. Passage of the angioscope through the venous valves is possible by the use of sudden powerful calf compression with simultaneous momentary cessation of irrigation (33). For venous valvular repair, angioscopy provides direct visual and

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A

B

C

FIGURE 21.12 Technique of percutaneous angioscopy. (A) Percutaneous angioscopy of the superficial femoral and popliteal arteries with proximal occlusion balloon and external compression using an occluding cuff. (B) Percutaneous angioscopy of the iliac arteries with single proximal ipsilateral occlusion balloon. (C) Percutaneous angioscopy of the iliac arteries with double balloon occlusion from both ipsilateral and contralateral femoral arteries. (Reproduced with permission from Miller A, Sacks B. Angioscopy in Interventional Surgery: diagnostic use and therapeutic application in endovascular procedures. In Pearce JS, Ya WH, ed. Techniques in Vascular Surgery. Stamford, CT: Appleton & Lange, 1997.)

functional information of the competence of the valve repair without the necessity of venotomy.

Percutaneous Angioscopy Although successful percutaneous angioscopy has been achieved in the coronary (34) and peripheral vessels (Fig. 21.12A–C) (35–37), the inherent limitations of angioscopy, the need to clear blood from view, and the inability to quantitate the image make this more of a research tool than an essential clinical tool at this time. The information obtained is particularly valuable to our understanding of the underlying pathology and results of interventional techniques. For clinical decisions regarding stent placement or angioplasty, standard angiography, and intraluminal ultrasound provide more relevant quantitative data.

References 1. Miller A, Jepsen S. Technique of Intraoperative Angioscopy In Lower Extremity Revascularization. In Yao JST, Bergan JJ, ed. Techniques in Arterial Surgery. Philadelphia, PA,: W.B. Saunders Co., 1989. 2. Miller A, Lipson W, et al. Intraoperative angioscopy: Principles of irrigation and description of a new dedicated irrigation pump. Am Heart J 1989; 118: 391–9. 3. Kwolek C, Miller A, et al. Safety of saline irrigation for angioscopy: results of a prospective randomized trial. Ann Vasc Surg 1992; 6: 62–68.

4. Wilson Y, Follett D, et al. Quantitative endoluminal measurements during angioscopy: an innovative technique. Eur J Endovasc Surg 1995; 9: 319–326. 5. Miller A, Campbell D, et al. Routine Intraoperative Angioscopy in Lower Extremity Revascularization. Archives of Surgery 1989; 124: 604–608. 6. Miller A, Stonebridge P, et al. Continued experience with intraoperative angioscopy for monitoring infrainguinal bypass grafting. J Vasc Surg 1991; 109: 286– 293. 7. Gilbertson J, Walsh D, et al. A blinded comparison of arteriography, angioscopy, and duplex scanning in the intraoperative evaluation of in situ saphenous vein bypass grafts. J Vasc Surg 1992; 15: 121–9. 8. Miller A, Jepsen S, et al. New angioscopic findings in graft failure during infrainguinal bypass grafting. Arch Surg 1990; 125: 749–755. 9. Marcaccio E, Miller A, et al. Angioscopically directed interventions improve arm vein bypass grafts. J Vasc Surg 1993; 17: 994–1004. 10. Miller A, Hölzenbein T, Gottlieb N. Routine Angioscopy for Vascular Access Surgery. In Henry ML and Ferguson MR, ed. Vascular Access for Hemodialysis — IV: WL Gore & Associates, Inc. Precept Press, Inc, 1995. 11. Hölzenbein T, Pomposelli Jr. F, et al. Results of a policy with arm veins used as the first alternative to an unavailable ipsilateral greater saphenous vein for infrainguinal bypass. J Vasc Surg 1996; 23: 130–40. 12. Miller A, Stonebridge P, et al. Angioscopically directed valvulotomy: a new valvulotome and technique. J Vasc Surg 1991; 13: 813–21. 13. Thörne J, Danielsson G, et al. Intraoperative angioscopy may improve the outcome of in situ saphenous vein bypass grafting: A prospective study. J Vasc Surg 2002; 35: 759–765.

Chapter 21 Role of Angioscopy in Vascular Surgery 14. Mehigan J. Angioscopic preparation of the in situ saphenous vein for arterial bypass: Technical considerations. In White G, White R, eds. Angioscopy: vascular and coronary applications: Year Book Medical Publishers, Inc., 1989. pp. 72–5. 15. La Muraglia G, Cambria R, et al. Angioscopy facilitates a closed technique for in-situ vein bypass. J Vasc Surg 1990; 12: 601–604. 16. Maini B, Andrews L, et al. A modified, angioscopically assisted technique for in situ saphenous vein bypass: impact on patency, complications, and length of stay. J Vasc Surg 1993; 17: 1041–1049. 17. Rosenthal D, Dickson C, et al. Infrainguinal endovascular in situ saphenous vein bypass: ongoing results. J Vasc Surg 1994; 20: 389–95. 18. Miller A, Marcaccio E, et al. Comparison of angioscopy and angiography for monitoring infrainguinal bypass grafts: results of a prospective randomized trial. J Vasc Surg 1993; 17: 382–98. 19. Taylor L, Edwards J, Porter J. Present status of reversed vein bypass: Five year results of a modern series. J Vasc Surg 1990; 11: 207–215. 20. Veith F, Moss C, , et al. New approaches in limb salvage by extended extraanatomic bypasses and prosthetic reconstructions to foot arteries. Surgery 1978; 84: 764–774. 21. Hölzenbein T, Miller A, et al. Role of angisocopy in reoperation for the failing or failed infrainguinal vein bypass graft. Ann Vasc Surg 1994; 8: 74–91. 22. White J, Haas K, Comerota A. An alternative method of salvaging occluded suprainguinal bypass grafts with operative angioscopy and endovascular intervention. J Vasc Surg 1993; 18: 922–931. 23. Grundfest W, Litvack F, , et al. Intraoperative decisions based on angioscopy in peripheral vascular surgery. Circ 1988; 78: I-13–I-17. 24. Hölzenbein T, Miller A, et al. The role of routine angioscopy in vascular access surgery. J Endovasc Surg 1995; 2: 10–25. 25. Delorme J, Guidoin R, et al. Vascular access for hemodialysis: pathologic features of surgically excised ePTFE grafts. Ann.Vasc.Surg. 1992; 6: 517–524. 26. Puckett J, Lindsay S. Midgraft curettage as a routine adjunct to salvage operations for thrombosed polytetrafluoroethyline hemodialysis access grafts. Am J Surg 1988; 156: 139–143. 27. Mehigan J, DeCampli W. Angioscopic Control of Carotid Endarterectomy. In: Endovascular Surgery,

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33.

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39.

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second edition. Ed Ahn SS, Moore WS. W.B. Saunders, Philadelphia, 1992: 102–105. Gaunt M, Naylor A, et al. Role of completion angioscopy in detecting technical error after carotid endarterectomy. Br J Surg 1994; 81: 42–44. Raithel D, Kasprzak P. Angioscopy after carotid endarterectomy. Ann Chir Gyn 1992; 81: 192–195. Vollmar J, Hutschenreiter S. Vascular endoscopy for venous thrombectomy. In: Endovascular Surgery, 2nd edition. Eds. Ahn, S and Moore, W, W.B. Saunders, Philadephia 1992: 83–90. Gloviczki P, Merrell S, Bower T. Femoral vein valve repair under direct vision without venotomy: A modified technique with use of angioscopy. J Vasc Surg 1991; 14: 645–648. Welch H, McLaughlin R, O’Donnell T, Jr. Femoral vein valvuloplasty: Intraoperative angioscopic evaluation and hemodynamic improvement. J Vasc Surg 1992; 16: 694–700. Woelfle K, Bruijnen H, et al. Technique and results of vascular endoscopy in arterial and venous reconstructions. Ann Vasc Surg 1992; 6: 347–356. Forrester J, Litvack F, et al. A perspective of coronary disease seen through the arteries of living man. Circulation 1987; 75: 505–13. Beck A. Percutaneous Angioscopy. First reports on percutaneous transluminal angioplasty and local lysis under angioscopic conditions. Radiology 1987; 27: 555–559. Dietrich E, Yoffe B, et al. Angioscopy in Endovascular Surgery: Recent Technical Advances to Enhance Intervention Selection and Failure Analysis. Angiology 1992; 43: 1–10. Miller A, Sacks B. Angioscopy in Interventional Surgery: diagnostic use and therapeutic application in endovascular procedures. In Pearce JS, Ya WH, ed. Techniques in Vascular Surgery. Stamford, CT: Appleton and Lange, 1997. Miller A, Salenius J. The Impact of Endoluminal Pathology on Vein Graft The Role of Routine Angioscopy for Vein Preparation. In Whittemore A, ed. Advances in Vascular Surgery, Vol. 3. St. Louis: Mosby Year Book, 1995. Miller A, Stonebridge P, Kwolek C. The role of routine angioscopy for infrainguinal bypass procedures. Philadelphia: W. B. Saunders Co., 1992. Stonebridge P, Miller A, et al. Angioscopy of arm vein infrainguinal bypass grafts. Ann Vasc Surg 1991; 5: 171–175.

PART IV

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

Surgical Exposure of Vessels

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 22 Exposure of the Carotid Artery Henry Haimovici

Anatomic Review The carotid artery is located in the lateral region of the neck, bounded by the broad sternocleidomastoid muscle laterally, by the mastoid process above, and by the clavicle and upper sternum below. The major landmark that stands out in bold relief is the sternocleidomastoid muscle, which courses from the mastoid process to the medial end of the clavicle. Anterior to the muscle is the vascular groove, which separates the muscle from the anterior neck region. The superficial structures, running into a duplication of the superficial cervical fascia, are the external jugular vein and a few superficial branches of the cervical plexus. These structures are covered by the platysma muscle. The sternocleidomastoid muscle is held securely in place by duplication of the enveloping fascia of the neck. Its sternal and clavicular heads are separated by a triangular interval. The outer covering of the deep fascia is thick and fibrous above. The deep fascial covering separating the muscle from the subadjacent structures is thin. When the sternocleidomastoid muscle is retracted laterally, the internal jugular vein can be distinguished in the upper one-half or two-thirds of the exposed area. The lymph nodes disposed between the muscle and the vein adhere more or less intimately to both structures. Adhesions caused by pathologic changes above the glands may be so dense as to require removal of the sternocleidomastoid muscle and internal jugular vein during lymph gland dissection. The carotid sheath is the tubular investment of the deep cervical fascia, which encloses the common and in-

ternal carotid arteries, internal jugular vein, and the vagus nerve. Above the common carotid artery, the structure of the sheath is somewhat attenuated. Its posterior wall is adherent to the prevertebral fascia. The anterior wall fuses with and, to some extent, is derived from the pretracheal fascia. It is tenuous over the internal jugular vein but is thick and dense over the common carotid artery. The common carotid artery arises from the innominate trunk on the right and from the arch of the aorta on the left. It emerges from behind the sternoclavicular joint and ascends obliquely in the direction of the angle of the mandible. At the superior margin of the thyroid cartilage, the artery, after forming the carotid bulb, divides into its two terminal branches, the internal and external carotid arteries. The internal carotid continues in the direction of the common trunk. The common carotid artery has posterior relations with the sympathetic ganglia and its chain, the prevertebral fascia, underlying prevertebral muscles and the anterior surface of the transverse processes. Anteriorly, the common carotid is in relation with the areolar tissue of the neck in the upper two-thirds of its course and with the pretracheal fascia in the lower one-third. The internal carotid artery that begins at the level of the superior margin of the thyroid cartilage is situated a little posterolateral to the external carotid, but, as it ascends, it passes to its medial side toward the lateral wall of the pharynx. The external carotid artery is directed upward and backward to the angle of the jaw. Its branches supply the upper neck and extracranial soft parts of the head. The internal jugular vein is the principal venous trunk of the neck and is the direct downward continuation

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of the transverse lateral sinus. The vessel is rarely seen surgically in its upper portion, which lies deep to the styloid process and the parotid compartment. It descends in the carotid sheath and may be recognized easily by its bluish gray color. It runs to a point a little lateral to the sternoclavicular joint, where it unites with the subclavian vein to form the innomminate vein. The common facial vein is the most important contributing branch of the internal jugular. The trunk is

formed at about the level of the submaxillary gland by the union of the anterior and posterior facial veins. It passes backward and downward to pierce the carotid sheath and enter the internal jugular vein opposite the great horn of the hyoid bone. It receives the thyroid and lingual veins and might be termed the thyrolingual–facial trunk. The vagus nerve lies between the internal jugular vein and common carotid artery and passes through the neck to its terminations in the thorax and abdomen.

FIGURE 22.1 (A) Exposure of carotid artery. Position of the head and shoulders and the line of skin incision in the neck. (B) Lateral retraction of the sternocleidomastoid muscle, exposing the carotid sheath. Note the descending branch of the hypoglossal nerve entering the carotid sheath and its relation with the common facial vein and its tributaries. (C) Lateral retraction of the internal jugular vein after division of the facial vein, thereby exposing the carotid artery and the ansa hypoglossi nerve. (D) Further mobilization of the common, internal, and external carotid (see text for further details).

Chapter 22 Exposure of the Carotid Artery

The hypoglossal or motor nerve to the tongue is an occupant of this region only in its proximal portion, where it lies deep to the parotid gland and descends between the internal carotid artery and the internal jugular vein.

Technique of Carotid Exposure Position The patient is placed in the supine position, with the head turned slightly away from the side to be operated on. The head is in slight hyperextension to expose the carotid groove. An inflatable pillow is placed under the shoulders. Marked hyperextension of the head and neck should be avoided if there is associated basilar arterial insufficiency (Fig. 22.1).

Skin Incision The classic line of incision extends from the tip of the mastoid and is directed obliquely to the sternoclavicular joint. The skin incision for the exposure of the common carotid artery and its bifurcation is made only in the upper half of this line (Fig. 22.1A). The incision is carried down through the subcutaneous tissue and the platysma. After the division of the external jugular vein, the sternocleidomastoid fascia is opened anteriorly and longitudinally, and the muscle

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is retracted laterally, thus exposing the neurovascular bundle.

Exposure of the Carotid The carotid sheath is opened near the bulb after having infiltrated the bifurcation with a local anesthetic (Fig. 22.1B). The internal jugular vein is dissected carefully from the artery. The common facial vein is ligated and divided. The internal jugular vein is then retracted laterally. Similarly the ansa hypoglossi nerve is retracted laterally (Fig. 22.1C). The common carotid artery is exposed and mobilized for about 2 to 3 cm below its bifurcation. The artery is carefully dissected from the vein and the vagus nerve. A tape is passed around the carotid below the bifurcation. The dissection is then continued distally to expose the hypoglossal nerve, which courses over the internal and external carotid arteries. As this is the motor nerve to the tongue, it should be dissected free, and its injury is to be avoided. The superior thyroid artery is freed and mobilized. Dissection is then carried to the internal and external carotid arteries.

Exposure of the Carotid Artery at its Origin on Aortic Arch This exposure may require a sternotomy or a left thoracotomy (for details, see Chapter 66).

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 23 The Vertebrobasilar System: Anatomy and Surgical Exposure Ronald A. Kline and Ramon Berguer

The vertebrobasilar system is unique in its anatomic layout. The two vertebral arteries converge into a major trunk of supply, the basilar artery, a situation not encountered elsewhere in the arterial tree with the exception of the origin of the anterior spinal artery. The vertebrals ascend the neck through an osteomuscular conduit formed by the transverse foramina of the cervical vertebrae and, between the foramina, by the musculotendinous cover of the spinal musculature. The vertebral artery is conventionally divided in four segments. The first segment (V1) starts at its origin in the subclavian artery and extends to the transverse process of C6, where the artery usually penetrates the cervical spine. The vertebral artery originates from the subclavian artery, usually from the posteromedial aspect of the latter. In 7% of cases, the vertebral artery on the left side originates directly from the arch of the aorta. When the left vertebral artery originates directly from the aortic arch, its entrance into the spinal canal usually takes place one or two levels above C6. On the right side, the vertebral artery may take origin from either the innominate or the common carotid artery in the rare cases in which there is a retroesophageal right subclavian artery. Immediately after its origin from the subclavian artery, the vertebral artery is in close relation to the lower cervical ganglion (or to the stellate ganglion, which represents the fusion of the lower cervical and first thoracic ganglia). A few millimeters after its origin, the artery is surrounded by a sympathetic loop made of connections between the middle (sometimes called intermediate) cer-

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vical ganglion and the lower cervical or stellate ganglia. In this first segment the vertebral artery is accompanied by a single overlying vertebral vein. The artery passes under the tendon of the longus colli before entering the transverse process of C6. This tendon can be stout and in some cases may compress the artery during rotation of the neck or abduction of the arm. The second segment (V2) of the vertebral artery extends from its penetration in the transverse foramen of C6 (occasionally the penetration may take place in C5 or C4) up to its exit from the transverse foramen of C2. During its ascent in the cervical spine, the artery is surrounded by a plexus of vertebral veins that eventually form a single vertebral vein below C6. In the spaces between the transverse processes, the vertebral artery is in a posterior relation with the intervertebral joint and the nerve roots. The latter lie immediately behind the artery and occasionally show the imprint of the latter as a small groove. The third segment (V3) starts at the top of the transverse foramen of C2 and ends at the point where the vertebral artery transverses the atlanto-occipital membrane, becomes intradural, and enters the foramen magnum. In this third segment the vertebral artery has some extra length, a redundancy that some have described as a “safety loop.” The reason for this extra length is that approximately 50% of neck rotation occurs between C1 and C2. The artery is bound by its adventitia to the periosteum of the transverse processes of C2 and C1, and, as the latter displays a wide arch during rotation, the vertebral artery needs extra length to accommodate the varying

Chapter 23 The Vertebrobasilar System: Anatomy and Surgical Exposure

distances existing between C2 and C1 at different angles of rotation of the neck. In this third portion, the vertebral artery is prone to injury by sudden rotation of the head, as happens in automobile accidents and falls. The wide range of rotational motion between C1 and C2 is a likely explanation for the fact that many dissections and traumatic arteriovenous aneurysms occur in this third segment. The V3 segment is particularly interesting to the surgeon because the artery is easily accessible between C1 and C2, the widest segment between transverse foramina at any level of the neck. In addition, the extra length of the artery at this level (the safety loop) provides for wider exposure of the vertebral artery for anastomosis. As it emerges from the top of the transverse process of C1, the vertebral artery runs over the arch of the atlas and penetrates the atlanto-occipital membrane. At this level the artery may be compressed by the atlas or the occipital bone by extension or rotation of the neck. On rare occasions the vertebral artery loops around, rather than going through the transverse process of C1. This imperforation of the transverse process of C1 can be presumed by noticing the absence of a transverse foramen in images of the atlas obtained by fine cut-computed tomography. The fourth segment (V4) of the vertebral artery comprises its intradural course and extends from the atlantooccipital membrane to the junction with the opposite vertebral artery to form the basilar artery. In this segment the artery gives off two important branches: the anterior spinal artery, which joins with a similar branch from the opposite vertebral artery to form a single vessel supplying the anterior half of the spinal cord, and the posterior– inferior cerebellar artery. As the vertebral artery becomes intradural, it experiences histologic changes similar to those noted in the carotid artery when it penetrates the temporal canal. The artery wall becomes thin and its adventitia disappears. Only the internal elastic lamina remains. These changes are important to the surgeon because the wall of the artery at this level is susceptible to perforation or rupture by manipulation with dilators or balloon catheters.

Exposure of the Vertebral Artery Surgical exposure of the vertebral artery is most commonly done in its first (V1) and third (V3) segments. Exposure in the second segment is limited to control of bleeding, usually from knife or gunshot injuries. With the availability of endovascular occlusive techniques, it has become exceedingly rare to approach the vertebral artery in its V2 segment.

Approaches to the V1 Segment Exposure of the first segment varies with the planned procedure. For the most commonly performed reconstruc-

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tion, the transposition of the vertebral artery to the common carotid artery, the exposure is medial to the scalenus anticus, which is neither cut nor exposed. If the operation planned is a subclavian-to-vertebral artery bypass or a transposition of the vertebral artery to another subclavian site, the subclavian artery needs to be exposed in its retroscalene segment, and for this the lateral approach is used. This lateral approach that exposes the subclavian artery behind the scalenus anticus muscle is also used for surgical control of traumatic bleeding and for resection of an aneurysm or arteriovenous fistula of the V1 segment of the vertebral artery. The lateral approach provides the control of the parent subclavian artery needed for these operations. Medial Approach For the medial approach, the incision is oblique, starting in the head of the clavicle and extending posterolaterally along the line that bisects the angle formed by the anterior edge of the sternomastoid muscle and the top of the clavicle. The incision is prolonged along the natural cleavage plane between the two heads of the sternomastoid. The omohyoid muscle is divided. The jugular vein and the common carotid artery are exposed, and the dissection proceeds between them with the vagus and internal jugular vein laterally and the common carotid artery medially. The common carotid artery is isolated and freed from its attachments into the mediastinum. The thoracic duct is identified, ligated, and divided. On the left side, one may find more than one thoracic duct. On the right side, accessory ducts should be identified and ligated. The thoracic duct arises from behind the common carotid artery and curves laterally to empty into the confluence of the left internal jugular and subclavian veins. The next step is the identification of the vertebral vein, which, once isolated, is divided between ligatures. The vertebral artery is found below the vertebral vein. The artery is freed from its origin up to the tendon of the longus colli, sparing the sympathetic trunks that cross it anteriorly. Lateral Approach The lateral approach is used for exposure of the retroscalene portion of the subclavian artery and of the vertebral artery. The incision is drawn in an oblique fashion almost parallel to the superior border of the clavicle. The omohyoid is divided, and the prescalene fat is dissected and freed except for a pedicle, and it is reflected to the lateral corner of the wound. The transverse scapular artery and vein within the prescalene fat pad are usually divided. The phrenic nerve is identified as it crosses diagonally from lateral to medial over the scalenus anticus muscle. The nerve is freed from the underlying fascia, and the medial and lateral edges of the scalenus anticus are exposed. The muscle is divided and the subclavian artery is exposed. The thyrocervical trunk is identified and, more medially, the vertebral vein is divided between ligatures exposing the subjacent vertebral artery.

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Approaches to V3 Segment The approach to V3 is used to isolate the vertebral artery in its C2–1 segment for bypass or transposition at this level. The position of the patient and the incision are similar to those used for carotid endarterectomy. The sternomastoid muscle is retracted posteriorly. Rather than reflecting the internal jugular vein posteriorly, the dissection proceeds between it and the sternomastoid muscle to identify the accessory spinal nerve, located approximately 3 cm below the tip of the mastoid (Fig. 23.1). The nerve is looped and freed cranially up to the point where it crosses over the transverse process of C1, a bony prominence that can be easily identified by palpation. The feel is that of the blunt end of a metal scalpel. The anterior and posterior edges of the levator scapula muscle are identified below its insertion on the transverse process of C1. The two branches of the anterior ramus of C1 can be seen as they emerge beneath the anterior edge of the levator. Using this anterior ramus as a guide, the muscle is divided below its insertion on C1 (Fig. 23.2). This permits exposure of the anterior ramus and visualization of the vertebral artery, which crosses vertically immediately behind this ramus. The ramus is divided over the artery (Fig. 25.3), which is still covered with small vertebral veins. These are isolated away from the artery by reflecting them medially and laterally, and the artery is looped (Fig. 23.4). Bipolar electrocautery is always required to perform this procedure.

Care must be taken during the dissection of the artery not to injure a collateral that frequently emerges from its posterolateral wall at this level. Suboccipital Approach The vertebral artery may have to be exposed as it travels over the posterior arch of the atlas. This is done to free the

FIGURE 23.2 Division of the levator scapula. The clamp was slid between the anterior ramus of C2 and the muscle.

FIGURE 23.1 Exposure of the accessory spinal nerve (looped) between the internal jugular vein and the sternomastoid muscle.

FIGURE 23.3 Division of the anterior ramus of C2 to expose the underlying vertebral artery.

Chapter 23 The Vertebrobasilar System: Anatomy and Surgical Exposure

FIGURE 23.4 The vertebral artery is isolated from its accompanying veins. The anterior stump of the divided C2 ramus is held away by a suture.

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artery from intermittent extrinsic compression at the suboccipital level or to repair aneurysms of the artery that extend into the suboccipital region. For this the patient is placed in the “parkbench” position. A racket-shaped incision is made with the upper end parallel to the occipital bone and the descending part of the incision following the posterior edge of the sternomastoid muscle. The splenius capitis muscle is divided. The lateral process of C1 is identified by palpation. After dividing the obliquus capitis superior and rectus capitis lateralis muscles, the artery can be visualized surrounded by a venous plexus. Bipolar cautery is again needed for hemostasis. To gain better exposure or to eliminate the extrinsic compressive agent, it may be necessary to do a laminectomy, removing part of the posterior arch of the atlas. The artery is not dissected into its subdural segment. During the laminectomy, one usually encounters bleeding from the epidural venous plexus. Care is taken not to injure the cervical root C2 at the bottom of the field. Bipolar cautery and packing with thrombin-soaked oxycellulose or collagen powder patties is usually all that is required to control epidural venous bleeding.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 24 Extrathoracic Exposure for Distal Revascularization of Brachiocephalic Branches Henry Haimovici

Historical Background Surgical correction of the arterial lesions involving the branches of the aortic arch was originally carried out by direct transthoracic arterial reconstruction. (1). After introduction of extra-anatomic bypasses for the management of aortoiliac lesions, similar principles were applied for the brachiocephalic lesions. Thus, extrathoracic approaches were devised for lesions in the proximal segments of the brachiocephalic arterial systems. The carotid–subclavian bypass was introduced as the first extrathoracic procedure (2,3). Although it obviates a thoracotomy and is easier to perform, it is applicable only for subclavian lesions but not when the occlusion is in the innominate artery. In addition, although carotid–subclavian bypass had found a wide degree of acceptance, theoretical concerns of possible compromise of the carotid flow led to the search for alternative extrathoracic approaches. Subclavian–subclavian (4,5) and axillary–axillary (6–8) bypasses appeared to offer greater ease of anatomic exposure with no concern of interfering with the carotid circulation. These approaches have gained greater acceptance in management of this condition.

Clinical Background Subclavian steal syndrome was first noted in 1960 by Controni, an Italian radiologist, who called attention to the occluded proximal subclavian artery as a cause of re-

versal of flow from the vertebral artery into the subclavian (9). Reivich et al., in 1961, demonstrated this reversal of blood flow through the vertebral artery and described its effects on cerebral circulation (10). An editorial in the New England Journal of Medicine, in the same issue as Reivich’s paper, drew attention to this new entity and called it “the subclavian steal syndrome” (11). Although North et al., in 1962, described the same syndrome under the name of “brachial-basilar insufficiency,” the steal stigma attached to it prevailed (12). Stenosis or complete occlusion of the subclavian or innominate arteries is due in almost all instances to an atheromatous plaque. However, a congenital cause and an embolic occlusion have been reported in a few rare instances (13–15). The left subclavian artery was involved in 72% of reported cases, whereas the right was found to be the cause in 16%, with the innominate the cause in 10% to 12% (2,3). The lesion of the affected arteries is located proximal to the vertebral artery and is accompanied by vertebral–basilar transient ischemic attacks or ischemic manifestations of the upper extremity or both (Fig. 24.1). The cerebral symptoms are usually characterized by headaches, dizziness, and blurring of vision, often occurring during all sorts of activities of the involved upper extremity. The upper extremity manifestations are those of intermittent claudication characterized by weakness, numbness, and paresthesias. The two syndromes may occur alone or together, the cerebral symptoms being by far the more common.

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Chapter 24 Extrathoracic Exposure for Distal Revascularization of Brachiocephalic Branches

FIGURE 24.1 Transfemoral arch aortogram of a 50year-old woman who developed ischemia of the left hand with no cerebral manifestations. The atherosclerotic stenosing plaque of the subclavian artery was located proximal to the origin of the vertebral artery. A 6-mm segment of Goretex graft was used for the bypass.

Carotid–Subclavian Bypass Technique For the carotid–subclavian bypass, the patient is placed in the supine position, with the shoulders being elevated in the usual fashion and the head rotated slightly to the opposite side. The upper extremity is kept in adduction, close to the body. The cervical segment of the subclavian artery is somewhat deeper on the left than the right. In the left region, the thoracic duct empties into the left innominate vein at the angle of the union of the internal jugular and subclavian veins. The skin incision is made 1 cm above the clavicle and extends from the sternoclavicular joint to the lateral portion of the supraclavicular region for about 8 to 10 cm (Fig. 24.2A). The cutaneous incision extends through the subcutaneous tissue, the platysma, and the superficial cervical fascia. Laterally, the external jugular vein is exposed, divided, and ligated. Medially, the posterior border of the sternocleidomastoid muscle is exposed, and the clavicular head is divided about 1 cm above its insertion on the clavicle. If medial extension is necessary, the sternal head may be divided subsequently during the procedure. The middle cervical fascia behind the sternocleidomastoid is divided, and the anterior scalene muscle is exposed behind the latter muscle. The adipose mass in front of the anterior scalene is identified. The subclavian vein

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that crosses in front of this muscle should be carefully mobilized, since the thoracic duct enters the junction between the internal jugular and the subclavian veins at that level. To expose the retroscalene portion of the subclavian artery, the muscle is divided after the subclavian and internal jugular veins are retracted gently downward and medially. As the muscle is transected, its proximal portion retracts spontaneously. The phrenic nerve, which crosses the scalene muscle from above downward and from the lateral to the medial side, must be identified before section of the muscle so that it can be preserved. A siliconized vessel loop is passed around it and retracted upward and laterally. The subclavian artery is then exposed in its third portion. Because the medial portion of the subclavian has to be mobilized for the purpose of exposing the vertebral artery, the sternal head of the sternocleidomastoid muscle must be divided at the same level as the clavicular head. To achieve this, the dissection of the branches of the subclavian at this level is mandatory. The posterior scapular, the thyrocervical, and the internal mammary arteries must be identified and mobilized, and tapes placed around them. Exposure of the carotid artery is then carried out. The carotid sheath is opened near and above the subclavian artery. The internal jugular vein is dissected carefully from the artery and is retracted laterally. Similarly, the vagus nerve is carefully handled and kept out of the area of carotid mobilization. The carotid artery is then isolated and surrounded with vessel loops. A segment of satisfactory length and caliber for the bypass is exposed. At this point, temporary occlusion of the carotid artery is carried out. Two methods are available for handling the sharp hemodynamic alterations of the distal carotid artery after its clamping: 1.

2.

Monitoring the electroencephalogram (EEG) changes and measuring the systolic, diastolic, and mean pressures distal to the occlusion—a mean pressure near 50 mmHg or above is acceptable for maintaining adequate intracerebral function. Use of an internal carotid shunt for continuous cerebral perfusion, during graft implantation. This second method is, of course, mandatory if the EEG or the mean arterial pressure appears to be below a safe level.

The graft material used for the bypass may be a saphenous vein or any commonly available synthetic graft; my preference is a polytetrafluoroethylene (PTFE, Goretex) graft. The implantation of the graft is first carried out in the subclavian artery through an end-to-side anastomosis using No. 6–0 suture material. After completion of the end-to-side routine anastomosis in the subclavian, the graft is tunneled toward the carotid artery. The carotid graft anastomosis is similarly carried out by end-to-side

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Part IV Surgical Exposure of Vessels FIGURE 24.2 A left carotid–subclavian graft bypass. (A) The arch with its brachiocephalic branches. (B) Exposure of the subclavian and carotid areas (for details, see text). Note that the graft crosses the jugular vein anteriorly. (C) Diagram indicating the position of the bypass graft in relation to the supraclavicular region.

A

B

anastomosis using No. 6–0 suture material (Fig. 24.2C). Before completion of the anastomosis into the carotid, flushing of the carotid as well as of the subclavian is carried out to remove any possible thrombi that might have occurred during the procedure. Heparin is administered to the patient before and throughout the completion of the bypass (Fig. 24.3). The wound is closed in layers in the usual fashion. The divided muscles are reattached except for the scalene. Careful handling of the phrenic nerve is essential to avoid any paralysis of the diaphragm. Correction of the subclavian lesion by carotid– subclavian bypass has raised the theoretical risk of siphoning blood from the distal common carotid artery, which would then constitute a carotid steal induced by the procedure. Several investigators have reported that no

carotid steal was detected during controlled experiments (16).

AxiIIary–AxiIIary Bypass Graft Technique The axillary artery is divided into three segments. The first extends from the outer border of the first rib to the medial border of the pectoralis minor muscle. This segment of the axillary artery is free of major branches and is the most desirable for the use of graft implantation. The second segment lies behind the pectoralis minor muscle and provides the thoracoacromial trunk and lateral thoracic branches. The third segment extends from the lateral border of the

Chapter 24 Extrathoracic Exposure for Distal Revascularization of Brachiocephalic Branches

A

311

pectoralis minor to the lower border of the teres major. A subclavicular horizontal approach is used for exposure of the first segment. A skin incision 8 to 10 cm long is made parallel to the inferior border of the clavicle corresponding to its middle portion (Fig. 24.4A). The pectoralis major muscle is transected progressively until the clavipectoral axillary fascia is exposed. Incision of its anterior sheath and of the subclavius muscle is done along its entire length. Retraction of the subclavius muscle proximally allows incision of the posterior sheath of the clavipectoral axillary fascia. At this point, the nerve of the pectoralis major crossing the anterior surface of the artery must be identified. This approach affords exposure and mobilization of the initial segment of the axillary artery, which is above the origin of its main collateral branches. The axillary vein, which is also free of tributaries at this level, is retracted upward. The exposure is most suitable for the anastomosis of the axillary–axillary bypass, as well as for the axillofemoral. After exposure of both axillary arteries, a subcutaneous tunnel is developed between the two areas. The tunnel is anterior to the sternal region. Implantation of the graft starts in the recipient site. After the axillary vein is mobilized by dividing several inferior tributaries, it is greatly elevated, revealing the underlying axillary artery. An autogenous saphenous vein or PTFE (Goretex) graft 6 mm in diameter is sutured end-toside into the recipient artery. The graft is then passed through the tunnel anteriorly to the sternum for the donor anastomosis, also carried out in an end-to-side fashion (Fig. 24.4C). Care is taken to flush the proximal ends of the recipient artery back through the graft to remove any clots or atheromatous debris that may have accumulated during the procedure. The patient, as mentioned already, is heparinized systemically during the entire period of clamping.

Subclavian–Subclavian Bypass

B FIGURE 24.3 Pulse–volume recording tracings taken before and after the bypass graft. (A) Before the carotid–subclavian bypass. Note abnormal and decreased amplitude of pulse waves on the left side and lower systolic pressure at the arm and forearm. (B) Postoperative recordings (day 7 after the bypass) indicate return to normal systolic pressure of upper arm and forearm with normal pulse waves.

The subclavian–subclavian bypass is carried out through bilateral supraclavicular incisions. The operative exposure is achieved through a 3-inch incision, one fingerbreadth above the clavicle and extending posteriorly from the sternocleidomastoid muscle (Fig. 24.5A). The external jugular vein is divided, the sternocleidomastoid muscle is retracted anteriorly, and the phrenic nerve is isolated. The scalenus anticus muscle is divided, allowing more complete inspection of the vessel and the thoracic outlet. After systemic heparinization is achieved, one subclavian artery is cross-clamped, and a vein graft or PTFE (Goretex) tube 6 mm in diameter is anastomosed to the vessels with a running fine No. 6–0 suture material. After the graft has been anastomosed to the recipient vessel, the graft is tunneled subcutaneously into the anterior tissues

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A

B FIGURE 24.4 An axillary–axillary bypass. Note the subclavicular skin incisions (broken line) for the approach to the axillary arteries. (A) Below, bilateral exposure of the axillary regions. Note the major structures from lateral to medial: brachial plexus, axillary artery hidden by axillary vein and its cephalic tributary. (B) Diagram of the bypass.

of the neck, and the donor anastomosis is carried out (Fig. 24.5C). The divided scalenus anticus muscle is not reapproximated. The graft pulsation is visible and palpable above the manubrium.

Conclusion The extrathoracic procedures have gained in popularity and, in most cases, have superseded the earlier direct ap-

proach of the intrathoracic procedure. Although the latter may still be indicated for innominate arterial lesions and may produce excellent hemodynamic results, thoracotomy is fraught with greater risk, especially in patients with mild or chronic chest disease or cardiovascular problems. Extrathoracic bypasses are technically much simpler and more expeditious than are the intrathoracic procedures. The type of bypass to be used in a given case will depend on the individual circumstances. Carotid–subclavian bypass may not be applicable on the right side if the innomi-

Chapter 24 Extrathoracic Exposure for Distal Revascularization of Brachiocephalic Branches

313

FIGURE 24.5 A subclavian–subclavian bypass. (A) Note the supraclavicular skin incisions (broken line). (B and C) Right and left exposures of the subclavian arteries in the supraclavicular region. Note the brachial plexus laterally, the vertebral and internal mammary branches, the divided muscles, and jugular vein (medially). (D) Diagram of the position of the subclavian–subclavian bypass.

A

C

B

D

nate artery is involved. In addition, if there is stenosis or complete occlusion of one carotid, the carotid–subclavian bypass may be hazardous without first correcting the internal carotid lesion Under those circumstances, any decrease in carotid blood flow may be totally undesirable. The axillary–axillary bypass is indicated in the majority of cases for revascularizing the upper extremity and correcting the vertebrobasilar insufficiency (17). Variants of the axillary–axillary bypass have also been reported (18–20). Potential disadvantages of the superficial subcutaneous bypasses may be related to cosmetic and mechanical problems. As the bypasses are at the base of the neck or just at the upper portion of the chest, they may not interfere with the cosmetic appearance of these anatomic re-

gions. On the other hand, mechanically they are less prone to compression than the axillofemoral or femorofemoral bypasses, which have proved not to be subjected to much mechanical stress. The long-term results are encouraging and have established these procedures as the most appropriate ones for the management of the occlusive process of the brachiocephalic branches.

References 1. Crawford ES, DeBakey ME, et al. Thrombo-obliterative disease of the great vessels arising from the aortic arch. J Thorac Cardiovasc Surg 1962;43:38. 2. Diethrich EB, Garrett RE, et al. Occlusive disease of the common carotid and subclavian arteries treated by

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3. 4.

5.

6. 7.

8.

9.

10.

Part IV Surgical Exposure of Vessels carotid–subclavian bypass. Analysis of 125 cases. Am J Surg 1967;114:800. Hafner CD. Subclavian steal syndrome: a 12-year experience. Arch Surg 1976;111:1074. Finkelstein NM, Byer A, Rush BR. Subclavian– subclavian bypass for the subclavian steal syndrome. Surgery 1972;71:142. Forrestner JE, et al. Subclavian–subclavian bypass for correction of the subclavian steal syndrome. Surgery 1972:71:136. Myers WO, Lawton BR, Sautter RD. Axillo-axillary bypass graft. JAMA 1971;217:826. Mozersky DJ, Sumner DS, et al. Subclavian revascularization by means of a subcutaneous axillary–axillary graft. Arch Surg 1973;106:20. Jacobson JH, Mozersky DJ, et al. Axillary–axillary bypass for the “subclavian steal” syndrome. Arch Surg 1973;106:24. Contorni L. Il circolo collaterale verebrale nella obliterazione dell’ arteria succlavia alla sue origine. Minerva Chir 1960;15:268. Reivich M, et al. Reversal of blood flow through the vertebral artery and its effect on cerebral circulation. N Engl J Med 1961;265:878.

11. A new vascular syndrome: the subclavian steal [editorial]. N Engl J Med 1961;265:912. 12. North RR, Fields WS, et al. Brachial-basilar insufficiency syndrome. Neurology 1962;12:810. 13. Massumi RA. The congenital variety of the subclavian steal” syndrome. Circulation 1963:28:1149. 14. Levine S, Serfas LS, Rusinko A. A right aortic arch with subclavian steal syndrome (atresia of left common carotid and left subclavian arteries). Am J Surg 1966;111:632. 15. Dardik H, Gensler S, et al. Subclavian steal syndrome secondary to embolism: first reported case. Ann Surg 1966;164:171. 16. Lord RSA, Ehrenfield WK. Carotid–subclavian bypass: a hemodynamic study. Surgery 1969;66:.521. 17. Mozersky DJ, Sumner DS, et al. The hemodynamics of the axillary–axillary bypass. Surg Gynecol Obstet 1972; 135:925. 18. Sproul G. Femoral-axillary bypass for cerebral vascular insufficiency. Arch Surg 1971;103:746. 19. Moseley HS, Porter IM. Femoral-axillary bypass for arm ischemia. Arch Surg 1973;106:347. 20. Jacobson JH, Baron MG. Axillary-contralateral brachial artery bypass for arm ischemia. Ann Surg 1974;179:827.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 25 Trans-sternal Exposure of the Great Vessels of the Aortic Arch Calvin B. Ernst

Extrathoracic arterial reconstructive procedures for treatment of symptomatic occlusive arterial disease of the vessels from the aortic arch evolved because of the perceived greater morbidity and mortality accompanying transthoracic arterial reconstruction (1). Extrathoracic extraanatomic procedures such as carotid–subclavian bypass, carotid–subclavian transposition, subclavian–subclavian bypass, carotid–carotid bypass, and axillary–axillary bypass may be preferred, especially when thoracotomy or mediastinotomy and exposure of the origins of the innominate, subclavian, and common carotid vessels poses undue risk to the patient. However, exposure of the great vessels from the aortic arch may be required when managing proximal arteriosclerotic lesions if no brachiocephalic inflow source is adequate for extrathoracic reconstruction, and direct transsternal repair now appears to be the operation of choice (2–4). Furthermore, knowledge and techniques of such exposure are mandatory when managing injuries to the great vessels. Although arterial reconstruction for severe arm ischemia may represent only 2% of all vascular surgical procedures (5), revascularization by trans-sternal exposure of the arch vessels is by no means outdated, and continues to be an important part of the armamentarium of the vascular surgeon. Transsternal reconstructive procedures may be required for approximately 30% of patients with multiple great vessel involvement (6). The great vessels arising from the aortic arch are relatively inaccessible, not only because they are obscured by bone but also because most surgeons have no experience with exposing

them. Although arterial reconstruction for the various lesions encountered may require innovative bypass and endarterectomy procedures, the common denominator to successful outcome is adequate exposure of inflow and outflow vessels, the subject of this chapter.

Left Subclavian Artery The most common indication for exposure of the left subclavian artery is trauma. Aneurysmal and occlusive lesions are less frequent. Various techniques for gaining exposure to the left subclavian artery have been provided since Halsted performed the first successful excision of a subclavian arterial aneurysm on May 10, 1892 (7). In that operation, Halsted resected the medial two-thirds of the clavicle. Since that time, other alternatives to clavicular resection have been advocated, including anterior third-interspace left thoracotomy as well as standard fifth-interspace posterolateral thoracotomy, with or without combined supraclavicular subclavian artery exposure (8,9). When managing brachiocephalic occlusive disease, exposure of the intrathoracic left subclavian artery is rarely required because priority is given to reconstructing the innominate and left common carotid vessels, and the left subclavian artery is left alone. In the event that left subclavian arterial reconstruction is required, exposure of its supraclavicular segment is usually adequate for a bypass graft originating from an innominate bypass graft,

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for carotid–subclavian bypass, or for carotid–subclavian transposition. Therefore, intrathoracic left subclavian artery exposure is reserved almost wholly for management of traumatic lesions. The left subclavian artery may be exposed through a supraclavicular incision for distal lesions or through an anterior third-interspace thoracotomy for proximal lesions (Figs. 25.1 and 25.2). Because the left subclavian artery arises posterolaterally from the aortic arch, median sternotomy does not provide adequate exposure from its aortic origin to its exit from the thorax at the first rib. An anterolateral third-interspace thoracotomy is required (Fig. 25.2). For exsanguinating hemorrhage from penetrating subclavian trauma, this third-interspace incision can be made to achieve proximal arterial control either

with a vascular clamp or by manual pressure tamponade (Fig. 25.1). Although third-interspace thoracotomy provides exposure of the intrathoracic left subclavian artery for expeditious proximal control, it is not adequate for repair of distal intrathoracic traumatic lesions, particularly those immediately proximal to the first rib. To expose the distal subclavian artery, another left supraclavicular incision is necessary. Division of the clavicular head of the sternocleidomastoid muscle and the anterior scalene muscle is required, taking care to identify and protect the phrenic nerve and thoracic duct. Through both incisions, after ligating and dividing the internal mammary and thyrocervical branches, sufficient length of subclavian artery may be mobilized to deliver it into the supraclavicular wound for repair. The vertebral artery must be identified and preserved (Fig. 25.1). Blunt injuries or nonexsanguinating left subclavian injuries are best exposed through a standard left posterolateral fifth-interspace thoracotomy (8). It is important to prepare a wide area and drape the left arm free so it may be maneuvered about in the event that supraclavicular exposure is also required (Fig. 25.3). Dual-incision exposure may be necessary, particularly for injuries immediately proximal to the first rib. Proximal left subclavian and juxta-aortic exposure require fifth-interspace left posterolateral thoracotomy (8). An anterior third-interspace incision is not appropriate, except under the most extreme circumstances requiring immediate proximal control to prevent exsanguination, because it compromises exposure for subsequent arterial repair. Under such circumstances, when optimal posterolateral thoracotomy is precluded by the urgency of the situation, retroclavicular subclavian exposure may be facilitated by dividing and excising a segment of the clavicle (Fig. 25.4). The medial one-third of the clavicle may be removed subperiosteally. The transverse scapular vessels lie close to its undersurface and may be injured if the periosteum is disrupted. After clavicular excision, the subclavian artery, as it emerges from the chest, is exposed, taking care to protect the phrenic nerve and thoracic duct.

Innominate, Right Subclavian, and Common Carotid Arteries FIGURE 25.1 Anterolateral third-interspace limited thoracotomy through which proximal occlusion of a lacerated left subclavian artery is obtained. Exposure of the distal subclavian artery is obtained through a separate transverse supraclavicular incision. The sternocleidomastoid and anterior scalene muscles are divided. The internal mammary and thyrocervical arteries are ligated and divided, but the vertebral artery is preserved. The phrenic nerve is retracted medially. (Reproduced by permission from Ernst CB. Exposure of inaccessible arteries: Part I carotid and arm exposure. Surgical Rounds 1985;8:21–29).

Whereas atherosclerotic occlusive lesions involving the origin of the left subclavian artery seldom require direct exposure, intrathoracic exposure and reconstruction of the innominate and left common carotid vessels provide viable options to extrathoracic reconstruction for occlusive disease involving those vessels. Among appropriately selected patients and in expert hands, intrathoracic reconstruction is comparable in morbidity and mortality to extrathoracic reconstruction, and the durability of direct transthoracic reconstruction is superior to that achieved

Chapter 25 Trans-sternal Exposure of the Great Vessels of the Aortic Arch

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FIGURE 25.2 Exposure of the proximal left subclavian artery through a full third-interspace anterior thoracotomy. Vagus and phrenic nerves are retracted medially using elastic loops. The subclavian artery distal to the internal mammary branch is obscured by the first rib. View is from the left side looking up into the apex of the chest as the internal mammary branches from the inferior surface of the subclavian artery. (Reproduced by permission from Ernst CB. Exposure of inaccessible arteries. Part I carotid and arm exposure. Surgical Rounds 1985;8:21–29.)

by extra-anatomic methods, making transsternal exposure the procedure of choice (2–4,6,10–12) Indications for transsternal exposure of the innominate, right subclavian, and both common carotid vessels are similar to those for left subclavian exposure, with trauma predominating. Optimal exposure of these vessels is obtained through a full-length median sternotomy extended transversely into the right supraclavicular area just above and parallel to the clavicle (Fig. 25.5). Following sternotomy and placement of a standard self-retaining sternal retractor, the anterior mediastinum is widely exposed (Fig. 25.5). The contents of the upper mediastinum must be carefully dissected from the posterior surface of the sternum to allow atraumatic and expeditious median sternotomy using a power saw. Periosteal bleeding is minimized by scoring a vertical line down the center of the sternum using electrocautery. Bleeding from the divided sternum is not usually a problem but may be controlled by placing thin strips of thrombin-soaked absorbable gelatin sponge along the cut edges. Foreign materials such as bone wax are rarely used. The thymic remnant is divided, and using blunt dissection the anterior edges of the pleura are swept laterally.

The innominate vein may be divided with impunity, particularly if urgent proximal control for traumatic injury is necessary. However, when possible, and depending upon the location of the occlusive lesion being treated, the innominate vein may be preserved and mobilized and retracted cephalad. When the prosthesis originates from the ascending aortic arch, it is tunneled behind the innominate vein. The vagus and recurrent laryngeal nerves must be identified at the innominate bifurcation and protected (Fig. 25.5). Lateral extension of the supraclavicular incision with division of the origin of the sternocleidomastoid, anterior scalene, and strap muscles provides excellent exposure of the right subclavian artery to the point where it passes over the first rib. The clavicle is not transected but retracted laterally as a unit while attached to the manubrium. The phrenic nerve, as it courses over the anterior scalene muscle from lateral to medial, must be identified and protected. When managing traumatic injuries, not only does median sternotomy provide excellent exposure of the innominate, proximal common carotid, and proximal right subclavian arteries, but it avoids the chest wall morbidity associated with other approaches, such as the trap door or book

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Part IV Surgical Exposure of Vessels FIGURE 25.3 Exposure of the proximal lacerated left subclavian artery and distal aortic arch through a fifth-interspace posterolateral thoracotomy. The left innominate vein and the vagus and phrenic nerves are retracted with elastic loops. The left arm is draped free to facilitate access to the supraclavicular region in the event distal subclavian artery exposure is required. (Reproduced by permission from Ernst CB. Exposure of inaccessible arteries. Part I carotid and arm exposure. Surgical Rounds 1985;8:21–29.)

thoracotomy originally described by Sencert and popularized by Steenburg and Ravitch (13). Variations of the book thoracotomy, which have no advantages over median sternotomy, include resection of the medial one-third of the clavicle along with a median sternotomy to the third or fourth interspace. Usually, when managing traumatic lesions, innominate exposure is required for proximal arterial control rather than reconstruction. However, occasionally the origin of the innominate artery is injured, which requires prosthetic graft replacement (14) (Fig. 25.6). Under these circumstances, the distal innominate artery is exposed just proximal to its bifurcation into the subclavian and common carotid arteries. When repairing such injuries, protective shunting of the cerebral circulation is not necessary. Elective transsternal exposure for reconstruction of occlusive lesions, although less hurried than when managing traumatic lesions, is no less demanding of meticulous technique. The innominate vein may be divided or retracted, as seems appropriate, for adequate exposure of the arteries in question.

Innominate endarterectomy is preferred if the occlusive process extends to the bifurcation but does not involve its origin (2,15). Endarterectomy of the innominate osteum requires side-biting clamp occlusion of the innominate origin with the occasional requirement of occluding the adjacent left common carotid artery (in 3% to 5% of patients) or interrupting blood flow in the left common carotid artery because it originates from a common brachiocephalic trunk (in 10% to 20%) (16). Furthermore, endarterectomy of the innominate origin requires extending the arteriotomy and endarterectomy into the aortic arch with the attendant hazard of an aortic dissection developing. Consequently, when the origin of the innominate is involved, most surgeons prefer aortobrachiocephalic grafting with a prosthetic tube or a bifurcation aortosubclavian–common carotid bypass graft as first described in 1958 by DeBakey and his colleagues (3,4,17). The bypass should originate from an undiseased segment of the ascending aorta. This is best accomplished by opening the pericardium at the aortic root for a short distance and using the intrapericardial segment of the aortic arch for the proximal anastomosis. Any

Chapter 25 Trans-sternal Exposure of the Great Vessels of the Aortic Arch

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A

B

C FIGURE 25.4 (A) Incision for exposure of right subclavian artery using clavicular resection. This is equally applicable for left retroclavicular subclavian exposure. (B) Exposure of the subclavian artery after subperiosteal resection of the medial one-third of the clavicle. (C) The pectoralis minor is transected to expose the underlying second portion of the axillary artery.

deeply troughed side-biting aortic clamp provides adequate inflow occlusion during the proximal anastomosis and also permits uninterrupted aortic blood flow. Varieties of bypass reconstruction are limited only by the surgeon’s imagination and the extent of occlusive disease being treated (Figs. 25.7 and 25.8). It is important to avoid too great a bulk of prosthesis, which may occur with a bifurcation graft, by fashioning side branches from a tube graft, in order to prevent superior mediastinal compression phenomena when the sternotomy is wired closed.

Conclusions For management of traumatic lesions of the great vessels of the aortic arch, there is no alternative to trans-sternal exposure and repair. Management of atherosclerotic lesions of the aortic arch vessels, however, has undergone significant evolution. In the 1950s transthoracic operations were associated with a 20% to 40% mortality. Now, with better selection of patients and improved operative techniques, contemporary mortality rates approximate 5% for elective transsternal arterial reconstruction

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Part IV Surgical Exposure of Vessels FIGURE 25.5 Exposure of the innominate, right subclavian, and common carotid arteries through a full median sternotomy. Extending the skin incision transversely and parallel to the clavicle provides additional exposure of the distal subclavian artery. The clavicle is not resected but retracted laterally with the sternum. The vagus, recurrent laryngeal, and phrenic nerves must be identified and protected. The innominate vein may be mobilized to expose the origins of the innominate and left common carotid arteries. (Reproduced by permission from Ernst CB. Exposure of inaccessible arteries. Part I carotid and arm exposure. Surgical Rounds 1985;8:21–29.)

A

B

C FIGURE 25.6 Aortoinnominate interposition graft for traumatic lesion at the innominate origin. The proximal innominate artery is oversewn, and the graft is anastomosed to the intrapericardial segment of the ascending aorta. (Reproduced by permission from Mattox KL. Aortic arch and proximal brachiocephalic penetrating injury. In: Ernst CB, Stanley JC, eds. Current therapy in vascular surgery. Philadelphia: BC Decker, 1987:262–265.)

FIGURE 25.7 (A) Aortosubclavian and right common carotid bifurcation graft bypass. (B) Aortoinnominate and left common carotid bifurcation graft bypass. A minimally diseased segment of intrapericardial aortic arch is used for the proximal anastomosis. (Reproduced by permission from Brewster DC, Moncure AC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985;2:99–112.)

Chapter 25 Trans-sternal Exposure of the Great Vessels of the Aortic Arch

3.

4.

5.

A

B

FIGURE 25.8 (A) Aortosubclavian bypass graft with side arm to right common carotid artery. (B) Aortoinnominate bypass graft with side arm to left common carotid artery. These bypass graft configurations may be required to decrease the bulk of prosthetic material occupying anterior superior mediastinum in order to prevent compression phenomena. A minimally diseased segment of intrapericardial aortic arch is used for the proximal anastomosis. (Reproduced by permission from Brewster DC, Moncure AC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985,2:99–112.)

6.

7.

8.

9. 10. 11.

(2–4,6,10,11). Furthermore, transsternal reconstruction is more durable than extrathoracic repair (3,4,6,10). Consequently, a less than perfect result should not be compromised by inappropriate use of extrathoracic extra-anatomic arterial reconstruction, recognizing that lesions requiring transthoracic arterial reconstruction are rarely encountered.

12.

13.

14.

References 1. Crawford ES, DeBakey ME, et al. Surgical treatment of the occlusion of innominate, common carotid, and subclavian arteries: ten years’ experience. Surgery 1969;65:17–31. 2. Cherry KJ Jr, McCullough JL, et al. Technical principles of direct innominate artery revascularization: a com-

15.

16. 17.

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parison of endarterectomy and bypass grafts. J Vasc Surg 1989;9:718. Corimer F, Ward A, et al. Long-term results of aortoinnominate and aortocarotid polytetrafluoroethylene bypass grafting for atherosclerotic lesions. J Vasc Surg 1989;10:135. Reul GJ Jr, Jacobs MJHM, et al. Innominate artery occlusive disease: surgical approach and long-term results. J Vasc Surg 1991;14:405. Whitehouse WM Jr, Zelenock GB, et al. Arterial bypass grafts for upper extremity ischemia. J Vasc Surg 1986;3:569–573. Crawford ES, Strowe CL, Powers RW. Occlusion of the innominate, common carotid, and subclavian arteries: long-term results of surgical treatment. Surgery 1983;94:781–791. Halsted W. Ligation of the first portion of the left subclavian artery and excision of a subclavian artery aneurysm. Bull Johns Hopkins Hosp 1892;3:93. Schaff HV, Brawley RK. Operative management of penetrating vascular injuries of the thoracic outlet. Surgery 1977;82:182–191. Ernst CB. Exposure of inaccessible arteries: Part I. Carotid and arm exposure. Surg Rounds 1985;8:21–29. Vogt DP, Hertzer NR. et al. Brachiocephalic arterial reconstruction. Ann Surg 1982:196:541–552. Zelenock GB, Cronenwett JL, et al. Brachiocephalic arterial occlusions and stenoses: manifestations and management of complex lesions. Arch Surg 1985;120: 370–376. Brewster DC, Moncure AC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985;2:99–112. Steenburg RW, Ravitch MM. Cervicothoracic approach for subclavian vessel injury from compound fracture of the clavicle. Ann Sur 1963;157:839–846. Johnston RH Jr, Wall MJ Jr, et al. Innominate artery trauma: a thirty-year experience. J Vasc Surg 1993;17:134. Carlson RE, Ehrenfeld WK, et al. Innominate endarterectomy: a 16-year experience Arch Surg 1977;112:1389–1393. Hewitt RL, Brewer PL, Drapanas T. Aortic arch anomalies. J Thorac Cardiovasc Surg 1970;60:746–753. DeBakey ME, Morris GC, et al. Segmental thrombobliterative disease of branches of aortic arch. JAMA 1958;166:988–1003.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 26 The Upper Extremity Henry Haimovici

Exposure of Subclavian Artery Anatomic Review The anatomic structures surrounding the subclavian artery are the supraclavicular region and the suprasternal fossa. The supraclavicular region is a depressible space above the clavicle. Its base rests on the dome of the pleura and is in broad communication with the sternomastoid, mediastinal, and axillary regions. The anterior wall of the supraclavicular region is composed of a fairly loose aponeurosis, which passes over and is adherent to the clavicle, from where it extends into the thoracic region as the pectoral fascia. The posterior wall is composed of groups of muscles that extend downward and outward from the cervical column. The scalenus medius and posterior muscle, although fused in their upper portions, form most of the anterior segment of the floor of the region and are attached to the first and second ribs. The subclavian artery and the trunks of the brachial plexus, as they emerge from the cleft between the anterior and middle scalene muscles, lie on the floor of the region. The anterior scalene muscle arises from the transverse processes to the third, fourth, fifth, and sixth cervical vertebrae and runs downward and laterally to insert on the scalene tubercle and ridge on the medial margin of the first rib. The subclavian vein lies between the anterior scalene muscle and the clavicle and grooves the upper portion of the first rib. Behind this muscle lie the subclavian artery and the large nerve trunks of the brachial plexus. The right subclavian artery is a subdivision of the innominate, whereas the left subclavian artery arises directly from the arch of the aorta. The right artery begins at the point deep to the sternoclavicular joint. The left, the

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longer of the two, arises within the thorax on the left side of the trachea. Both arteries run in a lateral direction in an arching course across the root of the neck, grooving the pleural dome. Each artery is conveniently divided into three segments: medial, posterior, and lateral to the anterior scalene muscle. Unlike the neighboring common carotid, the subclavian artery gives off a considerable number of widely distributed branches. The subclavian vein is a direct continuation of the axillary, or main, vein of the upper extremity. The individual nerves that make up the brachial plexus derive from the anterior roots or primary divisions of the fifth, sixth, seventh, and eighth cervical and first thoracic spinal nerves. These roots emerge between the anterior and middle scalene muscles and appear in the lower part of the posterior triangle of the neck. The skeletal structures in this region are the clavicle and the first rib. The sternal extremity of the clavicle has posterior relations with the innominate vein. On the right, it is related to the bifurcation of the innominate artery and, on the left, to the common carotid artery. The body of the first rib is placed so that its superior surface is almost flat. In its middle portion, it presents two transverse grooves, one for the artery and the other for the vein.

Exposure of Cervical Segment of Subclavian Artery The cervical portion of the subclavian artery is situated deeply in the supraclavicular region and is in direct contact with the first rib. Because of the different origins of the subclavian on the right and left, a description of the exposure will deal separately with each side.

Chapter 26 The Upper Extremity

Exposure of Left Subclavian Artery The left cervical segment of the subclavian artery (Fig. 26.1) is somewhat deeper than on the right. In this region, the thoracic duct empties into the left innominate vein at the angle of the union of the left internal jugular and subclavian veins. The patient is placed in the supine position, with the shoulders elevated in the usual fashion and the head turned to the opposite side. The upper extremity is in adduction close to the body.

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The skin incision is made 1 cm above the clavicle and extends from the sternoclavicular joint to the lateral portion of the supraclavicular region for about 8 to 10 cm (Fig. 26.1A). The cutaneous incision extends through the subcutaneous tissue, the platysma, and the superficial cervical fascia. Laterally, the external jugular vein is exposed, divided, and ligated. Medially, the posterior border of the sternocleidomastoid muscle is exposed, and the clavicular head is divided about 1 cm above its insertion on the clavicle (Fig. 26.1B). If medial extension is necessary, the

FIGURE 26.1 Exposure of the left subclavian artery. (A) Position of the head and the line of skin incision. (B) Lines of incision of sternocleidomastoid and omohvoid muscles and divided external jugular vein. (C) Dissection of the second deep layer, showing the line of anterior scalene muscle transection and protection of the phrenic nerve. Note, in front, the thoracic duct at the subclavian–jugular angle and, in the background behind the scalene muscle, the subclavian artery. (D) Subclavian artery freed, with the phrenic nerve retracted laterally. (E) Further cephalad retraction of divided muscles, allowing better exposure and mobilization of the subclavian artery.

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sternal bead may be divided subsequently during the procedure. The middle cervical fascia behind the sternocleidomastoid is divided, and the anterior scalene muscle is exposed behind the latter muscle. The adipose mass in front of the anterior scalene is identified. The subclavian vein that crosses in front of this muscle should be carefully mobilized, since the thoracic duct enters the junction between the internal jugular and the subclavian at that level. To expose the retroscalene portion of the subclavian artery, the muscle is divided after the subclavian and internal jugular are gently retracted downward and medially. As the muscle is transected, its proximal portion retracts spontaneously. The phrenic nerve, which crosses the scalene muscle from above downward and from the lateral to the medial side, must be identified before section of the muscle and preserved (Fig. 26.1C). A rubber vessel loop is passed around it and retracted upward and laterally. The subclavian artery is then exposed in its third portion. Should the medial portion of the subclavian have to be mobilized for the purpose of exposing the vertebral artery, division of the sternal head of the sternocleidomastoid muscle would have to be done by transection at the same level as the clavicular head. To achieve this, the dissection of the branches of the subclavian at this level is mandatory (Fig. 26.1D). The posterior scapular, the thyrocervical, and the internal mammary arteries must be identified and mobilized and tapes placed about them (Fig. 26.1E). If further exposure is hampered by the adjacent structures, resection of the clavicle may be necessary (see below). Exposure of Right Subclavian Artery The prescalene segment of the right subclavian is short, the bifurcation of the brachiocephalic being behind the sternoclavicular joint. Exposure of the right subclavian artery can be achieved almost completely in most instances through the cervical approach. If a wide exposure of the initial segment of the right subclavian is necessary, a thoracocervical exposure is indicated. Figure 26.2A depicts the position of the patient and the skin incision above the clavicle. Figure 26.2B shows the exposure of the subclavian before the anterior scalene muscle has been divided. Figure 26.2C shows the retraction of the internal jugular medially and the phrenic nerve laterally. The vertebral and the internal mammary arteries are seen in the prescalene portion of the subclavian. Variant Techniques of Subclavian Exposure Exposure of the intrathoracic portion of the left subclavian artery and of the left common carotid is best approached through a left-sided thoracotomy in the third or fourth intercostal space. For lesions of the innominate, of the first portion of the right subclavian, and of the intrathoracic portion of the common carotid arteries, surgery is best carried out by a median sternotomy. This approach allows a

FIGURE 26.2 Exposure of the right subclavian artery. (A) Position of the head and the line of skin incision. (B) Note the thyrocervical trunk emerging from the subclavian artery medially to the scalene muscle and coursing anterior to the latter. (C) Exposure of the subclavian artery, similar to Figure 26.1E.

less traumatic dissection and a smoother postoperative convalescence than does partial median sternotomy with extension of the incision into the third intercostal space. Exposure of Subclavian Artery with Resection of the Clavicle The approach to the subclavian artery may be greatly facilitated by the resection of a portion of the clavicle, especially if a combined subclavian and axillary exposure is indicated. The incision is made over the portion of the clavicle to be excised and is then extended into the axillary region, as

Chapter 26 The Upper Extremity

indicated in Figure 26.3. After the skin incision and its retraction, the periosteum of the medial two-thirds of the clavicle is incised and stripped. The portion of the clavicle to be excised is divided with a Gigli saw and removed subperiosteally. The transverse scapular vessels run close to its posterior surface and may easily be injured if the layer of periosteum is torn. The sternal end of the incision allows exposure of the innominate and carotid vessels. Its central portion allows exposure of the subclavian vessels and brachial plexus. The anterior scalene muscle is transected, thereby facilitating the exposure of the subclavian artery as well as that of the origin of the vertebral and thyrocervical trunk. If the axillary vessels are to be exposed, the incision is extended into the axillary region (see below). As is well known, excision of a portion of the clavicle does not interfere with motion of the shoulder and produces no noticeable deformity. Replacement of the resected segment is, therefore, not necessary.

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Exposure of Axillary Artery Anatomic Review The axillary region is the space between the upper lateral aspect of the chest wall and the proximal part of the upper limb. The apex of the pyramid-shaped region transmits the large vessels and nerves from the root of the neck to the upper extremity. The anterior wall consists of two main layers. The pectoralis major muscle with its enveloping fascia forms the outer layer, and the pectoralis minor muscle with the costocoracoid membrane of the clavipectoral fascia forms the deeper layer. The pectoral fascia attaches above to the clavicle and medially to the sternum. It closes the superficial deltopectoral triangle laterally and is continuous below with a fascial covering of the serratus anterior and external oblique muscles. The medial or costal wall of the space corresponds to the five upper ribs and their intervening spaces.

A

B

C FIGURE 26.3 Exposure of the subclavian artery with resection of the clavicle. (A) Line of skin incision for the subclavian–axillary approach. (B) Exposure of the subclavian and proximal axillary vessels after resection of the clavicle. (C) Exposure of the subclavian artery and of the entire length of the axillary vessels after transection of pectoralis major and minor muscles.

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The lateral wall of the space, to which the important axillary vessels and nerves are related, is formed by the coracobrachialis and biceps muscles, the proximal part of the shaft of the humerus, and the medial aspect of the shoulder joint. The axillary artery is the direct continuation of the subclavian artery. It extends from the outer margin of the first rib to the lower border of the teres major muscle, beyond which it is known as the brachial artery. Throughout its course, it is accompanied closely by the axillary vein and has intimate, although changing, relations with the nerves of the brachial plexus. The artery is divided into three segments, corresponding to the part of the vessel situated proximal, behind, and inferior to the pectoralis minor muscle. The axillary vein is formed from the union of the basilic and the two brachial veins. Its principal branch is the cephalic vein, which enters a short distance below the clavicle through the crease between the pectoralis major and deltoid muscles. The various nerves of the brachial plexus surround the third segment of the axillary artery. The median nerve is recognized by its great size and its two heads of origin. The ulnar nerve may be difficult to distinguish from the medial cutaneous nerve of the forearm, since both arise from the median cord and are overlaid by the axillary vein at their origin. The ulnar nerve is the larger and more posterior. The radial nerve is the direct continuation of the posterior cord and differs from the ulnar nerve in its posterior position and greater size. Axillary lymph nodes are embedded in the areolar adipose tissue occupying the axillary space.

Technique of Exposure of Axillary Artery The approach for the exposure of the axillary artery can be through the anterior wall or through the base of the axillary space. Anterior Approach The anterior approach to the axillary artery allows one to expose the artery either at its origin or in its entirety from the apex to the base of the axillary space. Subclavicular Horizontal Approach The skin incision, 8 to 10 cm long, is parallel to the inferior border of the clavicle, corresponding to its middle portion (Fig. 26.4). The pectoralis major muscle is transected progressively until the clavipectoral axillary fascia is exposed. Incision of its anterior sheath and of the subclavius muscle is done along its entire length. Retraction of the subclavius muscle proximally allows incision of the posterior sheath of the clavipectoral axillary fascia. At this point, the nerve of the pectoralis major crossing the anterior surface of the artery must be identified. This approach affords the exposure and mobilization of only the initial segment of the axillary artery above the origin of its collateral branches. The exposure is most suitable for ligation of the vessel in the event of its injury but is less suitable if arterial reconstructive surgery is to be carried out at this level.

A

B FIGURE 26.4 Subclavicular horizontal approach. (A) Position of the shoulder and the line of skin incision. (B) Anatomic structures to be divided for exposing the proximal segment of the axillary artery and the adjacent vein and brachial plexus.

Chapter 26 The Upper Extremity

Deltopectoral Approach The patient is placed in the supine position, with the upper extremity in slight abduction and external rotation. The technique of this exposure (Fig. 26.5) is based on the simple anatomic landmarks indicated by the deltopectoral groove extending from the middle of the clavicle down to the junction of the pectoralis major and deltoid, at its lowest segment. The skin incision extends from the clavicle down to the distal edge of the pectoralis major along the deltopectoral groove. In the upper part of the groove, the cephalic vein is present and must be dissected out and preserved. The pectoralis major is retracted medially, which allows exposure of the pectoralis minor and its pectoral axillary fascia. The latter is incised vertically, close to the coracobrachial inner edge on the coracoid process. At this point, the tendon of the pectoralis minor is transected and retracted medially. The neurovascular bundle appears in view and is surrounded by cellular adipose tissue. The artery is the central structure with its collateral branches. The vein, somewhat larger, is medial to the artery. The brachial plexus is divided in its terminal branches at this level. This approach allows exposure of all the neurovascular structures of the axillary region. However, retraction of the muscles is somewhat limited, making it difficult to obtain an adequate exposure. Should it be necessary because of extensive vascular lesions, the deltopec-

A

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toral approach can be extended, as indicated in Figure 28.6. Combined Approach: Deltopectoral–Subclavicular This approach is a combined procedure of the two previously described techniques. Either it can be carried out as a secondary enlargement of the previous procedure, or it can be done deliberately as a primary exposure, as indicated in Figure 28.6. The skin incision, as indicated in Figure 28.6A, is both subclavicular and deltopectoral, using a hockey-stick incision. After the pectoralis major has been transected below the clavicle, the rest of the exposure is similar to the one in the deltopectoral approach. Transpectoral Approach The transpectoral approach (Fig. 26.7) is used for limited access to the vessels for the purpose of exposure of the axillary artery and vein. The patient is placed in the supine position, with the shoulder slightly elevated and the upper extremity in a horizontal position at a 90° angle with the body. The skin incision extends from the middle of the clavicle to the anterior axillary line in the direction of its apex. The pectoralis major is divided along its fibers near its insertion on the humerus. The vessels are exposed after the pectoralis minor is divided near its insertion on the coracoid process.

B

C FIGURE 26.5 Deltopectoral approach. (A) Position of the shoulder and the line of skin incision. (B) Exposure of the deltopectoral groove and cephalic vein. (C) Retraction of the deltoid and pectoralis major muscles, transection of the pectoralis minor, and exposure of axillary vessels and the brachial plexus.

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A B

C FIGURE 26.6 Combined deltopectoral–subclavicular approach. (A) Position of the shoujder and the line of skin incision. (B) After division of the clavicular portion of the pectoralis major, the tendon of the pectoralis minor is transected. (C) The clavipectoral fascia is opened, thus exposing the neurovascular structures.

Subpectoral–Axillary Approach This exposure (Fig. 26.8) leads to the distal axillary artery and affords an easy extension toward the brachial artery without having to divide the pectoralis major. The patient is placed in the supine position, with the shoulder slightly elevated and the arm in abduction at 90° with the body. The skin incision follows the inferior border of the pectoralis major and is 8 to 10 cm in length. The pectoralis major is then retracted upward and medially. The sheath of the coracobrachialis is opened at its medial border, and the muscle is retracted laterally. The median nerve is then encountered. It is mobilized and placed under the protection of a rubber or umbilical tape. The artery is then exposed. It is surrounded by collateral veins coursing its surface from the satellite veins, and other structures of the brachial plexus are situated posteriorly and laterally. This exposure is fairly simple—requiring little dissection, being relatively atraumatic, and having few disadvantages. Its main indication, however, is an approach for proximal control of the brachial artery and less a routine exposure of the axillary vessels. The incision usually results in an invisible scar, although it may be troublesome if a keloid develops.

Exposure of Brachial Artery Anatomic Review The brachial is the main artery of the arm and is part of the neurovascular bundle situated on the medial aspect of the bicipital sulcus. The latter begins in front of the posterior axillary fold and descends along the inner aspect of the arm as far as the lower third, where it inclines obliquely forward, terminating at the center of the bend of the elbow. It separates the coracobrachialis and biceps muscles in front from the triceps muscle behind. The sulcus indicates the course of the basilic vein toward the brachial vein and is the superficial guide to the brachial vessels and the median nerve. The deep fascia of the arm furnishes its complete investment and is continuous with the deep fascia of the forearm. From the deep surface of this ensheathing layer are derived the lateral and the medial intermuscular septa, dividing the arm into anterior and posterior osseoaponeurotic compartments (Fig. 26.9). The medial intermuscular septum extends from the epicondyle to the insertion of the coracobrachialis muscle. The neurovascular bundle is situated in this compartment. The brachial artery, a continuation of the axillary, extends from the lower border of the teres major muscle to

Chapter 26 The Upper Extremity

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A

B

C FIGURE 26.7 Transpectoral approach. (A) Line of skin Incision medial to the deltopectoral groove. (B) Division of the pectoralis major along its fibers and the line of transection of the pectoralis minor (C) Exposure of the axillary neurovascular structures.

the antecubital fossa, just distal to the skin crease at the bend of the elbow. The artery is divided into three segments. The proximal third is beneath the deep fascia, bounded laterally by the coracobrachialis muscle and partly separated from it by the median nerve, the medial (internal) cutaneous nerve of the forearm, and the ulnar nerve, separated from the basilic vein. The middle third inclines gradually forward and outward and is overlapped by the medial border of the biceps muscle. It is overlaid by the median nerve, which crosses it obliquely. The distal third is overlapped by the medial border of the biceps muscle, but near its termination it lies medial to its tendon, overlaid by the bicipital fascia. Medial to it lies the median nerve. The brachial artery is accompanied by two satellite veins that receive the basilic vein at their upper segment. The latter vein is extrafascial in the lower half of the arm but becomes subfascial in its upper segment.

Exposure of Upper Half of Brachial Artery The patient is placed in the supine position, with the upper extremity in abduction and slight external rotation. A medial longitudinal incision is made along the bicipital groove (Fig. 26.9A). The incision follows the medial border of the biceps along its groove, which separates the biceps anteriorly from the triceps posteriorly. An incision 6 to 8 cm long is adequate for exposure of the artery. If necessary, proximal or distal extension of the incision can be easily achieved. The skin incision should be made anterior to the basilic vein. The incision is carried down to the fascia of the biceps after identifying its medial border. The muscle is then retracted laterally, and with the elbow slightly flexed, the neurovascular bundle appears under a thin aponeurotic sheath, which is then opened. The median nerve is exposed, mobilized, and placed under slight traction on a rubber strip and is retracted

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A

B FIGURE 26.8 Subpectoralaxillary approach. (A) Line of skin incision just at the distal edge of the pectoralis malor (B) Exposure of axillary–brachia vessels and their relations with the adjacent structures.

A

B

C FIGURE 26.9 Exposure of the proximal brachial artery. (A) Position of the arm and the line of skin incision along the bicipital groove. (B) Cross section of the arm, upper third. (C) Exposure of the neurovascular structures in the groove formed by the biceps and triceps muscles.

Chapter 26 The Upper Extremity

laterally, thus exposing the artery (Fig. 26.9C). Sometimes the brachial artery bifurcates quite high, in which case two arteries are found at this level. The cubital nerve is separated from the artery by the intermuscular septum. At this level, the artery is surrounded by two satellite veins and their communicating branches. The basilic enters into one of the brachial veins at its proximal end.

Exposure of Distal Brachial Artery and its Bifurcation The arm is positioned in abduction at 90°, with the forearm in extension and in supination. The antecubital fossa is delineated by flexing the elbow joint and by identifying the medial border of the bicipital tendon. A longitudinal incision of the skin should be avoided because of possible keloid scarring and subsequent retraction of the skin. Instead, an S-shaped or Z-shaped incision

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is recommended, as indicated in Figure 26.10A. The subcutaneous incision should preserve the veins and, as much as possible, the nerve fibers. The basilic vein should be avoided and retracted posteriorly, but it may sometimes be necessary to ligate it at its extrafascial level. The aponeurotic extension of the biceps (bicipital aponeurosis) is then divided, thereby exposing the brachial artery and its two branches, the radial and ulnar arteries (Fig. 26.10C). Like the proximal segment, the artery is surrounded by two satellite veins, with a plexus of communicating branches surrounding it anteriorly. The median nerve is located medial to the vascular bundle and should be retracted medially under the protection of a rubber band. The radial and ulnar divisions of the brachial artery are found at the distal angle of the exposure, with the radial being along the axis of the brachial and the ulnar plunging deeply under the median nerve and under the pronator muscle. Extension proximally or dis-

A

B

C FIGURE 26.10 Exposure of the distal brachial artery. (A) Lines of skin incision; S-shaped incision is preferable to straight incision. (B) Exposure of the biceps muscle and the bicipital aponeurosis. (C) After section of the bicipital aponeurosis exposure of the distal brachial artery and its bifurcation is easily achieved.

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tally of this exposure can be easily achieved, depending on the necessities of the surgical procedure.

Exposure of Radial and Ulnar Arteries Anatomic Review The forearm, containing the radial and ulnar arteries, extends three fingerbreadths below the level of the elbow to the bend of the wrist. In terms of arterial exposures, the forearm is placed in the supine position, with the palm of the hand facing forward. The deep antebrachial fascia invests the forearm completely and is continuous with a deep fascia of the arm and hand. The deep fascia is reinforced anteriorly by the bicipital fascia, which is an extension from the biceps tendon. At the wrist, the deep fascia is continuous with the transverse, carpal, or annular ligaments. From its deep surface, the fascia furnishes attachment to several muscles and sends intermuscular septa to the radius and ulna. The radial artery runs a fairly straight course through the forearm. In its upper two-thirds, it lies under

cover of the brachioradialis muscle and crosses the supinator muscle. In the distal third, the artery is subcutaneous and lies on the radius and on the flexor pollicis longus muscle. The ulnar artery is the larger of the two terminal trunks of the brachial artery. From its origin, it descends through the anterior surface of the forearm and crosses the transverse carpal ligament on the radial side of the pisiform bone. In the lower two-thirds of the forearm, the course of the artery is straight and is indicated by a line drawn from the front of the medial epicondyle to the radial surface of the pisiform bone with the forearm in full supination. The artery lies on the flexor digitorum profundus muscle between the flexor carpi ulnaris muscle medially and the flexor digitorum sublimis muscle laterally. It gradually becomes superficial toward the wrist. In the upper one-third of the forearm, the vessel is placed deeply between the superficial and deep layers of the anterointernal musculature. The nerves of the forearm are the median, the ulnar, and the radial with its superficial and deep branches. Each artery is accompanied by two satellite veins, which send communicating branches across the artery, as in the vessels previously described.

FIGURE 26.11 Exposure of the radial artery. (A) Lines of skin incision for exposure of the radial artery. (B) Proximal exposure. (C) Distal exposure.

B

A

C

Chapter 26 The Upper Extremity

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FIGURE 26.12 Exposure of the ulnar artery. (A) Lines of skin incision for exposure of the ulnar artery. (B) Proximal exposure. (C) Distal exposure.

B

A

C

Exposure of Radial Artery The radial artery may be exposed in its upper or lower third. The line of skin incision (Fig. 26.11A) is an extension of the antecubital one for the lower third of the brachial artery along the edges and the groove of the pronator teres muscle and the brachioradialis muscle (Fig. 26.11B). After incision of the deep fascia, these two muscles are retracted. A thin fascial layer is then incised over the vascular bundle, and the artery is identified and separated from the adjacent two satellite veins. The lower third of the radial artery is more superficial, although subfascial, and is situated laterally to the flexor carpi radialis tendon (Fig. 26.11C).

Exposure of Ulnar Artery As is true for the radial artery, exposure of the ulnar artery (Fig. 26.12) can be carried out proximally or distally. The patient is placed in the supine position, with the arm in abduction and slight external rotation. The forearm is in supination, with slight flexion for relaxing the flexor muscles and with the hand in hyperextension and abduction. The anteromedial approach to the ulnar artery offers

good access to this vessel on the line that extends from the epicondyles to the lateral border of the pisiform bone. The proximal third exposure is carried out through a skin incision 8 to 10 cm long that begins three to four fingerbreadths below the epicondyle. After incision of the deep fascia, the flexor carpi ulnaris muscle is exposed. The ulnar nerve is medial to the vessels, and the artery is surrounded by two satellite veins. In the lower third of the forearm the ulnar artery is more superficial. The approach to it is carried out by the same incision about 4 to 5 cm distal to the previous one. After incision of the fascia and the retraction of the tendons of the flexor carpi ulnaris and of the flexor carpi radialis, the exposure of the vessel and the ulnar nerve is achieved (Fig. 26.12). The radial artery, the interosseous branch, and especially the ulnar artery above the wrist are often used for shunts in dialysis.

Exposure of Carotid Artery See Chapter 22.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 27 Transperitoneal Exposure of Abdominal Aorta and Iliac Arteries Henry Haimovici

Anatomic Review The abdominal aorta extends from the aortic hiatus of the diaphragm, in front of the lower border of the twelfth thoracic vertebra, and ends on the body of the fourth lumbar vertebra by dividing into the two common iliac arteries. The projection of the bifurcation of the aorta to the anterior abdominal wall corresponds to the midpoint of a line joining the two iliac crests. Generally, this point is about 2 to 3 cm below the umbilicus (Fig. 27.1). The length of the abdominal aorta is about 13 cm, and its diameter, variable according to pathologic conditions, ranges between 25 and 40 mm under normal conditions. The abdominal aorta is situated in the retroperitoneal space and, because of its relations with a large number of viscera and vascular structures, its surgical access may be difficult. From a surgical point of view, the abdominal aorta may be conveniently divided into infrarenal and suprarenal segments. Anteriorly, the abdominal aorta is covered by the lesser omentum and stomach, behind which are the branches of the celiac artery and the celiac plexus. Below these structures, the aorta is covered by the splenic vein, the pancreas, the left renal vein, the inferior part of the duodenum, the mesentery, and the aortic plexus. Posteriorly, it is separated from the lumbar vertebrae and intervertebral fibrocartilages by the anterior longitudinal ligament and left lumbar veins. On the right side, above, it is in relation with the azygos veins, cisterna chyli, thoracic duct, and right crus of the diaphragm, the last separating it

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from the upper part of the inferior vena cava and from the right celiac ganglion; below, the inferior vena cava is in closer contact with the aorta. On the left side are the left crus of the diaphragm, the celiac ganglion, the ascending part of the duodenum, and some coils of the small intestine. The aorta gives off a large number of visceral and parietal branches. The visceral branches comprise the celiac, superior and inferior mesenteric, renal, spermatic, and ovarian arteries. The relation between point of origin of the visceral branches of the abdominal aorta and the vertebrae is highly variable. The parietal branches are the paired inferior phrenic and lumbar arteries. The latter are arranged in four pairs. At the medial border of the psoas muscle, each lumbar artery divides into dorsal branches, which supply the muscles of the spine, and ventral branches, which supply the muscles of the abdominal wall. Of the vascular structures in close contact with the aorta, the inferior vena cava and its tributaries have a significant surgical relation. The inferior vena caval system receives the veins of the lower extremities and those from the abdominal and pelvic cavities, except the veins of the portal system. At the level of the fifth lumbar vertebra, from its origin with the two common iliac veins, the inferior vena cava increases in size from below upward, with the accession of the various tributaries, and becomes the largest of the body veins. It maintains a close relation with the abdominal aorta through the major part of its course. Laterally, it lies in contact with the right psoas major mus-

Chapter 27 Transperitoneal Exposure of Abdominal Aorta and Iliac Arteries

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Anomalies of the abdominal aorta and of its major branches, although infrequent, may assume important surgical significance. Its bifurcation, instead of being at the level of the fourth lumbar vertebra, may be more proximal. The more frequent anomalies are found among its branches, especially of the renal arteries (see Chapter 74).

Transperitoneal Infrarenal Aortic Exposure

FIGURE 27.1 Topography of the abdominal aorta and iliac arteries.

cle and is related closely to the descending duodenum, the head of the pancreas, and the medial margin of the right kidney. Variations in the caval patterns, although infrequent, may be striking, and have important surgical implications. Figure 27.2A is an example of doubling of the inferior vena cava, the two vessels being of approximately the same caliber. Figure 27.2B shows a left-sided inferior vena cava, which on occasion can be even larger than the right normal vein. Figure 27.2C indicates a doubling of the inferior vena cava, the left renal vein being retroaortic. Figure 27.2D indicates that, although the inferior vena cava is in its normal position, the iliac veins are preaortic. Figure 27.2E indicates that the left renal vein is double and appears as a circumaortic venous collar. These vena caval anomalies, as well as others, and their surgical management will be reviewed in more detail in Chapter 59. Lymphatic structures are situated in the retroperitoneal space and form a chain extending from the inguinal ligaments to the diaphragm. The lumboaortic nodes are remarkable for their large number. They lie in superficial and deep grooves about the aorta and inferior vena cava and receive the efferents of the intestines and their mesenteries. The lumbar sympathetic ganglia lie in the retroperitoneal space, anterior to the lumbar vertebrae and medial to the psoas major muscle. The left lumbar chain is concealed partially by the aorta, the right by the vena cava.

Exposure of the infrarenal abdominal aorta is best achieved by a transperitoneal approach. An extraperitoneal exposure as an alternative may be indicated in some instances. The transperitoneal approach may be median or paramedian. The median xiphopubic celiotomy is the incision of choice (Fig. 27.3A). It is carried out from the xiphoid process to the pubic symphysis and goes through the subcutaneous tissue down to and including the linea alba. The rectus muscles form bulging bands on each side of the linea alba. As depicted in Figure 27.3A, the incision starts from the upper end and is carried straight down, except that the umbilicus is skirted in an elliptical fashion. The linea alba is first opened above the umbilicus where it is broadest. Below, because the rectus muscles approach the midline, the inadvertent opening of their sheaths is occasionally unavoidable, as the incision is carried toward the pubis. The properitoneal fat is separated to expose the peritoneum, and the two layers are then opened with scissors. Although the midline incision may be made more rapidly, the left paramedian incision (Fig. 27.3B) is considered to offer a more secure closure, because there are two layers of fascia with an intervening layer of muscle. In addition, the nerve supply to the rectus muscle is preserved because the muscle is mobilized from medial to lateral. As shown in Figure 27.3B, the skin incision starts from the lateral border of the xiphoid process and is extended laterally to the midline by about 2 to 4 cm and then downward to the pubic symphysis. The incision is deepened to the anterior rectus sheath, which is opened in line with that of the skin. The rectus muscle is reflected from medial to lateral, and the posterior rectus sheath and peritoneum are opened in line with the previous incision. The anatomic structures of the posterior sheath are different in its upper two-thirds from those below. The rectus is closed in a sheath formed by the aponeuroses of the three lateral muscles, which are arranged in such a way that, from midway between the umbilicus and the symphysis pubis, the posterior wall of the sheath contains no aponeurosis of the three muscles, since they all pass in front of the rectus. As a result, the posterior sheath ends in a thin curved margin, the linea semicircularis, the concavity of which is directed downward. The rectus, in the situation where its sheath is deficient below, is separated from the peritoneum by the transversalis fascia. Figure 27.3C depicts a cross-section of the abdominal wall: 1) above the umbilicus it indicates the anterior and posterior sheath;

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B

A

C

D

E

FIGURE 27.2 Inferior vena cava anomalies (see text).

and 2) below, there is only the anterior sheath, whereas posteriorly there are the fascia transversalis and peritoneum. Immediately upon entering the peritoneal cavity, before exposing the aorta, it is mandatory to explore and verify the conditions of all the intra-abdominal viscera (stomach, gallbladder, liver, pancreas, colon, and small bowel). In addition, the major visceral branches of the aorta should be explored for the possibility of associated vascular lesions by determining the presence of a thrill or diminished pulsation. Next, the small bowel is eviscerated and placed in a sac or on the upper right side of the abdomen and protected with wet towels. The posterior parietal peritoneum overlying the abdominal aorta is then incised (Fig. 27.4A). The peritoneal layer is lifted up with forceps lateral to the duodenojejunal angle. The first jejunal loop is put under slight

tension to facilitate the section of the ligament of Treitz. The peritoneal incision is extended toward the lower part of the abdominal aorta into the pelvic area. In the process, the third and fourth portions of the duodenum are separated from the aortic surface toward the right. The preaortic sheath is then incised, care being taken at this point to carry out hemostasis of the small vessels found at this level. Dissection of the peritoneum is continued toward the pelvic cavity, staying to the right of the mesosigmoid. The preaortic sheath is then opened in the same direction. Exposure of the left renal vein is carried out after completing the incision of the preaortic sheath. Avoidance of excision of the preaortic autonomic plexus may help prevent postoperative sexual dysfunction. The left border of the aorta is dissected after identifying the inferior mesenteric artery and vein, the latter near the angle of Treitz.

Chapter 27 Transperitoneal Exposure of Abdominal Aorta and Iliac Arteries

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C FIGURE 27.3 (A) Xiphopubic midline incision. (B) Xiphopubic left paramedian incision. (C) (1) Cross-section of the abdominal wall proximal to the umbilicus. (2) Cross-section of the abdominal wall midway between the umbilicus and pubic symphysis (below the linea semicircularis).

The inferior mesenteric artery, in cases of an abdominal aortic aneurysm, must be ligated and divided (Figs. 27.5A and 27.5B). Care must be taken to ligate it close to its origin from the abdominal aorta. Before doing so, it is essential to identify its bifurcation and to determine the presence or absence of a pulsation in its distal and proximal segments. If necessary, the inferior mesenteric vein may be ligated and divided above the left renal vein as it crosses this vessel proximally (Fig. 27.5C).

In isolating and mobilizing the left renal vein, the spermatic or ovarian veins should be identified and their origin and course be ascertained. To expose the renal arteries, the left renal vein must be retracted proximally by passing a rubber vessel loop about it (Fig. 27.5D). Mobilization and freeing of the posterior wall of the aorta is a more tedious step, requiring greater care than for the anterior surface. On the right, its separation from

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FIGURE 27.4 (A) Posterior parietal peritoneal incision. (B) Incision of peritoneal and aortic sheath layers. (C) Section of the ligament of Treitz at the duodenojejunal angle. (D) Inset indicating the relative positions of the abdominal structures during aortic exposure.

the adjacent inferior vena cava may be more hazardous and must be done with extreme care. The proximal mobilization of the aorta below the renal vessels should be carried out after identifying the retroaortic vessels, namely, the lumbar veins, in order to avoid their injury.

Mobilization of the bifurcation of the aorta is best carried out distal to it, around the common iliac arteries close to the latter’s division into internal and external iliac vessels. The reason for this maneuver stems from the fact that the normal confluence of the two iliac veins behind the bifurcation of the aorta renders its dissection at this

Chapter 27 Transperitoneal Exposure of Abdominal Aorta and Iliac Arteries

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FIGURE 27.5 (A) Exposure of the inferior mesenteric artery. (B) Ligation and section of the inferior mesenteric artery. (C) Ligation and section of the inferior mesenteric vein, proximally to the left renal vein. (D) Exposure of renal arteries by proximal retraction of the left renal vein.

level more difficult and dangerous. In mobilizing the bifurcation of the common iliac, it is necessary to identify the ureter to avoid its injury. Other pitfalls to be avoided, as already mentioned above, are 1) injuries to the lumbar veins, 2) difficulties that may arise in the presence of a left-sided or retroaortic inferior vena cava, 3) a horseshoe kidney, or 4) a lower-pole renal artery. This approach to the infrarenal abdominal aorta has the advantage of affording distal extension for exploring the iliac or femoral arteries. Proximal extension of the exposure may be more difficult and would afford reaching the superior mesenteric artery only by retracting the left renal vein and exposing the suprarenal viscera.

Exposure of the suprarenal abdominal aorta through the lesser omentum is somewhat more difficult, especially in heavy-set individuals. In these instances, a thoracoabdominal approach is the method of choice (see Chapter 58).

Physiopathologic Considerations in Aortic Surgery Clamping of the infrarenal abdominal aorta is well tolerated in the majority of cases. Occasionally, however, serious ischemic manifestations of the spinal cord, intestines,

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and kidney may be noted. Clamping of the suprarenal abdominal aorta, by contrast, may be fraught with serious to fatal complications if necessary precautions are not undertaken during the surgical procedure. Ischemia of the spinal cord and of the colon, and renal failure, are described in detail in Chapter 58.

Transperitoneal Exposure of Iliac Arteries In the presence of markedly diseased or completely occluded common iliac vessels, exposure of the external iliac arteries also becomes necessary and is carried out at the level of the iliac fossa. The decision to expose the external iliac arteries depends on their patency, as determined previously by arteri-

ography and by the palpatory findings during this stage of surgery.

Exposure of Right External Iliac Exposure of the right iliac fossa is achieved by retracting upward the cecum and the terminal ileum (Fig. 27.6). The posterior parietal peritoneum is incised along the iliac axis. The external iliac runs from the sacroiliac to the lateral side down to the inguinal ligament, where it becomes the femoral artery. The two branches of the external iliac, the inferior epigastric and the deep circumflex iliac, arise from its terminal segment. After incision of the peritoneum both proximally and distally, a short segment of about 4 to 5 cm needs to be mobilized. Proximally, toward the bifurcation of the common iliac, care should be taken not to injure the ureter, which crosses the vessels at that

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C FIGURE 27.6 Transperitoneal exposure of the right external iliac artery (see text).

Chapter 27 Transperitoneal Exposure of Abdominal Aorta and Iliac Arteries

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level. After opening the vascular sheath, the artery is mobilized and tapes are placed about it.

Exposure of Left External Iliac Artery The descending colon and the sigmoid are retracted upward and medially, exposing the iliac fossa. The exposure of the left external iliac (Fig. 27.7) is carried out in a fashion similar to that on the right side. As mentioned above, exposure of the external iliac arteries through the transperitoneal approach is usually carried out as part of an aortoiliac procedure. A retroperitoneal tunnel between the aorta and external iliac arteries on both sides is then developed. On the right, it is devel-

FIGURE 27.7 Transperitoneal exposure of the left external iliac artery (see text).

oped under the posterior parietal peritoneum, and on the left it is made under the mesosigmoid. In developing the retroperitoneal tunnels, it is important to bear in mind the presence of the ureter and the vessels originating from the iliac artery and the satellite veins, and to avoid their injury. The ureters, once identified, should be allowed to remain in situ. Should exposure of the external iliac prove to be inadequate for implantation of a graft or for a thromboendarterectomy, exposure of the femorals becomes mandatory. In these cases, passing of the graft is greatly facilitated through the tunnel of the iliac fossa extended to the femoral canal.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 28 Retroperitoneal Exposure of Abdominal Aorta Calvin B. Ernst

Since the first successful aortoiliac bypass for occlusive disease by Oudot on November 14, 1950, and the first successful abdominal aortic aneurysm repair by Dubost and his colleagues on March 21, 1951, innumerable reconstructive procedures have been performed on the abdominal aorta (1,2). It is somewhat ironic that retroperitoneal exposure of the abdominal aorta, used by both Oudot and Dubost in their first successful aortic reconstructive procedures, has not been widely adopted. In part this is because the retroperitoneal approach is unfamiliar to general and vascular surgeons, who, by nature of their training and by being comfortable working in the abdomen, have continued to expose the aorta transabdominally. That the transabdominal approach is highly effective has been widely documented, and, understandably, the retroperitoneal approach has few advocates. Nonetheless, under certain circumstances it is equal in effectiveness to the transabdominal approach, and under some circumstances it is preferred. It has been suggested that retroperitoneal aortic reconstruction is less stressful for the patient with less postoperative ileus, less third-space fluid shifts, and fewer pulmonary complications than transperitoneal aortic reconstruction (3–5). Consequently, retroperitoneal aortic reconstruction has been recommended for elderly high-risk patients. However, in a prospective randomized study contrasting these two approaches, investigators could not document any important physiologic advantages of the retroperitoneal approach over the transperitoneal approach (6). Indications for retroperitoneal aortic exposure include small infrarenal aneurysms localized to the aorta, suprarenal or juxtarenal aneurysms, aortic reconstruc-

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tion requiring left renal arterial or mesenteric revascularization, and it is indicated for patients with horseshoe kidneys, patients with right-sided ostomies, and some morbidly obese individuals. It is also indicated for patients who have a hostile abdomen resulting from extensive intra-abdominal adhesions, radiation therapy, or inflammatory processes, and those undergoing secondary aortic reconstruction. Contraindications to use of the retroperitoneal approach include need for right renal arterial reconstruction, need to assess intra-abdominal organs, and extensive aneurysmal involvement of the right iliac system. A relative contraindication is the need to expose the right groin vessels. To the uninitiated, several pitfalls exist when performing retroperitoneal aortic reconstruction. All may be avoided, and when one anticipates such problems, alternative approaches are available, including variations on the transabdominal approach. One of these is the transperitoneal-retroperitoneal approach, which offers the advantages of retroperitoneal exposure, particularly to the visceral vessels (7).

Retroperitoneal Infrarenal Aortic Exposure Several authors have provided detailed descriptions of retroperitoneal infrarenal aortic exposure utilizing transverse (8), midline (9), or perimedian incisions (10). A variety of incisions are available, all capable of providing access to the aorta and proximal common iliac arteries.

Chapter 28 Retroperitoneal Exposure of Abdominal Aorta

Positioning the patient is very important. The left thorax should be elevated 45° to 60°. In order to have access to the right groin, the hips should lie as flat as possible. Flexing the table and maintaining the patient’s position with an air-vacuum styrofoam bean bag causes the wound to spiral open (Fig. 28.1). The midpoint between the right costal margin and the right iliac crest is centered over the table flexion point. With the surgeon standing on the left, the table may be rotated away (during dissection of the aorta) or toward him or her (if groin incisions are required). During closure of the incision, the table is flattened, bringing the wound edges into apposition. A transverse skin incision is made from the edge of the rectus sheath, midway between the umbilicus and symphysis pubis, 8 to 10 cm into the 11th intercostal space (Fig. 28.1). The abdominal wall and intercostal muscles are divided in the line of the incision, taking care not to injure the 11th and 12th dorsal neurovascular bundles. Damage to these nerves denervates the abdominal wall musculature leading to muscle weakness manifest by an asymmetric abdominal contour with unsightly bulging (11). Excising a short segment of 12th rib facilitates wound closure. The retroperitoneal space is entered at the tip of the resected 12th rib, and using blunt dissection the peritoneum is stripped from the underlying iliac fossa and psoas muscle. Peritoneum is also stripped from the undersurface of the abdominal wall, taking care, as the linea semilunaris is approached, to avoid tearing the peritoneum, which thins out and is adherent to the transversalis fascia as the midline is approached. Posterolaterally, the peritoneum is stripped from the flank, psoas muscles, and inferior surface of the diaphragm. The peritoneum and its contents are swept and retracted anteromedially. A dissection plane is developed along the lumbodorsal fascia behind the left kidney and ureter, which are further mobilized and retracted anteriorly (Figs. 28.2 and 28.3).

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Alternatively, dissection may proceed anterior to the left kidney and ureter, but a major advantage of the retroperitoneal approach is partially lost because, by leaving the kidney in situ, the left renal vein obscures the juxtarenal aorta.

FIGURE 28.1 Patient position for retroperitoneal aortic exposure. Flexing the operating table causes the incision to spiral open. (Reproduced by permission from Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449.)

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FIGURE 28.2 Transverse section at the level of left renal artery. (A) Peritoneum depicted by bold line. (B) Dissection plane is developed along the lumbodorsal fascia behind the left kidney, which is mobilized anteromedially and to the right. (Reproduced by permission from Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449.)

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FIGURE 28.3 Aneurysm exposed by retracting the mobilized peritoneum and left kidney anteromedially and to the right. Lumbar branch of left renal vein (arrowhead) serves as a marker to the left renal artery (open arrow). Ureter (closed arrow) is swept anteromedially. (Reproduced by permission from Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449.)

With the kidney and ureter retracted anteromedially, the aorta is exposed from the level of the left renal artery to the aortic bifurcation. Any self-retaining retractor firmly attached to the operating table simplifies and maintains fixed exposure and is key to maintaining such exposure. By exposing the aorta from its bifurcation to the level of the left renal vein, the left renal artery is identified at the level of the lumbar branch of the left renal vein. The lumbar branch of the left renal vein is a fairly constant structure and serves as a marker to the origin of the left renal artery (Fig. 28.3). After ligating and dividing the lumbar branch of the left renal vein, the infrarenal aorta comes into complete view. Retroperitoneal aortic exposure for occlusive disease requires limited infrarenal dissection, preserving the inferior mesenteric artery. When managing a large aneurysm, however, sometimes the inferior mesenteric artery must be ligated and divided flush with the aneurysm to gain access to the right common iliac vessels. For aneurysms confined to the aorta, the inferior mesenteric artery is kept intact, and distal dissection proceeds posterior to the inferior mesenteric artery origin. Dissection of the aortic bifurcation from the underlying vena cava and iliac vein confluence must proceed with caution lest venous injury occur. At this level and through the retroperitoneal approach, venous repair, particularly on the right of the aorta, is very difficult if not impossible. Distal arterial control is facilitated by dissecting the common iliac arteries individually, thus avoiding the hazardous aortic bifurcation caval area. Large aneurysms

FIGURE 28.4 Proximal aortic occlusive clamp is placed just cephalad to celiac trunk; line of incision into aneurysmal sac is posterolateral to visceral vessels (top). Occlusion balloon catheter is passed through opened aneurysm to control backbleeding from celiac trunk, superior mesenteric artery, and right renal artery (only orifice shown with catheter); left renal artery and left common iliac artery are occluded with vascular clamps; and right common iliac artery backbleeding is controlled with intraluminal occlusion balloon catheter (bottom). (Reproduced by permission from Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449.)

requiring extensive right iliac dissection are a relative contraindication to the retroperitoneal approach. Required dissection of the right common iliac bifurcation is challenging because of marginal exposure. Dissection and mobilization of the right iliac arterial system under such circumstances is hazardous and should be avoided. Distal control and occlusion of the right iliac artery during aneurysm repair should be obtained by a balloon occlusion catheter threaded through the opened aneurysm (Fig. 28.4). Some authors recommend extending the abdominal incision across the midline to the right lower quadrant to facilitate right iliac arterial exposure (4). Dissection of the left common iliac artery, however, is easy because this vessel, along with its branches, is apparent throughout its entire length. Whether managing aneurysmal or occlusive disease, circumaortic dissection is unnecessary for proximal aortic clamping. Only small tunnels anterior and posterior to the infrarenal aorta are required, just sufficient to accommodate the blades of a vascular clamp. Caval injury is not a concern at this level because it is not immediately adjacent to the aorta, as it is at the aortic bifurcation.

Chapter 28 Retroperitoneal Exposure of Abdominal Aorta

Retroperitoneal Approach for Juxtarenal and Suprarenal Aortic Exposure The retroperitoneal approach is ideal for juxtarenal or suprarenal aortic exposure because the obscuring left renal vein and body of the pancreas are not limiting factors as they are with the transperitoneal approach. Occasionally, however, a combined transperitoneal– retropetitoneal approach may be required, particularly for large juxtarenal aortic aneurysms with extensive iliac arterial involvement or when right renal artery reconstruction is also necessary (7). The transperitoneal component of the exposure facilitates iliac dissection and right renal artery dissection, and the retroperitoneal component facilitates suprarenal aortic exposure. As with dissection of the infrarenal aorta, positioning the patient is most important to ease of exposure. Positioning is the same as when exposing the infrarenal aorta, with the exception that left chest elevation must be closer to 75° than 60°. A transverse skin incision begins at the lateral border of the rectus sheath, starting between the umbilicus and symphysis pubis, and extends 15 to 20 cm into the ninth or tenth intercostal space (12). Through such an incision, the supramesenteric aorta may be adequately exposed. Exposure of the celiac segment of the aorta requires an incision

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into the eighth intercostal space and a formal thoracoabdominal incision (Fig. 28.5). The abdominal wall and intercostal muscles are divided in the line of the incision. The retroperitoneal space is entered near the tip of the tenth rib, and using blunt dissection the peritoneum is stripped from the underlying iliac fossa and psoas muscle, developing a plane along the lumbodorsal fascia behind the left kidney and ureter, which are mobilized and retracted anteromedially. By sweeping the retroperitoneum cephalad and medial, the undersurface of the diaphragm is exposed. The lateral extent of the incision is deepened into the left thorax, and a short length of diaphragm is incised radially, which facilitates proximal exposure. After appropriate packs are placed, the peritoneal sac and wound edges are retracted by any self-retaining retractor firmly attached to the operating table. Dissection proceeds as for infrarenal exposure described above, with the addition of further cephalad exposure of the suprarenal aorta by dividing the diaphragmatic crus enveloping the aorta. Suture ligation of areolar tissue adjacent to the origin of the superior mesenteric artery prevents or minimizes lymphatic leaks. After dividing the diaphragmatic crus, further sharp dissection exposes the superior mesenteric artery 1 to 2 cm proximal to the left renal artery. If supraceliac aortic clamping is anticipated, the dissection is extended 2 to

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B FIGURE 28.5 Incision for retroperitoneal supraceliac aortic exposure. (A) An eighth-interspace incision is required to adequately expose the aorta proximal to the celiac trunk. (B) Transperitoneal–extraperitoneal approach by which the descending colon, spleen, stomach, and pancreas are mobilized anteromedially to the right. (Reproduced by permission from Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449.)

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4 cm cephalad. Circumferential aortic dissection is not required for suprarenal, supramesenteric, or supraceliac aortic occlusion. Only narrow tunnels anterior and posterior to the aorta are made, just sufficient to accommodate the blades of a vascular clamp. After opening the aneurysm, backbleeding from the right renal, superior mesenteric, and celiac orifices may be controlled by threading intraluminal balloon occlusion catheters into the respective ostia or by small bulldog clamps placed individually on the celiac, superior mesenteric, and left renal arteries (Fig. 28.4). As the right renal artery is obscured, clamping is not possible. Therefore, an occlusion balloon catheter may be used, or alternatively the operative field may be kept dry by cell saver suction and reinfusion of blood lost from the right renal orifice. In the time required to construct the aortic anastomosis, only a small amount of blood is lost from the right renal artery. In addition, no more than 28 minutes is usually required for suprarenal occlusion, an ischemic interval well tolerated by the kidneys. Consequently, no special precautions are taken to cool the kidneys or infuse solutions into the renal arteries. Anticipating prolonged suprarenal occlusion, however, demands renal protection by infusing 200 to 280 mL of iced Ringer’s lactate solution (containing mannitol, heparin sodium, and sodium bicarbonate) into each renal artery. Closure of incisions for both infrarenal and suprarenal aortic exposure is straightforward and facilitated by flattening the table. If the left chest has been entered, a 20-Fr. catheter is placed during closure and removed after evacuating air from the chest.

Pitfalls of Retroperitoneal Aortic Reconstruction Certain pitfalls of retroperitoneal aortic reconstruction deserve comment. These include injury to the vena cava, which is very difficult to manage through the retroperitoneal approach. Vigorous retraction in the upper aspects of the operative field may lead to unrecognized splenic trauma. This should be minimized by using self-retaining retractors. The lumbar branch of the left renal vein must be identified not only because it serves as a marker to the left renal artery but also to avoid injuring it. Similarly, although rare, a retroaortic left renal vein or circumaortic left renal vein may cause problems if not recognized. During mobilization of the retroperitoneum, it is important to identify the left gonadal vein so that in the course of sweeping the retroperitoneum anteriorly the gonadal vein is not avulsed from the left renal vein. A left pneumothorax may occur and be unrecognized, particularly if the left 11th-space incision is not made carefully. Both the inferior mesenteric and the left renal arteries are swept anteriorly when retrorenal dissection is performed, and they must be identified to prevent injury.

To preserve continuity of the inferior mesenteric artery, it is important to incise the aneurysm posterior to its origin. The left ureter must be identified and swept anteriorly with the kidney and retroperitoneal structures to avoid injury. One should be aware that the left ureter is particularly vulnerable to traction injury during secondary aortic procedures because it may be tethered in the pelvis and not as mobile as it might be in a virgin retroperitoneum. Postoperative problems following retroperitoneal aortic reconstruction include the potential for development of an aortoenteric fistula, if the aneurysm sac is not imbricated over the prostheses or if the duodenum lies on the graft following aortic reconstruction for occlusive disease. Excessive blunt retroperitoneal dissection may tear small veins, causing subsequent oozing with postoperative retroperitoneal hematoma formation. Precise dissection and careful hemostasis prevent this. Some have suggested closed suction drainage for 24 hours to minimize retroperitoneal hematoma formation (3,10). However, I have an aversion to placing drains near a fresh aortic graft. A left flank hernia may develop if precise multiple-layer closure of the wound is not performed.

References 1. Oudot J. La greffe vasculaire dans les thromboses du carrefour aortique. Presse Med 1951;59:234–236. 2. Dubost C, Allary M, Oeconomos N. Resection of an aneurysm of the abdominal aorta: reestablishment of the continuity by a preserved human arterial graft, with result after five minutes. Arch Surg 1952;64: 405–408. 3. Shepard AD, Scott GR, et al. Retroperitoneal approach to high-risk abdominal aortic aneurysms. Arch Surg 1986;121:444–449. 4. Sicard GA, Freeman MB, et al. Comparison between the transabdominal and retroperitoneal approach for reconstruction of the infrarenal abdominal aorta. J Vasc Surg 1987;5:19–27. 5. Williams GM, Ricotta J, et al. The extended retroperitoneal approach for treatment of extensive atherosclerosis of the aorta and renal vessels. Surgery 1980;88:846–855. 6. Cambria RP, Brewster DC, et al. Transperitoneal versus retroperitoneal approach for aortic reconstruction: a randomized prospective study. J Vasc Surg 1990;11: 314. 7. Ernst CB. Exposure of inaccessible arteries: Part II. Abdomen and leg exposure. Surg Rounds 1985;8:26–41. 8. Rob C. Extraperitoneal approach to the abdominal aorta. Surgery 1963;53:87–89. 9. Shumacker HB. Midline exposure of the abdominal aorta and iliac arteries. Surg Gynecol Obstet 1972;135:791–792. 10. Taheri SA, Sawronski S, Smith D. Paramedian approach to the abdominal aorta. J Cardiovasc Surg 1983;24:529–531.

Chapter 28 Retroperitoneal Exposure of Abdominal Aorta 11. Gardner GB, Josephs LG, et al. The retroperitoneal incision: an evaluation of postoperative flank “bulge”. Arch Surg 1994;129:753. 12. Nypaver TJ, Shepard AD, et al. Repair of pararenal abdominal aortic aneurysms: an analysis of operative management. Arch Surg 1993;128:803.

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13. O’Mara CS, Williams GM. Extended retroperitoneal approach for abdominal aortic aneurysm repair. In: Bergan JJ, Yao JST, eds. Aneurysms: diagnosis and treatment. New York: Grune & Stratton, 1982:327–343.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 29 Retroperitoneal Exposure of Iliac Arteries Henry Haimovici

Anatomic Review Access to the iliac arteries by the retroperitoneal approach is obtained through incisions made through the anterolateral abdominal wall. The skin of the abdomen at this level is attached loosely to the subjacent structures except at the umbilicus, where it adheres firmly. The superficial fascia of the lower abdomen is divided into two layers: the superficial, called Camper’s fascia, which lies in the bulk of the subcutaneous fat, and the deep layer, called Scarpa’s fascia, which is denser and is applied more closely to the abdominal muscles. The flat muscles of the abdomen and the recti are the main structures of the abdominal wall protecting its contents (Fig. 29.1). The most superficial of the flat muscles is the external oblique, which lies on the lateral and anterior parts of the abdomen. It is broad, thin, and irregularly quadrilateral, its muscular portion occupying the side, and its aponeurosis occupying the anterior wall of the abdomen. The fleshy fibers of this muscle proceed in various directions, some of which are inserted into the anterior half of the outer lip of the iliac crest, with others ending in an aponeurosis. The aponeurosis of this muscle is a thin but strong membranous structure, the fibers of which are directed downward and in a medial direction. The portion of the aponeurosis that extends between the anterior superior iliac spine and the pubic tubercle is a thick band, folded inward, that continues below with the fascia lata. It is called the inguinal ligament, or Poupart’s ligament. The second flat muscle is the internal oblique, which is thinner and smaller than the external, beneath which it lies. It is an irregularly quadrilateral form and is situated

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at the lateral and anterior part of the abdomen. It arises by fleshy fibers from the lateral half of the grooved upper surface of the inguinal ligament, from the anterior two-thirds of the middle of the iliac crest, and from the posterior lamella of the lumbodorsal fascia. From its origin, the fibers diverge. Those from the inguinal ligament, few in number and paler in color than the rest, arch downward and medialward across the spermatic cord or the round ligament of the uterus. The fibers from the anterior third of the iliac origin are horizontal in their direction and, becoming tendinous along the lower fourth of the linea semilunaris, pass in front of the rectus abdominis to be inserted into the linea alba. The fibers arising from the middle third of the origin run obliquely upward and medialward and end in an aponeurosis. The transversus muscle, so-called from the direction of its fibers, is the most internal of the flat muscles of the abdomen, being placed immediately beneath the internal oblique muscle. The muscle ends in front of a broad aponeurosis. It passes horizontally to the middle line and is inserted into the linea alba. Its upper three-fourths lies behind the rectus and blends with the posterior lamella of the aponeurosis of the internal oblique. Its lower onefourth is in front of the rectus. The rectus abdominis is a long, flat muscle that extends along the whole length of the front of the abdomen and is separated from its fellow of the opposite side by the linea alba. The rectus is enclosed in a sheath formed by the aponeuroses of the two oblique and transversus muscles. This arrangement of the aponeurosis originates from the costal margin, extending to midway between the umbilicus and the symphysis pubis, where the posterior wall of

Chapter 29 Retroperitoneal Exposure of Iliac Arteries

FIGURE 29.1 The anterolateral muscles of the abdomen.

the sheath ends in a thin, curved margin, the linea semicircularis, the concavitv of which is directed downward. Below this level, all three muscles pass in front of the rectus. The transversalis fascia is a thin aponeurotic membrane that lies between the inner surface of the transversalis muscle and the extraperitoneal fat. It forms part of the general layer of fascia lining the abdominal wall and is directly continuous with the iliac and pelvic fasciae.

Iliac Arteries The abdominal aorta, as stated above, divides on the left side of the body of the fourth lumbar vertebra into the two common iliac arteries, each about 5 cm in length. The right common iliac artery is usually somewhat longer than the left and passes more obliquely across the body of the last lumbar vertebra. In front of it are the peritoneum, the small intestines, branches of the sympathetic nerves, and, at its point of division, the ureter. Behind, it is separated from the body of the fourth and fifth lumbar vertebrae and the intervening fibrocartilage by the terminations of the two common iliac veins and the commencement of the inferior vena cava. Laterally, it is in relation, above, with the inferior vena cava and the right common iliac vein and, below, with the psoas major. Medial to it, above, is the left iliac vein. The left common iliac artery is in relation, in front, with the peritoneum, the small intestines, branches of the

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sympathetic nerves, and the superior hemorrhoidal artery. At this point it is crossed by the ureter. The left common iliac vein lies partly medial to and partly behind the artery. Laterally, the artery is in relation with the psoas major. The external iliac artery, a continuation of the common iliac, passes obliquely downward and lateralward along the medial border of the psoas major, midway between the anterior superior spine of the ilium and the symphysis pubis, where it enters the thigh and becomes the femoral artery. Its relations, in front and medially, are with the peritoneum, subperitoneal areolar tissue, the termination of the ileum, and, frequently, the vermiform process on the right side; on the left side, the external iliac artery is in relation to the sigmoid colon and a thin layer of fascia, derived from the iliac fossa, that surrounds the artery and vein. Behind, it is in relation with the medial border of the psoas major. Laterally, it rests against this muscle, from which it is separated by the iliac fascia. Numerous lymphatic vessels and lymph glands lie on the front and on the medial side of the vessel. Besides several small branches, the external iliac artery gives off two collaterals of considerable size: the inferior epigastric artery and the deep iliac circumflex artery. Both of these branches arise from the external iliac immediately above the inguinal ligament. The hypogastric artery (internal iliac artery) arises at the bifurcation of the common iliac artery, opposite the lumbosacral articulation, and divides into two large trunks, an anterior and a posterior. This artery supplies the walls and viscera of the pelvis, the buttock, the generative organs, and the medial side of the thigh. It is a short, thick vessel, smaller than the external iliac, of about 4 cm in length.

Exposure of External Iliac Artery The patient is placed in the supine position (Fig. 29.2). A rolled sheet or a small sandbag is placed under the buttocks to elevate this area by about 10° to 15°. A skin incision is made parallel with and about 1 cm above the inguinal ligament, the incision being in the middle third of a line extending from the anterior superior iliac spine to the pubic symphysis and slightly curved proximally (Fig. 29.2A). After hemostasis of subcutaneous vessels is carried out, the aponeuroses of the external oblique, internal oblique, and transversus muscles are incised, always parallel to the inguinal ligament. These three structures are then reflected upward and medialward, the transversalis fascia is opened, the properitoneal adipose tissue is retracted gently in the same direction as the muscles, and the retroperitoneal space is entered. The external iliac artery is exposed, its sheath opened, and a tape placed about it. On its anterior surface one finds two small, fragile venules that are branches of the satellite veins. This anatomic feature indicates the necessity for dissection of the external iliac artery above this point, where it presents no other

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C FIGURE 29.2 Extraperitoneal exposure of the right external iliac artery.

than the external iliac vein as the only important anatomic relation.

Extraperitoneal Exposure of Iliac Axis There are several approaches to the iliac axis. Our personal preference is indicated in Figure 29.3, which illustrates the exposure of the right iliac vessels. The patient is placed in the supine position, with a hard pillow under the right thoracolumbar region, thus elevating the body by about 10° to 15°. Figure 29.3A shows the skin incision, which begins at the level of the anterior

axillary line at the midpoint between the subcostal margin and the iliac crest. From there, it continues in an S-shaped line, the first part being directed toward the umbilicus, and the second portion parallel to the inguinal ligament and about 3 cm above it. The skin incision exceeds slightly the lateral border of the rectus abdominis. The incision is then carried down to the external oblique (Fig. 29.3B). The lateral edge of the skin flap is retracted laterally and downward. Incision of the external oblique is done closer to the inguinal ligament than to the lateral border of the rectus abdominis. The aponeurotic portion of the muscle is incised along its fibers. Then the muscular portion is elevated and separated from the underlying structures, and the incision is extended proximally along its fibers. Figure 29.3C and D indicate the section of the internal oblique and the transversus. Transection of these two muscles may require sacrificing two or three minor neurovascular bundles encountered during the cutting of these structures. Proximal and medial retraction of the three sectioned muscles, as well as retraction of the lateral edges of the same structures, exposes the properitoneal adipose tissue (Fig. 29.3E). Detachment of the abdominal contents, starting toward the lower angle of the exposure, facilitates the separation of the peritoneum from the psoas muscle. One should avoid separating the abdominal contents by entering the retroperitoneal space at the upper angle of the incision, which may lead to the quadratus lumborum muscle. After the abdominal contents are retracted and protected with moist laparotomy sheets, the iliac vessels are ready to be exposed (Fig. 29.3F). Two wide retractors of the Deaver type are adequate for retraction and exposure of the entire iliac axis. The ureter must be identified and protected from any undue injury in the course of retraction. Injury to the lymph nodes and lymphatics should be avoided. If they are injured, ligation should be done routinely to prevent lymphorrhea, which may be troublesome. Retraction of the upper angle may be difficult, especially in an obese patient, if the aorta is also to be exposed. If necessary, section of the lateral border of the rectus abdominis may facilitate the retraction. The advantage of this approach is its easy and clear exposure not only of the iliac axis but also of the bifurcation of the aorta. Pitfalls to be avoided during the mobilization of the iliac artery are injuries to the inferior vena cava or the satellite iliac veins. Another pitfall may be related to the inadvertent sacrifice of the nerves of the internal oblique and transversus muscles. Closure of the abdominal wall should be meticulous, although hernias after this procedure occur extremely rarely. Exposure of the left iliac axis is illustrated in Figure 29.4. The approach to the left iliac vessels is similar, if not identical, to the approach to those on the right side. The only difference in exposure is that the aortic bifurcation is more accessible and much easier to mobilize on the left side.

Chapter 29 Retroperitoneal Exposure of Iliac Arteries

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FIGURE 29.3 Extraperitoneal exposure of the right iliac vessels, including the terminal abdominal aorta.

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FIGURE 29.4 Extraperitoneal exposure of the left iliac vessels, including the terminal abdominal aorta.

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Part IV Surgical Exposure of Vessels

In both right and left exposure, a concomitant lumbar sympathectomy can be achieved through these extraperitoneal approaches.

Combined Iliac and Femoral Exposures The iliac and femoral vessels can be approached either by two separate incisions or by a combined abdominal–thigh incision. A

Separate Abdominal and Thigh Incisions If separate incisions are to be made (Fig. 29.5), the two separate approaches to the femoral and iliac vessels are carried out as previously described. Since this combined exposure is normally intended to revascularize the lower extremity through the femoral artery, it is wise to start first by exposing this (see Femoral Artery section in Chapter 30). The iliac exposure is carried out after the quality of the femoral vessels is ascertained. In this combined procedure, a tunnel between the iliac and femoral regions must be developed for passage of a graft. Proper dilation of the femoral canal is important in preventing a possible constriction at this level.

Combined Abdominal and Thigh Incision If a combined abdominal–thigh incision is to be used, the skin incision is as indicated in Figure 29.6A. It starts at the anterior axillary line and is directed toward the angle between the lateral border of the rectus abdominis and the inguinal ligament. At this point, it is redirected distally and curved slightly, with its convexity lateral along the femoral vessels. The thigh incision is slightly lateral to the femoral as it is extended along the medial border of the sartorius. The abdominal incision is first completed in a fashion similar to the extraperitoneal exposure of the iliac vessels (Fig. 29.6B). The external oblique is divided along its fibers. The internal oblique and transversus muscles are transected parallel to the inguinal ligament, and the retroperitoneal space is entered after the abdominal contents are retracted superiorly and medially. The inguinal ligament is transected about 1 cm lateral to the femoral artery (Fig. 29.6C). It is important to identify the anatomic planes: the aponeurosis of the external oblique, the inguinal ligament, and the iliopubic ramus. In dividing the inguinal ligament, one should avoid injuring the inferior epigastric and the circumflex iliac arteries found behind this structure. A few smaller arterioles, supplying the adjacent lymph nodes, and a few small venules can be sacrificed without any adverse effect. In dissecting the distal end of the external iliac artery, one may encounter enlarged lymph nodes because of chronically infected ischemic lesions of the foot. Undue

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FIGURE 29.5 Combined iliac and femoral exposures with separate approaches used.

trauma to these lymph nodes should be avoided for obvious reasons (lymphorrhea). In the course of this combined approach to the iliofemoral arteries, extraperitoneal exposure of the terminal abdominal aorta is also possible, being much easier to achieve on the left side. By contrast, on the right side, this approach offers better control of the origin of the inferior vena cava, whereas that of the bifurcation of the aorta is less adequate.

Chapter 29 Retroperitoneal Exposure of Iliac Arteries

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FIGURE 29.6 Combined iliofemoral exposure with division of the inguinal ligament.

Exposure of the femoral vessels is carried out in similar fashion, as previously described (Fig. 29.6). One of the critical steps in this combined iliofemoral exposure may be at the time of closure of the inguinal ligament. The anatomic reconstitution must be meticulous and must avoid any stricture of the femoral canal. The advantages of this combined iliofemoral expo-

sure are obvious. First, all these vessels can be handled under direct vision. Second, should it be necessary to expose the superficial femoral or popliteal artery, the previous incision can be easily extended. Note See the Bibliography at the end of Chapter 30.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 30 The Lower Extremity Henry Haimovici

Femoral Artery

Exposure of Femoral Artery in Scarpa’s Triangle

Anatomic Review

The patient is placed in the supine position, with the thigh in abduction and slight external rotation. A curved skin incision is made, extending from above the inguinal ligament and with a concavity medialward, along the medial border of the sartorius (Fig. 30.2A). The incision is carried through the subcutaneous tissue at the site of retraction of the lateral edge of the skin to avoid injuring the lymphatic vessels or the lymph nodes. Should some of the lymphatics or lymph nodes be divided, they should be ligated or cauterized to avoid any lymphorrhea in the postoperative period. The incision of the deep fascia is then carried out medial to the medial border of the sartorius (Fig. 30.2B). This incision is extended upward toward Poupart’s ligament and distal to the apex of the region. The arterial sheath is then opened along its entire length, thus enabling the artery to be mobilized (Figs. 30.2C and 30.2D). This sheath, a sleeve-like prolongation of the fascial envelopment of the abdomen, passes downward into the thigh behind the inguinal ligament. It extends downward as far as the origin of the profunda femoris artery, where it fuses with the outer coat of the femoral vessels. Two septa divide the sheath into arterial, venous, and lymphatic compartments. In the mobilization of the common femoral artery proximally, care should be taken to avoid injuring the epigastric and the deep circumflex iliac arteries, the latter two branches being at the junction between the femoral and the external iliac arteries under Poupart’s ligament. After the common femoral is mobilized, umbilical or rubber vessel loops are placed about it (Fig. 30.2E). Next, the superficial femoral artery is mobilized just 1 to 2 cm below the origin of the

The femoral artery (Fig. 30.1), a direct continuation of the external iliac artery, enters the thigh behind the inguinal ligament (Poupart’s ligament) midway between the anterior superior iliac spine and the pubic tubercle. From this point, the artery follows an almost straight course, gradually inclining from the anterior to the posteromedial aspect of the thigh. As a result of this direction, the initial segment of the femoral artery is comparatively superficial, but its terminal portion becomes deeply located. In its proximal part, it is located in what is known anatomically as the femoral triangle or the triangle of Scarpa. In its distal portion, it is located in an anatomic area known as the adductor or Hunter’s canal. The anatomic landmarks of Scarpa’s triangle include the soft parts of the root of the thigh. This region is bounded proximally by the inguinal ligament, laterally by the sartorius muscle, and medially by the pectineus and adductor muscles. Distally, the apex of the triangle is formed by the overlapping of these muscles. The roof of this area consists of the fascia lata, which completely covers the space anteriorly. The floor is made up of two inclined planes, which form a well-marked medium groove at their junction. The laterally inclined plane consists of the iliopsoas muscle invested by a thin layer of fascia. In this compartment are included the femoral vessels and nerve and their large branches. Among the latter structures are the termination of the great saphenous vein and the deep subinguinal lymph vessels and glands embedded in a quantity of loose fat tissue. This space communicates with the abdomen through the lacuna vasorum.

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Chapter 30 The Lower Extremity

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Exposure of Superficial Femoral Artery in Hunter’s Canal Brief Anatomic Review

FIGURE 30.1 The femoral artery and its divisions (Scarpa’s triangle, Hunter’s canal).

The superficial femoral artery is contained in the adductor or Hunter’s canal, which extends from the apex of the femoral triangle to the tendinous hiatus of the adductor magnus muscle. This canal is an intermuscular space on the medial aspect of the middle third of the thigh. Its main structures are the femoral vessels and the saphenous nerve. The boundaries of this canal include the lateral wall formed by the vastus medialis muscle and the posterior wall formed by the adductor longus muscle proximally and the adductor magnus muscle distally. The roof of the canal is a layer of deep fascia running from the adductor longus and magnus muscles to the vastus medialis. The sartorius muscle covers the space. The femoral artery is bound closely by connective tissue to the femoral vein, which at first lies posterior to and then slightly to the lateral side of the artery. The superior genicular artery (anastomotica magna) branches off from the femoral near its termination. Distal to it, when the artery goes through the adductor hiatus, the artery becomes the popliteal. The saphenous nerve crosses anterior to the femoral artery, and from the tendinous hiatus it passes downward under the sartorius muscle to the distribution over the medial aspect of the leg and ankle. Exposure of Superficial Femoral Artery

profunda, and a tape is placed about it in a similar fashion. Slight traction on these two tapes will facilitate the location of the origin of the profunda femoris artery, which is then mobilized by further opening of the sheath that extends around its origin. The profunda emerges posteriorly and usually courses laterally to the main trunk. Anterior to the origin of the profunda there is a fibrous band that has to be incised in order to mobilize it. In so doing, care must be taken not to injure the branches of the profunda femoris vein, which pass in front of the artery. These may be clamped, divided, and ligated. A tape is placed about the origin of the profunda and around some of its major branches. In addition to the common, superficial, and profunda vessels, the epigastric, circumflex iliac, and a few other branches that may come off the common or superficial femoral also have to be controlled before the surgery of the vessel is undertaken. In retracting these structures after the exposure of the vessels, it is important that the lymphoadipose tissue situated between Scarpa’s fascia and the deep fascia be retracted medially out of the operative field. Through the same incision, if the saphenous vein is to be used as a bypass graft, the procedure shifts to the medial aspect, and the dissection of the vein starts at that level.

For exposure of the superficial femoral artery (Fig. 30.3), the patient should be in the supine position, with the lower extremity placed in external rotation and the knee flexed (Fig. 30.3A). The skin incision is made along a line extending from the apex of the femoral triangle to the adductor tubercle. The incision is deepened through the superficial fascia overlying the sartorius (Fig. 30.3B). The saphenous vein is retracted medially. The muscle is then mobilized from its fascial investment, and the roof of the canal is exposed (Fig. 30.3C). The strong fascia is opened, and the femoral vessels are exposed, with the saphenous nerve lying on its anterior surface (Fig. 30.3D). The saphenous nerve is then protected by placing a tape around it and retracting it medially without too much tension. The artery is surrounded by a network of venules that may hamper its dissection and mobilization at this level (Fig. 30.3D). Several muscle branches emerge from the superficial femoral artery at this point, and they may have to be spared. Especially important is the highest genicular artery, located at the lower angle (Fig. 30.3E). Distal to it is the adductor hiatus, which may have to be opened for greater access to the junction between the superficial femoral and popliteal arteries. Usually, at this level there are marked arteriosclerotic changes of the artery. Variants of these exposures depend on the extent of the pathologic findings in the vessels proximally or

356

Part IV Surgical Exposure of Vessels FIGURE 30.2 Exposure of the femoral artery in Scarpa’s triangle.

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distally. If the external iliac artery is also involved, and if it is necessary to expose it, an extraperitoneal approach is indicated (see Chapter 27). Should it be necessary to expose the entire femoral artery, the incision is made from the groin down to the adductor tubercle, with the two incisions combined as described.

Popliteal Artery Anatomic Review The popliteal artery is situated behind the structures of the knee joint and constitutes the longitudinal axis of

the region. The popliteal fossa is a lozenge-shaped space consisting of an upper, or femoral, and a lower, or tibial, triangle. The popliteal artery, a continuation of the superficial femoral artery, enters the superior and medial part of the popliteal space through the tendinous part of the adductor magnus muscle (adductor magnus hiatus). As it passes through the popliteal space, it inclines laterally along the outer border of the semitendinosus muscle until it reaches the middle of the limb. It then descends vertically to the distal border of the popliteus muscle and terminates by dividing into the anterior and posterior tibial arteries. The popliteal artery throughout its course is placed deeply and lies in direct contact with the posterior ligaments of the knee joint.

Chapter 30 The Lower Extremity

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FIGURE 30.3 Exposure of the superficial femoral artery in Hunter’s canal.

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Three pairs of arteries branch off the popliteal artery at three different levels and are distributed mainly about the bony part of the knee. The superior genicular arteries, lateral and medial, originate at the level of the femoral condyles. The middle genicular artery pierces the oblique popliteal ligament and supplies the ligaments and synovial membrane in the interior of the articulation. The inferior genicular arteries, lateral and medial, wind around the front of the knee and anastomose with each other deep to the patellar ligament. The popliteal vein, formed by the junction of the anterior and posterior tibial veins, lies superficial to the artery, medial to it distally, and lateral to it proximally. The short saphenous vein, which pierces the deep fascia in the lower part of the popliteal space, divides into two branches, one entering the popliteal vein and the other the great saphenous. The popliteal vein and artery are bound wall to wall in a resistant connective tissue sheath, a relation that explains their simultaneous injury and the formation of an arteriovenous fistula. The sciatic nerve, with its two branches (tibial and common peroneal), is found at the upper angle of the

popliteal space. The two branches continue in their known direction, the tibial along the popliteal vessels, and the peroneal leaving the popliteal space at its lower end. From a surgical point of view, the popliteal artery is divided into proximal and distal segments. Each of these segments can be exposed alone, or it may be necessary sometimes to expose the vessel in its entirety.

Exposure of Popliteal Artery There are three different approaches to exposure of the popliteal artery: medial, posterior, and mixed posteromedial. The medial exposure may be used for the proximal or distal or the entire popliteal artery. Medial Approach to Proximal Popliteal Artery The patient is placed in the supine position, with the lower extremity in slight external rotation and the knee in 30° flexion and supported by a rolled sheet (Fig. 30.4A). The skin incision is made in the lower third of the thigh along the anterior border of the sartorius muscle and is carried through to the superficial fascia (Fig. 30.4B), care being

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FIGURE 30.4 Medial exposure of the proximal popliteal artery. (A) Position of the lower extremity, knee flexed and supported by a bolster. (B) Deep fascia incision, anterior to the sartorius muscle. (C) Exposure of the proximal popliteal artery and adductor magnus tendon. (D) Closeup view of the adductor magnus covering the proximal end of the artery. (E) Division of the adductor magnus tendon for better exposure of the vessel. (F) Popliteal artery freed of the venous plexus and mobilized between two tapes.

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taken not to injure the long saphenous vein, which is located slightly posterior outside the sartorius. After the deep fascia is opened, the sartorius muscle is retracted medially. The dissection is continued from the angle of the upper incision, which is bordered by the vastus medialis laterally and the sartorius medially and posteriorly. By retracting these two muscles, one encounters the tendon of the adductor magnus (Fig. 30.4C and D), which hides the most proximal portion of the popliteal artery at its emergence from the adductor canal. The highest genicular artery pierces the deep fascia; it should be identified and preserved (Fig. 30.4E). The tendon of the adductor magnus at its insertion on the femur is divided to facilitate exposure of the popliteal vessels. A thin fascial structure covering a layer of adipose tissue surrounds the vascular

bundle. The vascular sheath is opened longitudinally. The two satellite popliteal veins are located lateral and posterior to the artery. Often, communicating venous tributaries between the medial and lateral popliteal veins cross the artery, necessitating their division and ligation (Fig. 30.4C). The popliteal artery is then freed in its segment chosen for the selected surgical procedure. Usually a 3- to 4-cm length is suitable for its control (Fig. 30.4F). In exposing the popliteal vessels, it is essential to identify the saphenous nerve and retract it out of the field. The thick adipose tissue layer must be disassociated from the vascular bundle, which is relatively deep and is situated behind the lower portion of the femur shaft. The adipose layer is covered by a thin aponeurotic sheath, which has to be opened before the blood vessels are reached.

Chapter 30 The Lower Extremity

The vascular sheath is common to the artery and vein. The vein has a thick wall and may be confused at times with the artery, to which it is intimately attached by a dense perivascular tissue. Because of this tissue, the separation of the two vessels may sometimes be difficult. The artery is usually surrounded by the venous plexus formed by collateral veins between the two medial and lateral popliteal veins. The advantages of medial exposure stem from the fact that the supine position of the patient affords easy access also to the femoral artery and to the saphenous vein without any difficulty and with relatively little trauma.

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A

Medial Approach to Entire Popliteal Artery As in the previous exposure, the patient is placed in the supine position, with the extremity in slight external rotation and the knee in a 30° flexion, supported with a rolled sheet placed under it. A curved skin incision is made along the anterior border of the sartorius muscle in the lower one-third of the thigh and extended across the knee joint along the posteromedial edge of the tibia (Fig. 30.5A). The deep fascia is incised anteriorly to the sartorius muscle, and the popliteal space is entered below the adductor magnus tendon, in the lower angle of which four muscles are identified and mobilized at their lower insertions. The sartorius, semimembranosus, gracilis, and semitendinosus muscles are inserted in that order and are transected near the tibia (Fig. 30.5B). Next, the origin of the medial head of the gastrocnemius muscle is divided near the medial femoral condyle through its musculotendinous portion. After division of these muscle insertions, the exposure of the popliteal vessels from the proximal end through their division into anterior and posterior tibial arteries becomes easy. As in the previously described procedure, the adipose tissue layer and its thin fascia are displaced until the vascular bundle is exposed. The artery lies medial to it, and the veins are posterior and lateral to it. A venous plexus is usually present around the artery after the sheath has been opened. These communicating vessels between the two popliteal veins have to be dissected away from the arterial wall for free access to the artery (Fig. 30.5C). The distal portion of the popliteal may not be entirely accessible, in which instance the soleus muscle may have to be split open to expose the bifurcation of the artery. After the vascular procedure is completed, the tendons and muscular structures are reconstituted, with interrupted mattress sutures used for the approximation of the divided ends. Of these, the reconstitution of the medial head of the gastrocnemius is most important. Because catgut ligatures may not hold, it is important that the sutures be of nonabsorbable material. With this type of repair, there is no weakness of or difficulty with the knee joint postoperatively. Although the operative time is prolonged because of the reconstitution of the divided musculotendinous structures, the technical requirements for good exposure of the popliteal artery at this level justify the extra effort put into it.

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C FIGURE 30.5 Medial exposure of the entire popliteal artery. (A) Position of the extremity and the line of incision. (B) IdentificatIon of divided muscles covering the popliteal artery: (1) semitendinosus, (2) gracilis, (3) sartorius, and (4) semimembranosus muscles. (C) Popliteal artery exposed, freed, and mobilized between two tapes.

Medial Approach to Distal Popliteal Artery For exposure of the distal popliteal artery (Fig. 30.6), the patient is placed in the supine position, with the knee flexed about 30° and supported by a rolled sheet under it. A medial exposure is used, as for the previous two approaches to the popliteal artery. The skin incision starts about 1 cm below the posterior border of the medial condyle of the femur and is extended parallel to the posteromedial border of the tibia and about 1 cm behind it (Fig. 30.6A). The length of the incision is about 8 to 10 cm. In carrying out the skin incision, one should take care to avoid injury to the saphenous vein except for its branches, which are divided and ligated.

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Part IV Surgical Exposure of Vessels

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FIGURE 30.6 Medial exposure of the distal popliteal artery. (A) Position of the limb, knee flexed, and the line of skin incision. (B) Exposure of the crural fascia and the line of incision. (C) Fascia incised, exposing the vascular bundle. (D) Exposure of the distal popliteal vessels and the arcade of the soleus muscle. (E) Popliteal freed and mobilized.

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The crural fascia is exposed and incised below the tendons of the semitendinosus and gracilis. After the deep fascia is incised from end to end, the medial head of the gastrocnemius is retracted posteriorly and medially, thus exposing the soleus muscle and the neurovascular bundle (Fig. 30.6D). The latter is usually situated deep against the bony surface, which is covered by the popliteus. The vascular sheath is opened, and the first structures in the bundle to appear are usually two popliteal veins, one posteromedial and the other anterolateral. As in the previous segments of the popliteal, a number of communicating veins between the two popliteals are present, necessitating their division and ligation to expose the artery. Its distal dissection and mobilization may have to be achieved by division of the arcade of the soleus muscle, which covers the bifurcation of the popliteal at this level. The tibial nerve, which lies medial and posterior to the vessels, should be protected against any possible injury during the retraction of the artery. Tapes are placed about the popliteal artery (Fig. 30.6E). By a combined motion of slight elevation and medial traction, the artery comes into view. Advantages of exposing the distal popliteal artery are that at this level there are usually no significant collateral vessels arising either from the popliteal or from the posterior tibial and anterior tibial arteries below. Although this segment is smaller than the proximal popliteal, the

infragenual segment is of sufficient caliber for easy graft attachment. This segment tends to be better preserved than and is usually free of atheromatous degenerative changes relative to the proximal popliteal. Should the exposure just described be insufficient, a proximal extension of the incision with division of the tendons may be necessary, as described previously for the exposure of the entire popliteal artery. Posterior Approach to Popliteal Artery The classic approach to the popliteal artery is the posterior approach (Fig. 30.7). The neurovascular structures appear superficial, and their exposure necessitates no muscle sections. If the vascular procedure is confined to the popliteal artery, this approach to the vessel is obviously advantageous. However, under other circumstances, there are a number of disadvantages that contraindicate its exposure through the posterior incision. The patient is placed in a prone position, with the leg slightly flexed and supported by a small pillow under the ankle. The length of the skin incision may depend on whether only the proximal or the entire popliteal is exposed. In the former, a median vertical incision above the popliteal fold is carried out. For the lower popliteal, the skin incision starts from the middle of the flexion fold of the knee and extends distally in a straight

Chapter 30 The Lower Extremity

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FIGURE 30.7 Posterior approach to the popliteal artery. (A) Lines of incision. (B) Popliteal fascia with its line of incision and short saphenous vein accompanied by the medial sural cutaneous nerve. (C, D) Transfascial exposure of the neurovascular bundle.

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line in the depression between the two heads of the gastrocnemius. Exposure of the entire popliteal artery requires an extended skin incision both above and below the knee flexion fold (Fig. 30.7A). The classic median skin incision crossing the flexion fold of the joint perpendicularly may result in a retractile scar, thus preventing a full extension of the knee joint. Because of this possibility, an S-shaped skin incision is used in most instances, as indicated in Figure 30.7A. After the skin flaps are reflected, the deep fascia is opened longitudinally in the midline. The short saphenous vein pierces the fascia at this level, as does the posterior cutaneous nerve of the thigh (Fig. 30.7B). After the deep fascia is opened, the tibial and peroneal nerves are identified. The sciatic nerve can also be identified at a more proximal level where the nerve usually divides into the two branches. The neural structures

are the most superficial and lateral. The popliteal vein is medial to the nerve and can be exposed easily by following the short saphenous vein. The sheath surrounding the vessels is opened in the same fashion as in the exposure described above. The artery lies medially and is the deepest structure of the three in the neurovascular bundle. The distal portion of the popliteal artery is usually surrounded by a venous plexus resulting from the communicating branches between the two popliteal veins. The two heads of the gastrocnemius must be retracted to allow access to the distal portion of the popliteal. If more distal dissection is necessary, the soleus muscle must be exposed, because the neurovascular bundle plunges under it. After incision of the latter, the bifurcation of the popliteal artery into the anterior tibial and the tibioperoneal trunk and its bifurcation into the posterior tibial and peroneal can be easily exposed.

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Part IV Surgical Exposure of Vessels

Leg Arteries Anatomic Review The leg arteries are situated between the inferior part of the tuberosity of the tibia and the bases of the malleoli. The neurovascular bundles of the leg are situated in compartments provided by the deep crural fascia and its septa. Figure 30.8 depicts a cross-section through the upper third of the leg. As indicated in this diagram, the leg has four compartments: 1) anterior, 2) lateral, 3) superficial posterior, and 4) deep posterior. The anterior compartment is bounded anteriorly by the enveloping fascia, posteriorly by the interosseous membrane and the anterior surface of the fibula, medially by the lateral surface of the tibia, and laterally by the anterior intermuscular septum. It contains the anterior tibial, extensor digitorum longus, extensor hallucis longus, and peroneus tertius muscles, the anterior tibial vessels, and the anterior tibial nerve (deep peroneal). The lateral compartment is the smallest and is situated between the peroneal intermuscular septa. It contains the termination of the common peroneal nerve, the superficial peroneal nerve, and the peroneal longus and brevis muscles. The superficial posterior compartment comprises the gastrocnemius, soleus, and plantaris muscles. The combined tendons of the two previous muscles are the tendo calcaneus, or Achilles tendon, which inserts into the distal half of the posterior surface of the calcaneus. The deep posterior compartment is demarcated from the superficial muscles by a fascial septum that extends between the fibula and the medial border of the tibia. The posterior tibial muscle arises from the interosseous membrane and adjoining part of the tibia and fibula. In addition, the flexor digitorum longus and flexor hallucis

longus arise from the posterior surface of the tibia and fibula, respectively. The posterior tibial and the peroneal arteries and their satellite veins, as well as the tibial nerve, are situated in the deep posterior compartment.

Exposure of Posterior Tibial Artery Proximal Segment For the exposure of the proximal posterior tibial artery, a 10-cm skin incision is made at mid-calf level behind the posteromedial border of the tibia (Fig. 30.9A). After incision of the deep fascia (Fig. 30.9B), the gastrocnemius muscle is retracted posteriorly. Exposure of the posterior tibial vessels can be carried out either through a transsoleus division or by detaching the latter muscle from its tibial insertion. Our preference is the former approach. The soleus is transsected along its fibers, and the posterior tibial vessels are easily exposed (Fig. 30.9C). The artery is freed from its surrounding venous plexus and its two satellite veins. Care should be taken to avoid injury to the posterior tibial nerve in the process of mobilizing the vessels (Fig. 30.9D). Distal Segment Exposure of the distal posterior tibial artery is carried out in the lower third of the leg above the internal malleolus (Fig. 30.10A). After incision of the superficial fascia, the Achilles tendon is mobilized and retracted posteriorly. The deep fascia is then incised anteriorly, thus exposing the posterior tibial vessels (Fig. 30.10B). The flexor digitorum longus and flexor hallucis longus are situated posterior to the vessels. As in the preceding technique, the artery is freed after division of the communicating veins between the two tibial veins (Fig. 30.10C). The posterior tibial nerve in the lower third is situated posterior to the vascular bundle and should be carefully retracted to avoid any possible injury to it. Exposure of Anterior Tibial Artery The anterior tibial artery is composed of two distinct segments: 1.

2.

the upper third, or arched, segment, situated behind and immediately medial to the neck of the fibula and crossing the interosseous membrane; and the anterior tibial trunk proper, coursing the entire length of the anterior tibial compartment.

Exposure of the arched segment of the anterior tibial artery is best carried out through the transfibular approach (see below). Exposure of Upper Segment FIGURE 30.8 Cross-section through the upper third of the leg, depicting the location of the three major neurovascular bundles and the four compartments: (1) anterior, (2) lateral, (3) superficial posterior, and (4) deep posterior.

The patient is placed in the supine position, with the knees slightly flexed and supported by a rolled sheet, the foot being maintained in slight internal rotation. A long skin incision of about 8 to 10 cm is made along the classic line for the ligature of the artery (Fig. 30.11A). Proximally,

Chapter 30 The Lower Extremity

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FIGURE 30.9 Medial exposure of the proximal posterior tibiaI artery. (A) Line of skin incision. (B) Exposure of the deep fascia and its line of incision. (C) Transsoleus muscle exposure of the vascular bundle. (D) Freeing and mobilization of the posterior tibial artery.

this line starts medial to the head of the fibula and ends in the middle of the anterior surface of the ankle on the lateral visible edge of the tendon of the anterior tibial muscle. The skin incision is carried down to the fascia. It is important to determine, by digital palpation, the groove between the anterior tibial and extensor digitorum longus. With the index finger, one separates the interspace of the muscles until it reaches the neurovascular bundle located on the anterior surface of the interosseous membrane. The vessels are located deep to the extensor and lie slightly lateral to the incision. By gentle retraction of the muscles, the neurovascular bundle is exposed. The dissection of the artery from the satellite veins and anterior tibial nerve can then be achieved (Fig. 30.11). The mobilization of the various components of the neurovascular bundle may sometimes be difficult when the muscles are heavy and bulging. So that any undue pressure and trauma can be avoided, it is best to extend the incision both proximally and distally to release the pressure from the adjacent structure. Exposure of Distal Segment The skin incision, 6 to 8 cm long, follows the same line for the exposure of the anterior tibial artery (Fig. 30.12A), as mentioned above.

The superficial fascia is opened along the same line as the skin incision. The tendon of the anterior tibial muscle is identified, mobilized, and retracted medially, and the tendon of the extensor digitorum longus is retracted laterally (Fig. 30.12B). The neurovascular bundle is situated lateral to the anterior tibial muscle and medial to the extensor digitorum longus. The tibial artery is situated in the background and is accompanied by its two veins. The anterior tibial nerve is located medial to it. At this level, the artery is more superficial and access is easy. Extension of the exposure can be carried out proximally by extending the incision and separating the muscles as indicated or, if necessary, distally toward the dorsalis pedis by dividing the annular ligament of the ankle (Fig. 30.12C).

Combined Exposure of Distal Popliteal Artery and Its Trifurcation Exposure of the distal popliteal artery and of the posterior tibial and peroneal arteries can be achieved by the medial approach, as described above. Although this approach offers easy access to the distal popliteal and posterior tibial, exposure and mobilization of the peroneal may be

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difficult in some instances. Under these circumstances, a lateral exposure may offer greater advantages. Medial Exposure The distal popliteal artery and the tibioperoneal trunk, the latter a direct continuation of the former, frequently display a combination of lesions of variable degrees, which, if inadequately repaired, may be the main cause of femoropopliteal reconstructive failures. In atherosclerotic lesions, the popliteal–tibioperoneal trunk junction is often the site of stenotic or occlusive changes. This arterial segment as it enters the deep compartment of the leg is in contact with the tendinous arch of the soleus. As a result of its passage through the arch, this arterial segment undergoes chronic microtrauma that leads to mural changes, not unlike the arteriosclerotic changes in the femoral–popliteal junction in Hunter’s canal. Palma coined the term “soleus syndrome” for the arterial lesion of the popliteal–tibioperoneal junction, thus identifying its initiating cause. The technique for combined exposure of the distal popliteal and its leg branches includes the following steps:

A

B 1. 2. 3.

4. C FIGURE 30.10 Line of skin incision and medial exposure of the distal posterior tibial artery.

5.

medial leg exposure of the infragenual popliteal as described under Exposure of Distal Popliteal Artery; extension of the skin incision by 10 to 12.5 cm and exposure of the soleus muscle; splitting of the arcade of the soleus and part of its muscular portion to allow adequate access to the neurovascular bundle (a variant of transecting of the soleus over the neurovascular structures is detachment of the muscle from its insertion on the tibia and retracting it laterally); freeing of the tibioperoneal trunk from its satellite veins and posterior tibial nerve, and excision of the venous plexus surrounding the artery for its adequate mobilization; and identifving and mobilizing the trifurcation (Fig. 30.13).

FIGURE 30.11 Anterolateral exposure of the proximal anterior tibial artery. (A) Line of skin incision. (B) Exposure of the neurovascular bundle. (C) Mobilized anterior tibial artery and retraction of the anterior tibial nerve.

A

B

C

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FIGURE 30.12 Line of skin incision and anterolateral exposure of the distal anterior tibial artery.

A

B

C

tal popliteal, it is often difficult, if not impossible, to direct the catheter into the anterior tibial because of its nearly right-angle takeoff. To obviate this difficulty whenever indicated, one should perform the arteriotomy on the titioperoneal trunk opposite the origin of the anterior tibial. Lateral or Transfibular Exposure

FIGURE 30.13 Combined exposure of the distal popliteal artery and its trifurcation.

In popliteal artery embolism with propagating thrombosis into the tibioperoneal trunk and beyond, complete exposure of these critical vessels will allow a thromboembolectomy under direct vision, especially if the thrombus extends into the anterior tibial artery. When the Fogarty catheter is introduced, even as close as the dis-

This approach offers easy access not only to the peroneal but also to the distal popliteal and the anterior and posterior tibials. Exposure through the lateral approach by the transfibular route (Fig. 30.14) follows essentially the method described by Henry, to which a few minor modifications were introduced subsequently by others. The patient is placed in the supine position, with the leg semiflexed and internally rotated. The skin incision begins over the lower part of the biceps tendon and is carried distally below the knee over the length of the fibula for approximately 12 to 15 cm. It begins 5 to 6 cm above the head of the fibula and continues about the same length distally (Fig. 30.14A). The landmarks for the skin incision are the cord of the biceps tendon above the head of the fibula in the center, and the groove that separates the soleus from the fibular head distally. This groove is the key to the plane of cleavage between the peroneal and calf muscles. After the skin and superficial fascia are divided at the upper end of the incision, the deep fascia is opened at the medial edge of the biceps tendon. The common peroneal nerve is exposed and is placed on a rubber vessel loop for gentle traction. The division of the deep fascia is carried downward along the course of the nerve along the posterior margin of the biceps tendon. The fascial origin of the peroneus longus muscle lies directly over the groove in which the nerve passes forward across the neck of the fibula. This fascia is divided. A definite plane, the lateral intermuscular septum, between the soleus muscle posteriorly and the peroneus longus muscle anteriorly, is easily developed, and, when the muscles are separated, the later-

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Part IV Surgical Exposure of Vessels FIGURE 30.14 Transfibular approach to the distal popliteal artery and its three branches. (A) Line of skin incision. (B) Transsoleus exposure and freeing of the fibuIa. (C) Resected fibula and exposure of the distal popliteal artery, anterior tibial artery, tibioperoneal trunk, and the peroneal artery.

al border of the fibula is immediately exposed (Fig. 30.14B). By the use of sharp dissection and a periosteal elevator, the periosteum can be readily stripped from the fibula and its division accomplished by means of a Gigli saw (Fig. 30.14C). Although the fibula head can be removed without causing any instability of the knee joint, adequate exposure of the distal popliteal artery and its three branches can be achieved without removing it. The upper third or half of the fibula is resected subperiosteally, distal to its head. The ends of the severed fibula are smoothed with rongeurs or beveled laterally to avoid any injury to the adjacent structures, especially to the peroneal nerve. The medial aspect of the periosteum is incised. Proximal and distal dissection reveals the presence of the lower popliteal segment and its three branches. Mobilization of the selected artery is achieved as previously described in the other techniques for the leg arteries. The entire arterial tree is now easily accessible, which thus makes possible the direct evaluation of the entire outflow tract of the leg. Pitfalls to be avoided are injury to the peroneal nerve and the adjacent veins or arteries. Resection of the fibula per se does not result in any subsequent difficulties.

Advantages of this exposure are multiple. The arch of the anterior tibial, deeply situated, is accessible without resulting in injury to it or in subsequent hemorrhage, which may occur through another approach. With the retraction of the soleus muscle posteriorly and the peroneus longus muscle anteriorly, the vessels are easily seen. The resected portion of the bone is not replaced. Another advantage of this approach is that the procedures involving bypass grafts from the femoral or popliteal levels can be carried out with the patient in the supine position as indicated. It also offers the possibility of performing a local endarterectomy under direct vision with good control of the upper and lower parts of the vessel, a method that cannot be easily achieved by the medial approach.

Dorsalis Pedis Anatomic Review The dorsalis pedis artery is a continuation of the anterior tibial and passes forward from the ankle joint along the medial (tibial) side of the dorsum of the foot to the proximal part of the first intermetatarsal space, where it

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gives off the second, third, and fourth dorsal metatarsal arteries. The first dorsal metatarsal artery, the termination of the dorsalis pedis, courses forward on the first interosseous space and, at the cleft between the first and second toes, divides into two branches, one of which passes beneath the tendon of the extensor hallucis longus and is distributed to the medial border of the great toe. The other bifurcates to supp]y the adjoining side of the great and second toes. The deep plantar artery descends into the sole of the foot between the two heads of the first interosseous dorsalis and unites with the termination of the lateral plantar artery to complete the plantar arch. It sends a branch along the medial side of the great toe and continues forward along the first interosseous space as the first plantar metatarsal artery, which bifurcates for the supply of the adjacent side of the first and second toes.

Exposure of Dorsalis Pedis

FIGURE 30.15 Dorsalis pedis artery and its major branches.

divides into two branches, the first dorsal metatarsal and the deep plantar (Fig. 30.15). In its course, the vessel rests on the articular capsule of the ankle joint, the talus, navicular, and second cuneiform bones. Near its termination, it is crossed by the first tendon of the extensor digitorum brevis. On the medial (tibial) side is the tendon of the extensor hallucis longus, and on its lateral (fibular) side, the first tendon of the extensor digitorum longus. The artery is accompanied by two satellite veins and is covered by the skin, fascia, and cruciate ligament; near its termination, it is crossed by the first tendon of the extensor digitorum brevis. Branches On its medial side, the branches are thin walled and usually connect with the plantar branches of the posterior tibial. On the lateral side, the branches are much larger (Fig. 30.15). The medial tarsal arteries are two or three small branches that ramify on the medial border of the foot and join the medial malleolar network. The lateral tarsal artery passes in an arched direction laterally and supplies the extensor digitorum brevis and the joints of the tarsus. The arcuate artery arises a little anterior to the lateral tarsal artery and passes laterally to anastomose with the lateral tarsal and lateral plantar arteries. This vessel

Exposure of the dorsalis pedis is carried out close to the ankle and extends about 5 to 7.5 cm distally (Fig. 30.16). The incision is carried down through the skin, subcutaneous tissue, fascia, and the cruciate ligament. As mentioned, the artery is accompanied by two satellite veins and the termination of the deep peroneal (anterior tibial) nerve. In mobilizing the artery care should be taken to avoid damaging the collaterals, which not only supply the dorsum of the foot but in the absence of a posterior tibial provide also the main inflow to the plantar arteries. In reconstructing the leg arteries in occlusive arterial disease of the infrainguinal arteries, it is essential to determine the patency of the pedal vessels, both dorsal and plantar, and the degree of patency, an important index for achieving successful revascularization of the most distal part of the limb.

Plantar Arteries Anatomic Review The posterior tibial artery in its most distal parts approaches the medial side of the leg. At its bifurcation, it is situated midway between the medial malleolus and the medial process of the calcaneal tuberosity. Here it divides beneath the origin of the abductor hallucis into the medial and lateral plantar arteries. The medial plantar artery, much smaller than the lateral, passes forward along the medial side of the foot. At the base of the first metatarsal it passes along the medial border of the first toe, anastomosing with the first dorsal metatarsal artery (Fig. 30.17). Small superficial digital branches accompany digital branches of the medial plantar nerve and join the plantar metatarsal arteries of the first three spaces.

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Part IV Surgical Exposure of Vessels FIGURE 30.16 Exposure of the dorsalis pedis (see text for details).

FIGURE 30.17 Major arteries and branches of the foot seen in the lateral position.

The lateral plantar artery, much larger than the medial, passes laterally and forward to the base of the fifth metatarsal bone. It unites with the deep plantar branch of the dorsalis pedis artery, thus completing the plantar arch. The arch is deeply situated and extends from the base of the fifth metatarsal bone to the proximal part of the first interosseous space to complete the plantar arch. It is con-

FIGURE 30.18 Exposure of posterior tibial artery and its bifurcation (see text for details).

vexed forward and lies below the base of the second, third, and fourth metatarsal bones and the corresponding interossei muscles. The plantar arch, besides distributing numerous branches to the muscles, skin, fasciae, and the

Chapter 30 The Lower Extremity

sole, gives off the perforating and plantar metatarsal branches.

Exposure of Terminal Posterior TibiaI Artery and Origin of Plantar Arteries Revascularization of the plantar structures via the plantar branches can be achieved by implanting the graft behind the medial malleolus (Fig. 37.18). By division of the laciniate ligament, which covers the tendons, the blood vessels and the nerve are exposed at the junction between the heel and the plantar surface. In the presence of complete occlusion of the posterior tibial, indirect revascularization of the plantar flap can best be achieved by revascularizing the dorsalis pedis, provided the collaterals of the lateral plantar artery anastomose with the plantar branches. Repair of plantar arteries may be indicated in traumatic lesions and may require microvascular technique, these branches being otherwise too small for reanastomosis.

Bibliography Anson BJ, McVay CB. Surgical anatomy, 5th ed. Philadelphia: WB Saunders, 1971:1241. Arnulf C, Benichoux R. Découverte large de la fémoropoplitée (tiers inférieur de la fémorale et totalité de la poplitée). Lyon Chir 1949;44:203.

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Cormier JM, Sautot J, et al. Nouveau traité de technique chirurgicale. Artéres Veines Lymphatiques 1970;5:628. DeBakey ME, Creech O Jr, Morris GC. Aneurysm of thoracoabdominal aorta involving the celiac, superior mesenteric and renal arteries. Ann Surg 1956;144:549. Elkin DC. Exposure of blood vessels. JAMA 1946;130:421. Elkins RC, DeMeester TR, Brawley RK. Surgical exposure of the upper abdominal aorta and its branches. Surgery 1971;70:622. Feller I, Woodburne RT. Surgical anatomy of the abdominal aorta. Ann Surg (Suppl) 1961;154:239. Fiolle J, Delmas J. Découverte des vaisseaux profonds par des voies d’accès larges. Paris: Masson et Cie, 1940. Haimovici H. Arterial circulation of the extremities. In: Schwartz CJ, Werthessen NT, Wolf A (eds). Structure and function of the circulation, vol 1. New York: Plenum Press, 1980:425–485. Haimovici H, Steinman C, et al. Excision of a saccular aneurysm of the upper abdominal aorta involving the major branches, iliac-visceral revascularization via bypass graft. Ann Surg 1964;159:368. Henry AK. Extensile exposure, 2nd ed. Baltimore: Williams & Wilkins, 1957:300. Palma EC. The soleus syndrome: hemodynamic arteriosclerosis of the posterior tibial artery and its two branches treatment. J Cardiovasc Surg 1978;19:615. Rob C. Extraperitoneal approach to the abdominal aorta. Surgery 1963;53:87. Shumacker HB Jr. Midline extraperitoneal exposure of the abdominal aorta and iliac arteries. Surg Gynecol Obstet 1972;135:791.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART V Occlusive Arterial Diseases

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury Walter N. Durán, Peter J. Pappas, Mauricio P. Boric, and Robert W. Hobson II

Management of acute limb ischemia continues to be a formidable challenge for the vascular surgeon. Although use of the Fogarty balloon embolectomy catheter facilitates extraction of arterial emboli and thrombus (1), and the administration of heparin limits distal propagation of thrombus beyond the point of vascular obstruction and reduces the incidence of recurrent embolus and thrombosis, high rates of limb loss and mortality continue to be documented (2). Improved efficiency of thromboembolectomy, as confirmed by operative arteriography and vascular endoscopy (3), has been reported. In addition, operative use of intra-arterial lytic therapy has expanded our ability to recanalize distal vascular beds and salvage ischemic limbs (4). A better understanding of the pathophysiology of limb ischemia–reperfusion also may result in opportunities for further therapeutic intervention. This chapter reviews the pathophysiology of skeletal muscle ischemia–reperfusion injury in acute limb ischemia as well as opportunities for clinical intervention. Regardless of the etiology of ischemia (Table 31.1) as caused by embolus, thrombosis, or trauma, a period of devascularization or ischemia and a following period of revascularization or reperfusion are of central importance in understanding the complications of this syndrome. Several factors influence the course of subsequent events. The

level and severity of vascular obstruction are crucial, resulting in the often-quoted golden period of 6 to 8 hours of profound ischemia, after which irreversible cellular death may occur regardless of intervention. Limb loss due to the status of the limb as well as the patient’s underlying cardiovascular disease has been reported in 15% to 40% of cases, and the mortality rate has been as high as 25% to 50% (2). Historically, complications associated with ischemia secondary to untreated embolus (Table 31.2) have been characterized and emphasize the value of current methods of management in successfully salvaging ischemic limbs (5). Acute limb ischemia caused by embolism is associated with a cardiac origin in more than 75% of cases, and 80% of these emboli lodge in the aortoiliac or femoral arteries (6). Recent acute myocardial infarctions with mural thrombus or arterial fibrillation account for a substantial number of emboli. The morbidity and mortality of operations in patients with recent myocardial infarction will exceed those for patients who undergo operations for emboli without associated acute myocardial infarction (7,8). Acute arterial thrombosis is another major cause of limb ischemia (Table 31.1), frequently related to peripheral atherosclerotic disease. Central factors including congestive heart failure and shock contribute to

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TABLE 31.1 Etiology of acute limb ischemia Embolus Cardiac Atrial fibrillation Valvular heart disease Endocarditis Myocardial infarction (with mural thrombus) Aortic and peripheral arterial aneurysms Ulcerated atherosclerotic plaque with intraplaque hemorrhage Paradoxical embolus Atrial myxoma Cardiomyopathy Thrombosis Atherosclerotic occlusive disease Aortic and peripheral arterial aneurysms Intraplaque hemorrhage with arterial stenosis and occlusion Hypercoagulable states (c or S protein deficiencies) Entrapment syndromes Stasis/low-flow state Drugs of abuse Trauma Penetrating Blunt Interventional vascular procedures Reproduced by permission from Hobson RW. Acute limb ischemia. Semin Vasc Surg 1992;5:1–3.

the incidence of these occlusions. In addition, intraplaque hemorrhage as described in carotid occlusive disease also contributes to peripheral vascular occlusions (9). Consequently, the reported range of mortality from acute limb ischemia due to embolus or thrombosis frequently relates to not only the type and severity of the peripheral occlusive disease, but also the severity of underlying cardiac disease and the ill effects of delayed reperfusion. The clinical presentation of acute limb ischemia and reperfusion was described accurately by Haimovici as the myonephropathic–metabolic syndrome. Blaisdell observed these changes when revascularization of the acutely ischemic limb was performed beyond the range of 6 to 8 hours, resulting in the following systemic effects: acidosis; hyperkalemia as intracellular potassium was lost due to further tissue injury and accelerated tissue death, possibly leading to cardiac arrest; elevated creatine phosphokinase and serum glutamic–oxaloacetic transaminase levels; myoglobinemia–myoglobinuria, possibly leading to renal failure; activation of the clotting cascade, resulting in accumulation of extracellular fluid and, in some instances, cases of acute pulmonary insufficiency (10). Renal failure due to tubular deposition of myoglobin occurred and contributed to the development of multiorgan failure with its high mortality rate. In patients with profoundly ischemic limbs reflected clinically by the presence of pain, paralysis, and neural damage, as well as those corresponding to the classic description of the blue mottled extremity (10), the surgeon must exercise considerable judgment in defining the indications for revascularization, as primary amputation must be considered in these circumstances.

TABLE 31.2 Complications of untreated arterial embolism Gangrene Anischemic embolism Chronic ischemia Marked ischemia and early death Silent embolism Undetermined

27% 25.3% 18.3% 13% 5.7% 10.7%

Modified from Haimovici H. Peripheral arterial embolism. A study of 330 unselected cases of embolism to the extremities. Angiology 1950;1:20.

Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury The basis for tissue injury during ischemia depends on depletion of tissue oxygen and energy substrates with the predominance of anaerobic metabolism. Adenosine triphosphate (ATP) stores are maintained at the initial level for up to 3 hours, as a result of the depletion of creatine phosphate with conversion of creatine phosphate to creatine and inorganic phosphate (11). With more prolonged ischemia, there is a progressive fall in the ATP level, glycogen continues to be metabolized to lactate, and finally the continued consumption of ATP exceeds its production. The microvasculature is a susceptible target for ischemia, with cellular injury occurring after intervals of as short as 30 minutes of ischemia, as evidenced by changes in cellular membrane permeability (Fig. 31.1) and progressive cellular edema (12,13), as well as early changes of the no-reflow phenomenon (13). Irreversible changes in skeletal muscle occur after 4 to 6 hours of ischemia. However, the injury associated with acute arterial occlusion is not limited to the period of ischemia alone. The observation that reperfusion induces further damage has led to the concept of oxygen-derived free radical injury (14–16). The proposed sequence of events leading to microvascular injury upon reperfusion of ischemic tissue appears to be caused by the reintroduction of molecular oxygen and the subsequent production of oxidants derived from xanthine oxidase (Fig. 31.2). In the presence of ironcontaining compounds such as transferrin, lactoferrin, or hemoglobin (17,18), this iron-catalyzed Haber–Weiss reaction, or the so-called superoxide-driven Fenton reaction, occurs by the interaction of the superoxide anion and hydrogen peroxide, resulting in the formation of the toxic hydroxyl ion (◊OH). No endogenous scavengers exist for the hydroxyl ion, which then initiates lipid peroxidation, resulting in altered membrane permeability as well as the chemoattraction of leukocytes. The leukocytes are then capable of releasing oxygen-derived free radicals and proteases, leading to further microvascular injury (Figs. 31.2 and 31.3). Support for the role of oxygen-derived free radicals and microvascular dysfunction comes from experiments using free radical scavengers. Compounds

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FIGURE 31.2 Proposed sequence of events leading to microvascular injury observed on reperfusion of ischemic tissue. (Reproduced by permission from Kubes P, Kvietys PR, Granger DN. Ischemia–reperfusion injury. In: Morillaro NA, Taylor AE, eds. The Pathophysiology of the Microcirculation. Boca Raton, FL: CRC Press, 1994.)

FIGURE 31.1 Microvascular permeability alterations in ischemia–reperfusion injury in striated muscle. The rat cremaster muscle was prepared for intravital microscopy as described by Suval et al. (1987). The animal received fluorescein isothiocyanate–dextran-150, a fluorescent macromolecular tracer. (A) Control observation; note that the fluorescent macromolecule is confined to the vascular compartment. (B) Observations made within 10 minutes of onset of reperfusion; the fluorescent macromolecular tracer has extravasated into the interstitial space, and there are few microvessels showing signs of the no-reflow phenomenon (dark vessels on right-hand side). (Reproduced by permission from Suval WD, Durán WN, et al. Microvascular transport and endothelial cell alterations precede skeletal muscle damage in ischemia–reperfusion injury. Am J Surg 1987;154:211–218.)

such as superoxide dismutase, catalase, mannitol, allopurinol, and deferoxamine have proved to be efficacious in reducing changes in microvascular permeability (19), and in reducing the severity of skeletal muscle infarction (20). These oxygen-derived free radicals depend upon the generation of superoxide anion through endothelial cell and leukocyte-stimulated chemical reactions. A major contribution comes from the conversion of xanthine dehydrogenase to xanthine oxidase. Endothelial cells have been

identified as a major site of localization of xanthine oxidase (21), while skeletal muscle cells appear to have a low concentration of xanthine dehydrogenase (22). However, based on measurements of xanthine dehydrogenase activity in isolated endothelial cells, it is estimated that skeletal muscle cells contain a significant amount of xanthine dehydrogenase. The significance of the endothelial cell in the microvascular dysfunction in skeletal muscle ischemia– reperfusion injury is underscored by the report that the conversion of xanthine dehydrogenase to xanthine oxygenase proceeds at a slow rate in skeletal myocytes (23). Nitric oxide (NO) has recently been implicated as one of the substances produced by vascular and perivascular cells that may play a role in microvascular injury induced by ischemia–reperfusion. Beckman et al. postulated that superoxide reacts with NO to yield secondary cytotoxic species including the hydroxyl radical. As a product of the metabolism of L-arginine, NO can be produced by most cells. Under normal conditions, NO is a strong vasodilator (23), enhances the transport of macromolecules across postcapillary venules (24), and may serve as an antiadhesive substance to protect the endothelium against leukocyte adherence (25). In this framework, the L-arginine-NO pathway represents an alternative or additional mechanism to produce hydroxyl radicals. It must also be kept in mind that peroxynitrite (ONOO-), the reaction product of superoxide and NO, is potentially more toxic than either superoxide or hydroxyl radical alone (26). However, its role in ischemia–reperfusion injury remains ill-defined and requires further investigation. In studying the pathophysiology of microvascular dysfunction in skeletal muscle ischemia–reperfusion, it is convenient to categorize changes related to the endothelium, the leukocyte, and their interactions at the microcirculatory level. Ultimately, these events are linked to

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FIGURE 31.3 Interactions between leukocyte (L) and endothelium (E) in ischemia–reperfusion injury. During ischemia, parenchymal cell energy stores are depleted. Macrophages or mast cells (M) may influence the process by the production and release of cytokines (e.g., IL-1). The endothelium appears to be the site capable of significantly converting xanthine dehydrogenase (XDH) to xanthine oxidase (XO) during ischemia and to be responsible for the formation of oxygen-derived free radicals (superoxide anion, O2; OH, hydroxyl radical). The endothelium also releases PAF. The adherent leukocyte also forms oxygenderived free radicals and through its myeloperoxidase (MPO) generates hypochlorous acid (HClO). Weak adhesion (rolling) is the result of interactions between P-selectin (P-sel; endothelium) and L-selectin (L-sel; leukocyte). Upon stimulation by PAF, the CD11/CD18 adhesion complex interacts with the endothelial ICAM-1, leading to firm adhesion. (Reproduced by permission from Durán WN, Suval WD, et al. In: Veith FJ, Hobson RW, et al., eds. Vascular Surgery: principles and practice. New York: McGraw-Hill, 1993.)

ischemia–reperfusion injury, and a better understanding of these pathophysiologic mechanisms may provide opportunities for successful clinical interventions.

Role of the Endothelium The endothelium participates in several functions in the maintenance of vascular homeostasis. Endothelial cells are involved in the control of blood flow, microvascular permeability, vessel contractility, angiogenesis, coagulation, leukocyte traffic, and immunity. These endothelial functions are modulated exquisitely by endogenous and exogenous factors (endocrine, paracrine, and intracrine regulation). Deviations from the normal balance owing to a deficiency or an excess of the regulatory factors may lead

to pathologic states. Blood flow regulation depends to a large extent on the presence of an intact endothelium. In responses to several agonists, endothelial cells produce NO, a substance closely related, or perhaps identical, to endothelium-derived relaxing factor (EDRF) (27), which stimulates cyclic guanylate cyclase and leads to vascular smooth muscle relaxation (28). The endothelium also produces endothelin, a powerful vasoconstrictor agent. Physical and chemical denudation or damage of the endothelium results in the loss of the ability to produce these vasoactive compounds. Microvascular permeability is controlled by a variety of chemical mediators that are activated by ischemia– reperfusion damage. These substances include plateletactivating factor (PAF), histamine, and bradykinin. These compounds can alter microvascular permeability to macromolecules by themselves or by a priming interaction between them (29). Their actions are also exerted both directly and through the activation of other vasoactive agents. They have in common the activation of intracellular calcium mobilization or calcium entry or both (30), and possibly of protein kinase C (31). The changes in endothelial cytosolic calcium levels also result in the release of the powerful vasoactive agents such as NO and endothelin. The endothelial lining normally offers a noncoagulant surface for blood flow. This is achieved by catalyzing the formation of antithrombin III and by the presence of surface thrombomodulin (32,33). It is well known that endothelial cells also prevent coagulation by synthesizing prostacyclin, which antagonizes the plateletaggregating activity of thromboxane A2. The endothelium also participates in maintaining patent blood vessels by reducing clots through the conversion of plasminogen to plasmin, which results in dissolution of fibrin clots. Conversely, endothelial cells decrease their production of anticoagulating agents and are stimulated to produce procoagulating substances during the injury. This endothelial cell anticoagulant-coagulant function is germane to ischemia–reperfusion injury, inasmuch as microvascular thrombi may be in part responsible for the no-reflow phenomenon reported in the literature. Endothelial cells participate in the immune response primarily through expression of antigens after activation by cytokines. Interleukin 1 (IL-1), tumor necrosis factor (TNF), and interferons are able to modulate immune responses on the endothelial cell surface. The relation between cytokines and endothelial cell biology was elegantly and extensively reviewed by Pober and Cotran (34). Control of endothelium–leukocyte adhesion is a main step in the regulation of transvascular traffic of leukocytes in inflammatory and immune responses. This critical step is the result of complex interactions between adhesion molecules expressed on the surface of the endothelium and of the leukocyte. The endothelium plays a major role in determining the adhesion of leukocyte to its surface. It is accepted that endothelium–leukocyte adhesion can occur by two processes: endothelium-dependent adhesion

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury

and leukocyte-dependent adhesion. The adhesive status of the endothelium can be modulated by fast processes (within approximately 15 minutes) and slow processes (within about 2 hours). Thrombin, leukotriene B4, and leukotriene C4 produce an increase in endothelial cell adhesiveness within 5 minutes (35,36). The fact that these are endothelialdependent adhesion processes is shown by the failure of monoclonal antibodies to the CD18 adhesion molecules on the leukocyte surface to prevent the heightened adhesive state produced by thrombin or leukotriene C4. Fast endothelial-dependent adhesion may be related to translocation of P-selectin (granule membrane protein 140, GMP-140), an adhesion molecule apparently stored in the Weibel–Palade bodies of endothelial cells (37). This hypothesis is supported by the fast surface expression of P-selectin induced by substances such as thrombin, histamine, and phorbol ester. Slow induction of endothelial adhesiveness to leukocytes involves the expression of an endothelium– leukocyte adhesion molecule (E-selectin, ELAM-1) (38). When human cultured endothelial cells are incubated with IL-1, a maximal increase in adhesive state is obtained after 4 hours. E-selectin is induced by several cytokines, including IL-1 and TNF. The induction of E-selectin, which is absent in unstimulated endothelial cells, requires de novo protein synthesis.

Role of the Neutrophil Although the pathologic changes occurring at the level of the endothelium result in increased membrane permeability and changes associated with reperfusion, evidence demonstrates that inflammatory neutrophils play an essential role in the pathophysiology of ischemia– reperfusion injury. Neutrophils produce superoxide anions by the activity of their membrane-bound nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which in the presence of molecular oxygen converts cytoplasmic NADPH to NADP+, H+, and 2O2. The oxygen-derived free radicals can then participate in subsequent production of the injurious hydroxyl ion. One method for observing the appearance of granulocytes in postischemic skeletal muscle injury has been the analysis of a granulocyte-specific enzyme, myeloperoxidase. Myeloperoxidase utilizes H2O2 produced by neutrophils to form hypochlorous acid (HClO), which is locally more toxic than superoxide or H2O2. Measurement of myeloperoxidase levels in skeletal muscle is interpreted as evidence for the participation of leukocytes in the ischemia–reperfusion injury process. The level of myeloperoxidase has been found to remain constant during the ischemia and to increase after 15 minutes to 1 hour of reperfusion (39). However, these observations do not necessarily confirm a cause-and-effect relation. To address this issue, however, several investigators have used leukocyte-depleted models to demonstrate

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a correlation between depletion and decreased severity of skeletal muscle injury. This has included use of leukopak filters (40), irradiated animal models (41), chemotherapeutically treated animal models (42), and monoclonal antibodies (38,43). These investigations have confirmed reduction in the severity of skeletal muscle injury when white blood cell depletion has been introduced into the model. Depletion also attenuates myocyte membrane injury and muscle contractile dysfunction and reduces the extent of postischemic lipid peroxidation and muscle necrosis (43). It also appears that neutrophil depletion attenuates ischemia–reperfusion-induced microvascular membrane injury and the leukocyte plugging that may be responsible in part for the capillary no-reflow phenomenon and the unevenness of reperfusion in some areas after an ischemic insult.

Endothelial Cell–Leukocyte Interactions The pathophysiology of ischemia–reperfusion injury involves a sequence of events requiring endothelial and leukocyte interaction (Fig. 31.3). The reduction in cellular energy stores and the release of oxygen-derived free radicals on introduction of molecular oxygen during reperfusion also results in the chemoattraction of leukocytes to the site of injury. This may also initiate the release of other chemoattractants such as PAF or leukotriene B4. These oxidants alter the adhesion properties of the endothelial cell surface by allowing the expression of intercellular adhesion molecules (ICAM-1, ICAM-2). The molecules are inducible proteins on the surface of the endothelium that modulate neutrophil adhesion in areas of inflammation. The leukocytes also have membrane-bound proteins designated as the CD11/CD18 complex, a so-called B-2 integrin, which is involved in regulating leukocyte– endothelial cell adhesion. The mechanisms that link xanthine oxidase-mediated oxygen free radical production to reperfusion-induced leukocyte activation, adhesion, and extravasation form the foundation for the events that are described in the ischemia–reperfusion injury. Firm adhesion of leukocytes to endothelium is preceded by a weak adhesion, also termed “rolling,” as observed during intravital microscopy. This weak adhesion occurs under rheologic conditions of relatively high shear rate. Nonetheless, leukocytes roll along the venular walls at rates about 100-fold slower than the local flow (44). The use of monoclonal antibodies to L-selectin has demonstrated its relation to leukocyte rolling (44) and, by inference, to the initiation of the leukocyte-endothelium adhesion process. On the endothelium, evidence obtained in vitro in laminar flow chambers under conditions mimicking venular shear rates confirms that P-selectin modulates leukocyte rolling (45). Importantly, histamine and thrombin are among the chemical mediators that modulate the translocation of P-selectin to the endothelial cell

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membrane. Strong adhesion requires the involvement of integrins and ICAM-1 and possible E-selectin. The adhesion molecules involved in successful migration have not been completely elucidated even though it is believed that E-selectin is not an absolute requirement for migration. Further insight has been derived from the administration of monoclonal antibodies prior to the induction of the ischemia–reperfusion protocol in animal models. Under baseline conditions, only a few leukocytes adhere to venular endothelium (two to four leukocytes per 100 mm vessel length). Upon reperfusion of postischemic tissue, the number of adherent leukocytes increased severalfold (46,47). The monoclonal antibody 60.3, which is directed against the b-chain of the CD18 complex, inhibited neutrophil adherence and attenuated extravasation of plasma proteins in the intestinal mucosa (48). Similarly, monoclonal antibody IB4, also directed against the CD11/CD18 glycoprotein adhesive complex, successfully inhibited the adhesion of leukocytes to venular endothelium induced by PAF in the intestine (49). In canine gracilis muscle, IB4 administered prior to ischemia has the ability to diminish the ischemia–reperfusion-induced increases in the microvascular solvent drag reflection coefficient (50). Similar results regarding leukocyte adherence and microvascular permeability to macromolecules have been reported by our group, using monoclonal antibodies against CD11b and CD18 in the rat cremaster muscle model (43). In addition, a linkage between adherence of neutrophils and severity of parenchymal injury was established in these experiments. Taken together, these studies suggest that prevention of leukocyte adherence and migration stabilizes the architecture of the endothelial cell as well as reducing the severity of post-reperfusion injury, and may represent a useful new therapeutic approach to ameliorate ischemia–reperfusion injury. Chemotactic agents have been implicated also in the attraction of neutrophils to the ischemic injury site. It is conceivable that oxygen free radicals, in combination with some plasmogen, mediate reperfusion-induced neutrophil infiltration. Nevertheless, if a plasmogen does exist that in combination with oxidants and iron would promote leukocyte adhesion, its identity remains unknown (38). One other potential direction for resolving this investigation may be the observation that peroxide can oxidize phospholipids that will then promote leukocyte adhesion. Leukotriene B4, a product of arachidonic acid metabolism, is a potent chemoattractant that is frequently implicated as a mediator of reperfusion-induced neutrophil infiltration. Several studies have demonstrated significant increase in leukotriene B4 production in tissue as well as in plasma following ischemia–reperfusion (51). Zimmerman et al. reported that pretreatment with either a lipoxygenase inhibitor or leukotriene B4 antagonists decreases the magnitude of reperfusion-induced granulocyte infiltration assessed by myeloperoxidase activity, providing the first direct linkage that leukotriene B4 accumulation, particularly in the intestinal vasculature, is a cause (rather than effect) of reperfusion-induced infiltration (52). Simi-

lar observations have been made in the rabbit model of lower torso ischemia–reperfusion injury (53). Experimental evidence supports a role for PAF in ischemia–reperfusion-induced damage of the vasculature (38,54). The concentration of PAF increases dramatically after 5 minutes of reperfusion of the ischemic canine intestine (55). Under certain conditions, substances similar to PAF may cause neutrophil infiltration and adhesion to postischemic venules. PAF is a short-lived phospholipid, a vasoconstrictor, a strong promoter of microvascular permeability, and a powerful chemoattractant for leukocytes.

Chemical Mediators and Signaling Molecules Eicosanoids have been considered as important chemical mediators in ischemia–reperfusion injury. However, no clear picture is currently available regarding the involvement or importance of these arachidonic acid derivatives in either the genesis or the consequences of ischemia– reperfusion. Thromboxane A2 has been implicated in causing microvascular alterations in the lung following reperfusion of ischemic canine hindlimb (56). Most of the evidence from this interpretation comes from transient elevations in thromboxane A2 associated with a transient, self-resolved increase in lung water. These events are prevented by the use of thromboxane A2 inhibitors prior to the onset of ischemia. In the specific instance of changes in microvascular permeability, no clear correlation appears to exist between ecosanoid levels and transport of macromolecules in postischemic striated muscle (57). Prostaglandins have physiologic and pharmacologic properties that may be useful in the attempts to ameliorate the consequences of ischemia–reperfusion. In particular, prostacyclin is a vasodilator; it prevents platelet aggregation and may inhibit leukocyte adhesion to endothelium. Stable analogues of prostacyclin, such as Iloprost, have also shown some degree of protection against microvascular alternations in postischemic muscle (58), as well as protection against platelet sequestration and infarct size (59). Similar protection against ischemia–reperfusion damage has been afforded by Iloprost in the myocardium (60). Calcium, a universal signaling molecule, plays an important role in the pathophysiology of ischemia– reperfusion injury to skeletal muscle and associated microvascular injury. Both calcium entry and calcium mobilization are involved. With regard to muscle damage, muscle function is impaired in part due to a slower calcium uptake by the sarcoplasmic reticulum, which is partially prevented by pretreatment with scavengers of oxygen-derived free radicals (61). In regard to microvascular dysfunction, calcium ions modulate the activity of leukocytes as well as the contractile properties of endothelial cells. The impact of calcium entry on microvascular

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury

dysfunction is supported by the prevention of changes in microvascular permeability to macromolecules afforded by verapamil, a calcium-channel blocker (57). One of the most attractive putative mediators of ischemia–reperfusion currently being investigated is platelet-activating factor. Even though it is not constitutively present in endothelial cells, PAF can be quickly synthesized upon stimulation with thrombin, histamine, and other agonists, including PAF itself. This short-lived phospholipid (1-O-alkyl-2-acetyl-sn-3-phosphocholine) is a vasoconstrictor (62), a strong promoter of microvascular permeability (63,64), and a powerful chemoattractant for neutrophils at concentrations of 10-11 mol/L and 10-9 mol/L (64,65). It is worth noting that the actions of PAF on microvascular permeability are mediated by nitric oxide synthase (66). Evidence based on the use of chemically different inhibitors of PAF receptors indicates that some of these microvascular functions of PAF are mediated by different receptors in the precapillary and postcapillary segments (67). Pharmacologic advances based on this finding may make it possible to block the activity of PAF differentially so as to prevent or counteract the damage of ischemia–reperfusion. In vitro studies provide strong support for a role for PAF in ischemia–reperfusion. It is possible that the production of H2O2 serves as the stimulus for the synthesis of PAF. Primary cultures of bovine pulmonary artery endothelium and human umbilical vein endothelium synthesize PAF when stimulated with H2O2 (68). This PAF synthesis is associated with an increase in intracellular Ca2+, suggesting that a transmembrane Ca2+ flux may serve as a signal to initiate PAF production. Furthermore, H2O2 also induces endothelial cell-dependent adhesion of neutrophils to human umbilical vein endothelial cell monolayers. Current theories indicate that PAF synthesized by activated endothelial cells is expressed on the cell surface and binds to a receptor on the polymorphonuclear leukocyte (69,70). This interaction causes upregulation of CD11a/CD18 and CD1111b/CD18k, leading to firm adhesion of polymorphonuclear leukocytes to endothelial cells. The role of PAF in mediating endothelial cell– leukocyte interaction in vivo has been studied in inflamed and in reperfused tissues. Exogenously administered PAF, an agonist for PAF synthesis by microvascular endothelial cells, increases leukocyte adherence at concentrations of 10-9 mol/L and enhances permeability at 10-7 mol/L in the hamster cheek pouch (65). The possibility that H2O2 may be the stimulus for PAF synthesis in ischemia–reperfusion is indirectly supported by experiments in which human recombinant superoxide dismutase administered intravenously caused a 30% decrease in polymorphonuclear leukocyte adherence (46). In isolated autoperfused segments of feline intestine, reperfusion after 1 hour of ischemia increased the adhesion and extravasation of leukocytes, and pretreatment with intravenous doses of the PAF-receptor antagonists BN 52021 or WEB 2086 reduced the rates of leukocyte adhesion and extravasation

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during reperfusion (71). These results suggest that PAF plays a role in mediating the adhesive interaction between the leukocyte and the endothelial cell during ischemia–reperfusion, and promotes extravasation. Success has been achieved in providing protection against increased leukocyte adherence by administration of WEB 2086 just prior to reperfusion (72). In addition to strengthening the viewpoint of PAF’s role in ischemia–reperfusion-induced leukocyte adhesion, this finding may provide a valuable basis for developing therapeutic approaches applicable to acutely ischemic patients at the critical step of starting reperfusion. PAF may also play a paracrine role in ischemia– reperfusion-induced increases of leukocyte adhesion. In models of focal ischemia–reperfusion in which other areas of the tissue remain perfused at normal flow rates, the number of adherent leukocytes tends to increase in the nonischemic, normally perfused areas (47,72). These observations have been tentatively interpreted to indicate the release of a soluble chemical mediator by the ischemic area, which in turn diffuses to the normal microcirculation and stimulates the increment in leukocyte adhesion. The possibility that PAF is a paracrine chemical mediator derives from in vitro data in which the supernatant of hypoxic-reoxygenated endothelial cells increased leukocyte adhesion in normoxic endothelial cells (73) and from the in vivo demonstration that soluble PAF is a powerful chemoattractant for leukocytes (64,65).

Mechanisms of Signal Transduction in Hyperpermeability Nitric oxide (NO) has emerged as a major signaling molecule in the last decade (89–91). The role of NO in the regulation of vasorelaxation is well established. Indeed, NO and its endothelial synthase may even play an important role in the genesis of hypertension (92). However, current information highlights controversial reports on the impact of nitric oxide in the control of microvascular permeability, and thus on its potential importance in ischemia–reperfusion. Evidence in tissues and in isolated venules indicates that the activity of endothelial constitutive NO synthase (eNOS) increases microvascular permeability to macromolecules in response to inflammatory agents (66,93–96). Other reports indicate that NOS activity prevents increases in permeability (97–99). These controversial results may be due to species differences or to different mechanisms operating under the experimental conditions. With regard to possible mechanistic approaches, eNOS trafficking or translocation has emerged as being potentially important (100–102). Our work and the reports of others are consistent with the hypothesis that eNOS activity and release of NO serves to increase microvascular permeability. The signaling pathways for several inflammatory agents involve the activation of PKC and NOS (66,94–96,103–108,146). It is assumed that NO, under these conditions, is the product of eNOS because of the short duration of the stimulus and

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the brief delay (seconds to minutes) between stimulus and permeability response. These reactions are presumably followed by synthesis of cGMP (95,109). Experiments in isolated microvessels also support the concept that stimulation of NOS and production of cGMP leads to changes in permeability to small and large solutes (95,110,111). However, other investigators report that NO serves to maintain a tight microvascular barrier. In contrast to the cited studies, inhibition of NOS with L-arginine analogs increases leakage of macromolecules in the intestine (99). In addition, the maintenance of a tight microvascular barrier characteristic is thought to be a function of cGMP (112).

Basis for the Significance of Phosphorylation of eNOS and NO Production in Signaling The genes encoding for human and bovine endothelium eNOS have been characterized and their cDNA have been cloned (91,113–118). While the gene sequence is highly conserved among species, the post-translational regulatory modalities may vary in different species (119,120). The regulation of eNOS by phosphorylation is supported by its deduced amino acid sequence. However, whether phosphorylation leads to activation or inactivation of eNOS activity is contradictory. Bradykinin stimulates phosphorylation of eNOS and an increase in its activity in bovine aortic endothelial cells (BAEC) (102). In contrast, an elevation in NO-related nitrites was reported in BAEC after either pharmacologic inhibition of PKC (121). The rate of shear stress also causes opposite responses in eNOS phosphorylation (122). Shear stress at 25 dyne/cm2 (a rate found in arteries) elicits eNOS phosphorylation in BAEC, while shear stress at 5 dyne/cm2 (a rate observed in microvessels) did not cause phosphorylation in arterial EC (122). The preceding studies have investigated mainly PKC as the putative kinase involved in the phosphorylation of eNOS. Recently, elegant studies have demonstrated that protein kinase B (PKB) phosphorylates eNOS and leads to NO production (123–125). The impact of the available data on eNOS phosphorylation on our knowledge of microvascular transport, i.e., at the tissue level, is difficult to evaluate. The majority of available molecular biology data comes from experiments designed to investigate the function of eNOS and of NO in control of blood flow and blood pressure (121,122), and performed in endothelial cells (EC) derived from large vessels. To reconcile this difficulty, our laboratory has investigated the role of the eNOS–NO cascade in hyperpermeability using both tissue culture (HUVEC: human umbilical vein endothelial cells) assessments and tissues amenable to intravital microscopy. The latter afford an opportunity to investigate more directly the relationship between permeability alterations and biochemical regulation of eNOS in vivo. Because of their

rapid adaptation to changing environmental conditions, these tissues produce a measurable change in permeability in response to short stimulation. Based on our finding that a difference in PAF receptors exists between the pre- and postcapillary segments (67), we hypothesized that a difference in signal transduction may also exist between these microvascular segments. Thus, we asked: What biochemical pathways are involved in agonist-induced in vivo intracellular signaling? Based on the explicit assumption that cells use similar signaling for different targets, we proposed a pathway, taking into consideration existing biochemical data, and tested it experimentally. Briefly, the interactions of PAF with its specific receptors, as well as with tyrosine kinase (126), lead to activation of phospholipases (PL) A2, C and D, as well as Ca2+ channels. PLA2 exerts a dual action. Through the lipoxygenase pathway, PLA2 activation leads to formation of leukotrienes, particularly C4, which activate NOS and elevate permeability (105). Through the cyclooxygenases pathway, PLA2 activates thromboxane synthase and is mainly responsible for the vasoconstrictor effect of PAF (62,64). Another important phospholipase is PLC. To examine its role in microvascular permeability, we evaluated its impact with specific inhibitors. Inhibition of PLC reduces the impact of PAF on microvascular transport (127). Importantly, the activity of PLC and PLD leads to activation of PKC, an important element in the signal transduction associated with PAF and microvascular permeability (146). Our data support this schematic pathway for VEGF (vascular endothelial growth factor) in vivo and in vitro (128,129,146) and we speculate that it may be extended to nearly any agonist of hyperpermeability. We evaluated the role of PKC as a biochemical pathway for PAF action by using inhibitors of the catalytic (sphingosine, iso H-7) and regulatory (calphostin C) domains of the enzyme. The inhibitors were applied topically for 10 min before the topical 3-min challenge with 10-8 mol/L PAF. These experiments demonstrated a reduction in PAF-induced hyperpermeability (146). To examine more directly the regulatory role of PKC in microvascular permeability in vivo, we stimulated PKC with phorbol esters: phorbol dibutyrate (PDBu) at 10-7 mol/L, 10-6 mol/L, and 10-5 mol/L and phorbol myristate acetate at 10-6 mol/L and 5 ¥ 10-7 mol/L. Both phorbol esters increased microvascular leakage in a dosedependent fashion. Calphostin C inhibited PDBu-induced macromolecular leakage. Our results support the role of PKC as a signaling pathway in the in vivo regulation of microvascular transport by PAF (146). The preceding studies led us to postulate that signaling from these upstream kinases may converge on nitric oxide synthase in the modulation of microvascular permeability. We tested this hypothesis by two approaches. In one set of experiments, we used L-arginine analogs (NGnitro-L-arginine methyl ester [L-NAME] and NGmonomethyl-L-arginine [L-NMMA]) to block NOS activity. These inhibitors were applied continuously

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury

through the suffusate. Acetylcholine (ACh) at 10-6 mol/L served to test the inhibition of eNOS in the microvessels. Pretreatment with 10–5 mol/L and 10–6 mol/L L-NAME and with L-NMMA at 10–4 mol/L and 10–5 mol/L resulted in mild vasoconstriction, but had no significant effect on postcapillary venular permeability. Both L-NAME and LNMMA attenuated the ACh-induced vasodilation. ACh alone did not have any effect on permeability. In the presence of NOS inhibitors, PAF produced arteriolar constriction. Both NOS inhibitors reduced PAF-stimulated increase in vasopermeability. Our results demonstrate that L-arginine–NO synthesis pathway plays a role in PAF-stimulated microvascular permeability (66). The second approach was to test directly the relationship between PKC and NOS activity in the modulation of microvascular transport. To test our hypothesis, we stimulated PKC topically with PDBu at 10–7 mol/L. PDBu significantly increased transport of macromolecules, as demonstrated by the elevation in integrated optical intensity (IOI) from 5 ± 1 units to 46.8 ± 6.3. Pretreatment with L-NMMA at 10–4 mol/L nearly abolished the PDBustimulated net transport (IOI = 10.8 ± 0.9). These results suggest that PKC increases macromolecular transport by a mechanism involving NOS activity (94). Even though we and other investigators (66,95,105) have strong pharmacologic evidence that NOS plays an important role in the control of microvascular transport, we felt it was important to demonstrate the presence of NOS in microvessels by independent methods. As a first step to initiate our approach to integrate molecular basis and physiologic regulation, we chose to localize eNOS by immunocytochemistry. To this end, the hamster cheek pouch was fixed in Bouin solution and embedded in Paraplast. Immunostaining was accomplished with a polyclonal eNOS antibody (pAb; Transduction Laboratories, Lexington, KY) and detected by the peroxidase– antiperoxidase reaction. The results, which show reaction product in the endothelium, confirm the presence of eNOS in the hamster cheek pouch postcapillary venules (130).

PAF-induced NOS Phosphorylation An important question in evaluating the role of eNOS in the control of permeability is: How is the enzyme regulated? We hypothesized that eNOS phosphorylation in vivo is an important step in the regulation of microvascular permeability. To address this question, we determined whether or not PAF, a hyperpermeability-stimulating agent, could induce eNOS phosphorylation (130). The test assay consisted of immunoprecipitation coupled to Western blotting, using pAb to eNOS. To this end, the hamster cheek pouch was prepared as usual for intravital microscopy and [32P]-orthophosphoric acid was applied in a buffered solution to the pouch and incubated for 2 hours. Then, the tissues were harvested in a solution containing antiproteases and antiphosphatases, frozen in liquid nitrogen and processed for immunoprecipitation. A

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band that migrated with the mobility of the positive eNOS control was observed in the control and in the PAF-treated hamster cheek pouches. Comparison of the net band intensities by image analysis yields a mean PAF/control ratio of 1.6 ± 0.1 (SEM; n = 5). Since total protein was the same in control and PAF-treated pouches, and the amount loaded per lane was also the same, these initial results demonstrate that PAF increases eNOS phosphorylation, and are consistent with our central hypothesis (130).

Nitric Oxide Production in the Hamster Cheek Pouch Two important assumptions in the pharmacologic approaches to evaluate the role of NOS in microvascular permeability are that NO is produced in response to the agent, and that NOS-blocking agents inhibit NO production. We tested these assumptions by measuring global NO production in the hamster cheek pouch (130). We applied 10–7 mol/L PAF to evaluate whether or not NO is produced in response to this vasoconstricting, hyperpermeability-enhancing dose of PAF and demonstrated a significant increase in tissue NO production in response to PAF.

Nitric Oxide and Permeability Changes in Ischemia–Reperfusion The health-related significance of the new knowledge acquired regarding the signaling mechanisms of eNOS resides in its potential application to microvascular diseases, in particular those involving permeability alterations such as inflammation and ischemia–reperfusion injury. The role of eNOS in ischemia–reperfusion injury is unresolved. There is compelling evidence that inhibition of eNOS ameliorates the impact of ischemia–reperfusion on hyperpermeability, and also persuasive evidence that inhibition of eNOS leads to enhanced leukocyte adhesion and exaggerated macromolecular leakage. We have demonstrated that the increased permeability associated with ischemia–reperfusion injury is, at least partially, mediated by PAF and NOS (130). Blockade of PAF with a specific receptor antagonist or inhibition of NOS with LNMMA decreases the impact of ischemia–reperfusion on microvascular permeability (131). Importantly, these inhibitory agents are efficacious when applied either before the onset of ischemia or at the time of reperfusion (131). Evidence obtained by other investigators indicates that inhibition of NOS leads to an indirect increase in permeability due to enhanced leukocyte adhesion (132). The difference in results may be due in part to the specific model of ischemia applied to the tissue under examination. We have investigated models of global ischemia in the hamster cheek pouch (47,131) and in rat striated muscle (12,13,133), while other investigators have studied partial ischemia in the rat and cat mesentery (132). The differences in degree of ischemia and oxygen availability

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may lead to variations in the biochemical and physiologic mechanisms of the signaling sequence that stimulates NOS under the specific experimental conditions. A major missing step is to elucidate the translation of these findings to the care of patients.

seems that the needs of the tissue or information regarding the function to be performed drive the synthesis or release of specific growth factors and their associated signalamplifying cascades. These issues are to be considered in planning new approaches to solve the revascularization of ischemic organs.

Microvascular Permeability and Tissue Remodeling Do permeability alterations represent a pathologic inflammatory reaction or a beneficial inflammatory reaction in preparation for tissue remodeling? Current data suggest that vascular endothelial growth factor (VEGF) may play a significant role in tissue remodeling subsequent to ischemic injury. VEGF is the most powerful vascular permeability promoting factor (134) reported to date. It is possible that VEGF plays a role in the increase in vasopermeability after prolonged injury and after reperfusion. Because the normal level of VEGF ranges from 2 to 7 pmol/L (135,136) and increases to the nanomolar range in disease (135), it is plausible that VEGF involvement would require protein synthesis, a process that takes at least 45 minutes in normothermia. Considering that short periods of ischemia increase permeability to a similar extent as 2–4 hours of ischemia, it seems reasonable that the contribution of VEGF to postischemic hyperpermeability is not crucial. In fact, we have demonstrated that PAF, a phospholipid quickly generated by biological membranes, is responsible for large changes in permeability and in association with ischemia–reperfusion (66,72). We have also demonstrated that new synthesis of protein plays a role in the sequelae of 4 hours of ischemia and 1 hour of reperfusion (133). Indeed, inhibition of protein synthesis abolishes the impact of tumor necrosis factor in striated muscle. In this particular case, it seems that the ischemic muscle initiates a process that is greatly amplified at a systemic level (133). The significance of protein synthesis and its impact on permeability may reside in its role in tissue remodeling and adaptation to the ischemic insult. An important effect of elevated VEGF is angiogenesis, defined as neoformation of capillaries resulting in increased capillary density. It is claimed that enhanced angiogenesis significantly improves organ perfusion in animal models as well as in patients (137–141). Newly developed arborization of the vasculature has been reported; however, there is much concern regarding the primary evidence for this conclusion as the data may depend on the heterogeneity of the prevailing transit times. While arteriogenesis would be a highly desired result for distribution of blood flow to ischemic organs, it seems clear that VEGF does not induce growth of new arteries, but it may contribute to the utilization of preexisting vessels, i.e., opening of collateral vessels. The mechanisms linking microvascular permeability, angiogenesis, and tissue remodeling are still under investigation. Angiogenesis coupled to increased permeability is stimulated by VEGF, while angiogenesis lacking hyperpermeability is driven by angiopoietin (142–144). Thus, it

Clinical Recommendations and Future Directions Current management of acute limb ischemia is based on the restoration of blood flow to the ischemic extremity as rapidly as possible so as to reduce the degree of ischemic injury. Universal use of heparin is recommended in the absence of clinical contraindication. Using heparin in acute limb ischemia was recommended by Blaisdell and colleagues as an alternative to operative intervention in patients with limb-threatening ischemia (2). These authors reported a mortality of 7.5% (2), as compared with the 25% or more in their review of the literature, and recommended heparinization followed by further elective surgical intervention as required. Heparin reduces the incidence of recurrent emboli and limits extension of thrombus into the distal circulation. In addition, heparin has a beneficial effect on reducing microcirculatory dysfunction, as reported in the canine gracilis muscle experimental model (75). Furthermore, investigations have confirmed that heparin’s role may be independent of its acknowledged anticoagulant effects (76). Sternbergh and associates demonstrated that standard mucosal heparin attenuated endothelial cell dysfunction as measured by release of NO (77). Sternbergh and coworkers have investigated a chemically modified heparin having negligible anticoagulant activity and reported in postischemic endothelial dysfunction (78), confirming previous reports suggesting that heparin’s mechanism of action was independent of its anticoagulant activity. Iloprost, the stable analog of prostacyclin, is another drug that may be useful in the clinical management of ischemia–reperfusion injury. Belkin and colleagues reported on the use of Iloprost and demonstrated a reduction in the size of skeletal muscle infarcts in a canine gracilis muscle model (79). No decrease in platelet sequestration was observed, suggesting its protective mechanism of action was independent of its known antiplatelet effects. Selective lytic therapy is also recommended as an important adjunct to the treatment of acute limb ischemia. Used preoperatively with balloon angiodilation or intraoperatively as an adjunct to thrombectomy, urokinase has emerged as the lytic agent of choice (80). In a prospective and randomized comparison of initial operative intervention versus initial lytic therapy, Ouriel and colleagues reported comparable results for limb salvage (81). However, cumulative survival was significantly improved for patients randomized to thrombolysis, and these

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury

authors suggested its initial usage, relegating operative intervention to a complementary role. Finally, consideration of primary amputation for irreversible limb ischemia (class III patients) is recommended. Blaisdell has described these patients’ extremities as no longer being waxy white, but becoming blue and mottled and associated with rigor and tenderness on palpation of specific muscle groups (10). In this group of patients, revascularization is associated with high mortality, and primary amputation must be considered. Superimposed on this algorithm are proposed uses of other pharmacologic agents and nonpharmalogic methods for reducing ischemia–reperfusion injury (20). Pharmacologic agents included potential use of anti-inflammatory drugs such as dexamethasone (82), antioxidants as outlined in this chapter and including mannitol, dimethylsulfoxide, allopurinol, catalase, and superoxide dismutase. All have been reported to reduce microcirculatory dysfunction, and in some instances to reduce the severity of parenchymal skeletal muscle infarction. Nonpharmacologic methods relate to the basic recommendation for prompt revascularization and adjunctive use of fasciotomy, as indicated clinically. Controlled reperfusion may also have a role, as suggested by observations from the canine gracilis muscle preparation (83,84). Avoidance of reperfusion hyperemia during the first hour after ischemia correlated with significantly reduced skeletal muscle infarction. Beyersdorf et al. demonstrated similar results regarding controlled reperfusion in an experimental rat hindlimb preparation (85), as well as a clinical report on lower limb ischemia in patients (86). Beyersdorf also modified the composition of the reperfusate to include analyses of antioxidants, PO2, pH, and osmolality during a 30-min controlled limb reperfusion using femoral arterial and venous cannulation. This technique has been recently applied in North America (145). This innovative approach also uses control of temperature, as hypothermia was reported to reduce skeletal infarction upon reperfusion after ischemia in an experimental model (87). Depletion of leukocyte by irradiation (41), chemotherapy (42), Leukopak filtration (40), or monoclonal antibodies (43) in the reperfusate has also produced salutory results and reduced microcirculatory disruption and skeletal muscle infarction. All of the techniques require efficacy assessments by randomized clinical trials. These trials await development of more objective techniques for determining the severity of ischemic injury and subsequent determination during and after reperfusion. The evidence presented also supports the concept that a significant portion of the ischemia–reperfusion injury occurs during reperfusion as a result of activation and infiltration of neutrophils and their interaction with endothelial cells. Indeed, available information indicates that modulation of leukocyte–endothelial cell interaction is of foremost importance in order to attenuate the degree of injury after ischemia–reperfusion. There have been great expectations from approaches that would adminis-

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ter antibodies directed against cell adhesion molecules [such as endothelial cell surface (ELAM-1, ICAM-1, ICAM-2) or the neutrophil membrane glycoprotein CD18], or employ therapeutic interventions designed to interfere with protease activity in order to limit neutrophil-mediated postischemic injury, and other applications of newly developed molecular biology-based innovations. Whether any of these methods of providing additional protection against ischemia–reperfusioninduced cell injury will gain clinical applicability still depends on obtaining further knowledge as to their potential adverse systemic affects. For example, a barrier yet to be overcome in the potential application of monoclonal antibody therapy is the improvement of their site specificity so as not to jeopardize host defenses in other organs. The implementation of clinical trials to determine the effciacy of new modalities is greatly impaired by the lack of an improved, clinically applicable method for the objective measurement of the severity of skeletal muscle injury. The double jeopardy facing the vascular surgeon is that unattended ischemia leads to necrosis, making prompt restoration of blood flow a must, but reperfusion compounds the problem, and its consequences may interfere significantly with survival of the organ and the patient. Furthermore, any therapy that is instituted must be delivered effectively and quickly to the site of injury and its potential benefits assessed objectively. The best way to deliver substances to parenchymal cells is via the microcirculatory system of convection and exchange vessels. When no reflow is present, the ability to deliver therapeutic agents via the bloodstream is greatly impaired. Therefore, in addition to developing more refined chemical therapeutic agents, it may be advisable to improve upon ways of recanalizing or bypassing the obliterated arterial segments so as to access the compromised microcirculation and contribute to salvaging viable tissue. This formidable task still presents an exciting challenge to skilled vascular surgeons and physiologists.

References 1. Fogarty TJ, Cranley JJ et al. A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963; 116: 241. 2. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surg 1978; 84: 822. 3. Glick D, Grundest WS. Intraoperative decisions based on angioscopy. Circulation 1988; 78 (Suppl 1, No. 3): 13. 4. Cohen LH, Kaplan M. Bernhard VM. Intraoperative streptokinase: An adjunct to mechanical thrombectomy in the management of acute ischemia. Arch Surg 1986; 121: 708. 5. Haimovici H. Peripheral arterial embolism. A study of 330 unselected cases of embolism to the extremities. Angiology 1950; 1: 20.

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6. Thompson JE, Sigler L, et al. Arterial embolectomy: A 2-year experience with 163 cases. Surgery 1970; 67: 212. 7. Thompson JE, Weston AS, Sigler L. Arterial embolectomy after acute myocardial infarction: A study of 31 patients. Ann Surg 1970; 171: 979. 8. Satiani B, Evans WE. Immediate prognosis and five-year survival after arterial embolectomy following myocardial infarction. Surg Gynecol Obstet 1980; 150: 41. 9. Lusby RJ, Wylie EJ. Acute lower extremity ischemia: Pathogenesis and management. Word J Surg 1983; 7: 340. 10. Blaisdell FW. The reperfusion syndrome. Microcirc Endothelium Lymphatics 1989; 5: 127. 11. Harris K, Walker P, et al. Metabolic response of skeletal muscle to ischemia. Am J Physiol 1986; 250(19): H213– H220. 12. Suval WD, Hobson RW II, et al. Assessment of ischemia reperfusion injury in skeletal muscle by macromolecular clearance. J Surg Res 1987; 42: 550–559. 13. Suval WD, Durán WN, et al. Microvascular transport and endothelial cell alternations precede skeletal muscle damage in ischemia–reperfusion injury. Am J Surg 1987; 154: 211–218. 14. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med 1985; 312: 159. 15. Granger DN, McCord JM, et al. Xanthine oxidase inhibitors attenuate ischemia-induced vascular permeability changes in the cat intestine. Gastroenterology 1986; 90: 80. 16. Granger DN. Role of xanthine oxidase and granulocytes in ischemia–reperfusion injury. Am J Physiol 1988; 255: H1269. 17. Del Maestro RF. An approach to free radicals in medicine and biology. Acta Physiol Scand 1980; 492 (Suppl): 153. 18. Halliwell B, Gutterridge JMC. Oxygen toxicity, oxygen radicals, transition metals and disease. Biochem J 1984; 219: 1. 19. Durán WN, Dillon PK. Effects of ischemia–reperfusion injury on microvascular permeability in skeletal muscle. Microcirc Endothelium Lymphatics 1989; 5: 223– 239. 20. Wright JG. Pharmacological and nonpharmacological methods for preservation of skeletal muscle viability; mechanisms and potential clinical applications. Semin Vasc Surg 1992; 5(1): 28–41. 21. Jarasch ED, Grund C, et al. Localization of xanthine oxidase in mammary gland epithelium and capillary endothelium. Cell 1981; 25: 67. 22. Parks DA, Williams TK, Beckman JS. Conversion of xanthine dehydrogenase to oxidase in ischemic rat intestine; a re-evaluation . Am J Physiol 1988; 254: G768. 23. Ignarro LJ. Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein. Circ Res 1989; 65: 1. 24. Yuan Y, Granger HJ, et al. Flow modulates coronary venular permeability by a nitric oxide-related mechanism. Am J Physiol 1992; 263: H641. 25. Kubes P, Granger DN. Nitric oxide modulates microvascular permeability. Am J Physiol 1992; 262: H611. 26. Beckman JS, Beckman TW, et al. Apparent hydroxyl radical production by peroxynitrite implications for endothelial injury from nitric oxide and superoxide. Proc Natl Acad Sci USA 1990; 87: 1620.

27. Furchgott RF, Vanhoutte PM. Endothelium-derived relaxing and contracting factors FASEB J 1989; 3: 2007–220018. 28. Ignarro LJ, Byrns RE, Wood KS. Endothelium-dependent modulation of cyclic GMP levels and intrinsic smooth muscle tone in isolated bovine intrapulmonary artery and vein. Circ Res 1987; 60: 82–92. 29. Tomeo AC, Egan RW, Durán WN. Priming interactions between platelet activating factor and histamine in the in vivo microcirculation. FASEB J 1991; 5: 2850–2859. 30. Colden-Stanfield M, Schilling WP, et al. Bradykinininduced increases with cytosolic calcium and ionic currents in cultured bovine aortic endothelial cells. Circ Res 1987; 61: 632–640. 31. Murry MA, Heistad DD, Mayhan WG. Role of protein kinase C in bradykinin-induced increases in microvascular permeability. Circ Res 1991; 68: 1340–1348. 32. Rosenberg RD, Rosenberg JS. Natural anticoagulant mechanisms. J Clin Invest 1984; 74: 1–5. 33. Esmon CT, Owen WG. Identification of an endothelial cofactor for thrombin-catalyzed activation of protein. Proc Soc Natl Acad Sci USA 1981; 78: 2249–2252. 34. Pober JS, Cotrain RS. Cytokines and endothelial cell biology. Physiol Rev 1990; 70: 427–451. 35. Zimmerman GA, McIntyre TM, Prescott SM. Thrombin stimulates the adherence of neutrophils to human endothelial cells in vitro. J Clin Invest 1985; 76: 2235–2246. 36. Zimmerman GA, McIntyre TM. Neutrophil adherence to human endothelium in vitro occurs by CDw18 (Mol MAC/LAF-1, GP150, 95) glycoprotein-dependent and independent mechanisms. J Clin Invest 1988; 81: 531–537. 37. McEver RP, Bechstead JH, et al. GMP-140, a platelet granule membrane protein, is also synthesized by vascular endothelial cells and is localized in Weibel-Palade bodies. J Clin Invest 1989; 84: 92–99. 38. Kubes P, Kvietys PR, Granger DN. Ischemia–reperfusion injury. In: Mortillaro NA, Taylor AE, eds. The pathophysiology of the microcirculation. Boca Raton, FL: CRC Press, 1994. 39. Smith JK, Grisham GB, et al. Free radical defense mechanisms and neutrophil infiltration in postischemic skeletal muscle. Am J Physiol 1989; 256: H789–H793. 40. Korthius RJ, Grisham GB, Granger DN. Leukocyte depletion attenuates vascular injury in post-ischemic skeletal muscle. Am J Physiol 1989; 24454: H283–H287. 41. Belkin M, LaMorte WL, et al. The role of leukocytes in the pathophysiology of skeletal muscle ischemic injury. J Vasc Surg 1989; 10: 14–19. 42. Breitbart GB, Dillon PK, et al. Leukopenia reduces microvascular clearance of macromolecules in ischemia–reperfusion injury. Curr Surg 1990; 47: 8– 12. 43. Ferrante RJ, Hobson RW II, Miyasaka M, Granger DN, Durán WN. Inhibition of white blood cell adhesion at reperfusion decreases tissue damage in postischemic striated muscle. J Vasc Surg 1996; 24: 187–193. 44. Ley K, Gaehtgens P, et al. Lectin-like cell adhesion molecule 1 mediates leukocyte rolling in mesenteric venules in vivo. Blood 1991; 77: 2553. 45. Lawrence MB, Springer TA. Leukocytes roll on a selection at physiologic flow rates: Distinction from and

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56. 57.

58.

59.

60.

61.

62.

63.

prerequisite for adhesion through integrins. Cell 1991; 65: 859. Kubes P, Suzuki M, Granger DN. Modulation of PAFinduced leukocyte adherence and increased microvascular permeability. Am J Physiol 1990; 259: G859. Yasuhara H, Hobson RW II, et al. A new model for studying ischemia–reperfusion injury in the hamster cheek pouch. Am J Physiol 1991; 261: H1626–1629. Hernandez LA, Grisham MB, et al. Role of neutrophils in ischemia–reperfusion-induced microvascular injury. Am J Physiol 1987; 253: H699. Kubes P, Suzuki M, Granger DN. Platelet-activating factor-induced microvascular dysfunction: The role of adherent leukocytes. Am J Physiol 1990; 258: G158. Carden DL, Smith JK, Korthuis RJ. Oxidant-mediated, CD-18-dependent microvascular dysfunction induced by complement-activated granulocytes. Am J Physiol 1991; 260: H1144. Mangino MJ, Anderson CB, et al. Mucosal arachidonate metabolism and intestinal ischemia–reperfusion injury. Am J Physiol 1989; 257: G299. Zimmerman BJ, Guillory DJ, et al. Role of leukotriene B4 in granulocyte infiltration into the postischemic feline intestine. Gastroenterology 1990; 99: 1. Goldman G, Welbourn R, et al. Ischemia induced neutrophil activation and diapedesis are lipoxygenase dependent. Surgery 1990; 107: 428. Durán WN, Suval WD, et al. Microcirculatory dysfunction in the pathophysiology of skeletal muscle ischemia. In: Veith FJ, Hobson RW, et al, eds. Vascular Surgery: Principles and Practices. New York: McGraw-Hill, 1993: 388–396. Filep J, Herman F, et al. Increased levels of plateletactivating factor in blood following intestinal ischemia in the dog. Biochem Biophys Res Cmmun 1989; 158: 353. Blaisdell FW. The reperfusion syndrome. Microcirc Endothel Lymph 1989; 5: 127. Paul J, Bekker AY, Durán WN. Calcium entry blockade prevents leakage of macromolecules induced by ischemia–reperfusion in skeletal muscle. Circ Res 1990; 66: 1636. Blebea J, Cambria RA, et al. Iloprost attenuates the increased permeability in skeletal muscle after ischemia and reperfusion. J Vasc Surg 1990; 12: 657. Belkin M, Wright JG, Hobson RW II. Iloprost infusion decreases skeletal muscle injury after ischemia– reperfusion. J Vasc Surg 1990; 11: 77. Simpson PJ, Michelson J, et al. Iloprost inhibits neutrophil function in vitro and in vivo and limits experimental infarct size in canine heart. Circ Res 1990; 60: 666. Cronenwett JL, Lee KR et al. The effect of ischemia–reperfusion derived oxygen free radicals on skeletal muscle calcium metabolism. Microcirc Endothelium Lymphatics 1989; 5: 171. Dillon PK, Ritter AB, Durán WN. Vasoconstrictor effects of platelet-activating factor in the hamster cheek pouch microcirculation: Dose-related relations and pathways of action. Circ Res. 1988; 62: 722. Dillon PK, Durán WN. Effect of platelet-activating factor on microvascular permselectivity: Dose-response relations and pathways of action in the hamster check pouch microcirculation. Circ Res 1988; 62: 732.

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64. Durán WN, Dillon PK. Acute microcirculatory effects of platelet-activating factor. J Lipid Mediat 1990; 2: S215. 65. Dillon PK, FitzPatrick MF, et al. Effect of plateletactivating factor on leukocyte adhesion to microvascular adhesion. Inflammation 1988; 12: 563–573. 66. Ramírez, M.M., Quardt, S.M., et al. Platelet-activating factor modulates microvascular permeability through nitric oxide synthesis. Microvasc Res 1995; 50: 223–234. 67. Tomeo AC, Durán WN. Resistance and exchange microvessels are modulated by different PAF receptors. Am J Physiol 1991; 261: H1648. 68. Lewis MS, Whatley RE, et al. Hydrogen peroxide stimulates the synthesis of platelet-activating factor by endothelium and induces endothelial cell-dependent neutrophil adhesion. J Clin Invest 1988; 82: 2045. 69. Zimmerman GA, McIntyre TM, et al. Endothelial cellassociation platelet-activating factor: a novel mechanism for signaling intercellular adhesion. J Cell Biol 1990; 110: 529. 70. Lorant DE, Patel KP, et al. Coexpression of GMP-140 and PAF by endothelium stimulated by histamine or thrombin: A juxtacrine system for adhesion and activation of neutrophils. J Cell Biol 1991; 115: 223. 71. Kubes P, Ibbotson G, et al. Role of platelet-activating factor in ischemia–reperfusion-induced leukocyte adherence. Am J Physiol 1990; 259: G300. 72. Durán, W.N., Milazzo, V.J., et al. Platelet-activating factor modulates leukocyte adhesion to endothelium in ischemia–reperfusion injury. Microvasc Res 1996 51: 108–115. 73. Yoshida N, Anderson DC, et al. Anoxia/reoxygenationinduced neutrophil adherence to cultured endothelial cells. Am J Physiol 1992; 252: H1891. 74. Simpson PJ, Todd RF, et al. Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (Anti Mo1, Anti-CD116) that inhibits leukocyte adhesion. J Clin Invest 1981; 68: 1394–1403. 75. Hobson RW II, Wright JG, et al. Heparinization reduces endothelial permeability and hydrogenion accumulation in a canine skeletal muscle ischemia–reperfusion model. J Vasc Surg 1988; 7(4): 585–591. 76. Sternbergh WC III, Makhoul RG, Adelman B. Heparin prevents post-ischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity. J Vasc Surg 1993; 17: 318–3227. 77. Sternbergh WC III, Makhoul RG, Adelman B. Nitricoxide mediated endothelial-dependent vasodilation is selectively attenuated in the post-ischemic extremity. Surg 1993; 114: 960–967. 78. Sternbergh WC III, Sobel M, Makhoul RG. Heparinoids with low anticoagulant potency attenuate post-ischemic endothelial cell dysfunction. J Vasc Surg 1995; 21: 477–483. 79. Belkin M, Wright JG, Hobson RW II. Iloprost infusion decreases skeletal muscle ischemia–reperfusion injury. J Vasc Surg 1990; 11: 77–83. 80. Quiñones-Baldrich WJ. Surgical management of acute limb ischemia: intraoperative considerations. Semin Vasc Surg 1992; 5: 42–51. 81. Ouriel K, Shortell CK, et al. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–1030.

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82. Breitbart GB, Dillon PK, et al. Dexamethasone attenuates microvascular ischemia–reperfusion injury in the rat cremaster muscle. Microvasc Res 1989; 38: 155–163. 83. Wright JG, Fox D, et al. Rate of reperfusion blood flow modulates reperfusion injury in skeletal muscle. J Surg Res 1988; 44: 754–763. 84. Anderson RJ, Cambria R, et al. Sustained benefit of temporary limited reperfusion in skeletal muscle following ischemia. J Surg Res 1990; 49: 271–275. 85. Beyersdorf F, Mitrev Z, et al. Controlled limb reperfusion as a new surgical technique to reduce postischemic syndrome. J Thorac Cardiovasc Surg 1993; 106: 378–380. 86. Beyersdorf F. Protection of the ischemic skeletal muscle. Thorac Cardiovasc Surg 1991; 39: 19–28. 87. Wright JG, Araki CT, et al. Postischemic hypothermia diminishes skeletal muscle reperfusion edema. J Surg Res 1989; 47: 389–396. 88. Rutherford RB. Acute limb ischemia: clinical assessment and standards for reporting. Semin Vasc Surg 1992; 5: 4–10. 89. Furchgott, RF, Zawadski, JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 1980; 288: 373–376. 90. Ignarro LJ. Biosynthesis and metabolism of endotheliumderived nitric oxide. Ann Rev Pharmacol Toxicol 1990; 30: 535–560. 91. Pollock JP, Forstermann U, et al. Purification and characterization of particulate endothelium-derived relaxing factor synthase from cultured and native bovine aortic endothelial cells. Proc Natl Acad Sci USA 1991; 88: 10480–10484. 92. Shesely EG, Maeda N, et al. Elevated blood pressure in mice lacking endothelial nitric oxide synthase. Proc Soc Natl Acad Sci (USA) 1996; 93: 13176–13181. 93. Ialenti A, Ianaro A, et al. Modulation of acute inflammation by endogenous nitric oxide. Eur J Pharmacol 1992; 211: 177–182. 94. Ramirez MM, Kim DD, Durán, W.N. Protein kinase C modulates microvascular permeability through nitric oxide synthase. Am J Physiol 1996; 271: H1702–H1705. 95. Yuan, Y, Granger, HJ, et al. Histamine increases venular permeability via a phospholipase C-NO synthaseguanylate cascade. Am J Physiol 1993; 264: H1734H1739. 96. Wu, H.M., Yuan, Y., et al. Role of phospholipase C, Protein kinase C, and calcium in VEGF-induced venular hyperpermeability. Am J Physiol 1999; 276: H535– H542. 97. Kurose I, Kubes P, et al. Inhibition of nitric oxide production: Mechanisms of vascular albumin leakage. Circ Res 1993; 73: 164–171. 98. Kurose I, Wolf R, et al. Microvascular responses to inhibition of nitric oxide production: role of active oxidants. Circ Res 1995; 76: 30–39. 99. Kurose I, Wolf R, et al. Modulation of ischemia/ reperfusion-induced microvascular dysfunction by nitric oxide. Circ Res 1994; 74: 376–382. 100. Goetz RM, Thatte HS, et al. Estradiol induces the calcium-dependent translocation of endothelial nitric oxide synthase. Proc Natl Acad Sci USA 1999; 96: 2788–2793. 101. Michel T, Feron O. Nitric oxide synthases: which, where, how, and why? J Clin Invest 1997; 100: 2146–2152.

102. Michel T, Li GK, Busconi I. Phosphorylation and subcellular translocation of endothelial nitric oxide synthase. Proc Natl Acad Sci USA 1993; 90: 6252–6256. 103. Hood JD, Meininger CJ, et al. VEGF upregulates ecNOS message, protein, and NO production in human endothelial cells. Am J Physiol 1998; 274: H1054– H1058. 104. Huang, Q, Yuan, Y. Interaction of PKC and NOS in signal transduction of microvascular hyperpermeability. Am J Physiol 1997; 273: H2442–H2451. 105. Mayhan WG. Role of nitric oxide in leukotriene C4induced increases in microvascular transport. Am J Physiol 1993; 265: H409–H414. 106. Mayhan WG. Nitric oxide accounts for histamineinduced increases in macromolecular extravasation. Am J Physiol 1994; 266: H2369–H2373. 107. Mayhan WG. VEGF increases permeability of the bloodbrain barrier via a nitric oxide synthase/cGMPdependent pathway. Am J Physiol 1999; 276(5 Pt 1): C1148–53. 108. Murray, MD, Heistad, DD, Mayhan, WG. Role of protein kinase C in bradykinin-induced increase in microvascular permeability. Circ Res 1991; 68: 1340–1348. 109. He P, Zeng M, Curry FE. cGMP modulates basal and activated microvessel permeability independently of [Ca2+]i. Am J Physiol 1998; 274: H1865–H1874. 110. Huxley VH, Tucker VL, et al. Increased capillary hydraulic conductivity induced by atrial natriuretic peptide. Circ Res 1987; 60: 304–307. 111. Meyer DJ, Huxley VH. Capillary hydraulic conductivity is elevated by cGMP-dependent vasodilators. Circ Res 1992; 70: 382–391. 112. Kubes P. Nitric oxide-induced microvascular permeability alterations: a regulatory role for cGMP. Am J Physiol 1993; 265: H1909–H1915. 113. Janssens SP, Shimouchi A, Quertermous T, Bloch DB, Bloch KD. Cloning and expression of a cDNA encoding human endothelium-derived relaxing factor/ nitric oxide synthase. J Biol Chem 1992; 267: 14519–14522. 114. Lamas S, Marsden PA, et al. Endothelial nitric oxide: Molecular cloning and characterization of a distinct constitutive enzyme isoform. Proc Natl Acad Sci USA 1992; 89: 6348–6352. 115. Nishida K, Harrison DG, et al. Molecular cloning and characterization of the constitutive bovine aortic endothelial cell nitric oxide synthase. J Clin Invest 1992; 90: 2092–2096. 116. Schmidt HHHW, Murad F. Purification and characterization of a human NO synthase. Biochem Biophys Res Comm 1991; 181: 1372–1377. 117. Sessa WC, Harrison JK, et al. Molecular cloning and expression of a cDNA encoding endothelial cell nitric oxide synthase. J Biol Chem 1992; 267: 15274– 15276. 118. Venema RC, Nishida K, et al. Organization of the bovine gene encoding the endothelial nitric oxide synthase. Biochim Biophys Acta 1994; 1218: 413–420. 119. Garcia-Cardena G, Fan R, et al. Endothelial cell nitric oxide is regulated by tyrosine phosphorylation andinteracts with caveolin-1. J Biol Chem 1996; 271: 27237–27240.

Chapter 31 Pathophysiology of Skeletal Muscle Ischemia–Reperfusion Injury 120. Garcia-Cardena G, Oh P, et al. Targeting of nitric oxide synthase to endothelial cell caveolae via palmitoylation: Implications for nitric oxide sigaling. Proc Natl Soc Sci 1996; 93: 6448–64553. 121. Ohara Y, Sayegh HS, et al. Regulation of endothelial constitutive nitric oxide synthase by protein kinase C. Hypertension 1995; 25: 415–420. 122. Corson MA, James NL, et al. Phosphorylation of endothelial nitric oxide synthase in response to fluid shear stress. Circ Res 1996; 79(5): 984–991. 123. Dimmeler S, Fleming I, et al. Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation. Nature 1999; 399: 601–605. 124. Fulton D, Gratton JP, et al. Regulation of endotheliumderived nitric oxide production by the protein kinase Akt. Nature 1999; 399: 597–601. 125. Gallis B, Corthals GL, et al. Identification of flowdependent endothelial nitric-oxide synthase phosphorylation sites by mass spectrometry and regulation of phosphorylation and nitric oxide production by the phosphatidylinositol 3-kinase inhibitor LY294002. J Biol Chem 1999; 274: 30101–30108. 126. Kim D, Durán WN. Platelet-activating factor stimulates protein tyrosine kinase in the hamster cheek pouch microcirculation. Am J Physiol 1995; 268: H399– H403. 127. Kim DD, Ramirez MM, Durán WN. Platelet-activating factor modulates microvascular dynamics through phospholipase C in the hamster cheek pouch. Microvasc Res; 59: 7–13. 128. Lal BK, Varma S, et al. VEGF increases permeability of endothelial cell monolayers by activation of PKB/akt, endothelial nitric oxide synthase and MAP kinase pathways. Microvasc Res 2001; 62: 252–262. 129. Varma S, Breslin JW, Lal BK, et al. p42/44 MAP kinase regulates baseline permeability and cGMP-induced hyperpermeability in endothelial cells. Microvasc Res 2002; 63: 172–178. 130. Durán WN, Seyama A, et al. Stimulation of NO production and of eNOS phosphorylation in the microcirculation in vivo. Microvasc Res 2000; 60: 104–111. 131. Noel AA, Hobson RW II, Durán WN. Platelet-activating factor and nitric oxide mediate microvascular permeability in ischemia–reperfusion injury. Microvasc Res 52: 210–220, 1996. 132. Kurose I, Anderson DC, et al. Molecular determinants of reperfusion-induced leukocyte adhesion and vascular protein leakage. Circ Res 1994; 74: 336–343. 133. Takenaka H, Oshiro H, et al. Microvascular transport is associated with tumor necrosis factor plasma levels and

134.

135.

136.

137.

138.

139. 140.

141.

142.

143.

144.

145.

146.

387

protein synthesis in postischemic muscle. Am J Physiol 1998; 274: H1914–H1919. Dvorak HF, Nagy JA, et al. Vascular permeability factor/vascular endothelial growth factor and the significance of microvascular hyperpermeability in angiogenesis. Curr Top Microbiol Immunol 1999; 237: 97–132. Kraft A, Weindel K, et al. Vascular endothelial growth factor in the sera and effusions of patients with malignant and nonmalignant disease. Cancer 1999; 85: 178–187. Kranz A, Rau C, et al. Elevation of vascular endothelial growth factor-A serum levels following acute myocardial infarction. Evidence for its origin and functional significance. J Mol Cell Cardiol 2000; 32: 65–72. Isner JM. Angiogenesis: a “breakthrough” technology in cardiovascular medicine. J Invasive Cardiol 2000; 12 Suppl A: 14A-17A. Isner JM. Arterial gene transfer of naked DNA for therapeutic angiogenesis: early clinical results. Adv Drug Deliv Rev 1998; 30(1–3): 185–197. Asahara T, Kalka C, Isner JM. Stem cell therapy and gene transfer for regeneration. Gene Ther 2000; 7: 451–457. Yang HT, Yan Z, et al. VEGF(121)- and bFGF-induced increase in collateral blood flow requires normal nitric oxide production. Am J Physiol Heart Circ Physiol 2001; 280: H1097–1104. Hopkins SP, Bulgrin JP, et al. Controlled delivery of vascular endothelial growth factor promotes neovascularization and maintains limb function in a rabbit model of ischemia. J Vasc Surg 1998; 27(5): 886–894. Thurston G, Suri C, et al. Leakage-resistant blood vessels in mice transgenically overexpressing angiopoietin-1. Science 1999; 286 (5449): 2511–2514. Gale NW, Yancopoulos GD. Growth factors acting via endothelial cell-specific receptor tyrosine kinases: VEGFs, angiopoietins, and ephrins in vascular development. Genes Dev 1999 May 1; 13(9): 1055–1066. Papapetropoulos A, Garcia-Cardena G, et al. Direct actions of angiopoietin-1 on human endothelium: evidence for network stabilization, cell survival, and interaction with other angiogenic growth factors. Lab Invest 1999; 79(2): 213–223. Ihnken K, Wildhirt S, et al. Skeletal muscle reperfusion injury: reversal by controlled limb reperfusion: a case report. Vasc Surg 2001; 35: 149–155. Kobayashi I, Kim D, et al. Platelet-activating factor modulates microvascular transport by stimulation of protein kinase C. Am J Physiol 1994; 266: H1214–H1220.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 32 Arterial Embolism of the Extremities and Technique of Embolectomy Henry Haimovici

Arterial embolectomy, designed to restore patency of an acutely occluded vessel by a thromboembolus, is one of the earliest known reconstructive arterial procedures. Although attempted since 1895 by several surgeons, it was not until 1911 that the first successful embolectomy was performed by Georges Labey and reported by Mosny and Dumont (1). In their comments on this case, it is of interest to note the authors’ clear perception of what the ideal indications ought to be for a successful procedure. They stated that to be acceptable, it is important that “the operation should be undertaken without delay, that the embolus be aseptic and easily accessible, that the patient be young and his arteries healthy.” Obviously, these principles were then and still are today most applicable to ideal situations. However, the wide spectrum of clinical forms deals with less favorable conditions, as has been illustrated abundantly since 1911. Shortly after this first success, the procedure was extended to include patients of all ages and different clinical and pathologic circumstances. Because of the pioneering efforts of Einar Key of Sweden, this procedure gained increasing acceptance (2). The publications in the ensuing three to four decades pointed out, among other factors, the necessity of early operative intervention to avoid irreversible intimal damage and secondary thrombosis distal to the embolic occlusion (3,4). Very likely, incomplete removal of the secondary or propagated thrombi often contributed to its poor results. Among the attempts to overcome this technical difficulty was the introduction of

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retrograde arterial flushing with saline for the removal of the propagated thrombi (5–7). This technique, however, often failed to achieve its goal. A more significant advance in the management of arterial embolism was the introduction in 1940 of anticoagulant agents, especially heparin, used during and after surgery (8,9). However, it was not until 1963 that a most notable advance in the performance of arterial embolectomy was achieved by the introduction of the balloon catheter by Fogarty et al. (10). This simple instrument represents an important landmark in the history and management of arterial embolism, as well as in vascular surgery in general. Concurrently, further progress has been accomplished by better understanding of the hemodynamics of embolic occlusion, by greater awareness of the possibility of metabolic complications associated with severe ischemia of skeletal muscle (11–13), and by wider use of open heart surgery for cardiovalvular repair. In spite of all these advances responsible for the current higher rate of limb salvage and reduced mortality in some groups of patients previously considered high-risk surgical groups, the concept of arterial embolism and its management is still undergoing changes (14–16). It seems that while progress was being achieved in one area, a few old challenges continued to persist and new ones emerged. Thus, despite the fact that the balloon catheter has greatly improved the technique of embolectomy, limb loss and mortality rates still remain high in some patients. The car-

Chapter 32 Arterial Embolism of the Extremities and Technique of Embolectomy

diac nature of the emboligenic factors and the extent of the ischemic impact on the involved tissues (especially the skeletal muscles) with the metabolic repercussions are among the features responsible for the persistent severity of an arterial embolism. Its etiology and the clinical, metabolic, and operative aspects will be reviewed here to provide some answers to the persisting, challenging problems engendered by arterial embolism.

Clinical and Pathologic Data Arterial embolism is a complication of a severe cardiopathy. The heart is the source of embolism in 90% to 96% of the published cases (17–19). The relative incidence of the types of the cardiopathy has changed in recent years. Rheumatic valvular disease is no longer as preponderant as before (16), in contrast to a greater etiologic role played by arteriosclerotic heart disease and myocardial infarction. Although atrial fibrillation is common in both the rheumatic and arteriosclerotic heart diseases, its relative incidence in the latter group has increased in the decades since 1950 (Table 32.1). Mural thrombi associated with myocardial infarction, occurring about 11% of the time, may sometimes embolize long before clinical and electrocardiographic evidence of their origin becomes available. In such cases of silent myocardial infarction, the differential diagnosis of embolism from arterial thrombosis may be difficult or even impossible (19). Arterial embolism may occur at any age, although the peak incidence is in the fifth, sixth, and seventh decades. The sex incidence varies with the cardiopathy. In a group with rheumatic heart disease, 78.3% were women,

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whereas in a group with myocardial infarction, 73.6% were men (19). The natural clinical course of a peripheral arterial embolism (Fig. 32.1) depends upon the location of the occlusion, the completeness of the luminal obliteration, the extent of secondary thrombosis, and the degree of spontaneous restoration of the collateral circulation. Among these, secondary thrombosis is one of the most important local factors. Indeed, by its occurrence, from an initial short segmental obstruction induced by the embolus, the secondary thrombus extends the occlusion distally to the main arterial trunk and its collaterals (Fig. 32.2). Thus, the latter, by involving a long segment, is a lesion far more dangerous to the viability of the limb than is the original relatively small embolus. Multiple emboli are known to occur either in the same extremity or at different arterial sites. It is usually assumed that they are the result of a shower of emboli and occur at about the same time (Fig. 32.3). The possibility of multiple embolic occlusions in the same extremity or at different locations including the visceral arteries, although well known, is not always appreciated (Fig. 32.4). Failure to do so may be responsible for the unsuccessful results in some cases of embolectomy (19–23). Recurrent emboli may occur in different locations or in the same vessel. In the latter case, one may suspect the possibility of in situ thrombosis, a differential diagnosis

TABLE 32.1 Nature of cardiopathy in arterial embolism Percentage Heart Disease Etiology Rheumatic Arteriosclerotic Arteriosclerotic: rheumatic

Before 1960

After 1963

(228 patients)* 40.4 50.8 1.25

(83 patients)† 7.7 84.0 10.5

*Data from Haimovici H. Peripheral arterial embolism: A study of 320 unselected cases of embolism of the extremities. Angiology 1950;1:20. †Data from Haimovici H, Moss CM, Veith FJ. Arterial embolectomy revisited [editorial]. Surgery 1975;78:209.

FIGURE 32.1 Natural course of 300 cases of surgically untreated arterial embolism of the extremities. (Based on data from Haimovici H. Peripheral arterial embolism: A study of 320 unselected cases of embolism of the extremities. Angiology 1950;1:20.)

FIGURE 32.2 Note the small size of a femoral embolus (light color) involving the bifurcation and the long secondary thrombus (dark color) removed from the superficial femoral and popliteal arteries.

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a

FIGURE 32.4 (A) Saddle aortic and right common femoral emboli. (B) Specimens removed during surgery.

FIGURE 32.3 (A) Right iliac and popliteal emboli. (B) Specimens of emboli removed during the same surgical procedure.

that should be kept in mind. The interval of recurrence may take a few days to several months. The possibility of recurrent embolization emphasizes the necessity for eradicating its source, whether it be valvular disease, atrial thrombosis, or some other cause of vascular or nonvascular origin. Atheroembolism, arterial embolism of atheromatous material, has been reported with increasing frequency (24–28). It may occur as microemboli following release of cholesterol crystals or other atheromatous debris from an ulcerated plaque, and as macroemboli resulting from major atheromatous plaques mixed with thrombi and cholesterol crystals that lodge in major systemic arteries. These atheroemboli may originate in an abdominal aneurysm or a nonaneurysmal lesion of the aorta or may follow surgical manipulation of the latter. Their differential diagnosis from a cardiogenic embolism is usually helped by the absence of any emboligenic heart condition. The clinical picture varies with the location of the involved arterial segment. The atheroemboli may go unrec-

ognized or unsuspected, especially in the group of microemboli. Greater awareness of the source of atheroembolism is basic for recognition of this entity (28).

Topographic Diagnosis The site of an embolic occlusion is generally easily identifiable (Fig. 32.5). The clinical criteria are: 1. 2. 3. 4. 5.

the site of the initial pain; the level at which the normal pulsation disappears; the noninvasive diagnostic modalities; the extent of the circulatory disturbances; and knowledge that emboli usually lodge at bifurcations.

Unfortunately, in a certain number of cases, especially in those with preexisting occlusive disease, the exact localization of the embolus may be difficult to determine without arteriography. Indeed, the presence of an atherosclerotic stenosis, either proximal to or distal from bifurcations, may represent a potential site of entrapment of the embolus. Because of this possible unconventional location of an embolus, it is essential that preoperative

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FIGURE 32.6 Sites and incidence of visceral emboli in 96 cases out of 228 patients. (Based on data from Haimovici H. Peripheral arterial embolism: A study of 320 unselected cases of embolism of the extremities. Angiology 1950;1:20.)

often undetectable or remain unsuspected, whereas major embolic occlusions display significant and often rapidly irreversible and lethal changes when occurring in cerebral, mesenteric, renal, or coronary vessels. FIGURE 32.5 Incidence of location of peripheral emboli in a series of 320 cases. (Based on data from Haimovici H. Peripheral arterial embolism: A study of 320 unselected cases of embolism of the extremities. Angiology 1950;1:20.)

arteriography be carried out in patients suspected of having associated preexisting arterial lesions.

Differential Diagnosis The recognition of a peripheral arterial embolism is usually simple. Although a sudden onset is quite characteristic, occurring in 81% of cases (19), in one in five cases there may be a progressive onset. Lack of routine evaluation of the extremities in patients with advanced heart disease may sometimes be responsible for the failure of prompt recognition of an arterial embolism. Conditions that may otherwise be confused with peripheral embolism are phlegmasia cerulea dolens, acute arterial thrombosis, acute thrombosis of a popliteal aneurysm, acute thrombosis of a nonarteriosclerotic artery, low-flow syndrome due to circulatory failure, dissecting aortic aneurysm, and arterial spasm. Awareness of these entities is essential in the differential diagnosis.

Associated Visceral Arterial Embolism Visceral emboli, isolated or associated with peripheral emboli, occur with greater frequency than is generally recognized (Fig. 32.6). It is well known that there is a considerable discrepancy between their clinical diagnosis and autopsy findings. Clinically, visceral emboli, if small, are

Indications for Embolectomy It is hardly necessary to point out that conservative measures (heparin, vasodilator drugs, fibrinolytic agents) are only adjuncts to, not substitutes for, arterial embolectomy, which is the method of choice and is applicable in almost all cases. Percutaneous aspiration thromboembolectomy has been described as an alternative in cases below the femoral bifurcation (29). Early embolectomy, 8 to 12 hours after onset— considered the optimal time for this procedure since the first successful case performed in 1911—is still a valid principle today. However, in late cases, the physiologic state of the limb, rather than the elapsed time from the onset of the occlusion, will determine operability. Late arterial embolectomy thus may still be indicated and is often successful if the limb still exhibits signs of viable tissues. Analysis of the clinical and pathologic data of late arterial embolectomies suggests that four factors govern their successful outcome: 1. 2. 3. 4.

a relatively damage-free arterial intima; nonadherence of the embolus and secondary thrombus to the intima; a patent distal arterial tree prior to embolization; and pretreatment with anticoagulants.

These factors facilitate a more complete extraction of the secondary thrombi, essential for achieving adequate revascularization of the limb. A contraindication to a late arterial embolectomy is frank gangrene involving part of the extremity (30).

392

Part V Occlusive Arterial Diseases FIGURE 32.7 (A) Right transfemoral aortogram (Seldinger technique). Embolic occlusion of the left common femoral artery in a 58-year-old woman who had mitral stenosis and auricular fibrillation. Note the smooth outline of the arterial tree. (B) The same arteriographic study disclosed an embolic occlusion of the right popliteal.

A

B

Grading of Embolic Ischemia of Lower Extremity In its simplest form, an arterial embolus by itself occludes only a short segment of an artery, and in the absence of spasm or secondary thrombosis, the distal circulation may be restored through collateral channels. However, a peripheral arterial embolism usually occurs in a more complex clinicopathologic setting. On the basis of our previous study concerning the degree of spontaneous restoration of the circulation in a series of untreated cases (19), the grading of arterial embolism is as follows: Grade I

Moderate ischemia with early pulse return: anischemic embolism (29.5%). Grade II Advanced ischemia with only partial late recovery: chronic postembolic ischemia (22.2%). Grade III Severe ischemia leading to variable degrees of gangrene, often with metabolic complications (28%). Grade IV Very severe ischemia with early fatal outcome, mainly the result of advanced heart failure or associated visceral emboli (11.3%).

Preoperative Evaluation Evaluation of an embolic occlusion and its ischemic manifestations is based on examination of the pulses, skin temperature and color changes, motion and sensory deficits, and the degree of contracture of the calf or forearm. Paralysis and anesthesia of the distal or entire limb are

ominous signs. Embolectomy may still be attempted but not without some reservation, especially if limb rigidity is present. If the location of the embolus and the preembolic status of the distal arterial tree are in doubt, and if Doppler evaluation is equivocal, arteriography appears essential (Fig. 32.7). Assessment of the underlying heart disease, the source of the embolism, and its correction should be undertaken without delay. The cardiac condition may determine, to some extent, how aggressively one should treat the arterial complication. In the presence of myocardial infarction, heart failure, or shock, a vigorous treatment should be instituted prior to embolectomy. During the few hours necessary to correct to an acceptable degree the cardiac function, heparin should be administered intravenously. Fibrinolysins, if available, may be injected directly into the involved artery. Their value, however, is still not well established. Routine blood chemistry analyses, a hematologic profile, and examination of urine for myoglobin may be of value in cases with early rigidity of calf or forearm muscles.

Anesthesia and Monitoring of Patient During Surgery In the majority of cases, local anesthesia can be used to great advantage. Since the introduction of the balloon catheter, this method is applicable in almost all cases of embolectomy. However, a light general anesthesia or additional sedation can be used if the patient is apprehensive. Epidural or spinal anesthesia may be advisable if the

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Exposure of Femoral Vessels Exposure should be adequate to afford easy access to the common, superficial, and deep femoral vessels. A longitudinal incision is carried out over the course of the femoral artery and is extended slightly superiorly above Poupart’s ligament and inferiorly by approximately 7.5 to 10 cm. The femoral artery occluded by an embolus appears fusiformly dilated and slightly bluish. Proximally, there is a vigorous pulsation, whereas distally, pulsation is usually completely absent. However, a transmitted pulsation may be perceived occasionally by palpation. This should not mislead one into the belief that the occlusion is more distal. Gentle palpation of the vessels may identify the exact extent of the embolic or thrombotic occlusion, except for a recent soft thrombus that may be difficult to feel. After the femoral sheath is opened, the vessels are easily mobilized. Double-looped nontraumatic occluding clamps with Silastic pads (Vesseloops, Med General) are placed around the superficial, profunda, and common femoral vessels. To prevent migration or breaking off of the embolus and propagated thrombus through the profunda or superficial femoral artery, the double-looped tapes are not tightened or are only moderately tightened, without occluding the vessel completely (Fig. 32.9). Arteriotomy

FIGURE 32.8 Sites of embolectomy.

procedure entails exposure not only of the groin vessels but also of the popliteal and leg arteries. Monitoring of the patient’s electrocardiogram, blood pressure, and blood gases of the involved limb may be helpful, especially in late cases of embolectomy with possible involvement of skeletal muscles.

Operative Techniques Since the introduction of the balloon catheter, the technique of embolectomy has been simplified, and the approach to the various vessels has been reduced to a few critical areas. Although in most instances the latter provide access to any occluded vessel, direct exposure of the involved arteries may nevertheless be necessary in some cases (Fig. 32.8). The technique of embolectomy will be described for femoral, aortic bifurcation, iliac, popliteal, and upper limb arteries.

A longitudinal incision about 1.0 to 1.5 cm long is carried out in the common femoral artery down to the origin of the profunda. This type of incision is preferable, especially if the artery is arteriosclerotic. A transverse arteriotomy may be indicated if the artery seems devoid of mural lesions. Extraction of Embolus and Secondary Thrombus Upon completion of the arteriotomy, the embolus tends to extrude by itself. A balloon catheter of an appropriate size (5 Fr.) is then introduced into the superficial femoral artery. In the absence of preexisting arteriosclerotic occlusion, the passage of the catheter usually reaches the tibial vessels easily. After achieving patency of the main arterial axis, a 4-Fr. catheter is introduced into the profunda femoris. Each of its primary branches is catheterized until all suspected thrombi are removed. A 6-Fr. catheter is then passed proximally toward the iliac artery or aorta for removal of a possible unsuspected thrombus. The balloon catheters may have to be passed more than once in all vessels to obtain a normal flow. Upon completion of the embolectomy, or rather thromboembolectomy, the arteries are copiously irrigated with a 5% heparinized saline solution. The femoral vessels are reclamped and the arteriotomy is closed (Fig. 32.10).

Femoral Embolectomy Preparation of Limb

Closure of Arteriotomy

Although the procedure may be confined to the groin at the level of Scarpa’s triangle, it is essential also to prepare the abdomen and the entire lower extremity.

Closure can be carried out either by a continuous running stitch, using No. 5 or No. 6 synthetic (polypropylene) suture material, or by interrupted stitches, especially in a

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return in the profunda and superficial femoral arteries, indicative though the pulses may be, does not, however, guarantee the patency of the popliteal and tibial arteries. Although backbleeding during the procedure may be considered a significant sign of distal patency, it does not necessarily indicate absence of residual thrombi. It should be pointed out that the retrograde bleeding may originate from a proximal major collateral. Because of these considerations, it is important, before leaving the operating room, to ascertain the presence of the popliteal and pedal pulses. Their restoration can be anticipated only in those patients in whom the arterial tree was patent in the preembolic episode. However, if there is a history of preexisting arteriosclerotic occlusive disease, unless there is a return of distal pulses, the nature of the restoration of the arterial tree cannot be ascertained on clinical grounds alone. If in doubt, arteriography may then allow identification of the distal arterial lesion. This is particularly true in a late arterial embolectomy (see below). Closure of Incision This procedure is carried out in layers in the usual fashion. A correct closure of the incision is obviously important to prevent any possible collection of serum, blood, or lymph, all of which may lead to infection. Heparinization During the procedure, the patient is heparinized either systemically by the intravenous route or directly through the involved arterial tree. In addition to the heparinized solution used during the procedure, 3000 to 5000 units of heparin is also injected before closure of the incision. Postoperative Clinical Evaluation

FIGURE 32.9 Femoral embolectomy. (A) Right common femoral embolus (stippled area) with secondary thrombosis both proximal and distal to it. (B) Balloon catheter being withdrawn from the external iliac and pushing out the embolus and thrombus.

transverse arteriotomy. Irrespective of the type of closure, it is essential to prevent stenosis of the artery by careful approximation of the arteriotomy edges or by vein patch angioplasty, if indicated. Checking Reestablishment of Patency The proximal patency is usually easily ascertained by the presence of a vigorous pulsation. The more difficult evaluation of patency is confined to the distal pulses. Their

Immediately after arterial restoration, the pain disappears, together with return of motor and sensory functions and of normal color and warmth of skin. In patients with incomplete restoration of arterial circulation, it may be several hours before partial or complete return of these signs and symptoms can be expected. The cardiac condition responsible for the peripheral embolism dominates to a large extent, in most cases, the postoperative care. It is essential to monitor the cardiopathy, restore cardiac rhythm, and use heparin postoperatively as prophylaxis against further embolization.

Aortic Bifurcation Embolectomy Embolic occlusion of the aortic bifurcation results in a dramatic clinical picture and usually occurs in a critically ill patient. Its incidence is about 10% of all emboli of the extremities. The prognosis for both limb and life before the present era was extremely poor, whether with or without surgery. Use of the retrograde technique has improved the overall outcome substantially.

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FIGURE 32.10 Extraction of embolus and secondary thrombus. (A) Balloon catheter in the superficial femoral artery being withdrawn through the arteriotomy and achieving extrusion of secondary thrombus. (B) Backbleeding from the superficial femoral after thrombectomy. (C) Balloon catheter being withdrawn from the profunda femoris together with the secondary thrombus. (D) Backbleeding from the profunda femoris after thrombectomy. (E) Closed arteriotomy.

A

C

B

D

E

Diagnosis of an aortic saddle embolism is relatively simple. The presence of cardiopathy with the suddenness of bilateral ischemia with paraplegia leaves little doubt about the diagnosis. A dissecting aortic aneurysm, rather rarely encountered, may mimic an embolic syndrome and should be suspected in the presence of an atypical clinical picture (31). At the other end of the diagnostic spectrum, an incomplete aortic occlusion may be mistaken for a more distal embolism (Fig. 32.11). A translumbar or intravenous aortogram, usually optional, may be helpful in such cases in settling the diagnosis. Several technical approaches are available for aortic embolectomy: 1) transfemoral or retrograde, the most commonly used; 2) transperitoneal; and 3) retroperitoneal. The last two are rarely indicated nowadays. Retrograde or Transfemoral Embolectomy Since the introduction of the Fogarty balloon catheter (Fig. 32.12), the results of disobstruction of the aortic bi-

FIGURE 32.11 A riding aortic embolus, incompletely occluding the aortic bifurcation.

396

Part V Occlusive Arterial Diseases FIGURE 32.12 Aortic embolectomy. (A) Balloon catheter maximally distended in the abdominal aorta above the embolus. (B) Catheter being withdrawn through the right femoral arteriotomy together with the aortic embolus.

A

B

furcation have improved considerably because of a more complete and easier retrieval of the embolus and the propagated thrombi. Advantages The advantages of the retrograde technique are: 1. 2. 3. 4.

simple groin exposure of the femorals under local anesthesia; direct evaluation of distal propagated thrombi and of preexisting femoral arteriosclerotic lesions; lack of operative shock; and usually uncomplicated postoperative course.

Disadvantages Being a blind procedure, a successful embolectomy may sometimes be difficult to achieve in cases of: 1. 2. 3. 4. 5.

severe atherosclerotic lesions of the aortoiliac segment; marked iliac tortuosity; coexistence of visceral emboli, especially of the mesenteric artery; emboli of the hypogastric vessels, the latter being missed through this approach; and an undetected, acutely thrombosed, small aortic aneurysm.

These conditions are fortunately not common. The advantages of the retrograde approach outweigh by far the occasional pitfalls, which may be avoided if one bears in mind such possibilities.

Technique Although the technique consists of a bilateral transfemoral approach, it is essential also to prepare the abdominal region and both lower extremities. This wide operative field preparation may be necessary if a different or additional arterial exposure is required. Both femoral arteries in the groin are exposed through the standard longitudinal incision. Local anesthesia and monitoring of the patient are similar to those previously described for a simple femoral embolectomy. The common, superficial, and profunda femoris vessels are mobilized, and tapes are placed about them. After careful palpation of the vessel to determine the presence of either arteriosclerotic lesions or thrombotic material, the distal branches may not be clamped or only partially closed by incompletely tightening the tapes. The best and most expeditious way for handling the two groins is by two surgical teams. Arteriotomy is carried out in one common femoral artery, preferably on the side where the ischemia is most pronounced. On the opposite side, the superficial and profunda femoris vessels are occluded by atraumatic tapes. Disobliteration of the distal vessels is carried out first, by means of a Fogarty catheter of an appropriate caliber (4 or 5 Fr.), starting with the superficial femoral artery and then checking the profunda femoris. After obtaining a good or acceptable backflow, the two vessels are irrigated with heparinized solution. Proximal disobliteration is carried out with a largecaliber catheter (6 Fr.), which is introduced up to the renal vessels. The balloon is then inflated until an elastic resistance is perceived. At this point, the catheter is with-

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FIGURE 32.13 Aortic (A) and popliteal (B) embolectomy through a common femoral arteriotomy. Note the inflated balloon in the aorta (A) and posterior tibial trunk (B).

A

B

drawn through the arteriotomy. As the balloon catheter passes from the aortic level to the iliac, the balloon must be slightly deflated in order to readjust it to the diameter of the iliac. This maneuver may have to be repeated until one obtains a vigorous systolic flow. After a good pulsation is obtained above the arteriotomy, the attention is shifted to the opposite side. A good pulsation should be obtained on the contralateral femoral artery as determined by palpation. Should there be the slightest suspicion of a thrombus at this level, exploration of the femoral artery is mandatory. A similar set of maneuvers is then carried out, first in the superficial and profunda femoral vessels, and then proximally in the iliac artery and aorta. When patency of both sides is achieved, the arteriotomy of both femoral arteries is closed in the usual fashion (Fig. 32.13). Distal Arterial Patency Immediately after the arteriotomies are closed, the distal pulses must be ascertained. Their appearance, in addition to return of the normal color of the skin and filling of the superficial veins, is indicative of good flow. Intraoperative use of Doppler pulse determination of the peripheral vessels may be quite helpful. If unsatisfactory, intraoperative arteriography should be used. Any doubt about the quality of patency of the dis-

tal arterial tree in one or both lower extremities requires mandatory reexploration of one or both. Immediately postoperatively, the abdomen should also be examined clinically and, if necessary, radiologically in order to determine whether there is any involvement of the mesenteric vessels. Pitfalls The preceding technique is simple and easy to carry out in the presence of normal arteries or arteries at least devoid of any major arteriosclerotic changes. However, in the presence of severe mural lesions or of secondary thrombosis involving the distal arterial tree, it becomes necessary to explore the superficial femoral or the popliteal artery (Fig. 32.13). Transperitoneal Aortic Embolectomy Indications for this approach are rare nowadays. However, in the presence of an incomplete disobliteration through the femoral arteries, it is necessary to expose the aortic bifurcation directly. The reason for this difficulty resides primarily in the associated stenotic arteriosclerotic changes of the bifurcation. Advantages of such an exposure are obvious, as the lesions of the aortic bifurcation and of the iliac arteries can be properly evaluated and dealt with. Disadvantages,

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however, include a more extensive surgical exposure, necessitating general or spinal anesthesia. The operative risk is obviously much greater than in the previous approach. Technique The technique consists of a median or left paramedian incision extending from the pubis to above the umbilicus and, if necessary, up to the xiphoid process. The small bowel is eviscerated, and the posterior parietal peritoneum is incised along the aortic pulsation down to the pelvis. The abdominal aorta is mobilized below the inferior mesenteric artery. The two common iliac arteries are mobilized, and tapes are placed about them. An arteriotomy is carried out, preferably in one of the common iliac arteries, through which the embolus and the thrombus are extruded, including the one from the opposite side, if present. The distal arterial tree is cleared through the arteriotomy by means of a Fogarty catheter. Should any suspicion exist about the opposite side, its patency should be ascertained through a separate arteriotomy. After the arteriotomies are closed and the arterial flow is reestablished, the abdominal closure is carried out in the usual fashion. Retroperitoneal Aortic Embolectomy The aorta and its bifurcation may be exposed through a left retroperitoneal approach, using the technique described in Chapter 30. Advantages of this exposure, especially in a thin individual, are obvious. The operative risk is certainly less than with the transperitoneal approach. Disadvantages, especially in an obese individual, may be due to inadequate exposure of the right iliac artery. However, incision of the left rectus abdominis may facilitate the exposure, and an arteriotomy can be done without too much difficulty. Technique The embolectomy is carried out through an arteriotomy in the left common iliac artery, as previously described. The patency of the distal arterial tree on this side is easily evaluated by means of an appropriate balloon catheter. On the opposite side, if necessary, a catheter can be introduced through a separate arteriotomy in the contralateral common iliac. Should there be any need, this exposure also offers easy access for a lumbar sympathectomy. This may be particularly indicated if there is a history of preexisting arteriosclerotic lesions of the distal arterial tree. Postoperative Care Special attention must immediately be directed toward both the cardiopulmonary function and the lower extremities. The patient is transferred to the intensive care unit, where cardiac monitoring and pulmonary function are closely supervised. Anticoagulation may be deferred for 12 to 24 hours to avoid hematomas because of the extensive abdominal or retroperitoneal dissections. After this period, intravenous heparin is administered in order to prevent any

further embolization and possibly distal rethrombosis. Aspirin and dipyridamole are administered as soon as feasible postoperatively. Oral anticoagulation should be instituted and maintained for life. The lower extremities are checked carefully for pulses or for any sign of recurrence of ischemia. Doppler ultrasonic technique is most helpful, short of arteriography, for ascertaining patency and arterial flow. Revascularization complications should be watched for very closely (see below).

Iliac Embolectomy The embolus usually blocks the common iliac artery and extends into the external and internal iliac arteries. The clinical picture is that of major sudden ischemia of one lower extremity. Bilateral iliac embolism is indistinguishable from the clinical picture of a saddle embolus of the aorta. The technical approaches available for an iliac embolectomy are transfemoral or retrograde, the most commonly used, and retroperitoneal. Retrograde or Transfemoral Embolectomy Despite the fact that this is a unilateral procedure through the groin, it is important to bear in mind two possibilities: 1. 2.

difficulty of complete removal of the embolus and propagated thrombus; and inadvertent proximal dislocation of the thrombotic material into the aorta and the opposite iliac artery.

Consequently, a wide preoperative preparation of the abdomen and of both thighs is mandatory should it become necessary to expose directly the iliac or the opposite femoral artery. Local anesthesia and the various steps of the techniques are identical with those described for aortic embolectomy. Retroperitoneal Embolectomy Although local anesthesia can be used, because of discomfort it is most often desirable to use spinal or epidural or even general anesthesia. A wide retroperitoneal exposure of the iliac vessels as well as of the aortic bifurcation is necessary for an adequate procedure. The arteriotomy, whether longitudinal or transverse, is best carried out in the common iliac artery just above its division into the internal and external branches. This affords easy access to the latter for thrombectomy, if indicated. A possible difficulty may result from the thrombus propagated into the femoral artery, especially into its superficial and profunda vessels. Exposure of the femoral artery may then become necessary.

Popliteal Embolectomy A popliteal embolism may carry a more serious prognosis than that of a femoral artery. This is especially true in

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FIGURE 32.14 Popliteal embolectomy. (A) Skin incision (dotted line) for the lower third medial-thigh approach to the popliteal artery. (B) Balloon catheter embolectomy being done through a longitudinal arteriotomy.

A

B

older patients with preexisting arteriosclerotic lesions of the tibial arteries, primarily in diabetic patients in whom the leg arteries are much more severely involved than in nondiabetic persons. Early embolectomy appears mandatory, therefore, to avoid secondary thrombosis in the most distal branches and thereby help salvage the limb. A preoperative femoral arteriogram, with special emphasis on visualizing the popliteal and leg arteries, is essential. The popliteal embolus may be approached indirectly through the femoral artery in the groin or directly through a medial exposure of the lower third of the thigh above the knee (Fig. 32.14). Although these conventional approaches may be suitable in some cases, in most instances it is best to expose the infragenual popliteal artery for its direct access together with the origin of the tibial arteries (anterior tibial and tibioperoneal trunk with its two branches). One of the advantages of exposing the distal popliteal artery is the absence of significant collaterals arising from it or its branches. Although this segment is smaller than the proximal popliteal, the infragenual segment is of sufficient caliber for easy graft attachment. In addition, this segment tends to be better preserved and is usually free of artheromatous degenerative changes, in contrast to the proximal popliteal. Exposure of the distal popliteal is achieved through a medial paratibial route. The anatomic details of this exposure are described in Chapter 30. Essentially, the steps for this exposure consist of a skin incision 8 to

10 cm long, parallel to the posterior medial border of the tibia, opening of the crural fascia below the tendons of the semitendinosus and gracilis, exposure of the neurovascular bundle, which is usually situated quite deep against the bone surface covered by the popliteus muscle, opening of the vascular sheath surrounding the vessels, freeing of the popliteal artery from its satellite veins, section and ligation of the network of venules surrounding the artery, and division of the soleus muscle for exposure of the distal segment of the popliteal with its branches. The arteriotomy of the popliteal is carried out in its distal segment facing the origin of the anterior tibial and extended down to the tibioperoneal trunk (Fig. 32.15). This arteriotomy facilitates the insertion of the Fogarty catheter into the anterior tibial artery through direct vision of its ostium, as well as the introduction of the catheter into the posterior tibial and peroneal arteries (see Chapter 30). Should the thromboembolic material not be retrieved completely, a retrograde irrigation of these vessels through the retromalleolar incision of the posterior tibial artery may be attempted, although this procedure has given very few positive results. In a popliteal embolectomy, perhaps more than in any other, caution should be exercised in inflating the balloon catheter. Overdistention may cause damage to the intima or even its avulsion, especially in diabetic patients with arteriosclerotic lesions of the tibial arteries. Removal of the catheter should be done with great gentleness, with neither overdistention nor underdistention.

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plications may be due to ischemic rhabdomyolysis and the revascularization syndrome (see Chapter 40). In the assessment of rates of limb salvage, amputation, and mortality, it appears that the published criteria are far from standardized. Hence, these reports contain a number of built-in statistical errors inherent in the method of estimating the various postoperative findings. In evaluating the results of embolectomy, it is essential to properly identify gradations of the severity of ischemia along with the systemic factors. Finally, in reporting limb salvage, it is important to indicate whether rates are calculated for the survivors or for the entire series, a fact not always mentioned. As useful as they may be, statistical compilations may not provide an accurate and meaningful picture of the underlying factors that govern results of an arterial embolectomy. Therapeutic guidelines derived from such widely diverse statistics are nevertheless compelling. Treatment without delay remains the mandatory principle. Early arterial embolectomy and heparinization, either alone or combined, along with management of the patient’s cardiopulmonary and metabolic problems, are the best means at our disposal for improving limb salvage and patient survival rates.

Arterial Embolectomy for Upper Limb Embolism

FIGURE 32.15 Medial leg exposure of below-knee popliteal artery and its trifurcation branches. (See text for embolectomy procedure at this level.)

Results of Embolectomy of Lower Extremity The many factors that may determine the outcome of an embolectomy are not always uniformly interpreted in the published reports (21,32). The relative significance of the individual factors may vary substantially. In a review of 35 collected series, Blaisdell et al. (17) found 14 reports with mortality rates ranging from 15% to 24%, 11 reports with rates between 30% and 48%, and a median group of 10 series reporting mortality rates of 25% to 29%. The same wide range holds true for limb salvage, with rates between 40% and 81%. The entire series included 3,320 embolectomies, with an average limb salvage rate of 63% and an average mortality rate of 28%. The highest mortality rate is due to congestive heart failure and acute myocardial infarction, with pulmonary embolism being the second major cause. The other factors are strokes, mesenteric infarction, hepatic coma, and miscellaneous etiologies. In reporting causes of mortality, the literature rarely mentions that metabolic and renal com-

The relative incidence of upper limb emboli as related to the total number of peripheral emboli is variably reported and ranges between 16% and 32.6%. These percentages indicate that this embolic location is less infrequent than had been reported earlier (19,32–39). The nature of the cardiopathy, which is the source of emboli, has changed radically during the past three decades, as indicated earlier in this chapter. Distribution of emboli assumes a rather constant pattern. Their relative distribution is shown in Table 32.2. These data are based on the compilation of seven statistical studies. As can be seen, the greater incidence in the brachial artery suggests that the majority of upper limb emboli are of small size. Symptomatology varies according to the arterial level involved. In a subclavian–axillary artery embolism, the proximal pulsation is usually found in the supraclavicular fossa, with ischemic manifestations detectable to midarm level. In a brachial artery embolism, the occlusion may occur either in the upper third of the arm, just above the profunda brachii, in the midarm at the origin of the superior ulnar collateral artery, or at the bifurcation of the brachial artery in the antecubital fossa. Therefore, the brachial pulse may be felt either at the distal axillary, or at midarm or above the antecubital fossa. In these cases, the ischemic manifestations involve the hand and forearm up to or below the elbow (Fig. 32.16). In an embolic occlusion of the radial or ulnar arteries, clinical manifestations are usually less pronounced and remain localized to the distal forearm and hand.

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TABLE 32.2 Distribution of emboli of upper extremity Reference Haimovici (39) Daley et al. (22) Baird and Lajos (32) Darling et al. (20) MacGowan and Mooneeram (35) Raithel (36) Savelyev et al. (38) Totals (%)

Subclavian

Axillary

Brachial

Radial

Ulnar

— — 10 4 2 4 47 67 (11.7)

15 3 22 20 3 5 66 134 (23.4)

30 36 64 44 17 15 143 349 (61.0)

4 — 4 — 2 — 3 13 (2.3)

4 — 4 — — — 1 9 (1.6)

FIGURE 32.17 Brachial arteriogram indicating a massive occlusion between the distal axillary and antecubital fossa. FIGURE 32.16 Diagram indicating the three major locations of brachial emboli (upper, middle, and antecubital brachial).

Evaluation of the degree of viability of the hand or forearm may be determined by the color, temperature of skin, motion of fingers or wrist, sensory perception, degree of muscle edema, or rigidity. Noninvasive procedures, such as pulse volume recording (PVR) and Doppler pulse recording, may be helpful in assessing the level of arterial blockage. However, arteriography is the decisive diagnostic means, especially when clinical and noninvasive evaluation cannot identify the presumptive locations and extent of the occlusive process (Fig. 32.17). An intra-

operative arteriogram often may be necessary for assessing the result of the embolectomy. When properly performed, arteriography carries few risks as measured against the valuable information it may provide.

Prognosis Although the potential hazards to the viability of the upper limb are thought to be less than those of an embolism of the lower limb, morbidity and mortality rates in these cases are far from negligible (Table 32.3). Thus, in an earlier reported series of untreated surgical patients, 11 of

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TABLE 32.3 Natural course of nonsurgically treated arterial embolism of upper extremity based on location Location

Cases (%)

Gangrene and Early Death (%)

Gangrene and Amputation

Recovery (%)

Axillary Brachial Radial–ulnar

13 (28.3) 25 (54.3) 8 (17.4)

4 (30.8) 4 (16.0) 0 (0)

1 (7.7) 1 (4.0) 1 (12.5)

8 (61.5) 20 (80.0) 7 (87.5)

46, or 24%, died either with gangrene or before development of necrosis of the hand. In addition, gangrene occurred in 7% of the survivors, requiring a major amputation either of the hand or arm, thus raising the total percentage of gangrene to 31%. Furthermore, a number of patients developed functional impairment of the limb associated with occasional gangrene of one or several fingers. Several recent publications and our own experience clearly show that either persistent postembolic ischemic changes or frank gangrene of fingers or hand may occur in a rather substantial percentage of unoperated patients.

Indications The indications for embolectomy, which is usually performed under local anesthesia, are widely applicable, while contraindications are minimal and practically confined to a few seriously ill patients. Technique of embolectomy needs no elaboration except for reemphasis of its preferential use in certain anatomic areas of the arterial tree (Figs. 32.18 and 32.19). Subclavian–axillary embolectomy can be performed through a skin incision of the upper third of the arm using a medial approach to the brachial artery. The balloon catheter is first passed proximally until a forceful systolic jet is obtained behind the removal of the embolus. The catheter is then passed distally for retrieval of secondary thrombi. However, for anatomic reasons, the catheter may not reach the distal thromboembolic material through a midbrachial artery exposure. The procedure is then carried out through a distal brachial arteriotomy. Removal of emboli through the distal brachial artery is best achieved by its exposure in the antecubital fossa and is the most adequate approach not only for this location but also for the axillary-subclavian embolectomy. It provides also a better access to the peripheral arterial tree in the event that other thromboemboli occurred distally. The antecubital fossa is exposed in the usual fashion, and the artery is mobilized with its bifurcation of the radial and ulnar. Fogarty catheters of 2 and 3 Fr. can be introduced under direct vision into the two branches and thus help retrieve most of the peripheral thromboembolic material. Embolectomy of the proximal palmar arch may be attempted in certain instances when the hand remains

partially symptomatic in spite of the presence of wrist pulses (Fig. 32.20). Fasciotomy may be indicated in a small number of cases only if the edema of the muscles is severe enough to produce tension in the forearm. In general, the edema of the forearm in patients with restoration of arterial flow subsides within a few days. Results of arterial embolectomy for upper limb embolism are indicated in Table 32.4, which reviews 322 instances compiled from six reports. Briefly, successful embolectomies were divided into those with return of wrist pulses and complete circulatory restoration (55%) and those with salvage of the limb without return of wrist pulses (23.9%), making a combined limb salvage rate of 78.9%. Gangrene occurred in 9.3%, and mortality in 11.8%. In general, mortality following embolectomy was related primarily to the gravity of the cardiopathy and least related to the surgical procedure per se.

Special Problems in Arterial Embolism Associated Atherosclerosis of the Arterial Tree Preexisting arteriosclerotic occlusion of the superficial femoral artery is not an unusual finding in patients with arteriosclerotic heart disease. The latter is more prevalent today as a cause of peripheral emboli than in the past; therefore, it is not surprising that these patients may have associated arteriosclerotic lesions of the peripheral arterial tree. Many of these patients may have past histories of intermittent claudication, clearly suggesting the coexistence of this associated occlusive disease. Furthermore, asymptomatic arteriosclerosis due to mild or moderate stenosis is often found in such patients. In these cases, the results of embolectomy can be adversely affected by such lesions, especially in diabetic patients. In a specific example in which an occlusion of the superficial femoral artery is present but not detected preoperatively, an awareness of an embolus to the common femoral bifurcation may result in more dramatic ischemic and neurologic changes than in an uninvolved peripheral arterial tree (Fig. 32.21). Because of the simultaneous embolic blockage of the profunda femoris, thrombosis of the popliteal artery may

Chapter 32 Arterial Embolism of the Extremities and Technique of Embolectomy

403

A

A B

B C

C FIGURE 32.18 Subclavian–axillary embolectomy. (A) Skin incision (dotted line) for the upper third medialarm approach of the brachial artery. (B) Subclavian– axillary passage of a balloon catheter for removal of an embolus. (C) Distal brachial passage of the catheter for removal of secondary thrombi.

occur distal to the existing arteriosclerotic occlusion of the superficial femoral (Fig. 32.22). In such instances, if the femoral embolectomy is unable to restore the collateral supply to the leg and foot, it is necessary to explore the popliteal artery, either by means of an arteriogram or by direct exploration of the popliteal artery through a medial approach in the lower third of the thigh. Often, a soft thrombus may be found in it, the removal of which may be crucial for a successful outcome of the femoral embolectomy. It should be reemphasized that intraoperative arteriography is essential to properly manage the situation.

Results of Late Arterial Embolectomy Reported results of late arterial embolectomy, i.e., beyond 10 hours after onset, indicate that even if the operation is

FIGURE 32.19 Brachial artery embolectomy at the antecubital level. (A) Skin incision (dotted line). (B) Balloon catheter being withdrawn from the radial artery together with an embolus and secondary thrombus. (C) Catheter being withdrawn from proximal arteries (brachial and axillary) together with a thrombus.

performed one or several days beyond the accepted optimal time, complete or adequate restoration of arterial flow to the limb may be achieved, although morbidity and mortality are usually increased. Thus in my series of 28 cases of embolectomy performed after a delay ranging from 22 hours to 21 days after onset (30), revascularization was achieved in 18 cases, or 64.3%. Limb salvage reported by others ranged between 55.5% and 77% (40–42). Although early embolectomy remains the best treatment, indications for late arterial embolectomy should be based primarily on the physiologic state of the limb, and to a lesser extent on the chronologic factor. The absolute percentages of limb salvage and mortality reported for late arterial embolectomy series may not be entirely dependable, since patients with such conditions may have survived arterial embolic occlusions that only moderately threatened the viability of their limb. With a less select group, it is possible that limb loss and mortality rates could be much higher than in the isolated

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published reports, especially if they are not considered in the context of the total group of embolic cases.

Complications Complications associated with arterial embolectomy may be related to venous thromboembolism, technical pitfalls, and metabolic effects.

Venous Thromboembolism Venous thrombosis of the extremity involved with arterial embolism is perhaps more frequent than the literature would indicate, this being especially true in cases with late or prolonged occlusions. In an early study, this condition was noted in 7% of our cases (19). Fogarty et al. reported a 27% incidence of active venous thrombosis in their series (10). After a successful embolectomy, the limb may not be salvageable if there is an associated massive venous thrombosis. Routine inspection of the adjacent vein for presence of thrombosis is recommended. If such a lesion is suspected, a venotomy should be carried out and the venous tree explored with a venous Fogarty catheter, introduced both proximally and distally, to ascertain its patency. Venous aspiration, if required, should be accompanied by heparinization of the limb on the operating table. This maneuver may avert pulmonary embolism (43,44).

Technical Pitfalls Clamping Clamping of an arteriosclerotic and calcific artery may result in damage to the wall, which may necessitate an endarterectomy to prevent local thrombus formation. Before clamping the artery, therefore, it is recommended to avoid areas of mural calcification and to attempt to place the clamps in soft areas or use Vesseloops or nontraumatic clamps with Silastic pads. Complications Associated with Embolectomy Balloon Catheters These have been noticed ever since the introduction of balloon catheters in the management of occlusive arterial disease. Though the great advantages of the balloon catheter are well recognized, its use is indeed not always free of potential hazards (45–48). Several possible complications associated with its use are: 1. FIGURE 32.20 Proximal hand and wrist arteriograms indicating emboli of the radial and ulnar arteries of left hand.

2.

perforation of the arterial wall, followed by extravasation of blood in varying degrees; intimal dissection, which may result in ulceration with secondary thrombosis;

TABLE 32.4 Results of arterial embolectomy of the upper extremity Reference

Salvage with Pulses

Salvage without Pulses

Gangrene

Operative Mortality

7 17 20 52 101 20 105 322

4 15 10 26 28 14 80 177 (55%)

3 1 10 15 42 3 3 77 (23.9%)

0 1 0 4 19 3 3 30 (9.3%)

0 0 0 7 12 0 19 38 (11.8%)

冧

Champion and Gill (34) Baird and Lajos (32) MacGowan and Mooneeram (35) Darling et al. (20) Savelyev et al. (38) Sachatello et al. (37) Savelyev et al. (38) Totals

No. of Cases

78.9%

Chapter 32 Arterial Embolism of the Extremities and Technique of Embolectomy

A A

B

FIGURE 32.21 (A) Mild stenosing atherosclerosis (a) of the superficial femoral artery. (B) Embolic occlusion of the common femoral and its bifurcation (a), and thrombotic occlusion of the superficial femoral (b).

3. 4. 5.

6.

avulsion of atherosclerotic plaques; breakage of a catheter, with its retention in the arterial lumen; impaction of an embolus or thrombus into the distal arterial tree or shifting of the thrombus from one branch to another, which may lead to severe ischemia; and arteriovenous fistulas.

Although some of these complications may not always jeopardize the viability of the limb, their repair in most instances is mandatory as soon as they are recognized. Prevention Knowledge of the nature of the vascular pathology, especially the association of thromboembolism with arteriosclerosis, and a clear understanding of the function and limitations of the balloon catheter are essential for avoiding some of the more common hazards. Gentle manipulation of the catheter is the key to avoiding pitfalls and complications. After the uninflated catheter is introduced as far as is necessary, the balloon is slowly inflated until the feeling of complete occlusion of the lumen is deemed to be sufficient. At that point, withdrawal of the balloon is started (Fig. 32.23), and its volume is adjusted in accordance with the diameter of the artery either from the proximal to the distal or from the distal to the proximal area of its introduction. For instance, in passing the catheter into the aortoiliac

405

B

FIGURE 32.22 (A) Secondary thrombosis of the popliteal artery (c). (B) Reestablishment of patency of the common femoral by embolectomy and of the popliteal by thrombectomy.

segment, the balloon is inflated until complete obliteration of the lumen is achieved. Then, as the catheter is being withdrawn toward the femoral artery, the tension in the balloon must be progressively reduced. Conversely, if the catheter is first introduced distally into the tibial vessels, the volume of the balloon has to be gently and cautiously increased as it travels from the ankle toward the popliteal and into the femoral artery. The initial withdrawal of the catheter should be effected with extreme caution and gentleness, with progressive inflation for complete removal of the distal thrombus and embolus. Although the passage is usually smooth in the presence of a free and normal distal or proximal arterial tree, associated stenotic arteriosclerotic arterial changes may present serious hazards. Most complications occur in this type of arterial setting. Progression of the withdrawal of the balloon catheter during embolectomy in an atherosclerotic artery should, therefore, proceed with greater caution to adjust periodically the distention of the balloon to the luminal diameters. This can be effected only by manual appraisal of the pressure of the balloon through the ease with which it passes from one area to another in its withdrawal. To achieve this goal, it is essential that the surgeon control the degree of balloon distention and deflation throughout the withdrawal of the catheter.

Metabolic Complications Associated with Severe Embolic lschemia Reestablishment of arterial flow to an extremity following an acute embolic occlusion results in morphologic and functional recovery in a large percentage of patients; however, in a small number of instances (7.5% to 15%), even

406

Part V Occlusive Arterial Diseases FIGURE 32.23 (A–D) Progression of withdrawal of the balloon catheter during embolectomy in an atherosclerotic artery. Note the changes in the degree of balloon inflation matching the luminal diameters.

A

B

C

D

if arterial patency is achieved, a complex myopathicnephropathic-metabolic syndrome may be observed, often leading to loss of limb and life (11–13,49). The manifestations of this syndrome are divided into three stages: 1. 2. 3.

the ischemic or devascularization phase; the revascularization phase; and the reperfusion of the ischemic muscles.

In the first phase, the clinical imprint of four outstanding findings characterizes the ischemic or devascularization phase: excruciating pain, pronounced ischemia of tissues, rigidity of the limb, and massive edema. Besides the degree of pain, the most striking of these signs is the rigidity (rigor mortis) of the extremity. This sign, which I consider the most important alarm signal, is always present many hours before other clinical and laboratory findings, and is highly suggestive of the nature of the underlying pathologic condition. Within 10 to 12 hours after the onset of the acute arterial occlusion, the patient displays oliguria, azotemia, and myoglobinuria, together with variable degrees of metabolic acidosis. During the revascularization phase, the clinical picture and the metabolic changes, even if unnoticed during the acute phase, appear extremely severe. Shortly after blood flow is reestablished, massive edema and huge blis-

ters of the limb occur, together with rewarming of the skin, although distal gangrene and necrosis of the calf appear. Often even after a successful embolectomy, the muscles remain edematous. Because of the unyielding fascial compression around the calf muscles, the latter may turn into frank gangrene in such cases. It is then imperative to perform one or several fasciotomies to relieve the tension and release the edema from the muscles. This may be a limb-saving procedure. During the reperfusion of the ischemic muscles, metabolic studies indicate a decreased blood pH, an effluent low venous oxygen tension (PO2), an effluent high venous carbon dioxide tension (PCO2), elevation of serum potassium and creatine phosphokinase (CPK) concentrations, and alterations of other enzymes related to the striated muscle, such as lactic dehydrogenase (LDH) and serum glutamic oxaloacetic transaminase (SGOT). Because of the sequence of the clinicopathologic events, I have proposed the term myonephropathic– metabolic syndrome for this condition (11–13,49) (see Chapter 40). Management of these metabolic complications depends essentially on their immediate recognition. It is imperative to reestablish the electrolyte balance, especially to reduce serum potassium to normal levels by oral or rectal administration of exchange resins and, if necessary, by hemodialysis. Alkalinization of the patient

Chapter 32 Arterial Embolism of the Extremities and Technique of Embolectomy

to combat acidosis should be carried out without delay. This treatment is all the more mandatory if myoglobinuria is present or suspected, since myoglobin precipitates readily in the renal tubules in an acid milieu. Use of bicarbonates is essential in the prevention of the renal complication. In the presence of renal failure, hemodialysis should be used until kidney function is restored. Fasciotomies should be carried out in the presence of muscle edema as mentioned above. The CPK serum level is usually high. Its degree is an index of the extent of muscle necrosis. Mannitol and tromethamine (THAM) are to be used without delay, to avoid further metabolite release. Amputation, so often necessary because of massive gangrene, may be indicated even in the presence of ischemic lesions without frank gangrene as a prophylactic measure to remove the source of the metabolites from the necrosed skeletal muscles.

References 1. Mosny E, Dumont J. Embolie femorale au cours d’un restrecissement mitral pur. Arteriotomie. Guerison. Bull Acad Med (Paris) 1911;66:358. 2. Key E. Embolectomy in the treatment of circulatory disturbances in the extremities. Surg Gynecol Obstet 1923;36:309. 3. Key E. Embolectomy of the vessels of the extremities. Br J Surg 1936;24:350. 4. Haimovici H. Les embolies arterielles des membres. Paris: Masson et Cie, 1937. 5. Lerman J, Miller FR, Lund CC. Arterial embolism and embolectomy. JAMA 1930;94:1128. 6. Crawford ES, DeBakey ME. The retrograde flush procedure in embolectomy and thrombectomy. Surgery 1956;40:737. 7. Kartchner MM. Retrograde arterial embolectomy for limb salvage. Arch Surg 1972:104.532. 8. Murray DWG, Best CH. The use of heparin in thrombosis. Ann Surg 1938;108:163. 9. Murray DWG. Heparin in thrombosis and embolism. Br J Surg 1940:27:567. 10. Fogarty TJ, Cranley JJ, et al. A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963;116:241. 11. Haimovici H. Arterial embolism with acute massive ischemic myopathy and myoglobinuria: evaluation of a hitherto unreported syndrome with report of two cases. Surgery 1960;47:739. 12. Haimovici H. Arterial embolism, myoglobinuria and renal tubular necrosis. Arch Surg 1970;100: 639. 13. Haimovici H. Muscular, renal and metabolic complications of acute arterial occlusions: myonephropathicmetabolic syndrome. Surgery 1979;85:461. 14. Freund U, Romanoff H, Floman Y. Mortality rate following lower limb arterial embolectomy: causative factors. Surgery 1975;77:201. 15. Green RM, DeWeese JA, Rob CG. Arterial embolectomy before and after the Fogarty catheter. Surgery 1975;77:24.

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16. Haimovici H, Moss CM, Veith FJ. Arterial embolectomy revisited [editorial]. Surgery 1975;78:209. 17. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surgery 1978;84:822. 18. Warren R, Linton RR. The treatment of arterial embolism N Engl J Med 1948;238:421. 19. Haimovici H. Peripheral arterial embolism. A study of 320 unselected cases of embolism of the extremities. Angiology 1950;1:20. 20. Darling RC, Austen WG, Linton RR. Arterial embolism. Surg Gynecol Obstet 1967;124:106. 21. Haimovici H. Arterial embolism: peripheral and visceral. In: Haimovici H, ed. The surgical management of vascular diseases. Philadelphia: JB Lippincott, 1970:71. 22. Daley R, Mattingly TW, et al. Systemic arterial embolism in rheumatic heart disease. Am Heart J 1951;42:566. 23. Hara M, Williams GO. Multiple arterial emboli. Surgery 1966;60:804. 24. Gore I, Collins DP. Spontaneous atheromatous embolization: review of the literature and a report of 16 additional cases. Am J Clin Pathol 1960;32:415. 25. Wagner RB, Martin AS. Peripheral atheroembolism: confirmation of a clinical concept, with a case report and review of the literature. Surgery 1973;73: 353. 26. Kwaan JHM, Conolly JE. Peripheral atheroembolism. Arch Surg 1977;112:987. 27. Kempczinski RF. Lower extremity arterial emboli from ulcerating atherosclerotic plaques. JAMA 1979;241:807. 28. Haimovici H. Atheroembolism. In: Haimovici H, ed. Vascular emergencies. New York: Appleton-CenturyCrofts, 1982:205. 29. Turnipseed WD, et al. J Vasc Surg 1986;3:437. 30. Haimovici H. Late arterial embolectomy. Surgery 1959;46:775. 31. Amer NC, Schaefer HC, et al. Aortic dissection presenting as iliac arterial occlusion: aid to early diagnosis. N Engl J Med 1962;266:1040. 32. Eriksson I, Holmberg JT. Analysis of factors affecting limb salvage and mortality after embolectomy. Acta Chir Scand 1977;143:237. 33. Baird RJ, Lajos TZ. Emboli to the arm. Ann Surg 1964;160:905. 34. Champion HR, Gill W. Arterial embolus to the upper limb. Br J Surg 1973;60:505. 35. MacGowan WAL, Mooneeram R. A review of 174 patients with arterial embolism. Br J Surg 1973; 60:11. 36. Raithel D. Surgical treatment of acute embolization and acute arterial thrombosis: a review of 342 cases. J Cardiovasc Surg 1973;61. 37. Sachatello CR, Ernst CB, Griffen WO. The acutely ischemic upper extremity: selective management. Surgery 1974;76:1002. 38. Savelyev VS, Zatevakhin II, Stepanov NV. Artery embolism of the upper limbs. Surgery 1977;81:367. 39. Haimovici H. Cardiogenic embolism of the upper extremity. J Cardiovasc Surg 1982;23:3. 40. Ammann J, Seiler H, Vogt B. Delayed arterial embolectomy: a plea for a more active surgical approach. Br J Surg 1976;63:73.

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41. Robbs JV, Baker LW. Late revascularization of the lower limb following acute arterial occlusion. Br J Surg 1979;66:129. 42. Jarrert F, Dacumos GC, et al. Late appearance of arterial emboli: diagnosis and management. Surgery 1979;86:898. 43. Jackson BB. Venous aspiration as an adjunct in the management of late arterial embolectomy. Surgery 1965;57:358. 44. Blaisdell FW, Lim RD Jr, et al. Pulmonary microembolism: a cause of morbidity and death after major vascular surgery. Arch Surg 1966;93:776. 45. Foster JH, Carter JW, et al. Arterial injuries secondary to the use of the Fogarty catheter. Ann Surg 1970;171:971.

46. Rob C, Battle S. Arteriovenous fistula after Fogarty catheter thrombectomy. Arch Surg 1972;105:90. 47. Dainko EA. Complications of the use of the Fogarty balloon catheter. Arch Surg 1972;105:79. 48. Byrnes G, MacGowan WAL. The injury potential of Fogarty balloon catheters. J Cardiovasc Surg (Torino) 1975;16:590. 49. Haimovici H. Metabolic syndrome secondary to acute arterial occlusions. In: Haimovici H, ed. Vascular emergencies. New York: Appleton-Century-Crofts, 1982:267.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 33 Fluoroscopically Assisted Thromboembolectomy Evan C. Lipsitz, Frank J. Veith, and Takao Ohki

Historical Perspective There is now almost a century-long experience with arterial thromboembolectomy. The first such successful embolectomies of the femoral arteries were performed in 1911 by Kee in Stockholm and Labey in Paris (1). Developments in several areas of medicine have advanced the treatment of vascular pathology and specifically have improved the ability to perform successful thromboembolectomy. These developments include the use of heparin for anticoagulation, the introduction of antiplatelet agents, and improved surgical instrumentation and suturing techniques, as well as improvements in the anesthetic and critical care management of patients with vascular disease. Thromboembolic disease and its associated conditions carry a significant morbidity and mortality. Operative mortality rates for the treatment of acute arterial thromboembolism have been reported to range from 10% to 50% (2–6). The cost of caring for patients with this condition, including those of prolonged hospitalization, rehabilitation, and potential limb loss can be substantial. The treatment of acute limb ischemia secondary to thromboembolic disease has become significantly more complex over the past several decades for a number of reasons. Most important is the substantial decrease in the number of younger patients presenting with rheumatic valvular disease and/or atrial fibrillation. This group of patients tends to have relatively normal arteries and intact pulses except for the affected extremity. In these patients, the diagnosis and management of thromboembolic events is significantly less complicated than for older patients in the setting of advanced generalized atherosclerosis. Addition-

ally, in this setting, emboli are generally soft and only loosely adherent to the arterial wall, permitting easy retrieval. Conversely, there has been a marked increase in the proportion of elderly patients with advanced atherosclerosis presenting with this far more complex disease pattern. These older patients also have multiple medical comorbidities, which greatly complicate the operative and perioperative management of thromboembolic disease. Finally, there is a large population of patients with prosthetic bypass grafts, to and from both large and small vessels. The need to treat graft thrombosis and occlusion, which may be due to inflow, outflow, or conduit lesions, has become increasingly common as more of these grafts are placed and represents another challenging area. Fogarty et al. first introduced the balloon embolectomy catheter in 1963 (7). The introduction of this catheter permitted the extraction of clot from remote sites through one or more small arteriotomies, rather than opening the affected portion of the artery directly. Over the past 20 years, the development of thrombolytic agents has permitted the treatment of some arterial and graft occlusions without mechanical thrombectomy. Although some new thrombectomy technologies have been developed and are being used increasingly, these have not superseded the balloon catheter. Neither the surgical technique for thromboembolectomy nor the catheter designs have changed significantly over the intervening four decades since its introduction. However, the use of intraoperative fluoroscopy and the performance of fluoroscopically assisted thromboembolectomy (FATE) greatly improves the results of this treatment in many cases. Intraoperative fluoroscopy facilitates the performance of a

409

410

Part V Occlusive Arterial Diseases

A

B

FIGURE 33.1 (A) Tapering of contrast-filled balloon catheter at an area of extensive intimal hyperplasia. (B) Narrowing of contrast-filled balloon catheter in a less diseased segment.

more controlled thrombectomy and helps to determine the need for adjunctive procedures such as angioplasty and stenting or bypass. These procedures can then be performed at the time of the thromboembolectomy, resulting in more effective, complete, and simpler treatment.

Fluoroscopically Assisted Thromboembolectomy There are multiple reasons why standard thromboembolectomies might be suboptimal. 1. 2. 3.

4. 5.

6.

It may not be possible to pass the balloon catheter through tortuous, diseased arteries. It may be difficult to assess the adequacy of thrombectomy. Given the complex nature of this process, underlying lesions that may be responsible for the thrombosis can be missed. In such a situation, there is a good possibility that a recurrent episode of in situ thrombosis will occur, especially when there is a potential for damage caused by the thrombectomy itself. Traction on an overinflated balloon catheter can damage both normal and diseased arterial segments. Without fluoroscopic visual control, a subintimal catheter insertion or dissection, or the displacement of a large atherosclerotic plaque, may go undetected. Finally, these procedures can be associated with such late complications as aneurysms or arteriovenous fistulae when injuries occurring at the time of thromboembolectomy are not identified and treated (8).

There are several corresponding advantages to the performance of FATE. First, the likelihood of creating a major dissection or plaque disruption within the vessel is greatly reduced. This is because, should such a problem occur, it can generally be identified early while under fluoroscopic control and the extent of injury limited. More-

over, if a serious dissection occurs, it can be treated by balloon angioplasty and stenting. Although the smaller balloon catheters have a spring tip designed to prevent the creation of a dissection plane, these mechanisms are not infallible, especially in small, diseased vessels. Second, with the balloon partially inflated with contrast, the catheter can be directed to the occlusion and areas of disease within the vessel can be identified by distention or tapering of the contrast-filled balloon (Fig. 33.1A and B). If there is any resistance to retrograde catheter passage, which can be evidenced under fluoroscopy by bending of the catheter, the catheter can be withdrawn, the tip reshaped, and another attempt at passage performed. FATE also allows the identification and localization of concurrent atherosclerotic lesions as well as organized residual clot. As a contrast-filled balloon is brought through the artery, it will deform according to the shape of the underlying vessels. Lesions can be further identified and characterized by angiography. These lesions can then be immediately treated either by repeat thromboembolectomy or balloon angioplasty with or without placement of intravascular stents (Fig. 33.2A–D). If necessary, a bypass operation can be performed using the target vessels identified by the intraoperative fluoroscopic angiography. FATE can also help determine the nature of an underlying lesion. With atherosclerotic lesions, deformation of the balloon tends to have sharp borders. A chronic thrombus may cause a more gentle deformation of the balloon, which tends to be more rounded in appearance. A fresh thrombus tends not to cause any deformity of the balloon catheter. These findings are of course, variable and only roughly estimate the cause of the underlying lesion. Perhaps the most significant advantage of FATE is that it allows the operating surgeon to directly view and control the amount of balloon inflation, greatly reducing the risk of arterial damage (Fig. 33.3). This visualization complements the operator’s sense of friction with the balloon as it is pulled across the intima of the vessel. If there is no visualization and the operator depends only on the sensation

Chapter 33 Fluoroscopically Assisted Thromboembolectomy

A

B

C

D

411

FIGURE 33.2 FATE performed for iliac artery thrombosis occurring one week following angioplasty and stenting. (A) Deformation of the contrast-filled balloon at the proximal aspect of the stent. (B) Retrograde arteriogram demonstrates an apparent intimal flap just proximal to the iliac stent (arrow). (C) A second stent is deployed tacking the flap to the vessel wall. (D) Completion arteriogram shows correction of the defect and good flow through the artery.

of resistance to traction on the catheter shaft, significant overdistension of the arterial wall may occur before this sensation becomes apparent, as shown in the study by Parsons et al. (9). Estimation of vessel size can also be made when performing thromboembolectomy under fluoroscopic control using a marker catheter or guidewire, or an angioplasty balloon. Intraoperative fluoroscopy can also facilitate identification of suitable inflow and target vessels for either immediate or subsequent arterial bypass procedures. Completion digital angiography in the operating room

also allows for assessment of completeness of the thrombectomy. Without fluoroscopy, efficacy of the thrombectomy is dependent on subjective evaluation of the thromboembolic specimen, inflow, and outflow. A smoothly tapered thrombus is usually indicative of a complete thrombectomy while a thrombus with an abrupt cutoff is indicative of an incomplete thrombectomy. In some diseased arteries this may not be the case. Completion angiography also permits assessment of the adequacy of the outflow tract and provides an estimate of flow through native arteries or bypass conduits themselves.

412

Part V Occlusive Arterial Diseases FIGURE 33.3 Balloon thromboembolectomy catheters, in an in vitro system, distended to varying profiles with contrast material under fluoroscopy. (A) With minimal inflation the balloon assumes an ovoid profile which approximates but does not directly contact the vessel lumen. (B) On further inflation the balloon begins to transform into an elongated, rectangular structure that closely apposes the vessel wall. (C) After overdistension the balloon assumes a true rectangular profile and exerts significant radial force on the vessel wall.

Technique Operating Room Setup The successful performance of FATE is dependent on having the appropriate equipment and operating room setup. As vascular surgeons continue to embrace endovascular therapies and incorporate them into vascular surgical practice, many centers are well prepared to perform FATE. In fact, compared to many endovascular procedures such as endovascular abdominal aortic aneurysm repair and percutaneous transluminal angioplasty with or without stenting for occlusive disease, the equipment required for FATE is relatively simple. However, because these procedures can become complex it is preferable to have available a full armamentarium of sheaths, catheters, guidewires, balloon catheters, and stents. Obviously the availability of a high-quality digital fluoroscope in the operating room is mandatory. This unit should have last image hold, playback cine-loop, subtraction, and roadmapping capabilities as well as being available at all times. The surgeon must be facile in the operation of the fluoroscope and not dependent on a radiology technician. Since many of these cases present at nights and on weekends, when the operating room may not be fully staffed, this is an important requirement. A radiolucent operating table which can be controlled by the surgeon with a foot pedal or handle is also important. A floating table can simplify positional movements under fluoroscopy but is cumbersome in terms of its width and limited ability to provide height and tilt adjustments should a more complex open procedure be required.

Arterial Thromboembolectomy After making a longitudinal arteriotomy, the appropriate size balloon catheter is selected and advanced proximally

in an attempt to establish inflow. If the catheter passes without resistance the balloon is inflated under fluoroscopic control with one-quarter to one-half strength contrast material (Fig. 33.4). This permits visualization of the balloon along its course. If there is resistance or if the catheter cannot be passed, a guidewire and directional catheter are used to cross the lesion under fluoroscopic and angiographic control. When the lesion has been crossed, an over-the-wire balloon embolectomy catheter can then be placed (Fig. 33.5). Alternatively, a sheath may be advanced over the wire and positioned beyond the point of obstruction. The dilator is then removed and a single lumen balloon embolectomy catheter placed alongside the guidewire through the sheath (Fig. 33.6A–C). The contrast-inflated balloon and sheath are then retracted under fluoroscopic control. Once the balloon is inflated it is carefully withdrawn, paying close attention to the sense of friction on the balloon as well as to the fluoroscopic image. Indents on the balloon profile are noted and marked on the screen. Once optimum clot removal has been achieved, completion angiography is performed and any hemodynamically significant residual underlying lesions are treated. Once inflow has been established, the embolectomy catheter (generally a smaller one) is placed distally and the procedure repeated as needed under fluoroscopic control. Even greater care must be taken in the smaller, more distal vasculature to prevent balloon overdistension and damage to the vessel. In an experimental canine study, Parsons et al. (9) found that without the use of fluoroscopic guidance there was a substantial overdistension of the vessel being treated by surgeons at all levels of experience. The smaller the vessel, the greater the percentage of overdistention (23% in the iliac arteries and 40% in the superficial femoral artery). In several instances the embolectomy

Chapter 33 Fluoroscopically Assisted Thromboembolectomy

FIGURE 33.4 Balloon embolectomy catheter passes easily through the area of thrombus. The balloon is inflated and thromboembolectomy performed.

A

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FIGURE 33.5 The lesion has been crossed using a guidewire and directional catheter through a sheath. An over-the-wire balloon embolectomy catheter is then advanced past the thrombus and thromboembolectomy performed.

C

FIGURE 33.6 (A) A sheath is passed over the wire and beyond the lesion. (B) The balloon embolectomy catheter is then passed through the sheath and alongside the wire. (C) Both the sheath and the balloon embolectomy catheter are then withdrawn, leaving the wire in place.

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A

B

C

D

FIGURE 33.7 FATE performed for acute ileofemoral venous thrombosis with limb threat. (A) Initial venogram showing occlusion of the left iliac veins. (B) Following thrombectomy, flow is restored through the iliac veins into the inferior vena cava; however, a residual defect is noted at the iliac–vena caval confluence. (C) This area was refractory to thrombectomy and was treated by angioplasty and stenting. (D) Completion venogram shows improved flow through the iliac veins into the inferior vena cava. Only left-sided injections are shown for illustrative purposes.

catheter was observed to have been erroneously placed into aortic branch vessels, a dangerous situation of which the operator was unaware. Finally, marked deformation of the balloon was observed as the catheter was withdrawn from the aorta into the smaller iliac artery, indicating that significant radial force was being applied to that vessel.

In some cases, there is densely adherent, laminated thrombus within the artery. This may be especially true in larger vessels such as the iliacs. In such cases a balloon catheter may not generate enough force to dislodge the clot, making thrombectomy a less attractive option (10). In these situations it may be necessary to utilize a device such as an Adherent Clot Catheter (Baxter Vascular

Chapter 33 Fluoroscopically Assisted Thromboembolectomy

Systems, Irvine, CA) (11). This device has an adjustable pitch latex-covered corkscrew wire at its distal tip. The pitch of the wire is controlled by an adjustable knob. Because this device is considerably stiffer than a standard balloon catheter, it is able to dislodge a thrombus that the balloon catheter cannot. By the same token, the risk of damage to the artery is proportionally increased. The use of fluoroscopy with this device allows for more control and permits inspection of the distal end of the catheter during thrombectomy, hopefully permitting adequate thrombectomy while minimizing the risk of damage to the vessel.

Graft Thrombectomy Graft thrombosis is a frequent complication of prosthetic grafts. Another specialized catheter, the Graft Thrombectomy Catheter (Baxter Vascular Systems, Irvine, CA) was designed to remove the densely adherent neointimal material that develops in these grafts. This catheter is composed of two bare, helical wires that are spiraled around the shaft. A lever is used to control the expansion of the wires. Once again this device permits more aggressive clot removal, but risks damage to the grafts and to the native vessel when used near the anastomosis. Fluoroscopy during these procedures can also help minimize arterial and graft injury. There are many new devices becoming available for the performance of percutaneous mechanical thrombectomy (11,12). These include devices for aspiration thrombectomy, pullback and trapping thrombectomy, rotational and hydraulic recirculation thrombectomy, and nonrecirculating mechanical thrombectomy devices. These devices have various advantages and disadvantages but because of their percutaneous design all are used with fluoroscopic guidance. They may also be used in the venous system (13). Experience gained with the use of FATE may facilitate use of these systems.

Venous Thrombectomy Acute limb ischemia can also result from acute deep vein thrombosis, especially ileofemoral thrombosis. While uncomplicated phlegmasia cerulea dolens responds to elevation and anticoagulation therapy alone in the majority of cases, fasciotomy and venous thrombectomy are required when there is a loss of neurologic function or impending gangrene. In these situations, venography should be performed. If surgical thrombectomy is to be undertaken, FATE can be helpful and should be used in the majority of cases of venous thrombectomy for reasons similar to those outlined for arterial thromboembolectomy (14,15). The technique is similar to that outlined for arterial FATE except that in general a transverse venotomy just proximal to the saphenofemoral junction is used. Residual defects in the venous system are also often amenable to

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treatment with angioplasty and stenting (16). Many of these defects are found in cases of “acute on chronic” thrombosis (Fig. 33.7A–D). The more distal clot in these cases is removed by wrapping the leg from the foot upwards with an Esmarch bandage.

Summary As patients presenting with thromboembolic disease become increasingly complex in terms of both their anatomy and comorbidities, they demand a more rigorous and carefully planned approach to ensure successful treatment and to reduce morbidity and mortality. Although it is difficult to prove that FATE improves the ultimate outcome of thromboembolectomy, fluoroscopic guidance is being used with increasing frequency for these and other vascular procedures. In many cases there are tremendous advantages both in the performance of the thromboembolectomy itself and in the planning of concurrent or future adjunctive procedures.

References 1. Braithwaite BD, Earnshaw JJ. Arterial embolectomy: a century and out. Br J Surg 1994; 81: 1705–1706. 2. Kendrik J, Thompson B, et al: Arterial embolectomy in the leg: results in a referral hospital. Am J Surg 1981; 142: 739–743. 3. Panetta T, Thompson J. et al: Arterial embolectomy: a 34-year experience with 400 cases. Surg Clin North Am 1986; 66: 339–353. 4. Abbott W. Maloney R, et al: Arterial embolism: a 44-year perspective. Am J Surg 1982; 143: 460–464. 5. Green R. DeWeese J, Rob C: Arterial embolectomy before and after the Fogarty catheter. Surgery, 1975; 77: 24–33. 6. Haimovici H, Moss C, Veith F: Arterial embolectomy revisited. Surgery 1975; 78: 409–410. 7. Fogarty T, Cranley J, et al: A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963; 116: 241–244. 8. Albrechtsson U, Einarsson E, Tylen U. Complications secondary to thrombectomy with the Fogarty balloon catheter. Cardiovasc Intervent Radiol 1981; 4(1): 14–16. 9. Parsons RE, Marin ML, et al: Fluoroscopically assisted thromboembolectomy: an improved method for treating acute arterial occlusions. Ann Vasc Surg 1996; 10: 201–210. 10. Radoux JM, Maiza D, Coffin O. Long-term outcome of 121 iliofemoral endarterectomy procedures. Ann Vasc Surg 2001; 15(2): 163–170. 11. Hill BB, Fogarty TJ. Thrombectomy catheters: basic concepts, design, and types. In Endovascular Surgery, 3rd edn. (Eds: Moore WS, Ahn SS). Philadelphia, PA: WB Saunders, 2001: 75–86. 12. Kasirajan K, Marek JM, Langsfeld M. Mechanical thrombectomy as a first-line treatment for arterial occlusion. Semin Vasc Surg 2001; 14(2): 123–131.

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13. Delomez M, Beregi JP, et al. Mechanical thrombectomy in patients with deep venous thrombosis. Cardiovasc Intervent Radiol 2001; 24(1): 42–8. 14. Comerota AJ. Venous thromboembolism. In Vascular Surgery, 4th edn. (Ed: Rutherford RB). Philadelphia, PA: WB Saunders, 1995: 1785–1814. 15. Eklof B, Kistner RL. Surgical treatment of acute

iliofemoral thrombosis. In Current Therapy in Vascular Surgery, 3rd edn. (eds Ernst CB, Stanley JC). St Louis, MO: Mosby, 1995: 932–935. 16. Semba CP, Dake MD: Catheter-directed thrombolysis for iliofemoral venous thrombosis. Semin Vasc Surg 1996; 9: 26–33.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 34 Percutaneous Aspiration Thromboembolectomy Rodney A. White

Percutaneous aspiration thrombectomy is one of several techniques that can be used to remove thrombus and atheromatous debris from the lumen of a vessel. Aspiration thrombectomy is performed less frequently than the more popular technique of thrombolysis for dissolving acute and chronic thrombus; it is usually used during an interventional procedure when the embolized material can be directly engaged with an aspiration thrombectomy catheter. The aspiration thrombectomy techniques are most effective for soft thrombotic material, which occurs during angioplasty or administration of thrombolytic therapy (1), compared with the pulverized pieces of organized thrombus, fibrous tissue, or atherosclerotic plaque that are produced during atherectomy. Although the simplest approach to aspiration thrombectomy involves impacting a thrombus and aspirating part or all of the material into the lumen of a hollow catheter, modifications of this technique have developed including transluminal extraction atherectomy (Transluminal Extraction Catheter, Interventional Technologies, San Diego, CA), or other methods to pulverize or emulsify thrombus including ultrasonic energy or waterjet devices (2). This chapter focuses on the methods available to perform aspiration thrombectomy and briefly reviews the reported series documenting utility.

Thromboemboli During Endovascular Procedures Arterial embolization has been noted to occur in approximately 5% of angioplasty procedures (3), and in as many

as 12.5% to 25% of local lytic treatments with streptokinase or urokinase infusion (4). Thromboemboli occur more frequently during dilation of occlusive lesions because the soft thrombus that accumulates near recent occlusions is easily fractured and dispersed distally. Symptoms suggestive of recent occlusion of an arterial lesion should increase awareness of this possible complication if angioplasty is planned. Systemic anticoagulation and frequent flushing of the catheters during percutaneous procedures helps prevent thromboembolic complications. Fibrinolytic therapy prior to angioplasty procedures has been proposed by some as a means of decreasing the incidence of thromboemboli during the procedure (5), although others are concerned about the hemorrhagic complications of these agents when used in this application.

Percutaneous Transcatheter Aspiration Technique Percutaneous transcatheter aspiration embolectomy is performed using large-bore catheters for removal of peripheral emboli, or by specially designed catheter devices for pulmonary applications. Peripheral application of the technique is advocated only for arterial occlusions below the inguinal ligament; thus patients considered candidates for percutaneous embolectomv should have a patent iliac artery and palpable femoral pulses. Access to the pulmonary circuit is obtained transvenously through either the femoral or jugular vein, using local anesthesia and fluoroscopy.

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Part V Occlusive Arterial Diseases FIGURE 34.1 The percutaneous aspiration thromboembolectomy technique. (A) The aspiration catheter is advanced to the site of the embolus, preferably over a guidewire that is imbedded in the lesion. (B) Upon contact of the catheter with the lesion, the thrombus is aspirated. (C) The thrombus is withdrawn while the operator continues to aspirate through the catheter lumen. (D) Sequential aspirations may be performed for residual material.

A

B

C

The catheter for peripheral aspiration thromboembolectomy is best inserted through an antegrade femoral artery puncture over a guidewire and should be done through an arterial sheath to prevent damage to the arterial wall. When crossing newly recanalized lesions, extreme care is necessary to prevent dissections or perforations. Hand injection of dye through the catheter lumen is recommended during catheter advancement. Once the thrombus is encountered, a wire should be embedded into the clot, if possible, and the catheter impacted before aspirating the thrombus into the catheter lumen using a hand-drawn 30- to 50-mL syringe. Once the thrombus is engaged, the catheter is withdrawn while maintaining suction to hold the thrombus (Fig. 34.1). At the puncture site, the thrombus may become entrapped in the introduction sheath and cause reembolization. Aspiration through the sheath during removal helps prevent this complication.

Clinical Experience Percutaneous Peripheral Arterial Thromboembolectomy In 1984, Sniderman et al. reported the use of percutaneous embolectomy by transcatheter aspiration as a means to remove significant emboli that occurred during percutaneous transluminal angioplasty (PTA) (3). Upon recognizing an embolus at arteriography, the decision to attempt transcatheter embolectomy was made by clinical judgment of the radiologist and consultant vascular surgeon. Distal emboli were detected in 14 (4%) of 339 attempted PTA procedures in this series. Transcatheter embolectomy by aspiration through a nontapered 8-Fr. catheter passed over a guidewire that had been advanced into the embolus was technically successful in five of six attempts. The procedure was combined with successful PTA in three of five patients. The authors emphasized that extreme care must be made in recrossing a recently dilated

D

area to avert subintimal dissection and possible further damage. They concluded that this method could be attempted prior to surgical embolectomy as an alternative to local fibrinolytic therapy. Subsequent reports by Starck et al. (6) and Turnipseed et al. (7) detailed their experience with urgent percutaneous aspiration thromboembolectomy in 41 patients (45 treatments), alone or in combination with balloon dilation or local lytic therapy or both. The majority of treatments were in the femoral (21%), popliteal (30%), and tibial (40%) arteries, although thrombi of the superior mesenteric, renal, iliac, and profunda femoris arteries were included. The majority of the occlusions (75%) were acute (< 72 hours). Of the total, 31% were treated by aspiration alone, 27% underwent lysis and aspiration, 20% underwent balloon dilation plus aspiration, and 22% underwent lysis, balloon dilation, and aspiration. Aspiration was performed preferentially if the occlusion was a soft thrombus, whereas lysis and dilation were needed for more organized, stenotic lesions. For longer occlusions, balloon dilation was performed initially to fragment the clot. This theoretically increases the surface area for effective thrombolytic therapy, limiting the complications of lyric therapy associated with prolonged infusions, and enhances the success of aspirations. The length of occlusions treated varied from 1 to 50 cm, mean length 9.5 cm. The investigators used a custom-designed, minimally tapered catheter and a sheath with a detachable hemostatic valve to prevent dislodgment of the thrombus at this site during removal. A total of 37 (86%) of the patients had limb-threatening occlusions; of these, the majority improved and none was worse because of the procedure. The early limb salvage rate was 94% at follow-up from 1 week to 2.5 years. The authors concluded that the Fogarty catheter technique remains the method of choice for removing thromboemboli within the aortoiliac region, but in smaller peripheral arterial occlusions that are primarily iatrogenic (i.e., subsequent to angioplasty procedures), or in

Chapter 34 Percutaneous Aspiration Thromboembolectomy

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FIGURE 34.2 Pulmonary embolectomy catheter with a radiopaque cup attached to a steerable catheter and control handle. (Illustration courtesy of Medi-Tech, Inc., Watertown, MA.)

selected high-risk patients, the method may be an alternative to surgical embolectomy.

Percutaneous Pulmonary Embolectomy Massive pulmonary embolus causes approximately 50,000 deaths per year in the US (8). Partial cardiopulmonary bypass followed by total bypass and pulmonary embolectomy is occasionally useful to salvage moribund patients, but has not significantly improved survival. Because of the high mortality rate with surgery, thrombolytic agents have been investigated in this setting. However, thrombolytic therapy is of little help to patients who have had massive emboli and require pressors for support and who frequently die before they can be prepared for surgery. Greenfield et al. described a stainless-steel cup device that was used successfully in a canine model to remove lethal pulmonary emboli (9). The device was a 7-mm cup on the tip of a balloon catheter that was passed transvenously into the pulmonary circuit. Using fluoroscopic guidance, the cup was placed proximal to the embolus and the balloon was inflated. With the aid of pulmonary venous backpressure, syringe suction on the cup successfully enabled removal of the majority of 7- to 14-day-old thrombi in their experimental preparation. Unsuccessfully removal was attributed to fragmentation and distal movement of clot fragments beyond the site of possible retrieval. This work demonstrated the feasibility of removing life-threatening emboli, or at least attempting removal, while the patients were being stabilized or prepared for surgical embolectomy. Figure 34.2 illustrates the current commercially available percutaneous pulmonary embolectomy device. Figure 34.3 schematically demonstrates the catheter’s function. Subsequent to the initial successes in the experimental model, Greenfield extracted emboli from 86% of his patients using the cup device on a steerable catheter (10). Overall survival using this method was 64% (14 of 22 patients). To achieve these results, the entire unit was withdrawn with each aspiration, and the procedure was repeated until the pulmonary artery pressure fell toward normal levels and the cardiac output improved. An updated review of this series documents successful extrac-

tion of emboli in 29 (91%) of 32 patients, with 25 (78%) surviving (11). This report also reviews extensively the diagnosis, indications, and management of pulmonary embolism using this method.

Discussion The experimental use of percutaneous aspiration of thrombi was first reported by Greenfield et al. in 1969 (9). Subsequent to this report both peripheral and pulmonary applications have developed. Neither method has been widely adopted even though impressive success rates have been demonstrated. In the pulmonary embolus setting, the slow development may be related to the need for initiating the intervention in patients with acute vascular collapse who require significant monitoring and additional therapeutic interventions to maintain viability. Mobilizing patients to enable fluoroscopically guided aspirations can be cumbersome, at best, particularly in the group that would benefit most from the technique. Peripheral vascular application of the method is also limited to settings in which fluoroscopic guidance is available. For this reason, the initial experience has been by radiologists as a means to retrieve thromboemboli produced during angioplasty procedures, or as an attempt to remove thrombus during arteriography which is being performed to document the site and extent of occlusions in acute thromboembolic events. Operative experience with this method may develop as more surgeons begin to use percutaneous endovascular angioplasty devices. During open surgical procedures, aspiration thrombectomv is unlikely to achieve widespread use because most surgeons are able to retrieve embolic material from any size vessel using conventional Fogarty balloon devices. The limitations of percutaneous aspiration thrombectomy are related to the imaging issues and to complications of the procedure. Morbidity is approximately 17% and consists of groin hematomas, some of which have required transfusion, have produced femoral false aneurysms, and have caused cholesterol embolus (rashes and petechiae) (7). The technique is also limited to use by physicians who have expertise with percutaneous devices and methods. Extreme care is

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B

A

C

FIGURE 34.3 (A) The pulmonary embolectomy catheter is introduced through either the femoral or jugular vein and positioned in the pulmonary artery where the embolus was seen on arteriography. Inset shows syringe vacuum technique. (B) Proximity of the embolus is confirmed by injection of a small bolus of contrast medium. (C) Syringe suction is then applied to capture a portion of the embolus in the cup. (Reproduced by permission from Greenfield U. Complications in surgery and trauma, 2nd edn. Philadelphia: JB Lippincott, 1990;443–444.)

required to prevent vessel dissections, perforations, and distal embolization. The advantages of percutaneous aspiration thromboembolectomy are that it can be easily instituted at angiography and can be combined with other percutaneous angioplasty tools including balloons, lytic agents, lasers, and atherectomy devices. The method also provides an alternative therapy for thromboembolic disease when thrombolytic drugs are contraindicated and surgery is not desirable in the high-risk group of patients who have been identified as having increased mortality rates following surgical procedures (12).

References 1. Waltman AC, Greenfield LJ, et al. Transluminal angioplasty of the iliac and femoropopliteal arteries. Current status. Arch Surg 1978:117:1218–1221. 2. White RA, White GH. Color atlas of endovascular surgery. London: Chapman & Hall. 1990:92–93. 3. Sniderman KW, Bodner L, et al. Percutaneous embolectomy by transcatheter aspiration. Radiology 1984;150:357–361.

4. Hess H. Clot lysis in peripheral arteries. In: Dotter CT, Gruntzig AR, et al., eds. Percutaneous transluminal angioplasty. New York: Springer, 1983:145–153. 5. Katzen BT, Breda A. Low dose streptokinase in the treatment of arterial occlusion. Am J Roentgenol 1981:136:1171–1178. 6. Starck EE, McDermott JC, et al. Percutaneous aspiration thromboembolectomy. Radiology 1985:156:61–66. 7. Turnipseed WD, Starck EE, et al. Percutancous aspiranon thromboembolectomy (PAT): an alternative to surgical balloon techniques for clot retrieval. J Vasc Surg 1986;3:437–441. 8. Consensus Development Panel. Prevention of venous thrombosis and pulmonary embolus. JAMA 1986:256:744. 9. Greenfield LJ, Kimmell GO, McCurdy, WC. Transvenous removal of pulmonary emboli by vacuum-cup catheter technique. J Surg Res 1969;9:347–352. 10. Greenfield U. Pulmonary embolism: pathophysiology and treatment. In: Glenn WWL, ed. Thoracic and cardiovascular surgery. 4th edn, Norwalk, CT: AppletonCentury-Crofts, 1983:1283–1284. 11. Greenfield U. Catheter embolectomy for pulmonary thromboembolism. In: Veith FJ, ed. Current critical problems in vascular surgery. St Louis: Quality Medical Publishing, 1991:156–161. 12. Abbott WM, Maloney RD, et al. Arterial embolism: a 44 year perspective. Am J Surg 1982;143:460–474.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 35 Vascular Trauma Asher Hirshberg and Kenneth L. Mattox

Even at the beginning of the twenty-first century, injuries to major blood vessels still remain the most challenging aspects in the care of the injured patient. These injuries present a unique array of problems and dilemmas in all phases of trauma care (1). Contemporary trauma surgery focuses on correct priorities, the first of which is to save the patient’s life. Herein lies the fundamental difference between the two major types of vascular trauma: truncal vascular trauma is usually an immediate threat to life, whereas an injured extremity vessel is more often a threat to the viability of the limb. One of the fundamental principles to keep in mind when discussing vascular injuries in the context of multi-trauma is that bleeding and ischemia are different priorities. Vascular trauma is almost invariably associated with injuries to other organ systems and with marked physiologic derangements. Many patients with vascular trauma are critically ill, and while control of hemorrhage is lifesaving and usually rapid, vascular reconstruction often is neither. Complex truncal vascular reconstructions in the critically wounded make for elegant textbook illustrations—but may cost the patient’s life. More than in other fields of peripheral vascular surgery, it is important to remember that in vascular trauma not all that is technically feasible is in the patient’s best interest. The amazingly rapid progress in vascular surgery over the past decade, with the new imaging modalities and endovascular interventions, has translated into new concepts in the management of vascular trauma. The repair of the injured blood vessel always hinges on general technical principles that are taken from elective and emergency work in the field. However, the most significant advance in the last decade has been the realization that the patient’s physiology, and not the anatomic integrity of the repair, is

the key outcome determinant in operations for major vascular injuries. The translation of these basic concepts into the practicalities of patient care is the subject of this chapter.

General Operative Principles Initial Exposure and Control Control of external hemorrhage is usually obtained by direct pressure over the site of bleeding, using digital or manual pressure. Attempts at blind clamping in a pool of blood are ineffective and may damage adjacent structures. Tourniquets should also be avoided because they interrupt collateral circulation. Manual compression of the external bleeding site must occasionally be maintained until proximal and distal control are formally obtained in the operating room. The compressing hand or instrument is thus prepared as part of the operative field. Balloon catheter tamponade is also a very useful means of obtaining temporary control of torrential bleeding in inaccessible sites such as zones I and III of the neck, deep in the pelvis, or in the groin. A Foley catheter passed through the wound tract or into a bleeding cavity provides extraluminal compression when the balloon is inflated, whereas a Fogarty catheter inserted into the vessel through the injury site provides intraluminal occlusion (2) (Fig. 35.1). When approaching an injured vessel within a contained hematoma, the cardinal principle is to first obtain proximal and distal control. In the limbs and neck, control is obtained using standard methods of vascular exposure. Vascular control in the chest hinges on correct selection of

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ration. A patient with gunshot injuries to the liver, duodenum, colon, inferior vena cava, and right renal artery, even though seemingly “stable” after initial control of hemorrhage and blood replacement, has in fact sustained a major insult. After an hour of surgery, transfusion of some 10 units of blood, and a core temperature decreased to 32 °C, an attempt at renal revascularization will be lethal to this patient.

The “Damage Control” Strategy

FIGURE 35.1 Drawing depicting an injury to the subclavian artery, controlled using a Foley balloon inserted into the stab wound site.

incision, whereas in the abdomen the key is adequate visceral mobilization.

Assessing the Injury and the Patient There are several patterns of vascular trauma, depending on the wounding mechanism (3). In penetrating trauma, a simple laceration, partial wall loss, and complete transection represent increasing severity of injury. Blunt trauma may result in intimal flap, partial or complete wall disruption, and avulsion of branches off major vessels. The cavitation effect of high-velocity missiles and stretch injury from blunt trauma lead to intimal damage and subsequent thrombosis (3). The true extent of damage may not be fully appreciated from the external appearance of the injured vessel, which may be misleading. Injured arteries, especially following blunt trauma, need to be opened to fully assess the extent of the intimal damage. The direction and extent of the arteriotomy is dictated by the size of the vessel and the anatomic circumstances. The injured wall is then conservatively debrided, and a decision is made regarding the appropriate repair technique. Selection of vascular repair technique is based not only on the circumstances within the operative field, but also on a careful overall assessment of the patient’s physiology. A patient who is nearly exsanguinated from a stab wound to the brachial artery and arrives in the hospital unresponsive with a barely palpable pulse and a pH of 6.9 is clearly not a candidate for any type of vascular explo-

“Damage control” is a surgical strategy for the staged management of multivisceral trauma that represents a major paradigm shift in trauma surgery. With this approach, the traditional single definitive operation for trauma is replaced by a staged repair, whereby a rapid “bail out” operation (to control hemorrhage and intestinal or urine spillage) is followed by a delayed reconstruction after the patient’s physiology has been stabilized. In the last decade, this approach became part of the standard repertoire of trauma surgeons when operating on their most critically wounded patients. The underlying premise of “damage control” is that the operating room is a hostile environment for the physiology of the severely injured patient. Prolonged operations and massive blood replacement result in a triad of hypothermia, acidosis, and coagulopathy that is selfpropagating and lethal (4). The current trend in trauma surgery is to avoid crossing these physiologic boundaries by an early decision to “bail out.” This is done by using rapid temporary measures to control bleeding and spillage of bowel content or urine (5). Packing, ligation of bowel without resection, ureter exteriorization, and stapled nonanatomic lung resection are examples of the application of this principle. The operation is then rapidly terminated by temporary closure of the cavity, and the patient is stabilized and rewarmed in the intensive care unit. Planned reoperating and definitive repair are undertaken 24–48 hours later, when the patient’s condition has been optimized (6). Major vascular trauma is often part of an injury complex in patients with exsanguinating hemorrhage in whom the “damage control” strategy represents the patient’s only hope of survival. In this context, it is vital to distinguish between simple and complex vascular repair techniques. Simple repairs are rapid and include ligation, lateral repair, and temporary shunt insertion. Complex repairs are more time-consuming and include patch angioplasty, end-to-end anastomosis, and graft interposition (3). While simple repairs are feasible even under adverse physiologic circumstances, complex repairs usually are not. However, the decision not to restore vessel continuity may force the surgeon to accept tissue loss (such as a kidney in renal artery injury or even a limb in iliac artery injury) in order to save the patient’s life. These are some of the most difficult decisions in trauma surgery.

Chapter 35 Vascular Trauma

Simple Repair Techniques Ligation Ligation is a valid technical option when the injured vessel is inaccessible, reconstruction is difficult, or the patient’s physiologic reserves are waning. Many injured vessels (especially veins) can be ligated at the cost of postoperative edema (7). The external carotid artery, celiac axis (in nonatherosclerotic patients), and internal iliac arteries can be ligated with impunity. The risk of amputation following ligation of the femoral vessels was 81% for the common femoral and 55% for the superficial femoral artery, based on data from World War II (before the advent of fasciotomy) (8). Unfortunately, for some visceral vessels such as the portal vein and proximal superior mesenteric vessels, which are difficult to repair, the risk of ligation is not as well defined. Lateral Repair The technical keys to accomplishing a direct lateral repair of an injured vessel (especially an artery) are conservative debridement of the damaged wall, and directing the repair perpendicular to the vessel axis to avoid stenosis whenever possible. Most surgeons would consider a mural defect of more than half the arterial circumference to be the upper limit of damage amenable to direct repair, but, in fact, as long as some of the posterior wall is present and the transverse orientation of the repair is maintained, it is possible to reapproximate even large defects without tension. Temporary intraluminal shunts The insertion of an intraluminal shunt is a simple temporary vascular reconstructive option that is valid for patients who approach the boundaries of their physiologic envelope (9–11). In the hypothermic coagulopathic and grossly unstable patient, a carotid shunt, endotracheal suction catheter, or a piece of sterile nasogastric tube trimmed to the appropriate length can be inserted into both ends of a disrupted vessel and held in place with ties of Rummel tourniquets. The shunt is flushed prior to insertion of the distal part, and the distal artery is examined for signs of reconstituted flow. There are four indications for shunt insertion: 1.

2. 3.

4.

maintenance of limb perfusion in a patient with a peripheral vascular injury requiring transfer from a remote facility to a trauma center where vascular reconstruction will be undertaken; maintenance of limb perfusion while other lifethreatening injuries (e.g., in the trunk) are addressed; maintenance of limb perfusion while skeletal alignment is accomplished prior to vascular repair in an ischemic limb; maintenance of limb perfusion as a “damage control” technique in patients who require complex repairs but have exhausted their physiologic reserves.

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Shunts have very good short-term patency (3–6 hours), and limited data document patency of up to 24–36 hours.

Complex Repair Techniques End-to-end Anastomosis In clinical practice, end-to-end repairs of injured arteries are used only infrequently. This is because after adequate debridement the vessel ends retract and it is often very difficult to bring them together into a tension-free anastomosis. Mobilization of an artery by tying off branches in order to “gain length” is time consuming and often insufficient. Many surgeons maintain a very low threshold for insertion of a substitute conduit when an artery is completely transected. The technical principles of vascular anastomosis apply equally well to direct end-to-end anastomosis and to graft interposition: arterial ends smaller than 1 cm in diameter should be beveled, Fogarty balloon thrombectomy should be performed distally and proximally, and both segments should be flushed with heparinized saline. Systemic heparin is not used. Vascular Grafts An interposition conduit is used for extensive vessel destruction when the simpler reconstructive options are inappropriate. Considerable discussion, debate, and research have focused on the use of synthetic versus autogenous conduits. This debate comes down to only two locations: the superficial femoral and the subclavian arteries. In the trunk (including the neck), use of PTFE or Dacron prostheses is an issue of size match and durability. In the distal extremities and smaller truncal arteries, the size match of currently available prostheses are unacceptable and use of a saphenous vein is most appropriate. Currently, for vessels of 5 mm or less in diameter, the use of a saphenous vein graft is the only practical option (12). The use of prosthetic material in the presence of infection or contamination is also a subject of considerable debate. One option is to use ligation and extra-anatomic routing around the contaminated area. The classical example of this approach is ligation of the iliac artery in an abdomen with gross fecal spillage and performance of a femorofemoral graft. In some instances, such as reconstruction of an injured abdominal aorta, it is virtually impossible to avoid reconstruction in an area of contamination (13). In other instances, infection is not a consideration until a graft is later exposed, or a secondary infection or abscess sets in. Another argument has been whether or not venous or arterial autografts are “living” at the time that the conduit is harvested and translocated to another anatomic area. A major advantage in the use of synthetic grafts is speed. Expediting the operative procedure is an important consideration for severely injured patients or for those with complex vascular injuries in the same extremity, in

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whom early restoration of perfusion is critical for limb salvage. The two technical pitfalls in graft interposition for arterial trauma are inappropriate size selection and inadequate graft protection. The arteries of young trauma victims are often surprisingly small, especially in the patient who is hypotensive and vasoconstricted. A conscious effort should be made to select a slightly larger graft size to avoid a hemodynamically unfavorable “bottlenecking” when the native artery dilates. Graft protection is a fundamental principle in vascular surgery that is especially relevant to trauma. Associated soft tissue or visceral injuries often create unfavorable local circumstances in the operative field that may jeopardize the graft. The graft needs to be routed through noncontaminated tissue planes, adequately covered and protected from mechanical trauma. Considerations of graft protection often dictate the sequencing of the operative procedure. In the abdomen, repair of hollow visceral injuries and thorough irrigation should precede graft placement. Similarly, soft tissue debridement and bone alignment should be performed prior to vascular repair in a traumatized limb.

Vascular Injuries in Specific Anatomic Locations The Neck Vascular injuries to the neck frequently pose an immediate threat to life because of either external hemorrhage or airway obstruction by a cervical hematoma. In the presence of active external bleeding or an expanding hematoma, local pressure and immediate awake intubation to protect the airway are two important maneuvers to keep in mind during the initial management. Probing a nonbleeding wound or missile tract in the neck may prove fatal (14). The anatomic configuration of the neck consists of two lateral neurovascular bundles and midline airway and digestive tract structures, all in close proximity within a small space. As a result, injuries to the cervical vasculature are common and often associated with trauma to aerodigestive structures. There is general agreement that stable patients with penetrating injuries to the base of the neck (zone I) should undergo angiography to define the injury and help plan the operative approach. The same applies to penetrating injuries above the angle of the mandible (zone III), where both exploration and distal vascular control are technically difficult or impossible and therefore an interventional angiographic solution may be the only feasible course of action. The major controversy revolves around asymptomatic zone II injuries, in which significant trauma can be ruled out either by routine exploration (a straightforward and low-morbidity procedure), or by a combination of four-vessel angiography, esophagoscopy, and barium swallow. Both alternatives are acceptable (15).

The most frequently injured major cervical vessel is the internal jugular vein, which is usually amenable to lateral repair or ligation. The carotid arteries, and to a lesser extent the vertebral arteries, are the focus of clinical interest. Carotid Artery Trauma Carotid artery injuries account for 5% of vascular injuries, with penetrating trauma accounting for 80% of these. The standard exposure of the carotid artery is via an incision along the anterior border of the sternocleidomastoid. However, proximal control of the common carotid artery at the base of the neck may require a median sternotomy, and a high injury at the base of the skull may require division of the digastric muscles and occasionally anterior mandibular subluxation. But even with these adjunctive maneuvers, exposure and control of internal carotid injuries at the base of the skull may be impossible. Initial control of bleeding by balloon catheter tamponade followed by ligation and division of the internal carotid artery at the carotid bifurcation and removal of the balloon 3 days later, is a simple solution to this difficult problem, albeit at a much increased risk of stroke (Fig. 35.2). The optimal utility incision for neck exploration is along the anterior border of the sternocleidomastoid. When the cervical wound is bleeding externally, direct digital pressure is applied and maintained while dissection proceeds around the compressing finger. A Foley balloon catheter inserted into the missile tract and inflated is a very useful adjunct for obtaining temporary control of hemorrhage. Once the platysma is divided and the sternocleidomastoid is retracted laterally, a large hematoma and active bleeding obscuring the cervical anatomy are often encountered. The key anatomic landmark at this stage is the internal jugular vein. Dissection along the anterior border of the vein leads the surgeon to the facial vein. The facial vein is “the gateway to the neck” because, once it is ligated and divided, access to the content of the carotid sheath and the carotid bifurcation opens up for the surgeon. At this point, it is important to keep in mind the cardinal principle of obtaining proximal control prior to addressing the injured segment. This can usually be done by isolating and controlling the common carotid artery below the hematoma. When the neck is penetrated by several missiles, the surgeon has to reconstruct the presumed trajectories either preoperatively (by thorough physical examination and plain films of the neck and chest) or intraoperatively. Like in any other anatomic cavity violated by penetrating trauma, the trajectories of the missiles must “make sense” to the surgeon, because a discontinuous nonlinear trajectory, an uneven number of esophageal perforations in the presence of a trajectory across the neck, or a bullet wound that is unaccounted for are all markers of potential missed injuries. Revascularization of most common carotid and internal carotid injuries is usually achieved using lateral repair,

Chapter 35 Vascular Trauma

425

FIGURE 35.2 Technique of extravascular balloon occlusion of uncontrolled bleeding from a high neck gunshot wound. Balloon was deflated and removed without incident on postoperative day 3.

B

A C

end-to-end anastomosis or graft interposition. External carotid injuries are usually ligated. Transposition of the external carotid artery to serve as an autogenous conduit that replaces an extensively injured internal carotid artery is an oft-cited technical solution that is nevertheless time consuming and applicable only when the anatomic arrangement of the external carotid is favorable (Fig. 35.3). The major debate in carotid trauma revolves around the management of patients with a fixed neurologic deficit (14). Currently, most authors strongly advocate revascularization regardless of the patient’s neurologic status, accepting that patients with a profound neurologic deficit (i.e., coma) have a poor outcome with either reconstruction or ligation (16). The only exception to the recommendation may be the patient with a fixed grave neurologic deficit and no retrograde flow from the open distal stump. Concern over possible distal embolization after revascularization serves as strong argument in favor of ligation of these patients (17). Blunt Carotid Artery Injuries Blunt carotid artery injury is an underdiagnosed entity that has focused considerable attention in recent years (18,19). The reported incidence is less than one patient per 1000 admitted to a major trauma center. But the injury carries the potential for a devastating neurologic deficit (up to 15–30% of the patients in some series). The mechanism of injury can be a direct cervical trauma, hyperextension or flexion and rotation of the neck. The underlying pathophysiology is that of intimal damage with subsequent dissection of the carotid artery, leading to

A B FIGURE 35.3 Technique of mobilizing noninjured external carotid artery to provide autogenous conduit for injured internal carotid artery.

partial or complete luminal obstruction, distal embolization, pseudoaneurysm formation, or a carotid-cavernous fistula. Blunt carotid injury should be suspected in the presence of a hemispheric neurologic deficit that is in-

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compatible with computed tomography (CT) findings. A salient clinical feature of this injury is that in at least onehalf of patients there is a latent period of hours or days before the neurologic deficit sets in. There is evidence to suggest that early institution of heparin anticoagulation in an asymptomatic patient improves outcome. Once diagnosed, management of blunt carotid injury is largely conservative. Full anticoagulation is the mainstay of therapy. The roles of endovascular carotid stenting or operative repair for acute symptomatic dissection are not well defined. Vertebral Artery Injuries Vertebral artery injuries are rare, except in series reported from trauma centers that routinely use four-vessel angiography to screen asymptomatic patients with penetrating neck injuries (20). This fact suggests that the majority of vertebral artery injuries may have a benign natural history even if left untreated. The major difficulty with these injuries is the inaccessibility of the artery within the bony canal formed by the transverse processes of the cervical vertebrae and the associated ligaments. Nowhere in vascular trauma is the discrepancy between elegant drawings depicting elaborate exposures and the harsh reality of the operating room more striking than with a bleeding vertebral artery encountered during neck exploration. Thus, when one is not forced to operate urgently to stop active bleeding, either nonintervention or angiographic embolization is a wise decision. Although Henry’s approach to the vertebral artery within the transverse processes of the cervical vertebrae has been advocated by some authors (21), this involves an elaborate dissection and the risk of injury to the vertebral vein, sympathetic nerves, and suboccipital venous plexus. A simple alternative is the application of two median-sized metal clips, pushed firmly and blindly onto the artery above and below the injury through the same interspace, and then closed (22). This can be done over the intertransverse ligament without exposing the artery in its bony canal, and by guiding the clip applier over the palpating index finger into the appropriate space between the transverse processes. Another simple option that works is filling the vigorously bleeding hole in the transverse process with bone wax.

The Chest Positioning and Choice of Incision The two major areas of interest in thoracic vascular trauma are blunt injuries to the descending thoracic aorta and penetrating injuries to the thoracic inlet. Injuries to other thoracic vascular structures, such as the vena cava and the pulmonary vasculature, are rare and frequently lethal. Patient positioning and the choice of thoracotomy incision can determine the success or failure of an operation for thoracic vascular trauma. An incorrectly placed incision may result in prolonged struggle to obtain control, con-

verting a relatively straightforward repair into a technical nightmare. In stable patients, the choice of incision is dictated by the angiographic findings. But in the actively bleeding patient in shock, choice of an incision is based on clinical judgment. The incision of choice for the unstable patient with ongoing hemorrhage into the pleural cavity is an anterolateral thoracotomy through the fourth or fifth intercostal space. This approach does not require special patient positioning and does not limit access to the contralateral chest or to the abdomen. The only exception is a penetrating injury to the right lower chest (below the nipple) where bleeding most commonly emanates from an injured liver, hence the initial operative approach should be through a midline laparotomy. In the agonal patient, a resuscitative left thoracotomy provides access not only to the left lung and pulmonary hilum, but also to the heart, descending thoracic aorta, and proximal subclavian artery. A left thoracotomy incision can be extended across the sternum (“clam shell incision”) to provide maximal exposure of the heart, mediastinal vessels, and right chest, albeit at the cost of additional morbidity. The main pitfall with transsternal extension is the tendency to make it too low. It should be carried upward to the third intercostal space on the right to afford easy access to the innominate artery and its bifurcation. Blunt Aortic Injury Thoracic aorta disruption maintains a unique place in vascular trauma surgery because of the lethal consequences of diagnostic delays and the devastating spinal complications that haunt the surgeon even after the most technically perfect repair. More than 80% of traumatic aorta disruptions occur just distal to the origin of the left subclavian artery, and only some 15% of these patients arrive at the hospital alive (23). Patients with a contained rupture are usually stable enough for a rapid diagnostic evaluation and urgent surgical repair. Although the mortality of untreated aortic disruption is reported to be around 1% per hour during the first 48 hours, the majority of deaths occur within the first few hours, thus emphasizing the urgency of the situation. Diagnosis Multiple radiologic clues suggest thoracic aortic disruption on the plain chest film. Although none of these signs is highly sensitive or specific and some are subtle and missed in the presence of more apparent injuries, a normal chest radiograph seen by an experienced radiologist has a 98% negative predictive value (24). In practice, the timely diagnosis of thoracic aortic disruption hinges on a high index of suspicion and a low threshold for thoracic aortography. The purpose of aortography is not to demonstrate the size of the tear of the false aneurysm, but merely to make the diagnosis and help plan the operative approach. Two classic congenital conditions that occasionally lead to a negative thoracotomy are ductus diverticulum and vascular ring remnant.

Chapter 35 Vascular Trauma

The role of computed tomography in the diagnosis of blunt aortic injury has been the focus of debate. Conventional CT may show mediastinal hematoma and is mainly useful as a screening modality in patients with a normal mediastinum on chest x-ray or with questionable mediastinal widening due to technical factors in obtaining the chest film (such as gross obesity or inability to sit the patient up) and clinical suspicion of a blunt aortic injury. Demonstration of a mediastinal hematoma, however, does not obviate the need for subsequent aortography to define the site and extent of injury. Helical CT angiography is rapidly becoming an imaging modality that rivals aortography because it is more expedient and noninvasive. Three-dimensional reconstructions of the aorta provide accurate anatomic detail that obviates the need for a subsequent aortography. However, three-dimensional reconstructions are labor intensive and time-consuming. As this technology becomes increasingly available in trauma centers, and data regarding accuracy accumulate, helical CT angiography is likely to replace aortography as a definitive imaging modality for blunt aortic injuries in the trauma patient. Current Management Options The management of blunt aortic injury is prompt operative repair of the injured aortic segment. In some patients, a purposeful delay of surgery or even nonoperative management may be indicated. Patients with severe head injury, complex multi-system trauma, and those about to breach their physiologic envelope are bad candidates for an aortic reconstruction, and a risk of free rupture of 1% per hour compares favorably with the risk of aortic repair under these circumstances. Evidence is now accumulating that, in stable patients, purposeful delay of surgery combined with pharmacologic control of the blood pressure (similar to the management of a nontraumatic type B aortic dissection) and careful monitoring of the mediastinal hematoma may be an acceptable course of action. This purposeful delay will allow the surgeon to assess the total injury burden of the patient and select the optimal timing for operative intervention. In addition, “minimal” blunt aortic injuries, such as a small intimal flap or a small pseudoaneurysm, may be amenable to nonoperative management. However, the long-term behavior of these lesions is still not well defined, and careful follow-up is required. The option of endovascular stent-grafting of blunt aortic injuries is the focus of much interest, especially with chronic post-traumatic false aneurysms. A need to address the occlusion of the left subclavian artery by the stent-graft, and the high incidence of endoleaks, are two technical problems that currently present an obstacle to the increasing use of this modality. This technique cannot therefore be recommended as a practical alternative to operative repair in the acute situation at this time. However, the concept is certainly valid, and with further experience

427

this technique will certainly become a therapeutic option available to surgeons. The descending thoracic aorta is approached through a left posterolateral thoracotomy in the fourth intercostal space. The standard operative repair of aortic injuries (25) uses clamp and direct reconstruction and can be achieved by using one of three adjuncts: pharmacologic control of central hypertension, a temporary passive shunt, or pump-assisted atriofemoral bypass (26,27). The last can be achieved either by a traditional pump bypass (which requires full heparinization) or using a centrifugal pump without heparin. The use of temporary shunts or pump bypass is more complex than direct reconstruction with pharmacological control (Fig. 35.4). While more and more surgeons tend to favor the use of a shunt or partial bypass and there is evidence that this may improve morbidity and mortality, no clear-cut advantage over the clamp repair technique has been demonstrated. Thus, all three technical variations should be part of the surgeon’s armamentarium, and the technique chosen for an individual case should be tailored to the specific clinical and operative circumstances. Proximal control is obtained by encircling the subclavian artery and the aortic arch (between the carotid and left subclavian arteries). This maneuver is the most diffi-

A

C

B

FIGURE 35.4 Technique of repair of descending aortic injuries using claim and repair (A), left heart bypass (B), or shunt (C).

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Part V Occlusive Arterial Diseases

cult part of the dissection. The pleura between the vagus and phrenic nerves is incised, and using a combination of blunt and sharp dissection a plane is developed between the pulmonary artery and the inferior aspect of the aortic arch. A large curved vascular clamp can then be carefully brought around the aorta, making just enough space for passage of an umbilical tape and later an aortic clamp. The distal descending aorta is encircled after opening the mediastinal pleura, taking care not to injure an intercostal vessel. Clamps are placed on the isolated vessels, and extreme blood pressure fluctuations are avoided by careful pharmacologic control during aortic clamping and declamping. After clamping, the hematoma is entered and the extent and configuration of the tear is assessed through a careful longitudinal aortotomy. It is not possible to assess the full extent of the injury until the aorta has been opened. Direct primary repair is possible in only 15% of patients, while the rest require an interposition graft. The reported operative mortality of blunt aortic injury repair is 5% to 25% and is related not only to the procedure but also to the presence of associated injuries. The major devastating complication is paraplegia or paraparesis, occurring in approximately 8% of patients. The incidence of spinal cord damage is affected neither by choice of operative technique nor by the method chosen to deal with central hypertension and distal ischemia. There is also no direct proven correlation between aortic cross-clamp time and the incidence of spinal cord damage. The use of intraoperative adjuncts such as monitoring of spinal somatosensory-evoked potentials is still debatable and is not a standard part of the operative procedure. The Thoracic Inlet Vascular injuries to the thoracic inlet are rare, accounting for less than 3% of vascular trauma cases. In stable patients, angiographic definition of the injury enables the surgeon to plan the operative approach, but actively bleeding patients present a real challenge. After initial control digitally or with a balloon catheter inserted in the wound tract, the appropriate incision is determined. Both subclavian arteries can be approached through supraclavicular incisions and the exposure expedited by removal of the medial third of the clavicle. However, proximal control, which is the prime consideration, may be difficult through this limited exposure. The first part of the left subclavian artery is intrapleural and more posterior than is generally appreciated, and the safest and quickest way to control it is through a separate left anterolateral thoracotomy in the third intercostal space. Similarly, the safest route to proximal control of the first part of the right subclavian artery is through a median sternotomy, as is also the case with active bleeding from the suprasternal area. The second most common blunt thoracic vascular injury is a tear at the origin of the innominate artery off the aortic arch. The current approach to this injury employs

A

B

C FIGURE 35.5 Technique of innominate artery injury revascularization. Knitted Dacron or PTFE grafts are preferred.

the bypass and exclusion principle, eliminating the need for cardiopulmonary bypass, shunts, or heparinization (28) (Fig. 35.5). After median sternotomy, the ascending aorta is exposed intrapericardially and, using a partially occluding clamp, a Dacron graft of 8 to 12 mm is sewn end-to-side to the normal aorta away from the injury. The distal innominate artery is exposed and clamped, and bypass is completed. The injury is then oversewn by placing a pledgeted suture line on the aortic arch. In penetrating injuries to the innominate vessels and proximal carotid arteries, the surgeon encounters a mediastinal hematoma, and, much as in the retroperitoneum, plunging into this hematoma without proximal control is a recipe for disaster. Proximal control of arterial injuries can be obtained intrapericardially, where the anatomy is not obscured by the hematoma. An injured innominate vein may be ligated with impunity. Injuries to the subclavian vessels present several technical problems, the first of which is accessibility (29). Although an experienced surgeon may be able to control and repair most of these injuries through a limited supraclavicular incision, there should be no hesitation to improve exposure by either removing the medial third of the clavicle or extending the incision into a median sternotomy (for the right subclavian artery) or a “book” thoracotomy (for the left). The key to a rapid clavicular resection is early subperiosteal division of the bone as laterally as needed, grasping it with a towel clip and lifting it upward out of its

Chapter 35 Vascular Trauma

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bed. The subclavian artery is in close proximity to the brachial plexus and is also very friable, a fact not always appreciated by the inexperienced. Limited dissection and graft interposition (preferably using knitted Dacron) is thus preferable to extensive mobilization and attempted end-to-end anastomosis. The mortality rate associated with subclavian artery injuries is around 6%, and is due not only to associated injuries, but also to exsanguination, thus attesting to the heavy toll of difficulties in obtaining control of these injuries.

rential arterial hemorrhage. Aortic clamping can be performed at several sites:

The Abdomen

2.

1.

General Principles Abdominal vascular trauma presents either as free intraperitoneal hemorrhage or as a contained retroperitoneal hematoma. Several injury patterns such as a bullet trajectory across the abdominal midline (trans-axial trajectory) were shown to be associated with abdominal vascular trauma. In most patients the indications for an urgent laparotomy is clear, and the diagnosis is made at operation. Time should not be wasted on unnecessary diagnostic tests or futile attempts to stabilize the patient. Vigorous fluid resuscitation in the hypotensive patient with uncontrolled bleeding is of no benefit, and has actually been shown to adversely affect outcome in penetrating torso trauma (30).

3.

Laparotomy and Initial Control Laparotomy is performed through a midline incision. Rapid evisceration and evacuation of blood enables quick assessment of injury patterns. The first priority is to control bleeding. If the vascular injury itself is the source of hemorrhage, then it must be addressed. However, if the presumed vascular injury is contained within a stable retroperitoneal hematoma and there are other sources of bleeding or gross spillage, these must be addressed first. Free hemorrhage is controlled initially by digital or manual pressure. Once the bleeding is temporarily controlled, the surgical team should halt. To ensure that vascular repair is performed under optimal conditions, especially when dealing with relatively inaccessible vessels or complex repairs, time should be taken to summon a full range of vascular instruments, sufficient blood, an autotransfusion device, and competent assistance. This is the time to formulate an operative plan, including the necessary exposure maneuvers and approach to associated injuries, as well as to coordinate the surgical effort with the anesthesia team. The same principle applies to a stable retroperitoneal hematoma, which should not be opened without first obtaining proximal (and preferably also distal) control away from the area of injury. Aortic Cross-clamping Aortic clamping is traditionally used both as an adjunct to resuscitation and a means of partially controlling tor-

4.

5.

The descending thoracic aorta can be clamped above the diaphragm through a left anterolateral thoracotomy. Used mainly as one of the steps in resuscitative thoracotomy, it also enables the surgeon to gain aortic control before laparotomy. However, because it entails opening another visceral compartment, with the inevitable loss of time and body heat, clamping of the descending thoracic aorta is rarely performed in the context of abdominal vascular trauma. The supraceliac aorta can be approached through the lesser omentum and clamped at the diaphragmatic hiatus (31). The peritoneum anterior to the esophagus is opened, and the esophagus is rapidly mobilized to the patient’s left. An opening is made bluntly in the left diaphragmatic crus, and the aorta is clamped through it, thus avoiding the thick periaortic tissue below the diaphragm. Using this technique, the clamped aortic segment is in fact the lowermost portion of the thoracic aorta. The supraceliac aorta may also be exposed by medial visceral rotation, as described below. The suprarenal aorta can be clamped or compressed directly through an opening in the lesser sac, or approached in the retropancreatic area by performing an extended Kocher maneuver and retracting the duodenum and pancreas toward the patient’s left shoulder (32). The infrarenal aorta is clamped beneath the left renal vein after a rightward reflection of the small bowel, division of the ligament of Treitz, and incision of the posterior peritoneum overlying the aorta (Fig. 35.6). The aorta can also be occluded by retrograde insertion of an occluding balloon from the groin, via the femoral and iliac arteries (33).

Aortic clamping through the lesser sac is not always quick and easy, especially when performed in a pool of blood. Meticulous dissection is often impossible, proper positioning of the clamp is made difficult by the dense periaortic tissue, and iatrogenic injury (to the celiac axis, esophagus, left gastric artery, and the aorta) may also occur. Therefore it is often advisable to use firm digital pressure to compress the aorta through the lesser sac against the vertebral body instead of formal clamp placement. Another problem with aortic clamping is its physiologic effect. It dramatically changes the numbers on the monitor screen, but the sudden afterload augmentation and peripheral ischemia are detrimental to the patient’s already borderline physiologic reserves. Although at times a lifesaving maneuver vital for the rapid control of aortic injuries in a “crashing” patient, its use as a resuscitative adjunct should be judicious and not reflexive.

430

Part V Occlusive Arterial Diseases FIGURE 35.6 Retroperitoneal rightward reflection of the abdominal viscera to expose the retroperitoneal abdominal aorta (Mattox maneuver).

Abdominal Exposure Maneuvers The major abdominal vascular structures are retroperitoneal and relatively inaccessible. The key to correct exposure of these vessels is rapid mobilization of the overlying peritoneal viscera. This can be achieved using two visceral rotation maneuvers that swing the peritoneal content off the retroperitoneal structures. Medial rotation of the left-sided abdominal viscera (Mattox maneuver) (34) affords rapid access to the entire intra-abdominal aorta and its branches, except the right renal artery (Fig. 35.6). It is the key to exposing the supramesocolic aorta and its branches, an area that is otherwise almost inaccessible. The correct plane is entered by incising the lateral peritoneal attachment of the sigmoid and left colon at the level of the pelvic brim, and the hand is swept upward lateral to the left colon, kidney, and spleen. The plane of blunt digital dissection is rapidly developed in front of the left common iliac vessels and behind the kidney, with the hand sliding on the posterior abdominal wall muscles, thus bringing the viscera (left colon, kidney, spleen, and pancreas) to the midline. The presence of a retroperitoneal hematoma greatly facilitates the dissection, which can be completed in 30 seconds. Right-sided medial visceral rotation (extended Kocher or Cattel–Braasch maneuver) consists of medial reflection of the right colon and duodenum by incising their lateral peritoneal attachments (Fig. 35.7). Continuing the dissection medially to detach the posterior attachments of the small bowel mesentery and reflecting the small bowel onto the lower chest provides wide exposure of the infrarenal cava, aorta, and their bifurcations. This technique also exposes the superior mesenteric vessels and the entire length of the right iliac vessels as well as the

proximal part of the left iliac vessels. Access to the left iliac vessels more distally requires mobilization of the sigmoid mesocolon.

Approach to Specific Injuries Although management of most abdominal vascular injuries follows the principles outlined above, several types of injuries merit a detailed discussion. These injuries present either special technical problems or controversies in management. Iliac Vessels Trauma to the iliac vessels carries a mortality of approximately 30%, mostly from uncontrollable hemorrhage, thus attesting to the difficulties in obtaining control of these inaccessible vessels (35). This is particularly true for the iliac veins that lie hidden behind the arteries, the internal iliac vessels that dive deep into the pelvis, and the distal external iliac vessels in which distal control is difficult (but may be facilitated by a Deaver retractor “toed in” over the lower part of the abdominal incision and unto the vessels). Often the pelvic hematoma is so large it is impossible even to be sure which side is injured. The key to approaching extensive iliac vascular injuries is, therefore, obtaining initial control away from the injury (i.e., clamping or compressing the aorta, vena cava, and the external iliac vessels) in combination with direct pressure on the site of bleeding (Fig. 35.8). With subsequent dissection, the clamps can be sequentially advanced closer to the injury until all backbleeding is eliminated. Occasionally, the only way to provide access to an injured iliac vein is to divide the overlying common iliac artery and reconstruct

Chapter 35 Vascular Trauma

431

FIGURE 35.7 A right-sided medial rotation of the viscera to expose the right-sided abdominal vasculature.

it after the venous repair. Another problem in iliac artery injuries is gross fecal contamination from associated colorectal injuries. In this situation, if a synthetic graft is an unavoidable necessity, an extra-anatomic bypass (such as femorofemoral) is a safe technical solution. Renal Vascular Injuries The traditional approach to renovascular trauma contained within a stable perinephric hematoma is to obtain proximal control by “midline looping” of the ipsilateral renal artery and vein close to the aorta and vena cava. However, when active bleeding is present or when speed is important, the injured kidney can be rapidly mobilized by incising the posterior peritoneum and Gerota’s fascia lateral to the kidney, elevating it medially, and clamping the renal pedicle en masse, in a manner similar to a rapid splenectomy. Penetrating renovascular trauma is usually associated with other injuries and more often than not results in nephrectomy because the patient’s condition does not allow for complex renovascular reconstructions (36). Only the proximal left renal vein can be ligated with impunity. Deceleration injury to the renal pedicle is usually asymptomatic and discovered when the kidney fails to opacify on intravenous pyelogram or CT scan. It is perhaps the only abdominal vascular injury to require angiographic proof for diagnosis. Angiography may reveal a spectrum of injuries ranging from a minimal tear to complete thrombosis of the main renal artery. Renal revascularization for a deceleration-type injury is very controversial (37). The combination of an asymptomatic lesion with other associated life-threatening injuries, as is often the case, makes renal revascularization

FIGURE 35.8 Control of iliac vascular injury by direct compression against the posterior pelvic wall.

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an unrealistic option in the majority of these patients, and translates into significant delays in those few who may be suitable candidates. Opinions differ regarding the time limit that precludes a successful revascularization, considering that a viable but damaged kidney can be the source of renovascular hypertension. Most surgeons will not revascularize a kidney with a renal artery that has been totally occluded for more than 4 to 6 hours. Mesenteric and Portal Injuries Injury to the proximal (suprapancreatic and retropancreatic) superior mesenteric artery presents as a supramesocolic hematoma or bleeding and is approached using left-sided medial visceral rotation. A more distal (infrapancreatic) injury is approached directly through the base of the mesentery, after pulling the small bowel downward and to the left. Rarely, pancreatic transection is required to obtain access and control. Approximately one-half of the patients in the Ben Taub General Hospital series (38) were managed by simple arteriography, while the other half required complex vascular repairs. The key to aortomesenteric graft protection is keeping the proximal suture line away from associated pancreaticoduodenal wounds by placing it in the distal aorta and covering it with retroperitoneal tissue. Ligation is theoretically possible for the suprapancreatic segment of the artery because collateral flow via the pancreaticoduodenal arcade should in theory suffice to maintain midgut perfusion. However, this is not always the case in the shocked and vasoconstricted trauma patient. Therefore every effort should be made to revascularize the superior mesenteric artery, and when ligation is employed in a critical patient in order to avoid a complex repair, a planned “second look” exploration should also be seriously considered if the patient survives. Injuries to the superior mesenteric vein and portal vein both present accessibility problems (39), and are almost invariably associated with other grave injuries to the pancreatoduodenal region. Exposure of the proximal superior mesenteric vein may require pancreatic transection (over a finger insinuated from the root of the mesentery toward the portal triad) (Fig. 35.9). Control of the portal vein is difficult because vigorous backflow requires a “double Pringle” maneuver with clamping above and below the injury. In practice, the hepatoduodenal ligament is often too short to accommodate two clamps. And the portal vein must be repaired with less than optimal control using a combination of the Pringle maneuver and direct digital pressure (40). When lateral repair of the portal vein or superior mesenteric vein is impossible, ligation is an option, especially with the latter. Ligation requires aggressive postoperative fluid resuscitation to counteract the resulting massive splanchnic sequestration (41). The Retrohepatic Vena Cava Injuries to the retrohepatic vena cava and hepatic veins are rightfully considered the most challenging of all abdominal vascular injuries. Fortunately rare and almost always

FIGURE 35.9 Exposure of the proximal portal vein.

associated with high-grade hepatic trauma, retrohepatic caval injuries present as vigorous bleeding from somewhere behind the liver, a hemorrhage that is not diminished by a Pringle maneuver. Usually, by the time the nature of the injury is realized, the patient has already lost a massive amount of blood and is in critical condition. Thus survival is possible only if the injury is recognized early and temporary control is accomplished either by direct pressure or by pulling the divided falciform ligament downward, which tilts the liver parenchyma backward to compress the bleeding vein. Once temporary control is obtained, time is taken to stabilize the patient and make all necessary preparations to optimize surgical attack on the injury. Retrohepatic IVC injury is perhaps the most lethal and most challenging abdominal vascular injury. The typical operative findings are massive venous bleeding from the posterior aspect of a severely injured liver that is unaffected by a Pringle maneuver. Usually, by the time the injury is identified, the patient has already sustained massive blood loss and is in critical condition. Temporary control is accomplished by either direct pressure or pulling the divided falciform ligament downward, thus tilting the liver backward to compress the bleeding vein. Once temporary control is obtained, time is taken to stabilize the patient and make all necessary preparations for a well-planned surgical attack on the injury. Several techniques have been used to approach the retrohepatic vena cava. Full mobilization and medial rotation of the right or left hepatic lobe affords limited access, which may suffice to repair a small laceration. Hepatic vascular isolation entails a Pringle maneuver in conjunction with infrahepatic and suprahepatic (transdiaphragmatic) caval clamping (42). Unfortunately, the critically injured hemodynamically unstable patient often will not tolerate the sudden preload

Chapter 35 Vascular Trauma

reduction associated with caval clamping. A direct transhepatic approach to the injured IVC has also been described (43), using rapid hepatic transection in the principal plane to directly expose the injury from within the liver. The most widely published technique is the atriocaval shunt described by Schrock, which uses either a chest tube or an endotracheal tube to exclude the injured segment without compromising cardiac preload. This technically demanding procedure requires familiarity with cardiac cannulation and is usually performed by two teams working simultaneously in the chest and abdomen. It is therefore not surprising that this technique, usually employed in dire circumstances, carries a reported mortality in excess of 80%. Since there is no good technical solution for the challenge of retrohepatic IVC trauma, a recent anatomic analysis of these injuries suggests that it makes much more sense to try and contain these injuries by hepatic or perihepatic packing (44) than to try and repair them. If performed early and effectively, this simple solution may prove a more practical approach to injuries in this low-pressure system than the more heroic and technically complex alternatives. Retroperitoneal Hematoma As a general rule, retroperitoneal hematoma from penetrating trauma requires exploration, with two exceptions. A stable perinephric hematoma in a patient whose preoperative CT scan does not show major urine extravasation is best left undisturbed. A stable retrohepatic hematoma should also not be explored, because of the very high mortality of retrohepatic venous injuries (45). The approach to a retroperitoneal hematoma resulting from blunt trauma varies according to its location. A central hematoma (either supramesocolic or inframesocolic) is explored routinely, even if stable. Every effort should be made to avoid opening a pelvic hematoma except when a major vascular injury is suspected within it or when access is required to repair a bladder injury.

Peripheral Vascular Trauma General Principles The management of extremity trauma is a team effort, involving vascular, orthopedic, and plastic aspects. The arrest of hemorrhage and reconstitution of limb perfusion usually take priority, but orthopedic manipulation may disrupt the vascular repair, and soft tissue cover considerations may dictate an alternative route (46). Thus the extent and sequencing of the vascular, orthopedic, and plastic procedures should be carefully planned and orchestrated. If the extremity is not ischemic, bone alignment is usually achieved before vascular repair. In an ischemic limb, a temporary intraluminal shunt can be inserted across the injured arterial segment, or the vascular repair can be performed first. In the latter case, the risk to the graft from subsequent orthopedic manipulation

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can be reduced markedly if it is “guarded” by the active presence of the vascular surgeon during the orthopedic procedure. Two important adjuncts to the management of extremity vascular trauma are balloon catheter tamponade to temporarily control external bleeding, and angiographic embolization to control extravasation from a nutrient artery (such as branches of the deep femoral artery or relatively inaccessible vessel (such as one distal leg artery).

“Minimal” Vascular Injuries Not all arterial injuries require operative management. Intimal flaps, segmental narrowings, small false aneurysms, and small arteriovenous fistulas comprise a group of “minimal” nonocclusive and asymptomatic injuries that generally have a benign natural history, and do not require operative repair. Contrary to previous belief, data from prospective follow-up studies show that only about 10% of minimal injuries progress with time and require eventual operative repair. Nonoperative management and careful follow-up is therefore a safe and cost-effective option in these patients. However, currently no objective criteria have been established to precisely define what constitutes a “minimal” lesion. The mechanism of injury, size of the angiographic defect and, most importantly, the patient’s availability for follow-up are the key factors to consider in the decision to treat a minimal lesion nonoperatively. In rare instances when a nonocclusive “minimal” injury progresses and eventually requires surgical intervention, morbidity is not increased by the delay.

Diagnosis Clinical Diagnosis The clinical diagnosis of peripheral vascular trauma in an injured extremity is classically associated with a diligent search for “hard” and “soft” signs. “Hard” signs are an absolute indication for vascular exploration, whereas “soft” signs are an indication for angiography or sonography to rule out an injury. Two aspects of the clinical diagnosis of extremity vascular injuries require emphasis. First, a complete neurologic examination of the injured extremity is essential, not only because neurologic deficit is a sign of possible vascular trauma, but also because the exploration of traumatized neurovascular bundles always carries the risk of iatrogenic damage. Documentation of the preoperative neurologic status therefore has important medicolegal implications. Another, often underemphasized, aspect of the clinical diagnosis is the presence of associated truncal injuries. It may well be impossible to diagnose limb ischemia in a shocked, hypothermic, and vasoconstricted patient. In fact, whenever one finds it difficult to decide whether or not a wounded patient’s limb is ischemic compared with the opposite limb, immediate reassessment of the management priorities is indicated,

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because limb ischemia is an irrelevant issue in a shocked patient exsanguinating from a truncal injury. Noninvasive Imaging The ankle-brachial index is a very reliable screening modality for significant arterial obstruction following both blunt and penetrating trauma, but there are no welldefined quantitative guidelines for a critical value below which arteriography is indicated. The hand-held Doppler is also useful in assessing severity of ischemia by determining presence of an arterial and venous Doppler signal. Absence of the latter signifies grave ischemia. Duplex scanning is a reliable screening tool for peripheral vascular trauma, with an accuracy rate of around 98% in detecting clinically significant injuries. It can also detect “minimal” arterial injuries such as intimal flaps and small pseudoaneurysms. However, hopes that this technology will replace exclusion arteriography for “soft” signs have not been realized, because the routine use of duplex ultrasonography in the acute admission area of many trauma centers is limited by logistic constraints such as cost and the availability of trained personnel. It remains a very valuable tool for follow-up of patients with suspected or “minimal” vascular injuries, postoperative patients, and those with late complications of vascular trauma such as pseudoaneurysm and arteriovenous fistula. Arteriography Arteriography is the gold standard in the diagnosis of extremity vascular injuries. The indications for arteriography differ in patients with “hard” and “soft” signs. In the former, arteriography is indicated when the information gained may alter or facilitate the operative approach. Typical examples are penetrating injury to the thoracic outlet and multiple penetrating wounds in the same extremity, where precise localization of vascular injury may eliminate the need for extensive exploratory dissection. For patients with “soft” signs, arteriography is indicated to rule out a vascular injury. Evidence suggests that Doppler pressure measurement may be a noninvasive substitute for angiography in these patients (47). Thus, for the patient with normal peripheral pulses, many surgeons do not use angiography any more “to rule out” an arterial injury, because the incidence of injuries that will require operative intervention is so small. Single-shot arteriography using manual injection of contrast material through an 18-gauge plastic intravenous catheter is a rapid, accurate and cost-effective technique that is immediately available in the resuscitation area, thus bypassing the time-consuming logistics of formal arteriography (48).

Special Management Problems Complex Groin Injuries High-velocity shotgun blast injury to the groin results in a fiercely bleeding cavity in which major arterial and venous

disruption is combined with extensive soft tissue loss. Unless a determined and effective effort is made to control bleeding in the field or in the emergency room, these patients die of exsanguination. A pressure dressing, a wide blood pressure cuff, an inflated Foley balloon or a fist should be used to temporarily control bleeding. Blind groping and attempted clamping under less than optimal conditions is likely to have a fatal result. Formal vascular control is obtained in the operating room using the inguinal ligament (when identifiable) as a guide to dissection. The first priority is to reestablished flow in the common and superficial femoral arteries and to ensure distal perfusion by liberal use of four-compartment fasciotomy. The second priority is soft tissue coverage of the vascular graft or repair. In the stable patient, a large contaminated soft tissue defect that requires debridement and open management is an indication for extra-anatomic routing of the graft underneath healthy soft tissue (49). However, most patients with groin injuries need a more expeditious solution, and temporary cover by a porcine xenograft followed later by a rotational muscle flap (or myocutaneous flap) is one such solution (50). Restoration of venous flow is a low priority, and in most patients with serious groin injuries who just survived an exsanguinating hemorrhage, a complex venous repair using interposition graft, with its high occlusion rate, is a dangerous (and often futile) exercise.

Popliteal and Tibial Vascular Injuries Trauma to the popliteal artery leads to limb loss more often than any other extremity vascular injury. Amputation rates as high as 20% to 30% are not uncommonly reported, especially in battlefield injuries from high-velocity projectiles, and in blunt trauma (51,52). The fate of the limb is often determined not by technical aspects of the arterial repair, but rather by the extent of associated damage to bone, nerve, and soft tissue and by delays in diagnosis and management. Following bone and soft tissue trauma, the very limited collateral circulation around the knee is disrupted, and viability of the distal lower limb is jeopardized if early revascularization is not achieved. The key to early detection of blunt popliteal artery trauma is a high index of suspicion and a low threshold for arteriography even in asymptomatic patients with knee dislocation, displaced fractures, or “bumper” automobile injuries. The operative management of popliteal artery injuries follows the principles outlined above. The contralateral saphenous vein is the conduit of choice, but an externally supported 6-mm PTFE graft is an acceptable alternative. Several traditional dogmas unsupported by good objective evidence have strongly influenced the management of popliteal and lower leg vascular trauma. Repair or reconstruction of the popliteal vein is traditionally held to be important for limb salvage (52), but this belief is not based on sufficient evidence. Similarly, the necessity of

Chapter 35 Vascular Trauma

maintaining patency of at least two shank arteries following blunt trauma is unproved (53). Any surgeon who has ever attempted to identify, dissect, and reconstruct a shank artery in the hostile operative field created by a compound fracture knows that this can be a long and tedious procedure that, in the presence of one patent artery, may well be unnecessary.

Fasciotomy Fasciotomy is the most important adjunct to the surgical repair of extremity arterial trauma. An elusive diagnosis even under optimal circumstances, compartment syndrome is even more difficult to diagnose in a vasoconstricted, edematous, and hypothermic patient. A host of local and systemic factors such as extensive soft tissue trauma, prolonged hypothermic patient, and substantial delays between injury and revascularization all combine to create a set of circumstances favoring the rapid development of increased compartment pressures (54). Arbitrary definitions of ischemic times (6 or 8 hours) are poor guidelines for the need for a fasciotomy. Pressure measurement, although occasionally useful in borderline cases, provides information about one point in time, and in the labile, severely traumatized patient, this is clearly not enough. Maintaining a very low threshold for fasciotomy in injured limbs is always in the patient’s best interest. Fasciotomy should precede revascularization in patients with preoperative signs of compartment syndrome. Patients with several hours’ delay between injury and arterial repair, those with compromised venous outflow, and those with extensive soft tissue destruction should have a fasciotomy even in the presence of normal compartment pressure, because the risk of developing a compartment syndrome far exceeds the added morbidity of the procedure.

Primary Amputation The decision to amputate a severely mangled limb rather than attempt to salvage it is difficult and emotionally charged, and until recently, objective data on which to base it were lacking. Despite several attempts to develop objective criteria, severity scales, and indications for primary amputation (55,56), this remains very much a matter of judgment. However, several principles have emerged to guide the surgeon facing this decision. First, decision to amputate a limb without reconstruction is a joint venture in which the vascular injury may well be the least important component. This is so because with modern vascular reconstructive techniques, the fate of the limb is often decided by the extent of neural, bony, and soft tissue damage, as these elements are less amenable to reconstruction than the artery. Second, except for obvious near-total amputations, the decision to amputate is always made intraoperatively. The mangled limb should be examined meticulously under the optimally controlled conditions of the operat-

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ing room. This is the only reliable way to assess the full extent of the damage, especially to nerve continuity, a critical factor in the decision. The “mangled extremity syndrome” is defined by involvement of at least three of the four major tissue systems of the extremity: soft tissue, nerve, vessel, and bone (55). As a general guideline, totally interrupted distal innervation, extensive soft tissue destruction, and bone loss exceeding 6 cm portend a grave prognosis of the limb. The patient’s hemodynamic stability and associated injuries are also important factors (57). But even with the availability of indexes and grading systems, the decision to amputate must be individualized and remains challenging and problematic.

References 1. Rich NM, Spencer FC. Vascular trauma. Philadelphia: WB Saunders, 1978. 2. Feliciano DV, Burch JM, et al. Balloon catheter tamponade in cardiovascular wounds. Am J Surg 1990; 160:583–587. 3. Schickler WJ, Baker RJ. Chapter 3. Types of vessel injuries and repairs. In: Flanigan DP, ed. Civilian Vascular Trauma. Philadelphia: Lea & Febiger, 1992; 36–43. 4. Ferrara A, MacArthur JD, Sright HK. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg 1990; 160: 515–518. 5. Burch JM, Ortiz VB, et al. Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg 1992; 215:476–482. 6. Morris JA, Jr., Eddy VA, et al. The staged celiotomy for trauma: issues in unpacking and reconstruction. Ann Surg 1993; 217:576–586. 7. Timberlake GA, O’Connell RC, Kerstein MD. Venous injuries: to repair or ligate, the dilemma. J Vasc Surg 1986; 553–558. 8. DeBakey ME, Simeone FA. Battle injuries of the arteries in World War II. Ann Surg 1946; 123:534–579. 9. Johansen K, Bandyk D, et al. Temporary intraluminal shunts: resolution of a management dilemma in complex vascular injuries. J Trauma 1982; 22:395–401. 10. Nichols JG, Svoboda JA, Parks SN. Use of temporary intraluminal shunts in selected peripheral arterial injuries. J Trauma 1986; 26:1094–1096. 11. Kahlil IM, Livingston DH. Intravascular shunts in complex lower limb trauma. J Vasc Surg 1986; 4:582–587. 12. Feliciano DV, Mattox KL, et al. Five year experience with PTFE grafts in vascular wounds. J Trauma 1985; 25:71–78. 13. Lim RC, Jr, Trunkey DD, Blaisdell FW. Acute abdominal aortic injury: an analysis of operative and postoperative management. Arch Surg 1974; 109:706–712. 14. Thal ER, Meyer DM. Penetrating neck trauma. Curr Prob Surg 1992; 29:1–56. 15. Asensio JA, Valenziano CP, et al. Management of penetrating neck injuries: the controversy surrounding zone II injuries. Surg Clin North Am 1991; 71:267–296.

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16. Brown MF, Graham JM, et al. Carotid artery injuries. Am J Surg 1982; 144:748–753. 17. Thal ER, Snyder WH, et al. Management of carotid artery injuries. Surgery 1974; 76:955–961. 18. Martin RF, Eldrup-Jorgensen J, et al. Blunt trauma to the carotid arteries. J Vasc Surg 1991; 14:789–795. 19. Perry MO, Snyder WH, Thal ER. Carotid artery injuries produced by blunt trauma. Ann Surg 1980; 192:74–77. 20. Reid JDS, Weigelt JA. Forty-three cases of vertebral artery trauma. J Trauma 1988; 28:1007–1012. 21. Henry AK. Extensile exposure. 2nd edn. Edinburgh: Churchill Livingstone, 1973:58–74. 22. Hatzitheofilou C, Demetriades D, et al. Surgical approaches to vertebral artery injuries. Br J Surg 1988; 75:234–237. 23. Parmley LF, Mattingly TW, Marion WC. Nonpenetrating traumatic injury to the aorta. Circulation 1958; 17:1086–1101. 24. Mirvis SE, Bidwell JK, et al. Imaging diagnosis of traumatic aortic rupture: a review and experience at a major trauma center. Invest Radiol 1987; 11:187–196. 25. Mattox KL, Holzman M, et al. Clamp-repair: a safe technique for treatment of blunt injury to the descending thoracic aorta. Ann Thor Surg 1985; 40:456–463. 26. Verdant A, Cossette R, et al. Acute and chronic traumatic aneurysms of the descending thoracic aorta: a 10-year experience with a single method of aortic shunting. J Trauma 1985; 25:601–607. 27. Oliver HF, Jr., Maher TD, et al. Use of the BioMedicus centrifugal pump in traumatic tears of the thoracic aorta. Ann Thor Surg 1984; 38:586–591.. 28. Johnston RH, Wall MJ,Jr., Mattox KL. Innominate artery trauma: a thirty-year experience. J Vasc Surg 1993; 17:134–139. 29. Graham JM, Feliciano DV, Mattox KL. Management of subclavian vascular injuries. J Trauma 1980; 20:537–544. 30. Martin RR, Bickell WH, et al. Prospective evaluation of preoperative fluid resuscitation in hypotensive patients with penetrating truncal injury: a preliminary report. J Trauma 1992; 33:1–9. 31. Veith FJ, Gupta S, Daly V. Technique for occluding the supraceliac aorta through the abdomen. Surg Gynecol Obstet 1980; 151:427–429. 32. DeLucia A, III, Fromm D. Retropancreatic control of the suprarenal aorta. Surg Gynecol Obstet 1988; 166:475–476. 33. Gupta BK, Khaneja SC, et al. The role of intra-aortic balloon occlusion in penetrating trauma. J Trauma 1989; 29:861–865. 34. Mattox KL, McCollum WB, et al. Management of upper abdominal vascular trauma. Am J Surg 1974; 128:823–828. 35. Burch JM, Richardson RJ, et al. Penetrating iliac vascular injuries: recent experience with 233 consecutive patients. J Trauma 1990; 30:1450–1459. 36. Carroll PR, McAninch JW, et al. Renovascular trauma: risk assessment, surgical management and outcome. J Trauma 1990; 30:547–552. 37. Brown MF, Graham JM, et al. Renovascular trauma. Am J Surg 1980; 140:802–806.

38. Accola KD, Feliciano DV, et al. Management of injuries to the superior mesenteric artery. J Trauma 1986; 26:313–318. 39. Feliciano DV, Burch JM, Graham JM. Abdominal vascular injury. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. Norwalk CT: Appleton & Lange, 1988:519–536. 40. Graham JM, Mattox KL, Beall AC, Jr. Portal venous system injuries. J Trauma 1978; 18:419–422. 41. Stone HH, Fabian TC, Turkleson ML. Wounds of the portal venous system. World J Surg 1982; 6:335– 341. 42. Heaney JP, Stanton WK, et al. An improved technique for vascular isolation of the liver: experimental study and case reports. Ann Surg 1966; 163:237–241. 43. Patcher HL, Spencer FC, et al. The management of juxtahepatic venous injuries without an atriocaval shunt. Surgery 1986:569–575. 44. Beal SL. Fatal hepatic hemorrhage: an unresolved problem in the management of complex liver injuries. J Trauma 1990; 30:163–169. 45. Feliciano DV. Management of traumatic retroperitoneal hematoma. Ann Surg 1990; 211:109–123.. 46. Martin RR, Mattox KL, et al. Advances in treatment of vascular injuries from blunt and penetrating limb trauma. World J Surg 1992; 16:930–937. 47. Lynch K, Johansen K. Can Doppler pressure measurement replace “exclusion” arteriography in the diagnosis of occult extremity arterial trauma? Ann Surg 1991; 214:737–741. 48. Itani KMF, Burch JM, et al. Emergency center arteriography. J Trauma 1992; 32:302–306. 49. Feliciano DV, Accola KD, et al. Extra-anatomic bypass for peripheral arterial injuries. Am J Surg 1989; 158:506–510. 50. Ledgerwood AM, Lucas CE. Biological dressings for exposed vascular grafts: a reasonable alternative. J Trauma 1975;15:567–571. 51. Conkle DM, Richie RE, et al. Surgical treatment of popliteal artery injuries. Arch Surg 1975; 110:1351–1354. 52. Snyder WH, III. Vascular injuries near the knee: an updated series and overview of the problem. Surgery 1982; 91:502–506. 53. Keeley SB, Snyder WH, III., Weigelt JA. Arterial injuries below the knee: fifty-one patients with 82 injuries. J Trauma 1983;23:285–290. 54. Matsen FA, III. Compartment syndrome: a unified concept. Clin Orthop 1975; 113:8–14. 55. Gregory RT, Gould RJ, et al. The mangled extremity syndrome (M.E.S.): a severity grading system for multisystem injury of the extremity. J Trauma 1985; 25:1147–1150. 56. Russell WL, Sailors DM, et al. Limb salvage versus traumatic amputation: a decision based on a seven-part predictive index. Ann Surg 1991; 213:473–480. 57. Johansen K, Daines M, et al. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma 1990; 30:568–572.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 36 Fasciotomy Calvin B. Ernst, Bruce H. Brennaman, and Henry Haimovici

Fasciotomy is designed to decompress the neurovascular elements and the skeletal muscles encased in a rigid osteofascial compartment, to prevent neuromuscular ischemia and necrosis. A variety of pathologic conditions may lead to vascular compromise of skeletal muscles and to ischemic impairment of neural function in such a closed system. The most common entities that may require decompressive fasciotomy are the revascularization procedures, especially those for severe acute ischemia and for severe traumatic lesions of the extremities of both an orthopedic and vascular nature. Following the description by Volkmann in 1881 of the traumatic ischemic contracture (1), a number of investigators reported similar clinical and pathologic findings resulting from acute arterial occlusions (2,3). These reports dealt primarily with the morphologic effects of ischemic muscle damage, swelling of the muscle fibers leading sometimes to fibrosis, and resulting contracture (3,4). The pathogenic mechanism of Volkmann contracture remained unclear, although Volkmann believed that it was due to skeletal muscle anoxemia. The first investigative work that brought this problem into proper focus was published by Jepson in 1926 (5). He demonstrated experimentally in dogs that considerable edema in the muscles can result from constriction of an extremity. Jepson found that drainage of edema from the intermuscular spaces relieved the muscle swelling and restored the extremity to a normal state. His experimental data suggested that intrinsic pressure was responsible for the ischemic condition, and he concluded that drainage of edema was essential for preventing the necrotic changes and contracture.

Jepson’s contribution provided both the pathogenic mechanism—that is, the increased pressure of the compartment—and its management. However, this contribution was slow to gain recognition and make the necessary clinical impact. One of the earliest clinical applications of fasciotomy was reported by Dennis in 1945 for acute massive deep venous thrombosis (6). In the same year, Horn described the syndrome of acute ischemia of the anterior tibial compartment (7). Subsequently, fasciotomy was performed for arterial injuries in civilian and military practice, as well as for other vascular entities (8,9). Recent investigations of the role of compartment pressure and the need for a more comprehensive decompression of more than one compartment have provided better understanding of the pathogenesis of the compartment syndrome and its treatment (10,11).

Clinical and Pathologic Data The main vascular and allied disorders for which fasciotomy is indicated are acute occlusive arterial diseases, massive venous thrombosis, functional anterior tibial syndrome, limb fractures, crush injuries, and replantation of limbs. With the use of more sophisticated and more readily available street weapons among the civilian population, the incidence of compartment compression syndromes secondary to severe soft-tissue injury without significant vascular damage appears to be increasing. Arterial diseases that may require fasciotomy include all forms of acute occlusion likely to induce muscle edema and hematoma such as embolism, acute thrombosis, arte-

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rial reconstruction, and arterial injuries (12). Venous diseases include phlegmasia cerulea dolens, venous gangrene (13), acute injuries of major limb veins, and combined arterial and venous injuries. Crush injuries (14), limb fractures, circumferential burns, and replantation of limbs are other conditions that frequently lead to muscle ischemia and edema. Another group of patients who must be closely observed for onset of compartment syndromes are those suffering from drug-induced coma or stupor and subsequent positional compression of an extremity.

Pathogenic Mechanism lrrespective of the vascular lesion, compromise of blood supply is one of the main factors that may initiate a chain of hemodynamic events resulting in edematous muscle tamponade of the nutrient (capillary) bed. First there is a rise in pressure in the compartment due to the increased muscle bulk resulting from edema. Then there is fluid retention and associated small hemorrhages, which in turn interfere further with the vascular supply, and a vicious positive-feedback cycle develops. If unrelieved by fasciotomy, the changes occurring in the compartment will lead to compression myopathy, with ensuing necrosis. Occlusion of the arteries and veins or their injury does not fully explain the pathogenic mechanism of compartment syndrome, however, since it may occur in the absence of vascular injury or occlusion. Therefore other factors must influence the development of the compartment syndrome. Regardless of the injury or ischemic insult, the response of the muscles and their supporting vascular beds in any affected compartment is to develop edema, which is thought to be the result of an increase in capillary permeability in the nutrient bed of the muscle. The end results are an increase in muscle bulk within the restricted confines of the fascial compartment and a rise in compartmental pressure. With increased pressure, there is a relative decrease in nutrient bed capillary perfusion and resulting ischemia. An increase in capillary permeability and a further increase in muscle bulk and intercompartmental pressure follow. The pressure at which nutrient blood flow ceases approximates the critical closing pressure of the capillary bed and has been estimated to be about 35 to 40 mmHg. At compartment pressures above the critical closing pressure, perfusion of muscle essentially ceases, leading to the above-mentioned chain of ischemic events. Decompressive fasciotomy breaks this self-perpetuating ischemic cycle and allows reperfusion of muscle by venting it. At the cellular level, the changes occurring at the onset of the self-perpetuating compartment compressions cycle may be related to ischemia–reperfusion phenomena. The exact mechanisms responsible for the increase in capillary permeability are unknown. However, certain biochemical processes have been identified that can partially account for the increase. The increase in capillary permeability seen in an ischemia–reperfusion model in dogs was

closely associated with the generation of oxygen-derived free radicals (O2-,OH˙) (15). Using both direct and indirect measurements of capillary permeability and capillary pressure, Korthuis et al. found that capillary permeability was significantly increased in the presence of oxygenderived free radical scavengers (15). A pathway by which generation of free radicals may arise in the ischemia– reperfusion phenomenon was developed (Fig. 36.1) (15). Resistance or vulnerability to ischemia appears to be related to tissue content of xanthine dehydrogenase and speed of conversion of this enzyme to xanthine oxidase, the source of the superoxide radical. Superoxide species are toxic to the intercellular matrix and cell membranes. Thus it appears that the use of oxygen-derived free radical scavengers such as allopurinol, mannitol, catalase, dimethylsulfoxide, and superoxide dismutase to suppress or eliminate cytotoxic oxygen metabolites would be potentially useful in the treatment of compartment syndrome. Further evidence for the presence of oxygen-derived free radicals in ischemia–reperfusion injury has been provided by Lee et al. (16). During episodes of ischemia, skeletal muscle sarcoplasmic reticulum has a depressed ability to transport intracellular calcium. Using this model in ischemic rat hindlimbs and later in reperfused limbs, Lee demonstrated that pretreatment with superoxide dismutase and catalase significantly increased calcium uptake by skeletal muscle sarcoplasmic reticulum when compared with untreated ischemic-reperfused controls. However, treatment with free radical scavengers did not return calcium uptake to a level consistent with nonischemic hindlimbs, suggesting that other mechanisms may be at play in the development of compartment syndrome. Heppenstall et al. investigated the biochemical and histologic changes that occurred in two models of skeletal muscle ischemia in dogs (17). They studied a tourniquetinduced ischemia–reperfusion model and a compartment syndrome model of ischemia–reperfusion. At the biochemical level, the compartment syndrome group demonstrated decreases in high-energy phosphate supply, with a significant delay in resynthesis of these high-energy phosphates. Also, intracellular pH measurements were significantly more acidotic in animals with compartment syndrome, and had slower return toward normal levels upon reperfusion. Ultrastructural damage to skeletal muscle cells was also noted to be more intense in the animals made ischemic by induction of compartment syndrome. In summary, it would appear that the initiating events in the development of compartment syndrome revolve around an ischemia–reperfusion phenomenon and may be partially induced by the development of oxygenderived free radicals. With the onset of intracompartment pressure elevation, a synergistic relationship may develop, resulting in more severe myopathy than seen with ischemia–reperfusion alone.

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FIGURE 36.1 Possible mechanism for oxygen free radical production in ischemic skeletal muscle. O2- represents the superoxide anion; H2O2 represents hydrogen peroxide; and OH- represents the hydroxyl radical. (Reproduced by permission from Korthuis RJ, Granger DN, et al. The role of oxygen-derived free radicals in ischemia-induced increases in canine skeletal muscle vascular permeability. Circ Res 1985;57:536.)

Clinically, it appears that oxygen-derived free radical scavengers may reduce the amount of muscle damage induced by the compartment syndrome. Compounds such as mannitol, allopurinol, catalase, dimethylsulfoxide, and superoxide dismutase have been used with success to reduce the damage caused by ischemia in the heart, intestine, pancreas, kidney, and brain (18–20). Walker and associates used controlled oxygen delivery alone and in combination with mannitol, superoxide dismutase, and catalase in a dog model of ischemia–reperfusion (21,22). Both methods were successful in significantly reducing the degree of muscle necrosis when compared with untreated ischemic controls. Although these studies are encouraging, further investigation will be required before the treatment of compartment syndrome will routinely include the use of free radical scavengers.

Indications Early fasciotomy is essential to prevent irreversible changes. The compression myopathy of the forearm and the leg compartments displays varying degrees of impending ischemia. The course of this compartment syndrome may be divided into three stages: Stage 1 Stage II

Pain, swelling, and paresthesias; Neurologic deficit, absent pulses, and early focal necrosis of the muscles; Stage III Advanced necrosis of the muscles and the overlying skin. Clinical criteria for indications for fasciotomy, although well established, are still controversial because of their lack of reliability. Classically, there are six clinical

findings that have been recognized in the diagnosis of compartment syndrome: 1. 2. 3. 4.

5. 6.

pain in the affected extremity that generally is out of proportion to the injury or condition of the extremity; pain induced by passive stretch of the muscles in the affected compartment; paralysis or paresis of the muscles in the affected compartment; hypesthesia or paresthesia in the cutaneous distribution of the nerves that traverse the affected compartment; induration or inflammation or both of the affected compartment; diminished or absent distal pulses.

That clinical manifestations are sometimes inadequate to make the diagnosis of compartment compression is documented by the frequent finding of severe irreversible myonecrosis even when fasciotomy is performed soon after the onset of symptoms. This finding suggests that the clinical manifestations of the syndrome become manifest late in the course of the disease, and emphasizes the need for early recognition and aggressive management. The use of compartment pressure measurements has been suggested as a more reliable indicator of the need for decompressive fasciotomy (11,23,24). Initial efforts in this area left much to be desired because of technical difficulties in obtaining accurate tissue pressure measurements (25). Recent studies and technology have improved the reproducibility and reliability of the compartment pressure measurement as a clinical indicator of the need for fasciotomy (26–29). The use of compartment pressures is based on the concept of critical closing pressure. In the skeletal muscle bed, the critical closing pressure has

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been experimentally estimated in humans to be about 40 mmHg (30,31). Based on this estimate, a net perfusion pressure of less than 40 mmHg would result in neartotal cessation of capillary bed perfusion in the affected compartment. Therefore tissue pressure measurements greater than 40 mmHg strongly suggest the need for fasciotomy. Other investigators have used a compartment pressure within 30 mmHg of the patient’s diastolic blood pressure as an indication for fasciotomy (24,26). Still other investigators have used absolute compartmental pressure measurements ranging from 30 to 45 mmHg as an indicator to perform decompressive fasciotomy

FIGURE 36.2 To measure compartment pressure, apparatus is assembled as shown to aspirate column of sterile saline in extension tubing. (Reproduced by permission from Whitesides TE, Haney TC, et al. A simple method for tissue pressure determination. Arch Surg 1975;110:1311.)

(27,28). Lack of uniformity and the individual variations between patients have hampered the use of compartment pressures as a uniformly reliable indicator for fasciotomy. Many different techniques for the measurement of compartment pressure have been described (26–28,32). Different catheters have been developed for the continuous measurement of compartment pressures. Use of these catheters requires experience, and sophisticated measuring methods complicate evaluation. Whitesides et al. reported a simplified technique for measurement of compartment pressures that can be performed with readily available equipment (32). The assembled system is shown in Figure 36.2. The 20-mL syringe is assembled with its plunger withdrawn to the 15-mL mark. The threeway stopcock is turned off to the needle before its insertion into the compartment. After insertion of the needle into the desired compartment, the system is modified as shown in Figure 36.3, and the stopcock is turned so as to open all three ports of the stopcock simultaneously. The syringe plunger is then slowly depressed, causing an observable rise in the mercury manometer. When the saline meniscus begins to move, the pressure is noted and recorded as the compartmental pressure. This technique provides a simple method to assess compartment pressures in patients who do not show overt clinical signs of compartment syndrome. The needle is inserted at about the junction of the upper one-third and lower two-thirds of the leg. The anterior compartment is entered at a point approximately one fingerbreadth lateral to the lateral border of the tibia. The lateral compartment is entered approximately three fingerbreadths from the lateral border of the tibia. The deep posterior compartment is approached about one finger’s breadth posterior to the posterior border of the tibia on the medial surface of the leg, sliding the needle parallel to the patient’s bed until it is just behind the tibia. The superficial posterior compartment pressure is measured

FIGURE 36.3 Tissue pressure is measured by determining the amount of air pressure within this closed system that is required to barely overcome the pressure within the closed compartment and to inject very slowly a minute quantity of saline. (Reproduced by permission from Whitesides TE, Haney TC, et al. A simple method for tissue pressure determination. Arch Surg 1975;110:1311.)

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as the needle is withdrawn from the deep posterior compartment. It is best to inject a small amount of saline (1 mL) when the catheter is placed, to clear tissue from the end of the needle. Gentle pressure on the leg will give a small pressure wave if the catheter is clear and functioning well. In summary, clinical diagnosis of compartment syndrome requires a high index of suspicion. Clinical signs and direct measurements of compartment pressure are not consistently diagnostic when used alone. Together, however, they are complementary. The major complications of the compartment syndrome come from procrastination in performing fasciotomy, resulting in a “too little and too late” phenomenon (10).

Anatomy of the Compartments Any anatomic location in which muscles are enveloped in an osteofascial sheath has the potential to develop a compartment syndrome. The compartments of the leg and the forearm are of most interest to the vascular surgeon, with the former being most important. A brief anatomic description of only these compartments is given. The forearm contains two clinically significant compartments: the volar and dorsal. The volar compartment includes the flexors of the wrist and fingers and has the radial and ulnar vasculature traversing the compartment. Its boundaries are the radius laterally and the ulna medially, with the intervening interosseous membrane as its deep border and the deep fascia of the forearm more superficially. The ulnar and median nerves traverse the compartment and provide innervation to its muscles, the intrinsic muscles of the hand, and the skin over the palmar surface of the hand. The dorsal compartment contains the extensors of the wrist and fingers, with blood supply through the posterior interosseous artery and the muscular branches of the radial artery. The radial nerve traverses the compartment and innervates the skin of the dorsum of the hand and the muscles of the compartment. It is bounded by the radius, ulna, and interosseous membrane, as well as its own deep fascia. The leg contains four osteofascial compartments: anterior tibial, lateral peroneal, superficial posterior, and deep posterior (Fig. 36.4). The anterior tibial compartment includes the tibialis anterior, the extensor digitorum longus, the extensor hallucis longus, and the peroneus tertius muscles. Their functions are to evert and dorsiflex the foot and to extend the toes. The anterior tibial neurovascular bundle traverses the anterior compartment and lies on the interosseous membrane. The lateral compartment contains the peroneus longus and peroneus brevis muscles. The lateral compartment also contains the deep peroneal nerve. The superficial posterior compartment contains the gastrocnemius and soleus muscles. The deep posterior

FIGURE 36.4 Cross-section of the four compartments of the leg: 1) anterior tibial; 2) lateral peroneal; 3) superficial posterior; and 4) deep posterior.

compartment contains the tibialis posterior, the flexor digitorum longus, and the flexor hallucis longus muscles. The posterior tibial and peroneal vessels and the posterior tibial nerve lie in the deep posterior compartment. The enveloping fasciae of all these compartments, especially those of the anterior and lateral compartments, are quite rigid (Fig. 36.4). The most commonly affected compartment is the anterior tibial. The greater occurrence of the anterior tibial compartment syndrome can be explained by a combination of anatomic and physiologic factors. The arterial supply to the muscles of this compartment consists of end-type branches with very little collateral circulation.

Technique The major requirement for relief of the compartment syndrome is adequate decompression of all involved compartments. A variety of methods are described below, all of which, when performed properly, will provide the needed decompression of an involved compartment. The choice of technique is dependent on the suspected severity of the compartment syndrome and the number of compartments requiring decompression.

Anesthesia Fasciotomy of an isolated compartment compression can usually be carried out using local anesthesia. If several compartments are involved, which is the usual case, it is best to perform decompression using epidural, spinal, or even general anesthesia.

Short Skin Incisions This method of fasciotomy is suitable for an isolated compartment syndrome. Two short skin incisions are made at

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A

B

C

B D

A E FIGURE 36.5 Skin incisions for different types of fasciotomies. (A) Incision of fascia and bulging muscle through its aperture. (B) Short skin incisions of the leg for the anterior (continuous line) and posterior (broken line) compartments. (C) Fasciotomy performed with straight scissors subcutaneously between the two short skin openings. (D) Long skin incisions of the leg for anterior (continuous line) and posterior (broken line) compartments. (E) Long skin incision of the leg and thigh.

both ends of the compartment (Fig. 36.5) and are carried through the subcutaneous tissue down to and including the fascia. Straight scissors are used for the incisions of the fascia. Specifically designed instruments with a curved cutting edge have been described by Mozes et al. (33) and Rosato et al. (34). The procedure is performed subcutaneously between the two areas of exposure (Fig. 36.5A). As soon as the fascia is opened, the underlying muscle bulges through the incision. The muscle may appear as grayish or congested tissue and is sometimes pale, having a fish-flesh appearance. The fascia is left open, whereas the skin may be closed with a few interrupted stitches. Should there be a great amount of edema, the skin must be completely incised over the fascial incision by connecting the short skin incisions. Such a skin incision is left open and is closed secondarily 4 to 5 days later. In the event that difficulty is encountered in approximating the edges, a split-thickness skin graft is applied to the defect.

FIGURE 36.6 (A) Embolic occlusion of the popliteal artery and its three branches. (B) Cross-section at the midleg level, indicating necrosis of the anterolateral compartment.

It must be emphasized that if adequacy of the decompression is questionable because of a limited fasciotomy, a more extensive skin incision is used without hesitation. Complete decompression of all involved compartments is necessary, especially in cases of unyielding phlegmasia cerulea dolens and in post-traumatic compartment compression.

Long Skin Incision Lower Extremity The anterolateral compartment of the leg is entered through an extensive skin incision (Fig. 36.5D and E). The fascia is incised from below the knee to above the ankle. The muscles encountered at that level, namely the extensor digitorum and the peroneal muscles, are separated to the level of the entry of the deep peroneal nerve into the lateral compartment. In localized muscle necrosis of the anterolateral compartment, wide excision of its contents may be indicated, to be followed by skin grafting (Figs. 36.6 and 36.7).

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times indicated, especially in patients with severe trauma of massive edema associated with phlegmasia cerulea dolens. The incisions are carried out on both the medial and lateral aspects from the shoulder down to the elbow.

Parafibular Four-compartment Decompression

FIGURE 36.7 Healed leg in which the entire anterolateral compartment was excised because of muscle necrosis. Healing was completed through use of a skin graft.

The superficial posterior compartment is entered by a long incision (see Fig. 36.5D) placed somewhat medially and going through the gastrocnemius down to and including the soleus. For the deep posterior compartment, the incision is carried beyond the soleus and enters the deep group, including the tibialis posterior, the flexor digitorum longus, and the flexor hallucis longus. At that level one finds the neurovascular bundles, the posterior tibial and the peroneal arteries with two satellite veins, and the posterior tibial nerve. It may be necessary in some cases also to split the posterior tibialis muscle down to the interosseous membrane. Combined extensive fasciotomy in the thigh may sometimes be required, especially in patients with phlegmasia cerulea dolens (13). Such incisions are made on both the medial and lateral aspects of the thigh in the same direction as those in the leg (see Fig. 36.5E). Upper Extremity The incisions in the forearm are made from the elbow through the wrist, incising the fascia overlying the volar and dorsal compartments. Such incisions allow exploration of the vessels and the nerves, together with evaluation of the degree of muscle ischemia. As in the lower extremity, extensive fasciotomies of the arm are some-

For parafibular four-compartment decompression, a long lateral skin incision is made directly over the fibula and runs its length from just below its neck to a point 3 to 4 cm above the lateral malleolus (24,25,35). The anterior compartment is opened by retracting the anterior skin flap, and it is opened over its entire length. Care is taken to avoid injury to the common peroneal nerve at the neck of the fibula and the superficial peroneal nerve at the lower level (junction of the upper two-thirds and the lower onethird of the leg). The lateral compartment is opened directly beneath the skin incision, which is deepened to incise fascia overlying the peroneal muscles. The edge of the skin flap overlying the posterior compartment is retracted, and it is opened over its entire length. The superficial posterior compartment, after the fibular origin of the soleus muscle is detached, is thus exposed. The gastrocnemuis-soleus group is then retracted posteriorly to expose the deep posterior compartment, which is opened over its entire length. In the deep compartment, care should be taken to avoid injury to the posterior tibial and peroneal vessels and the posterior tibial nerve. The wound is left open and is covered with fine-mesh gauze and a dry bulky dressing. After 7 to 14 days, the wound may be closed, or delayed closure may be carried out by using a split-thickness skin graft within 1 to 2 weeks.

Four-compartment Fasciotomy with Fibulectomy Four-compartment fasciotomy with fibulectomy was used during the Vietnam conflict for vascular injuries (10). As the fibula has no weight-bearing function, its excision would result in few, if any, untoward effects. Only the distal fibula is essential because of its participation in providing stability of the ankle joint. Exposure of the fibula and of the four compartments is identical to the preceding technique without fibulectomy (Fig. 36.8). With the introduction of the perifibular procedure, fibulectomy–fasciotomy has been used less frequently, since the former modality accomplishes the four-compartment fasciotomy without the bone resection. It is mentioned briefly here because of the rare need for its application. The four-compartment decompression is useful in certain well-defined conditions. Its greatest value lies in its use for extensive vascular injuries with massive tissue damage rather than in other vascular entities affecting the leg compartments.

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Part V Occlusive Arterial Diseases FIGURE 36.8 (A) Cross-section showing entrances for decompression of the four compartments of the leg: (1) anterior tibial; 2) lateral peroneal; 3) superficial posterior; and 4) deep posterior. (B) Fibulectomy–fasciotomy technique (see text).

Pitfalls and Complications The most serious pitfall is delayed recognition of the leg and forearm compartment syndromes that require early and urgent fasciotomies. Inadequate decompression by limited skin incisions in the presence of markedly swollen muscles may be a significant error. Likewise, partial debridement of damaged muscles may lead to further infection and secondary amputation. Long skin incisions, so necessary to decompress several edematous muscles, with their edges left unapproximated for several days may leave neurovascular structures, vascular grafts, or tendons unprotected. Every effort must be made to cover these structures with either the adjacent tissues or a splitthickness skin graft when appropriate (36). If the muscle ischemia is too far advanced, fasciotomy may not always achieve its therapeutic goal. In cases of ischemic venous thrombosis with incipient gangrene, for example, results of fasciotomy may be mediocre because of protracted wound healing due to the delayed procedure and superimposed infection. In the majority of cases, however, in promptly recognized compartment syndromes, fasciotomy properly

performed will reduce morbidity, save limbs, and have few, if any, complications.

References 1. Volkmann RV. Die ischaemischen muskellahmungen und kontraktuten. Zentralbl Chir 1881;8:801 2. Brooks B. Pathologic changes in muscle as a result of disturbances of circulation: an experimental study of Volkmann’s ischemic paralysis. Arch Surg 1922;5:188. 3. Griffiths DL. Volkmann’s ischemic contracture. Br J Surg 1940;28:239. 4. Jacobs AL. Arterial embolism in the limbs. Edinburgh: Churchill Livingstone, 1959:60. 5. Jepson PN. Ischemic contracture experimental study. Ann Surg 1926;84:785. 6. Dennis C. Disaster following femoral vein ligation for thrombophlebitis; relief by fasciotomy; clinical case of renal impairment following crush injury. Surgery 1945; 17:265. 7. Horn CF. Acute ischemia of the anterior tibia muscle and the long extensor muscles of the toes. J Bone Joint Surg 1945;27:615.

Chapter 36 Fasciotomy 8. Chandler JG, Knapp RW. Early definitive treatment of vascular injuries in the Viet Nam conflict. JAMA 1967: 202:136. 9. Patman RD, Thompson JE. Fasciotomy in peripheral vascular surgery. Report of 164 patients. Arch Surg 1970;101:663. 10. Ernst CD, Kaufer H. Fibulectomy-fasciotomy: an important adjunct in the management of lower extremity arterial trauma. J Trauma 1971;11:365. 11. Matsen FA, Krugmire RB. Compartmental syndromes. Surg Gynecol Obstet 1978; 147:943. 12. Haimovici H. Myopathic-nephrotic-metabolic syndrome associated with massive acute arterial occlusions. J Cardiovasc Surg 1973;14:589. 13. Haimovici H. Phlegmasia cerulea dolens. Venous gangrene. In: Ischemic forms of venous thrombosis. Springfield, IL: Charles C Thomas, 1971. 14. Weeks RS. The crush syndrome. Surg Gynecol Obstet 1968;127:369. 15. Korthuis RJ, Granger DN, Ct al. The role of oxygen derived free radicals in ischemia-induced increases in canine skeletal muscular vascular permeability. Circ Res 1985;57(4):536. 16. Lee KR, Cronenwett JL, et al. Effect of superoxide dismutase plus catalase on Ca2+ transport in ischemic and reperfused skeletal muscle. J Surg Res 1987,42:24 17. Heppenstall RB, Scott R, et al. A comparative study of the tolerance of skeletal muscle to ischemia. J Bone Joint Surg 1986:68A(6):820. 18. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med 1985:312:159. 19. Parks DA, Buckle GB, Graiger DN. Role of oxygen-derived free radicals in digestive tract diseases. Surgery 1983,94:415. 20. Saufey H, Bulkley GB, Cameron JL. The pathogenesis of acute pancreatitis: the source and role of oxygen-derived free radicals in three experimental models. Ann Surg 1985;201:633. 21. Labbe R, Lindsay T, Walker PM. The extent and distribution of skeletal muscle necrosis after graded periods of complete ischemia. J Vasc Surg 1987;6:152. 22. Walker PSI, Lindsay TF, et al. Salvage of skeletal muscle with free radical scavengers. J Vasc Surg 1 1987;5:68. 23. Whitesides TE, Haney TC, et al. A simple method for tissue pressure determination. Arch Surg 1975;110:1311. 24. Mubarak SJ, Woen CA, et al. Acute compartmental syndromes: diagnosis and treatment with the aid of the Wick catheter. J Bone Joint Surg (Am) 1978;60:1091. 25. Rollins DL, Bernhard VM, Towne JB. Fasciotomy: an appraisal of controversial issues. Arch Surg 1981;116:1474. 26. Whitesides TE, Haney TC, et al. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:43. 27. Russell WL, Apyan PSI, Burns RP. Utilization and wide clinical implementation using the Wick catheter for compartment pressure measurement. Surg Gynecol Obstet 1985;160(3):207. 28. Matsen FA, Winquist RA, Krugmire RB. Diagnosis and management of compartmental syndromes. J Bone Joint Surg 1980;62A(2):286.

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29. Allen MJ, Stirling AJ, et al. Intracompartmental pressure monitoring of leg injuries. J Bone Joint Surg 1985; 67B(1):53. 30. Ashton H. Critical closure in human limbs. Br Med Bull 1963; 19(2):149. 31. Jennings ASIC. Some observations of critical closing pressures in the peripheral circulation of anesthetized patients. Br J Anesth 1964;36:683. 32. Whitesides TE, Haney TC, et al. A simple method for tissue pressure determination. Arch Surg 1975; 110:1311. 33. Mozes NI, Ramon Y, Jahr J. The anterior tibial syndrome. J Bone Joint Surg 1962:44A:730. 34. Rosato FE, Barker CF, et al. Subcutaneous fasciotomy: description of a new technique and instrument. Surgery 1966:59:383. 35. Matsen FA. Compartmental syndromes. New York: Grune & Stratton, 1980:163. 36. Ledgerwood AM, Lucas CE. Massive thigh injuries with vascular disruption: role of porcine skin grafting of exposed arterial vein grafts. Arch Surg 1973;107:201.

Selected Readings Ascer E, Strauch B, et al. Ankle and foot fasciotomy: an adjunctive technique to optimize limb salvage after revascularization for acute ischemia. J Vasc Surg 1989;9(4):594–597. Fasciotomy of the ankle and foot should be considered for compartment syndrome unrelieved by standard leg fasciotomy. Fowl RJ, Akers DL, Kempczinski RE. Neurovascular lower extremity complications of the lithotomy position. Ann Vasc Surg 1992;6(4):357–361. Perioperative monitoring of the lower extremity circulation and compartment pressures are essential in these patients. Kikta RJ, Meyer JP, et al. Crush syndrome due to limb compression. Arch Surg 1987:122(9):1078–1081. Extensive open fasciotomy and dialysis for severe acute renal failure should provide good functional results in the majority of patients. Pedowitz RA, Hargens AR, et al. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990;18(1):35–40. Criteria to be diagnostic of chronic compartment syndrome of the leg are 1) a preexercise pressure greater than or equal to 15 mmHg, 2) a 7-minute postexercise pressure of greater than or equal to 30 mmHg, or 3) a 5-minute post-exercise pressure greater than or equal to 20 mmHg. Ris HB, Furrer M, et al. Four-compartment fasciotomy and venous calf-pump function: long-term results. Surgery 1993;113(1):55–58. Fasciotomy does not lead to venous pump dysfunction, irrespective of whether the wound is closed by delayed suture or skin grafts. Rosfors S, Bygdeman S, Wallensten R. Venous circulation after fasciotomy of the lower leg in man. Clin Physiol 1988;8(2):171–180. The results of the study indicate that an intact muscle fascia is of importance for venous return and venous pump function. Rush DS, Frame SB, et al. Does open fasciotomy contribute to morbidity and mortality after acute lower extremity ischemia and revascularization? J Vasc Surg 1989;10(3):343–350. Limb loss and death resulted from

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persistent ischemia and underlying systemic disease processes or injuries, but not from open fasciotomy wound complications. Turnipseed W, Detmer DE, Girdley F. Chronic compartment syndrome: an unusual cause for claudication. Ann Surg

1989;210(4):557–562; discussion 562–563. Patients treated by open fasciotomy instead of subcutaneous fasciotomy had fewer early postoperative wound complications (6% vs. 11%) and fewer late recurrences (2% vs. 11%).

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 37 Ankle and Foot Fasciotomy for Compartment Syndrome of the Foot Enrico Ascher and Elke Lorensen

Compartment syndrome of the extremities is known to occur in a variety of clinical settings that lead to the development of increased pressures within the defined space of an osseofascial compartment. These settings include soft-tissue injuries, complex fractures, arterial or venous injuries, arterial revascularization, limb reimplantation, and circumferential burns. The elevation in compartment pressure occurs either directly from hemorrhage and tissue edema incited by a traumatic event, or indirectly from the edema that results when an ischemic extremity is reperfused and there is increased endothelial cell permeability and the formation of reactive free oxygen species. A compartment syndrome results when intracompartmental pressures are produced that exceed venous pressures and impair venous return, leading to further production of edema and pressure, until the arteriovenous gradient is reduced so that arterial inflow is compromised. Myoneural ischemia subsequently develops and progresses to irreversible damage unless fasciotomy is performed to relieve pressures and allow capillary filling to recur. Although compartment syndrome of the leg due to crush injury or ischemia and reperfusion of the skeletal muscle is a well-described phenomenon, a compartment syndrome of the foot has only recently been recognized (1). Foot compartment syndrome was first described following a direct traumatic injury to the foot with hemorrhage, edema, and fractures (2). The adverse sequelae, if fasciotomies were not performed, were permanent myoneural dysfunction leading to claw toes, loss of motor

function, and chronic pain. It was recognized that compartment syndrome of the leg could follow arterial revascularization for acute ischemia; however, there were no reports of a similar syndrome occurring in the foot in this clinical scenario. Considering that the foot communicates with the deep posterior compartment of the leg, relies on the same arterial supply, and contains several discrete osseofascial compartments, it could logically follow that reperfusion injury following revascularization of an ischemic leg could lead to a concurrent compartment syndrome in the foot as well. The first cases of compartment syndrome in the foot following revascularization of arterial injuries were reported by Ascher et al. in 1989 (1). Compartment syndrome of the foot was diagnosed on the basis of signs of foot ischemia, recurrent thrombosis of arterial repairs, and elevated foot compartment pressure. The performance of extended ankle and foot fasciotomies alleviated ischemia, allowed repairs to remain patent, and decreased foot compartment pressure. Potential consequences of foot compartment syndrome in the setting of arterial repair are not only the myoneural sequelae described above, but also the thrombosis of a bypass graft secondary to outflow obstruction from foot intracompartmental pressures that are elevated. Thus it is essential to be cognizant that a compartment syndrome in the foot can develop concurrently with one in the leg, and to diagnose and treat it expeditiously by appropriate fasciotomy, to prevent these consequences.

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Clinical Presentation The patients who subsequently developed compartment syndromes of the foot had all initially presented with an arterial injury necessitating emergent repair. The type of injuries and the repairs were as follows. 䊏

䊏

䊏

䊏

Five patients had occlusion of the superficial femoral artery or popliteal artery secondary to blunt or penetrating injury. Three underwent a primary arterial repair, and two underwent repair with an interposition vein graft. Three patients sustained penetrating injury to all three infrapopliteal vessels and underwent tibiotibial vein bypass. Two patients had a thrombosed common femoral artery secondary to injury from an intra-aortic balloon pump underwent thrombectomy and patch angioplasty. One patient had a traumatic leg amputation that was successfully reimplanted.

Immediately following revascularization and during the same operation, all patients underwent fourcompartment leg fasciotomy by a single long lateral incision and skeletonization. The indications for fasciotomy were prolonged ischemic time (mean 8.5 hours), concomitant venous injury and calf swelling, and tenseness. In six patients, a compartment syndrome of the foot was diagnosed at the first operation, whereas in the remaining five, the diagnosis was made up to 6 hours postoperatively, on the basis of the signs and symptoms described in the section below.

Signs and Symptoms The signs and symptoms of foot compartment syndrome are parallel to those of a compartment syndrome of the leg: 䊏

䊏 䊏 䊏 䊏

䊏

swelling and tenseness over dorsal or medial aspects of the foot; pain on passive dorsiflexion of the toes; sensory deficits along dorsal nerve distribution; weakness of intrinsic foot muscles; excessive muscle edema and bulging at leg fasciotomy; graft thrombosis.

There may be pain out of proportion to what is expected for the clinical situation. Sensory deficits in the distribution of the nerves affected by the ischemic process occur. In the foot parasthesias, the more subtle loss of twopoint discrimination and sensation to pin prick are seen, especially in the dorsal nerve distribution on the toes. Weakness of the muscles contained in the involved compartment occurs. There may be pain upon passive stretch

of involved muscles. In the foot there is classically pain upon dorsiflexion of the toes. Swelling and tenseness occur over the dorsal and medial aspects of the foot. There is pain to palpation of the involved compartments. Pallor, complete loss of sensation, and absence of detectable pulses are late findings, not valuable for making an early diagnosis. Specific to our group of patients, the most common finding was swelling and tenseness over the medial compartment. In awake patients, there was pain to palpation of the dorsum of the foot, the inability to spread the toes (secondary to ischemia of the interrossei muscles) and parasthesias. In three patients, concurrent compartment syndrome of the foot was suspected on the basis of excessively swollen and edematous muscle seen upon leg fasciotomy. An important and remarkable finding was the recurrent thrombosis of two of the infrapopliteal vein bypass grafts despite leg fasciotomy, thrombectomy, and demonstration of good flow on completion angiogram.

The Role of Compartment Pressure Measurements The role of intracompartmental pressure measurements in the diagnosis of foot compartment syndrome has not been completely delineated. They are now routinely used to make the diagnosis in cases involving direct traumatic injury to the foot (3). However, in these cases there is often such myoneural damage that clinical examination for diagnosis is completely unreliable. Thus the diagnosis must be made on the basis of pressure measurements. We did measure compartment pressures in three of our patients using the Wick catheter technique, and found elevated pressures of 58, 65, and 67 mmHg. There are no data on the actual pressures that the foot can tolerate, but it is assumed these are equal to the pressures tolerated by the leg. Foot fasciotomy is recommended once the compartment pressure is greater than 30 mmHg or if it is 10 to 30 mmHg below diastolic pressure. Compartment pressures were not measured in all our patients as we felt that the clinical signs of a foot compartment syndrome in patients who had already undergone leg fasciotomy were the most important indicators of ongoing elevated pressures. Subsequent management would not have been altered by any objective data. Whether routine measurements in the foot after leg fasciotomy would enable an earlier diagnosis of foot compartment syndrome before the clinical signs occur remains to be investigated.

Compartments of the Foot Until 1990, it was believed that the foot contained four osseofascial compartments: the medial, central, lateral, and interrosseous. Nine compartments have now been identi-

Chapter 37 Ankle and Foot Fasciotomy for Compartment Syndrome of the Foot

FIGURE 37.1 Ankle and dorsal foot fasciotomies performed through two separate incisions.

fied by dye injection studies (4). The medial, superficial, and lateral compartments traverse the entire foot. The calcaneal compartment is limited to the hindfoot, and the interrossei and adductor compartments are in the forefoot. The medial compartment contains the abductor hallucis and flexor hallucis brevis muscles; the lateral, the flexor digiti minimi and the abductor digiti minimi muscles. The flexor digitorum brevis, flexor digitorum longus, and lumbricales are in the superficial compartment. The calcaneal compartment contains the quadratus plantae muscle and the posterior tibial nerve and vessels, as well as the lateral plantar neurovascular bundle. Fascial extensions circumscribing the ankle also provide the potential for detrimental swelling to occur here in continuity with the leg and foot. The fascia overlying the ankle consists of the superior and inferior extensor retinaculum anteriorly, and the flexor retinaculum medially. Considering foot compartment syndrome a continuum with that in the leg, ankle fasciotomy should be included in the treatment of these syndromes.

Foot Fasciotomy Essentially, the two original approaches to foot fasciotomy are still used despite the recognition of five more compartments to be released (Fig. 37.1). Foot fasciotomy can be approached via a medially placed incision or by two dorsally placed incisions. There are problems associated with doing only one approach when all nine compartments need to be released, and it is recommended that, if this is the case, a modification of both approaches be used. The dorsal approach enables only a slow and sometimes

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inadequate decompression of the calcaneal compartment. A disadvantage to the medial approach is the risk of injuring the lateral plantar vessel and nerve when release of all compartments is attempted. To perform a fasciotomy by the medial approach, a 6-cm incision is made on the medial aspect of the foot, parallel to and 3 cm above the plantar surface, beginning 4 cm from the heel. The adductor hallucis muscle fascia is divided, releasing the medial compartment. After retraction of the adductor hallucis muscle superiorly, an inferior fascial incision will open the superficial compartment. A more superiorly placed incision in the intermuscular septum will release the calcaneal compartment. The lateral compartment can be opened from the proximal portion of the superficial compartment. The flexor retinaculum can also be opened from the proximal end of this incision. The dorsal approach ideally utilizes two incisions on the dorsum of the foot to minimize subcutaneous dissection: one, medial to the second metatarsal; the other, lateral to the fourth metatarsal. All four interrossei compartments are released, taking care not to injure the dorsal veins. The adductor compartment is decompressed as well by entering the space deep to the first interrosseus compartment after retracting the interrosseous muscle from the second metatarsal.

Ankle Fasciotomy A short incision of 3 to 5 cm is made on the posterior aspect of the ankle. Under direct vision, the superior and inferior extensor retinaculums are divided so as not to injure the anterior tibial vessels. To divide the flexor retinaculum, the proximal end of the medial fasciotomy is used and extended if necessary. If not already present, a separate retromalleolar incision of 2 to 3 cm is used. Care must be taken in this case not to disturb the posterior tibial vessels.

Approach to Extended Ankle and Foot Fasciotomy In the case of concurrent leg and foot compartment syndromes following delayed revascularization, it is advisable to extend fasciotomies into both the ankle and foot. To approach the dorsal compartments we actually used a single curvilinear incision between the second and third metatarsals (Fig. 37.2). With the need to decompress both the ankle and foot, this enabled us to limit out skin incisions and avoid potential skin necrosis. Fasciotomies via the medial incision were first performed on all patients, and then the foot was reevaluated for the persistence of symptoms or signs. In only 6 of 11 patients was it necessary to also decompress via the dorsally placed incision. In five of these patients, we observed obvious swollen and bulging muscles upon the second fasciotomy.

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intention. Within the follow-up period, up to 28 months postoperatively, limb salvage and skin healing were maintained. There were no myoneural deficits detected and no foot deformities; only moderate foot edema was noted in three patients.

Conclusion

FIGURE 37.2 Plantar and medial ankle fasciotomies performed through a single skin incision.

Compartment syndrome of the foot can occur following a direct traumatic injury to the foot or revascularization of an acutely ischemic limb. In the latter situation, it occurs concurrently with compartment syndrome of the leg. Elevated pressures can also occur in the foot owing to the presence of discrete osseofascial compartments, its communication with the posterior compartment of the leg, and its dependence on the same arterial supply. Potential consequences of a foot compartment syndrome after arterial reconstruction are not only long-term myoneural dysfunction, but also the thrombosis of a bypass graft with the subsequent threat of limb loss. The recognition of a compartment syndrome of the foot in this circumstance and the performance of timely ankle and foot fasciotomies can lead to improved limb function and salvage.

Results All arterial reconstructions remained patent. Of significance, the two infrapopliteal reconstructions that had rethrombosed after thrombectomy remained patent after ankle and foot fasciotomy was performed concurrently with repeat thrombectomy. Ten of eleven cases resulted in limb salvage. There was one below-knee amputation for rupture of one tibiotibial bypass graft secondary to severe infection. Two other infections were superficial and responded to local debridement and antibiotics. One-half of the wounds were closed by skin grafting 1 to 2 weeks after fasciotomy, and the other half closed by secondary

References 1. Ascher E, et al. Ankle and foot fasciotomy: an adjunctive technique to optimize limb salvage after revascularization for acute ischemia. J Vasc Surg 1989;9:594–597. 2. Bonurti PM, Bell GR. Compartment syndrome of the foot: a case report. J Bone Joint Surg 1986;68A: 1449–1451. 3. Manoli A. Compartment syndromes of the foot: current concepts. Foot Ankle 1990;10:340–344. 4. Manoli A, Weber TA. Fasciotomy of the foot: an anatomic study. Foot Ankle 1990;10:267–275.

PART VI

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

Chronic Arterial Occlusions of the Lower Extremities

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity Henry Haimovici

It is well recognized that the pathologic features of atherosclerosis are variable from individual to individual and from one arterial segment to another. As a result, the patterns emerging from the innumerable combinations of lesions are varied and complex. However, in terms of location and extent of the atherosclerotic process, it is possible to identify a certain number of broad patterns. Thus, the arteriographic findings may lend themselves to an overall classification of three major groups (Fig. 38.1): 1) aortoiliac, 2) femoropopliteal, and 3) tibioperoneal.

Methods of Study Computerized technology has been used recently for visualization of the entire vascular system (1). Achieved by intravenous injection of standard contrast agents, this method can be carried out as an outpatient procedure and in general does not entail the hazards of conventional intra-arterial injections. The results of this new technique, while helpful as a screening method, do not as yet yield the same qualitative details as standard arteriography for the lower extremities, especially when excellent information about the arterial lesions is needed. (See Chapter 5 for the correlation of the two methods.) Duplex ultrasonography, the newest modality for arterial imaging, may enable better evaluation of arterial patterns (Chapter 5). The data to be described herein were obtained with

standard conventional arteriography and are the basis for the classifications of arteriosclerotic patterns. When one deals with any one of the three patterns, it is essential that evaluation of the arterial lesions include the entire vascular tree from its origin to its final ramifications. A comprehensive assessment must therefore be based on the study of the inflow and outflow tracts of the arterial lesions from the infrarenal abdominal aorta to the pedal arterial network (2). Serial angiography is a prerequisite for proper evaluation of the arterial lesions (Fig. 38.2). Principles of angiography will not be reviewed here, since they are fully described in Chapter 5. It is sufficient to mention only briefly that aortoarteriography of the lower extremity can be achieved either by translumbar aortography or by the transfemoral retrograde and anterograde method. The latter can be carried out either by bilateral puncture of the femoral artery, using appropriate needles, or, preferably, by means of the catheter method. General or local anesthesia, especially the latter, because the newer radiopaque substances are generally painless, may be used in nearly all cases. In any case, optimum arteriographic outlines of the vasculature are essential.

Aortoiliac Patterns The atherosclerotic process of the aortoiliac segment may begin at the bifurcation or, most frequently, in one or both

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FIGURE 38.1 The three major arteriographic patterns of the lower extremity.

common iliac arteries. The development of these lesions is slow, insidious, and progressive. From a clinicopathologic standpoint, it may be emphasized that this syndrome may go through two distinct phases: stenotic and occlusive. If the terminal abdominal aorta or its bifurcation or the two common iliac arteries become occluded, the thrombotic process progresses proximally toward the renal arteries. The site of origin of the atherothrombotic process is not always easy to pinpoint. However, analysis of the arteriographic data strongly suggests that two major sites of origin may determine the evolution of the lesions and their subsequent patterns: 1) the aortic bifurcation and 2) the iliac arteries.

Aortic Bifurcation Progression of the lesions that begin at the bifurcation may extend proximally up to the renal arteries, but rarely above. Consequently, one may expect to find at least three patterns of such lesions: 1. 2.

3.

at the bifurcation itself, which includes the terminal abdominal aorta and the origin of both iliac arteries; in the distal segment, including the bifurcation and the terminal aorta up to the inferior mesenteric artery; and in the entire aortic segment up to the renal arteries.

The relative frequency of these three patterns is difficult to assess. The lesions range from moderate to marked steno-

FIGURE 38.2 Aortography of the lower extremity by the serial angiographic technique using a bilateral transfemoral method. This procedure affords evaluation of the entire arterial tree from the abdominal aorta to the pedal vessels. Note the complete occlusion of the right common iliac artery and a few minor lesions in the left leg (arrows).

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

sis (Figs. 38.3 and 38.4), to complete occlusion (Figs. 38.5, 38.6, and 38.7). In a study of 100 aortograms, Watt found the aorta to be completely occluded in 10% and the aortic bifurcation stenosed in 24% (3). DeBakey et al. found, in a series of 448 cases, complete occlusion of the aortoiliac segment in 44% and aortoiliac stenosis in 56% (4). As already alluded to, the aortic occlusion is confined most often below the renal artery origin because the large flow in these vessels often prevents the obstruction from progressing higher. Nevertheless, stenotic atherosclerotic lesions associated with complete obstruction or stenosis of the terminal abdominal aorta are not unusual in the renal arteries (5). It should be pointed out that, in cases of aortoiliac stenosis, narrowing of the origin of the two iliac arteries is not always identical. For example, stenosis may either be absent or be more pronounced on one side than on the other.

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Stenosis or occlusion of the common iliac artery, without aortic involvement, is the commonest form. Watt found that common iliac lesions accounted for 43% of the total group of 142 lesions of the aortoilac segment (3). Of these, stenosis was slightly more frequently encountered than complete occlusion. The site at which the lesion occurred was also variable: 1. 2. 3.

near the bifurcation of the aorta (Fig. 38.8); in the course of the artery itself (Figs. 38.9 and 38.10); or at the level of its bifurcation (Fig. 38.11).

The lesions of the iliac may involve the common, the external, or the internal. In some cases, there is a combination of two or three of these occlusions.

Although it is not always easy to assess the exclusive or specific site of the iliac involvement, arteriographically one can reasonably determine the exact location and extent in most cases. It should be pointed out, however, that in the case of stenosis, the lesions found at surgery appear much more extensive than the arteriographic image would indicate. Bilateral common iliac distribution of the lesions is relatively common. Although the lesions are not always symmetric, the rate of progression of the two sides does not appear to be synchronous.

A

B

Iliac Arteries

FIGURE 38.3 (A)Aortogram indicating aortoiliac stenosis of significant hemodynamic degree. (B) An aortoiliac endarterectomy is necessary.

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FIGURE 38.4 Segmental stenosis of the terminal abdominal aorta above its bifurcation.

FIGURE 38.6 Complete abdominal aortic occlusion distal to the inferior mesenteric artery, indicating also the pathways of collateral circulation from the inferior mesenteric artery through the pelvic vessels.

Occlusion and stenosis are less frequent in the external iliac artery than in the common iliac. When the occlusion occurs, it extends distally to the origin of the inferior epigastric artery, thus leaving the common femoral patent. Occlusion and stenosis of the internal iliac artery often remain asymptomatic. However, they are more commonly found in combination with the other iliac occlusions and are incidental findings in the course of the aortoiliac exploration. When an isolated lesion is present, its clinical manifestations are often not fully appreciated. The symptoms resulting from this lesion are buttock claudication and thigh and calf claudication, produced by occlusion of the main arterial channel. The latter type of claudication may overshadow the former. Combined lesions of the common, external, and internal iliac arteries may involve two or three of these vessels. The most frequent combination of lesions is found in the common and external iliac arteries, whereas the internal iliac is often spared.

Other Associated Vascular Lesions FIGURE 38.5 Aortogram showing complete occlusion of the terminal abdominal aorta below the inferior mesenteric artery and of both common iliac arteries.

Aortoiliac lesions are often associated with atherosclerotic stenosis or occlusion of the femoropopliteal or tibioperoneal vessels (Fig. 38.2). DeBakey et al. noted that, in a

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

457

A

FIGURE 38.7 (A) Complete abdominal aortic occlusion distal to the renal arteries. (B) Serial aortogram, 5 and 7 seconds later, indicating reestablishment of collateral supply from the superior to the inferior mesenteric artery and from the latter to the pelvic area and thence to the external iliac, femoral, and popliteal arteries.

certain proportion of their cases, the aortoiliac lesions were associated with peripheral arterial occlusive disease (4). Thus, in a series of 448 cases, 78 (18%) had such involvement of the femoropopliteal segment. In the majority of these cases, the peripheral occlusive process was also

B

segmental, involving primarily the superficial femoral artery with a patent lumen in the popliteal. In reviewing aortograms of 600 patients, Valdoni and Venturini found 830 occlusive lesions (6). Of these, 24% involved the aortic bifurcation and the iliac arteries. In 50% of the

B

FIGURE 38.8 (A) Severe aortoiliac stenosis most marked on the left side, with the patient having disabling intermittent claudication. (B) Tracings from intrabrachial and intrafemoral arterial pressures obtained from the artery whose aortogram is shown in A. Upper tracing is from the right brachial artery; middle tracing is from the right femoral artery, which shows moderate stenosis; lower tracing is from the left femoral artery, which shows marked stenosis. A

(Reproduced by permission from Haimovici H, Escher DIW. Aortoiliac stenosis, diagnostic significance of vascular hemodynamics. Arch Surg 1956,72:107.)

FIGURE 38.10 Complete occlusion of the right common iliac artery (see Figure 38.2).

FIGURE 38.9 Translumbar aortogram indicating complete occlusion of the origin of the left common iliac artery and stenosis of the right midcommon iliac artery.

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

aortoiliac lesions, they found the superficial femoral artery to be involved, whereas the popliteal appeared to be patent.

Collateral Circulation in Aortoiliac Occlusive Disease When aortic obstruction occurs just below the renal arteries, the most important anastomosis occurs between the superior mesenteric by way of its middle colic branch to the left colic and thence to the inferior mesenteric artery (Fig. 38.7B). If the distal aorta is patent at and below the origin of the inferior mesenteric, it is common for it to be fed directly in this fashion. If the origin of the inferior mesenteric is occluded, the flow proceeds distally into the inferior mesenteric and superior rectal (superior hemorrhoidal) arteries, then to the anastomosing pelvic visceral and parietal branches, including the internal pudendals, lateral sacrals, vesicals, and obturators, then to the internal, common, and external iliac arteries, and then to the lower extremity (Fig. 38.7B). The collateral vessels that provide flow to the main vessels below the occlusion develop from existing vessels and networks. The collaterals that occur in the occlusion of the aortic bifurcation are determined by a well-known anastomotic setup known as Winslow’s anastomotic system. These include, in addition to the arteries described

FIGURE 38.11 Marked stenosis of the junction between the common and external iliac arteries (arrow).

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above, the intercostals, the internal mammary, and the external iliac via the inferior epigastric artery. Riolan’s arc is seen in the same type of occlusion when the marginal artery in the mesentery develops into an important link in blood supply of the lower extremity by way of the superior mesenteric artery, middle and left colic, and inferior mesenteric, and thence to the superior rectal, hypogastric, and external iliac or deep femoral arteries. Awareness of this anastomotic network becomes important when resection of the left colon has to be considered in a patient with advanced aortoiliac disease.

Femoropopliteal Patterns The extent and location of lesions in the femoropopliteal segment are extremely variable. In one study (2), six subpatterns were identified on the basis of site and extent of occlusion (Fig. 38.12). Although almost half of the

FIGURE 38.12 Femoropopliteal patterns showing their six divisions: 1) distal superficial femoral, 2) proximal superficial femoral, 3) entire superficial femoral, 4) entire femoral and popliteal, 5) profunda femoris, and 6) diffuse atherosclerosis with multiple stenotic areas.

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B

A

FIGURE 38.13 (A) Arteriogram indicating multiple stenoses of femoral, popliteal, and tibial vessels (site of arrows). (B) Note the excellent arterial supply to the leg and foot below these stenotic lesions.

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

FIGURE 38.14 Almost complete occlusion of the superficial femoral artery at its junction with the popliteal. The arterial tree is otherwise completely normal from aorta to feet.

arterial lesions of the lower extremity were seen in the femoropopliteal area, they were rarely confined to this segment alone. However, isolated femoropopliteal lesions are encountered more often in nondiabetic atherosclerotic patients than in diabetic patients. Initial lesions (Fig. 38.13) are characterized by mild to severe stenosis. One of the most common locations of such lesions is at the junction between Hunter’s canal and the initial segment of the popliteal artery, as well as in the distal popliteal or below the origin of the anterior tibial artery. A complete or nearly complete occlusion often occurs as an initial lesion at the level of the foramen adductor magnus area (Fig. 38.14). A short segmental lesion in the common femoral artery is not unusual (Fig. 38.15). A complete occlusion of the common femoral from its origin at the external iliac artery to the bifurcation (Fig. 38.16) and an associated occlusion of the superficial femoral are more advanced patterns (Fig. 38.17). In these cases, the collateral supply is established between the internal iliac

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FIGURE 38.15 Short segmental occlusion of the common femoral artery.

branches and those of the profunda femoris, as shown by the arteriogram in Figure 38.17. A complete occlusion of the superficial femoral artery may occur distally at the adductor magnus hiatus or may extend up to the bifurcation of the femoral (Figs. 38.18 and 38.19). Such lesions may often occur bilaterally, as seen in Figure 38.20. These lesions were all confined to the femoral segment. However, the incidence of isolated lesions is much smaller than that of those combined with the proximal or distal arterial tree (see below). The popliteal lesions, like those in the femoral, are initially segmental and confined to a small area. Most often, the lesion appears either as a stenosis or complete occlusion in its midportion behind the condyles or just proximal to them (Figs. 38.21 and 38.22). A more extensive occlusion of the popliteal occurs as a result of progression of the lesion proximally, from the condyles toward Hunter’s canal (Fig. 38.23). Occlusion of the entire popliteal artery, including its tibial segment, may occur in patients with diabetes or with Buerger’s disease (Fig. 38.24).

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FIGURE 38.17 Complete occlusion of the right common femoral artery as well as the superficial. Note that the distal arterial flow of the limb is provided by the profunda femoris and the channels from the internal iliac artery, mainly through the obturator artery.

Associated Aortoiliac Lesions

FIGURE 38.16 Complete occlusion of the common femoral artery from the external iliac to the profunda. Note that the superficial femoral artery, as well as the rest of the arterial tree, is completely patent.

In a study previously cited, the incidence of a femoropopliteal segment as an isolated lesion was seen in only 10.4%, whereas the combined femoropopliteal– tibial patterns were present in 49.2% of a total of 321 cases (2).

In the presence of a segmental femoropopliteal occlusion, it is essential to determine the condition of the outflow and inflow tracts. The concept of a segmental nature of atherosclerotic disease is an attractive one and has been propounded and propagated through the literature, but this concept may lead one to oversimplify the true features of the atherosclerotic process. By the use of the panangiographic method, we have been able to demonstrate that intimal lesions are widespread and affect certain segments with greater predilection than others. In contrast to the extent of intimal lesions, the occlusive process is usually segmental only at an early phase of the disease. As the disease progresses, the intimal lesions may increase in size and become a significant hemodynamic lesion. In the presence of a reducing inflow, especially proximal to implantation of a graft, it is important to detect such silent lesions before undertaking the distal arterial reconstruction. An angiographic survey of the femoropopliteal segment, reported earlier, disclosed a relatively high incidence of 27% of associated aortoiliac lesions (7). Four basic patterns of associated lesions may be present: 1. 2. 3. 4.

aortoiliac stenosis; iliac occlusion (unilateral); aortoiliac aneurysms; and tortuosity of the aortoiliac segment.

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FIGURE 38.19 Complete occlusion of the entire superficial femoral artery from the profunda to the popliteal.

FIGURE 38.18 Complete occlusion of the right superficial femoral artery at its distal half. Note the patency of the popliteal and tibial vessels.

These aortoiliac patterns and their respective incidence are illustrated in Figure 38.25. Aortoiliac stenosis cannot always be accurately estimated from the arteriogram alone. Hemodynamic tests, previously described by us (8) and confirmed by others (9), may help to identify the critical stenotic lesions. Figure

38.26B indicates a severe lesion in the right iliac artery, both at its origin and above its bifurcation, in addition to the midfemoral arterial lesion indicated in Figure 38.26A. In this study, complete iliac occlusion (unilateral) (Fig. 38.10) was found to be of low incidence, although investigation of the common iliac artery as the site of the primary lesion reveals a higher incidence of associated femoropopliteal involvement. Aortoiliac aneurysms associated with the femoropopliteal segment are often not detectable clinically and are revealed only by a transfemoral aortogram. Figure 38.27 indicates a small abdominal aneurysm above its bifurcation, associated with stenosis of the iliac arteries. Figure 38.28 depicts an aortoiliac aneurysm associated with bilateral femoropopliteal occlusive disease. The associated aneurysm is usually unsuspected and is found only on arteriographic examination or aortosonography or computed tomography scan. At surgery, these lesions are found to consist of small fusiform dilations of the aorta or iliac vessels. In some cases, only a small anterior saccular dilation is present. These aneurysms are often associated with either tortuosity or stenosis of the iliac arteries. Such combined lesions lead to further impairment of the arteri-

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al inflow to the already involved femoropopliteal segment. Figure 38.29 indicates a segmental occlusion of the distal superficial femoral associated with stenosis and tortuosity of the ipsilateral iliac vessels and with severe lesions of the internal iliac artery.

Tibioperoneal Patterns

FIGURE 38.20 Bilateral superficial femoral occlusion with patency both proximally and distally. Right common iliac artery (arrow) is inadequately opacified.

Occlusion of leg arteries alone occurred in 85 of 321 cases, or 26.5%, in our own study. The incidence in nondiabetic and diabetic cases was 23.9% and 29.2% respectively. Combined occlusions of leg arteries with other arterial segments occurred in all arterial patterns. Comparison of the incidence of various patterns in nondiabetic and diabetic groups shows that the atherosclerotic process is more discrete in the former and more diffuse in the latter group. Involvement of a single artery was noted in 65% of cases of atherosclerosis and in only 31.1% of cases of atherosclerosis and diabetes (Fig. 38.30). Conversely, occlusion of two or all three leg arteries occurred in 68.9% of the cases in the latter group as compared with 35% in the nondiabetic patients (Figs. 38.31–38.34). This difference between the two groups holds true, though to a lesser degree, in the cases with combined leg and other occlusive patterns. This difference is further demonstrated when the two groups with occlusion of the leg arteries alone are evaluated in terms of incidence of associated intimal lesions of the proximal arterial tree. These mural alterations may range from simple plaques to significant stenosing lesions. Analyzed from this angle, isolated leg arterial patterns occurred in 37.5% of cases of simple atherosclerosis and in only 4.6% of cases of atherosclerosis and diabetes. These figures indicate, therefore, that practically all diabetic patients with tibial occlusions displayed intimal lesions of the proximal arterial tree from the popliteal up to the aortoiliac area, with the highest percentage (40%) in the femoropopliteal segment (Fig. 38.35). A further breakdown of the findings concerning the length of occlusion in the various arteries showed that in atherosclerosis the process is more segmental in comparison with cases of atherosclerosis and diabetes, in which the process often involved the entire vessel. It may be of some interest that the overall incidence of peroneal arterial occlusion is the lowest of the three arteries and that in the diabetic group, with only leg arterial involvement, the peroneal was never found occluded, although some degree of intimal change might be present. In these cases, the caliber of the peroneal appeared enlarged, obviously compensating for the absent tibials. Finally, pedal arteries per se rarely have isolated lesions. Figure 38.36 illustrates such an example, in which the plantar arteries were involved bilaterally, together with some involvement of the dorsalis pedis. Combined occlusions of leg arteries with those of other arterial segments occurred in all patterns, as

B

A

FIGURE 38.21 (A) Three times magnification of the occluded segment. The arterial tree is otherwise normal proximally and distally. (B) Segmental occlusion of the mid popliteal artery (arrow).

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 38.22 Three times magnification of the occluded segment. The arterial tree is otherwise normal proximally and distally. Short segmental occlusion of the left popliteal artery in the supracondylar region. Note fusiform dilation of a symmetric segment on the right side.

mentioned above. Comparison of the incidence of various patterns in nondiabetic and diabetic groups shows that the atherosclerotic process is more discrete in the former but more diffuse in the latter group.

Collateral Circulation in Occlusive Patterns of Femoropopliteal and Tibioperoneal Segments The collateral pathways compensating for the various patterns of occlusion found in the femoropopliteal and tibioperoneal segments areas may be classified into five major groups (10): 1. 2. 3. 4. 5.

the profunda femoris–iliac group; the profunda femoris–genicular group; the genicular–tibial group; the profunda femoris–genicular–tibial group; and the genicular–tibial–peroneal groups.

Profunda Femoris–Iliac Group In occlusion of the common femoral artery, collateral vessels that bypass the arterial occlusion originate from the common, internal, and external iliac branches. Of these, the iliolumbar, the superior gluteal, the inferior gluteal, the obturator, and the deep iliac circumflex will anastomose with the branches of the profunda femoris, namely, with the lateral circumflex, the medial circumflex, and the branches of the latter.

Profunda Femoris–Genicular Group In occlusion of the superficial femoral artery, the collateral vessels compensating for the arterial occlusion originate from one or more branches of the profunda femoris artery and anastomose with branches of the genicular systems (Fig. 38.37). The branches of the profunda femoris most frequently assuming the role of major collaterals noted in our studies were 1) the descending branch of the lateral circumflex or the rectus femoris collateral and 2) the perforating branches, mostly the third and fourth. The branches of the genicular system most concerned in the anastomosis with the above collaterals originate from either the highest genicular or the lateral superior genicular artery. In complete occlusion of the superficial femoral artery, anastomoses between the obturator and superior gluteal arteries, along with the lateral and medial femoral circumflex arteries, supply the important link between the internal iliac and profunda femoris arteries, as in the preceding group.

Genicular–Tibial Group In occlusion of the popliteal artery, the major collateral vessels arise from: 1. 2.

the highest genicular artery, with its musculoarticular and saphenous branches; and the profunda femoris artery, with its fourth perforating branch and the descending branch of the lateral femoral circumflex.

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

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FIGURE 38.23 Segmental occlusion of the left popliteal artery. Note corkscrew collateral vessels compensating between the superficial femoral and distal popliteal arteries with normal leg and foot arteries.

FIGURE 38.24 Occlusion of the proximal popliteal artery with abundant collateral vessels and a fair runoff.

These collaterals anastomose with the genicular arteries and, via this network, with the recurrent tibial arteries (Fig. 38.38). About half of our cases belong to this genicular–tibial group (10). Although the number and

size of collaterals vary with the occlusion pattern, the saphenous branch of the highest genicular, the descending branch of the lateral circumflex, and the fourth perforating branch are the most developed and constant ones.

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Profunda Femoris–GenicuIar–TibiaI Group In combined occlusion of the superficial femoral and popliteal arteries, collateral vessels from the profunda femoris artery anastomose with branches of the genicular network, which in turn anastomose with branches of the tibial arteries (Fig. 38.39). In this group, as in the profunda femoris–genicular group, the profunda femoris receives anastomotic branches from the internal iliac artery.

Genicular–Tibial–Peroneal Group In the group of cases of leg artery occlusions, the origin, distribution, and anastomosis of the collateral vessels are not always as well outlined as in the foregoing groups. Three sets of branches provide the anastomotic network: the genicular, the sural, and the terminal branches of the anterior and posterior tibial and peroneal arteries.

The genicular arteries form a rich but fragile network around the knee, which has connections with the collateral system from the lower third of the thigh and is linked to the anterior compartment of the leg via the anterior tibial recurrent artery. These vessels primarily supply the ligaments and joint structures of the knee. The sural arteries, which arise from the posterior aspect of the popliteal artery, supply the gastrocnemius muscle and have only sparse anastomoses with other muscular vessels of the leg. The collateral vessel from the anterior tibial artery is the anterior tibial recurrent, which is a major link between the genicular system and the anterior compartment. The posterior tibial recurrent is of relatively minor importance because of its size and location. The posterior tibial artery provides collateral vessels that occur near the ends of the vessel and do not primarily FIGURE 38.25 Diagrams illustrating the four aortoiliac patterns associated with femoropopliteal-tibial occlusive disease.

FIGURE 38.26 (A) Segmental occlusion of the right superficial femoral artery associated with (B) two marked stenotic areas (arrows) of the right common iliac artery.

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FIGURE 38.27 Bilateral common iliac stenosis (arrows) and aneurysm of the abdominal aorta proximal to its bifurcation.

supply muscular tissue. There is a constant communicating artery that links the posterior tibial artery and the peroneal artery, usually about 5 cm above the level of the malleoli. The peroneal artery is sometimes regarded as the termination of the popliteal, having the tibial arteries as side branches. There seems to be a reciprocal relation between these vessels so that, at the ankle, the peroneal may replace the anterior tibial and produce the dorsalis pedis via a large perforating branch, or it may replace the lower posterior tibial artery via a communicating branch in certain cases.

FIGURE 38.28 Severe occlusive arterial disease of both lower extremities with aortobiiliac aneurysm (unsuspected clinically).

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A

B

FIGURE 38.29 (A) Segmental occlusion of the left superficial femoral. (B) Associated tortuosity and stenosis of the ipsilateral iliac vessels. Note the nearly complete occlusion of the internal iliac artery.

FIGURE 38.30 Comparative incidence of atherosclerotic lesions of the tibial and peroneal arteries alone and combined with other patterns. ASO, arteriosclerosis obliterans.

䉴 FIGURE 38.31 Arteriograms of leg and foot arteries, indicating the absence of the right peroneal artery, whereas all the other vessels are normal, 5 seconds after injection of radiopaque material into the femoral arteries.

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FIGURE 38.32 Arteriograms showing the absence of right and left anterior tibiaI, normal posterior tibiaI, and plantar vessels, a left peroneal artery giving off a small-caliber dorsalis pedis artery. The patient is nondiabetic.

FIGURE 38.33 Bilateral femoral arteriogram showing diffuse atherosclerotic disease in a diabetic patient. Note patency of peroneal arteries only.

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FIGURE 38.34 Arteriogram of a diabetic patient’s leg, showing occlusion of the distal popliteal and all three leg arteries except for the distal half of the anterior tibial. Note the tenuous extensive calf collateral vessels and diffuse intimal lesions of the proximal popliteal and superficial femoral vessels.

FIGURE 38.35 Unilateral transfemoral arteriogram of a diabetic patient. Note a nearly normal iliac and common femoral artery, complete occlusion of the superficial femoral, and diffuse disease of leg arteries, with only the peroneal artery patent.

Chapter 38 Arteriographic Patterns of Atherosclerotic Occlusive Disease of the Lower Extremity

FIGURE 38.36 Bilateral diffuse disease of the plantar arteries (arrowheads).

FIGURE 38.38 Genicular–tibial group of collateral vessels.

FIGURE 38.37 Profunda femoris–genicular group of collateral vessels.

The arteries of the foot (dorsalis pedis and plantar arteries) provide the pedal anastomotic networks. These two major arteries provide malleolar, tarsal, and arcuate arteries and anastomose freely with each other and with the arteries of the plantar system. The main arterial arch of the foot is completed in a dorsoplantar direction. The plantar arch of the foot gives rise to plantar metatarsal arteries in each metatarsal space. Ischemic necrosis and rest pain involving the foot must be due to more than any one of the above arteries (11).

FIGURE 38.39 Profunda femoris–genicular–tibial group of collateral vessels.

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References 1. Turnipseed WD, Crummy AK, et al. Computerized intravenotis arteriography: a technique for visualizing the peripheral vascular system. Surgery 1981;89:118. 2. Haimovici H. Patterns ot arteriosclerotic lesions of the lower extremity. Arch Surg 1967;95:918. 3. Watt JK. Pattern of aorto-iliac occlusion. Br Med J 1966;2:979. 4. DeBakey ME, Crawford ES, et al. Surgical considerations of occlusive disease of the abdominal aorta and iliac and femoral arteries: analysis of 803 cases. Arch Surg 1958;148:306. 5. Gomes MMR, Bernatz PE. Aurtoilial occlusive disease: extension cephalad to origin of renal arteries with surgical considerations and results. Arch Surg 1970;1:161. 6. Valdoni P, Venturini A. Considerations of late results of vascular prostheses for reconstructive surgery in congenital and acquired arterial disease. J Cardiovasc Surg 1964;5:509.

7. Haimovici H, Steinman C. Aortoiliac angiographie patterns associated with femoropopliteal occlusive disease: significance in reconstructive arterial surgery. Surgery 1969;65:232. 8. Haimovici H, Escher DJW. Aortoiliac stenosis: diagnostic significance of vascular hemodynamics. Arch Surg 1956;72:107. 9. Brener BJ, Raines JK, et al. Measurement of systolic femoral arterial pressure during reactive hyperemia: an estimate of aortoiliac disease. Circulation 1974;49:50. (Suppl II):259. 10. Haimovici H, Shapiro JH, Jacobson HG. Serial femoral arteriography in occlusive disease: clinical-roentgenologic considerations with a new classification of occlusive patterns. Am J Roentgenol Radium Ther Nucl Med 1960;83:1042. 11. Haimovici H. Arterial circulation of the extremities. In Schwartz CJ, Werthessen NT, Wolf S, eds. Structure and function of the circulation. New York: Plenum Press 1980;425–485.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 39 Nonatherosclerotic Diseases of Small Arteries Henry Haimovici and Yoshio Mishima

The nonatherosclerotic diseases of small arteries include a large variety of vascular entities, many of which are still poorly understood. Their pathologic features are varied and include organic and vasospastic diseases. They may affect the vessels of both upper and lower extremities, as well as those of many vital organs. The definition of small artery disease, in terms of vessel diameter, is often more speculative than precise. It may therefore be useful to delineate the group of arteries preferentially involved in these entities. The small arteries are generally defined as the unnamed branches of the cognate medium-sized arteries. Included in this definition are also the arterioles and their branches, the diameters of which range from 30 to 100 mm. In the extremities, the small vessels are found distal to the medium-sized arteries of the popliteal and the brachial and represent functionally the distributive division of the arterial tree. Although the term “diseases of small arteries” would suggest entities exclusively localized therein, it should be emphasized that the lesions may be associated in the extremities with those of the more proximal arteries, especially in the group of organic vascular diseases. Furthermore, arterioles and their smaller branches are also frequently, if not preferentially, affected in organic diseases, as well as in vasospastic and collagen diseases. This chapter will deal only with the distinctive clinical, pathophysiologic, and therapeutic features limited to the most common entities. The diseases causing the most common occlusive and vasospastic disorders of these vessels are listed in Table 39.1.

Small and Medium Vessels For the sake of clarifying the complex clinicopathologic nature of the various entities, it appeared necessary to deal with them in separate sections. These will be divided into two major groups: 1. 2.

Takayasu’s and Buerger’s diseases; and the large group of the various entities indicated in Table 39.1.

The disease entities to be discussed in this chapter are distinct from those of medium and large arteries, which are due to an arteriosclerotic process. The latter represent most surgical vascular problems. Diseases of small arteries are less frequent and are rarely treated by operative procedures. Another major difference between these two groups is the pathogenesis of the small artery diseases, which is generally variable and is still poorly defined in general. These differences are particularly relevant in connection with two diseases: Takayasu’s disease and Buerger’s disease. They are of the greatest interest in terms of temporal and geographic evolution characteristics of the disease process. Whereas Takayasu’s disease originated in Japan and is still predominantly found in the Orient, Buerger’s disease was first recognized in Western countries and until recently was predominantly found in the West. Within the past three decades, for unknown reasons, Takayasu’s disease is no longer exclusively seen in the Orient. By contrast, Buerger’s disease is at the same time more frequent there while it is on the wane in Western

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TABLE 39.1 Nonatherosclerotic diseases of small arteries Organic diseases Takayasu’s arteritis Thromboangiitis obliterans (Buerger’s disease) Acute thrombosis of small arteries Arterial microemboli Arterial lesions of undetermined cause Collagen diseases (immune arteritis) Periarteritis nodosa (polyarteritis) Lupus erythematosus Scleroderma Behçet’s disease Vasospastic diseases Raynaud’s disease or syndrome Acrocyanosis Livedo reticularis Frostbite Mixed organic and vasospastic diseases Raynaud’s phenomenon and preexisting occlusive arterial disease Post-traumatic occupational Raynaud’s phenomenon Occupational trauma and secondary occlusive arterial disease of the hand Hematologic disorders Polycythemia vera Cryoglobulinemia This table includes only the most common entities, usually amenable to corrective therapy.

countries. Whether geographic or socioeconomic factors underlie these evolutional changes is not evident. Regardless, these two entities appeared different in the Orient and the West. A common comprehensive review could emphasize both the similarities and the disparate features of these two diseases. The approach may appear unconventional, I believe that the Western and the Oriental experiences with these diseases could be presented independently. Thus a Japanese scholar, Professor Yoshio Mishima, will discuss the diseases from the Oriental vantage point, and I will discuss the Western experience, especially with Buerger’s disease, inasmuch as I have had experience with this disease since my training days in France and later at Mt Sinai Hospital in New York, where Leo Buerger studied and described the disease that bears his name. Consequently, two versions each of Takayasu’s and Buerger’s diseases, one by Mishima and the other by me, will attempt to provide an overview of the present status of these diseases in the two geographic regions. As a result of this presentation by two different authors, there unavoidably will be repetition of some of the clinicopathologic findings.

Takayasu’s Arteritis: the Western Experience Initially, Takayasu’s arteritis was thought to be confined mostly to the Orient, as already stated, more specifically

to Japan. Subsequent reports indicated that this entity may affect all races and is worldwide in distribution. The early reports were limited to the description of vascular lesions of the aortic arch and its branches, but later findings showed that such abnormalities may affect any segment of the aorta, with its major branches, and the pulmonary artery branches as well. Depending on the location and extent of the lesions of the branches of the aorta, Takayasu’s disease is classified into four types, to be discussed in Mishima’s sections of this chapter. Although atherosclerosis is recognized as the most common cause of the vascular process involving the aortic arch and its branches, Takayasu’s disease was identified later as an aortitis syndrome. It was found also in the Western world as a rare but distinct possibility of a clinical and pathologic entity. Originally, as is well known—and as stated by Mishima in his discussion—in 1908 Takayasu, a Japanese ophthalmologist, noted in younger female patients a condition of peculiar ocular manifestations consisting of capillary flush with arteriovenous anastomoses and cataracts, which could lead to blindness. A large number of papers appeared subsequently in Japan. Among these was a paper by Shimizu and Sano in which, in addition to the above syndrome, they described the absence of pulses in the upper extremities and attributed all the manifestations to an obliterative process of the aortic arch and its main branches. They named this syndrome “pulseless disease.” The name of Takayasu attached to this syndrome remained, nevertheless, the accepted term. But besides this name, other synonyms have been used for the description of this entity: aortic arch syndrome, Martorell’s syndrome, atypical coarctation, brachiocephalic arteritis, and idiopathic aortitis. In the present chapter, the discussion of Takayasu’s disease will be limited to type 1. As stated earlier, most of the lesions of this type that are described in the Western literature are due to intimal atherosclerotic plaques that partially or completely obstruct the vessels. In contrast, Takayasu’s arteritis has rarely been identified in the past in the Western world. On the other hand, besides Japan, even in Mexico, South America, and Africa, atherosclerosis is infrequently diagnosed in this anatomic location. Thus, Kimoto in Japan found an 83% incidence of aortitis syndrome versus a 14% incidence of arteriosclerosis, and Paramo Diaz et al. in Mexico found a similar ratio of 73% versus 13%, respectively. In the Western world, Lande et al. and Crawford, on the basis of their personal experience, believe that most unusual lesions of the aorta and its branches, especially in young female patients, are actually due to the aortitis type, identified otherwise as Takayasu’s disease. Clinical Manifestations Clinical manifestations progress from an early systemic phase to a late occlusive phase. Systemic manifestations

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

include malaise, fever, leukocytosis, elevation of the erythrocyte sedimentation rate, and an increase in Creactive protein. The incidence of these symptoms varies (35% to 53%). Studies implicate immunologic factors in the development of this disease. The onset of the occlusive phase may vary from months to years after the systemic phase. Stenosis or occlusion of one or more of the aortic arch branches may produce a wide range of neurologic or ocular symptoms, including headaches, syncope, hemiplegia, hypertension, and claudication of the upper extremities. Pathology The nature of the disease is that of an inflammatory process of unknown origin. The arterial changes involve all layers of the arterial wall and are characterized by infiltration of giant cells in the acute phase. According to activity and duration of the inflammatory process, there may be thickening of the vessel wall, thickening of the intima, fibrosis of the media, or scarring and fibrotic reaction of the adventitia. Occlusion is associated with extension of intimal proliferation and with fibrosis of the media and adventitia. The lesions of the aorta and its branches may progress to stenosis or occlusion and, depending on the vessel, to coarctation or aneurysm. Stenosis or occlusion of the subclavian, carotid, and vertebral arteries, in various combinations, is responsible for a multiplicity of cerebral and visual disturbances. The brachiocephalic lesions, with their neurologic and ophthalmologic manifestations, have been well described since Takayasu’s initial observations. Depending on the affected vessels, a variety of clinical syndromes may emerge. Arteriographic Findings Various arteriographic patterns of the arch and its branches may be present, depending on the specific lesions. Carotid stenosis may be confined to the origin of the vessel. Not infrequently, especially in advanced cases, the stenosis may extend for a variable distance along the axis of the vessel. In these instances, it is not unusual to find a filiform narrowing extending from the aorta to the base of the skull. In general, occlusion of the brachiocephalic trunks occurs near the orifice of the artery. A flame-shaped termination of the vessel appears to be characteristic of Takayasu’s arteritis. In extreme forms of brachiocephalic arteritis, all or most of its trunks are occluded. In these instances, the circulation to the brain may be provided by collateral circulation, originating from a number of neck and spinal vessels. Obstruction of the subclavian arteries may produce a subclavian steal syndrome with symptoms of cerebellar insufficiency. Some of the arteriographic characteristics should alert the clinician to the possible diagnosis of Takayasu’s disease. Lande et al., among others, urge a total aortography to confirm the exact diagnosis of this disease.

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Treatment If the disease is diagnosed early, during the systemic phase, the treatment consists of the use of steroids, which may relieve symptoms in a large majority of cases. Concomitantly, arterial hypertension and heart failure are controlled by medical means, irrespective of surgical indications for the occlusive arterial lesions. Principles and techniques of arterial reconstructive methods affecting the aortic arch branches are similar to those described earlier in this text for atherosclerotic occlusive disease. Although steroids may relieve early symptoms, they do not affect the course of the established occlusive lesions. The most applicable reconstructive methods are resection with graft interposition and bypass operations. Experience with endarterectomy has yielded poor results in most patients. The reason for the difficulties and poor outcome of endarterectomy is the lack of a cleavage plane between the thick, fibrous obstruction and the media of the wall because of the specific type of arteritis with its inflammatory lesions. Most of the reconstructive procedures will be described in detail later in this chapter. Further descriptions of these methods may be found in Kimoto’s presentation; his experience with Takayasu’s disease is extensive. Kimoto emphasizes that the best indications for reconstructive surgery are found in patients with moderate symptoms. He further states that the degree of retinal change, especially if severe, is an important guideline. In the presence of retinal changes, serious postoperative complications, such as glaucoma, retinal bleeding, or cerebral hemorrhage, could present problems.

Takayasu’s Arteritis: the Japanese Experience In 1908, Takayasu reported the peculiar ocular manifestations seen in a young female patient with attacks of blindness and syncope. Thereafter, in 1951, Shimizu and Sano described the clinical triad of this disease, including absence of pulsation of radial arteries, arteriovenous anastomosis in the ocular fundi, and hypersensitive carotid sinus due to obliterative process of the aortic arch and its main branches. They called the syndrome “pulseless disease.” Because of developments in clinical and laboratory studies, the concept of this disease has definitely changed, and in 1963 it was categorized as “aortitis syndrome” in Japan by Ueda et al., because the disease process involved not only the aortic arch and its branches but also the entire aorta and its branches, sometimes extended into pulmonary arteries. Takayasu’s arteritis was formerly considered almost exclusively a disease of women. In more recent years, however, there seems to have been a relative increase in the incidence of the disease among men. In our research, approximately 10% of patients with this disease are men. The number of living patients having this disease in Japan

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is considered to be approximately 3000, and the annual increase of new cases is estimated to be about 100. Pathology From the histologic investigation of 76 autopsy cases collected over the last 16 years, Nasu (1977) classified this lesion histopathologically into three types: granulomatous inflammation type, diffuse productive inflammation type, and fibrosis type. Granulomatous Inflammation Type (28%) Granulomas, often accompanied by Langerhans’ giant cells and foreign body giant cells, are formed with or without the presence of small necrotic foci and microabscesses. Diffuse Productive Inflammation Type (14%) Diffuse infiltration of lymphocytes and plasma cells, along with proliferation of connective tissue and new growth of blood vessels, is seen in the media. A few solitary giant cells are found scattered in rare cases. Fibrosis Type (58%) This type was observed in a large majority of cases and was thought to be the sequela of the inflammatory changes. The severe fibrosis occurred chiefly in the media, because of scar formation after granulomatous and productive inflammation. Fibrosis of the adventitia is thought to be a protective reaction against passive distention due to diminished elasticity of the weakened media. Secondary fibrosis was also detected in the intima, and its severity depended mostly on the duration of the disease process. In the autopsy cases, pulmonary artery involvement was detected in 45%. Pathophysiology Clinical pictures of Takayasu’s arteritis are extremely variable because of the distribution of the arterial lesions. There has not yet been a definite classification of the disease; however, we have classified it into three types according to hemodynamic characteristics (Fig. 39.1). Type 1 A classic pulseless disease that manifests hypotension of the head and upper extremities. Dizziness, syncope, impaired vision, and claudication of the upper extremity are the commonly noted chief complaints. Type 2 Characterized by the presence of systemic hypertension or hypertension of the upper half of the body, simulated by signs and symptoms caused by coarctation of the aorta. Type 3 A mixed type, in which types 1 and 2 are combined, characterized by hypotension of the upper extremity and head, hypertension above the coarctated segment, and, less frequently, systemic hypertension Further, aneurysm formation can be classified as type 4 disease.

Type 1

Type 2

Type 3

FIGURE 39.1 Classification of hemodynamic characteristics of Takayasu’s arteritis.

The triad pointed out by Shimizu and Sano is no longer considered to be representative of the disease. For example, the ischemic change of the ocular fundi reported by Takayasu is not so prominent as was believed, except in cases categorized as having a type 1 lesion. The erythrocyte sedimentation rate is accelerated in the majority of cases, especially in the active stage of the disease. An increase in serum levels of a2-globulin and gglobulin is frequently noted. C-reactive protein is also frequently detected. These findings results from an active inflammatory process and are helpful for differentiating Takayasu’s arteritis from other conditions. The electrocardiogram frequently reveals evidence of left ventricular hypertrophy, often associated with changes in the ST segment and the T wave. They are presumably due to hypertension, or aortic insufficiency, or both, although a contribution from lesions of the coronary arteries and myocardium is not ruled out. Cardiac enlargement is a common finding on the chest x-ray film. Calcification of the aorta is also seen in some cases. Arteriography Aortography is the most valuable diagnostic examination and should be performed in every suspected case. Total aortography, including all brachiocephalic vessels, is useful for delineation of the full extent of the disease (Figs. 39.2 and 39.3). Usually, the involved arteries reveal stenosis or obstruction, but prestenotic or poststenotic dilation may also be seen. Occasionally, aneurysm formation is recognized. In type 1 disease, as stated above, the lesions are located mostly in the aortic arch and its branches. The ascending aorta may also be affected, resulting in aortic insufficiency in some cases. In many cases, lesions of the pulmonary arteries are detected. They are also demonstrated by pulmonary scintiscan. Diagnosis There are no pathognomonic symptoms of Takayasu’s arteritis. Onset is often overlooked and may mimic a

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TABLE 39.2 Guidelines for diagnosis of Takayasu’s arteritis Major signs and symptoms Symptoms related to cerebral ischemia Symptoms related to ischemia of upper extremities Hypertension Visual disturbance Pain at the neck, back or hip General symptoms Important diagnostic findings Decreased brachial artery pulse or blood pressure Increased or decreased femoral artery pulse Bruit over the neck, back or abdomen Cardiac murmur (aortic valve regurgitation) Ophthalmologic changes

FIGURE 39.2 Aortogram of a 26-year-old woman showing occlusion of the brachiocephalic and both the carotid and subclavian arteries. Both vertebral and axillary arteries are patent through the collateral vessels.

Contributory laboratory findings Inflammatory reaction: elevated erythrocyte sedimentation rate, positive C-reactive protein, leukocytosis, increased gglobulin Anemia Immunologic abnormalities: increased immunoglobulin, increased C3 and C4, antiaortic antibody Increased coagulopathy HLA specificity: A9-BW52, DW-12 Characteristic image findings Calcification: chest radiography, CT Occlusive arterial lesions: angiography, MRI, CT Dilative arterial lesions: angiography, ultrasound, CT Pulmonary arterial lesions: MRI, angiography Diagnostic points Predominant in young females Arteriogram for definite diagnosis Differential diagnosis Atherosclerosis, giant cell arteritis, collagen disease, Behçet’s disease, congenital vascular anomaly, Buerger’s disease Research Committee, 1992.

rheumatic or nonspecific illness with acute systemic symptoms in many cases. General weakness and fatigability are common, especially in the initial stage of the disease. Usually, after an asymptomatic quiescent stage of variable duration, the inflammatory lesion of the arteries becomes manifest, most commonly in the brachiocephalic vessels, with pain and tenderness of the neck, shoulders, or anterior portion of the chest. Presumably the pain is of vascular origin. The complaints more frequently noted are due to impaired cerebral circulation, such as dizziness, headache, and visual disturbances. Ischemic symptoms of the upper extremity, such as numbness, cold sensation, and claudication, are also encountered frequently. Recently, the Research Committee in Japan revised the guidelines for diagnosis as shown in Table 39.2. Clinical Course and Prognosis

FIGURE 39.3 Aortogram of a 29-year-old woman showing atypical coarctation of the aorta.

The natural history of the disease is not yet fully understood. The prognosis is greatly influenced by the severity of hypertension. Aortic insufficiency is frequently associated with hypertension and is also inherent to the

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prognosis. Of 1210 women patients, 664 (54.9%) have been pregnant and 622 (50.2%) have delivered a normal baby. Treatment Treatment currently consists of long-term steroid therapy. Subjective symptoms together with abnormal laboratory findings improve rapidly in most cases with administration of steroids, especially in active stage. Itoh reported that an initial dose of 30 mg of prednisolone per day is usually sufficient. Then the dose is reduced gradually to reach withdrawal of steroids. However, long-term administration of a small dose, 5 to 10 mg per day, is often required to maintain the therapeutic effects. Other medical treatment includes control of hypertension, congestive heart failure, angina pectoris, and so on. Arterial reconstructive surgery is indicated for cerebral ischemia, especially for that with progressive visual impairment, for severe hypertension, and for aneurysm with impending rupture. Aortic valve replacement may be considered in cases of severe aortic regurgitation. Surgical intervention should preferably avoid active inflammatory episodes, and the best guide is the erythrocyte sedimentation rate (ESR). However, emergency operation may be performed even if inflammatory changes persist, maintaining the ESR under 40 mm per hour with continuous administration of steroids. The reconstruction of extracranial vessels is indicated for the cases with 75% or more stenosis in the main extracranial arteries accompanied by progressive cerebral ischemic symptoms (visual disturbance, syncope, and so on) or small retinal aneurysms. Far-advanced cases with arteriovenous retinal fistulas are contraindicated. In the cases combined with hypertension due to atypical coarctation or renal artery stenosis, a detailed discussion of the operative procedure is necessary. The best technique is resection with autovein grafting or aortocarotid or subclavian-carotid (interbranch) bypass. Usually it is satisfactory to reconstruct flow on only one side, even if the bilateral arteries are involved. For atypical coarctation, surgery is indicated when systolic blood pressure is higher than 180 mmHg at rest. Patients who respond well to medical treatment may be followed without surgical intervention. The procedure of choice is aortoaortic bypass with synthetic graft. The indication for renal artery stenosis is systolic hypertension above 180 mmHg or diastolic hypertension above 110 mmHg. A renin ratio of more than 1.5 between involved and uninvolved renal vein samples, or a renal vein–peripheral vein renin coefficient of 0.24 or higher, are also indications for surgery. Transluminal angioplasty is the first choice; however, its initial success rate is only 50%. Failure is an indication for aortorenal bypass with autovein or synthetic graft. For patients with deteriorated renal function, nephrectomy may be required.

For cases of aortic regurgitation, surgery is indicated when regurgitation is more than Seller’s tertiary classification and the left ventricular ejection fraction is more than 0.40. The best procedure is valve replacement including Betall’s technique. Reconstruction of the subclavian artery is indicated only for the cases of prominent subclavian steal syndrome. Interbranch bypasses such as carotid–subclavian or subclavian–subclavian are the preferred technique. The indications for coronary artery involvement are similar to those in atheromatous disease. Percutaneous angioplasty is the first choice; however, the success rate is lower than in atheromatous disease. Failure is the indication for aortocoronary bypass. Because of the high risk of rupture, saccular aneurysms are an absolute indication for urgent surgery. Fusiform aneurysm with pain or increasing in size is also an indication for surgery. The treatment of choice is resection and synthetic graft replacement. From 1959 through 1991, Tada performed 93 arterial reconstructions for the cases with Takayasu arteritis, including 16 of type 1, 48 of type 2, 13 of type 3, and 16 of type 4. Nine operative deaths were observed, among which eight had been operated on before 1970. The most serious complication was aneurysm formation at the suture line, which was encountered in 10 cases. These aneurysms were often found long after the operation, and some of them developed after more than 20 years. Therefore, long-term postoperative observation is mandatory to improve the late survival rate. From 1981 through 1990, 774 operations were performed in the major institutions in Japan. Characteristically, the number of operations for aortic regurgitation greatly increased (Table 39.3).

Thromboangiitis Obliterans (Buerger’s Disease): the Western Experience As in the preceding section, there will be two versions of this discussion: one on the condition as seen at present in the United States and the remainder of the Western world and the second version on the Japanese experience with this disease. TABLE 39.3 Operated cases of Takayasu’s arteritis in Japan from 1981 to 1990 Aortic regurgitation Atypical coarctation Carotid arteries Renal arteries Aneurysm Subclavian arteries Coronary arteries Visceral arteries Pulmonary arteries Others

155 (18.4%) 134 (15.9%) 128 (15.2%) 110 (13.1%) 98 (11.6%) 76 (9.0%) 48 (5.7%) 38 (4.5%) 12 (1.4%) 43 (5.1%)

Total

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Research Committee, 1981–1990.

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

The nature of occlusive arterial disease in young individuals has continued to be a controversial subject since 1879, when von Winiwarter first described a vascular syndrome for which he proposed the name “endarteritis obliterans.” It was not until 1908, when Buerger published his classic paper, and later his book (1924), that this disease, for which he proposed the name “thromboangiitis obliterans” (TAO), became well recognized. More recently, however, the existence of this disease as an entity has been called into question, and the suggestion has been made that the cases described by Buerger were actually special examples of atherosclerosis. Subsequent critical reexamination disclosed that: 1. 2. 3.

the diagnosis of Buerger’s disease was probably too frequently made in the past; the disease occurs less frequently today than it did three decades ago; and the disease exists as a definite entity separate from atherosclerosis in a limited occurrence.

The cause of Buerger’s disease is unknown. It affects primarily men (95% of the cases). Although the disease was initially thought to occur predominantly in Jews of Eastern European origin, subsequent statistical studies have shown that no race or color is known to be immune. Heavy cigarette smoking appears to be the most important associated etiologic factor. The disease has a tendency to progress in spite of any other treatment if patients continue to smoke, whereas those who discontinue the use of cigarette smoking show improvement and

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seem to have no further exacerbation of the disease. A relation between recurrence of the disease and its progression with the resumption of tobacco smoking is characteristic. Although the deleterious effects of tobacco smoking may also be encountered in arteriosclerotic occlusive disease, its almost causal relation to the aggravation of the disease holds an unusually significant place among the diagnostic criteria for TAO. Although the age at clinical onset of the disease is known to be between 20 and 35 years, one of the common diagnostic errors still encountered is to place patients older than 35 years who have peripheral vascular disease in the TAO category. Although occasionally this diagnosis may be corroborated by pathologic findings in patients with clinical onset after the age of 35 or 40 years, it should he pointed out that in this age group, atherosclerosis is the most likely finding. Conversely, even in the group with an age at onset of 20 to 35 years, a number of patients may have early manifestations of atherosclerosis, as shown by findings during surgical exploration of such patients (Fig. 39.4). Migrating thrombophlebitis is encountered in about 40% of the patients and is regarded as a characteristic component of TAO. Involvement of all four extremities (Fig. 39.5) occurs in almost half the patients. Such distribution of the vascular lesions, although not constant, is definitely more characteristic of TAO than of any other arterial disease. Small vessels of the hand are more frequently involved by TAO than by arteriosclerosis obliterans (ASO) (Fig. 39.6). Arteriography may reveal distinctive features of TAO, of which the most significant is a smooth outline of

FIGURE 39.4 Arteriograms of both hands of a 39-year-old woman, a heavy cigarette smoker, with a 7month history of discoloration, pain, and right index minimal fingertip ulceration. Note dilation of ulnar artery, right more than left, occlusion of radial arteries, left more than right, and absence of opacification of most digital arterioles. Diagnosis of Buerger’s disease with Raynaud’s phenomenon was made. No evidence of thoracic outlet syndrome compression of vascular origin noted.

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FIGURE 39.6 Gangrene of the fingers of both hands due to acute thrombosis of digital arterioles. Wrist pulses were normal.

FIGURE 39.5 Bilateral gangrenous lesions of the toes in a woman with thromboangiitis obliterans involving all four extremities. Major peripheral arteries were patent.

the arterial tree, in contrast to the intimal irregularity so characteristic of atheromatous lesions (Fig. 39.7). These arteriographic signs are important in the differential diagnosis, but it should be pointed out that they are not pathognomonic. Histopathologic criteria deserve a critical evaluation. The disease begins in medium-sized or small arteries (posterior tibial, anterior tibial, radial, ulnar, plantar, palmar, or digital). The lesions are distinctly segmental and follow an episodic course. Larger arteries (popliteal, femoral, or brachial) may also be affected if the disease is severe and progressive. In the major arteries (aorta, iliac), true thromboangiitic lesions have rarely, if ever, been reported and have never been seen in our experience. This also holds true, with few exceptions, for the visceral vessels. The histopathologic features of the vascular lesions, as described by Buerger, have perhaps been the subject of the greatest controversy. This may be due partly to the relatively wide spectrum of lesions ranging from the acute stage to the healed thrombus. In the acute stage, Buerger described a process that consists of an acute inflammatory lesion involving all the coats of the vessel, with its lumen completely filled by a thrombus and with purulent and giant-cell foci in its periphery. These characteristic features disappear at the stage of healing (intermediate

stage). The thrombus becomes organized, cellular, and recanalized. Finally, in the “healed” stage, the lumen is occluded by connective tissue representing the end product of the above-mentioned lesion, which at this time may be extremely varied in its general appearance. Failure by some observers to demonstrate the acute special histologic lesion is one of the sources of skepticism concerning its true significance. Recent documentary evidence has reconfirmed these characteristic lesions. Association of TAO in the extremities with atherosclerotic changes of the aortoiliac segment or coronary or cerebral vessels is not unusual, particularly during the fifth and sixth decades of life (Fig. 39.8). Indeed, some of these patients have TAO in the medium-sized and small vessels in their young adulthood and then years later may develop atherosclerotic lesions of the major arteries or of the visceral vessels. The early peripheral vascular lesions and the late aortoiliac lesions are associated only temporally and are not related etiologically or pathogenetically. Thus it would be erroneous to attach a common label to the two vascular processes, inasmuch as a long interval separates their clinical onset (Fig. 39.9). In relation to pathogenesis, although the description presented above clearly indicates a local reaction of a thrombus and of the arterial wall, studies of patients with Buerger’s disease seem to have demonstrated specific cellular immunity against arterial antigens, formation of specific humoral antiarterial antibodies, and elevated levels of circulating immune complexes in many of these patients. It is necessary to point out that these studies are only of a preliminary nature and will have to be confirmed should an immunologic factor be involved in the etiology of Buerger’s disease. Diagnosis The differential diagnosis of TAO is usually not difficult in the presence of a typical clinicopathologic picture. How-

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

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B A

FIGURE 39.7 (A) Gangrene of all toes of left foot in a 28-year-old man who was a heavy smoker and had involvement of all four extremities of his arteries. He underwent an above-the-knee amputation of the other lower extremity. The gangrene of the left foot developed somewhat rapidly within a matter of 2 weeks. (B) Microscopic lesions indicate thrombosis of both artery and vein. There is a marked perivascular reaction between the artery and vein.

ever, it is always necessary to keep in mind the features of ASO and idiopathic arterial thrombosis as main differential diagnoses. The main criteria for differentiating TAO from these two conditions are as outlined above. Other vascular diseases, such as vasospastic syndromes (Raynaud’s disease, periarteritis nodosa, pernio, ergotism, frostbite) should not be difficult to rule out. The histologic evidence is ultimate proof in the differential diagnosis. In 50 patients in whom the diagnosis of TAO was made on clinical grounds, Brown et al. found only seven with clear evidence of small vessel inflammatory disease as described by Buerger. Prognosis The prognosis with respect to limb survival and life expectancy of patients with TAO, in comparison with those with atherosclerosis obliterans, is quite different. McPherson et al. reported a higher amputation rate in TAO in comparison with that of patients with ASO who have ischemic complications. By contrast, life expectancy appeared to be better in patients with TAO than in those with ASO.

Treatment The treatment will vary according to the stage at which the disease presents itself. At the early stage, the arrest of progress of the disease by tobacco abstinence is absolutely essential. Unfortunately, very few of these patients display any capability of discontinuing smoking. The use of vasodilators may be of little effectiveness. Lumbar or upper thoracic sympathectomy may be beneficial and persistent, provided that the patient continues to abstain from smoking. In spite of a lumbar sympathectomy, it is often necessary to add destruction of a sensory nerve of the leg to achieve complete relief of pain. Arterial reconstruction is most often not feasible in these patients. Although the posterior and anterior tibial or peroneal artery may still be patent, the multifocal lesions of the small arteries may negate the success of the bypass graft. Amputation of toes or fingers for limited lesions is often successful, but more extensive limb loss may be unavoidable because of pain and failure to heal.

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A

A B

B

FIGURE 39.8 Photomicrograph (A) and enlarged central detail (B) of a cross-section of posterior tibial vessels in a 70-year-old man who at the age of 30 years was treated for TAO. The lesions are consistent with this diagnosis. This case illustrates the possible association of Buerger’s disease, which occurred at an earlier age, and arteriosclerosis of the proximal arterial tree, which developed at a later age. Most of the arteriosclerosis developed at an advanced age.

Thromboangiitis Obliterans (Buerger’s Disease): the Japanese Experience In the past, most patients in Japan suffering from chronic arterial occlusion were regarded as having Buerger’s disease; however, recently the number of patients with

C

FIGURE 39.9 (A) Ischemic ulcers of right second, third, and fourth fingers of a 40-year-old patient with a long history of TAO. The patient was a heavy smoker and had involvement of all four extremities. The arteriogram disclosed occlusion of the radial and ulnar arteries just proximal to the wrist and involvement of the distal portions of the digital arteries. A left upper thoracic sympathectomy was carried out, followed later by amputation of the distal phalanx of the index finger. (B and C) Microscopic study of the small vessels of the digit showed lumina narrowed by proliferative endothelial lesions.

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

485

FIGURE 39.11 Subacute arterial lesions in the radial artery of a 32-year-old man. Proliferation of elastic fibers and fragmentations of the internal elastica in the organized thrombus are observed.

Migratory thrombophlebitis recurs frequently in extremities and occurs before, during, or after the onset of arterial lesions. The histologic changes in involved superficial veins are similar to those observed in the involved arteries. In the old lesion, the involved artery is occluded by well-organized thrombi with recanalization. They are categorized as follows: 䊏

䊏 䊏

FIGURE 39.10 Frequency of TAO and ASO every 5 years in Japan.

䊏

arteriosclerosis obliterans has increased significantly (Fig. 39.10).

䊏

Etiology The specific cause is not known. Secondary etiologic factors that have a positive effect on the disease include age, sex, race, hereditary factor (HLA antigen), autoimmune process, occupation, changes in the blood, and smoking. Smoking is the strongest secondary etiologic factor in this disease. Pathology Most authors agree that the inflammatory changes in all three layers of the involved vessel walls and thrombotic occlusion of the involved segments are characteristic, followed by recanalization. In the acute stage, there may be fibroblasts and lymphocytes, and sometimes a giant cell. The occluding thrombus is very cellular and contains many nuclei of fibroblasts. Usually, the disease affects primarily the medium-sized and small arteries in segments, with relatively normal arteries between involved segments (Fig. 39.11).

those with few changes in the arterial wall and involving organized thrombus and vascularization within thrombus; those with notable thickening of the intima; those with organized thrombus and with vascularization at and within the arterial wall; those with proliferation of elastic fibers and fragmentation of the internal elastic lamina in organized thrombus; those with fibroplasia, vascularization, and infiltration of round cells in arterial wall and thrombus.

Therefore it is generally difficult to determine the actual cause by means of a resected specimen obtained from an old lesion. Pathophysiology The symptoms are those which arise from the arterial occlusion, those which depend on the inflammatory nature of the lesions, and those resulting from the breakdown of the tissue rendered ischemic by the arterial occlusion. Frequently early symptoms include limping, caused by pain in the bottom of the foot, and gangrene, also limited to the feet. Intermittent claudication occurs but is less frequent than in arteriosclerosis obliterans, because the disease occurs mostly in the smaller vessels, such as the anterior or posterior tibial artery, often producing extensive tissue damage before claudication develops. This evidence is supported by arteriographic confirmation of the sites of arterial occlusion. In 91.9% of 322 upper extremities and in 98.7% of 1129 lower extremities, arterial occlusion

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was detected distal to the cubital and popliteal bifurcations, whereas atherosclerotic occlusion developed preferentially in such major channels as the iliac, femoral, and popliteal arteries (Table 39.4). The symptoms caused by the inflammatory nature of the disease are those of ischemic neuritis, producing rest pain and the associated thrombophlebitis. Generally, the thrombophlebitis occurs in short segments and in a migratory manner. In our series, recurrent episodes of segmental superficial thrombophlebitis were encountered in 21.9% of cases before, during, or after the onset of the ischemic symptoms (Table 39.5).

TABLE 39.4 Occlusive sites Upper extremities Brachial artery Radial or ulnar artery

322 (22.2%) 25 (1.7%) 297 (20.5%)

Lower extremities Aortoiliofemoral artery Popliteal artery Tibial artery

1129 (77.8%) 25 (1.7%) 334 (23.0%) 771 (53.1%)

Total

1451 limbs

Arteriography The artery proximal to the occlusion appears smooth and of even caliber in most cases. The most characteristic occlusive patterns on the arteriogram are tapering and abrupt occlusion with tree root configuration. There are usually abundant collateral networks around the occlusion, sometimes forming a corkscrew appearance. In some cases, however, there are circumscribed stenotic lesions limited to narrow segments, followed by thrombotic occlusion in a few years (Fig. 39.12). In patients who clinically show acute arteritis or phlebitis, especially young patients, a small, irregular filling defect is often observed proximal to the obstructed site (Fig. 39.13). This finding is considered to be the early picture of vasculitis. These lesions are often localized to a small area, but they may sometimes be extensive. The irregular filling defect frequently develops as a result of obstruction by a thrombus, and especially when such lesions extend to larger parts, they can easily cause acute obstruction. Thus, the arterial occlusion in Buerger’s disease develops not only in an ascending fashion but also as a skip lesion. These changes may represent early stages of the disease (Fig. 39.14). Diagnosis The diagnostic criteria used are as follows:

TABLE 39.5 Initial symptoms of Buerger’s disease 䊏

Coldness (Fontaine I) Claudication (Fontaine II) Rest pain (Fontaine III) Ulcer (Fontaine IV) Gangrene (Fontaine IV) Phlebitis

93.2% 78.4% 66.2% 55.2% 39.9% 21.9%

Total

1451 limbs

䊏

䊏

asymmetric, abnormal coldness of the skin in the extremities; impairment or absence of peripheral arterial pulsations; exclusion of cases involving, for example, hypertension, hypercholesterolemia, albuminuria, glycosuria, calcification, abnormal electrocardiogram, or retinal atherosclerosis; FIGURE 39.12 Angiographic characteristics in Buerger’s disease.

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

487

A

FIGURE 39.14 Arteriogram of a 32-year-old patient. Corkscrew appearance is due to development of collateral vessels.

Group 2 (39%) Those with recurrence of relatively mild clinical manifestations during the follow-up period. Group 3 (8%) Those with recurring acute episodes of severe clinical symptoms during the observation period, usually followed by major amputation. B

FIGURE 39.13 Arteriograms of a 21-year-old patient (A) and of the same patient at 23 years of age (B). In patients who clinically show acute arteritis or phlebitis, especially young patients, a small, irregular filling defect is often observed proximal to the obstructed site. This finding is considered to be the early picture of vasculitis. These lesions are often localized in small parts, but they may sometimes extend. The irregular filling defect frequently develops as the result of an obstruction due to thrombus; especially when such lesions extend to larger parts, they easily cause acute obstruction. 䊏

䊏

arteriographic findings, including tapering, abrupt occlusion, and corkscrew appearance of collateral vessels; exclusion of cases with atheroma formation.

The above-mentioned criteria are thought to be sufficient in making the clinical diagnosis, although they may include, in part, simple thrombosis or some type of nonmanifested atherosclerotic occlusions. Clinical Course and Prognosis From long-term observation, the cases may be classified into three groups. Group 1 (50%) Those with a relatively uneventful course after initial transient ischemic attacks.

Empirically noteworthy are the cases occurring at an early age and belonging to group 3 of our classification. In our series, the patients with Buerger’s disease had a practically normal survival rate, in comparison with a normal population of the same age and sex distribution. The survival curves in this series resemble those reported by McPherson et al., and both curves are distinctly better than those of the patients with arteriosclerosis obliterans. Treatment Suspicion of Buerger’s disease is the signal for complete abstinence from smoking and the institution of a variety of other supportive measures, although none of them is specific. To date, the vasodilating substances have been prescribed mainly for patients suffering from chronic arterial occlusive disease. In recent years, however, the rheologic study of microcirculatory disturbances in these cases has progressed both experimentally and clinically. Consequently, the agents that improve the deficient microcirculation have been noticed. In our multiclinical trials, an antiplatelet agent (Ticlopidine), an agent transforming the shape of the human red cell (pentoxifylline), and a defibrinating agent (Batroxobin) were similarly effective for the ischemic leg ulcer caused by chronic arterial occlusion. Surgical therapy for arterial diseases of the extremities consists of an indirect procedure for the release of vasospasm and direct arterial surgery for the reestablishment of arterial flow. In Buerger’s disease, conventional arterial reconstructive surgery rarely seems to be of value.

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occasionally abandoned, and even still-active inflammation is left untouched. Because of this operative difficulty, there still remain dangers of infection of the graft and of hemorrhage from the anastomosis, which sometimes lead to the formation of a new aneurysm at the anastomotic site. So far, it has also been well known that infection occurs so often in Behçet’s disease that great care should be taken before, during, and after surgery.

Acute Thrombosis of Small Arteries

FIGURE 39.15 Moth-eaten appearance of the medial layer of the aorta in a patient with Behçet’s disease.

Behçet’s Disease* The main symptoms of Behçet’s disease occur not only in the skin, mucosa, and eyes but also in the joints, digestive tract, vascular system, and nervous system. Its clinical course is characterized by a repeated cycle of acute exacerbation and remission in the incipient stage, and then it gradually becomes chronic. For many years, the known vascular complications in Behçet’s disease have been attributed to thrombophlebitis. But a considerable number of reports have been published relating to cases with aneurysm and arterial occlusion. These vascular involvements are considered to be essential pictures of the disease process, as a part of the wide variety of clinical manifestations of this systemic disease. Histologic changes of these arteries reveal derangements of the media, particularly of its elastic fibers (Fig. 39.15). Of the vascular changes in Behçet’s disease, aneurysms develop at a relatively early age and are extremely prone to rupture. Therefore an aggressive surgical approach, initiated as soon as the diagnosis of this disease becomes definite, is mandatory for aneurysm. At operation, the aneurysm usually adheres tightly to concomitant veins and to the perivascular tissues. It should be particularly noted that dissection from the inferior vena cava is difficult in the case of abdominal aortic aneurysm. Although all inflammatory areas should be surgically removed, the dissection from the inferior vena cava is so difficult in the case of abdominal aortic aneurysm that complete removal of the affected areas is *Editor’s note: Behçet’s disease is largely unknown in the West. According to Behçet, it consists of a “triad of iritis, oral and scrotal ulcerations.” Additional manifestations consist of vascular findings in the skin, joints, and elsewhere. This condition appears most frequently in the Middle and Far East. The most striking vascular findings are multiple central and peripheral arterial aneurysms. Bacterial infection is often associated with these vascular conditions Their surgical repair is an extremely hazardous undertaking—H. H.

Sudden and widespread occlusion of small arteries of the hands and feet may be due to acute thrombosis in the absence of atherosclerosis. The lesions are usually limited to toes and fingers, with no previous history of intermittent claudication or impairment of the hands. The peripheral pulsations are normal in the vast number of cases. The underlying abnormality is usually an occlusive process, due to thrombosis, of the digital arterioles. Jepson described 11 cases of acute arterial thrombosis of the small arteries of the hands and feet, often in the same individual, leading in some cases to gangrene. In all these patients, the acute episode was followed by a remarkable degree of recovery of the limb function, with little impairment and with Raynaud’s phenomenon recurring only rarely, at a later stage. The organic occlusion of the digital arteries produced marked cyanosis of the digits and in some instances proceeded to limited gangrene. Similar cases have been described previously under the title “symmetrical digital gangrene” and have been misdiagnosed as Raynaud’s disease. However; their clinicopathologic features and subsequent course do not fit the description of the latter entity. A differential diagnosis of these acute lesions from arterial embolic or venous gangrene is usually established easily by the absence of cardinal signs of a cardiogenic source for embolic lesions or by the absence of massive venous occlusion associated with gangrene (Fig. 39.16). In the presence of severe vasospasm with incipient digital gangrene, a cervicothoracic or lumbar sympathectomy is indicated in most instances, combined, when necessary, with digital amputation.

Arterial Microemboli Two types of microemboli may be responsible for acute occlusion of small arterial vessels: thromboembolism and atheroembolism. Thromboembolism Embolism resulting from a thrombus originating in a cardioarterial system (e.g., heart aortic aneurysm) and involving the small arteries of the extremities, and even the medium-sized vessels, is rare. In a previous study of 300 cases of peripheral arterial embolism, we found 18 emboli

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

FIGURE 39.16 Arteriogram of left hand of a 70-year-old man with an acute syndrome of sudden pain, cyanosis, and coldness of the fourth and fifth fingers. Note occlusion of distal half of digital arterioles of these two fingers, which led eventually to gangrene and partial amputation.

lodged in the anterior and posterior tibial arteries and eight in the radial and ulnar arteries, a total of 26 cases representing 8.7% of the entire series. The clinical manifestations, although often minimal, may lead to severe ischemia. Such an instance is illustrated in Figure 39.17, which shows an embolus of the left radial artery and its palmar arch. Even when microthrombi occlude small arteries, localized skin lesions may result. Furthermore, occlusion of a medium-sized artery, such as the anterior tibial, may occasionally lead to ischemic gangrene of the muscles of the anterior compartment in spite of embolectomy and fasciotomy. In one instance, excision of the entire anterolateral compartment was carried out to achieve salvage of the leg. Atheroembolism Atheromatous emboli may arrest in multiple organs (e.g., kidney, pancreas, spleen), and in the lower extremities as well. Most such microemboli originate in the infrarenal or terminal portion of the aorta. Their size ranges from cholesterol crystals to atheromatous plaques. Embolization,

489

FIGURE 39.17 Arteriogram of left hand of a 60-year-old man, with sudden coldness, numbness, and pain of 48 hours duration. Note embolic occlusion of the terminal segment of the radial artery extending into the palmar arch, with absence of opacification of digital arterioles. Symptoms were completely relieved after embolectomy.

primarily involving the legs, often produces a distinct clinical syndrome. Myalgia or simple muscle tenderness is frequent, and the appearance of cutaneous lesions, ranging from tender discoloration to necrosis and ulceration, is characteristic. Peripheral pulses are usually present with microembolization, although they may be absent if preexisting occlusive disease is associated with this syndrome. Although most atheromatous emboli may be spontaneous, some are iatrogenic in origin and occur after operation on the aorta or catheterization of the vessels. Depending on the size of the emboli, the resulting manifestations may range from a subclinical state to an obvious arterial occlusion. The diagnosis of arterial embolism in these cases may be difficult to resolve in the absence of a cardiogenic origin (atrial fibrillation, myocardial infarct) or the presence of a known abdominal aneurysm or of an aortogram indicating the presence of ulcerated lesions. Often the benign clinical manifestations are overlooked or do not receive adequate interpretation because of lack of evidence of the source of the embolism. Often, only awareness of the existence of such emboli would help one to make the correct diagnosis.

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Anticoagulation may be of little value in this condition. In the presence of an ulcerated atheromatous aorta or abdominal aortic aneurysm, its resection offers the best hope to prevent further embolism.

Arterial Lesions of Undetermined Cause As has been stated, lesions of small arteries are not always easy to identify. Frequent lack of specificity of the clinical and histopathologic features of these entities often makes it difficult to classify them with reasonable certainty. TAO is a classic example that has aroused a great deal of controversy concerning its identification and even its very existence. One of the results of this debate was reassessment and reclassification, as atherosclerosis, of many cases considered earlier to be TAO. It should be pointed out that certain pathologic features of some small vessel diseases are common to several entities, especially in the broad category of vasculitis. Thus nosologic identification of some cases is uncertain. Hardy et al. reported a typical case presenting complex thrombotic and inflammatory lesions of small arteries. The various diagnoses considered in that case range from Buerger’s disease to essential polyangiitis to possible collagen disease. Such unclassified lesions are probably not unusual. In connection with these cases of arterial lesions of undetermined cause, Inada et al., in 1974, reported on 11 patients with atypical Buerger’s disease in whom the available histologic material supported an inflammatory cause more complicated than a simple reaction to thrombosis. The cases thus reported were atypical of Buerger’s disease in comparison with other cases described in that article, in which 236 cases of a group of 375 were classified as Buerger’s disease and only 139 cases as arteriosclerosis. This unusual type of small artery thrombosis of undetermined origin occurred in 11 of these cases of so-called Buerger’s disease. There were definite inflammatory changes suggestive of the inflammatory origin of the occlusive lesion in these cases. These changes were not considered to be a reaction to simple thrombosis. The pathologic changes of Buerger’s disease differed according to the stage of the disease. Vaidya, of India, in commenting on the paper presented by Inada et al., stated that in India, Sri Lanka, and other countries of the Orient, occlusive arterial disease affecting the inferior extremity, seen predominantly in young males, frequently results in gradual vascular insufficiency, ischemia, and gangrene, similar to the cases described by Inada et al. It appears that the process of obliteration starts at the distal end and that the thrombus gradually ascends. It may stop short at any level; in the majority of patients it stops in the popliteal artery. There are no skip lesions. It is thought that some sort of infection may be entering through the bare skin of the feet, or perhaps some kind of reaction to tubercular infection may be occurring in the arterial tree. The presence of the Langerhans type of giant cells and calcification of the granulomatous inflam-

matory tissue surrounding the thrombus and also of the arterial wall point in this direction, although Mycobacterium tuberculosis has neither been seen nor cultured. The lesions described by Vaidya are almost identical to those described by Inada et al., as mentioned above. Their exact nature has not yet been established. Opinions have been expressed in favor of rheumatic, tubercular, and autoimmune origin, without substantial evidence. It resembles some collagen diseases in certain characteristics as well. I reported a case in which a 35-year-old white woman had pain in the toes of both feet and in the ankles, in association with swelling and difficulty in walking. Her condition began at the age of 14 years, and until the time of her admission to the hospital, she experienced intermittent attacks of pain and swelling of the distal portions of both lower extremities (Fig. 39.18). She finally underwent below-the-knee amputation because of spreading gangrene of the toes and severe pain. Cross-section of the posterior tibial artery and of the venae comitantes showed microscopic lesions consistent with the diagnosis of TAO. However, the gangrene of the right foot due to disseminated obliterative arteritis of undetermined origin involved not only the medium-sized arteries but also their tributaries of small vessels in the muscles and skin. The lesions appeared to be typical of TAO, but in the small muscular vessels they were consistent with the diagnosis of polyarteritis nodosa. Therefore, as Hardy and Alican emphasized in their article, the histopathologic diagnosis was based on this complex clinical picture as well as on the histopathologic findings. It appears that the lesions in this particular case simply represented a combined process of two independent entities: TAO and a mixed pathologic finding of collagen disease or polyarteritis nodosa. Therefore the term “undetermined cause” must still be applied to these cases, as described by Inada et al. and Vaidya —and as indicated by my own experience in this field.

Collagen Diseases (Immune Arteritis) Periarteritis Nodosa (Polyarteritis) Periarteritis nodosa is an inflammatory disease of the medium-sized and small arteries. Since the introduction of this term in 1866 by Kussmaul arid Maier, this entity has also been described by other terms; the most frequently encountered synonyms include necrotizing angiitis, polyarteritis, and panarteritis. This process may affect the arteries throughout the body. Its clinical manifestations are protean, often simulating an infectious disease with toxemia. The clinical course may be acute or chronic, with symptoms and signs referable to the organs and tissues affected. In order of decreasing frequency, the clinical features include arthralgia, skin lesions, cerebrovascular accidents, respiratory manifestations, myalgia, gastroin-

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

491

FIGURE 39.18 (A) Gangrene of right foot of nonsmoker, a 35-year-old woman, due to an undetermined cause. (B) Cross-section of posterior tibial artery and of venae comitantes. The microscopic lesions appear consistent with the diagnosis of thromboangiitis obliterans or arteritis of undetermined cause (elastin–van Gieson stain; ¥30). (C) Magnification of a portion of the posterior tibial artery , showing greater detail of the histologic changes (elastin–van Gieson stain; ¥60). (D) Photomicrograph of a section of an arteriole in the gastrocnemius muscle. Lesions are those of panarteritis.

A

C

B

D

testinal syndromes, cardiac lesions, renal manifestations, vascular lesions involving the veins as well as the arteries, and genital complications. The common denominator of all these clinical syndromes is the involvement of the medium-sized and small arteries, the outstanding pathologic change being a focal necrosis of the medial coat with perivascular inflammatory changes. When the process extends to the intima, the smaller vessels may become occluded. As a result, blood supply to various organs and tissues is markedly impaired, leading to necrosis, infarction, or fatty degeneration. Because of the multiplicity of the clinical manifestations, the diagnosis of periarteritis nodosa may be extremely difficult. The disease should be suspected in any patient who has an obscure illness suggesting the presence of a diffuse systemic process with involvement of several

organs and tissues, particularly joints, skin, kidneys, gastrointestinal tract, or peripheral nerves. Laboratory findings may be helpful, if positive, but often they are nonspecific. Rapid erythrocyte sedimentation rate, leukocytosis, hypertension, and often failure of the condition to respond to conventional treatment should provide enough evidence to justify suspecting this diagnosis. Biopsy diagnosis, when positive, is the most helpful procedure, but its interpretation may be limited because of the possible inadequacy of the specimen. Histologic examination of the tissues should establish the nature of the disease. Biopsy specimens of skin or muscle may often demonstrate involvement of the small vessels or arterioles. However, biopsy specimens of the liver or kidney are rarely helpful in establishing a diagnosis—and the biopsy procedure is hazardous. In general, random biopsies should be avoided because they

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Part VI Chronic Arterial Occlusions of the Lower Extremities

are of little value in establishing the nature of the vascular lesion. Periarteritis nodosa, or polyarteritis, is seen mostly in male patients in a ratio of 2:1; the peak incidence is in the fifth decade of life. Formation of aneurysms associated with the inflammatory destruction of the media is observed relatively often. Among more frequently involved organs are the kidney, heart, lung, liver, and gastrointestinal tract, as mentioned above. In a detailed arteriographic study of 17 patients with this condition, Travers et al. reported that 10 of the patients had multiple aneurysms involving the hepatic, renal, and mesenteric vessels. Obviously, ruptured aneurysms in these locations are often unrecognized and undiagnosed before surgical exploration or postmortem examination and therefore contribute to the death of the patient. This type of aneurysm limits considerably the options of the vascular surgeon, and experience gained with these cases has been limited as a result of these clinicopathologic complications. Therefore the prognosis for periarteritis nodosa is usually poor, although the condition is not invariably fatal. Of the criteria reflecting poor prognosis, the most significant are the visceral manifestations, especially hypertension, renal involvement, and rupture of aneurysms, as mentioned. The use of corticosteroids has greatly improved the overall outlook. Treatment must be instituted before widespread vascular damage occurs and should be intensive and prolonged. Frohnert and Sheps, in a long-term follow-up study of periarteritis nodosa, were able to demonstrate a 5-year survival rate of 48% of patients treated with steroids. Early diagnosis is of paramount importance for adequate management of this condition, which was formerly considered fatal in most instances.

Lupus Erythematosus The vascular manifestations associated with lupus erythematosus are varied and complex. The most common lesions involve the smaller arteries, most frequently the digital arterioles. In addition, both arterial and venous thrombosis of larger vessels is also seen. Venous thrombosis involving both superficial and deep veins and pulmonary embolism are not infrequently encountered in these patients. However, the typical vasculitis of small vessels is characteristic of lupus and is responsible for the skin infarction and the paroxysmal color changes, whereas the thrombosis of the larger arteries and veins is due to a different mechanism. Raynaud’s phenomenon is seen in about 20% of patients with systemic lupus erythematosus and seems to precede other vascular manifestations of the disease by several years. Gangrene is usually limited to the digits. Leg ulcers with systemic lupus erythematosus have been reported to be due to infarction of the skin as a result of vasculitis. Among the laboratory findings, the lupus erythematosus (LE) cell phenomenon is characteristic of this

syndrome. It is present in only about 75% of the patients with clinical systemic lupus erythematosus. During clinical remissions, either there is a reduction m the number of LE cells or the test result becomes negative. Active lupus erythematosus may be fatal within a matter of a few weeks. However, in the milder forms of the disease, the clinical course is prolonged and relatively benign. Treatment consists of large doses of corticosteroids. Continuous or intermittent steroid therapy may provide many years of remission.

Scleroderma Patients with scleroderma often have associated Raynaud’s phenomenon characterized by intermittent digital vasospasm or even persistent coldness and cyanosis. Raynaud’s phenomenon is sometimes the outstanding manifestation that first brings the patient to the attention of the physician. The pathologic skin changes in scleroderma that are associated with Raynaud’s phenomenon consist of increase and swelling of collagenous connective tissue with fragmentation and swelling of the elastic fibers in the dermis. Replacement of the subcutaneous tissue by abnormal connective tissue, both within the fibrils and in the ground substance, is specific to systemic scleroderma. The epidermis may be hyperkeratotic, with melanin often accumulated in the basal cells. The arteriolar changes in scleroderma consist of thickening of the intima, involving not only the arterioles in the skin but also those of the kidney, gastrointestinal tract, musculature, and central nervous system. The vascular manifestations seem to arise from a local fault similar to Raynaud’s disease. An increase in connective tissue surrounding blood vessels has been suggested as the cause of constriction of the vessels, leading to ischemia, at least of the skin of the affected region. Raynaud’s phenomenon associated with diffuse scleroderma is seen mostly in women. The chronology of the manifestations may be variable. In some cases, Raynaud’s phenomenon precedes the sclerodermal skin changes, whereas in other instances the stiffness and soreness of the joints antedate the functional organic vascular disease. As the disease progresses, the tips of the fingers or toes may become more pointed or shrunken. Occasionally, a limited gangrenous lesion of the distal phalanx of a finger or toe may be present. The prognosis of Raynaud’s phenomenon associated with diffuse scleroderma is variable. It is usually fatal in patients with renal, cardiac, and other visceral involvement. Management of Raynaud’s phenomenon associated with scleroderma includes protection against trauma or other injurious factors and use of measures to increase peripheral circulation, such as treatment with reserpine or methyldopa. Sympathectomy at the early stage of scleroderma associated with marked Raynaud’s phenomenon is advocated by some but has little value in general; especially in the late stages it has no value.

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

Vasospastic Diseases Raynaud’s Disease Since the original description in 1862 by Maurice Raynaud, the disease known by his name has undergone a wide reappraisal in regard to its clinical manifestations, which has led to a reclassification of this entity. Raynaud’s disease is defined as a purely vasospastic phenomenon involving mainly the digital arterioles of both hands and feet. It is characterized by a triad of intermittent color changes consisting of pallor, cyanosis, and rubor brought on by exposure to cold or by emotional stimuli. These symptoms are usually worse in the cold season and disappear or become less severe in the warm season. The onset of these manifestations is usually gradual. Originally only the tips of one or two fingers of both hands are involved, but at a later stage, involvement extends to the more proximal parts of the fingers. In the very late stages, although rarely, it may also extend to the rest of the hands. Involvement of the toes is less conspicuous but often occurs in conjunction with the vasomotor changes in the fingers and hands. The disease is progressive, especially among women, and may become severe and disabling. Ulceration of the tips of the fingers and occasionally gangrene may cause considerable pain and discomfort. Loss of tissue in Raynaud’s disease is exceptional, however, except for the distal phalanx and infected and progressively gangrenous lesions. The exact cause of primary Raynaud’s disease remains obscure. In about 80% or 90% of patients, it appears before 40 years of age. In men, it is much less severe in intensity. When Raynaud’s disease occurs in the later decades, organic vascular changes are usually associated with it. Pathology Virtually nothing is known about pathologic changes of the digital vessels in the early stages of Raynaud’s disease because biopsy specimens are not available. Lack of abnormality of the small vessels in primary Raynaud’s disease is such that description of the disease does not entirely meet the definition of this chapter. Nevertheless, it is described in this chapter mainly because it may occur in association with organic or traumatic lesions. As a consequence, one has to be aware of this association to understand the more complex features of Raynaud’s syndrome. Although no biopsy or pathologic evidence exists regarding the changes in the digital arterioles, the changes may be observed in persons aged 50 years or more without Raynaud’s disease, because of normal age-related changes of the arteries. At a later stage, with the advent of trophic skin lesions of the tip of the fingers, obstructive disease of the digital arteries may be present. Diagnosis Arteriography has been of little value in establishing the diagnosis because it has failed to demonstrate any distinctive arterial disease of the digital arterioles.

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Acrocyanosis Acrocyanosis is usually confused with Raynaud’s disease. Like Raynaud’s disease, it is prevalent in women and is characterized by painless and persistent coldness and cyanosis of the distal parts of the extremities. Its cause and physiopathology are obscure. Most authors tend to agree with Lewis and Landis that its disturbed physiology is reflected in the smaller vessels of the extremities. The local fault is attributed to increased vasomotor tone of the small arterioles, which leads to dilation of the capillaries and venules even at normal environmental temperature. Clinically, the patient notes constant coldness and bluish discoloration of the fingers and hands for many years. These signs and symptoms are more pronounced in the winter months but remain present, although to a lesser degree, in a warm environment. The color changes do not disappear on elevation of the hand. The major arteries are normal, and tropic changes do not occur in this condition. The differentiation of acrocyanosis from Raynaud’s disease should be easily determined if the triad of intermittent cold-induced color changes characteristic of the latter condition is carefully identified. Management of acrocyanosis remains largely that of protecting the patient from cold and using vasodilator drugs, which may be of some value. In severe cases, sympathectomy, either thoracic or lumbar, offers a better prospect of a good result than it does in the treatment of Raynaud’s disease. Prognosis is usually good in regard to viability of the limb.

Livedo Reticularis Livedo reticularis is a vasospastic condition characterized by bluish discoloration and by blotchy reddish blue skin; it is seen mostly in women. The basic physiologic abnormality consists of a narrowing, either organic or functional, of the arterioles, with dilatation of the capillaries and venules. The underlying vascular abnormality is characterized primarily by thrombosis of digital arteries with absence of involvement of the larger vessels. The histopathologic changes consist of proliferation of the intima and of the isolated arterioles and small arteries. Some of these vessels are occluded completely by the proliferative process or by thrombosis, or both, with similar lesions being found in a few of the larger veins. In the presence of ulcerations of the skin due to livedo reticularis, dilated subepidermal capillaries, lymph vessels, and venules often accompany the nonspecific infiltrate of the skin. The clinical manifestations consist of persistent bluish red mottling of the skin, not only of the lower extremities but often of the hands and arms, to a lesser degree, and occasionally of the lower part of the trunk. Coldness, numbness, dull aching, and paresthesia of the feet and legs are often present as well. Leg and foot ulcers associated with livedo reticularis are commonly recurrent

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during the winter months. These ulcers are usually painful and resistant to healing. Livedo reticularis as a result of periarteritis nodosa, systemic lupus erythematosus, cryoglobulinemia, microembolism, or arteriosclerosis obliterans is a distinct possibility and should be considered in the differential diagnosis. In mild forms of the disease, conservative management of the vasospastic condition and the ulceration may be helpful. Lumbar sympathectomy should be tried, because it may be effective in certain patients.

Frostbite Acute frostbite is the result of vasoconstriction, which, if unrelieved, may lead to severe ischemia as a result of superimposed thrombosis of smaller arteries. Although the cause of death of the tissue is not entirely elucidated, it is well known that marked intimal changes of small arteries and arterioles may develop at a later stage. The endothelium of the terminal capillaries may also be severely damaged, affecting the permeability of the capillary wall. Stasis thrombosis then occurs in terminal arterioles and capillaries. On the basis of the severity of tissue damage, frostbite has been classified, in a fashion similar to the classification of burns, into four degrees. However, classification into superficial and deep frostbite, as suggested more recently, appears to have more practical value. Superficial frostbite involves the skin and superficial subcutaneous tissue, whereas deep frostbite involves—besides the skin—subcutaneous tissue, muscle, and even bone. In the mild form there is numbness, yellowing of the skin, and prickling and itching sensations. At this initial stage, rewarming of the extremity may alter the situation within a few minutes to a few hours, and recovery may be permanent. In severe frostbite, paresthesia and stiffness are more marked than in the mild form, and there is complete loss of sensation to touch. Rewarming of the extremity is accompanied by reactive hyperemia, tenderness, burning pain, and possible formation of blisters. Necrosis or gangrene of the extremity may develop at this stage. Depending on the severity of the frostbite, the necrotic tissue may be more superficial than is suspected initially. The diagnosis of the severe degree of frostbite is usually not difficult. In patients whose age indicates probable arteriosclerosis, it is important to determine preexisting arterial occlusive disease. Obviously, the prognosis for frostbite associated with such disease is much less favorable than that of a similar degree of frostbite with normal circulation. A history of previous intermittent claudication, cold feet, or Raynaud’s phenomenon should be ascertained in each of these patients with frostbite. It may have medicolegal implications. Frostbite should be considered as an emergency, and treatment should be instituted without delay for better salvage of the involved extremity.

In mild frostbite, restoration of natural warmth to the skin should be achieved as quickly as possible. Rubbing of the affected part should be avoided, because it may result in trauma to the skin. Likewise, overheating of the skin should be completely avoided. In severe frostbite, avoidance of trauma and maintenance of asepsis are of great significance. On the basis of recent experience, rapid thawing is preferred to a slow rewarming. Vasodilator procedures and the use of heparin have been advocated by some and found to be of no value by others. In the presence of tissue damage and gangrene, amputation should be delayed as long as possible, because the lesions may be superficial. Conservative therapy and local debridement may result in healing without major loss of tissue.

Mixed Organic and Vasospastic Diseases Raynaud’s Phenomenon and Preexisting Occlusive Arterial Disease Raynaud’s phenomenon may occur in association with preexisting occlusive arterial disease. Vasospastic phenomena displaying the characteristics of Raynaud’s triad may be encountered in Buerger’s disease in about 30% of the cases, in arteriosclerosis obliterans in about 10% to 15%, and in embolic occlusions in about 10%. This association of organic occlusive disease and Raynaud’s phenomenon is generally not well recognized. It is usually precipitated by environmental coldness without emotional stimuli. It is more frequently observed in men, in contrast to Raynaud’s disease, which is prevalent in women. The presence of occlusive arterial disease and the usual absence of bilaterality provide the main criteria for the differential diagnosis.

Post-traumatic Occupational Raynaud’s Phenomenon Occupational injuries of various types, such as those occurring in pianists, typists, workers using the pneumatic hammer or vibrating tools, and machinists of all types, may induce Raynaud’s phenomenon. This phenomenon usually involves only one or two digits and, if severe enough, may result in occupational disability (Fig. 39.19). Protection from exposure to cold, which is invoked as a precipitating factor, avoidance of intermittent trauma, or readjustment in the technique of a pianist or typist may be helpful. If the condition is too severe and symptoms are frequent, leading to marked disability, the temporary cessation of the occupation or permanent discontinuance may be necessary. The use of vibrating tools has resulted in Raynaud’s phenomenon after repeated percussion on the hands, a syndrome also known as pneumatic hammer disease. The phenomenon is attributed to sensitization of digital arteri-

Chapter 39 Nonatherosclerotic Diseases of Small Arteries

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blunt trauma, may complain of pain, coldness, and color changes typical of Raynaud’s phenomenon. They may have cold fingers and painful ulcers as a result of the combined arterial occlusive disease of the fingers and repeated trauma. The arterial occlusive process in these patients is usually considered a result of chronic arterial injuries. Such patients may present a syndrome of ulnar occlusion due to trauma resulting from occupational use of the hypothenar portion of the hand. This latter condition is called hypothenar traumatic syndrome. A communication on 17 cases with long-term follow-up indicated the presence of thrombosis or aneurysm of the ulnar artery. Arteriography is essential for identifying the location and extent of the lesions. Local surgery may be necessary, and reconstructive vascular procedures may be feasible if involvement is confined to the proximal segment of the ulnar artery.

Hematologic Disorders PoIycythemia Vera

FIGURE 39.19 Arteriogram of right hand of a 53-yearold man who injured his hand 2 years before the onset of coldness, pain, cyanosis, and ischemic ulcer of all fingertips except the tip of the thumb. Note complete occlusion of the ulnar artery just proximal to the wrist joint and lack of opacification of most digital arterioles.

oles because of both rapid percussion and exposure to cold. If the occupation leads to intolerable disability, a sympathectomy may be justifiable if the occupation cannot be changed without undue hardship.

Occupational Trauma and Secondary Occlusive Arterial Disease of the Hand Workers who use vibrating tools, and machinists, laborers, and farmers, whose hands are subjected to repeated

As early as 1903, Osler recognized the frequency of vascular complications occurring in polycythemia vera. The most serious complications are thrombosis and hemorrhage. These occur in about one-third to one-half of the patients and are a significant cause of morbidity and death. The thrombotic sites are most frequently seen in the peripheral, cerebral, and coronary vascular systems, with mesenteric, splenic, hepatic, and portal venous occlusions occurring less commonly. Arterial thrombosis associated with polycythemia involves primarily the smaller arteries or the digital arterioles. The coexistence of polycythemia vera and vascular complications poses the question of their causal relation, because some of these entities may be coincidental. On the basis of a series of 98 cases of polycythemia with 34% vascular complications, Norman and Allen concluded that a cause-and-effect relation exists between these conditions. It is conceivable, however, that the presence of arteriosclerosis or TAO together with polycythemia may raise some doubts about the latter’s role in the causation of vascular complications. However, it appears that the treatment of polycythemia may sometimes improve the arterial lesions, lending support in such cases to the role of the hematologic disorder in their causation. Regardless of these combined or coincidental conditions, polycythemia vera per se will induce small-vessel thrombosis. A few examples from my experience will illustrate some of the associated clinical manifestations of polycythemia vera leading to ischemic lesions. 1.

A 40-year-old man developed gangrene of one toe of the right foot and cyanosis of all the other toes and the forefoot. Both pedal pulses were palpable, and an arteriogram disclosed only a short segmental stenosis of

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the midportion of the anterior tibial. In this case, the relation of small-vessel involvement and polycythemia appeared plausible. An 80-year-old man with atherosclerosis obliterans of the distal tibial arteries developed gangrene of the great toe, requiring its subsequent amputation. Concomitant active treatment of the hematologic condition seemed to relieve the ischemic manifestations of the rest of the foot. In this case, the polycythemia appeared as an aggravating factor rather than as its initiating cause. A 60-year-old man had a small ulceration of the right fifth toe, moderate arterial insufficiency, and severe burning pain due to erythromyalgia. Active treatment of the polycythemia, coupled with local management of the foot lesions, relieved the pain and helped heal the ulcer. In this case the causal relation among polycythemia, erythromyalgia, and the arterial complications seemed questionable.

It appears, therefore, that in the presence of vascular complications associated with polycythemia, active treatment of the latter is essential. Furthermore, in addition to the peripheral manifestations, awareness of the multiplicity of visceral involvement should evoke the possibility of these lesions in every patient with polycythemia vera. Once the diagnosis is reached, management with appropriate therapy should yield a satisfactory response.

Cryoglobulinemia Cryoglobulinemia is a result of the presence in plasma of abnormal proteins that precipitate on cooling. In 1933, Wintrobe and Buell reported such a case in a patient suffering from multiple myeloma. It was not until 1947 that Lerner and Watson suggested the name “cryoglobulins” to represent a group of proteins with a common property of precipitating from cold serum. They also noted that when the proteins are in a high concentration, they may precipitate spontaneously even at room temperature. The presence of cryoglobulins may lead to intravascular thrombosis. In addition, if cryofibrinogens are also present, both thrombosis and hemorrhage may occur. Many of the patients with this abnormal protein in the blood may have Raynaud’s phenomenon, acrocyanosis, or purpura with vascular manifestations in an unusual location or of an unusual type. In these cases, the patient should be tested for cryoglobulins, and if they are found, suspicion of the presence of multiple myeloma or similar hematologic conditions, such as leukemia, lymphoblastoma, or polycythemia vera, should be raised and the possibilities investigated. Because significant amounts of cryoglobulin may produce intravascular thrombosis, necrosis of the skin may develop, as reported by Hardy et al. Idiopathic cryoglobulinemia is usually less amenable to treatment. In the presence of an associated underlying disease process such as myeloma, treatment of the primary disease may be partially effective. In the presence of

ischemic necrosis, local treatment is obviously indicated in addition to the management of the dysproteinemia.

Bibliography Baur GM, Porter JM, et al. Rapid onset of hand ischemia of unknown etiology. Ann Surg 1977;186:184. Behçet H. Uber rezidivierende aphthose durch ein Virus verusachte Gersehwure Am Mund, Am Mauge und an den Genitalien. Dermatol Ubchenschr 1937;1 05:1152. Bengtsson B, Malmvall B. Giant cell arteritis. Acta Med Scand (Suppl) 1982:658:1. Bergan JJ, Coon J Jr, Tripel OH. Severe ischemia of the hand. Ann Surg 1971;173:301. Block KJ, Makin DG. Hyperviscosity syndromes associated with immunoglobulin abnormalities. Semin Hematol 1973:10:113. Brouet C, Clauvel J, Danon F. Biologic and clinical significance of cryoglobulins. Am J Med 1974:57:775. Brown H, Sellwood RA, et al. Thromboangiitis obliterans. Br J Surg 1969:56:59. Buerger L. Thrombo-angiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. Am J Med Sci 1908;136:567. Buerger L. The veins in thromboangiitis obliterans. JAMA 1909;111:1320. Buerger L. The circulatory disturbances of the extremities. Philadelphia: WB Saunders, 1924. Crawford ES, Crawford JL. Diseases of the aorta. Baltimore: Williams & Wilkins, 1984. Danaraj TJ. Primary arteritis of aorta causing renal artery stenosis and hypertension. Br Heart J 1963;25:153. deShazo R. The spectrum of systemic vasculitis. Postgrad Med 1975;58:78. Dible JH. The pathology of limb ischemia. St Louis: Warren H.Green, 1966. Downs AR, Gaskell P, et al. Assessment of arterial obstruction in vessels supplying the fingers by measurement of local blood pressures and the skin temperature response test: correlation with angiographic evidence. Surgery 1975,77:530. Dobois EL, Tuffanelli DL. Clinical manifestations of systemic lupus erythematosus: computer analysis of 520 cases. JAMA 1964;190:104. Duncan JM, Cooley DA. Surgical considerations in aortitis with surgical emphasis on Takayasu’s arteritis. Tex Heart Inst J 1983;10:233. Edwards PA. Postamputation radiographic evidence for small artery obstruction in arteriosclerosis. Ann Surg 1959;150:177. Fauci AS, Haynes BF, Katz P. The spectrum of vasculitis. Ann Intern Med 1978;89:660. Feldaker M, Hines EA Jr, Kierland RR. Livedo reticularis with ulcerations. Circulation 1956;13:196. Fitts WT, Melissinos EG. Polycythemia vera. In: Sabiston DC, ed. Textbook of surgery, 11th edn. Philadelphia: WB Saunders, 1977;146. Gulati SM, Singh KS, et al. Immunological studies in thromboangiitis obliterans (Buerger’s disease). J Surg Res 1979;27:287. Hachiya J. Current concepts of Takayasu’s arteritis. Semin Roentgenol 1970:5:245.

Chapter 39 Nonatherosclerotic Diseases of Small Arteries Haimovici H. Peripheral arterial embolism: a study of 330 unselected cases of embolism of the extremities. Angiology 1950;1:120. Haimovici H. Arterial embolism: peripheral and visceral. In: Haimovici H, ed. The surgical management of vascular diseases. Philadelphia: JB Lippincott, 1963. Haimovici H. Thromboangiitis obliterans: a nosologic reappraisal [editorial]. J Cardiovasc Surg 1963:4:83. Haimovici H. Ischemic forms of venous thrombosis, phlegmasia cerulea dolens, and venous gangrene. Springfield, IL: Charles C Thomas, 1971. Haimovici H. Diseases of small arteries of the extremities. In: Hardy Rhoades’ textbook of surgery, 5th edn. Philadelphia: JB Lippincott, 1977:1827. Haimovici H. Aortic arch syndrome: Takayasu’s arteritis. In: Cirugia Vascular (Spanish edition of Vascular surgery). Barcelona: Salvat, 1986:778. Hardy JD, Alican E. Ischemic gangrene without major organic vascular occlusion: an enlarging concept. Surgery 1961;50:107. Hardy JD, Conn JH, Fain WR. Nonatherosclerotic occlusive lesions of small arteries. Surgery 1965:57:1. Hill GL. A rational basis for management of patients with Buerger syndrome. Br J Surg 1974:61:476. Hill GL, Smith AH. Buerger’s disease in Indonesia: clinical course and prognostic factors. J Chronic Dis 1974;29:205. Hirai M, Shionoya S. Arterial obstruction of the upper limb in Buerger’s disease. Br J Surg 1979:66:124. Hutchinson J. Acro-scleroderma following Raynaud’s phenomena. Clin J 1896;7:240. Hutton M, Rhodes RS, Chapman G. The lowering of postischemic compartment pressures with mannitol. J Surg Res 1982;32:239. Inada K, Iwashima Y, et al. Nonatherosclerotic segmental arterial occlusion of the extremity. Arch Surg 1974:108: 663. Inada K, Shimizo H, Yokayama T. Pulseless disease and atypical coarctation of the aorta, with special references to their genesis. Surgery 1962:52:433. Isaacson C. An idiopathic aortitis in young Africans. J Pathol Bacteriol 1961:81:69. Ishikawa KK. Natural history and classification of occlusive thromboaortopathy (Takayasu’s disease). Circulation 1978;57:27. Ishikawa K, Kawase S, Mishima Y. Occlusive arterial disease in extremities, with special reference to Buerger’s disease. Angiology 1962:13:399. Jager BV. Cryofibrinogenemia. N Engl J Med 1962:266:579. Jenkins AM, Macpherson AS, et al. Peripheral aneurysms in Behçet’s disease. Br J Surg 1976:63:199. Jepson RP. Widespread and sudden occlusion of the small arteries of the hands and feet. Circulation 1956:14:1084. Kalbfleisch JM, Bird RM. Cryofibrinogenemia. N Engl J Med 1960;263:881. Kimoto S. The history and present status of aortic surgery in Japan, particularly for aortitis syndrome. J Cardiovasc Surg 1979:20:107. Lande A, Bard R, et al. Aortic arch syndrome (Takayasu’s arteritis). J Cardiovasc Surg 1978;19:507. Laroche GP, Bernatz PE, et al. Chronic arterial insufficiency of the upper extremity. Mayo Clin Proc 1976:51:180. Lerner AB, Watson CJ. Studies of cryoglobulins: 1. Unusual purpura associated with the presence of a high concen-

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tration of cryoglobulin (cold precipitable globulin). Am J Med Sci 1947;214:410. Lewis T, Landis EM. Observations upon the vascular mechanism in acrocyanosis. Heart 1930;15:229. Liechty RD, Iob V, McMath M. Cryoproteinemia: its relationship to peripheral vascular disease. Ann Surg 1961;154:319. Little AG, Zatins CK. Abdominal aortic aneurysm and Behçet’s disease. Surgery 1982;91:359. Lupi-Herrera E, Sanchez-Torres G, et al. Takayasu’s arteritis: clinical study of 107 cases. Am Heart J 1977;93:94. Maekawa M, Hayase S, et al. Obstructive aortitis with hypertension: Takayasu’s disease without the eye symptoms. Jpn Circ J 1963;27:730. Martorell F, Fabre J. El sindrome de obliterative de los troncos supraaorticos. Med Clin (Barc) 1944;2:26. McKusick VA, Harris WS, et al. Buerger’s disease: a distinct clinical and pathologic entity. JAMA 1962;181:5. McLoughlin FA, Helsby FR, et al. Association of H1A-AI and HLA-B5 with Buerger’s disease. Br Med J 1976:2: 1165. McPherson JR, Juergens JL, Cifford RW Jr. Thromboangiitis obliterans and arteriosclerosis obliterans: clinical and prognostic differences. Ann Intern Med 1963;59:288. Mozes M, Cahansky G, et al. The association of atherosclerosis and Buerger’s disease: a clinical and radiological study. J Cardiovasc Surg 1970;2:52. Nakao K, Ikida M, Kimata S. Takayasu’s arteritis: clinical report of eighty-four cases and immunologic studies of seven cases. Circulation 1967;35:1141. Norman IL, Allen EV. The vascular complications of polycythemia. Am Heart I 1937;13:257. O’Leary PA, Waisman M. Acrosclerosis. Arch Dermatol 1943:47:382. Oohashi S. Clinical, angiographical and pathological studies on Buerger’s disease especially in relation to arteriosclerosis. J Jpn Surg Soc 1975:76:491. Paramo Diaz M, Diaz Ballesteros F, et al. Sindrome de obliteracion de los troncos supraaorticos y enfermedad de Takayasu. Angiologia 1982;34:111. Perdue GD, Smith RD III. Atheromatous microemboli. Ann Surg 1966;93:71. Raddi HTV Thromboangiitis obliterans and/or Buerger’s disease in South India: a review of 70 cases. Int Surg 1974;59:555. Rivera R. Roentgenographic diagnosis of Buerger’s disease. J Cardiovasc Surg 1973;14:40. Sanding H, Welin G. Aortic arch syndrome with special reference to rheumatoid arteritis. Acta Med Scand 1961;170:1. Schatz JJ. Occlusive arterial disease in the hand due to occupational trauma. N Engl J Med 1963:268:281. Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs: surgical considerations: report of a case and review of the literature. Surgery 1956;40:398. Sheps SC, McDuffie EC. Vasculitis. In: Juergens IL, Spitell JA, Gairbairn Jr, eds. Peripheral vascular disease. Philadelphia: WB Saunders, 1980;493. Shimizu K, Sano K. Pulseless disease. J Neuropathol Exp Neurol 1951;1:37. Shionoya S, Ban I, et al. Diagnosis, pathology, and treatment of Buerger’s disease. Surgery 1974;75:695. Shionoya S, Ban I, Nakata Y. Vascular reconstruction in Buerger’s disease. Br J Surg 1976;63:841.

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Swinton NW, Cook GA. Systolic hypertension and cardiac mortality of Takayasu’s aortoarteritis. Angiology 1976;27:568. Takayasu M. Cases with unusual changes of the vessels in the retina. Acta Soc Ophthalmol Japan 1908,12:554. Taylor LM. Baur GM, Porter JM. Finger gangrene caused by small artery occlusive disease. Ann Surg 1981;193:453. Thieme WT, Strandness DE Jr, Bell JW. Buerger’s disease: further support for this entity. Northwest Med 1965;64:264. Travers RL, Allison DJ, et al. Polyarteritis nodosa: a clinical and angiographic analysis of 17 cases. Semin Arthritis Rheum 1979;8:184. Ueda H, Ito I, Okada R. Aortic arch syndrome with special

reference to pulseless disease and its variants. Jpn Heart J 1963,4:224. von Winiwatter F. Ueber eine eigenthumliche Form von Endarteritis and Endophlebitis mit Gangran des Fusses. Arch Kim Chir 1879;23:202. Wessler S, Ming SC, et al. A critical evaluation of thromboangiitis obliterans: the case against Buerger’s disease. N Engl J Med 1960;262:1149. Wintrobe MM, Buell MV. Hyperproteinemia associated with multiple myeloma with report of a case in which an extraordinary hyperproteinemia was associated with thrombosis of retinal veins and symptoms suggesting Raynaud’s disease. Bull Johns Hopkins Hosp 1933;52:156.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 40 Aortoiliac,Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases David C. Brewster

The infrarenal abdominal aorta and iliac arteries are among the most common sites of chronic obliterative atherosclerosis (1). Indeed, atherosclerotic narrowing or occlusion of these vessels, most commonly centered around the aortic bifurcation, occurs to varying degrees in almost all patients with symptoms of arterial insufficiency of the lower extremities severe enough to require consideration for surgical revascularization. Despite the frequency of multilevel occlusive disease, successful correction of proximal aortoiliac disease will usually provide adequate relief of ischemic symptoms. In addition, careful assessment of the adequacy of arterial inflow is important in patients who require infrainguinal revascularization procedures, if successful and durable results are to be obtained. The possibility of surgical intervention for relief of ischemic symptoms secondary to aortoiliac disease was first recognized by Leriche. Beginning in 1923, he published a series of observations of a syndrome occurring in relatively young men, consisting of bilateral intermittent claudication, diminished or absent femoral pulses, and sexual impotence. He termed this syndrome, which has subsequently come to bear his name, “aortitis terminalis,” and suggested that the ideal treatment would be excision and reestablishment of vascular continuity by means of an arterial graft (2). Thromboendarterectomy, as introduced by Dos Santos in 1947 (3), was firmly established in the aortoiliac

segment by Wylie in 1952 (4). Inspired by the pioneering work of Gross with thoracic homografts (5), resection and replacement of the diseased abdominal aorta began with arterial homografts (6–8). With introduction of fabric arterial grafts by Voorhees in 1952 (9), the era of prosthetic graft replacement or bypass began (10,11). Since then, tremendous advances have occurred in this area. Currently, a variety of methods exist to accurately evaluate aortoiliac occlusive disease and help in selection of patients for revascularization. Most importantly, a variety of operative approaches and methods of revascularization are available for use in differing clinical circumstances. In recent years, an increasing number of patients with aortoiliac disease are being treated with endovascular catheter-based interventions, including balloon angioplasty and stent insertion (see Chapters 18 and 19). With proper patient selection and a carefully performed procedure, a favorable outcome and low operative morbidity and mortality may be anticipated, making surgical management of aortoiliac occlusive disease one of the most rewarding areas of vascular surgical practice.

Clinical Manifestations The symptoms and natural history of the occlusive process are significantly influenced by its distribution and extent (Fig. 40.1). Truly localized aortoiliac disease (type

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FIGURE 40.1 Anatomic patterns of aortoiliac occlusive disease.

I), with occlusive lesions confined to the distal abdominal aorta and common iliac vessels, is seen in only 5% to 10% of operative candidates, and in the absence of more distally distributed disease rarely produces limb-threatening symptoms (12,13). In such localized aortic obstruction, the potential for collateral blood flow around the aortoiliac segment is great. Collateral pathways include both visceral and parietal routes, such as: internal mammary to inferior epigastric; intercostal to circumflex iliac; lumbar and hypogastric to common femoral and profunda branches; and superior mesenteric to inferior mesenteric and superior hemorrhoidal pathways via the marginal artery of Drummond and arc of Riolan. If patients with occlusive disease were to be studied arteriographically earlier in the course of their disease, patients with a localized type I pattern of aortoiliac disease would no doubt be more common than the 5% to 10% estimate noted above. These data are derived from angiographic examination in patients with symptomatology serious enough for them to be considered for surgical intervention. If more liberal indications for arteriography are employed, as may become more frequent with increased use of “less invasive” forms of treatment such as balloon angioplasty, localized aortoiliac disease may be observed more often. Patients with such segmental disease typically have varying degrees of claudication, most often involving the proximal musculature of the thigh, hip, or buttock areas. The symptoms may be equally severe in both limbs, although usually one leg is more severely affected than the other. More advanced ischemic complaints are absent unless distal atheroembolic complications have occurred. In men, impotence is an often-associated complaint, present in at least 30% of men with aortoiliac disease. Such patients are characteristically younger, with a relatively low incidence of hypertension or diabetes, but a

FIGURE 40.2 Transaxillary aortogram of patient with localized (type I) aortoiliac disease, confined to the region of the aortic bifurcation and proximal iliac vessels.

significant frequency of abnormal blood lipid levels, particularly type IV hyperlipoproteinemia (14,15). In contrast to the usual male predominance in chronic peripheral vascular disease, almost one-half of those patients with localized aortoiliac lesions are women (12). Indeed, the frequency of aortoiliac disease in women has been increasing substantially in recent years, coincident with the increased national incidence of cigarette smoking in women. Many female patients with localized aortoiliac disease constitute a characteristic clinical picture often referred to as the “hypoplastic aorta syndrome” (Fig. 40.2): typically a woman of about 50 years of age, invariably a heavy smoker, with angiographic findings of small aortic, iliac, and femoral vessels, a high aortic bifurcation, and occlusive disease often strikingly localized to the lower aorta or aortic bifurcation (15–18). Commonly, many such patients will have had an artificial menopause induced by hysterectomy or radiation. In more than 90% of symptomatic patients, disease will be more widespread, however. In our experience, approximately 25% will have disease confined to the abdomen (type II), and approximately 65% will have widespread occlusive disease above and below the inguinal ligament (type III). Patients in the latter group with such “combined segment” or “multilevel” disease are typically older, more commonly male (about 6 : 1 ratio) and much more likely to have diabetes, hypertension, and associated atherosclerotic disease involving cerebral, coronary, and visceral arteries. Progression of the occlusive process is also more likely in such patients

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

compared with those patients with more localized aortoiliac disease (17,19,20). For these reasons, the majority of patients with a type III pattern manifest symptoms of more advanced ischemia such as ischemic pain at rest or varying degrees of ischemic tissue necrosis, and more often require revascularization for limb salvage rather than relief of claudication alone. Not unexpectedly, patients with diffuse multilevel disease have a decrease in life expectancy of 10 or more years, whereas it may be near normal in patients with localized aortoiliac disease (21).

Diagnosis In most instances, an accurate and detailed history and carefully performed physical examination can unequivocally establish the diagnosis of aortoiliac disease. A reliable description of claudication in one or both legs, possibly decreased sexual potency in the man, and diminished or absent femoral pulses defines the characteristic triad often referred to as the Leriche syndrome. It should be remembered, however, that clinical grading of femoral pulses may sometimes be inaccurate, particularly in obese patients or in patients with groins scarred from previous surgery (22,23). Although proximal claudication symptoms in the distribution of thigh, hip, and buttock musculature are usually reliable indicators of clinically important inflow disease, a significant number of patients with aortoiliac disease will nonetheless complain only of calf claudication, particularly those with multilevel disease (24). Audible bruits may frequently be appreciated over the lower abdomen or femoral vessels with a stethoscope, particularly after exercise. Elevation pallor, rubor on dependency, shiny atrophic skin in the distal limbs and feet, and possible areas of ulceration or ischemic necrosis or gangrene may be noted, depending upon the extent of atherosclerotic impairment. In some instances, however, the diagnosis of aortoiliac occlusive disease may not be readily apparent, and pitfalls may exist in terms of certain complaints that may cause diagnostic confusion. In some cases, pulse evaluation and appearance of the feet may be judged entirely normal at rest, despite the presence of proximal stenoses that are physiologically significant with exercise. This is also often the case in patients presenting with distal microemboli secondary to atheroembolism, the so-called blue toe syndrome (25,26). In other instances, complaints of exercise-related pain in the leg, hip, buttock, or even low back may be mistaken for symptoms of degenerative hip or spine stenosis, diabetic neuropathy, or other neuromuscular problems. Many such patients may be distinguished from patients with true claudication by the fact that their discomfort is often relieved only by sitting or lying down, as opposed to simply stopping walking. In addition, the typical sciatic distribution of the pain and the fact that often their complaints are brought on by simply standing, as opposed to walking a certain distance, suggest nonvascular causes. However, in many such in-

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stances use of one or more noninvasive laboratory testing modalities may be extremely valuable (27,28). Use of noninvasive studies not only improves diagnostic accuracy, but also allows physiologic quantification of the severity of the disease process. This may be of considerable clinical benefit, for instance in establishing the likelihood of lesion healing without revascularization, or differentiating neuropathic foot pain from true ischemic rest pain. Noninvasive studies may also serve as a reliable and objective baseline by which to follow patients’ courses, and finally may often help in localization of the disease process. Doppler segmental limb systolic blood pressure measurements and pulse volume recordings before and after exercise have been found useful by most vascular laboratories (27,29). In some centers, duplex scanning has been utilized in recent years to evaluate patients with suspected aortoiliac disease (30). Such studies may help in establishing a diagnosis, localizing disease, and aid in determining its hemodynamic importance, but have not yet been widely utilized.

Arteriography If the patient’s symptoms and clinical findings indicate sufficient disability or threat to limb survival, angiography is the next step. It should be emphasized that arteriography is rarely used in a truly diagnostic sense; the presence or absence of occlusive disease as a cause of the patient’s symptoms can almost always be reliably established by clinical evaluation supplemented by noninvasive vascular laboratory studies before and after exercise. Rather, angiography is employed for the anatomic information it provides the surgeon in selecting and planning an operative procedure. On occasion, the angiogram may be the final bit of data involved in a decision whether or not to proceed with operation, or in other instances it may be employed to determine if occlusive disease is amenable for percutaneous transluminal balloon angioplasty. Neither of these is “diagnostic” in the usual sense of the word. In addition to noting the actual anatomic distribution of occlusive disease in the aortoiliac segment and distal vessels, the surgeon should examine the films for potentially helpful, or in some instances critical, anatomic variations or associated occlusive lesions in the renal, visceral, or runoff vessels. For example, an enlarged meandering left colic artery (Fig. 40.3) may often be an indicator of associated occlusive disease in the superior mesenteric artery, which can usually be appreciated only on a lateral view. Failure to recognize this may lead to catastrophic bowel infarction if the inferior mesenteric artery is ligated at the time of aortic reconstruction (31).

Approach Our general preference is for a retrograde transfemoral approach, feasible from the less involved side in most

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the possibility of distal infrapopliteal bypass grafting is considered likely. In such instances, when the amount of contrast material reaching these distal points may be significantly impaired by multilevel occlusive lesions, supplemental use of digital subtraction angiographic techniques may enhance visualization and definition of anatomy.

Imaging Alternatives

FIGURE 40.3 Aortogram demonstrating enlarged “meandering” inferior mesenteric and left colic arteries, an indicator of associated occlusive disease in the superior mesenteric or celiac axis.

patients. In patients with severe bilateral occlusive disease or total aortic occlusion, a translumbar or transaxillary route may be employed depending on the preferences of the angiographer or surgeon carrying out the study. A biplane study, providing oblique or lateral views, is highly desirable and often greatly enhances ability to determine the clinical importance of visualized lesions (22).

Extent of Study For most patients, a full and complete arteriographic survey of the entire intra-abdominal aortoiliac segment and infrainguinal runoff vessels is advisable. Even if proximal operation alone is planned, knowledge of the anatomy of runoff disease is important as it helps the surgeon anticipate the probable outcome of proximal operation alone, aids in more effective management of possible technical misadventures, and is important for future planning. Only by such complete studies will unusual but highly important variations in the occlusive process, which may critically affect the conduct and outcome of operation, be detected. Some have advised that aortography is not necessary in patients with complete absence of both femoral pulses. However, currently most vascular surgeons feel that angiographic study even in these cases is important to define the exact anatomic distribution and extent of occlusive disease, and facilitate selection and conduct of an appropriate arterial reconstruction. In general. runoff views are obtained to at least the level of the midcalf. In selected patients with obviously advanced distal disease and threatened limbs, more distal views may be advisable, including views of the foot itself if

In recent years, alternative imaging techniques have been developed which in selected circumstances may replace, or be used in place of, conventional catheter contrast arteriography. As previously mentioned, duplex scanning may be employed to identify patients with likely occlusive lesions in the aortoiliac system. Such studies are generally used more for screening purposes, however, and more detailed imaging generally required before actual intervention takes place. Three-dimensional spiral (helical) contrast-enhanced computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) with gadolinium are becoming increasingly helpful as technology and software improvements occur (32,33). Although such studies still do not usually match the visual clarity, detail, and spacial resolution of a standard contrast arteriogram, they may be particularly valuable in patients with renal dysfunction or other circumstances which increase the risk of conventional catheter angiography.

Hemodynamic Assessment of Multilevel Disease While an accurate assessment of occlusive disease is possible by traditional clinical evaluation and arteriography in most patients, difficulty may exist in some patients, particularly those with multilevel occlusive disease. Assessment of the hemodynamic distribution of occlusive disease at each segmental level is of critical importance in selecting an appropriate reconstructive procedure. Many atherosclerotic lesions may be of only morphologic significance on the arteriogram, with little or no actual hemodynamic importance. In such patients, proximal reconstruction alone may fail to relieve the patient’s symptoms. Furthermore, if proximal disease is only modest in the presence of associated severe distal disease, operative correction of both segmental lesions may be required in patients with manifestations of limb-threatening ischemia. Despite a wide array of noninvasive vascular laboratory testing methods, none is entirely accurate in determining the hemodynamic importance of aortoiliac inflow lesions, particularly in the patient with multilevel disease. All appear influenced by the presence of infrainguinal occlusive disease, and abnormal results may not always be reliably attributable to the proximal lesion. Deficiencies

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

of segmental limb Doppler ultrasound pressures or pulse volume recordings are well recognized in this regard (34). Analysis of femoral artery Doppler waveforms, or calculation of a pulsatility index, are also of uncertain accuracy in the presence of multisegment disease (22,35). Reliance upon the morphologic appearance of lesions on arteriograms also carries known hazards. There is marked observer variability associated with the interpretation of the functional importance of arterial lesions visualized on arteriograms (36). In addition, although the relation of a simple arterial stenosis and hemodynamic impairment is well documented, the multiplicity and complexity of lesions occurring in the aortoiliac system makes hemodynamic assessment based upon morphology alone often inaccurate (37). Some investigators have suggested use of duplex scanning for diagnostic evaluation, anatomic localization, and hemodynamic assessment of lower extremity occlusive disease (30). However, such examinations are time-consuming, require very experienced technicians, and may not successfully image all arterial segments. In addition, conclusive velocity criteria for hemodynamically significant iliac disease have not been firmly established to date. All of these factors currently limit the applicability of duplex scanning in the evaluation of aortoiliac disease. In such instances, actual measurement of femoral artery pressure (FAP) may be of considerable value (22,38–40). FAP measurements are usually obtainable in the arteriographic suite at the time of transfemoral

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catheter aortography. Separate arterial puncture by a relatively small-caliber (22-gauge) needle may occasionally be required if pressure determinations are needed in the femoral artery contralateral to the angiographic catheter insertion site. As illustrated in Figure 40.4, peak systolic pressure in the femoral artery is compared with distal aortic or brachial systolic pressure. A resting systolic pressure difference greater than 5 mmHg or a fall in PAP greater than 15%, with reactive hyperemia induced pharmacologically or by inflation of an occluding thigh cuff for 3 to 5 minutes, implies hemodynamically significant inflow disease. If revascularization is indicated in such patients, attention should be directed at correction of the inflow lesions. With a negative study, the surgeon may more confidently proceed directly with distal revascularization without fear of premature compromise or closure of a distal graft, and without subjecting the patient to an unnecessary inflow operation (41). Based upon such criteria, selection of patients for an inflow procedure is greatly facilitated and benefit accurately predicted. In our most recent review, 96% of patients with positive results of FAP studies had satisfactory clinical improvement in ischemic symptoms with proximal arterial reconstruction alone, despite uncorrected distal disease in the majority of patients. In contrast, 57% of patients undergoing proximal operation despite a normal FAP result experienced unsatisfactory relief of symptoms and required subsequent distal procedures (24). Other investigators have reported similar results using pressure determinations (42,43).

FIGURE 40.4 Femoral artery pressure (FAP) study, an accurate means of assessing the hemodynamic importance of aortoiliac occlusive lesions. A significant fall in peak systolic femoral pressure is demonstrated across the left iliac arterial segment (arrow).

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Indications for Operation Ischemic pain at rest or actual tissue necrosis, including ischemic ulcerations or frank gangrene, are well accepted as indicative of advanced ischemia and threatened limb loss. If untreated, most such patients will progress and require major amputation. Because of this, all surgeons agree that these symptoms are clear-cut indications for arterial reconstruction, if anatomically feasible. Age per se is rarely an important consideration. Even elderly, frail, or patients at high risk from multiple associated medical problems may generally be revascularized by alternative methods or balloon angioplasty if direct aortoiliac reconstruction is deemed inadvisable. Some disagreement remains concerning the advisability of operation for claudication symptoms alone. Such decisions must be individualized, with considerations of age, associated medical disease, employment requirements, and lifestyle preferences in each patient. In general, claudication that jeopardizes the livelihood of a patient or significantly impairs the desired lifestyle of an otherwise low-risk patient may be considered a reasonable indication for surgical correction, assuming that a favorable anatomic situation for operation exists. It is usually advisable for the surgeon to have followed such a patient conservatively for a while, and to have thoroughly discussed the merits and possible risks of any surgical procedure. The patient should have demonstrated commitment to the therapeutic program by control of appropriate risk factors, most importantly elimination of cigarette smoking and appropriate weight reduction, when required, by compliance with a low-fat, low-calorie diet. In general, most surgeons are more liberal in recommending surgical operation for patients with claudication alone if symptoms can be attributed to isolated proximal inflow disease, as opposed to more distal disease in the femoropopliteal segment. This seems logical and appropriate because of the generally excellent and long-lasting results currently achieved by aortoiliac reconstruction, at low risk to the patient. Another less frequent but well-recognized indication for aortoiliac reconstruction is peripheral atheromatous emboli from proximal ulcerated atherosclerotic plaques. As already described, clinical evidence of occlusive disease in such patients may be minimal, with little to no history of claudication. Recognition of the condition and complete angiography to investigate the presence of causative proximal lesions is important, however, to avoid repetitive episodes or even limb loss. No truly effective medical treatment for aortoiliac occlusive disease is currently available. Nonoperative care is aimed at limiting disease progression, encouraging development of collateral circulation, and preventing local tissue trauma or infection in the foot. With such care, spontaneous improvement may be noted in a few patients, although slow progression of symptoms may be anticipated in most. Progression of the atheromatous process may, in some instances, be slowed by altering the patient’s risk factors. Complete cessation of cigarette smoking is

paramount in this regard, and cannot be overemphasized to the patient. Weight reduction, treatment of hypertension, correction of abnormal serum lipid levels, and regulation of diabetes all seem desirable and logical, although definite benefit in terms of stabilization or improvement of occlusive symptoms is less well established. A regular exercise program, often involving no more than walking a specific distance on a daily basis, seems the best stimulant to collateral circulation. Good local foot care is extremely important, as trauma and digital infection are often the precipitating causes of gangrene and amputation, particularly in the diabetic patient. While several drugs are available for the claudicating patient, none has been shown to increase the exercising muscle blood flow in the claudicating extremity, the critical requirement for a truly effective agent in the treatment of claudication. A multi-institution double-blind placebocontrolled trial of pentoxifylline (Trental) in treatment of patients with claudication showed a significant increase in walking distance compared with placebo (44), and the drug has been approved by the US Food and Drug Administration for the treatment of claudication. Similarly, in the past few years Cilostazol (Pletal) has been demonstrated to have greater efficacy in alleviating claudication symptoms and increasing walking distance (45). In my own experience, perhaps 25% of patients may find some improvement in claudication symptoms. It is often difficult to know if this is attributable to the drug, however. Although such medications may be used in patients with moderate claudication, they do not appear to have changed the eventual need for surgical revascularization in patients with very severe claudication, resting ischemia, or more advanced symptoms. The role of percutaneous transluminal angioplasty (PTA) or stenting is discussed more fully in Chapters 18 and 19. Such catheter-based therapies may be a valuable treatment modality in properly selected patients with aortoiliac occlusive disease. However, patient selection is of paramount importance. To be appropriate for PTA or stenting, the lesion should be relatively localized, and preferably a stenosis rather than a total occlusion. A localized stenosis of the common iliac artery less than 5 cm in length is the most favorable situation for PTA, with excellent early and late patency rates (46,47). Such a situation may exist in 10% to 15% of patients with aortoiliac disease coming to arteriographic study (48). PTA is generally not recommended for patients with diffuse iliac disease, unless they are extraordinarily poor surgical candidates, or for totally occluded iliac arteries because of the higher incidence of complications or recurrent occlusion (47). Alternatives for revascularization in high-risk patients with such situations unfavorable to PTA almost always exist.

Surgical Treatment Currently, methods of direct aortoiliac reconstruction offer the most definitive and durable means of surgical

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

revascularization. Most often, aortofemoral bypass grafting is utilized, while in a limited number of cases aortoiliac endarterectomy may be feasible. Remote or “extra-anatomic” procedures are reserved for the limited number of truly high-risk patients unable to tolerate conventional anatomic reconstruction, or in circumstances of infection or other technical problems that may hamper standard direct operation. Such procedures are discussed more fully in Chapter 51. What is evident is that a variety of inflow procedures are available to the surgeon. The proper choice of operation depends upon the general condition of the patient, the extent and distribution of atherosclerotic disease, and the experience and training of the surgeon (49).

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allowed identification of a low-risk subset of patients, in whom no further evaluation or intensive intraoperative monitoring appears warranted. In contrast, a subset of high-risk patients can be identified, who often deserve preoperative coronary angiography and possible myocardial revascularization prior to their aortic operation. Alternatively, in high-risk cardiac patients it may be prudent to choose methods of revascularization other than direct aortic grafting, or operation may be deferred entirely unless limb-threatening indications exist.

Direct Operative Procedures Aortoiliac Endarterectomy

Preoperative Preparation In addition to angiographic assessment, evaluation of associated cardiac, renal, and pulmonary disease is routine. Any correctable deficiencies are best identified prior to operation, and appropriately treated. For instance, patients with compromised pulmonary reserve may benefit from a period of preoperative chest physiotherapy, bronchodilator medication, appropriate antibiotic treatment, etc. Diminished renal function also requires evaluation, with correction of any prerenal component due to dehydration, or treatment of other reversible deficiencies. Similarly, cardiac abnormalities demonstrated by clinical evaluation or electrocardiography are evaluated and treated appropriately; in many instances, consultation with a cardiologist may be helpful. Without question, the most important and controversial aspect of preoperative patient evaluation is the detection and subsequent management of associated coronary artery disease (50). Several studies have clearly documented that potentially important coronary artery disease exists in 40% or more of patients requiring peripheral vascular reconstructive procedures (51), and is quite clearly responsible for the majority of both early and late postoperative deaths. Significant coronary artery disease may be clinically “silent” in 10% to 20% of patients. However, most currently available screening methods lack sensitivity and specificity in predicting postoperative cardiac complications (50). Many patients with vascular occlusive disease cannot achieve adequate exercise stress due to claudification or infirmity. Even with coronary angiography, it is difficult to relate anatomic findings to surgical risk. In addition, coronary angiography is associated with its own inherent risks, and patients undergoing coronary artery bypass grafting or coronary angioplasty prior to needed aortoiliac reconstructions are subjected to the risks and complications of both procedures. In this regard, we and others have found use of preoperative dipyridamole–thallium 201 scintigraphy to be valuable in identifying the subset of preoperative vascular patients who may be at high risk of perioperative myocardial ischemic events and perhaps warrant more intensive preoperative evaluation, including coronary angiography and perhaps coronary bypass grafting (52–58). This has

Aortoiliac endarterectomy may be considered in the group of approximately 5% to 10% of patients with truly localized (type I) disease. Endarterectomy offers several theoretic advantages: 1. 2. 3.

4.

no prosthetic material is inserted; the infection rate is practically nonexistent; inflow to the hypogastric arteries, potentially improving sexual potency in the male, is perhaps somewhat better than with bypass procedures; finally, because the procedure is totally autogenous, and therefore more resistant to infection, it may be utilized in unusual circumstances in which reoperation in a contaminated or infected field requires innovative reconstructive methods (59).

Proper selection of patients for endarterectomy is important: disease should terminate at or just beyond the common iliac bifurcation, allowing the surgeon to achieve a satisfactory end point without extending more than 1 to 2 cm into the external iliac segment. Whether transverse or vertical arteriotomies are employed is of less importance than ensurance of a proper plane of endarterectomy at the level of the external elastic lamina and achieving a secure end point of endarterectomy, with or without the aid of tacking sutures. Primary closure of arteriotomies is generally feasible, although patch closure may occasionally be employed (Fig. 40.5). When properly performed in suitable patients, aortoiliac endarterectomy can provide excellent and durable results (12,60,61). Endarterectomy is definitely contraindicated in three circumstances: 1.

2.

Any evidence of aneurysmal change makes endarterectomy ill-advised because of possible continued aneurysmal degeneration of the endarterectomized segment in the future. If total occlusion of the aorta exists to the level of the renal arteries, simple transection of the aorta several centimeters below the renal arteries with thrombectomy of the aortic cuff followed by graft insertion is technically easier and far more expeditious.

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and few residents currently have much exposure to the procedure in their training. Therefore a bypass graft may be preferable even for localized disease if the surgeon does not have adequate experience with aortoiliac endarterectomy.

Aortofemoral Bypass Grafting

A

C

B

D

FIGURE 40.5 Aortoiliac endarterectomv. (A) Occlusive disease limited to distal aorta and common iliac arteries, with location of arteriotomies indicated by dotted lines. (B) A satisfactory endarterectomy plane is achieved, and the atheromatous material removed from the aorta from the level of the proximal clamp to the bifurcation. (C) Satisfactory end point of the endarterectomy is achieved at the iliac bifurcation, and endarterectomv continued proximally. Tacking sutures may be necessary to secure an adequate end point. (D) Closure of arteriotomies to complete procedure. See text for details.

3.

By far the most common consideration favoring bypass grafting will be extension of the disease process into the external iliac or distal vessels (types II and III). Difficulties with adequate endarterectomy of the external iliac artery as a result of its smaller size, greater length, somewhat more difficult exposure, and the more muscular and adherent medial layer are well documented, with a higher incidence of both early thrombosis and late failure as a result of recurrent stenosis.

For these reasons, extended aortoiliofemoral endarterectomy procedures have been generally abandoned and replaced by bypass grafting, which is simpler, faster, and associated with better late patency rates in patients with more extensive disease (12,62,63). In addition, aortoiliac endarterectomy is generally acknowledged to be more demanding technically than bypass procedures,

Over the past three decades, prosthetic graft insertion from the abdominal aorta just below the renal arteries to the femoral vessels in the groin has become the standard method of direct surgical repair for aortoiliac occlusive disease, being utilized in more than 90% of such patients by most vascular surgeons. Aortofemoral grafts offer the most definitive, durable, and expeditious reconstruction currently available (12,19,49,64–67). Although the technique of aortic graft insertion has been fairly well standardized, some differences in methods used do remain, and some are quite controversial (49). The proximal aortic anastomosis may be made either endto-end or end-to-side. End-to-end anastomosis is clearly indicated in patients with coexisting aneurysmal disease or complete aortic occlusion extending up to the renal arteries. Many vascular surgeons prefer it for routine use in most cases for several reasons. 1.

2.

3.

It appears more sound on a hemodynamic basis, with less turbulence, better flow characteristics, and less chance of competitive flow with still patent host iliac vessels. Such considerations have led to considerably better long-term patency of grafts done with end-to-end proximal anastomosis in some reported series (12,14,68,69), although none have been randomized prospective trials. Other studies, however, have not shown any significant difference in late patency between end-to-end and end-to-side grafts (70–73). Application of partially occluding tangential clamps for construction of an end-to-side anastomosis may often carry a higher risk of dislodging intra-aortic thrombus or debris that may then be irretrievably carried to the pelvic circulation or lower extremities. Resection of a small segment of host aorta and use of a short body of the prosthetic bifurcation graft for end-to-end anastomosis, as shown in Figure 40.6, allows the prosthesis to be placed directly in the area of the resected aortic segment, greatly facilitating subsequent tissue coverage and reperitonealization, and potentially reducing the incidence of aortoenteric fistula formation in subsequent years (12,14,70).

End-to-side anastomosis appears potentially advantageous in certain anatomic patterns of disease (Fig. 40.7). For instance, if a large aberrant renal artery arises from the lower abdominal aorta or iliac arteries, or if the surgeon wants to avoid sacrifice of a large patent inferior mesenteric artery, end-to-side proximal anastomosis pre-

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

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FIGURE 40.6 End-to-end aortofemoral graft insertion. (A) Schematic of preoperative aortogram. (B) Segment of diseased aorta resected, and distal aortic stump oversewn. (C) Completed procedure.

A

A

B

C

B

FIGURE 40.7 (A) Anatomic circumstances or patterns of occlusive disease favoring end-to-side proximal aortic anastomosis include low-lying accessory renal arteries, an enlarged patent inferior mesenteric artery, or occlusive disease confined largely to the external iliac arteries. (B) In such situations, these vessels may be preserved and flow maintained to the hypogastric arterial network by use of end-to-side graft implantation.

sumably will allow preservation of such vessels. Alternatively, they may be preserved by reimplantation into the body of the graft if end-to-end insertion is preferred. Most importantly, end-to-side anastomosis appears advisable if the occlusive process is located principally in the external iliac vessels. In such instances, interruption of the infrarenal aorta for end-to-end bypass to the femoral level effectively devascularizes the pelvic region, as no retrograde flow up the iliac arteries can be anticipated. This

may increase the incidence of erectile impotence in the sexually potent male (74,75). Such hemodynamic consequences may also increase the incidence of postoperative colon ischemia, severe buttock ischemia, or even paraplegia secondary to spinal cord ischemia (31,76,77). Troublesome hip claudication may also continue to plague the patient despite the presence of excellent femoral and distal pulses. Finally, should the limb of the graft occlude in later years, the resulting limb ischemia may be particularly severe and lead to difficulty with healing of even above-knee amputation should further revascularization not prove feasible. For these reasons, the surgeon may elect to use end-to-side proximal anastomosis in the anatomic circumstances described. At present, one can only conclude that this area is controversial, and both methods have experienced and highly skilled vascular surgeons as advocates (49). Irrespective of the method of proximal anastomosis, the principle of placing the proximal anastomosis high in the infrarenal abdominal aorta, relatively close to the renal arteries in an area almost always less involved with the occlusive process, is of paramount importance to minimize later recurrent difficulties. Although the distal anastomosis of the aortic graft may on occasion be accomplished at the level of the external iliac artery in the pelvis, it is almost always preferable to carry the graft to the femoral level, where exposure is generally better and anastomosis easier from a technical standpoint. With adequate personnel, both femoral anastomoses may often be done simultaneously. Most importantly, anastomosis at the femoral level provides the surgeon an opportunity to ensure adequate outflow into the profunda femoris artery. Experience has clearly demonstrated an increased late failure rate of aortoexternal iliac grafts, with a higher incidence of subsequent “downstream” operations as a result of progressive disease at or just beyond the iliac anastomosis (12,63,78). With meticulous surgical technique, proper skin prepara-

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tion and draping, and a limited period of prophylactic antibiotic coverage, the anticipated higher incidence of infection if grafts were extended into the groin has not been borne out by extensive experience (12,19,62,64–67). The importance of establishing adequate graft outflow at the level of the femoral artery anastomosis, usually via the profunda femoris artery in patients with disease or occlusion of the superficial femoral, has clearly emerged in early and late graft results (12,64,79,80). For these reasons, it is imperative that any lesion that might compromise profunda flow be carefully evaluated and corrected at the time of distal anastomosis. Preoperative arteriography should visualize the profunda orifice, particularly when occlusion of the superficial femoral artery is demonstrated. This is usually accomplished by oblique views of the groin. At operation, the surgeon must search for possible profunda origin stenosis by palpation, gentle passage of vascular probes, or direct inspection. If any stenosis of the profunda origin exists, it should be corrected by endarterectomy or patch angioplasty techniques. Our own preference is for extension of the arteriotomy down the profunda beyond the orifice stenosis, with subsequent anastomosis of the beveled tip of the graft as a patch closure (Fig. 40.8). This achieves hemodynamic correction and is preferable in most instances to formal endarterectomy, which we believe may lead to a higher incidence of late false aneurysm formation when the prosthetic graft is sutured to the endarterectomized arterial wall. Endarterectomy of the profunda will be required, however, if the vessel is heavily diseased. Others have pre-

A

B

FIGURE 40.8 (A) In patients with associated occlusion of the superficial femoral artery, graft runoff may be seriously impaired by associated occlusive disease at the profunda orifice. (B) Extension of common femoral arteriotomv into the proximal profunda, beyond significant occlusive disease, with anastomosis of tapered graft tip achieves patch angioplasty of profunda orifice. Improved outflow is associated with better long-term patency.

ferred to utilize autogenous arterial or saphenous vein patches for separate profundaplasty, then anastomosing the prosthesis to the common femoral artery above this. In any case, it is imperative that the surgeon use precise anastomotic technique at the end point of the profundaplasty to ensure an adequate profunda outflow tract. Some have suggested that the mere existence of an occluded superficial femoral artery in itself causes a “functional” stenosis even without any actual occlusive disease in the profunda itself (81). Most evidence suggests that this is not the case, however, and “routine” profundaplasty in all patients with a superficial femoral artery occlusion does not improve the hemodynamic result or late patency of inflow grafts unless profunda disease is in fact present and relieved (49,71). Use of a graft of appropriate size is clearly important (82,83); previously, many surgeons employed grafts too large in comparison to the size of outflow tract vessels, tending to promote sluggish flow in graft limbs and deposition of excessive laminar pseudointima in the prosthesis. This, in turn, may often have a propensity to later fragmentation or dislodgment, leading to occlusion of one or both limbs of the graft. For occlusive disease, a bifurcated graft 16 ¥ 8 mm is most often employed, with no hesitation to use a prosthesis 14 ¥ 7 mm or even smaller when appropriate, as is the case in some female patients. The limb size of such grafts will most closely approximate the femoral arteries of patients with occlusive disease, or more particularly the size of the profunda femoris, which often remains as the only outflow tract. In addition, it is now well recognized that many Dacron prosthetic grafts have a tendency to dilate 10% to 20% when subjected to arterial pressure (84). Selection of a smaller graft size will help compensate for this. Most surgeons continue to employ standard Dacron prostheses for direct aortic reconstruction. Knitted grafts are often preferred because of their desirable handling characteristics, but they have the disadvantages of need for preclotting and a greater propensity to possible late caliber dilatation. Stiffer low-porosity woven grafts have been considered by many surgeons to be inferior for reconstructions that must cross the inguinal ligament, but little if any factual data exists to support this bias. Many currently available, somewhat higher-porosity, woven grafts have good flexibility and suturability, and are easier to preclot. In recent years, grafts with various biologic coatings (collagen, albumin, gelatin, etc.) have been used with increasing frequency. The attractive feature of such grafts is the convenience of their zero implant porosity with no requirement for preclotting. They are more expensive, however, and no other long-term advantage has yet been established. Similarly, polytetrafluoroethylene (PTFE) aortic bifurcation grafts are impermeable, and have been improved in terms of handling characteristics. Some investigators feel that PTFE grafts have other possible advantages such as resistance to infection, less platelet adherence, and ease of thrombectomy (85,86). One may conclude that currently no single large-caliber prosthetic

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

graft is clearly superior and that long-term patency is more closely related to proper technical implantation and control of risk factors and disease progression than to the specific graft employed.

The Operative Procedure On the morning of surgery, preoperative antibiotics are administered along with other “on-call” medications before bringing the patient to the operating room. Broadspectrum antibiotics appear to be beneficial in instances of prosthetic vascular reconstruction (87–89). These are routinely continued for 24 to 48 hours postoperatively. On arrival in the operating room, appropriate intravenous lines and other anesthetic monitoring devices are secured. It is important that the vascular anesthetist be fully aware of the patient’s overall condition, and in particular associated vascular disease in coronary, carotid, or renal arteries that may influence intraoperative management. Intra-arterial radial artery catheter blood pressure monitoring is virtually routine for aortic reconstruction, with pulmonary artery Swan–Ganz catheter insertion utilized, at the discretion of the anesthesiologist, when the patient has potential cardiovascular instability, or when fluid shifts and blood pressure swings may present particular hazard. Liberal crystalloid intravenous fluids are administered during induction of anesthesia, as guided by the available monitoring lines, to ensure adequate vascular volume and promote good urine output. The patient is placed supine on the operating room table, and wide preparation and draping are carried out. In cases of isolated aortoiliac occlusive disease, the surgical field need not extend below the upper thigh, but in most instances it is advisable to prepare both legs to the ankles in the event of unsatisfactory results or technical misadventures that may require more distal arterial exploration or reconstruction. Because of our preference for intraoperative monitoring with a segmental plethysmograph, unsterile cuffs are placed at the calf or ankle level, and draped out of the operative field (90). If more distal sterile preparation is necessary, sterile intraoperative cuffs are utilized for preoperative baseline recordings. Both femoral arteries are first exposed, often simultaneously if experienced surgical assistants are available. Each common femoral artery is exposed from the inguinal ligament to 1 to 2 cm beyond its bifurcation, with separate control of both superficial femoral and deep femoral branches. At this time, the surgeon can review the preoperative arteriograms and combine this information with careful palpation of the femoral vessels, with particular attention to detect disease at the origin or proximal portion of the deep femoral artery. This is particularly important, of course, in patients with preexistent superficial femoral artery occlusion, in whom the profunda femoris must function as the principal outflow tract of the graft. The inguinal ligament is then partially divided to create space for comfortable passage of the graft. The lateral cir-

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cumflex iliac vein, crossing anterior to the distal external iliac artery, is often visualized and may be divided if this will interfere, or be traumatized, at the time of graft tunneling from the abdomen. At the conclusion of groin dissection, a moist sponge is placed in the groin wounds and self-retaining retractors are removed. The abdomen is then opened, generally employing a midline incision from xyphoid to within several centimeters of the symphysis pubis. The abdomen is explored, transverse colon elevated out of the wound, and the small bowel gathered and covered with a moist towel. This is then retracted to the right upper quadrant, either inside or outside the abdominal cavity. Use of large appropriately designed self-retaining retractors may facilitate exposure and reduce requirements for additional surgical or nursing personnel whose sole requirement is holding retractors. The importance of an adequate incision, and proper exposure, cannot be overemphasized. The retroperitoneum is then opened over the midinfrarenal abdominal aorta, between the duodenum and the inferior mesenteric vein. This will usually reveal the origin of the inferior mesenteric artery. Dissection is then continued slightly to the right, along the anterior wall of the aorta until the crossing left renal vein is identified. Distally, the retroperitoneum is opened over the right side of the aorta to approximately the level of the aortic bifurcation, to allow retroperitoneal tunneling to each groin incision. Dissection should be minimized in this region so as to spare the autonomic nerve fibers, which cross the aortic bifurcation and proximal iliac vessels in this region (75,91). Retroperitoneal tunnels to each groin incision are then constructed by blunt finger dissection from both incisions. This is usually most easily accomplished by gaining access to the avascular plane immediately anterior and just lateral to the common iliac arteries. It is important that the surgeon maintain this avascular plane immediately adjacent to the iliac artery, to ensure passage of the prosthetic graft posterior to the ureter in order to minimize the chance of ureteral compression or obstruction by the graft limb or later fibrotic reaction. A long clamp is then passed from the groin to meet the surgeon’s dissecting finger above, and advanced into the abdomen to complete creation of the tunnel. A Penrose drain is then grasped and drawn back through the tunnel, to facilitate later passage of the graft. On the left side, the presence of the sigmoid colon and mesocolon may make tunneling more difficult, and occasionally it is safer and easier to develop the tunnel in two stages, using a retroperitoneal incision in the left iliac fossa. If adjunctive lumbar sympathectomy is planned, this is carried out next, removing 5 to 10 cm of lumbar sympathetic chain on each side, usually encompassing the third and fourth lumbar sympathetic ganglia. If elected, this is best carried out before systemic heparinization. At this point, the surgeon must decide between endto-end and end-to-side proximal anastomosis, based on the criteria previously described. Final decisions in this re-

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 40.9 Use of interrupted mattress suture technique for proximal aortic anastomosis. (A) Double-armed suture is passed from graft to host aorta. (B) Posterior row of five such sutures is completed and tied over pledgets of Teflon felt. (C and D) Graft is then directed toward patient’s feet, and similar row of five anterior mattress sutures tied to complete the anastomosis.

gard are often made at the time of operation, however, when unexpected findings of aneurysmal change in the aorta, or more advanced disease or calcification of the anterior aortic wall than had been anticipated, render end-to-side anastomosis more difficult and less desirable. Unless special circumstances indicate the advisability of preserving the inferior mesenteric artery, this is then routinely divided flush with its origin from the aorta. This usually facilitates further exposure, graft insertion, and tunneling of the graft to the groins. If the inferior mesenteric artery needs be preserved, this is accomplished by either use of end-to-side proximal anastomosis above this vessel, or preservation of a button of aortic wall around its orifice for later reimplantation into the graft if an end-toend proximal anastomosis is utilized. Before systemic heparinization, an appropriately sized graft is selected, and if necessary preclotted with unheparinized blood. The patient is then systemically heparinized by the anesthesiologist, with 5000 to 7500 units of heparin being administered via a reliable intravenous line. After several minutes, to allow systemic circulation of heparin, the femoral arteries are gently occluded with bulldog clamps, to minimize chances of distal atheromatous embolization at the time of aortic clamp application. The proximal aortic clamp is then placed as close to the renal arteries as feasible. In general, this will be at the level of the crossing left renal vein, but occasionally the superior extent of the occlusive disease of calcification will require mobilization of the left renal vein and cephalad retraction, or even division, to allow placement of the proximal clamp immediately at the level of the renal arteries. The surgeon may or may not choose to first gain circumferential control of the aorta at the chosen level of proximal clamp application, with passage of a tape or rubber catheter. It is my general practice to do so unless this would be unusually difficult or hazardous due to extensive inflammatory reaction, prior surgery, or similar considerations. Distally, the aorta is occluded several centimeters above the aortic bifurcation by an angled vascular clamp. A segment of aorta 2 to 3 cm is then removed between the clamps if end-to-end anastomosis has been elected, as

A

B

FIGURE 40.10 (A) Aortic cuff endarterectomy. If thrombus, occlusive disease, or calcification is present in the stump of the divided aorta below the aortic clamp, thromboendarterectomy up to the proximal clamp (B) can facilitate construction of the aortograft anastomosis. (Reproduced by permission from Brewster DC. Technical features to simplify or improve aortofemoral or aortoiliac reconstructions. In: Veith RJ, ed. Current critical problems in vascular surgery, vol 5. St Louis: Quality Medical Publishing, 1993:278–289.)

is my preferred method (Fig. 40.6). Several pairs of lumbar arteries posteriorly will need to be divided and oversewn or occluded with metal clips. This segment is resected to within 1 to 2 cm of the proximal clamp. The distal cuff is then oversewn and the distal clamp removed. Proximal end-to-end anastomosis is then carried out to the cuff of aorta below the proximal clamp, with a running Prolene suture, or an interrupted mattress suture technique if the aorta is particularly diseased, fragile, or otherwise less well suited to a continuous suture technique (Fig. 40.9). Not infrequently, significant atheromatous disease and thickening will exist in the proximal cuff even if one is close to the renal arteries, and endarterectomy to the level of the proximal clamp is advisable to facilitate proximal anastomosis (Fig. 40.10). Because the remaining aortic wall below the clamp is then quite thin, I

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

believe use of interrupted mattress sutures, backed with Teflon pledgets, is definitely advisable. Upon completion of the anastomosis, the proximal graft limbs are occluded and the proximal clamp released, testing the hemostatic security of the anastomosis and further preclotting the graft. The proximal clamp is then reapplied, blood is evacuated from both limbs of the prosthesis, and the graft is withdrawn through the previously created retroperitoneal tunnels to each groin. If an end-to-side aortic anastomosis is preferred, this may be performed with use of partially occluding tangential clamps, or by total occlusion of the aorta by two clamps above and below the proposed level of anastomosis. I believe the latter method is usually preferable, facilitating creation of the anastomosis and, perhaps more importantly, evacuation of thrombotic material from this region. End-to-side anastomosis to each femoral artery is then performed. In the absence of significant disease in the superficial or deep femoral arteries, this is readily accomplished to each common femoral artery after creation of an arteriotomy approximately 2 cm in length. If the superficial femoral artery is occluded, and particularly if disease is palpated at the origin of the deep femoral artery, the arteriotomy is extended obliquely across the profunda and into the proximal aspect of this vessel, with the graft hood then sutured across this, as illustrated in Figure 40.8. If more extensive profunda disease exists, a separate profundaplasty may be required rather than an excessively long anastomosis of the beveled graft tip. The surgeon should ensure that appropriate tension is placed upon the graft limb prior to cutting it to a suitable length; excessive tension will increase the likelihood of later anastomotic aneurysm formation, while excessive redundancy may lead to kinking and subsequent occlusion of the limb. If adequate experienced surgical assistants are available, both femoral anastomoses can be accomplished simultaneously. Prior to completion of each anastomosis, the limb is first flushed in antegrade fashion, and then proximal and distal host arteries are backbled and probed. Upon completion of the anastomosis, distal clamps are left in place, and blood flow is restored in a retrograde fashion first. Subsequently, deep femoral and finally superficial femoral clamps are removed. If feasible, some means of ensuring adequate distal flow intraoperatively is advisable. It is our custom to obtain pulse volume recordings at this juncture to assess this (90). Some surgeons prefer to prepare and drape the feet in transparent bags to allow visualization of their color and appearance, but this is often a more subjective and uncertain method. Alternatively, distal Doppler pressures, or electromagnetic flow measurements through the opened graft limb may contribute information for this judgment. Once the surgeon is assured of a satisfactory technical result on both sides, protamine is administered and hemostasis secured. Closure of the retroperitoneum over the graft is next accomplished, ensuring complete coverage of the prosthe-

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sis and separation from the duodenum. This is greatly facilitated if end-to-end anastomosis has been utilized with a short body of the prosthetic graft, allowing this to sit in the bed of the resected aorta and avoiding the forward bulge that inevitably accompanies end-to-side construction. The groin wounds are carefully closed in at least two layers. Meticulous attention to groin closure cannot be overemphasized, in order to minimize chances of poor wound healing or breakdown, with the possible dreaded complication of graft infection.

Special Considerations Adjunctive Lumbar Sympathectomy The use of a concomitant lumbar sympathectomy at the time of aortic reconstruction remains unsettled and controversial. Although it is well accepted that sympathectomy does increase skin and total limb blood flow, there are few objective data to document more favorable longterm graft patency or improved limb salvage results (92,93). However, evidence does suggest that decreased pedal vasomotor tone and increased skin perfusion may be helpful as an adjunct to revascularization, particularly in patients with uncorrected distal disease and small superficial areas of toe or foot ischemic necrosis (92,94,95). Therefore, in such circumstances, limited (L2–3) lumbar sympathectomy may be helpful in conjunction with aortic reconstruction. This is easily and quickly accomplished and possibly beneficial to the patient with multilevel disease or limb-threatening ischemia.

The Totally Occluded Aorta Approximately 8% of our patients undergoing operation for aortoiliac occlusive disease have a totally occluded aorta (96). In about one-half, the occlusion has extended retrograde to the level of the renal arteries; in the remainder, the occlusion has involved only the distal infrarenal aorta, the proximal segment remaining open via runoff through a still patent inferior mesenteric artery or lumbar vessels (Fig. 40.11). Surgical management of the latter group is straightforward and similar to that for standard aortic graft insertion. With extension of the occluding thrombus to a juxtarenal level, however, the operative approach is more taxing, and possible complications are more likely, particularly those complications involving disturbance of renal function (96–98). Some surgeons feel that patients with juxtarenal complete aortic occlusion should undergo operation even if lower extremity ischemic symptoms are relatively mild, because of the potential for more proximal propagation of thrombus leading to compromise of neighboring renal or visceral arteries. The exact incidence of this is controversial, however. Some series have suggested that it is a real danger (99), while others have concluded that such propagation of clot to obstruct the renal

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 40.11 Angiographic examples of total aortic occlusion. (A) Total occlusion extending to the mid-infrarenal aorta, with patency of proximal aorta maintained by inferior mesenteric artery and lumbar branches. (B) Juxtarenal complete aortic occlusion, with retrograde thrombosis to the level of the renal arteries.

or mesenteric circulation is quite rare unless coexistent severe renal or mesenteric stenosis is also present (100,101). In almost all patients with juxtarenal occlusion, the bulk of the actual occlusive disease lies in the distal aorta, with the proximal occlusive material composed largely of secondary thrombus. This proximal plug may almost always be removed by simple thrombectomy followed by routine graft insertion. Adequate dissection should be carried out to allow temporary control of the renal arteries to minimize chances of renal embolization at the time of juxtarenal thrombectomy. Division of the left renal vein may facilitate exposure and is a benign procedure if carried out correctly near its insertion into the vena cava, thereby preserving collateral venous drainage. The completely occluded aorta should be opened through an arteriotomy placed several centimeters below the renal arteries. The suprarenal aorta is controlled by manual pressure, or suprarenal clamping, and thrombectomv of the aortic cuff to the level of the renal arteries is carried out with a blunt clamp. This is usually terminated by aortic pressure “blowing out” a typical organized cap of thrombus representing the apex of the thrombotic occlusion. The aorta is then flushed, the renal artery bulldog clamps are removed, and an appropriate vascular clamp is applied to the now patent infrarenal cuff. Graft insertion is then carried out in the routine fashion. Formal endarterectomy is best not carried out in most circumstances, as this plane may be difficult to terminate without compromise of the renal artery origins. Simple thrombectomy at this level is preferred, and it is sufficient in almost all cases.

Reconstruction can always be accomplished using several possible alterations. First, a high end-to-end proximal anastomosis is preferred. By carrying dissection to or just above the left renal vein following its division or cephalad retraction, one often finds the aorta immediately below the renal arteries less involved and more manageable. Second, endarterectomy of a 1- to 2-cm cuff of totally transected aorta to the level of the infrarenal aortic clamp is usually possible and removes the calcification that always lies in the diseased intima and media. This greatly facilitates subsequent end-to-end graft anastomosis. Although the cuff of the endarterectomized aorta, consisting of aortic adventitia and external elastic lamina, always appears fragile, it invariably proves adequate for graft anastomosis without later difficulties with bleeding, suture line disruption, or false aneurysm formation. The surgeon must employ a tapered (not cutting-tip) needle; and the use of an interrupted mattress suture technique, each suture backed with a pledget of Teflon felt as described above (Fig. 40.9), is to be particularly recommended. Clamping of such calcified vessels may also be problematic. This may usually be accomplished just below the renal arteries, where calcification is often less severe. Clamping in an anterior-to-posterior fashion, by use of an arterial clamp applied from a lateral direction or use of a Linton–Darling tourniquet clamp, may also be helpful. Finally, in truly difficult situations, the aorta may be clamped above the renal arteries at the level of the diaphragm, or intraluminal balloon occlusion methods may be used.

The Calcified Aorta

The Small Aorta

Occasionally, dense calcification of the infrarenal aorta appears to preclude successful insertion of an aortic graft and causes the surgeon to consider abandoning the procedure. This is particularly true of end-to-side anastomosis with use of tangential, partially occluding clamps.

In approximately 5% of patients, the infrarenal aorta, iliac, and femoral vessels will be small or hypoplastic, which may make aortic reconstruction technically difficult. Actual anatomic definition of the small aorta is arbitrary. Cronenwatt et al. have defined the syndrome as

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

characterized by infrarenal aortas measuring less than 13.2 mm just below the renal vessels, or infrarenal aortas smaller than 10.3 mm just above the aortic bifurcation. Iliac and femoral vessels are typically correspondingly small, with the common femoral vessels often only about 5 mm in size (15). These patients appear to form a unique and distinct subgroup, and are frequently characterized by the “hypoplastic aorta syndrome” (16–18). Preferred surgical methods for reconstruction in patients with small vessels remain somewhat controversial; some authorities think the small size of the aorta and iliac vessels makes endarterectomy unsuitable, while others favoring bypass techniques advocate the use of end-to-side proximal aortic anastomosis to avoid size discrepancies with the usual prosthetic grafts. In our experience, because the disease in such patients is frequently localized, aortoiliac endarterectomy may often still be utilized. Although the small size of the vessels demands greater care and occasionally requires the use of patch closures, endarterectomy in our hands has worked well. If the disease is more diffuse, bypass grafting to the femoral vessels is preferred. Although end-to-side anastomosis is favored by many surgeons to overcome size differences of graft and host aorta, we nonetheless still use end-to-end techniques most often. A smaller prosthesis should be chosen to avoid the consequences of inappropriately large grafts. In most cases, this will require the use of a bifurcation graft 14 ¥ 7 mm or even 12 ¥ 6 mm. The limbs of such grafts, although small, will also be much more appropriate for the smaller femoral and outflow vessels of these individuals. Again, greater technical care must be exercised, but with attention to technical detail, such grafts have not failed as a result of their small size; we much prefer the insertion of such grafts to the use of oversized prostheses. Burke and colleagues have suggested better results if PTFE aortic grafts are used for patients with small aortas (85), but their data are not definitive.

Simultaneous Distal Grafting A frequent practical concern is whether or not inflow operation alone will suffice in patients with multilevel occlusive disease. As already emphasized, such diffuse combined-segment disease (type III) is the most common pattern of occlusive disease, present in from one-half to two-thirds of the patients coming to surgery (12,62, 64–67). Traditional teaching has appropriately emphasized that patients with multilevel disease will generally be satisfactorily treated by initial aortofemoral bypass grafting alone, as long as good flow into the deep femoral system is established. Although this is indeed correct in most patients, prior reports have indicated that up to one-third of such patients who are treated by initial aortic reconstruction may fail to achieve adequate relief of ischemic symptoms with proximal operation alone (20,24,64,68, 71,102–106). Analysis depends somewhat, of course, on

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how much improvement is considered adequate or satisfactory for the procedure to be considered clinically successful. For instance, in our review, claudication symptoms were lessened in more than 80% of patients with multilevel disease by aortofemoral grafts, but only 35% were totally relieved of claudication (24). Some of these patients may feel disappointed at the outcome of the operation. Many patients with such unsatisfactory outcomes require subsequent distal bypass grafts. If this were known in advance, it would be easier and logical in many such patients to perform the distal graft at the same time as initial aortic operation. Identification of patients most likely to have insufficient relief of ischemic symptoms with an inflow procedure alone remains difficult, however. In this regard, we reviewed a 6-year experience with 181 patients with multilevel disease undergoing aortofemoral grafting (24). A well-performed inflow procedure will usually suffice if unequivocally severe proximal disease exists in the aortoiliac segment. Such clear-cut proximal disease is best identified by the findings of an absent or clearly reduced femoral pulse and obvious severe aortic or iliac disease on angiography, and it is confirmed, if necessary, by a positive femoral artery pressure study. Several intraoperative criteria may also be used. Restoration of an improved pressure–volume recording at the calf or ankle, compared with preoperative tracings, can give reassurance of satisfactory improvement in distal circulation. However, improvement of pressure–volume recordings or Doppler ankle pressures may not be immediately apparent in the presence of significant distal disease, especially in the cold, vasoconstricted limb. Another useful intraoperative guide in predicting a good clinical response is assessment of the anatomic size of the profunda femoris vessel itself. If the proximal profunda accepts a 4-mm probe, and if a No. 3 Fogarty embolectomy catheter can be passed for a distance of 20 cm or more, it is likely that the profunda femoris artery is well developed and will function satisfactorily as an outflow tract and collateral source. Possible benefits of simultaneous grafting include a more total correction of extremity ischemia and avoidance of the difficulties and potential complications associated with reoperation in the groin should later distal grafting prove necessary. Such advantages are usually outweighed by the greater magnitude of the synchronous two-level grafting and the fact that the majority of properly selected patients will benefit from proximal operation alone (76% in our series). Distal bypass may be carried out in the future, if necessary; it was required in 17% of the patients in our series followed up to 6 years (24). Such a figure is in agreement with previously reported experience (62,65,68,78,107). In some carefully selected patients with multilevel disease, synchronous proximal and distal reconstruction does seem appropriate (108). Combined procedures should be restricted to a relatively small group of patients, many of whom have advanced limb-threatening ischemic

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problems in the foot. Typically, such patients have only modest proximal disease, and because of the need for restoration of maximal flow to the foot due to significant distal disease, simultaneous reconstruction is elected. If the surgeon can reliably predict that a distal graft will almost certainly be necessary in the future for limb salvage, we believe simultaneous grafting is to be preferred, offering the best chance of limb salvage and avoiding a more demanding reoperation in the groin at a later time (108–111). Certainly the use of two surgical teams can minimize the additional operative time required, and in current practice the morbidity of synchronous reconstruction is not significantly increased (109). Although some success has been claimed with preoperative noninvasive hemodynamic studies in selecting such patients (24,108,112,113), other investigators have found tests of this type unreliable indicators of the need for concomitant distal bypass (71,78,102). Good clinical judgment remains extremely important, with reasoned and pragmatic decisions usually required.

Unilateral Iliac Disease Not infrequently, proximal occlusive disease may appear unilaterally, with fairly normal pulses and minimal to no symptoms in the contralateral extremity. Truly unilateral iliac disease is relatively infrequent, as the occlusive process is generally a more diffuse and eventually bilateral involvement. Progression of disease in the aorta of untreated contralateral iliac artery will necessitate later reoperation in some patients treated initially with unilateral operations for apparent one-sided disease, although the frequency of this occurrence remains controversial (63,114–116). Thus, the most definitive and optimal longterm management for most patients is bilateral reconstruction with a bifurcated prosthetic graft (117). For these reasons, most vascular surgeons have abandoned use of unilateral aortofemoral grafts. In our own experience, unilateral grafts were performed in 15% of patients undergoing proximal operation from 1963 through 1969, whereas only 4% of patients had such procedures from 1970 through 1978 (12). They are rarely performed today. In patients with a well-preserved aorta and contralateral iliac artery, femorofemoral grafts have become increasingly important, due to the ease of the procedure and the generally good long-term results (118,119). In certain instances, however; the surgeon may want to avoid the contralateral groin and confine reconstructive efforts to the ischemic side. For instance, the contralateral limb may be asymptomatic but inflow in the proposed donor limb of questionable reliability, and the patient not a good risk for standard aortobifemoral grafting. In other instances, use of the contralateral groin may be relatively contraindicated due to heavy scarring from prior operative procedures, possible infection, etc. In these situations, the ipsilateral iliac artery may be quite useful as an inflow source for an iliofemoral bypass (120–122). A retroperitoneal approach through a separate lower quadrant inci-

sion (Fig. 40.12) usually provides good exposure and can be carried out with low patient morbidity. Several reports have suggested that late patency of iliofemoral grafts may be somewhat better than femorofemoral long-term results (123,124). In similar situations, retroperitoneal iliac endarterectomy may also be employed for relatively localized disease, and is readily combined with concomitant profundaplasty or simultaneous distal bypass (125). If iliac disease is focal and distal revascularization necessary, iliac PTA may be used to provide inflow for infrainguinal grafts with good long-term results (126).

Associated Renal and Visceral Artery Occlusive Lesions Because of the recognized diffuse nature of atherosclerotic occlusive disease in most patients, it is not surprising that patients requiring aortic reconstruction for symptomatic lower extremity ischemia are often found to have associated occlusive lesions involving the renal or visceral arteries. Frequently these are unsuspected and detected only at the time of preoperative angiography. The dilemma of whether or not to attempt simultaneous correction of both abdominal aortic and other aortic branch lesions is commonly encountered and difficult to resolve (127–130). In these instances, each case must be considered individually, and no general recommendations are feasible or appropriate. Although theoretically appealing, it is clear that extending aortic reconstruction to include renal artery revascularization increases the complexity and magnitude of the operation, and hence is associated almost invariably with some increased morbidity and mortality (127,131). For these reasons, truly prophylactic revascularizations should generally be avoided. However, the natural history of renal artery stenoses associated with aortic disease indicates progression in more than 50% of patients, and approximately 10% go on to total occlusion and loss of functioning renal mass (128). Hence, functionally significant or severe preocclusive renal lesions should often be considered for simultaneous repair at the time of aortic reconstruction (127–129,132–134). If both renal and aortic lesions warrant repair but a staged correction of each lesion is preferred for a variety of reasons, the hepatic or splenic arteries are very useful for renal revascularization, preserving an unoperated field for aortic grafting (135,136). In the asymptomatic patient with visceral artery disease, careful evaluation of the anatomic pattern of disease on the preoperative arteriogram should indicate those patients at risk of postoperative intestinal ischemia if the visceral lesions are not dealt with. As emphasized by Ernst and others, avoidance of this catastrophic postoperative problem will require preservation of an important inferior mesenteric artery in those patients with celiac or superior mesenteric artery occlusive disease, or perhaps concomitant bypass grafting to the celiac or superior mesenteric artery in a small number of patients (31,130).

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

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FIGURE 40.12 Iliofemoral bypass graft, useful for unilateral iliac occlusive disease. (A) Lines of abdominal and groin incisions. (B) Retroperitoneal exposure of the distal aorta and iliac vessels, and exposure of right femoral vessels. (C) Iliofemoral bypass graft insertion being completed.

A

B

C

Results of Direct Aortoiliofemoral Reconstruction Currently, generally excellent early and late results of direct aortoiliofemoral reconstructions can be anticipated, and are achievable at highly acceptable patient morbidity and mortality rates. A consensus of several large series in the modern era clearly supports this, indicating that it is reasonable to expect approximately 85% to 90% graft patency at 5 years and 70% to 75% at 10 years (12,64–67,103). Perioperative mortality rates well under 3% are now commonplace in many centers. Mortality risk for direct reconstructions in patients with relatively localized aortoiliac disease can be expected to be extremely low, while those patients with multilevel disease and associated occlusive lesions in coronary, carotid, and visceral vessels will quite naturally have somewhat greater mortality risk. In this latter group of patients, it is hoped that continued improvement of screening methods for associated disease and continued refinements of anesthetic management, intraoperative monitoring, and postoperative intensive care can further reduce the risk of serious morbidity and mortality.

Long-term survival of these patients continues to be compromised, however. The cumulative long-term survival rate for patients undergoing aortoiliac reconstruction remains some 10 to 15 years less than that which might be anticipated for a normal population matched for sex and age. Overall, approximately 25% to 30% of patients will be dead at 5 years, and 50% to 60% at 10 years (21,65,66). Not unexpectedly, the majority of late deaths were attributable to atherosclerotic heart disease. Patients with more localized aortoiliac disease, who have a lesser incidence of coronary artery disease, distal occlusive disease, or diabetes, appear to have a much more favorable long-term prognosis, approaching that of a normal population at risk (21,103).

Postoperative Complications EarIy Complications Early complications following aortic reconstruction are largely technical and are infrequent when the procedure is carried out by an experienced surgeon and operative team

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(137). Postoperative hemorrhage severe enough to require reoperation is seen in only 1% to 2% of patients, and is usually due to failure to secure adequate hemostasis before wound closure, imprecise anastomotic techniques, inadequate reversal of intraoperative heparin, or dilutional coagulopathy associated with excessive blood loss and fluid replacement. Acute aortofemoral graft limb occlusion may occur in 1% to 3% of patients (138). Early graft thrombosis is similarly due to technical misadventures in most instances, most commonly at the femoral anastomosis of an aortofemoral graft. Occasionally, problems may be attributable to twisting or kinking of the graft limb in the retroperitoneal tunnel. Thromboembolic causes of acute limb ischemia following aortic operation are more frequent than previously recognized, but are usually treatable by prompt reoperation and use of embolectomy catheters (139,140). Truly distal atheroembolic complications, often termed “trash foot,” are difficult to deal with surgically, and are far better prevented by avoiding excessive manipulation of the aorta, use of full systemic heparinization during the procedure, careful placement of gentle vascular clamps on nondiseased portions of the vascular tree, and careful flushing of the reconstruction before restoring flow. Acute renal failure following aortic operation is now relatively uncommon after elective operation, largely due to recognition of the importance of administering adequate volumes of intravenous fluids during operation, and maintenance of optimal intravascular volume and cardiac performance by careful monitoring of filling pressures and avoidance of declamping hypotension (141–143). Acute postoperative bowel and spinal cord ischemia are more difficult to prevent but are, fortunately, relatively rare occurrences (31,76,137,144,145).

Late Complications Graft occlusion secondary to recurrent obliterative disease remains the most common late complication, reported in from 5% to 10% of patients at 5 years and 15% to 30% of patients followed 10 years or more (138, 146,147). Recurrent proximal disease extensive enough to cause failure of the entire reconstruction is unusual unless the original procedure was performed too low in the infrarenal abdominal aorta (82,137). Failure of the entire reconstruction will require another aortofemoral graft if the patient is an appropriate candidate (63), or extra-anatomic reconstruction for those patients felt to be less suitable for extensive reoperative surgery. In certain instances, the supraceliac aorta, descending thoracic aorta, or even ascending thoracic aorta may be utilized as an inflow source for such reoperations if direct reoperation on the infrarenal abdominal aorta is felt ill-advised or hazardous due to dense scarring, possible infection, etc. (148–151). Most commonly, one limb of an aortobifemoral graft will fail, with the other limb retaining patency. In most instances, thrombectomy of the

occluded graft limb can successfully restore inflow, and when combined with profundaplasty or femorodistal grafting, can maintain patency of the reoperated graft limb (138,151–154). If thrombectomy is not feasible, crossover femorofemoral grafting from the uninvolved limb is the most useful alternative. Direct aortic surgery for unilateral graft limb failure is infrequently indicated or necessary. Pseudoaneurysm formation may occur in 3% to 5% of patients, and is most often attributable to degeneration of the host arterial wall, with subsequent anastomotic dehiscence due to pulling through of the intact sutures (66,155,156). Faulty anastomotic technique or placement of the graft limb under excessive tension are contributing factors. Infection may be responsible, and must be carefully considered in each instance of anastomotic aneurysm. The great majority of anastomotic aneurysms will occur in the groin at the femoral anastomosis of an aortofemoral graft. Diagnosis in this location is readily achieved, and confirmed by angiography, which is indicated to evaluate possible occult associated pseudoaneurysm formation at the proximal aortic suture line. Reoperation is generally easily accomplished by use of a short additional segment of graft extended to a slightly more distal anastomotic site. The true incidence of intra-abdominal anastomotic aneurysms remains unknown. These were formerly thought to be infrequent, but their apparent low incidence is related in large part to difficulty in detection. The actual incidence of proximal pseudoaneurysms may be much higher than previously thought, as suggested by Edwards et al., who reported a 10% incidence at a mean follow-up interval of 12 years following initial operation (157). These data suggest that ultrasound or, more likely, computed tomography scans of the abdomen should be part of a late follow-up protocol of patients with aortic grafts. Preoperative sexual dysfunction is common in patients with aortoiliac occlusive disease, but postoperative iatrogenic impotence may occur in up to one-quarter of patients (75). Although the physiology of erection and ejaculation is complex, the incidence of sexual dysfunction may be minimized by recognition of the principles of nerve-sparing dissection, as well as maintenance of hypogastric artery and pelvic perfusion by a variety of reconstructive techniques (74,75,91,158,159). Late graft infection remains a dreaded complication, but fortunately is rare after elective aortoiliofemoral reconstruction. Prophylactic antibiotics are clearly indicated in vascular reconstructions and, together with meticulous sterile technique at the time of graft insertion, will minimize the chances of graft contamination. Once established, vascular infection will usually require removal of the prosthetic segment and revascularization via remote uncontaminated routes (160–165). Aortoenteric fistula formation is infrequent, but carries a high likelihood of death of the patient or loss of limb. Fistula formation usually involves the proximal suture line and overlying duodenum, although the small bowel

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases

and colon may less frequently be involved. Massive gastrointestinal hemorrhage almost always occurs at some point, although frequently lesser degrees of gastrointestinal bleeding occur initially, allowing time for diagnosis and management. The diagnosis may be difficult to establish, and sometimes exploration based upon a high index of suspicion is required. If present, treatment principles involve removal of the prosthetic graft, oversewing of the infrarenal aortic stump, closure of the gastrointestinal defect, and revascularization by extraanatomic means (166–169).

Conclusions Arteriosclerotic aortoiliac occlusive disease is a common cause of lower extremity ischemic symptomatology. In the majority of patients, occlusive lesions will be multifocal in nature, involving the lower abdominal aorta, both iliac arteries, and frequently the infrainguinal arterial tree. Because of such considerations, unilateral operations are infrequently performed, and most patients are best served by aortobifemoral grafting. Before proceeding with aortic reconstructive surgery, the surgeon must document the hemodynamic significance of inflow disease. This may often be accomplished by careful clinical examination, and supplemented with vascular laboratory hemodynamic data and good arteriographic studies. If any doubt remains, however, direct measurement of femoral artery pressures is helpful. Because the results of surgical reconstruction in this anatomic area are so satisfactory, operation may be considered on carefully selected patients with limiting claudication as their only symptom. More advanced limb-threatening ischemia is a clear indication for aortic reconstructions in appropriate patients. Aortoiliac endarterectomy may be utilized for a small group of patients, but, in most, aortofemoral grafting is the preferred procedure. The key features of aortofemoral grafting are high placement of the proximal anastomosis immediately distal to the renal arteries, and careful techniques of distal anastomosis, with or without profundaplasty, to achieve adequate flow into the deep femoral artery. Despite the presence of multilevel disease in the majority of patients, a properly performed inflow procedure can be expected to achieve satisfactory improvement of ischemic symptoms in 70% to 80% of cases. Approximately 10% to 15% of patients with advanced distal ischemia may be best managed with simultaneous inflow and outflow reconstructions, but careful patient selection is important. Clearly, no single option for inflow revascularization is optimal in all instances. In every patient, a decision about which method is best should be made through consideration of several factors: primary factors are the extent and distribution of disease and the anticipated risk of the possible alternatives that might be used. The likely success of various methods in terms of hemodynamic improvement, symptom relief, and sustained patency can

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usually be predicted with relative accuracy, and such estimates must be judged in the context of patient age, expected length of survival, and specific clinical needs of each patient. Durability must often be balanced against the possible advantages of safety and expediency. Alternative therapies have a well-established role in the management of occlusive disease of limited extent or lesser severity and in the treatment of patients in whom adverse technical challenges or high operative risk contraindicates conventional direct aortic reconstruction. However, for most patients with diffuse aortoiliac occlusive disease, aortobifemoral grafts remain the most durable and functionally effective means of revascularization and should continue to be rightfully regarded as the gold standard against which other options must be properly compared.

References 1. DeBakey ME, Lawrie GM, Glaeser DH. Patterns of atherosclerosis and their surgical significance. Ann Surg 1985;201:115. 2. Leriche RR, Morel A. The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg 1948; 127:193. 3. Dos Santos JC. Sur la desobstruction des thromboses arterielles anciennes. Mem Acad Chir 1947;73:409. 4. Wylie EJ. Thromboendarterectomy for arteriosclerotic thrombosis of major arteries. Surgery 1952;4.339. 5. Gross RE, Hurwitt ES, et al. Preliminary observations on the use of human artificial grafts in the treatment of certain cardiovascular defects. N Engl J Med 1948;239:578. 6. Oudot J. La greffe vasculaire dans les thromboses do carrefour aortique. Presse Med 1951;59:234. 7. Julian OD, Dye WS Jr, et al. Direct surgery of arteriosclerosis. Ann Surg 1952;136:459. 8. DeBakey ME, Creech O Jr, Cooley DA. Occlusive disease of the aorta and its treatment by resection and homograft replacement. Ann Surg 1954;140:290. 9. Voorhees AB Jr, Jaretzki A lII, Blakemore AH. Use of tubes constructed from Vinvon “N” cloth in bridging arterial defects: preliminary report. Ann Surg 1952;135: 332. 10. Edwards SW, Lyons C. Three years experience with peripheral arterial grafts of crimped nylon and teflon. Surg Gynecol Obstet 1958;107:62. 11. DeBakey ME, Cooley DA, et al. Clinical application of a new flexible knitted Dacron arterial substitute. Am Surg 1958;24:862. 12. Brewster DC, Darling RC. Optimal methods of aortoiliac reconstruction. Surgery 1978;84:739. 13. Brewster DC. Clinical and anatomic considerations for surgery in aortoiliac disease and results of surgical treatment. Circulation 1991;83 (Suppl l):42. 14. Darling RC, Brewster DC, et al. Aorto-iliac reconstruction. Surg Clin North Am 1979;59:565. 15. Cronenwett JL, Davis JT, Jr, et al. Aortoiliac occlusive disease in women. Surgery 1980;88:775. 16. DeLaurentis DA, Friedmann P, et al. Atherosclerosis and the hypoplastic aortoiliac system. Surgery 1978;83:27.

518

Part VI Chronic Arterial Occlusions of the Lower Extremities

17. Staple TW. The solitary aotroiliac lesion. Surgery 1968; 64:569. 18. Greenhalgh TM. Small aorta syndrome. In: Bergan JJ, Yao JST, eds. Surgery of the aorta and its body branches. New York: Grune & Stratton, 1979:183–190. 19. Moore WS, Cafferata HT, et al. In defense of grafts across the inguinal ligament. Ann Surg 1968;168:207. 20. Morersky DJ, Sumner DS, Strandness DL. Long-term results of reconstructive aortoiliac surgery. Am J Surg 1972;123:503. 21. Malone JM, Moore WS, Goldstone J. Life expectancy following aortofemoral arterial grafting. Surgery 1977;81:551. 22. Brewster DC, Waltman AC, et al. Femoral artery pressure measurement during aortography. Circulation 1979:60 (Suppl l):120. 23 Sobinsky KR, Borozan PG, et al. Is femoral pulse palpation accurate in assessing the hemodynamic significance of aortoiliac occlusive disease? Am J Surg 1984;148:214. 24. Brewster DC, Perler BA, et al. Aortofemoral graft for multilevel occlusive disease: predictors of success and need for distal bypass. Arch Surg 1982;117:1593. 25. Kempczinski RF. Lower extremity arterial emboli from ulcerating atherosclerotic plaques. JAMA 1979;241: 807. 26. Karmody AM, Powers FR, et al. “Blue toe” syndrome: an indication for limb salvage surgery. Arch Surg 1976;111: 1263. 27. Kempczinski RF. Clinical application of noninvasive testing in extremity arterial insufficiency. In: Kempczinski RF, Yao JST, eds. Practical noninvasive vascular diagnosis. Chicago: Year Book Medical Publishers, 1982: 343–365. 28. Goodreau JJ, Creasy JK, et al. Rational approach to the differentiation of vascular and neurogenic claudication. Surgery 1978;84:749. 29. Raines JK, Darling RC, et al. Vascular laboratory criteria for the management of peripheral vascular disease of the lower extremities. Surgery 1976:79:21. 30. Kohler TR, Nance DR, et al. Duplex scanning for diagnosis of aortoiliac and femoropopliteal disease: a prospective study. Circulation 1987;76:1074. 31. Ernst CB. Prevention of intestinal ischemia following abdominal aortic reconstruction. Surgery 1983;93: 102. 32. Cambria RP, Kaufman JA, et al. Magnetic resonance angiography in the management of lower extremity arterial occlusive disease: a prospective study. J Vasc Surg 1997; 25:30. 33. Raptopoulos V, Rosen MP, et al. Sequential helical CT angiography of aortoiliac disease. Am J Roentgenol 1996; 166:1347. 34. Rutherford RB, Lowenstein DH, Klein MF. Combining segmental systolic pressures and plethysmography to diagnose arterial occlusive disease of the legs. Am J Surg 1979;138:211. 35. Thiele BL, Bandyk DF, et al. A systematic approach to the assessment of aortoiliac disease. Arch Surg 1983;118: 477. 36. Slot HB, Strijbosch L, Greep JM. Interobserver variability in single plane aortography. Surgery 1981;90: 497.

37. Flanigan DP, Tullis JP, Streeter VL. Multiple subcritical arterial stenosis: effect on poststenotic pressure and flow. Ann Surg l977;186:663. 38. Moore WS, Hall AD. Unrecognized aortoiliac stenosis: a physiologic approach to the diagnosis. Arch Surg 1971; 103:633. 39. Brener BJ, Raines JK, et al. Measurement of systolic femoral artery pressure during reactive hyperemia: an estimate of aorto-iliac disease. Circulation 1974;49, 50 (Suppl 2):259. 40 Flanigan DP, Williams LR, et al. Hemodynamic evaluation of the aortoiliac system based on pharmacologic vasodilatation. Surgery 1983;93:709. 41. Kitka MJ, Flanigan DR, et al. Long-term follow-up of patients having infrainguinal bypass performed below stenotic but hemodynamically normal aortoiliac vessels. J Vasc Surg 1987;5:319. 42. Flanigan DP, Ryan TJ, et al. Aortofemoral or femoropopliteal revascularization? A prospective evaluation of the papaverine test. J Vasc Surg 1984;1:215. 43. Verhagen PF, Van Vroonhaven TJMV. Criteria from intra-arterial femoral pressure measurements combined with reactive hyperemia to assess the aortoiliac segment: a prospective study. Br J Surg 1984;71:706. 44. Porter JM, Cutler BS, et al. Pentoxifylline efficacy in the treatment of intermittent claudication: multicenter controlled double-blind trial with objective assessment of chronic occlusive arterial disease patients. Am Heart J 1982;104:66. 45. Dawson DL, Cutler BS, Meissner MH, et al. Cilostazol has beneficial effects in treatment of intermittent claudication: results from a multicenter, randomized, prospective, double-blind trial. Circulation 1998; 98:678. 46. Johnston KW, Rae M, et al. Five-year results of a prospective study of percutaneous transluminal angioplasty. Ann Surg 1987;206:403. 47. Morin JY, Johnston KW, et al. Factors that determine the long-term results of percutaneous transluminal dilatation for peripheral arterial occlusive disease. J Vasc Surg 1986;4:68. 48. Johnston KW, Colapinto RI, Baird RJ. Transluminal dilation: an alternative? Arch Surg 1982;117:1604. 49. Brewster DC. Current controversies in the management of aortoiliac occlusive disease. J Vasc Surg 1997; 25:365. 50. Brewster DC, Edwards JP. Cardiopulmonary complications related to vascular surgery. In: Bernhard VM, Towne JB, eds. Complications in Vascular Surgery. St. Louis: Quality Medical Publishing, 1991:23–41. 51. Hertzer NR, Beven EG, et al. Coronary artery disease in peripheral vascular patients: a classification of 1000 coronary angiograms and results of surgical management. Ann Surg 1984;199:223. 52. Boucher CA, Brewster DC, et al. Determination of cardiac risk by dipyridamole-thallium imaging before peripheral vascular surgery. N Engl J Med 1985;312:389. 53. Brewster DC, Boucher CA, et al. Selection of patients for preoperative coronary angiography: use of dipyridamolestress thallium myocardial imaging. J Vasc Surg 1985;2: 504. 54. Cutler BS, Leppo JA. Dipyridamole-thallium 201 scintigraphy to detect coronary artery disease before abdominal aortic surgery. J Vasc Surg 1987;5:91.

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases 55. Eagle KA, Coley CM, et al. Combining clinical and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med 1989;110:859. 56. Golden MA, Whittemore AD, et al. Selective evaluation and management of coronary artery disease in patients undergoing repair of abdominal aortic aneurysms: a 16year experience. Ann Surg 1990;212:415. 57. Cambria RR, Brewster DC, et al. The impact of selective use of dipyridamole-thallium scans and surgical factors on the current morbidity of aortic surgery. J Vasc Surg 1992;15:43. 58. Hollier LH. Cardiac evaluation in patients with vascular disease—overview: a practical approach. J Vasc Surg 1992;15:726. 59. Ehrenfeld WK, Wieber BC, et al. Autogenous tissue reconstruction in the management of infected prosthetic grafts. Surgery 1979;85:82. 60. Inahara T. Evaluation of endarterectomy for aortoiliac and aortoiliofemoral occlusive disease. Arch Surg 1975;110:1458. 61. van der Akker PJ, van Schilfgaarde R, et al. Long-term results of prosthetic and non-prosthetic reconstruction for obstructive aorto-iliac disease. Eur J Vasc Surg 1992;6:53. 62. Perdue GD, Long WD, Smith RB III. Perspective concerning aortofemoral arterial reconstruction. Ann Surg 1971,173:940. 63. Crawford ES, Manning LG, Kelly TE. “Redo” surgery after operations for aneurysm and occlusion of the abdominal aorta. Surgery 1977;81:41. 64. Malone JM, Moore WS, Goldstone J. The natural history of bilateral aortofemoral bypass grafts for ischemia of the lower extremities. Arch Surg 1975;110:1300. 65. Crawford ES, Bomberger RA, et al. Aortoiliac occlusive disease: factors influencing survival and function following reconstructive operation over a twenty-five year period. Surgery 1981;90:1555. 66. Szilagyi DE, Elliott JP Jr, et al. A thirty-year survey of the reconstructive surgical treatment of aortoiliac occlusive disease. J Vasc Surg 1986;3:421. 67. Nevelsteen A, Wouters L, Suy R. Aortofemoral Dacron reconstruction for aorto-iliac occlusive disease: a 25-year survey. Eur J Vasc Surg 1991;5:179. 68. Mulcare RJ, Royster TS, et al. Long-term results of operative therapy for aortoiliac disease. Arch Surg 1978;113:601. 69. Pierce GE, Turrentine M, et al. Evaluation of end-to-side v. end-to-end proximal anastomosis in aortobifemoral bypass. Arch Surg 1982;117:1580. 70. Dunn DA, Downs AR, Lye CR. Aortoiliac reconstruction for occlusive disease: comparison of end-to-end and endto-side proximal anastomoses. Can J Surg 1982;25:382. 71. Rutherford RB, Jones DN, et al. Serial hemodynamic assessment of aortobifemoral bypass. J Vasc Surg 1986; 4:428. 72. Ameli FM, Stein M, et al. End-to-end versus end-to-side proximal anastomosis in aortobifemoral bypass surgery: Does it matter? Can Soc Vasc Surg 1991;34:243. 73. Melliere D, Labastie J, et al. Proximal anastomosis in aortobifemoral bypass: end-to-end or end-to-side. J Cardiovasc Surg 1990;31:77.

519

74. Queral LA, Whitehouse WM Jr, et al. Pelvic hemodynamics after aortoiliac reconstruction. Surgery 1979;86: 799. 75. Flanigan DP, Schuler JJ, et al. Elimination of iatrogenic impotence and improvement of sexual function after aortoiliac revascularization. Arch Surg 1982;117:544. 76. Picone AL, Green RM, et al. Spinal cord ischemia following operations on the abdominal aorta.J Vasc Surg 1986;3:94. 77. Gloviczki P, Cross SA, et al. Ischemic injury to the spinal cord or lumbosacral plexus after aorto-iliac reconstruction. Am J Surg 1991;162:131. 78. Baird RJ, Feldman P, et al. Subsequent downstream repair after aorta-iliac, and aorta-femoral bypass operations. Surgery 1977;82:785. 79. Morris GC, Edwards W, et al. Surgical importance of profunda femoris artery: analysis of 102 cases with combined aortoiliac and femoropopliteal occlusive disease treated by revascularization of deep femoral artery. Arch Surg 1961;82:32. 80. Bernhard VM, Ray LI, Militello JP. The role of angioplasty of the profunda femoris artery in revascularization of the ischemic limb. Surg Gynecol Obstet 1976;142:840. 81. Berguer R, Higgins RE, Colton LT. Geometry, blood flow, and reconstruction of the deep femoral artery; Am J Surg 1975;130:68. 82. Robbs JV, Wylie EJ. Factors contributing to recurrent limb ischemia following bypass surgery for aortoiliac occlusive disease, and their management. Arch Surg 1981;193:346. 83. Sanders RJ, Kempczinksi RF, et al. The significance of graft diameter. Surgery 1980;88:856. 84. Nunn DB, Carter MM, et al. Postoperative dilation of knitted Dacron aortic bifurcation graft. J Vasc Surg 1990;12:291. 85. Burke PM, Herrmann JB, Cutler BS. Optimal grafting methods for the small abdominal aorta. J Cardiovasc Surg 1987;28:420. 86. Cintora I, Pearce DE, Cannon JA. A clinical survey of aortobifemoral bypass using two inherently different graft types. Ann Surg 1988;208:625. 87. Kaiser AB, Clayson KR, et al. Antibiotic prophylaxis in vascular surgery. Ann Surg 1978;188:283. 88. Pitt HA, Postier RG, et al. Prophylactic antibiotics in vascular surgery. Ann Surg 1980;192:356. 89. Hasselgren PO, Ivarsson L, et al. Effects of prophylactic antibiotics in vascular surgery: a prospective, randomized, double-blind study. Ann Surg 1984;200:86. 90. O’Hara PJ, Brewster DC, et al. The value of intraoperative monitoring using the pulse volume recorder during peripheral vascular surgery. Surg Gynecol Obstet 1981;152:275. 91. DePalma RG, Levine SB, Feldman S. Preservation of erectile function after aortoiliac reconstruction. Arch Surg 1978;113:958. 92. Barnes RW, Baker WH, et al. Value of concomitant sympathectomy in aortoiliac reconstruction: results of a prospective randomized study. Arch Surg 1977;112: 1325. 93. Satiani B, Liapis CD, et al. Prospective randomized study of concomitant lumbar sympathectomy in aortoiliac reconstruction. Am J Surg 1982;143:755.

520

Part VI Chronic Arterial Occlusions of the Lower Extremities

94. Imparato AM. Lumbar sympathectomy: role in the treatment of occlusive arterial disease in the lower extremities. Surg Clin North Am 1979;59:719. 95. Rutherford RB. The current role of sympathectomy in the management of infrarenal aortic occlusion. Semin Vasc Surg 1991;4:195. 96. Corson JD, Brewster DC, Darling RC. The surgical management of infrarenal aortic occlusion. Surg Gynecol Obstet 1982;155:369. 97. Liddicoat JE, Bekassy SM, et al. Complete occlusion of the infrarenal abdominal aorta: management and results in 64 patients. Surgery 1975;77:467. 98. Tapper SS, Jenkins JM, et al. Juxtarenal aortic occlusion. Ann Surg 1992;215:443. 99. Starrett RW, Stoney RJ. Juxta-renal aortic occlusion. Surgery 1974;76:890. 100. McCullough JL, Mackey WC, et al. Infrarenal aortic occlusion: a reassessment of surgical indications. Am J Surg 1983;146:178. 101. Reilly LM, Sauer L, et al. Infrarenal aortic occlusion: Does it threaten renal perfusion or function? J Vasc Surg 1990;11:216. 102. Sumner DS, Strandness DE Jr. Aortoiliac reconstruction in patients with combined iliac and superficial femoral arterial occlusion. Surgery 1978;84:348. 103. Martinez BD, Hertzer NR, Beven EG. Influence of distal arterial occlusive disease on prognosis following aortobifemoral bypass. Surgery 1980;88:795. 104. Hill DA, McGrath MA, et al. The effect of superficial femoral artery occlusion on the outcome of aortofemoral bypass for intermittent claudication. Surgery 1980;87:133. 105. Galland RB, Hill DA, et al. The functional result of aortoiliac reconstruction. Br J Surg 1980;67:344. 106. O’Donnell TF Jr, Lahey SJ, et al. A prospective study of Doppler pressures and segmental plethysmography before and following aortofemoral bypass. Surgery 1979;86:120. 107. Jones AF, Kempczinski RF. Aortofemoral bypass grafting: a reappraisal. Arch Surg 1981;116:301. 108. Brewster DC, Veith FJ. Combined aortoiliac and femoropopliteal occlusive disease. In Veith FJ, Hobson RW, et al., eds. Vascular surgery: principles and pratice, 2nd edn. New York: McGraw-Hill 1994:459:472. 109. Dalman RL, Taylor LM Jr, et al. Simultaneous operative repair of multilevel lower extremity occlusive disease. J Vasc Surg 1991;13:211. 110. Eidt J, Charlesworth D. Combined aortobifemoral and femoropopliteal bypass in the management of patients with extensive atherosclerosis. Ann Vasc Surg 1986;1:453. 111. Harris PL, Cave Bigley OJ, McSweeney L. Aortofemoral bypass and the role of concomitant femorodistal reconstruction. Br J Surg 1985;72:317. 112. O’Donnell TF Jr, McBride KA, et al. Management of combined segment disease. Am J Surg 1981;141:452. 113. Garrett WV, Slaymaker EE, et al. lntraoperative prediction of symptomatic result of aortofemoral bypass from changes in ankle pressure index. Surgery 1977;82: 504. 114. Levinson SA, Levinson HJ, et al. Limited indications for unilateral aortofemoral or iliofemoral vascular grafts. Arch Surg 1973;107:791.

115. Kram HB, Gupta SK, et al. Unilateral aortofemoral bypass: a safe and effective option for the treatment of unilateral limb-threatening ischemia. Am J Surg 1991; 162:155. 116. van den Dungen JJAM, Boontje AH, Kropveld A. Uniateral iliofemoral occlusive disease: long-term results of the semiclosed endarterectomy with the ringstripper. J Vasc Surg 1991;14:673. 117. Piotrowski JJ, Pearce WH, et al. Aortobifemoral bypass: the operation of choice for unilateral iliac occlusion? J Vasc Surg 1988;8:211. 118. Dick LS, Brief DK, et al. A twelve-year experience with femoro-femoral crossover grafts. Arch Surg 1980;115: 1359. 119. Kalman PG, Hosang M, et al. The current role for femoro-femoral bypass. J Vasc Surg 1987;6:71. 120. Couch NP, Clowes AW, et al. The iliac-origin arterial graft: a useful alternative for iliac occlusive disease. Surgery 1985;97:83. 121. Kalman PG, Hosang M, et al. Unilateral iliac disease: the role of iliofemoral graft. J Vasc Surg 1987;6:139. 122. Darling RC III, Leather RP, et al. Is the iliac artery a suitable inflow conduit for iliofemoral occlusive disease: an analysis of 514 aorto-iliac reconstructions. J Vasc Surg 1993;17:15–22. 123. Perler BA, Burdick JF, Williams M. Femoro-femoral or ilio-femoral bypass for unilateral inflow reconstruction? Am J Surg 1991;161:426. 124. Ricco J-B. Unilateral iliac artery occlusive disease: a randomized multicenter trial examining direct revascularization versus crossover bypass. Ann Vasc Surg 1992,6:209. 125. Taylor LM Jr, Freimanis IE, et al. Extraperitoneal iliac endarterectomy in the treatment of multilevel lower extremity arterial occlusive disease. Am J Surg 1986;1 52:34. 126. Brewster DC, Cambria RP, et al. Long-term results of combined iliac balloon angioplasty and distal surgical revascularization. Ann Surg 1989;210:324. 127. Dean RH, Keyser JE III, et al. Aortic and renal vascular disease: factors affecting the value of combined procedures. Ann Surg 1984;200:336. 128. Tollefson DFJ, Ernst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg 1991;14:327. 129. Perry MO, Silane MF. Management of renovascular problems during aortic operations. Arch Surg 1984;119: 681. 130. Connolly JE, Kwaan JHM. Prophylactic revascularization of the gut. Ann Surg 1979;190:514. 131. Tarazi RY, Hertzer NR, Beven EG. Simultaneous aortic reconstruction and renal revascularization: risk factors and late results in eighty-nine patients. J Vasc Surg 1987;5:707. 132. Brewster DC, Buth J, et al. Combined aortic and renal artery reconstruction. Am J Surg 1976;131: 457. 133. Stewart MT, Smith RB III, et al. Concomitant renal revascularization in patients undergoing aortic surgery. J Vasc Surg 1985;2:400. 134. Stoney RJ, Skioldebrand CG, et al. Juxtarenal aortic atherosclerosis: surgical experience and functional result. Ann Surg 1984;200:345.

Chapter 40 Aortoiliac, Aortofemoral, and Iliofemoral Arteriosclerotic Occlusive Diseases 135. Moncure AC, Brewster DC, et al. Use of the splenic and hepatic arteries for renal revascularization. J Vasc Surg 1986;3:196. 136. Brewster DC, Moncure AC. Hepatic and splenic artery for renal revascularization. In: Bergan JJ, Yao JST, eds. Arterial surgery: new diagnostic and operative techniques. Orlando, FL: Grune & Stratton, 1988:389–405. 137. Brewster DC. Complications of aortic and lower extremity procedures. In: Strandness DE, Van Breda A, eds. Vascular disease: surgical and interventional therapy. New York: Churchill Livingstone, 1994:1151–1178. 138. Brewster DC, Meier GH, et al. Reoperation for aortofemoral graft limb occlusion: optimal methods and long-term results. J Vasc Surg 1987;5:363. 139. Imparato AM. Abdominal aortic surgery: prevention of lower limb ischemia. Surgery 1983;93:112. 140. Starr DS, Lawrie GM, Morris GC Jr. Prevention of distal embolism during arterial reconstruction. Am J Surg 1979;138:764. 141. Diehl IT, Cali RF, et al. Complications of abdominal aortic reconstruction: an analysis of perioperative risk factors in 557 patients. Ann Surg 1983;197:50. 142. Castronuovo JJ, Flanigan DP. Renal failure complicating vascular surgery. In: Bernhard VM, Towne JB, eds. Complications in vascular surgery. Orlando, FL: Grune & Stratton, 1985:258–274. 143. Bush HL, Huse JB, et al. Prevention of renal insufficiency after abdominal aortic aneurysm resection by optimal volume loading. Arch Surg 1981;116:1517. 144. Brewster DC, Franklin DP, et al. Intestinal ischemia complicating abdominal aortic surgery. Surgery 1991;109: 447. 145. Elliott JP, Szilagyi DE, et al. Spinal cord ischemia: secondary to surgery of the abdominal aorta. In: Bernhard VM, Towne JB, eds. Complications in vascular surgery. Orlando, FL: Grune & Stratton, 1985:291–310. 146. Brewster DC, Cooke JC. Longevity of aorto-femoral bypass grafts. In: Yao JST, Pearce WH, eds. Long-term results in vascular surgery. East Norwalk, CT: Appleton & Lange, 1993:149–161. 147. Nevelsteen A, Suy R. Graft occlusion following aortofemoral Dacron bypass. Ann Vasc Surg 1991;5:32. 148. Baird RJ, Ropchan GV, et al. Ascending aorta to bifemoral bypass—a ventral aorta. J Vasc Surg 1986;3:405. 149. Canepa CS, Schubart PJ, et al. Supraceliac aortofemoral bypass. Surgery 1987;101:323. 150. McCarthy WJ, Rubin JR, et al. Descending thoracic aorta-to-femoral artery bypass. Arch Surg 1986;121:681. 151. Rosenfeld JC, Savarese RP, DeLaurentis D. Distal thoracic aorta to femoral artery bypass: a surgical alternative. J Vasc Surg 1985;2:747. 152. Bernhard VM, Ray LI, Towne JB. The reoperation of

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157.

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159.

160. 161.

162.

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164.

165.

166.

167. 168.

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choice for aortofemoral graft occlusion. Surgery 1977;82:867. Brewster DC. Surgery of late aortic graft occlusion. In: Bergan JJ, Yao JST, eds. Surgery of the aorta. Philadelphia: WB Saunders, 1989:519–538. Malone JM, Goldstone J, Moore WS. Autogenous profundaplasty: the key to long-term patency in secondary repair of aortofemoral graft occlusion. Ann Surg 1978:188:817. Satiani B. False aneurysms following arterial reconstruction: collective review. Surg Gynecol Obstet 1981; 152:357. Szilagyi DE, Smith RF, et al. Anastomotic aneurysms after vascular reconstruction: problems of incidence, etiology, and treatment. Surgery 1975;78:800. Edwards JM, Teefey SA, et al. Intraabdominal paraanastomotic aneurysms after aortic bypass grafting. J Vasc Surg 1991;15:344. Flanigan DP, Sobinsky KR, et al. Internal iliac artery revascularization in the treatment of vasculogenic impotence. Arch Surg 1985:120:271. Kempczinski RF. Impotence following aortie surgery. In: Bernhard VM, Towne JB, eds. Complications in vascular surgery. St Louis: Quality Medical Publishing, 1991:160–171. Bandyk DF. Aortic graft infection. Semin Vase Surg 1990;3:122. O’Hara PJ, Hertzer NR, et al. Surgical management of infected abdominal aortic grafts: review of a 25-year experience. J Vasc Surg 1986;3:725. Reilly LM, Lusky RJ, et al. Late results following surgical management of vascular graft infection. J Vasc Surg 1984;1:36. Quinones-Baldrich WJ, Hernandez JJ, Moore WS. Longterm results following surgical management of aortic graft infection. Arch Surg 1991;126:507. Yeager RA, Moneta GL, et al. Improving survival and limb salvage in patients with aortic graft infection. Am J Surg 1990;159:466. Schmitt DD, Seabrook GR, et al. Graft excision and extra-anatomic revascularization: the treatment of choice for the septic aortic prosthesis. J Cardiovasc Surg 1990;31:327. Bernhard VM. Aortoenteric fistula. In: Bernhard VM, Towne JB, eds. Complications in vascular surgery. Orlando, FL: Grune & Stratton, 1985:513–525. Connolly JE, Kwaan JHM, et al. Aortoenteric fistula. Ann Surg 1981;194:402. Perdue GD Jr, Smith RB III, et al. Impending aortoenteric hemorrhage: the effect of early recognition on improved outcome. Ann Surg 1980:192:237. Reilly LM, Ehrenfeld WK, et al. Gastrointestinal tract involvement by prosthetic graft infection: the significance of gastrointestinal hemorrhage. Ann Surg 1985;202:342.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 41 Percutaneous Interventions for Aortoiliac Occlusive Disease Edward B. Diethrich

Less than a decade ago, in the 1995 edition of this book, the author predicted the following regarding percutaneous interventions for abdominal aortic occlusive disease: “Without a doubt, the new subspecialty of endovascular surgery will, by the turn of the century, be the preferred therapeutic approach to peripheral vascular occlusive disease in almost every vascular bed.” Not only has that prediction been fulfilled, the young subspecialty of endovascular surgery has already undergone a new metamorphosis, with endovascular therapies conveying the all-encompassing momentum toward less invasive endoluminal therapies. Indeed, as anticipated, endovascular therapy has now shown promise in arterial beds from the cerebral cortex to the dorsum of the foot. Not every procedure or technique has shown equal success, and indeed, some arterial territories are just now being investigated. These progressions of the technology have, not surprisingly, resulted in a fair amount of conflict and controversy. Those opposed to deployment of the first Palmaz stent in the iliac artery were no less voracious in their attacks than the current opponents of angioplasty and stenting of the carotid artery bifurcation. In just over 5 years, however, angioplasty and stenting have become the new gold standard for treating iliac stenoses. It would not be unreasonable to believe the same will occur with the cervical procedure. Even today though, physicians are still referring patients for aortofemoral bypass to treat isolated lesions of the abdominal aorta and the common iliac arteries. That conventional surgical approach should now be reserved

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only for a select few patients, who are “unfit” for the endoluminal apparatuses available to us today (Fig. 41.1). The long-term results of endovascular therapy in the iliac arteries have been outstanding (1–6), with the current armamentarium incorporating thrombolysis, balloon dilation, stent implantation, and endoluminal grafting for treatment of ulcerative lesions, bifurcation disease, and occlusions and stenoses that compromise native arteries or prosthetic grafts. These procedures are so effective that the classic, open procedure is now obsolete. The exception here would be a situation in which there is extensive calcification in the small arteries (5–6 mm), particularly in the external iliac, where the long-term results of endovascular therapy (or even open surgery) are not exceptional. Angioplasty and stenting under these circumstances has yielded short-term positive results, but reintervention is frequently required. The numerous benefits we anticipated with endovascular procedures have certainly been borne out with the inauguration of stent technology. The ability to avoid extensive laparotomy and graft interposition in patients with abdominal aortic disease conveys numerous advantages and may reduce healthcare costs. No general anesthesia is usually required, shorter hospitalization is common, lower mortality can be anticipated, fewer complications related to infection will occur, and reapplication of the technique in the event of recurrent disease is simpler. In addition, in male patients, the likelihood of impotence following a catheter-based procedure is much lower than that observed after aortoiliac surgery.

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The single most important factor contributing to the progress of endovascular technology over the past decade is the intravascular stent developed by Julio Palmaz (Palmaz stent, Johnson & Johnson Interventional

Systems, Warren, NJ) (Fig. 41.2). His monumental work began in the iliac system and resulted in nearly parallel applications in the coronary arteries with the Palmaz-Schatz stent (Johnson & Johnson Interventional Systems). The results of stent application in long iliac vessels and improvements in delivery technology led to Food and Drug Administration (FDA) approval of the devices and a rapid introduction of the technology in the United States and abroad. Years later, we have documented long-term success with stents in the iliac region (1–6) that rival or better the results seen with open procedures. The iliac stent was not originally designed for application in the aorta, except for use in areas where “kissing” stents were to be deployed to overcome obstructive disease involving the distal abdominal aorta and the proximal common iliac arteries (Fig. 41.3). However, the early success with the stent led our surgical team to investigate

FIGURE 41.1 Angiogram illustrating a case, which in spite of advances in endovascular therapy, is best treated with classical aortofemoral bypass.

FIGURE 41.2 Photograph of the first Palmaz stent, which paved the way for all future developments in endovascular therapy for aortoiliac disease. FIGURE 41.3 Diagram (A) and angiogram (B) illustrating use of two Palmaz stents in a technique called “kissing” stents. This application of stents permits treatment of occlusive lesions involving the origins of the common iliac arteries and the distal abdominal aorta.

A

B

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 41.4 (A) Preoperative aortogram and (B) control angiogram following deployment of a Palmaz stent for isolated abdominal aortic occlusive disease. This was one of the first procedures of its kind, and it helped to establish the potential of stent therapy.

A

B

its potential in a variety of abdominal pathologies, leading to our initial report of stenting in the distal portion of the aorta (Fig. 41.4) (7). This work, expanded upon by many others, created the foundation for endovascular therapy in both isolated aortic disease as well as other aortoiliac pathologies. In this chapter, we discuss advances in treating aortoiliac disease with endovascular procedures. An overview of the necessary equipment is provided, and a review of current treatment options is presented.

Equipping the Endovascular Suite Large Equipment Performing high-quality percutaneous interventions requires a sophisticated “workshop.” High-resolution fluoroscopic imaging equipment is the hallmark of a well-designed endovascular suite and forms the foundation for development of a successful endovascular program. By far the most popular imaging system used by interventionists is the portable C-arm roentgenographic unit with an image enhancer that is integrated with a 3/4inch videotape recorder and monitors for contrast injection visualization. A second monitor with a digital storage disk is also needed to provide still images of selected arteriographic segments, facilitating “road mapping,” a tool essential to complex angioplasty procedures. For hardcopy documentation, a multiformat x-ray film camera or Polaroid film pack with adapters may be integrated with the equipment. There are a number of fluoroscopic units available worldwide with various modifications depending upon the manufacturer (e.g., Philips, GE, OEC, Siemens, Toshiba, etc.) The unit in our endovascular suite (ISS-2000 Plus Intraoperative Imaging System, International Surgical Systems, Phoenix, AZ) (Fig. 41.5) has been

FIGURE 41.5 Photograph of the ISS-2000 Plus Intraoperative Imaging System. The numerous advantages of the ceiling-mounted system have been demonstrated repeatedly as the concept has evolved over the past years.

designed and refined under our supervision to create a system that fulfills all the current and foreseeable requirements for endovascular surgery. The use of automated contrast injectors should be considered as the injection volume and precision required during a long injection may be difficult to achieve manually. Pressure injectors (Medrad, Indianola, PA) are available in a number of configurations, including both ceiling-mounted and floor-

Chapter 41 Percutaneous Interventions for Aortoiliac Occlusive Disease

based mobile units. These types of injector allow rapid delivery of contrast, which may be particularly important when high volumes are administered in large vessels such as the aorta. To optimize the usefulness of this radiographic equipment, nonmetallic, carbon fiber surgical tables are available for interventional techniques. Our preference is a thin but highly stable table (ISS-1000 Plus, International Surgical Systems) (Fig. 41.6) supported at only one end to provide complete clearance beneath for a panning x-ray system. Its telescoping pedestal allows vertical travel from 28 to 48 inches, 20° side-to-side roll, and 20° Trendelenburg tilt (standard and reverse). The table itself can be removed from the pedestal for exchange with other types of tabletop. Other models are available, each with their own specific characteristics. The crucial feature, however, is the unobstructed head-to-toe fluoroscopic imaging capability. Based on our extensive experience in intraprocedural imaging, we believe that at least two current assessment modalities should be available for intraluminal therapies: intravascular ultrasound (IVUS), mainly for lesions above the inguinal ligament, and angioscopy for small-caliber

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vessels. In the most modern suites, the images from these assessment techniques appear on several video monitors that are positioned so that all members of the endovascular team have an unobstructed view. Members of our group (8), as well as others (9), believe IVUS is a valuable tool for evaluating lesion characteristics and confirming accurate stent placement and deployment in the distal aorta and bifurcation. The importance of IVUS imaging cannot be underestimated, because it provides baseline luminal dimensions pre- and postangioplasty (intraluminal cross-sections and arterial circumferences) along with precise determination of arterial architecture and lesion pathology. In most cases, the IVUS examination following balloon dilation plays a significant role in both determining the need for stenting and assessing adequate deployment of devices (Fig. 41.7). Laser equipment is sometimes used for angioplasty. In particular, the excimer laser (Spectranetics, Colorado Springs, CO)—which is considered a “cool” source laser with photoablative capabilities—was introduced to treat restenosis and offer an alternative for recanalization following standard angioplasty or to open obstructed arteries. The laser procedures, however, have not gained FIGURE 41.6 Complete fluoroscopic and angiographic visualization can be obtained only when the procedure tables are free of opaque obstruction. This nonmetal, carbon-fiber table (photograph) permits unobstructed head-to-toe imaging.

FIGURE 41.7 Intravascular ultrasound examination showing (A) incomplete apposition of the stent to the arterial wall and (B) a positive outcome after expansion with a larger diameter balloon.

A

B

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general acceptance, most likely due to failure of early devices. The endovascular suite must also be equipped for accurate monitoring of the patient during the procedure. Because many patients will have systemic arterial disease—especially coronary artery obstructions— continuous electrocardiographic surveillance is imperative. Provision for central venous monitoring should be available for those patients who are at high risk in the more complex procedures. Frequent observation of urine output is also essential for cases involving the renal arteries and higher abdominal or thoracic aortic segments. Intra-arterial monitoring is useful in most cases, especially those in which pressure differentials play a role in assessing the performance of the procedure. Precise measurement of pressure differentials can easily be accomplished with 4-Fr. or 5-Fr., 65-cm, wire-guided, radiopaque-tipped catheters (MediTech/Boston Scientific, Natick, MA or Cook, Inc., Bloomington, IN) placed retrograde across the lesion. The exact proximal origination point of the gradient is determined by pulling the catheter back through the lesion and noting the level on fluoroscopy at which the radial artery and catheter pressures begin to differ. Use of ECG monitoring allows close observance of electrical changes and cardiac rhythm. Ventricular fibrillation is a rare but serious complication during some endovascular interventions, and the ECG provides early warning of significant rhythm changes. Inadvertent placement of a wire at the level of the valve in the ascending aorta may result in a serious arrhythmia that is easily detected by the ECG. Pulse oximetry is also a useful monitoring tool and is indicated when a patient receives conscious sedation during the procedure. Most endovascular procedures do not require the use of a general anesthetic. At the Arizona Heart Institute, we prefer a local anesthesia with mild sedation for percutaneous retrograde femoral interventions. It is possible to use agents that allow the patient to be completely comfortable and conversant during the procedure.

Disposable Equipment The rapid advancement in angioplasty techniques has placed a demand on equipment manufacturers to supply sheaths, catheters, wires, and balloons in a greater variety of dimensions and with more functional characteristics attuned to specific pathologic situations. Sheaths come in a multitude of lengths and diameters, with assorted sideports for infusion. As the technology advances, so does the continued reduction in profile of the equipment. It is now possible to perform most standard angioplasty procedures, including stent deployment, through 6-Fr. or 7 Fr. sheaths, which are available from many companies (e.g., Cordis/Johnson & Johnson Interventional Systems, Warren, NJ; Cook, etc.) Some sheaths (e.g., Super Flex Introducer, Arrow International, Reading, PA) are particularly useful in obese patients and those

with groins heavily scarred from previous interventions. For stent techniques using the retrograde brachial approach, the smallest sheath that can be used is 7 Fr. For antegrade infrarenal aortic deployment, long sheaths (7.5-Fr. and 8-Fr., 70 cm; Daige Corporation, Minnetonka, MN) protect the stent as it is being delivered to the designated location. Crossover sheaths, such as the Balkin Up & Over contralateral introducer sheath and dilator (Cook), facilitate positioning over the bifurcation and are flexible and relatively kink resistant. In guidewire technology, the advent of hydrophiliccoated guidewires (Glidewire, MediTech/Boston Scientific) has greatly increased the ease and safety of lesion traversal, and high-resolution fluoroscopic equipment assures better positioning of all wires. Steerable guidewires add another measure of control (and cost) but, in our experience, the nitinol alloy core of the Glidewire resists bending and kinking, making it functionally identical to the steerable wires in all but the most circuitous vessels. More recently, guidewire design has turned toward “activated” wires that bring us a step closer to the “wire through every lesion” ideal envisioned by many interventionists. Guiding catheters are not commonly used in lower limb interventions where tortuous pathways are not encountered. Instead, less expensive angiographic catheters can usually suffice to assist in lesion traversal. One that we like a great deal is a 5-Fr., 65-cm custom angiographic catheter with a radiopaque tip marker; this catheter is ideal for quantifying the location of pressure differentials. Balloon technology has perhaps shown the greatest headway in recent years, as manufacturers strive to lower the profile of their products, increase their performance capabilities with new balloon materials, and overcome some inherently traumatic aspects of the traditional overflagged balloon design. The decision as to which balloons to stock is largely based on experience and periodic evaluation of new designs. For peripheral interventions, catheter lengths from 65 cm to 150 cm are commonly inventoried for a variety of balloon dimensions. Balloon diameters range from 4 to 8 mm over lengths of 2 to 10 cm (Table 41.1). Larger diameter balloons (Cook) for aortic interventions are now available in 10 to 23 mm diameters with 3 to 5 cm lengths (Fig. 41.8). The stent’s presence in the modern endovascular surgery suite is a prerequisite for superior angioplasty results. There are many types of stent now available (Table 41.2) (Fig. 41.9). All have certain advantages and varying degrees of radiopacity that make high-resolution fluoroscopy mandatory. The characteristics of some of the more popular devices are described. The Wallstent (MediTech/Boston Scientific) is a favorite in peripheral interventions. The stent is a self-expanding design, and its flexible construction allows it to conform even in tortuous anatomy. The device’s dynamic radial force properties enable expansion to maximum lumen size, and it is reconstrainable for optimal positioning. The Symphony

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TABLE 41.1 Balloons and manufacturers Braun Z-Med 8 Fr. 9 Fr.

20 mm ¥ 4 cm 22 mm and 25 mm ¥ 4 cm 15 mm to 25 mm ¥ 2 cm and 4 cm Catheter length: 100 cm

Boston Scientific UDT (Ultrathin Diamond) 5–5.8 Fr. 3 mm to 8 mm ¥ 2 cm, 4 cm, and 10 cm Catheter lengths: 40, 75, and 120 cm Marshall 5–5.2 Fr. 5–5.8 Fr.

4 mm to 6 mm ¥ 2 cm, 4 cm, and 8 cm 7 mm to 10 mm ¥ 2 cm, 4 cm, and 8 cm

BMX (Blue Max 20) 5.8 Fr. 5 mm to 10 mm ¥ 4 cm to 10 cm (6-Fr. introducer) 8 mm ¥ 3 cm and 8 cm (7 Fr., 8-mm introducer) Catheter lengths: 90 cm

FIGURE 41.8 Photograph of a variety of newer balloons that are low profile and have been improved over the years for use in angioplasty procedures.

Olbert 4.8 Fr. 5.8 Fr.

TABLE 41.2 Stents and manufacturers

Smash 5 Fr. Cordis Opta LP 5 Fr.

6 mm and 7 mm ¥ 2 cm 5 mm to 14 mm ¥ 4 cm 5 mm to 10 mm ¥ 10 cm Catheter lengths: 75 and 90 cm 8 mm, 9 mm, and 12 mm ¥ 4 cm and 8 cm 4 mm to 9 mm ¥ 4 cm 4 mm to 10 mm ¥ 2 cm to 8 cm

Jupiter

4.5 mm to 6 mm ¥ 2 cm

Savvy Max

2 mm to 6 mm ¥ 2 cm to 4 cm 14 mm to 20 mm diameter

Cook Accent 6 Fr. Omega 8.5 Fr. 10.5 Fr.

10 mm, 12 mm, and 14 mm ¥ 4 cm Catheter lengths: 80 cm 18 mm and 20 mm ¥ 3 cm and 5 cm 23 mm and 25 mm ¥ 3 cm and 5 cm Catheter lengths: 65 cm and 100 cm

stent (MediTech/Boston Scientific), which is also selfexpanding, includes new radiopaque markers that allow clearer visualization during deployment. Again, radial strength of this stent is excellent, and its flexibility assists the operator accurate placement of the device. Sulzer Intratherapeutics, Inc. (St Paul, MN) has introduced a variety of new stents for peripheral use. The Protégé is a self-expanding nitinol stent designed to allow accurate deployment, while the IntraStent DoubleStrut ParaMount XS (extra support) is balloon-expandable and comes premounted on a Bard Opti-Plast balloon (CR Bard, Murray Hill, NJ). DoubleStrut technology combines parallel struts and a unique cell geometry. Nitinol coil stents (IntraCoil) are also available; these devices are conformable, yet maintain adequate compression resistance. The Memotherm stent (CR Bard) is also self-expanding and

Bard Memotherm (self-expanding) Boston Scientific Wallstents (self-expanding) Symphony (self-expanding) Cook Z-stents (balloon-expandable) Cordis Endovascular Palmaz stents (balloon-expandable) Smart stents (self-expanding) IntraTherapeutics Protégé (self-expanding) ParaMount (balloon-expandable) IntraStent Double Strut (balloon-expandable) IntraStent LP (balloon-expandable) IntraStent Intracoil (self-expanding) Medtronic (AVE) Bridge stent (balloon-expandable)

incorporates a flexible diamond shape that allows optimal anatomical configuration when the device is released. There are no sharp edges, and the stent may be dilated to a pre-programmed diameter. Endoluminal grafts (ELGs), or stent–grafts, allow percutaneous exclusion of aneurysms, iatrogenic perforations, ruptures, and arteriovenous fistulas. Some investigators are also using ELGs to treat atherosclerotic disease in iliac arteries. Such grafts have been particularly useful in treating patients with iliac artery aneurysms (Fig. 41.10). Commercially available grafts include the Wallgraft (Boston Scientific), the JoStent graft (JoMed, Amsterdam, NL), the Hemobahn (WL Gore and Associates, Flagstaff, AZ) and the aSpire covered stent (Vascular Architects, San Jose, CA), which is available in both open and closed configurations. The aSpire is the newest and most unique of the devices (Fig. 41.11), incorporating a

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spiral nitinol stent completely covered by a thin layer of polytetrafluoroethylene (PTFE), which provides greater lumen wall coverage and radial strength than metal stents. Unlike other covered stent grafts, the aSpire stent preserves many of the desired elements of the native lumen. It is available in lengths of 2.5, 5.0, and 10 cm and diameters from 6 to 14 mm.

Endovascular Treatment of Aortoiliac Disease Selection of the Patient FIGURE 41.9 A variety of stents have been developed since the original Palmaz stent. Increased flexibility of these devices has improved ease and accuracy of deployment.

Most manifestations of atherosclerotic involvement in the distal abdominal aorta or aortoiliac segment are potentially suited for percutaneous interventions. The need for open surgical exposure of the common femoral artery is FIGURE 41.10 (A) Preoperative angiogram showing aneurysm of the left common iliac artery, which was excluded with an endoluminal graft, and (B) 3-month postoperative control angiogram.

A

B

FIGURE 41.11 (A) Angiogram showing atherosclerotic disease at the origins of the common iliac arteries. These lesions were treated with the new aSpire covered stent. The control angiogram (B) confirms successful deployment of the stents.

A

B

Chapter 41 Percutaneous Interventions for Aortoiliac Occlusive Disease

limited to situations in which the artery or its distal branches require a concomitant operative intervention. A history of previous surgical (i.e., aortoiliac bypass) or percutaneous intervention does not preclude subsequent intraluminal therapy. Similarly, when comorbid factors that place a patient in a high-risk category with an open procedure are present, a less invasive percutaneous procedure is indicated. Since both local and epidural anesthesia are suitable for percutaneous entry at the groin, procedures may be offered to patients who have even extensive coronary and pulmonary comorbidities. The patient with impaired renal function who is not yet on dialysis does present a special problem since, during the course of most percutaneous procedures, potentially nephrotoxic contrast material is used. Special precautions can be applied, and in some circumstances, a procedure may be accomplished using fluoroscopy and intravascular ultrasound for guidance of stent deployment.

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Access for Percutaneous Procedures There are three basic approaches for percutaneous procedures in the aortoiliac system: 1. 2. 3.

retrograde femoral; transaortic; and retrograde brachial (Fig. 41.12).

Indications The signs and symptoms of aortoiliac occlusive disease may be difficult to pinpoint. For example, a patient with a blue toe and early gangrene may have a strong femoral pulse, indicating the possibility of embolization from a proximal aortic source. Another patient may have femoral pulses at rest that disappear with exercise testing, suggesting severe proximal occlusive disease. Compounding these diagnostic challenges is the likelihood of multiple lesion sites in the pelvic and limb arteries, where symptoms may be masked by the more proximal disease. Therefore, the diagnostic workup (beyond the routine history-taking and physical examination with emphasis on pulse status) should include resting and, usually, exercise Doppler ultrasound testing, duplex scanning, and either contrast or magnetic resonance angiography (MRA). Recently, MRA studies at some institutions have been used more routinely. Our preference continues to include a study that clearly demonstrates the arterial system, the location of the culprit lesion(s) and the distal runoff. As less invasive diagnostic studies become more sophisticated, the requirement for contrast imaging will undoubtedly decline. Patients who are candidates for percutaneous intervention usually present with one of three symptom complexes: 1.

2.

3.

Intermittent claudication is by far the most common complaint. It is not uncommon for the symptoms to be static for a period of time and then increase suddenly, indicating an acute exacerbation. This may also occur when an existing graft or site of a previous angioplasty fails. Aortoiliac lesions may produce critical limb ischemia, particularly when a stable occlusive plaque is superimposed with an acute thrombus. A third type of presentation may occur with distal embolization of either thrombotic material or fragmented plaque from a proximal ulceration.

A

B

C

FIGURE 41.12 Diagrams illustrating the three percutaneous approaches used for endovascular therapy: (A) retrograde femoral, (B) transaortic and (C) retrograde brachial.

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The retrograde femoral approach is by far the most commonly used for treatment of stenotic and occlusive disease. In the former, a variety of available wires make crossing the lesion successful in almost every case so that balloon dilation and stenting are possible. When the artery is occluded, retrograde wire passage can be more difficult and it may be necessary to use a guiding catheter to assist (Fig. 41.13). In these situations, a transaortic passage of the wire to the contralateral iliac may permit crossing the lesion. Again, a guiding catheter may be needed and, once the catheter is in position, a Balkin sheath (Cook) may provide a working conduit for laser, balloon, stent, or stent–graft deployment. Either of these approaches, as well as the retrograde brachial, are applicable to thrombolytic therapy as well. We usually reserve the brachial approach for cases in which the retrograde femoral or transaortic access methods have failed or are not completely satisfactory.

The Use of Thrombolysis Historically, patients presenting with symptoms of a thrombotic occlusion were treated with an initial regimen of thrombolysis to remove the clot prior to angioplasty. Thrombolysis results when plasminogen is converted to plasmin, a nonspecific proteolytic enzyme that degrades fibrin and other proteins. Acute arterial occlusion (10,11) and graft occlusion (12,13) are often indications for thrombolytic therapy. Acute thromboses or embolization that occurs within 24 hours is most amenable to thrombolytic therapy. Thrombolysis is also the preferred option for restoring graft patency in occlusions less than 14 days old, and preoperative use of thrombolytic therapy may be a safe and effective means of achieving limb salvage (14). In patients undergoing revascularization for severe limb ischemia, the use of intraoperative, intra-arterial thrombolytic therapy has also been successful in improving blood flow (15,16). Thrombolysis has a more limited role

in the treatment of chronic occlusion. Although some investigators prefer this technique even in longstanding occlusions, surgical intervention is generally preferred in these cases (17). Thrombolysis may be used adjunctively in endovascular procedures (Fig. 41.14) and may be valuable in treating complications, such as acute occlusion at the angioplasty site and distal embolization (18). First-generation thrombolytic agents, such as urokinase and streptokinase, were used for a number of years to activate free plasminogen. Urokinase, which was the most popular drug, is no longer available in the United States. More recently, tissue-type plasminogen activators (t-PA), have been introduced. These agents activate very little free plasminogen, and it has been suggested that their use might minimize interference with systemic clotting mechanisms, yielding fewer bleeding complications. Unfortunately, in practice, bleeding complications have not necessarily been less severe than those seen with the use of first-generation agents like streptokinase and urokinase. While t-PA is in current use, it is not as easy to administer and not as familiar to most clinicians as urokinase. Thus, t-PA is considerably less popular than urokinase was. Additionally, many lesions that were lysed initially with thrombolysis are now treated with stent deployment so that the offending intraluminal material is trapped against the arterial wall. When thrombus removal is required, both catheter-directed techniques and newer rheolytic procedures (Angiojet, Possis Medical, Inc., Minneapolis, MN) may be used. The Angiojet is designed to remove thrombi of any composition without damage to the arterial intima. The device, less than 1 mm in diameter, is inserted transfemorally through a standard microcatheter. After it is passed through the occlusion, the Angiojet is activated and pulled through the site of blockage. Thrombus is removed mechanically by the Venturi effect, which creates a low-pressure suction zone at the device’s tip. In some cases, patency may be restored more quickly than with conventional administration of thrombolytic agents alone.

The Role of Antiplatelet Medications

FIGURE 41.13 Photograph of a crossover catheter (Balkin Up & Over, Cook) that is used to facilitate a contralateral approach for endovascular techniques.

In the past, we had recommended that aspirin and dipyridamole (DuPont Pharmaceuticals Co., Billerica, MA) be given before and following endovascular procedures, especially if stents were deployed. Many patients today are already taking one aspirin per day, and there is no need to discontinue that regimen prior to the procedure. Many interventionists are now recommending 75 mg of Plavix (Sanofi, Bristol Myers Squibb, Newington, NH) daily, 3–5 days before stenting and for a period of 30 days following the procedure. In situations in which no antiplatelet therapy has been prescribed, a loading dose of 300 mg may be given at the time of the stenting procedure. While there are no comparative scientific data to support this practice, it is now fairly standard, based on the collective experience with Plavix in coronary stenting. We do not use the regimen in our institution, except in carotid stent-

Chapter 41 Percutaneous Interventions for Aortoiliac Occlusive Disease

C

B

A

D

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E

FIGURE 41.14 Case study illustrating the philosophical changes observed in the treatment of aortoiliac occlusive disease. (A) Preoperative angiogram showing occlusion of the infrarenal aorta—note the large contralateral vessels indicating the longstanding occlusive process. This patient would ordinarily be referred for a classical open procedure, but an endovascular approach was chosen. (B) A catheter was placed from the left brachial artery to the aortic occlusion to allow thrombolysis over 12–24 hours. (C) Using the guiding catheter, a straight hydrophilic wire was passed through the left common iliac artery into the common femoral artery. (D) A right femoral wire was passed successfully into the aorta, permitting kissing balloon dilation of the iliac arteries and the abdominal aorta. (E) The procedure was completed with the deployment of stents in these vessels and provided successful percutaneous therapy for this extensive disease process.

ing procedures. Glycoprotein IIb/IIIa inhibitors are also used as adjuncts to stenting in some institutions, but their benefits are similarly unproven in the aortoiliac region.

Angioplasty and Stenting Standard balloon angioplasty has been deemed “an acceptable procedure in selected patients as an alternative to bypass grafting” since the Council for Scientific Affairs of

the American Medical Association guidelines were published in 1984 (19) Around the same time, another recognized body—the Health and Public Policy Committee of the American College of Physicians—concluded that “the morbidity in the periphery is less than for surgery” (20). As indicated earlier in this chapter, balloon angioplasty has become the standard for percutaneous interventions in lower extremities, particularly in the iliac arteries because of its high safety and efficacy rates and cost-effective

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nature (21). While laser angioplasty, which uses short pulses of photons to vaporize plaque, may be used as an adjunct, stents have certainly proven to be the most important means of correcting complications such as dissection, occlusion, and restenosis.

Endoluminal Grafting Endoluminal grafting technology offers an important alternative treatment for excluding abdominal aortic aneurysms, but it is rarely used in smaller vessels. It is certainly true that isolated iliac aneurysms, iatrogenic perforations, ruptures, and arteriovenous fistulas can be successfully treated with the ELG, but in general the incidence of these lesions is fairly low. ELGs are sometimes used to treat atherosclerotic disease in iliac arteries (22–27), and grafts fashioned from Palmaz stents and PTFE have been the most common and successful designs to date (23–25).

Summary The New Gold Standard The pendulum of the last decade has swung predictably in favor of endovascular procedures over classic surgical approaches for treatment of aortoiliac occlusive disease. Likewise, endovascular techniques will undoubtedly figure decisively as a treatment of choice for aortoiliac aneurysmal disease in the future. The technological improvements and developments in the field of endovascular therapy have permitted a sweeping change not only in procedures themselves but in the types of physicians involved in performing them. Although intervention in the vessels was long the purview of vascular surgeons alone, interventions incorporating low-profile, catheter-based therapies, stents, and improved imaging equipment have opened the doors for a variety of other clinicians to join in treating vascular disease. Indeed, the scalpel and suture have given way to percutaneous delivery in many institutions. The dramatic reduction in the use of lytic agents has not impacted on our favorable results. When necessary, tPA is available and achieves optimum outcomes. Cool lasers are enjoying a resurgence over the “hot”-tip lasers of the past. Their role, however, is primarily ancillary in the aortic and iliac lumens. Endoluminal grafts have yet to achieve acceptance except in very specific circumstances. In extensive dissections, and certainly in treating ruptures, these devices are indispensable in preserving life and limb. Newer stent–grafts like the aSpire incorporate designs with “open areas” in the device and may prove useful for treating a variety of lesions. A wide array of new stents are also expected from manufacturers, and some are likely to incorporate materials that are more visible under fluoroscopy than those used in the devices currently available. At present, we do not know the role, if any, for

eluding stents (and we certainly do not yet know what materials will be used to cover them). Will such devices exhibit good patency without the propensity for myointimal proliferation that is currently observed with coronary stents? While many questions persist, one thing seems certain: percutaneous treatment of aortoiliac occlusive disease is now the gold standard of treatment. Still, it remains to be seen which specialists, whether surgeons, cardiologists, or radiologists, will administer the bulk of these treatments.

References 1. Cikrit DF, Dalsing MC. Lower-extremity arterial endovascular stenting. Surg Clin North Am 1998; 78: 617–629. 2. Marin ML, Hollier LH, et al. Varying strategies for endovascular repair of abdominal and iliac artery aneurysms. Surg Clin North Am 1998; 78: 631–645. 3. Murphy KD, Encarnacion CE, et al. Iliac artery stent placement with the Palmaz stent: Follow-up study. J Vasc Intervent Radiol 1995; 6: 321–329. 4. Martin EC, Katzen BT, et al. Multicenter trial of the Wallstent in the iliac and femoral arteries. J Vasc Intervent Radiol 1995; 6: 843–849. 5. Vorwerk D, Guenther RW, et al. Primary stent placement for chronic iliac artery occlusions: Follow-up results in 103 patients. Radiology 1995; 194: 745–749. 6. Nöldge G, Richter GM, Rören T. A randomized trial of iliac stenting versus PTA in iliac artery stenoses and occlusions: Updated 6-year results. (Abstract) J Endovasc Surg 1996; 3: 99–100. 7. Diethrich EB, Santiago O, et al. Preliminary observations on the use of the Palmaz stent in the distal portion of the abdominal aorta. Am Heart J 1993; 125: 490–501. 8. Diethrich EB. Endovascular treatment of abdominal aortic occlusive disease: the impact of stents and intravascular ultrasound imaging. Eur J Vasc Surg 1993; 7: 228–236. 9. Cavaye DM, Diethrich EB, et al. Intravascular ultrasound imaging: an essential component of angioplasty assessment and vascular stent deployment. Int Angiol 1993; 12: 214–220. 10. Abbott WM, McCabe C, et al. Embolism of the popliteal artery. Surg Gynecol Obstet 1984; 159: 533–536. 11. Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity. Arch Surg 1984; 119: 784–787. 12. Ouriel K, Veith FJ, Sasahara AA for the TOPAS Investigators. Thrombolysis or peripheral arterial surgery (TOPAS): phase I results. J Vasc Surg 1996; 23: 64–75. 13. Camerota AJ, Weaver FA, et al. Results of prospective, randomized trial of surgery versus thrombolysis for occluded lower extremity bypass grafts. Am J Surg 1996; 172: 105–117. 14. Greenberg R, Wellander E, et al. Aggressive treatment of acute limb ischemia due to thrombosed popliteal aneurysms. Eur J Radiol 1998; 28: 211–218. 15. Quinones-Baldrich WJ, et al. Intra-operative fibrinolytic therapy: an adjunct to catheter thrombembolectomy. J Vasc Surg 1985; 2: 319–326.

Chapter 41 Percutaneous Interventions for Aortoiliac Occlusive Disease 16. Patent FN, Berhard VW, et al. Fibrinolytic treatment of residual thrombus after after catheter embolectomy for severe lower limb ischemia. J Vasc Surg 1989; 9: 153–160. 17. The STILE Investigators. Results of a prospective, randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial. Ann Surg 1994; 220: 251–268. 18. Cleveland TJ, Cumberland DC, Gaines PA. Percutaneous aspiration thrombo-embolectomy to manage the embolic complications of angioplasty and as an adjunct to thrombolysis. Clin Radiol 1994; 49: 549–552. 19. Council on Scientific Affairs, American Medical Association. Percutaneous transluminal angioplasty. JAMA 1984; 251: 764–768. 20. Health and Public Policy Committee, American College of Physicians. Percutaneous transluminal angioplasty. Ann Intern Med 1983; 99: 864–869. 21. Vorwerk D, Gunther RW. Percutaneous interventions for treatment of iliac artery stenoses and occlusions. World J Surg 2001; 25: 319–26; discussion 326–7.

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22. Formichi M, Raybaud G, et al. Rupture of the external iliac artery during balloon angioplasty: endovascular treatment using a covered stent. J Endovasc Surg 1998; 5: 37–41. 23. Sanchez LA, Wain RA, et al. Endovascular grafting for aortoiliac occlusive disease. Semin Vasc Surg 1997; 10: 297–309. 24. Dorros G, Cohn JM, Jaff MR. Percutaneous endovascular stent–graft repair of iliac artery aneurysms. J Endovasc Surg 1997; 4: 370–5. 25. Quinn SF, Sheley RC, et al. Endovascular stents covered with pre-expanded polytetrafluouroethylene for treatment of iliac artery aneurysms and fistulas. J Vasc Interv Radiol 1997; 8: 1057–63. 26. Nevelsteen A, Lacroix H, et al. Stent grafts for iliofemoral occlusive disease. Cardiovasc Surg 1997; 5: 393–7. 27. Lammer J, Dake MD, et al. Peripheral arterial obstruction: prospective study of treatment with a transluminally placed self-expanding stent–graft. International Trial Study Group. Radiology 2000; 217: 95–104.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment Frank J. Veith and Henry Haimovici

The occlusive process of the femoropopliteal segment is the most common lesion of the lower extremity, especially in patients over 60. Its preponderance, exclusive of its combination with other arterial lesions, has been documented by several statistical surveys, with its incidence ranging from 47% (1) to 65.4% (2), with an intermediate figure of 55% as shown in Figure 42.1 (3). Our studies have also shown that these lesions in diabetics are more prevalent in the femoropopliteal-tibial vessels than in the aortoiliac segment (75.4% vs. 24.6%) (4). More recently, the therapeutic significance and frequency of intrapopliteal occlusive disease have been recognized, and improved methods to treat it have been developed (5). Currently the need for interventional procedures to extend below the popliteal artery parallels or exceeds the need to perform femoropopliteal bypasses. In 1972, it was estimated that of the 73,000 reconstructions of major arteries in the United States every year, more than 20,000 (over 27% of the total) are carried out in the femoropopliteal segment (6). Furthermore, in 1982, it was reported that, of a total of 339,000 major vascular procedures performed in 1978 (an increase of 117% over 1972), there were 163,000 peripheral reconstructions, thus constituting almost 50% of all vascular operations (7). Although no specific breakdown by category of peripheral procedures was available in that report, by excluding by far the less frequent endarterectomy and

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aneurysmectomy procedures, it is estimated that the largest increase had occurred in the bypass grafting category. It should be noted that percutaneous transluminal balloon angioplasty (PTA) has been used increasingly to treat stenoses and short occlusions in the superficial femoral and popliteal arteries over the past two decades. In general, these unconventional techniques, which are not as durable as bypass procedures, may be useful as adjunctive or stand-alone treatments. However, as the sole treatment of stenotic or occlusive femoropopliteal lesions, they have their greatest utility in early phases of the disease process, in intermittent claudication when conservative treatment is not a good option. However, PTA of these lesions will be considered elsewhere in this volume (Chapter 18), and the remainder of this chapter will deal with the open surgical treatment of femoropopliteal thrombotic occlusions. Historically, the introduction of thromboendarterectomy by J. Cid dos Santos (8) in 1947 and the bypass graft technique by Kunlin (9) in 1948 marked the beginnings of direct revascularization methods of the lower extremity. Of the two procedures, the bypass has gained wider acceptance and has largely superseded the former, as attested to by the vast worldwide literature on this subject. Although functional improvement and limb salvage are being achieved in a large number of patients, the results of these reconstructive procedures are the subject of

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

FIGURE 42.1 Distribution of the incidence of occlusive arteriosclerotic lesions in the lower extremities. Note the preponderance of femoropopliteal lesions. (Based on data from Valdoni P, Venturini A. Considerations on late results of vascular prostheses for reconstructive surgery in congenital and acquired arterial disease. J Cardiovasc Surg 1964;5:509.)

an ongoing review and analysis concerning the various factors involved. These factors, which may determine the operative indications and influence their results, will be reviewed first, before describing the surgical technique.

Clinical Background Clinical, hemodynamic, and arteriographic findings provide the basis for the criteria in selecting patients with femoropopliteal occlusive disease for reconstructive surgery. The clinical manifestations of these arterial lesions vary with their location and extent, as well as with the degree of other associated vascular lesions. They are divided into three major groups of increasing severity: 1. 2. 3.

disabling intermittent claudication; rest pain; and ischemic ulcers and gangrene.

Intermittent claudication, indicating an inadequate arterial blood supply to contracting leg or foot muscles, varies in intensity according to the degree of arterial involvement. Mild to moderate intermittent claudication is generally not considered an indication for PTA or reconstructive surgery. By contrast, marked intermittent claudication that greatly restricts the patient’s walking ability, often to the point of disability, is sometimes an indication,

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especially if this symptom is a serious handicap in the lifestyle of a younger individual. However, an older, inactive person whose livelihood is not threatened by this type of claudication is not considered a candidate for invasive treatment, especially if systemic manifestations of arteriosclerosis are present. The degree of intermittent claudication is largely related to the extent and progression of the arterial disease. In the course of the evolution of the arteriosclerotic process, a superimposed acute segmental occlusion may occur, not only causing a corresponding sudden aggravation of the claudication but also leading to gangrene and occasionally to foot or leg amputation. In such instances, arterial reconstruction may assume a more urgent indication than in the chronic stage. Rest pain is a clinical picture of a more advanced arterial insufficiency. The underlying hemodynamic fact is a fall in the blood flow below the level providing adequate arterial supply to the resting limb. Clinically, rest pain involves the toes and the adjacent metatarsal area and occurs mostly at night. The patient awakes and hangs the involved limb over the side of the bed to relieve his pain. If further dependency of the limb is necessary to improve the capillary flow, the patient walks about the room before he can return to sleep. In a more advanced stage, rest pain may become continuous and be present not only during the night but also during waking hours. Associated signs of end-stage ischemia often present are a cold anesthetic or a cold edematous and discolored foot. Ischemic ulcerative and gangrenous lesions, to be amenable to reconstructive arterial surgery, should be localized in the toes or the heel or a combination thereof. In these cases, there may be associated infection in the interdigital web or in fissures on the heel. Meticulous local management of these lesions combined with appropriate antibiotics and avoidance of any trauma will usually limit the lesions to a small area. However, spreading gangrene may occur if local infection is not controlled, especially in diabetic patients or if venous thrombosis is superimposed and if cardiac failure is present. In attempting to establish operative criteria, it is important to take into account: 1. 2. 3. 4.

the type of onset; the age of the patient; the pattern of occlusive arterial disease; and the presence of diabetes.

The mode of onset may be insidious, sudden without prior claudication, or sudden with prior claudication and a combination of associated trauma, venous occlusion, arterial embolism, and vasospastic conditions. As to age, the majority of patients fall within the sixth, seventh, and eighth decades, and over 80% are men. It is noteworthy that the relative age incidence in nondiabetic and diabetic patients varies inversely with the advancing decades. In our own study of vascular lesions in these two groups of patients, there were slightly more than 50%

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under age 60 in the nondiabetic group, whereas only 33% were found in the diabetic group. Conversely, after 60, the incidence in the latter group was 67% and 49% in the nondiabetic group (4).

Clinical Evaluation of Arterial Disease Before one undertakes arteriographic or other instrumental assessment, a clinical evaluation of the arterial disease is the most important part of the physical examination. The color of the limb, especially of the foot and toes, in the supine and dependent as well as elevated positions may provide a clue to the severity of the arterial ischemia at the microcirculatory level. The temperature of the skin, examined under basal conditions, may provide an indication of the degree and the location of the arterial impairment, especially if there is a difference between the two sides. Unilateral foot coolness or coldness is a manifestation of severe ischemia. In an occlusion of the distal superficial femoral or proximal and middle popliteal, the knee on the affected side is warmer than on the contralateral side. This finding, which we call the “hyperemic knee sign,” indicates an increased collateral circulation around the knee provided by the genicular system and branches of the profunda femoris artery (Fig. 42.2). The difference between the two knee temperatures may range from 2° to 5°F (Haimovici H, unpublished data). Systematic palpation of all the pulses from the abdominal aorta down to the foot should provide a first indication about the degree and location of the arterial occlusion. Auscultation along the arteries from the abdominal aorta down to the popliteal artery may also indicate the presence of marked stenosis when a systolic bruit is audible. The Doppler ultrasonic detector may provide semiquantitative information about the peripheral pulsations and their degree of amplitude. Of the noninvasive modalities, Doppler-determined segmental blood pressures and pulse–volume recordings (PVRs) are generally the most useful means for evaluating lower-extremity occlusive disease. In addition, these measurements are semiquantitative and provide a permanent record of the patient’s lowerextremity circulatory status at a given point in time. By comparing values at different times, the effect of interventional treatments may be assessed, and evidence of graft patency, failure, or the failing state may be obtained (10). Duplex ultrasonography imaging of the site of lesions may also be useful in deciding on the best treatment plan.

Clinical Assessment of General Condition A routine systematic evaluation of all the vital organs is essential for all patients being considered for arterial surgery and should include the following: cardiovascular status, cerebral history with special reference to the carotid arteries, renal function, especially in diabetic patients, chest films, blood pressure determinations over a

FIGURE 42.2 Arteriogram indicating occlusion of the superficial femoral and proximal popliteal arteries, with an enlarged saphenous branch of the highest genicular artery on the medial aspect of the knee.

period of several days, complete blood chemistries, and lipid profile. Of these evaluations, those pertaining to cardiac function and status are the most important since perioperative myocardial infarction and other cardiac problems are the common causes of perioperative and late morbidity and mortality (11). In fact, PTA or aortocoronary bypass may have to be performed before the patient’s peripheral lesion can be safely corrected by operation. (See Chapter 14).

Arteriographic Patterns A comprehensive assessment of the arterial lesions of the lower extremity should include the entire arterial tree from the terminal abdominal aorta to the pedal vessels (Fig. 42.3). This method is essential to provide information not only about the lesions of the femoral and popliteal arteries but also about the state of the aorta and iliac arteries (inflow tract), as well as about the tibial and pedal vessels (outflow tract). This can be achieved by serial aortoarteriography, performed preferably with local anesthesia, since new contrast agents are less painful. [Bilateral arteriography should be carried out in most cases since in the majority of instances the arteriosclerotic process involves both lower extremities (12).]

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FIGURE 42.4 Diagram of femoropopliteal arterial patterns (see text for details): (1) distal superficial femoral, (2) proximal superficial femoral, (3) entire superficial femoral, (4) entire femoral and popliteal, (5) profunda femoris, (6) diffuse atherosclerosis with multiple stenotic areas.

which the lesions are confined to the femoral and popliteal arteries is relatively low in the nondiabetic arteriosclerotic group and is even lower in patients with diabetes. Analysis of the data in the former group discloses that the lesions involve either the distal superficial femoral (about the adductor canal) or the femoropopliteal segment, with the latter extending on each side of the foramen of the adductor magnus. Occlusion of the entire superficial femoral artery is often noted. Involvement of the proximal superficial femoral artery alone is extremely rare. Diffuse stenosing atherosclerotic changes were found in approximately 20% of our series. Analysis of our arteriographic data indicates that 1) isolated femoropopliteal lesions occur primarily in nondiabetic atherosclerosis and 2) the lesions seem to be initiated at the foramen of the adductor magnus junction between Hunter’s canal and the origin of the popliteal artery. The latter interpretation is in accord with the prevailing opinion of several investigators as well as with our previous findings. FIGURE 42.3 Bitransfemoral aortoarteriogram of a 62year-old nondiabetic patient with bilateral occlusion of the superficial femoral artery. Note the right iliac displaying reduced opacification (arrow) due to an atherosclerotic lesion verified at surgery.

Femoral Arteries Our classification of the arterial disease in the femoropopliteal segment into six patterns is illustrated in Figure 42.4 and is based on the site and extent of the occlusion (13). The incidence of the pattern in

Popliteal Arteries The incidence of isolated popliteal occlusion appears to be low, especially in diabetics. The site of the occlusive process in this pattern is in the proximal half only, i.e., above the knee joint. A popliteal-tibial occlusion pattern is more common than that of the isolated popliteal lesion. In most of these cases, the site of the popliteal occlusion is in the lower half. The occlusive process appears to be in continuity with that of the leg arteries in more than half of the patients and occurs more often in diabetics than in nondiabetics.

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Aortoiliac Segment (Inflow Tract) Silent atherosclerotic lesions of the aortoiliac segment associated with occlusive disease of the femoropopliteal artery, as reported previously, are found in 27% of the cases (13). Four basic patterns of this segment are present: 1. 2. 3. 4.

aortoiliac stenosis; unilateral segmental iliac occlusion; aortoiliac aneurysms; and tortuosities of the aortoiliic segment.

The net hemodynamic effect of all these lesions is reduction of arterial inflow of the lower extremity. Such lesions are often detected only by a panangiographic evaluation of the arterial tree, as indicated previously. Tibial–Peroneal Segment (Outflow Tract) In the presence of femoropopliteal occlusive disease, the outflow tract is rarely intact. More often than not, there are combined occlusions of leg arteries in which a single artery or two or a combination of all three arteries may be involved (Fig. 42.5). Although the incidence of combined occlusive patterns of the tibioperoneal arteries is more prevalent in diabetics, it is of some interest to note that, of the three leg vessels, the peroneal is most often patent, although some degree of intimal changes may be present. Profunda Femoris The profunda femoris artery, the main collateral channel of the femoropopliteal segment, may play a significant role in the overall clinicopathologic picture, since it is often involved by arteriosclerotic lesions. In the nondiabetic it is usually less involved than in the diabetic. In the majority of instances, the arteriographic findings are those of stenosis and only rarely of complete occlusion. Interpretation of Arteriographic Findings From the foregoing brief description of the findings, it appears that the arterial lesions are rarely monosegmental and most often are multiple and complex. The complete occlusion of a segment is easily interpretable, but intimal lesions encroaching on the lumen are often difficult to assess in terms of their hemodynamic significance. The degree of stenosis assigned to an atheromatous lesion radiologically visible may often be misleading. Operative findings are usually more severe than the arteriographic outline would indicate, but sometimes the opposite is true. The nature of the lesions may range from a soft atheromatous to a hard fibrous or calcified plaque. The extent of the latter is rarely detectable from the angiographic image. To avoid possibly misleading interpretations, it is essential to obtain adequate opacification of the arteriographic outline of the entire vasculature. In the aortoiliac segment, a CT scan of the arteries may also prove helpful.

FIGURE 42.5 Femoral arteriogram showing occlusion of the superficial femoral, proximal popliteal, and anterior tibial arteries in a patient with moderately severe intermittent claudication.

Indications Based on clinical, hemodynamic, and arteriographic criteria for grading the degree of arterial insufficiency, three major indications are generally considered for femoropopliteal reconstruction: Grade I

Severe intermittent claudication in an active person that interferes with gainful employment if the patient cannot control his condition by lifestyle modification and if he accepts the risks of operation.

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

Grade II

Rest pain, moderate or severe, not relieved by nonsurgical conservative means. Grade III Nonhealing ulcers or gangrene, usually limited to toes or heel or both. The indications for grade I are generally for functional improvement. The indications for grades II and III are limb salvage. Femoropopliteal bypass grafting and thromboendarterectomy of the femoropopliteal segment are the two major procedures commonly used for reconstructing this arterial segment.

Femoropopliteal Bypass Graft Although Jeger (14) first described in 1913 the principle of bypass grafting for peripheral aneurysms (Fig. 42.6), it was not until 1948 that Kunlin independently introduced the procedure in the management of occlusive disease (9). The technique described by Kunlin consists of a parallel shunt with the occluded artery, using end-to-side anastomosis both proximally and distally. The rationale for this technique is the transporting of arterial blood around an occluded segment while avoiding operative trauma and interference with collaterals or damage to concomitant veins. This technique has been widely accepted in reconstructive peripheral arterial surgery and later for aortocoronary bypass grafts.

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Graft Materials After more than four decades of experience, autogenous veins still are the favored choice of graft material for the femoropopliteal bypass. Before the current era, at the start of the twentieth century, there were sporadic reports of the use of autogenous veins for arterial replacements, primarily for injuries or aneurysms. Goyanes, in 1906, replaced a popliteal aneurysm with the adjacent popliteal vein (15). Subsequently, Pringle (16), Bernheim (17), Lexer (18), and others reported successful transplants of veins for replacing arterial lesions. Kunlin must be credited with the reintroduction of the autogenous vein for reconstructive occlusive arterial lesions. The autogenous saphenous vein, when available, is considered the optimal graft material. It is obtained at the time of surgery and is prepared during the procedure. The availability of autogenous veins may be a problem in patients who have had previous surgical removal of their greater or lesser saphenous venous systems. Another problem may arise if an adequate length of saphenous vein is not available. Then, cephalic and basilic veins may be used successfully, either alone or combined with the saphenous vein (19–22). In the absence of autologous veins, use of fresh and cryopreserved homologous veins has been reported in the past by a few surgeons. Further experience with homologous vein grafts is necessary before their safety and feasibility are fully demonstrated. In any event, their absolute indications appear limited. This is especially true in light of newer graft material developments. Graft Material Developments

FIGURE 42.6 Bypass principle described by Jeger in 1913. (Reproduced by permission from Jeger W. Die Chirurgie der Blutgefasse und des Herzens. Berlin: A. Hirschwald, 1913.)

Among the grafts that either have gained clinical acceptance or are still being evaluated are expanded polytetrafluoroethylene, or PTFE (Gore-Tex and Impra), the glutaraldehyde-processed umbilical vein homograft (Meadox biograft), and a velour knit Dacron, which is a noncrimped and externally supported prosthesis (23). The detailed description of these various graft materials is found in Chapter 18, and we will mention only the highlights of each of these grafts. The PTFE graft is composed of expanded Teflon arranged as nodules connected by thin fibrils. It is a remarkably inert material, provoking little perigraft inflammation, and the inner surface has a strong electronegative potential, both features that very likely account for the graft’s resistance to thrombosis. Its clinical use, particularly in limb-salvage situations, has resulted in early patency rates comparable to those achieved with saphenous veins in femoropopliteal bypasses in both above- and below-knee positions. However, saphenous veins have better late primary patency rates below the knee, although limb salvage rates for vein and PTFE femoropopliteal bypasses remain comparable for more than 4 years (24).

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 42.7 (A) Position of patient for above-knee femoropopliteal bypass graft. (B, C, D) Note the interrupted skin incisions for harvesting the saphenous vein from the thigh and upper leg. Alternatively, a single long incision may be used.

A

B

C

D

The glutaraldehyde-stabilized human umbilical cord vein graft is covered with a netlike polyester mesh. The tanning agent molecule can establish crosslinks effectively and results in a stabilized graft that resists biodegradation. The umbilical vein graft is a collagenous tube lined by a thromboresistant basement membrane. Although patency rates of this graft compare equally or even favorably to those of PTFE grafts in the femoropopliteal position, the high incidence of aneurysmal degeneration that has been reported with this graft seems to contraindicate its widespread use (25–27). Dacron prostheses that are externally supported have been reported with a 78% patency rate at 4 years in the above-knee femoropopliteal site (23). These improved results contrast with the nonsupported external velour Weft-Knit Dacron that yielded a patency rate of 56% at 4 years and 40% at 10 years for the femoropopliteal above-knee position. The results with the Dacron grafts are encouraging and represent an additional concept in the development of vascular prostheses. In one prospective study, Dacron grafts used for aboveknee femoropopliteal bypass had 5-year patency rates equal to PTFE grafts (25).

Reversed Autogenous Vein Bypass* The femoropopliteal bypass graft may be carried out above or below the knee. Above-knee Procedure Position of Patient The patient is placed in the supine position with the thigh externally rotated and the knee flexed approximately 30° (Fig. 42.7A). This position affords easy exposure of the femoral and popliteal arteries, as well as of the saphenous vein. The skin of the abdomen, thigh, leg, and foot is prepared in the usual fashion. The medial aspect of the groin should be carefully draped and isolated from the adjacent perineal area by placing skin clips through the drapes and skin. The contralateral uninvolved extremity should be similarly prepared and draped in the event of the need for additional saphenous vein.

* Technique using the nonreversed in situ saphenous vein is described elsewhere in this book, although no proof of the superiority of in situ bypasses in the femoropopliteal position has been reported.

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

Incisions The skin incisions are made along the line of the femoral and popliteal arteries. Which artery should be exposed first depends on the arteriographic findings. If the supragenual popliteal artery appears of good caliber, the femoral is exposed first. However, should there be any question concerning the degree of involvement of the popliteal above the knee, it is best to start with its exposure. Exposure of Femoral Artery in the Groin A longitudinal, slightly curved skin incision, with the concavity facing the medial aspect, is made from above the inguinal crease and extended distally for 7.5 to 10 cm. (See Chapter 10 for exposure of the femoral artery.) The incision is made slightly lateral to the pulsation of the femoral to avoid the lymphatics as much as possible. Any minor bleeding or evidence of dividing lymphatics should be controlled by electrocoagulation or fine ligatures. Self-retaining retractors are placed and the lymphoadipose tissue is gently retracted medially. The deep fascia is opened along the femoral artery. The sheath of the artery is then opened along its axis. The common and superficial femoral are mobilized, and Silastic loops are placed about them. By elevating them slightly, the origin of the profunda comes into view laterally and posteriorly to the common femoral just proximal to the superficial femoral. Dissection of the origin of the profunda femoris should be carried out carefully to avoid injuring collaterals coming off at that level, as well as one or two branches of the satellite veins crossing the anterior portion of its initial segment. It is best to divide the latter and ligate them if mobilization of the profunda is difficult. Exposure of Proximal Popliteal Artery The surgeon stands at the opposite side of the table for the approach to the popliteal artery. The skin incision is made in the lower third of the thigh anterior to the sartorius muscle and is extended close to the medial aspect of the knee. The deep fascia anterior to the sartorius muscle is opened, and this muscle is detached from the vastus medialis and retracted posteriorly and medially. The posterior edge of the vastus medialis muscle is identified and retracted anteriorly. The popliteal artery is identified by palpation as the most superficial structure palpable through this exposure. The overlying fascia is incised, and the adipose tissue, usually present at this level, is dissected until the vascular bundle is reached. The sheath of the artery is opened. At this level, a network of venules surrounding the artery is almost always present and requires careful dissection from the arterial wall. This venous network is separated from the arterial adventitia, and the various branches are divided and ligated. The popliteal vein is then separated from the artery. This separation may sometimes be quite difficult because of the intimate connection between the two vessels. In separating them, it is important to avoid injuring any of

541

the genicular branches of the popliteal artery. The latter is freed over a length of approximately 3 to 5 cm, and loops are placed around it. Should the proximal popliteal artery appear markedly sclerotic and unsuitable for anastomosis to the graft, it is then necessary to extend the exposure to the midpopliteal. To do so, the hamstring muscles and their tendons should be mobilized and retracted posteriorly. Then the medial head of the gastrocnemius muscle should be divided close to the medial condyle of the femur. The sheath of the popliteal is then opened farther distally. The tributaries of the veins surrounding the artery must be further dissected away from the latter vessel. To facilitate the dissection of the midportion of the popliteal, flexion of the knee may be helpful in relaxing the artery, thus allowing it to be readily drawn closer to the surface of the wound. Harvesting of Saphenous Vein The saphenous vein may be obtained by means of a long single skin incision from the groin down to below the knee. However, our preference is to remove it through multiple skip incisions, as indicated in Figure 42.7B. Using shorter skin incisions offers the advantage of better healing with less danger of skin necrosis. Recently, endoscopic techniques have been used for vein harvest, and these have further diminished wound complications. The dissection of the saphenous vein is performed from the groin distally. The saphenofemoral junction is carefully mobilized, the vein is divided close to the femoral, and the proximal end is doubly ligated or oversewn. A small atraumatic bulldog clamp is placed on the distal end. The tributaries are ligated with fine silk close to their entrance into the main trunk, care being taken not to impinge on the wall of the latter. By careful dissection distalward and by elevating progressively the main trunk of the saphenous vein, all tributaries are identified and ligated. Below the knee, bifid trunks are often present and should be ligated and divided approximately 2.5 cm beyond their junction. They are removed with the main trunk to the used for an angioplastic procedure designed to enlarge the vein for the proximal anastomosis (see below). Before the vein is removed, placement of a marking suture of fine arterial silk through the adventitia may be useful for indicating its longitudinal position when it is placed through the tunnel (Fig. 42.8). Through the distal end of the divided vein, a small cannula is passed into it for irrigation with chilled Hanks’ solution or heparinized saline to expel any possible liquid blood or clots. The vein is then removed from its bed and placed immediately into a basin containing cold Hanks solution. The cannula is left in place to indicate the distal end of the graft, which has to be reversed when implanted into the artery. Studies have emphasized the role of optimum conditions for preparing the vein to prevent structural changes by suggesting the use of a balanced salt solution at 4°C and

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Part VI Chronic Arterial Occlusions of the Lower Extremities

FIGURE 42.8 Flushing and distention of the saphenous vein. Note the direction of valves and silk marking along the axis of the vein.

with a pH adjusted to 7.0 (28). Based on these data, these studies would indicate that structural alterations resulting from the type of handling of the vein may determine its ultimate biologic fate, although this remains to be proved. Developing Tunnel for Graft Before passing the graft from the femoral to the popliteal area, it is necessary to develop a tunnel that parallels the natural course of the arterial tree. It follows over the adductor longus tendon and Hunter’s canal beneath the sartorius muscle. A variety of tunnelers have been described and are available for developing a passage for the graft (29,30). Any of these tunnelers is satisfactory, provided one avoids trauma and twisting of the graft. Once the instrument has passed in the subsartorial region and the tunnel is developed, it is necessary to complete and enlarge the passage with digital dissection to destroy any strands of tissue that might interfere with the passage of the graft or produce a stricture through the tunnel. A red rubber catheter is then threaded through it to facilitate the placing of the graft later. Handling of Vein Graft The vein graft should be handled with extreme care. Application of arterial clamps on the trunk for any reason should be avoided to prevent injury to the intima or tears of branches at their junction with the wall of the vein. The ends of the graft may be clamped, provided they are later cut away. The vein should not be allowed to dry out while additional branches or rents are being repaired or while the anastomoses are being performed. The tributaries should be grasped by the end with a fine hemostat and sufficient traction applied upward. A fine No. 5-0 or 6-0 ligature is used to ligate the tributary at a point 1 or 2 mm distal to its junction with the main trunk. The ligature should not be placed too close to the wall, but neither should it be placed too far away from the junction with the main trunk. Implantation of the graft may be started in either the popliteal or femoral artery. Some surgeons do the distal anastomosis first, because it is usually the most difficult. Arteriotomy of Common Femoral Artery Administration of heparin before applying vascular clamps is routine.

A sharp No. 15 knife blade is used for a longitudinal arteriotomy into the anterior wall of the artery. A scalpel or iris scissors are used to enlarge the arteriotomy. If the edges of the latter are calcified and the atheromatous intima exceeds the cut edge, it is best to excise it by using arteriotomy scissors (31). (See Chapter 15). If the artery is diseased, we use a No. 15 blade to make the incision. The anastomotic opening of the artery should be long in relation to the diameter of the vessel. A 1.5–2 : 1 arteriotomyto-vessel diameter ratio is recommended. The reversed saphenous vein is then brought into the field. Its distal end becomes proximal for the anastomosis (Fig. 42.9). It is enlarged using a T incision to form a long anastomosis. Double-armed sutures are placed through the distal angle, with the needles going from the outside to the inside and then from the inside to the outside of the arteriotomy. Then a similar double-armed suture is passed through the proximal angle of the graft from outside to inside, and from inside to outside through the end of the arteriotomy. A running suture is used for approximating the edge of the vein to that of the arteriotomy, starting from the distal angle toward the proximal. After completion of one half of the anastomosis, the edge of the vein graft and that of the opposite side of the arteriotomy are separated for inspection of the inside of the lumen of the artery and of the appearance of the completed suture. A similar running suture is carried out from the distal end to the proximal for the other half of the anastomosis. The two sutures are tied together, thus completing the implantation of the graft (Fig. 42.9B). The graft is then distended by injecting heparinized saline solution into it to test for leaks from it or from the anastomotic site. A tunneler is then placed under the sartorius muscle and is brought out from the popliteal into the femoral area. The graft is attached at the end of the tunneler and is pulled through to the popliteal space. The black silk marker thread on the vein graft should help to orient the direction of the vein and thus avoid its twisting (Figs. 42.9C and 42.9D). Implantation of Graft into Popliteal Artery After it has been ascertained that the graft is properly oriented, it is important that it be placed posterior to the saphenous nerve. Before starting the distal anastomosis, one should ascertain the proper length of the graft to avoid redundancy. The vein wall opposite that of the artery is split in a fashion similar to that for the proximal end. After the corners are cut off, the graft is anastomosed to the arteriotomy of the popliteal artery. Its length, like that for the femoral artery, should be at least 1.5 to 2 times its diameter. The graft is attached by double-armed needks at its proximal angle and then in a similar fashion at its distal angle. The anastomosis is completed first in the center, since the ends are the most difficult and most critical to attach. The alternative is to start with the lateral edges of the graft, working from the proximal to the distal end. The

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FIGURE 42.9 (A) Completed exposure of the common femoral (1) and midpopliteal (2) arteries. (B) Proximal anastomosis of the vein into the common femoral artery. (C) Vein is pulled through the tunnel. Note the silk marking in the adventitial coat of the vein. (D) Graft is brought into the popliteal space. (E) Distal anastomosis of the graft is being completed.

B

C

A

D

E

anastomosis of the medial edges is then performed in a similar fashion (Fig. 42.9E). Before completing this anastomosis of the graft into the popliteal artery, routine distal flushing of the latter and then of the graft is carried out by releasing the respective occluding clamps in the proper sequence. Figures 42.10 and 42.11 show successful saphenous venous femoropopliteal bypasses, 1 year after surgery. Below-knee Procedure When the proximal and middle popliteal segments are unsuitable for implantation of the graft because of occlusion or marked stenosis, its infragenual portion, often uninvolved, may be selected for the distal anastomosis (Fig. 42.12). With the knee moderately flexed, a vertical incision of the skin is made just behind the posteromedial surface of the tibia. Care must be taken to avoid injuring the greater saphenous vein during the skin incision. The crural fascia is opened along its fibers, its distal attachments are separated from the semitendinosus and gracilis tendons, and the latter are mobilized pro-

ximally and may be divided if necessary. The medial head of the gastrocnemius muscle is retracted posteriorly to expose the popliteal artery and vein and posterior tibial nerve as these structures cross the popliteus muscle posteriorly. It should be noted that the distal popliteal artery has few branches below the inferior geniculate arteries, that atheromatous plaques are rarely present at this level, and that the arterial wall is often more suitable for graft implantation. The tunneling for the bypass from the femoral triangle to the infragenoal popliteal is carried out through the subsartorial space, the upper popliteal space, and then through the infragenual region behind the popliteus muscle. Although the exposure as described requires three separate incisions (see Fig. 42.12), it may also be carried out by only two incisions, using the upper femoral and a long medial one starting from the lower third of the thigh and extending all the way into the upper third of the leg 10 to 12.5 cm below the knee. Further exposure may be obtained by dividing the medial head of the gastrocnemius muscle. Except for the medial head of the gastrocnemius

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Part VI Chronic Arterial Occlusions of the Lower Extremities

FIGURE 42.10 Saphenous vein femoropopliteal bypass for occlusion of the superficial femoral and proximal popliteal arteries in a 54-year-old woman with ischemic lesions of the toes. Arteriogram taken 1 year postoperatively.

muscle, none of the other tendons is reconstructed at the end of the procedure. Because of occasional anatomic variations of the soleus in its proximal portion, it sometimes may be necessary to detach this from the tibia to expose the distal popliteal artery at its bifurcation. The first structure coming into view is the tibial nerve, which is closely associated with one or two popliteal veins accompanying the popliteal artery. After dissection and displacement of the tibial nerve and popliteal veins medially toward the surgeon, the popliteal artery is mobilized, freed, and brought out to a more superficial level. In doing so, it may be necessary to mobilize and sever one or more communicating venous tributaries connecting the two popliteal veins. Anastomosis of the vein graft into the distal popliteal then proceeds in a fashion similar to that in the aboveknee procedure.

FIGURE 42.11 Saphenous vein femoropopliteal bypass in a 58-year-old diabetic patient with gangrenous lesions of two toes and severe rest pain. Arteriogram taken 1 year postoperatively. Note minor redundancy of the graft. Lesions healed shortly after reestablishment of arterial flow.

Anatomic Variations, Pitfalls, and Safeguards Anatomic Considerations of Popliteal Bifurcation Anatomic variations in the division of the popliteal artery (Fig. 42.13), although infrequent, may be encountered in its infragenual portion. Recognition of such variations may assume important significance in the techniques used for anastomosing a vein graft into the popliteal artery or

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

545

FIGURE 42.12 Three separate skin incisions along the vascular axis (A) used for implantation of a saphenous vein below the knee (B).

FIGURE 42.13 Patterns of popliteal division into its branches: (1) popliteal, (2) anterior tibial, (3) posterior tibial or tibioperoneal trunk, (4) peroneal artery, and (5) posterior tibial. (A) Pattern 1. (B) Pattern 2. (C) Pattern 3. (D) Pattern 4. (See text for details.)

A

B

C

its branches. The localization of these branches by a good arteriogram is essential to preoperative planning. Morris et al. (32) and Bardsley and Staple (33) evaluated the variations in branching of the popliteal artery, based on several hundred arteriograms. From these studies it is possible to describe four main patterns of branching of the popliteal artery (see Fig. 42.13).

D 1.

2.

In approximately 90% of the cases, the most common pattern consists of the popliteal artery division more than 1 cm below the joint space into the anterior tibial and the tibioperoneal trunk, with the peroneal artery arising from the latter as a branch. A second pattern consists of a high division of the popliteal artery, usually behind the knee-joint space.

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Part VI Chronic Arterial Occlusions of the Lower Extremities

A third pattern consists also of a high division of the popliteal, as in pattern 2, but the peroneal arises from the anterior tibial. A fourth pattern consists of a trifurcation at a normal level but with the peroneal arising from the anterior tibial.

A

Although other minor variations are also described, from a surgical point of view it is well to remember that the normal pattern is present in almost 90% of the extremities. In patterns 2 and 3, instead of the infragenual popliteal, two tibial branches are present (32, 33).

B

Limitations Inherent in Veins as Grafts Limitations in the use of the saphenous vein may be related to the following factors: 1. 2. 3. 4. 5.

reduced diameter, below 3.5 mm; inadequate length; mural alterations of the vein due to dilatation or previous thrombosis; irreducible small diameter after attempted dilatation; or absence of the saphenous vein because of previous stripping (34,35).

C

FIGURE 42.14 Pitfalls related to improper ligation of tributaries of the main vein (see text for details).

Preoperative Saphenous Phlebography Clinical assessment of the saphenous vein for use as a bypass is not always possible. To obviate this uncertainty, preoperative phlebography, angioscopy, or duplex ultrasonography of the saphenous vein may help in determining its anatomic state, including its diameter, suitable length, valve competency, and venous anomalies, as well as the location of the last (36–38). Pitfalls in Preparing the Vein Graft Figure 42.14A1 indicates the placement of a ligature around a tributary, about 1 mm away from the main trunk. Figure 42.14A2 depicts the transection of the tributary after its ligation, and Figure 42.14A3 shows the length of its stump. Figure 42.14B1 indicates the use of a suture ligature, using a fine half-circle needle and No. 5–0 suture material. Figures 42.14B2 and 42.14B3 show the two steps for completing this figure-eight suture ligature. Figures 42.14A and 42.14B depict the correct methods for ligating tributaries. Figure 42.14C depicts improper ligatures of tributaries. Figure 42.14C1 shows a too-long stump of a tributary, resulting in its dilation. Figure 42.14C2 indicates a thrombus formation in the cul-de-sac, resulting from the improper length of the ligated tributary, although this problem is probably more theoretical than real. Figure 42.14C3 shows a ligature impinging on the wall of the vein, resulting in stenosis of the vessel at that level. Sometimes the stenosis may result from some of the adventitia of the main vessel being caught in the ligature. Eliminating

the point of constriction caused by the poorly placed ligature can sometimes be achieved by cutting away the adventitia at that level very carefully with a fine pair of scissors. Pitfalls Resulting from Incorrect End-to-side Anastomosis Figure 42.15A1 shows the two sutures at each end of the vein and arteriotomy. Figure 42.15A2 indicates completion of one row of anastomosis carried out in the direction of the arrow. The second row is started from the end of the previous one and is continued toward the first suture line. Figure 42.15B1 indicates completed anastomosis of the graft into the artery, showing a slight ballooning of the vein cuff. Figures 42.15A1 and 42.15B1 depict the correct appearance of an end-to-side anastomosis. Figure 42.15B2 shows bites too large in the vein graft, resulting in a stenosis of the graft anastomosis. This is an incorrect implantation into the artery. Figure 42.15B3 is another example of bites too large into the host artery, resulting in a stenosis of the latter at the anastomosis site. Figure 42.15B4 indicates an acute angle of implantation, with bites too large into the artery, also resulting in a stenosis of the artery. The last three types of anastomoses are incorrect. They can be prevented by avoiding bites too large into either the vein graft or host artery. These pitfalls may be partly prevented by excising some of the adventitia around the anastomosis.

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FIGURE 42.15 Correct end-to-side anastomosis and pitfalls resulting from incorrect end-to-side anastomosis (see text for details).

A

B

Angioplastic Technique for Improving Graft Diameter Although the distal anastomosis of a reversed saphenous vein is usually technically satisfactory because of its maximum width at that level, the proximal anastomosis, because of the smaller diameter of the vein, may result in a critical area of narrowing. Royle (39) described an improved technique for preparing the distal end of the reversed saphenous vein used for the proximal anastomosis (Fig. 42.16). The vein with a tributary is cut in a longitudinal direction, as indicated by the dotted line in Figure 42.16A1. Excess vein is excised to fit the arteriotomy. The corners of the opened vein are cut away (Fig. 42.16A2). After the adventitia around the edges of the vein has been trimmed away (Fig. 42.16A3), the anastomosis is carried out with a continuous suture, as shown in Figure 42.16A4. Use of a Bifid Saphenous Vein The two branches of the bifid vein are divided along the inner edges (Fig. 42.16B1). The anterior and posterior walls of the split branches are then sewed together, using fine suture material. This maneuver can be easily achieved by introducing a catheter of an appropriate diameter and suturing the two walls over this stent (Fig. 42.16B2). This angioplastic procedure is designed to obtain a greater length of the vein for a proximal anastomosis. Figure 42.17A1 indicates the splitting of the vein in the usual fashion and excision of the tips to provide an oval opening for an end-to-side anastomosis.

A

B

FIGURE 42.16 (A) An improved technique described by Royle for preparing the distal end of a reversed saphenous vein for proximal anastomosis. (Reproduced by permission from Royle JP. Autogenous vein bypass: an improved technique. Surgery 1966;60:795.) (B) Angioplastic

procedure for a bifid saphenous vein designed to obtain greater length for a proximal anastomosis (Linton’s procedure).

Techniques for Increasing Vessel Diameter To achieve a wider diameter, one may excise an area of bifurcation of the vein, as indicated in Figures 42.17B1 and 42.17B2. A variant of this technique for enlarging a diameter is shown in Figure 42.17C.

Use of Synthetic Prostheses for Bypass Grafts The indications for use of a synthetic prosthesis (Fig. 42.18) as a femoropopliteal bypass graft are essentially

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Part VI Chronic Arterial Occlusions of the Lower Extremities

A

B

B C

D

C

A FIGURE 42.17 Variants of the procedure for enlarging the diameter of veins, using their bifurcation branches (see text for details).

the absence of available autogenous vein, occasionally in cases of segmental occlusion of the superficial femoral with good popliteal-tibial runoff, and when there is urgent need for salvaging the limb with a questionable saphenous vein (24). Experience with some of the newer grafts such as PTFE and velour Dacron has shown that, in the aboveknee location, their patency rates and durability differ little from those of an autogenous vein. Although a longerterm experience with these newer grafts is not yet available to equate them with the 15- to 20-year statistics of the saphenous vein grafts, 3- to 5-year results are nevertheless encouraging. However, their use in the infrapopliteal leg arteries remains less than acceptable, thus leaving the autogenous saphenous vein the graft of choice (24). PTFE Bypass Graft The operative technique for PTFE bypass grafting is essentially the same as the standard one described for autologous saphenous vein grafting The graft size used generally for a femoropopliteal bypass graft is 6 mm in internal diameter. The shape com-

FIGURE 42.18 A synthetic prosthesis in femoropopliteal bypass graft above the knee (see text for details).

monly accepted is a straight tube. Experience with tapered tubes achieves less favorable hemodynamics than with a straight one, and as a result their use has been largely abandoned. The graft is beveled, with the length of the bevel being 1.5 to 2 times the diameter of the common femoral artery. The implantation of the graft may be started at either the proximal or the distal angle with Prolene 5–0 or 6–0. Care should be taken to avoid a disparity between the length of the bevel and the arteriotomy, which might otherwise result in a stenosis due to suture tension at the level of the anastomosis. It is important to ensure that the graft take off obliquely from the artery to avoid this pitfall. After its anastomosis is completed, the proximal clamp is momentarily opened to flush the graft. The subsartorial tunnel is prepared in the fashion described. The medial edge of the sartorius at the apex of the femoral incision is freed from its posterior connections. Similarly, the proximal angle of the popliteal exposure is enlarged, with the sartorius being retracted medially. A tunneler is introduced into the subsartorial region, with

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

549

FIGURE 42.19 (A) Left femoropopliteal PTFE 8-mm bypass graft implanted 3 days after an acute femoral and popliteal thrombosis in a borderline diabetic. This arteriogram was done 8 days postoperatively (July 1976). Note the arteriogram on the right side in which there is femoropopliteal occlusive disease for which a right lumbar sympathectomy was carried out 11 years before the left side’s acute arterial event. The then acute symptoms improved. Both limbs were salvaged. (B) The left femoropopliteal bypass graft 5 years (1981) after implantation of PTFE graft. Note some degree of tortuosity and layering of the graft. Clinically, the graft remains patent after 6.5 years.

A B

the graft being attached to it in the femoral area and pulled through into the popliteal space. Great care is taken to avoid any twisting or kinking of the graft during the passage through the tunnel. The exact length of the graft is then assessed and is beveled in the appropriate direction for its implantation into the popliteal. In performing a femoropopliteal bypass procedure, whether one should do the distal or proximal anastomosis first is a matter of personal preference. If the distal anastomosis is performed first, it is best to fill the graft with heparinized saline, which is left in the graft until the procedure is completed and bypass circulation restored. Because of its microstructure, the graft requires no preclotting. Air within the graft can be easily removed before institution of circulation by first releasing the occlusion at one end or the other until the graft fills with blood, since air is immediately displaced through its pores within the graft wall. Some sweating of serous droplets through the graft wall may be seen when circulation through the graft wall is begun. Such sweating is of no serious consequence and is in no way indicative of possible subsequent seroma formation postoperatively, because the serum protein in the graft wall will clot as soon as the heparin wears off or is neutralized.

After closure of the anastomoses, sometimes needlehole oozing or bleeding occurs, which can be controlled easily by application of Surgicel and pressure on the area for a few minutes. In general, oozing anastomoses are sealed as a result of gentle pressure rather than as a result of the hemostatic quality of the Surgicel (Figs. 42.19A and 42.19B). Use of Externally Supported Dacron Prostheses The technique used for implantation in the above-knee femoropopliteal position consists of placing the graft deep, with the length of the anastomosis about 2.5 to 3 times the diameter of the graft (Figs. 42.20 and 42.21). A 6-mm prosthesis is recommended for most patients. To reduce the thrombogenicity of the fibrin flow surface, it is necessary to inactivate thrombin through the action of heparin-activated antithrombin III in the fourth and final step of the preclotting procedure (23). Most of the experience with this type of graft has been reported by Kenney, Sauvage, and their group. The results for above-knee location of this graft are encouraging. Although the autogenous saphenous vein grafts remain the gold standard of graft materials for lowerextremity bypass procedures, the newer grafts offer a

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FIGURE 42.20 Dacron femoropopliteal bypass graft from the superficial femoral to the midpopliteal artery. Note the patency of all three leg arteries. The patient had ischemic and stasis ulcers of the leg, necessitating concomitant ligation and stripping of the saphenous veins. Arteriogram taken 5 years after surgery.

FIGURE 42.21 Dacron femoropopliteal bypass graft in a 66-year-old nondiabetic woman 6 years after its implantation. Note the patency of the peroneal artery.

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FIGURE 42.22 (A) A composite bypass graft, using a synthetic tube for the bypass around the superficial femoral artery occlusion, to the midpopliteal artery and a saphenous vein bypass from the midpopliteal to the distal popliteal artery below the knee. (B) Blowup of the distal anastomoses of the two grafts.

A B

number of advantages as a result of the time saved in preparing the vein graft, and their ready availability.

Sequential Grafting Lack of adequate length of autologous vein and the necessity for bypass grafting to the distal popliteal or to the infrapopliteal branches (small vessels) had led to the use of either a composite or sequential graft (Fig. 42.22). A composite graft consists of a combined proximal prosthetic (PTFE or Dacron) graft with a distal autologous vein. The prosthetic grafts are attached end-to-side proximally into the common femoral artery and distally into the above-knee popliteal artery. The reversed vein graft is preferably anastomosed first distally into the below-knee popliteal artery or into a leg artery, then the graft is tunneled in the usual anatomic fashion to above the knee for anastomosis into the prosthetic graft. The sequential technique, as defined originally by Edwards et al. (40), consists of a single graft (vein or PTFE) with multiple anastomoses for the purpose of reducing resistance and increasing flow. In this technique, the proximal and distal anastomoses are performed end-to-side, whereas the middle one or ones are side-to-side.

Both these concepts of composite and single bypass techniques have come to be known as “sequential grafting.” Several reports have shown that this concept of sequential bypass provides increased arterial flow, with improved hemodynamic results. Results of the sequential bypasses have been reported to improve distal perfusion in markedly ischemic limbs, leading to 1- to 8-year patency rates of 76% to 31%, respectively (41). When occlusion of the distal bypass occurs with continued patency of the proximal segment, it is due usually to poor distal runoff. Loss of limb in these cases may occur sometimes with a patent graft (42). Based on the reported experience, it is reasonable to attempt this technique in well-selected cases for the advantages, as pointed out above, that it offers.

Femoropopliteal Reconstruction in Diabetic Patients Peripheral arterial disease in diabetic patients is often associated with, and sometimes dominated by, two other important clinical manifestations: diabetic neuropathy and local infection. Their association, in varying degrees, lends to the lesions a truly characteristic clinical picture,

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often referred to as the “diabetic foot.” The clinical manifestations may thus be conveniently classified under the following four headings: 1. 2. 3. 4.

arteriosclerosis obliterans; peripheral neuropathy; infection; and combined lesions.

Accurate diagnosis and prompt treatment of circulatory disturbances seen in the extremities of diabetic patients, therefore, depend on determining the degree of participation of each of these three major causative factors. Thus it is essential to evaluate each patient from this triple point of view before deciding on the course to follow. Arteriographic patterns of diabetic versus nondiabetic patients have been reviewed in Chapter 38. Suffice it to state that usually the patient with diabetes has more involvement of the distal arterial tree (leg arteries and the popliteal artery) than the nondiabetic patient, in whom the lesions are more proximal but with frequent patent distal vessels, although this is by no means absolute, and diabetic patients with threatened limbs and ischemia have salvage rates comparable to those of nondiabetic patients (5,11). Careful selection of diabetic patients for reconstructive surgery is essential, although attempts at reconstruction in almost everyone with poor circulation are often rewarding (5,11). When selection of diabetic patients is based on good runoff of the popliteal and leg arteries, the patency rates of femoropopliteal reconstruction are no different from those obtained in nondiabetics (5,11). Wheelock and Filtzer (43) reported their experience with vein grafts in 100 diabetic patients with a 5-year cumulative patency of 72%. Even when cloth bypass grafts were used in diabetics, in the case of unavailability of saphenous vein, Harmon and Hoar (44) presented a 5-year cumulative patency of 59%. The latter results are similar to our own and others’ experience of 60% patency after 5 years or longer in patients in whom Dacron (Fig. 42.23) bypass grafts were used (45). Femoropopliteal endarterectomy has yielded generally poor results in this area. However, when endarterectomy is carried out for very short segments with good inflow and outflow tracts, the procedure is beneficial for limb-salvaging purposes. Such cases are best treated today by percutaneous transluminal angioplasty (PTA) (5,11).

Associated Intraoperative Measures The use of antiplatelet agents preoperatively and early postoperatively, before the use of anticoagulation, has been advocated. Anticoagulation Before temporary occlusion of the arteries, heparin sodium is administered intravenously, using 5000 to 7500 units, adjusted to the patient’s weight. In addition, heparin in solution with normal sodium chloride is used

subsequently for periodic irrigation of the graft or the distal arterial tree. Postoperatively, anticoagulants or dextran is not used unless a specific indication exists. Patency of the graft, as a rule, does not depend on such postoperative measures, although occasionally heparin or dextran may be used for prophylaxis of thromboembolic phenomena. Protamine sulfate may be administered after all occluding clamps are removed if the necessity for reversing the heparin effect is indicated. Otherwise, one should abstain from its routine use. These measures are discussed in Chapter 12. Intraoperative Arteriography At completion of the operative procedure, it is essential to evaluate the distal arterial patency. Testing the latter by the quality of backflow, graft pulsation, and Doppler flowmeter, although useful, may sometimes be misleading. If there is any question about outflow, arteriography is indicated. Presence of thrombi, distal anastomotic defect, or an intimal flap, detected intraoperatively by arteriography, can be easily managed or repaired. However, routine intraoperative arteriography may often be unnecessary and may unduly prolong the operating time. Its use should, therefore, be selective.

Complications Intraoperative and immediate postoperative complications include either thrombosis or hemorrhage. Early Thrombosis After completion of the anastomoses, pulsation of the graft and distal arteries should be observed while the proximal incision is being closed. The slightest decrease in the pulsation of the graft or of the distal arteries should immediately evoke the possibility of early thrombosis. There are three major areas where thrombosis may originate: 1. 2. 3.

the graft; the distal anastomosis; and the runoff.

Thrombosis in the graft may be due to inadequate clearance of fresh blood clots before completing the anastomosis. Accumulation of clotted blood in the graft is a serious pitfall and should be avoided during its implantation. Its palpation between the index finger and the thumb may help to identify the presence of the incipient blood clot. Its immediate recognition and management are essential before closing the operative wounds. If the distal anastomosis is the site of early thrombotic occlusion, it is usually due to a technical error or to an intimal distal flap. An arteriogram should help to delineate these lesions and provide a precise location for their proper repair. If leg arterial embolism or thrombosis is suspected, the balloon embolectomy catheter may be useful except for the anterior tibial artery that could not be reached because of its right-angle takeoff from the popliteal artery.

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

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B

C

A

It may then require a retrograde thromboembolectomy from the ankle level or direct exposure of this vessel (Chapter 32). Hemorrhage Intraoperative bleeding may occur as a result either of an untied small artery or vein branch, or of diffuse bleeding from the capillary bed. The former can easily be identified and the vessels ligated. The latter type, commonly associ-

FIGURE 42.23 (A) Femoropopliteal bypass, using a Dacron graft, in a 74-year-old diabetic patient. Note the absence of the distal popliteal, posterior tibial, and peroneal arteries and reentry of arterial flow into the anterior tibial artery. (B) Gangrene of the great toe, which separated 3 weeks later and was removed at bedside. (C) Intra-arterial pressures before and after the femoropopliteal graft. Note restoration of the pulsatile flow in the popliteal artery after graft implantation.

ated with heparin overdosage, can be controlled by reversing heparin’s effect with protamine sulfate. Immediate postoperative bleeding, after the wounds have been closed and exclusive of the above factors, may originate from the anastomotic sites or from the graft itself. Early reexploration is mandatory to avoid a tamponade effect from the accumulating blood, which may cause thrombosis of the graft. Only a few additional sutures of these areas are needed to control the bleeding.

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Hemorrhage occurring in the late postoperative period is usually due to infection or is associated with a false aneurysm. These two points are discussed later in this section. Postoperative Complications Lymphorrhea Inadvertent or unavoidable division of lymphatic vessels in the groin may result in drainage of cloudy, watery fluid. If drainage is minimal, the wound may heal spontaneously within 10 days. However, should the drainage be profuse and unyielding to daily dressings, one may have to open the wound and ligate any visible lymphatics or mass-ligate some areas of the subcutaneous tissue. Bedrest with the legs elevated, application of an elastic stocking, and antibiotics should be instituted. Edema Edema of the lower extremity is frequently observed, most often after successful reconstructive surgery of the femoropopliteal segment. It usually persists from a few weeks to several months postoperatively. Its mechanism is not entirely elucidated, although several theories have been advanced to account for it, such as deep venous thrombosis, sudden reestablishment of high arterial pressure with a compromised venous return, and postoperative lymphatic abnormalities. The role of deep venous thrombosis was based more on indirect evidence than on venographic data. The latter usually failed to demonstrate deep venous occlusion. Husni (46) studied this complication in 137 arterial reconstructions of the lower extremity in which phlebograms and pressure studies disclosed normal venous channels and hemodynamics. He believed that the postoperative hyperemia and edema were related to the degree of preexistent ischemia. He concluded that the edema is most probably attributable to an increased hydrostatic pressure and filtration at the capillary end, secondary to an overstretched precapillary arterial tree. On the other hand, Vaughan et al. (47), using lymphangiograms in 24 patients, found lymphatic abnormalities. Their study established that both superficial and deep lymphatic systems were damaged during the procedures. Although the mechanism of postarterial reconstructive edema is not entirely elucidated, the available evidence presented by the above and other investigators suggests that a combination of hemodynamic, lymphatic, and other yet unknown factors may account for this complication in the absence of venous thrombosis. Usually, in the mild form, the edema is self-limited after a few weeks. Infection Sepsis after a femoropopliteal bypass graft, although more frequently observed in the past, is fortunately seen today in less than 5% of the cases. A detailed account of the management of infection with vascular reconstruction is given in Chapters 53 and 62. Prophylactic measures consisting of antiseptic preparation of the skin in the groin for several days preceding surgery and use of antibiotics, especially if foot lesions are present, are of particular importance. If groin skin infection is present

before surgery, the latter should be postponed until the sepsis has been eradicated by local treatment and systemic antibiotics. Saphenous Neuropathy A not uncommon complication following a femoropopliteal bypass graft is saphenous neuropathy. The patient complains of pain along the medial aspect in the lower part of the thigh and the medial aspect of the leg. Its distribution coincides with that of the saphenous nerve dermatome. The severity of the pain varies from patient to patient. It may occur spontaneously, may be evoked by pressure on the involved region, or be aggravated by motion and exercise. It may appear as a mild transient discomfort or may assume a burning character; more rarely, it may be persistent and disabling. This pain is related to an operative injury to the nerve or may result from its entrapment in the scar tissue in the lower thigh. The neuropathy of the saphenous nerve can best be understood from the nerve’s anatomic relation to the femoral and popliteal vessels. It is exclusively a sensory nerve and originates in the distal part of the femoral triangle, lies close to the lateral side of the femoral artery, and thence descends in Hunter’s canal with the artery. At this point, it crosses superficially from the lateral to the medial side and then leaves the distal end of Hunter’s canal by piercing its aponeurotic roof. From there it passes to the tibial side of the knee and continues distally to the tibial side of the leg, accompanying the saphenous vein. Its terminal branches are distributed to the medial side of the leg and foot down to the level of the medial malleolus. The anatomic proximity of this nerve to the femoral and popliteal arteries accounts for the possibility of its injury in the course of the bypass procedure or during a thromboendarterectomy. Management of this neuropathy depends on the severity of the pain. For its mild form, injections of procaine in the area of maximum pain often permanently relieve the discomfort. The injections may have to be repeated several times until therapeutic effect is achieved. In the rare cases of entrapment in the scar, the nerve should be freed from the surrounding fibrous tissue. Prophylaxis against saphenous neuropathy should be achieved by protecting the nerve from any possible injury during the handling of the adjacent arteries. In closing the popliteal space, particular attention must be paid to the position of the nerve and avoidance of its inclusion in the suture line, either during the approximation of the sartorius to the vastus medialis or during suturing of the skin. Late Complications Graft Thrombosis Thrombosis of the graft may be related to 1) graft material, 2) proximal or distal progression of the underlying disease, or 3) anastomotic difficulties. Although considered the best available graft material, autogenous veins are far from being immune to failure because of a number of factors such as graft stenosis, anastomotic stenosis, anastomotic aneurysms, size of the vein,

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

and intimal hyperplasia or valve cusp stenosis (34,35). Most of these complicating factors can be identified if patients are followed at frequent regular intervals either by clinical evaluation or especially by Doppler and postoperative arteriograms. Correction of these lesions, preferably before thrombosis occurs, maintains patency in most patients. It has been estimated that the rate of thrombosis in vein grafts is approximately 3% per year (48). Even after vein and PTFE graft thrombosis has occurred, reoperation is remarkably effective in improving the arterial circulation and salvaging limbs that are threatened by the failure of the arterial reconstruction (49,50). False Aneurysms Late occurrence of false aneurysms is observed in both the femoral and popliteal areas, perhaps more frequently in the former location. Their detection and management are discussed in Chapters 64 and 65. Progression of Arterial Disease Progression of arterial disease may occur both proximal and distal to the femoropopliteal bypass (Fig. 42.24). Such lesions may be present before the bypass procedure but may remain undetected or hemodynamically not very significant. As the disease progresses, the intimal lesions may increase in size and become significant hemodynamically. In the presence of a decreasing inflow to the graft, it is important to detect such silent lesions first by a noninvasive method and to confirm them by an aortogram. In an angiographic survey of the femoropopliteal segment reported earlier, we found a rather high incidence of 27% of associated aortoiliac lesions (13). Lesions distal to the popliteal artery progressing after the implantation of the graft or after an endarterectomy have been demonstrated by a number of investigators (51,52). The morphology and rate of progression of the distal arterial outflow obstructions can be

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determined by preoperative and postoperative serial arteriograms (Fig. 42.25). Although progression of the disease either proximally or distally is sufficient to cause late failure of the graft, combined aortoiliac or tibial arteriosclerotic progression provides cumulative reasons for poor late prognosis. Downs and Morrow reported in 1972 on angiographic follow-up assessment of antogenous vein grafts and found proximal disease in 6 out of 56 cases and significant occlusive lesions in the distal outflow in 13 patients (53). If detected early enough, such lesions are remediable and allow graft salvage. Degenerative Changes of Graft Although autogenous venous bypass grafts in the femoropopliteal region have yielded good long-term functional results, a number of these grafts fail because of degenerative changes of the venous tissue itself. DeWeese et al. (54), Szilagyi et al. (55), and others have shown that these grafts may display histologic changes consisting of progressive thickening of the intima, progressive smooth muscle decrease of the media with an increase of collagen tissue, and increased vascularity extending from the adventitia. These changes are pressure-related, but atheromatous changes have also been observed by a number of investigators in recent years. These atherosclerotic changes are not unlike those observed experimentally in animals as reported by us (56) and other investigators (57,58). (See Chapter 39 for further details.) Of great significance are the potential causes of graft deterioration, when one considers that a third of the lesions observed by Szilagyi et al. (55) were seen over a period of 5 to 10 years. Thus, these defects may threaten the long-term function of the graft. Half of these defects may be preventable or remediable if detected early enough. Careful technique, avoiding traumatic and suture fibrosis, will prevent some of these

FIGURE 42.24 Superficial femoral occlusion (1) with involvement of the inflow (2) and outflow (3) tracts. (A) Segmental femoral occlusion with normal inflow and outflow tracts. (B) Inflow stenosis of the Iliac arteries. (C) Outflow stenosis of the poplitealtibial arteries. (D) Inflow and outflow tract involvement.

A

B

C

D

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FIGURE 42.25 Distal anastomosis of a femoropopliteal bypass graft with a marked stenosing plaque of the host popliteal artery distal to the graft.

complications. However, the intrinsic lesions to which the graft is susceptible, namely intimal thickening and atherosclerosis, are inherent in the new environment into which these grafts are placed (59,60). Subendothelial hypertrophy and mural layering are a major threat to patency whenever the distal hemodynamics are not satisfactory. Under these conditions, apparently the same process is destined to occur in the autogenous vein graft as has been observed abundantly in synthetic femoropopliteal prostheses (56–58). These degenerative changes may be difficult to prevent. Strict dietary control of lipid levels may delay the onset of this cause of late graft failure. Repeat examinations and duplex scans at periodic intervals may help in early detection of these lesions and their repair (10,61,62).

Neointimal (Graft) and Intimal (Recipient Artery) Hyperplasia In recent years, greater emphasis is being placed on anastomotic intimal hyperplasia as an important factor among the causes of graft failure. Indeed, in addition to progression of arteriosclerosis of the graft itself, much attention is being placed on the suture line reaction, mostly at distal

anastomoses. In many instances, these last changes occur without significant morphologic alterations in the remainder of the neointima of the graft. The anastomotic neointimal (graft side) and intimal (recipient artery) fibrotic hyperplasia has been observed in autogenous saphenous veins, with such plastic prostheses as Dacron, Teflon, and PTFE, and in endarterectomized arteries. It occurs in many arterial locations—femoropopliteal, infrapopliteal leg arteries, carotid, aortocoronary—but apparently has not been observed to be as common in the aortoiliac location. Failure of arterial grafts may occur early, within 30 days, or late, extending from a few months to a few years. In the peripheral circulation, it has been estimated that this complication is as high as 7%, whereas in the aortocoronary position, it is as high as 30% at 3-year followup. These changes may lead to complete occlusion of the graft, whether the intimal hyperplasia occurs proximal to the distal anastomosis or below it. The pathogenesis of this process, although not entirely understood, implicates a number of potential factors: arterial pressure and flow patterns (hemodynamics), shear stress forces, operative handling of the anastomosis, thrombogenicity of graft, and mechanical mismatch between graft and host artery (63–66). Prevention of these lesions is not always achievable because of their multifactorial nature. However, in recent years, use of antiplatelet drugs has been claimed to be effective in preventing the anastomotic neointimal fibrous hyperplasia. However, firm evidence that aspirin and dipyridamole inhibit its formation has not been presented in experimental or clinical data. The mechanism of action of these drugs is through blocking and the production of the prostaglandin endoperoxides PGG2 and PGH3 and thromboxane A2, thus inhibiting platelet aggregation. This effect is achieved only by low concentrations of aspirin. Higher doses of aspirin may actually have the opposite effect by promoting intravascular thrombosis. The administration of both aspirin and dipyridamole has a synergistic effect. These agents appear to prevent early thrombosis but probably do not prevent intimal hyperplasia (67).

Endarterectomy of the Femoropopliteal Segment Since the introduction of interventional radiology for managing stenotic and occlusive lesions for the femoral and popliteal arteries, endarterectomy has generally lost its usefulness in such cases. However, although PTA results are generally good in a substantial percentage of cases, endarterectomy or a bypass graft may be indicated if the PTA technique fails, since the failure may be due in part to inadequate correction of the small diameter of the vessels. Stents have not proved generally useful in the femoropopliteal segments of the arterial tree.

Chapter 42 Femoropopliteal Arteriosclerotic Occlusive Disease: Operative Treatment

References 1. Humphries AW, deWolfe VG, et al. Evaluation of the natural history and the results of treatment in occlusive arteriosclerosis involving the lower extremities. In: Wesolowski SA, Dennis C, eds. Fundamentals of vascular grafting. New York: McGraw-Hill, 1963:423. 2. Fontaine R, Kieny R, et al. Long-term results of restorative-arterial surgery in obstructive diseases of the arteries. J Cardiovasc Surg 1964;5:463. 3. Valdoni P, Venturini A. Considerations on late results of vascular prostheses for reconstructive surgery in congenital and acquired arterial disease. J Cardiovasc Surg 1964; 5:509. 4. Gensler SW, Haimovici H, et al. Study of vascular lesions in diabetic, nondiabetic patients. Arch Surg 1965;91: 617. 5. Veith FJ, Gupta SK, et al. Changing arteriosclerotic disease patterns and management strategies in lowerlimb-threatening ischemia. Ann Surg 1990;212:402. 6. DeWeese JA, Blaisdell FW, Foster JR. Optimal resources for vascular surgery. Committee on Vascular Surgery. Report of Inter-Society Commission for Heart Disease Resources. Circulation 1972;46:A-305. 7. Rutkow IM, Ernst CB. Vascular surgical manpower: Too much? Enough? Too little? Unknown? Arch Surg 1982; 117:1537. 8. Dos Santos JC. Sur la desobstruction des thromboses arterielles anciennes. Mem Acad Chir 1947;73:409. 9. Kunlin J. Le traitement de l’arterite obliterante par la greffe veineuse. Arch Ma Coeur 1949;42:371. 10. Veith FJ, Weiser RK, et al. Diagnosis and management of failing lower extremity arterial reconstructions prior to graft occlusion. J Cardiovase Surg 1984;25:381. 11. Veith VJ, Gupta SK, et al. Progress in limb salvage by reconstructive arterial surgery combined with new or improved adjunctive procedures. Ann Surg 1981;194:386. 12. Haimovici H. Patterns of arteriosclerotic lesions of the lower extremity. Arch Surg 1967;95:918. 13. Haimovici H, Steinman C. Aortoiliac angiographic patterns associated with femoropopliteal occlusive disease: significance in reconstructive arterial surgery. J Cardiovasc Surg 1969;65:232. 14. Jeger W. Die Chirurgie der Blutgefasse und des Herzens. Berlin: A. Hirschwald, 1913;262. 15. Goyanes J. Nuevos trabajos de chirugia vascular, substitucion plastica de las arterias por las venas o arterio plastia venosa, applicada como nuevo metodo, al tratamiento de los aneurismas. El Siglo Med 1906;53: 446,561. 16. Pringle JH. Two cases of vein grafting for the maintenance of direct arterial circulation. Lancet 1913;1:795. 17. Bernheim BM. The ideal operation for aneurysm of the extremity. Report of a case. Bull Johns Hopkins Hosp 1916;27:93. 18. Lexer E. Die ideale Operation des Arteriellen und des Arteriovenosen Aneurysmas. Arch Klin Chir 1907;83: 459. 19. Kakkar VV. The cephalic vein as a peripheral vascular graft. Surg Gynecol Obstet 1969;128:551. 20. Stipa S. The cephalic and basilic veins in peripheral arterial reconstructive surgery. Ann Surg 1972;175:581.

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21. Tice DA, Santoni E. Use of saphenous vein homografts for arterial reconstruction: a preliminary report. Surgery 1970;67:493. 22. Ochsner JL, DeCamp PT, Leonard GL. Experience with fresh venous allografts as an arterial substitute. Ann Surg 1971;173:933. 23. Kenney DA, Sauvage LR, et al. Comparison of noncrimped, externally supported (EXS) and crimped, nonsupported Dacron prostheses for axillofemoral and above-knee femoropopliteal bypass. Surgery 1982;92: 931. 24. Veith FJ, Gupta SK, et al. Six year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 1986; 3:104. 25. Bordik H, Wengerter K, Oin F, et al. Comparative decades of experience with glutaraldehyde-tanned human umbilical cord vein graft for lower extremity revasculaization: an analysis of 1275 cases. J Vasc Surg 2002;35:64. 26. Karkow WS, Cranley JJ, et al. Extended study of aneurysm formation in umbilical grafts. J Vasc Surg 1986;4:486. 27. Hasson JE, Newton WD, et al. Mural degeneration in the glutaraldehyde tanned umbilical vein graft. J Vasc Surg 1986;4:243. 28. Abbott WM, Weiland S, Austen WG. Structural changes during preparation of autogenous venous grafts. Surgery 1974;76:1031. 29. Lowenberg EL. An instrument to facilitate the long arterial bypass graft. Arch Surg 1960;80:306. 30. Jackson DR. An improved tunneling device for vascular reconstruction. Surgery 1969;66:807. 31. Haimovici H. Arteriotomy scissors. Surgery 1963;54: 745. 32. Morris GC, Beall AC, et al. Anatomical studies of the distal popliteal artery and its branches. Surg Forum 1960; 10:498. 33. Bardsley JL, Staple TW. Variations in branching of the popliteal artery. Radiology 1970;94:581. 34. Wengerter KR, Veith FJ. Influence of vein size (diameter) on infrapopliteal reversed vein graft patency. J Vasc Surg 1990;11:525. 35. Panetta TF, Veith FJ, et al. Unsuspected pre-existing saphenous vein disease: an unrecognized cause of vein bypass failure. J Vasc Surg 1992;15:102. 36. Sapala JA, Szilagyi DE. A simple aid in greater saphenous phlebography. Surg Gynecol Obstet 1975;140:265. 37. Veith FJ, Moss CM, et al. Preoperative saphenous venography in arterial reconstructions of the lower extremity. Surgery 1979;85:253. 38. Sales CM, Veith FJ, et al. Saphenous vein angioscopy: a valuable method to detect unsuspected venous pathology. J Vasc Surg 1993;18:198. 39. Royle JP, Autogenous vein bypass: an improved technique. Surgery 1966;60:795. 40. Edwards WS, Gerety E, et al. Multiple sequential femoral tibial grafting for severe ischemia. Surgery 1978;80:722. 41. Rosenfeld JC, Savarese RP, et al. Sequential femoropopliteal and femorotibial bypasses. Arch Surg 1981;116:1538.

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42. Flinn WR, Flanigan P, et al. Sequential femoral-tibial bypass grafting for limb salvage. Ann Surg 1976;80:722. 43. Wheelock FC, Filter HS. Femoral grafts in diabetics. Arch Surg 1969;99:776. 44. Harmon JW, Hoar CS Jr. Cloth femoral-popliteal bypass grafts in 29 diabetic patients. Arch Surg 1973;106:282. 45. Stipa S, Wheelock FC. A comparison of femoral artery grafts in diabetic and nondiabetic patients. Am J Surg 1971;121:223. 46. Husni LA. The edema of arterial reconstruction. Circulation 1967;35,36 (Suppl 1):169. 47. Vaughan BF, Slavotinek AH, Jepson RR. Edema of the lower limb after vascular operations. Surg Gynecol Obstet 1970;131:282. 48. Darling RC, Linton RR, Razzuk MA. Saphenous vein bypass grafts for femoropopliteal occlusive disease: a reappraisal. Surgery 1967;61:31. 49. Whittemore A, Clowes AW, et al. Secondary femoropopliteal reconstruction. Ann Surg 1981;193:35. 50. Veith FJ, Gupta SK, et al. Improved strategies for secondary operations on infrainguinal arteries. Ann Vasc Surg 1990;4:85. 51. Morton DL, Ehrenfeld WK, Wylie EJ. Significance of outflow obstruction after femoropopliteal endarterectomy. Arch Surg 1967;94:592. 52. Couch MP, Wheeler HB, et al. Factors influencing limb survival after femoropopliteal reconstruction. Arch Surg 1967;95:163. 53. Downs AR, Morrow IM. Angiographic assessment of autogenous vein grafts. Surgery 1972;72:699. 54. DeWeese JA, Terry R, et al. Autogenous venous femoropopliteal bypass grafts. Surgery 1966;59:28. 55. Szilagyi DE, Elliott JD, et al. Biologic fate of autogenous vein implants as arterial substitutes: clinical angiographic and histopathologic observations in femoropopliteal operations for atherosclerosis. Ann Surg 1973;178:232.

56. Haimovici H, Maier N. Autogenous vein grafts in experimental canine atherosclerosis. Arch Surg 1974;109:95. 57. Penn I, Schenk E, et al. Evaluation of the development of athero-arteriosclerosis in autogenous venous grafts inserted into the peripheral arterial system. Circulation 1965;31:192. 58. Scott HW Jr, Morgan CV, et al. Experimental atherosclerosis in autogenous venous grafts. Arch Surg 1970;101: 677. 59. Szilagyi DE, Hageman JH, et al. Autogenous vein grafting in femoropopliteal atherosclerosis: the limits of its effectiveness. Surgery 1979;86:836. 60. Haimovici H. Ideal arterial graft: an unmet challenge— scope and limitations. Surgery 1982;92:117. 61. Sanchez L, Veith FJ, et al. A ten-year experience with one hundred fifty failing or threatened vein and polytetrafluoroethylene arterial bypass grafts. J Vasc Surg 1991;14: 729. 62. Bandyk DF, Bergamini TM, et al. Durability of vein graft revision: the outcome of secondary procedures. J Vasc Surg 1991;13:200. 63. Imparato AM, Bracco A, et al. Intimal and neointimal fibrous proliferation causing failure of arterial reconstruction. Surgery 1972;72:1007. 64. Imparato AM, Baumann FG, et al. Electron microscope studies of experimentally produced fibromuscular arterial lesions. Surg Gynecol Obstet 1974;139:497. 65. Oblath RW, Buckley FO Jr, et al. Prevention of platelet aggregation and adherence to prosthetic vascular grafts by aspirin and dipyridamole. Surgery 1978;84:37. 66. Echave V, Koornick AR, et al. Intimal hyperplasia as a complication of the use of the polytetrafluoroethylene graft for femoral-popliteal bypass. Surgery 1979;85:395. 67. Chesebro JH, Clements IP, et al. A platelet-inhibitor-drug trial in coronary artery bypass operations. N Engl J Med 1982;307:73.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 43 In Situ Vein Bypass by Standard Surgical Technique Dhiraj M. Shah, R. Clement Darling III, Benjamin B. Chang, Paul B. Kreienberg, Philip S.K. Paty, Sean P. Roddy, Kathleen J. Ozsvath, and Manish Mehta

The concept of using the greater saphenous vein as a bypass by rendering its valves incompetent and leaving it within its subcutaneous bed was first introduced by Hall in 1962 (1). It provoked intermittent interest in both the western and the eastern hemispheres and was used and advocated by some vascular surgeons (2–6). More recently, the in situ vein bypass has gained widespread attention because of the introduction of the concept of producing valvular incompetency by valve incision and the development of effective instruments to accomplish this (7). This technique, plus the apparently superior results obtained when in situ bypasses are compared with reversed vein bypasses (8,9), has prompted many vascular surgeons to adopt the in Situ vein bypass for all infrainguinal reconstructions whenever possible (10,11). On the other hand, some surgeons have claimed that in situ vein bypass results appear superior only because they are compared with data from historical controls with reversed vein grafts, and that equally good results can be achieved with some of the more modern techniques of reversed vein grafting presented in Chapter 44 (12,13). The only prospective randomized studies of reversed vein grafts and in situ bypasses to date have produced conflicting results (14,15), probably because of critical

differences in the techniques used to prepare the in situ conduit.

Principles of the Method This chapter underscores the importance of the in situ vein bypass in the evolution of instruments for infrainguinal limb salvage surgery, and describes the techniques for performing it effectively. The popularity of the in situ vein bypass has prompted many vascular surgeons to attempt limb salvage arterial reconstructions that previously were being performed in only a few centers. The success of these in situ bypasses, often performed in disadvantageous circumstances, was due to the in situ nature of the bypass and to the careful semi-microtechniques used by those who have popularized this type of reconstruction. Since some patients not suitable for an in situ vein bypass will have ectopic vein available, thus for the present, a competent limb salvage surgeon should be capable of performing both in situ and reversed vein bypasses. Accordingly, this chapter describes the meticulous techniques that make in situ bypasses successful and does not attempt to answer the question of whether one is bet-

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ter than the other in a patient who could undergo either type of reconstruction.

Advantages and Disadvantages Despite these conflicting views, it is probable that endothelial preservation is paramount for optimal bypass function. This can be accomplished either by perfusion of the endothelium via the vasa vasorum or by continuous intraluminal flow. In the in situ bypass, both these routes are left intact during preparation of the bypass conduit; hence the preservation of this vital determinant is inherent in this technique. Therefore, conceptually, the problem can be viewed as largely logistic; that is, can a vein be harvested without inflicting other critical injuries, and can flow be reestablished before ischemic endothelial damage occurs? At present this goal is most consistently and completely achieved by leaving the vein in situ, provided the valves can be rendered incompetent without causing significant endothelial injury. With in situ vein bypass, the veins are left in their normal bed, so they cannot be twisted as they are placed in a new tunnel, a real threat with reversed vein grafts. However, care must be exercised to avoid twisting of the dissected proximal and distal ends of the in situ bypass. The in situ bypass is generally a better size match for anastomosis, with the larger end of the saphenous vein available for anastomosis to the femoral artery and the smaller distal end used for the small distal artery. However, we have not found size discrepancy a problem with reversed vein grafts, and occasionally a reversed vein graft will be smaller at its original central end than at its original peripheral end. Potential disadvantages of in situ vein bypasses include the possibility of leaving a partially competent valve, the slightly greater technical complexity, large AV fistula, and potential for twisting or kinking at the transition between mobilized and in situ segments. However, the operating time of in situ bypasses, as well as reversed bypasses, is more a function of the patient’s arterial and venous anatomy and disease than it is of the type of venous conduit preparation chosen for the arterial reconstruction.

Preoperative Assessment by Saphenous Phlebography In the early experience, preoperative assessment of the greater saphenous vein was limited to physical examination of its below-knee pathway. Saphenous phlebography was adopted after the encouraging report by Veith et al. of its safety and utility (16). It has proved invaluable in the preparation of the vein in situ and was mandatory if a valve cutter was to be used safely. Two methods have been used: preoperative phlebography, usually performed the day before surgery, and an intraoperative study, per-

formed in emergency situations or in those patients with impaired renal function. In more than 300 preoperative phlebograms using a remote vein on the dorsum of the foot of patients who have received heparin pretreatment, venography has proved safe while providing the relevant information for the efficient planning of this procedure. Currently, transcutaneous mapping of the saphenous vein by B-mode duplex ultrasound has been found to be an equally effective method for determining venous anatomy provided an experienced vascular laboratory is available (17). This noninvasive method provides a detailed three-dimensional map of the course of the saphenous vein that may be traced onto the overlying skin. This map aids in the placement of skin incisions and the location of venous access points for instrumentation. Furthermore, it avoids the risks associated with phlebography and can be routinely performed in approximately 30 minutes. Our initial experience with 345 limbs studied in this way demonstrates that, in more than 90% of patients, B-mode imaging is the optimum technique for venous assessment. In the less than 10% of cases in which complex systems are encountered, one may perform intraoperative phlebography because it provides additional information for accurate planning of the procedure. In spite of these considerations, many remain resistant to these preoperative assessments, preferring to determine anatomic variations at operation. However, such attempts to define them by surgical dissection may often be frustrating and ineffective. In addition, they may result in inappropriate excessive dissection, increasing the potential for spasm and other forms of injury to the vein, leading to failure and abandonment of the procedure, as well as to an increased incidence of serious wound complications.

Exposure of Saphenous Vein The primary concerns of most surgeons embarking on the use of the saphenous vein in situ for arterial bypass are identification and division of venous valves, as well as location and interruption of the large side branches that become arteriovenous (AV) fistulas when the vein is arterialized. These concerns have led to two technical approaches: 1.

2.

One method is to expose the vein over its length so that all technical maneuvers are in direct view, which is basic to operative surgery. This approach provides familiarity and confidence in performing this procedure when starting new (11). The alternative method, which we have arrived at through this “open” method, is to use the intraluminal valve cutter in the thigh portion of the vein, which is the largest and least tapered segment (18). This method allows safe use of this “blind” technique

Chapter 43 In Situ Vein Bypass by Standard Surgical Technique

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provided the vein is large enough for the cutter to be free-floating, thereby minimizing the potential for endothelial abrasion. As in all surgery there are trade-offs. With the open approach, there is a greater risk of injury to the vein directly and a greater chance of causing spasm and desiccation, in addition to an increase in wound healing problems. With the closed or blind approach, it is safe in 90% of cases provided the cutter is used on only the large segment of the vein (>3.5 mm) and that one has precise knowledge of the venous anatomy, gained either by ultrasound mapping or venography. It is tempting to extend this blind approach to the smaller-diameter portion of the vein below the knee. However, this extension exceeds the limit of this approach’s safety, because the risk of circumferential abrasion is greatly increased, not only because of decreasing vein size but also because of the propensity of these smaller veins to go into spasm when manipulated. The retrograde valvulotome, because of its minimal potential for endothelial contact, remains the safest instrument for valve incision in small veins, in open technique.

Angioscopy The use of an angioscope has been advocated by some as a means for cutting the valve leaflets under direct vision (19). Although perhaps comforting, its use is unnecessary because consistently safe and effective valve incision can be produced by the valvulotome or cutter. Furthermore, it is expensive and potentially injurious. The fear of a “missed” valve is more dependent on anatomy and experience than it is a function of currently available instrumentation.

Arteriovenous Fistulas in In Situ Saphenous Veins The effect of AV fistulas on in situ saphenous vein bypass hemodynamics and patency has been of great concern to some, even to the point of regarding them as a frequent cause of in situ bypass occlusion (20). From the outset more than 10 years ago, our practice has been to ligate only those fistulas that conduct enough dye during completion angiography to visualize the deep venous system (Fig. 43.1). The vast majority of the residual subcutaneous iatrogenic AV malformations will undergo spontaneous thrombosis. We have studied more than 200 such bypasses, using duplex ultrasound scanning to assess overall hemodynamic function. The results indicate a steady reduction in fistula flow, with no overall effect on distal perfusion (Fig. 43.2) (21). There is a small group in whom high fistula flow is poorly tolerated—usually they are patients with limited inflow capacity due to proximal

FIGURE 43.1 Identification of residual AV fistulas by intraoperative angiography using a needle grid.

stenosis or a small vein (<3 mm outside diameter). In most patients, however, the flow capacity of the in situ conduit far exceeds the sum demanded by the fistula and adequate distal perfusion. The allegation that fistulas are a potential cause of occlusive bypass failure is not true; rather, the probable cause of failure in this setting is endothelial injury in the distal vein, with that portion of the in situ conduit proximal to the fistula remaining patent because of flow to the fistula. Thus we regard fistulas as at most an annoyance to the patient and the surgeon, but not a crucial determinant of thrombosis of the bypass. Technically, the crucial issue in using the greater saphenous vein in situ and the primary reason for its excision and reversal for femoral-to-distal arterial bypass is to remove the valvular obstruction to arterial flow. In addition, its use in situ entails interruption of the venous side branches, which may become AV fistulas when the vein is arterialized, and the minimal mobilization of its ends for the construction of the proximal and distal anastomoses. The objective is to accomplish this with a minimum of operative manipulation of the vein and especially of the endothelial surface, with particular avoidance of circumferential longitudinal shear. The simplest, most expedient, and least traumatic method of rendering the bicuspid ve-

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FIGURE 43.2 Relation between distal bypass flow and fistula flow.

nous valve incompetent is to cut the leaflets in their major axes while they are held in the functionally closed position by fluid or arterial pressure from above. This is the essence of the valve incision technique (Fig. 43.3). Preparation for the operative procedure ideally should include the following: 1.

2. 3. 4.

preoperative digital arteriography, including the ankle and the foot, with multiplane views of the calf, not only to determine the true extent of disease in the vessels but also to accurately differentiate the anterior tibial artery from the peroneal artery; saphenous suitable duplex-generated map; marking the skin with the path of the saphenous vein below the knee; and assembling the operating table so that the foot is sufficiently extended to allow performance of all surgical manipulations from the knee down with the surgeon in a comfortable sitting position, with his arms resting on the table for proper use of microsurgical instruments.

In addition, the following equipment is necessary for the optimum performance of tibial artery bypasses: 1.

2.

operating loupes of at least 2.5 power (ideally 3.5 power) with an extended field, that is, a comfortable and easily accommodated field 7 to 8 cm in diameter and comparably deep; coaxial headlight, which provides ideal illumination required for optimal visual acuity;

FIGURE 43.3 Use of valve incision scissors with blunted tips.

3. 4. 5.

6.

7.

a Doppler ultrasound flow detector with sterile 8- or 10-MHz probe, preferably with a 3-mm tip; microsurgical instruments: forceps, needle holders, and Castroviejo scissors; a sterile orthopedic tourniquet cuff for use in place of occlusive vascular clamps or intraluminal balloons for control of calcified tibial vessels; calibrated handleless clips for truly atraumatic control of the saphenous vein and tibial arteries, for example, Yasargil or Weck microclips; items specific to the in situ procedure in addition to the valvulotomes and the cutter instruments: a sterile standard intravenous set; dextran 40 or 70 in a compliant plastic bag or a similar bag for drawing fresh blood; a pneumatic transfusion cuff; and papaverine hydrochloride (30 mg/mL).

After preparation and sterile draping of the entire extremity, warm papaverine solution (37 °C, 60 mg/500 mL of Plasma-lyte or normal saline) is injected percutaneously into the subcutaneous tissue adjacent to the saphenous vein along its course below the knee (22).

Chapter 43 In Situ Vein Bypass by Standard Surgical Technique

Techniques for Saphenous Implantation and Instrumentation The proximal saphenous vein, which lies immediately deep to the superficial fascia, is exposed, and papaverine solution is infiltrated into the surrounding tissue to minimize spasm. Although the common femoral artery has been considered the proper site for proximal anastomosis of all distal bypasses, there is evidence that use of the superficial femoral artery in some patients within the limb-salvage population is equally satisfactory (23). Furthermore, technical circumstances such as previous surgical use or exposure of the common femoral artery or its encasement with circumferential calcification make either the profunda femoris artery or the superficial femoral artery valid alternative inflow sources. Despite its less accessible anatomic location, the profunda femoris artery is usually less invested with thick or calcified plaque than either the common or superficial femoral arteries and, therefore, frequently provides the most satisfactory site for proximal anastomosis. It is best approached from the medial aspect (with the surgeon on the contralateral side of the table) by incision of the subcutaneous tissue immediately lateral to the saphenous vein down to the underlying investing myofascia. Dissection laterally in this fusion plane to the superficial femoral artery is bloodless. The fascia is incised over the superficial femoral artery, and, if it is occluded, a segment of 3 to 5 cm can be excised, thus facilitating exposure of the profunda femoris artery. The lateral circumflex femoral vein is divided, and the proximal profunda artery lies immediately deep to it. With the most satisfactory site of proximal anastomosis now determined, the length of the proximal saphenous vein required to reach the site is known. If the common femoral artery is to be used as the inflow source, complete dissection of the saphenous bulb and secure ligation of its branches is carried out. If additional length is required to facilitate anastomosis to the common femoral artery, a portion of the anterior aspect of the common femoral vein is removed in continuity with the saphenous bulb. An alternative to this approach is to preserve an appropriate length of the frequently present anterior branch at the saphenous bulb and to fillet it. The valve leaflets at the saphenofemoral junction are excised, removing only the transparent portion and leaving the usually prominent insertion ridge intact. The second valve invariably present 3 to 5 cm distal to this junction can be incised easily with a retrograde valvulotome through a side branch distal to the valve before the vein is divided, or, alternatively, it can be cut either with scissors or with an antegrade valvulotome through the open end of the vein, as is the valve immediately distal to the medial accessory branch. These

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valves are identified by gently distending the vein through its open end with dextran or heparinized blood and are cut with scissors, with the thumb and index finger around the shank of the scissor, while the valve is held in the functionally closed position by fluid trapped between the open end of the saphenous vein and the valve. The plane of closure of the valve cusps is invariably parallel to the skin. This position dictates the orientation of all instruments with relation to the valve cusps. If a valve cutter cannot be used, the location of the next valve site is determined by advancing a 6-Fr. catheter, with the infusion running under 200 mmHg of pressure until it impacts in the valve sinus. This location is marked on the skin, and the proximal anastomosis is carried out. The saphenous vein is thus arterialized. If the cutter is to be used, an incision of 3 to 5 cm is made 5 mm posterior to the position of the main saphenous vein, which was marked preoperatively on the skin, allowing identification of a predetermined branch seen on the venogram and using it to gain access to the lumen of the saphenous vein. A no. 3 Fogarty catheter is introduced into the saphenous vein through this side branch and is passed proximally, with the leg straightened, to exit through the open end of the vein. The catheter is then divided at an acute angle at the 20- or 30-cm mark, whichever is closest to the open end of the vein. The valve cutter is screwed onto the catheter; and an 8-Fr. catheter is then secured to the cutter with a loop of a fine suture. The leading cylinder of the cutter is drawn into the vein, providing a partial obturator obstruction to venous flow while permitting the visualization of the cutting blade and minimal resistance in torque, thus allowing precise orientation of the cutting edges at a 90° angle to the plane of closure of the valves, that is, to the plane of the overlying skin surface. The catheter–cutter assembly is then slowly drawn distally while the dextran solution or blood is introduced through the catheter at 200 to 300 mmHg pressure, with a pressure seal provided by a 1-mm Silastic rubber vessel loop secured by a small hemostat around the most proximal end of the saphenous vein. This pressurized fluid column snaps each successive valve to the closed position so that the cusps are efficiently engaged by the blades of the cutter (Fig. 43.4). A slight but definite resistance will be felt as the cutter encounters each valve and cuts the leaflets. Greater resistance than this should be managed by turning the cutter 45° and making another attempt at advancement. If this maneuver does not produce the desired result, the cutter should be withdrawn and dismounted, and the area of impaction should be exposed directly. The cutter is advanced through a predetermined safe distance, generally to the knee-joint level, and is then withdrawn to the femoral exposure. The cutter is dismounted, and the catheter is removed from the saphenous vein. Proximal anastomosis of the saphenous vein to the selected inflow artery is performed, and the pulsatile impulse thus pro-

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FIGURE 43.4 Mechanism of action of valve cutter.

FIGURE 43.6 Sites of distal anastomosis in 975 in situ arterial bypasses for limb-threatening ischemia.

FIGURE 43.5 Use of modified valvulotome.

vided will make the location of the next competent valve readily apparent. Continuity incision, exposing the full length of the saphenous vein, is necessary only if the cutter cannot be used and the combination of thick subcutaneous tissue, a small vein, and reduced pulsation due to the presence of an AV fistula makes the valve sites difficult to determine. The remaining valves are incised by means of a retrograde valvulotome introduced through a side branch or the distal end of the vein. This instrument is designed so that it will engage leaflets, center itself, and cut the leaflet in its longitudinal axis. It is then advanced again, carefully rotated through 180°, and withdrawn, thus engaging the remaining leaflet (Fig. 43.5). Before the cutting force is applied to the valvulotome tip, however, the valvulotome should be maneuvered toward the center of the vein lumen by depression of the vein itself, allowing division of the remaining leaflet without the risk of entering a side branch, which is invariably present and close to all valve sinuses. In passing the valvulotome intraluminally to and from a valve site, it is important that any pressure on the vein wall resulting

from the curving path be exerted on the shaft of the instrument rather than on the projecting blade tip. This precaution will lessen the likelihood of the blade becoming lodged in the branch and lacerating the vein wall. Unobstructed arterial pulsatile flow is thus brought to the desired level. Before transection and mobilization of the distal vein, exposure of the anticipated outflow anastomotic site is carried out. This exposure is desirable not only to minimize the warm ischemic time of the endothelium but also to assess the appropriate bypass length, always allowing an additional 1 to 2 cm so that the manipulated, and thus traumatized, terminal portion can be excised and discarded. After completion of the distal anastomosis, flow in the bypass, as well as in the outflow vessel, is confirmed, and a quantitative appraisal is made through use of the sterile Doppler ultrasound probe. A completion angiogram is then performed with radiopaque reference markers (e.g., 19-gauge needles in their plastic containers taped to the skin, a radiologic strip marker, or skin clips) to correlate the position of the fistulas as viewed on x-ray film with the surface anatomy. Most branches of the saphenous vein drain the superficial subcutaneous tissue, and their orifices are generally guarded by a competent valve, thus preventing flow away from the arterialized saphenous vein. Only valveless branches immediately become AV fistulas. However, they are usually small and generally undergo spontaneous thrombosis postoperatively. This thrombotic activity is signaled by the development of superficial phlebitis, the

Chapter 43 In Situ Vein Bypass by Standard Surgical Technique

extent of which is determined by the size of this iatrogenic AV malformation. Although occasionally a large area of induration results, it is sterile and self-limiting and invariably resolves within a few days. Even if these superficial veins remain patent, the loss of distal arterial flow is generally small and does not threaten the continued patency of a bypass. As a general rule, only those branches with sufficient flow to allow visualization of the deep venous system with radiopaque dye on the completion angiogram need be ligated. The normal closing mechanism in a symmetric venous valve is initiated by tension along the leading edge of the valve leaflet caused by expansion of the valve sinus from the raised intraluminal pressures. This tension brings the edge of the leaflet toward the center of the lumen so that flow forces it into the closed competent position. In any segment of vein in which a valve is mechanically opened from below by passage of an instrument (e.g., valvulotome or balloon catheter) in the proximal direction, there is potential for a valve leaflet to be pushed against the wall and to remain temporarily adherent to the valve sinus in the open position. This is most likely to occur in asymmetric valves. In asymmetric valves, the normal closing mechanism may not be operative so that the valve may remain open for an indefinite period of time. The subsequent closure, either spontaneous or induced, of the artificially opened valve leaflet by manipulation (e.g., palpation of the pulse in that area) results in partial or even complete obstruction of arterial flow. Therefore, before the operation is completed, deliberate attempts should be made to precipitate closure of any incompletely lysed valves by the following maneuver: with the distal vein open and free flow observed, a sponge is rolled along the in situ conduit from top to bottom. When the cutter is used, the most frequent location of a missed valve is in the segment immediately distal to the point of lowest cutter travel and at the level of exposure of the vein. This segment should be checked routinely with the valvulotome because, in the absence of flow, an undiminished pulse can be transmitted, even through an intact valve in a static hydraulic column.

Critique What appears to some as a disadvantage of the in situ technique is that, during preparation of the vein, its endothelial surface remains in constant contact with a static column of blood. However; the flow rate in the normal, nonarterialized saphenous vein is very low, approximately 5 to 10 mL per minute. In fact, in some areas the blood is actually stagnant for varying periods. Therefore the presence of a static column of blood in a conduit lined by viable endothelium is a normal physiologic state and does not result in thrombus formation provided that the endothelium has not been damaged. Such an injury is probably due to the shear forces caused by injudicious intraluminal instrumentation.

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Once endothelial disruption occurs, platelet adhesion and aggregation develop rapidly, particularly in areas of absent or low flow, and this buildup may subsequently jeopardize arterial flow. This buildup may first be detected by the loss or diminution of the pulse distally and by dampening of the Doppler velocity profile. Only temporary improvement follows the passage of the valvulotome to check for a residual valve leaflet. Buildup can also be confirmed by introducing a distal pressure-monitoring catheter and recording the pullback pressures or by finding a characteristic foamy surface filling defect on the operative angiogram. The simple expedient of assessing flow from the distal divided end of the saphenous vein before construction of the distal anastomosis is very reliable in detecting any proximal hemodynamically significant lesions. If there is steady, undiminished pulsatile flow, it is unlikely that such a lesion is present proximally. In practice, every effort should be made to prevent intimal injury and its resulting platelet aggregate. Instruments should be passed only when the vein is fully distended, preferably by arterialized blood and pressure, so that contact with the endothelium is prevented as much as possible. Particularly devastating is circumferential shear, especially in the distal mobilized segment, which is smallest in diameter and in which the protective effect of flowing blood through a coincident fistula before completion of the distal anastomosis is absent. Fortunately, this problem is infrequent with proper care of this critical segment—that is, strict avoidance of instruments exerting circumferential contact such as catheters, sounds, dilators, and cylindrical valve cutters of disruptors. When this shear does occur, the span of vein involved is usually short, and it can be easily corrected by removal, under direct vision, of the platelet debris from the area of injured endothelium and with the addition of an autogenous vein patch or by segmental replacement with a fresh segment of vein if the involved area is too long. In situ vein bypasses require careful preparation. Merely retaining the saphenous vein in situ does not compensate for sustained care, patience, and attention to detail, as well as consistent, meticulous surgical technique aided by optical magnification. Before attempting to adopt this technique, the surgeon should see it performed by an experienced operating team. In addition, familiarity with the use and feel of all instruments should be gained ex vivo on discarded valve-bearing vein segments obtained from aortocoronary bypass procedures, vein-stripping operations, or autopsy specimens.

Results An in situ bypass was attempted in more than 95% of the first 2000 consecutive patients in whom the ipsilateral greater saphenous vein was present requiring a distal arterial reconstruction for limb preservation. Of these attempts, less than 6% could not be reconstructed by the in situ technique; however, half of them were successfully

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TABLE 43.I Demographics Males Females Diabetics Smokers Mean age

2123 (63%) 1245 (37%) 1751 (52%) 1233 (37%) 69 (range 12–100 years)

completed using segments of autogenous vein grafts (a partial in situ bypass). In later years, in situ bypass vein availability dropped to 70% of patients requiring infrainguinal bypass. The incidence of perioperative occlusion has decreased steadily as greater care and control have been exercised to prevent endothelial injury, particularly in the distal mobilized vein segment. There is ample experimental and clinical evidence that endothelial integrity is best preserved by avoidance of the summation of a variety of injuries (i.e., spasm and the subsequent trauma from hydraulic dilatation required for its relief, particularly if a pressure exceeding 300 mmHg is used; exposure to nonhemic solutions; warm ischemic time exceeding 30 minutes; and the more obvious mechanical trauma of dissection, manipulation, and application of occluding clamps). Early detection of stenoses and correction of defects of in situ conduits before occlusion occurs can be achieved by a comprehensive follow-up program. Our patients are seen and examined every 3 months for the first 12 months, every 3 to 4 months up to the second year, and every 6 months thereafter. Each examination includes obtaining pulse-volume recordings and segmental pressures (ABI) and performing duplex assessment along the course of the bypass. More recently direct visualization of the conduit and estimates of volume flow by duplex ultrasound scanning, both at rest and after reactive hyperemia induced by 2 minutes of ischemia, have been used and evaluated. From 1975 to 2000, there were 6564 infrainguinal arterial reconstructions performed, of which 3368 (52%) were in situ bypasses, representing 62% (3368/5475) of all autogenous conduit in bypasses performed at our institutions. The percentage of autogenous bypasses suitable for in situ techniques has decreased over the years. Reasons include the use of the saphenous vein for cardiac revascularization, an increase in redo operations, and a willingness to use alternative and spliced vein in situations deemed unreconstructible earlier in this series (4,5). Demographic data is presented in Table 43.1. There was a predominance of males (nearly 2 : 1) and over half of patients were diabetic. Surgical indications are listed in Table 43.2. Indication for operation was predominantly limb salvage (88%) but the numbers for claudication have risen slightly over the years. The various sites used for the inflow artery and the outflow artery are presented in Tables 43.3 and 43.4 respectively. The common, superficial, and deep femoral arteries encompass the majority of inflow (38%, 35%, and

TABLE 43.2 Indications for in situ bypass Total Limb salvage Rest pain Tissue necrosis Claudication Aneurysm Trauma

3368 2953 (87.7%) 910 2043 300 (8.9%) 89 (2.6%) 26 (0.8%)

TABLE 43.3 Inflow sources Graft/iliac Common femoral Superficial femoral Profunda femoris Popliteal Tibial

127 (3.8%) 1286 (38.2%) 1177 (34.9%) 627 (18.6%) 142 (4.2%) 9 (0.3%)

TABLE 43.4 Distal outflow tract Above-knee popliteal Below-knee popliteal Tibioperoneal trunk Proximal anterior tibial Distal anterior tibial Dorsalis pedis Proximal posterior tibial Proximal peroneal Distal peroneal

50 (1.5%) 1015 (30.1%) 58 (1.7%) 299 (8.9%) 210 (6.2%) 307 (9.1%) 216 (6.4%) 622 (18.5%) 187 (5.6%)

19% respectively) while the below-knee popliteal artery (30%) is the most often used outflow. Of the tibial arteries, the peroneal was the most commonly used (24%) followed by the posterior tibial, anterior tibial, and dorsalis pedis arteries (18%, 15%, and 9%). Very few in situ bypasses were performed to the above-knee popliteal artery as there is an institutional preference to use prosthetic in the above-knee position or to go below the knee when the greater saphenous vein is used. Distal anastomoses to plantar and tarsal arteries are grouped with the distal posterior and dorsalis pedis groups and are not listed separately. Operative mortality was 3.3% and perioperative wound complications were 90 of 3368 (2.7%). Early occlusions occurred in 4.8%; early revisions occurred in 5.8% and included 43 fistulas and 54 retained valves. In long-term follow-up 381 patients required revision, 224 patients experienced late thrombosis, and 90 patients had limb loss, for the entire series. Primary patency at 5 and 10 years was 74% and 57% respectively and secondary patency is 84% and 69%. Patency was similar for all inflow arteries. Additionally, primary and secondary patency was independent of the distal sites. The dependence of in situ performance upon the vein diameter (outside diameter measured with full arterial pressure distention) was evaluated. Bypasses with vein 2.5 to 3.4 mm in diameter were compared to those 3.5 mm

Chapter 43 In Situ Vein Bypass by Standard Surgical Technique

and larger. Using log-rank analysis, veins ≥3.5 mm fared better, statistically, at 5 years and 10 years for both primary and secondary patency (5% difference). Subgroup analysis revealed this difference to be true at years 1 to 5 but not in years 6 to 10 of follow-up. The effect of demographic variables was examined. Specifically, these include gender and the presence of diabetes. No difference in secondary patency was seen through ten years of follow-up comparing men to women or diabetics to non-diabetics in all infrainguinal in situ reconstructions. Limb salvage rates were 99%, 96%, and 94% and cumulative patient survival was 96%, 68%, and 42% at 1, 5, and 10 years respectively. Notably, limb loss was almost nonexistent in the claudicant group, with one major amputation during 25 years. Not surprisingly, the limb salvage group had a relatively poor rate of survival. Conversely, fully a third of them were alive for 10-year follow-up, indicating that bypass performance is important for substantial numbers of patients beyond the 5-year window often reported.

Conclusion The major advantage of the saphenous vein when prepared in situ for an arterial bypass is the better preservation of a viable, physiologically active endothelium. The ability of such a conduit to maintain satisfactory longterm patency may make it possible to use smaller veins with limited outflow tracts that would otherwise be considered inadequate for use in other methods of reconstruction. Unquestionably, retaining the vein in situ decreases its accessibility. This procedure requires great care, patience, attention to detail, and meticulous surgical technique.

References 1. Hall KV. The great saphenous vein used in situ as arterial shunt after extirpation of the vein valves. A preliminary report. Surgery 1962; 51: 492. 2. Connolly JE, Harris JE, Mills W. Autogenous in situ saphenous vein bypass of femoral popliteal obliterative disease. Surgery 1964; 55: 144. 3. May AG, DeWeese JA, Rob CG. Arterialized in situ saphenous vein. Arch Surg 1965; 91: 743. 4. Connolly JE, Kwaan JHM. In situ saphenous vein bypass. Arch Surg 1982; 117: 1551. 5. Samuels PB, Plested WG, et al. In Sito saphenous vein arterial bypass: a study of the anatomy pertinent to its use as a bypass graft with a description of a new venous valvulotome. Am J Surg 1982; 34: 122.

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6. Gross JD, Bartels D, et al. Arterial reconstruction for distal disease of the lower extremities by the in situ vein graft technique. J Cardiovasc Surg 1982; 23: 231. 7. Leather RP, Shah DM, et al. Instrumental evolution of the valve incision method of in situ saphenous vein bypass. J Vasc Surg 1984: 1: 113. 8. Leather RP, Shah DM, Karmody AM. Infrapopliteal bypass for limb salvage: increased patency and utilization of the saphenous vein used in situ. Surgery 1981; 90: 1000. 9. Leather RP, Karmody AM. In situ saphenous vein arterial bypass for the treatment of limb ischemia. In: Mannick JA, ed. Advances in surgery, vol 19. Chicago: Year Book Medical Publishers, 1986: 175. 10. Levine AW, Bandyk DF, et al. Lessons learned in adopting the in situ saphenous vein bypass.J Vasc Surg 1985; 2: 146. 11. Fogle MA, Whittemore AD, et al. A comparison of in situ and reversed saphenous vein grafts for infrainguinal reconstruction.J Vasc Surg 1987; 5: 46. 12. Taylor LM, Phinney ES, Porter JM. Present status of reversed vein bypass for lower extremity revascularization. J Vasc Surg 1986; 3: 288. 13. Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage.J Vasc Surg 1985; 2: 552. 14. Harris PL, How TV, Jones DR. Prospectively randomized clinical trial to compare in situ and reversed saphenous vein grafts for femoropopliteal bypass. Br J Surg 1987; 74: 252. 15. Buchbindcr D, Singh JK, et al. Comparison of patency rate and structural changes of in situ and reversed vein arterial bypass. J Surg Res 1981: 30: 213. 16. Veith FJ, Moss CM, et al. Preoperative saphenous venography in arterial reconstructive surgery of the lower extremity. Surgery 1979; 85: 253. 17. Leopold PW, Shandall AA, et al. Initial experience comparing B-mode imaging and venography of the saphenous vein before in situ bypass. Am J Surg 1986; 152: 206. 18. Shah DM, Chang BB, et al. The anatomy of the greater saphenous venous system.J Vasc Surg 1986; 3: 273. 19. Fleischer HL, Thompson BW, et al. Angioscopically monitored saphenous vein valvulotomy. J Vasc Surg 1986; 4: 360. 20. Denton MJ. Hill D, Fairgrieve J. In situ femoropopliteal and distal vein bypass for limb salvage: experience of 50 cases. Br J Surg 1983; 70: 358. 21. Leopold PW, Kupinski AM, et al. Hemodynamic observations related to in situ bypass arteriovenous fistulac. Vasc Surg 1987; 21: 265. 22. LoGerfo FW, Quist WC, Crawshaw HW. An improved technique or endothelial morphology in view grafts. Surgery 1981; 90: 1015. 23. Veith FJ, Gupta SK, et al. Supcrficial femoral and popliteal arteries as inflow sites for distal bypasses. Surgery 1981: 90: 980.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage Frank J. Veith, Sushil K. Gupta, Evan C. Lipsitz, and Enrico Ascher

Over the past three decades, more aggressive attitudes have evolved concerning the performance of operations designed to salvage patient’s limbs when they are threatened by ischemic lesions due to arteriosclerosis below the inguinal ligament (1,2). Most of the developments reflecting these attitudes relate to interventions on arteries distal to the popliteal artery. However, some relate also to interventions on arteries between the inguinal ligament and the terminal end of the popliteal artery, and many of the latter deal with improvements in treatment that are possible when a primary arterial procedure has failed. This chapter deals with limb-salvage bypasses to the tibial and peroneal arteries, that is, so-called distal bypasses to so-called small arteries in the leg and foot. Since these bypasses are required and only justified in patients with threatened lower extremities and critical ischemia, they almost all have multisegment arteriosclerosis, usually with two or three levels of occlusive disease (1,2). Accordingly, in any consideration of distal bypasses, one cannot escape the fact that these operations are required in patients with severe generalized atherosclerosis and specifically in patients whose disease involves not only the tibial and peroneal arteries but also often the aorta, the iliac arteries, and the femoropopliteal system as well. Thus many of the points made in Chapter 42, Femoropopliteal Arteriosclerotic Occlusive Disease, apply equally well to the present chapter, which is

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designed to supplement the information provided in Chapter 42.

Developments Leading to Smallartery Reconstructive Surgery In the last two decades, several developments have occurred that have made distal bypasses to even diseased small arteries in the leg and foot possible (1,2). One was the evolution of arteriographic techniques, which routinely visualize all patent named arteries in the leg and foot. Only with accurate visualization and definition of all patent arteries and of the extent of occlusive and stenotic disease can bypasses to small distal arteries be planned appropriately. A second development was the evolution of instruments and methods for performing safe and effective surgery in small vessels. These specialized vascular techniques are not truly microvascular as they need not be performed through a microscope, although they may be facilitated with loop magnification and they draw heavily on the hardware and instruments developed for microvascular surgery. In this regard, fine forceps, Castroviejo needle holders, and fine atraumatic monofilament sutures with small swedged needles are particularly important. Of even greater importance is the realization by the surgeon that these operations cannot be

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

performed with standard vascular instruments or techniques but require specialized instruments, training, and methods with meticulous commitment to a myriad of details. A full discussion of all these technical details is beyond the scope of this chapter, which, however, does emphasize those details that are most important. Among the more important technical developments are those that facilitate surgical manipulations (occlusion, arteriotomy, and suturing), even in the presence of severe atheromatous involvement or heavy calcification (1–3), since many patients requiring these operations will have extensive disease in the patent segment of artery available for anastomosis. A third development that has contributed heavily to the evolution of limb salvage using small-artery distal bypasses and the present aggressive attitudes toward their use is the in situ vein bypass technique. This method was first introduced in 1962 by Hall (4) and has been popularized and strongly advocated by Leather and his colleagues (5), who have introduced improved instrumentation for rendering the vein valves incompetent. Although there are theoretic advantages to this form of vein preparation, which are fully discussed in Chapter 43, its superiority to comparable reversed vein bypasses performed with equal care has yet to be proved in a prospective controlled fashion (6). Moreover, many patients do not have a vein suitable for an in situ bypass but do have an ectopic vein that can be used for a reversed vein bypass (Fig. 44.1). However, the advocates of in situ bypasses deserve credit for promoting the careful semi-microtechniques that make small-artery bypasses successful. The increasing acceptance and effectiveness of these very distal procedures are probably due to this meticulous, careful technique rather than to whether the vein graft is of the in situ or reversed variety. Although in situ vein grafts may provide better patency rates than comparably performed reversed vein grafts when a very long graft with a small vein (<3 mm in diameter) is required, this remains to be proved. Moreover, the skilled limb-salvage surgeon should be capable of performing both types of bypass to small arteries since some patients may not be suitable for an in situ bypass and should not be denied an attempt at salvage of a threatened limb. A fourth development that has contributed to the evaluation and acceptance of small-artery bypasses is the short-vein bypass concept. Traditional practice dictated that all bypasses to the popliteal or more distal arteries should arise from the common femoral artery because of the frequency of disease in the superficial femoral artery. Since 1981 we have advocated use of more distal arteries, when suitable, as the sites of origin for all lower extremity bypasses (1,7,8). The superficial femoral, popliteal, and even tibial arteries have been used successfully in this capacity, with long-term patency rates that compare favorably with the standard longer bypasses. The use of shorter vein grafts clearly increases the availability of good quality autologous vein in many patients; it simplifies the operation. It allows the surgeon to avoid obese,

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FIGURE 44.1 Ectopic, short-vein graft used to perform a distal popliteal artery to proximal peroneal artery bypass. This patient had no usable vein in the ipsilateral extremity, and his opposite greater saphenous vein had been removed. The graft was from the short saphenous vein in the opposite leg. This arteriogram was performed 4 years after surgery.

scarred, or infected groins; and we have presented evidence that short-vein grafts have better patency than comparable long-vein grafts. Particularly when the bypass is to a disadvantaged outflow tract (Figs. 44.2 and 44.3) (2,8,23). A related development that has contributed to the evolution of small-artery reconstructions has been the realization that disadvantaged outflow arteries such as those connecting to incomplete plantar arches, those consisting of isolated or blind segments, and those with con-

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FIGURE 44.2 Intraoperative arteriogram of a shortvein bypass from the anterior tibial artery to the lateral tarsal branch of the dorsalis pedis artery for extensive foot gangrene. The plantar arch is incomplete. The graft was from the opposite leg since all ipsilateral veins had been used for aortocoronary bypass. This graft remains patent more than 3.5 years after operation. (Reproduced by permission from Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552.)

siderable disease or heavy calcification can sometimes serve as effective sites for bypass implantation (Figs. 44.2–44.6) (1–3,7,8). Thus almost all patients with a threatened limb will have some distal artery that can be used in a limb-salvage effort. This high operability rate is further increased by some of the recent improvements in anesthesiology and intensive care. With use of appropriate measures to improve and maintain the function of diseased hearts preoperatively, intraoperatively, and postoperatively, almost all patients, even those with severe heart disease, can, with reasonable safety, undergo even a long operation designed to save a limb (2).

FIGURE 44.3 Tibiotibial bypass to an isolated segment of anterior tibial artery. This arteriogram was obtained 6 months after operation. (Reproduced by permission from Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552.)

Interface of Small-artery Bypasses with More Proximal Revascularization Procedures Patients requiring distal bypasses frequently have, in addition to proximal occlusions in the infrapopliteal arteries, significant stenotic or occlusive disease involving the distal aorta, the iliac arteries, and the superficial femoral artery or the popliteal artery or both. Sometimes this disease may be segmental in nature so that these patients frequently have an isolated proximal patent segment distal to a hemodynamically significant stenosis or an occlusion. A patent common femoral artery distal to an iliac lesion

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

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FIGURE 44.4 Two views of an arteriogram performed 3 years after a posterior tibial-to-posterior tibial bypass. The bypass is inserted into an isolated segment of posterior tibial artery (i.e., the plantar arch is incomplete) and remains patent 6 years after operation. (Reproduced by permission from Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552.)

FIGURE 44.6 Postoperative arteriogram after a shortvein bypass on an isolated segment of dorsalis pedis or lateral tarsal artery that ends in a total occlusion. There is no plantar arch. Despite this lack, the graft is patent 2.5 years after operation. (Reproduced by permission from Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552.)

FIGURE 44.5 Arteriogram after a bypass from the tibioperoneal trunk to the posterior tibial artery at its bifurcation in the foot. Note small size of the vein graft. Despite this size, the graft is patent 3 years after operation. (Reproduced by permission from Veith FJ, Ascer E, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552.)

and outflowing into a normal deep femoral artery or a patent isolated or blind popliteal artery distal to a superficial femoral occlusion and with outflow only through patent collaterals are the two most common isolated segments. Clearly, any patient who is a candidate for a small-artery bypass should have any correctable, more proximal, stenosis or occlusion repaired first. Frequently this repair will be enough to obviate the need for the more difficult distal procedure because of the increased distal perfusion obtained from the “trickle-down effect” through collateral arteries. An example of this effect would be a patient with a hemodynamically significant stenosis of the left external iliac artery and occlusions of the superficial femoral, distal popliteal, and all proximal tibial arteries on the left. If this patient had only severe rest pain in the left foot, it would probably be relieved by an

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aortofemoral bypass or percutaneous transluminal angioplasty of the iliac artery stenosis. A bypass to the isolated popliteal segment might also be required if the iliac gradient were not large and would probably be required if the patient had significant foot gangrene. In this setting, the distal bypass should be performed only if a healed foot could not be obtained by performance of the simpler proximal procedures.

Isolated Popliteal Artery Segment Many patients who are candidates for a small-artery bypass by virtue of their having a patent tibial or peroneal artery with a continuous lumen extending into the foot will also have an isolated or almost isolated patent popliteal artery segment with flow only into the proximal portion of one tibial artery. The question of what operation to perform is clearly one of judgment and depends on many factors, including the quality and anatomy of the superficial veins as demonstrated by venography and duplex ultrasonography, the size and quality of the patent distal small artery, the extent of gangrene or infection in the foot, and, most importantly, the length and quality of the patent popliteal segment and the collateral arteries that arise from it (1,9,10). If the popliteal segment is fairly disease-free and long (>7 cm) and has good collaterals, and if the foot has little if any necrosis, we would advocate performing a femoropopliteal bypass. If, on the other hand, the patent popliteal segment was short but still greater than 7 cm in length and had poor collaterals, and the foot gangrene was extensive, a sequential femoro-topopliteal-to-small-vessel bypass should be performed primarily. If the patent popliteal segment is less than 7 cm in length, a primary small-artery bypass should be performed, although there may be exceptions. Occasionally after performing a femoropopliteal bypass to an isolated popliteal artery segment, a secondary distal bypass will be required to obtain healing of foot lesions (1,2,9). Judgment in these complex cases depends on these and a number of other variables, as well as on the surgeon’s and angiographer’s training and experience. It is precisely because of the complexity of this judgment and of the technical skills required to perform the operation that this form of limb-salvage vascular surgery requires special training, experience, and commitment. It is not a field that is well managed by the occasional or casual vascular surgeon.

Indications and Contraindications As bypasses to either of the tibial arteries or the peroneal artery are generally complex, difficult operations with a real incidence of early and late failure and some degree of operative morbidity and mortality, it is our opinion that these operations should rarely, if ever, be performed for intermittent claudication. Most patients with this symptom will readily accept the limitations it imposes on

their activity if they are told that an operation for claudication does not necessarily lower the risks of subsequent limb loss and that eventual failure of the operation may actually be associated with an increased risk to their limb. These facts mean that virtually all bypasses to arteries distal to the popliteal should be performed to save a limb that will otherwise be lost because of ischemia. Such critical ischemia is not always easy to determine, since patients with advanced ischemia and limited ischemic rest pain, small patches of gangrene, or ischemic ulceration may occasionally be improved through the use of analgesics and conservative measures, and this improvement may persist for protracted periods despite poor noninvasive indexes (11). These cases are rare. However, generally, these manifestations, if severe or extensive, will cause limb loss if the circulation is not improved by some form of arterial reconstruction or angioplasty. In cases in which the lesions are limited and the outcome uncertain, a trial period of hospitalization with conservative treatment may be warranted before undertaking a difficult distal bypass (11). Again, many factors influence this decision, and the experience and judgment of the surgeon are of paramount importance in deciding on the proper course of action. The need for such fine judgment is obviously not required to determine that operation is required for limb salvage when the patient has severe rest pain that interferes with nutrition and sleep or extensive enlarging gangrene or ulceration. It is more important, in the presence of such conditions and any significant distal ischemia as indicated by noninvasive tests, to avoid the performance of local ablative procedures on the toes or foot without first performing an appropriate arterial reconstruction, preferably one establishing direct pulsatile arterial flow to the foot. Only in this way will the circulation be adequate to control the necrosis and associated infection and to allow the foot to heal. Extensive gangrene in the foot, particularly gangrene of the heel, has long been regarded as a contraindication to performing a limb-salvage arterial bypass. Increasingly over the years, we have challenged this premise and have been able to show that functional remnants of foot can be obtained even when extensive necrosis and gangrene involve the bones and soft tissues of the forefoot or heel (1,2). A healed foot remnant, which can sometimes only be obtained with a split-thickness skin graft, will allow some of these aged, debilitated patients to ambulate far better than a below-knee amputation, even if the forefoot amputation is through the proximal tarsal bones or if the heel amputation involves the tuberosity of the os calcis and the Achilles tendon (1). Similarly, major amputation in preference to limbsalvage arterial reconstruction has been widely advocated for patients who are nonambulatory because of a previous contralateral amputation. However, we have found that these patients need their remaining lower extremity to transfer from bed to wheelchair to toilet and to be cared for by their family at home (1).

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

What then are contraindications to limb-salvage distal bypasses? Only such severe organic mental syndrome that the patient is completely out of contact with his environment, or gangrene and infection of the midportion of the foot, are absolute contraindications to attempts at limb salvage and indications for a primary major amputation. In some other cases, the patient’s cardiac status may be so precarious that operative risk for a bypass may be considered excessive. In such instances, our practice has been to discuss these risks with the patient and the immediate family and then to let them participate in the amputation versus limb-salvage decision. Invariably patients will opt for the limb-salvage attempt, even when the risks of failure or death are relatively large, and many of our advances in this field have been prompted by the wishes of courageous patients.

Surgical Techniques Distal bypasses to small infrapopliteal arteries are usually complex, technically demanding operations. They are time-consuming and require the surgeon to be committed to performing a variety of technical details with patience and expertise. Any flaw in any of these details can jeopardize the success of the procedure. The details that are described below represent one method for performing the operations. Undoubtedly there are other methods for accomplishing the same result. However, the methods presented do work, and the surgeon must remember that, regardless of which methods are used, there is no substitute for care, experience, and commitment to perfection.

Incisions and Approaches In virtually every instance, there are standard surgical approaches to all infrainguinal arteries, and there are unusual approaches which can be used when the standard approaches are impossible because of previous operative scarring or infection. The deep femoral and popliteal arteries may be used as sites of origin for bypasses to small arteries, in the presence of extensive groin scarring or infection. The second and third portions of the deep femoral artery can be approached directly through the medial or anterior thigh to provide an inflow site for a short-vein graft to a distal small vessel (12,13). In similar circumstances when the standard medial approaches to the popliteal artery are unusable, we have described lateral approaches to this artery both above and below the knee (14). In the usual circumstances, the surgical approaches to the femoral and popliteal arteries for the performance of distal bypasses are accomplished by the techniques described in Chapters 15 and 42. When the ipsilateral greater saphenous vein in the region of these arteries is to be used for the bypass, the incision is made over the vein (Fig. 44.7A), and the arteries are then reached by raising a subfascial flap (15).

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Tibioperoneal Trunk and Proximal Two-thirds of Posterior Tibial and Peroneal Arteries These vessels are usually approached through a medial incision below the knee (see Fig. 44.7A). The deep fascia is incised, and the popliteal fossa is entered. The arc of the soleus muscle must be defined and the soleus fibers cut to expose the distal popliteal artery, the tibioperoneal trunk, and the origin of the anterior tibial, the posterior tibial, and the peroneal arteries (Fig. 44.7B–D). Often the arteries are overlaid by the accompanying veins, and division of these veins or their branches is necessary to expose the arterial segment to be used for anastomosis. In Figure 44.7D the anterior tibial vein has been divided to provide arterial exposure. Direct exposure of the more distal segments of the posterior tibial or peroneal artery is obtained through a medial approach without first exposing the more proximal arteries. The soleus muscle is simply freed by incising its tibial attachments, and the vascular bundles are identified. The peroneal bundle approximates the medial border of the fibula. Once the bundle is found, careful dissection is required to separate the artery from the adjacent veins. No arterial branches, no matter how small, should be ligated or injured. Anterior Tibial Artery Except for its proximal 2.5 cm, which can be approached posteromedially with division of the interosseous membrane from its posteromedial aspect, this artery is best approached anterolaterally (Fig. 44.8). The incision is deepened into the muscle layers midway between the two bones. Accompanying veins can be used to trace a path to the artery, and the appropriate segment of artery is isolated by careful dissection, which often requires ligation and division of vein branches (Fig. 44.8C). Distal Peroneal, Anterior Tibial, Posterior Tibial, and Dorsalis Pedis Arteries These arteries are best approached through the incisions shown in Figure 44.9. The distal third of the peroneal artery is best accessed by removing a segment of overlying fibula as illustrated in Figure 44.9C. When approaching the distal anterior tibial or dorsalis pedis arteries, a gently curved incision is made, and a short skin and subcutaneous flap with a medial base is raised so that the artery and the anastomosis will be under the base of the flap rather than under the incision, in case incisional healing is imperfect (Fig. 44.9F,G). Unusual Approaches In case of medial scarring or infection or both, all three leg arteries can be reached through a lateral approach with fibula resection (13–17); the proximal anterior tibial artery can be reached from posteromedially with division of the interosseous membrane; the distal branches of the posterior tibial artery (i.e., the medial and lateral plantar

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arteries) can be reached in the sole of the foot (Figs. 44.5 and 44.10) (17); and the terminal branches of the dorsalis pedis artery (lateral tarsal artery and deep plantar arch) can be reached through an appropriate dorsal incision, sometimes with resection of one or more metatarsal bones (see Figs. 44.2 and 44.6) (17). All these vessels have been used successfully as bypass outflow sites (see Figs. 44.2, 44.5, 44.6, and 44.10). Moreover, the distal third of the peroneal artery can be approached and used for anastomosis by making a medial incision and dividing some of the long flexor muscles to aid in exposure. This approach is useful when an in situ vein graft is used.

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Graft Tunneling Bypass grafts are generally brought from inflow sites to outflow sites by subfascial tunnels if possible, minimizing graft exposure if wound breakdown occurs. The tunnels are constructed using a combination of finger and instrument dissection (Figs. 44.7E, 44.8D, and 44.9D). Particular care is required in transversing the interosseous membrane because of the abundance of vessels in the area. This membrane is best divided under direct vision from the front (see Fig. 44.8C). If subfascial planes are not readily available, subcutaneous tunnels may be used, and they are obligatory for bypasses to the distal anterior tibial and dorsal pedis arteries (Figs. 44.9D,E).

D C

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Clearly, autologous lower-extremity vein represents the best graft with which to perform bypasses to small leg and foot arteries. However, even autologous vein is far from an ideal graft for many reasons. Veins that appear large and healthy when first used may harbor unsuspected defects. Moreover, in some patients, even good veins, when used as a bypass, may for unexplained reasons develop focal or diffuse hyperplastic lesions that lead to their ultimate failure (18). We have observed the inexorable development of such lesions in both reversed and in situ grafts, even when the original operation was smooth and apparently flawless. If the stenosis is focal, detection and correction by percutaneous transluminal dilatation or operative patch angioplasty before graft thrombosis occurs can produce sustained good results (19,20). However, if the lesion containing a segment of the vein is superficial and easily approachable, we favor surgical correction. If the process is diffuse, detection in the failing state, that is, detection of

䉳 FIGURE 44.7 Technical steps for the medial approach to lower-extremity vessels, the harvest and preparation of the greater saphenous vein, arterial occlusion and incision, and anastomotic suturing. See text for details. (Reproduced by permission from Veith FJ, Gupta SK. Femoral-distal artery bypasses. In: Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

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C B B A

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FIGURE 44.8 Approach to the upper and middle thirds of the anterior tibial artery for performance of a distal bypass. Note details of cruciate incision in interosseous membrane and tunneling of the graft. See text for details. (Reproduced by permission from Veith FJ,

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Gupta SK. Femoral-distal artery bypasses. In: Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

a lesion before thrombosis occurs, is of little value, and graft occlusion is inevitable. Why some grafts in some patients behave this way remains an unanswered question and an important area for future investigation. When a patient’s ipsilateral greater saphenous vein is absent or too small (i.e., <3.5 mm in minimal distended external diameter for femoropopliteal bypasses or <3 mm for small-vessel bypasses) (21), the greater saphenous vein from the opposite extremity or the short saphenous vein may be used as the graft. We have found preoperative venography and duplex ultrasonography helpful in identifying usable vein segments and predicting their location and size (22). Unless their veins have been traumatized by previous surgery, most patients will have an adequate vein somewhere in their lower extremities, and this number can be increased by using the distal origin or short-vein graft concept whenever possible (7,8,23) When no usable lower-extremity vein exists, upperextremity veins (i.e., cephalic and basilic) can sometimes be helpful. However, these veins are generally thinwalled, have many fine branches, and, in our experience,

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FIGURE 44.9 Technical details in operations on the distal third of the three leg arteries. See text for details. (Reproduced by permission from Veith FJ, Gupta SK. Femoral-distal artery bypasses. In: Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

often have scarred, recanalized segments from previous venepunctures or intravenous infusions. Two undiseased segments may have to be anastomosed with an oblique union to provide a satisfactory graft. Prosthetic small-artery bypasses have been condemned by some vascular surgeons who have advocated a primary amputation as the treatment of choice when a patient, despite all efforts, truly does not have an autogenous vein graft and requires a bypass to a distal artery (24). We disagree with this recommendation and will perform a

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FIGURE 44.10 Postoperative arteriogram performed 1 year after a bypass to the lateral plantar branch of the posterior tibial artery.

prosthetic bypass with a polytetrafluoroethylene (PTFE) graft in this setting. Even though patency rates of these grafts are worse than those for vein grafts, some long-term patency can be obtained, and, more importantly, reasonable late limb-salvage rates can be achieved (25). Although glutaraldehyde-fixed umbilical vein grafts have been advocated as a vein alternative in this setting (26), the high incidence of aneurysm formation in this graft would seem to preclude its widespread use (27,28).

Technique for Reversed Vein Graft Preparation Although the relative merits of in situ and reversed vein grafts are discussed in Chapter 43, it is clear that some patients will have no vein suitable for an in situ graft. These patients usually will have an ectopic segment of usable vein, so all vascular surgeons should be proficient at techniques for harvesting and preparing a standard reversed vein graft. As with all aspects of distal bypass technique, patience and meticulous attention to detail are critical. As already mentioned, all incisions for approaching the involved arteries should be planned with vein harvest in mind. If the same incision is to be used for both procedures, it should be placed directly over the vein, and a subfascial flap should be raised to access the artery (see Fig. 44.7A). In this way, subcutaneous flaps can be avoided, and vein harvest complications minimized. We often use skip incisions for vein harvest. After the vein is exposed, it is carefully dissected free, and its branches are doubly ligated and divided so as not to cause any constriction by catching excess adventitia from the main vein. When the arterial dissections are completed and the vein graft is removed, all vein-harvest incisions are temporarily closed with skin staples to prevent desiccation of the subcutaneous fat. After completion of arterial anastomoses and reversal of heparin, these incisions are reopened, perfect hemostasis is obtained, and they are meticulously reapproximated in two layers.

As soon as the vein is removed from its bed, it is immersed in a 4°C Hanks’ solution, a balanced salt solution used in tissue culture. The vein is flushed with the same solution, using a long plastic cannula with a smooth end. This cannula is introduced progressively throughout the length of the vein, which is compartmentalized into segments of 4 to 5 cm by gentle finger pressure (Fig. 44.7F). These segments, with the end of the cannula lying within them, are gently distended with Hank’s solution. Any residual unligated branches or vein wall defects can be localized and carefully repaired over the stenting cannula with fine ligatures or No. 6-0 sutures. In this way, these sutures can obliterate the leaks without narrowing even small veins. The cannula is then advanced until the entire vein has been gently dilated and rendered leak-free. Although there may be theoretic reasons to avoid passage of the cannula through the entire lumen of the vein, we believe they are more than compensated for by the frequent nonocclusive intraluminal defects that occur and that can only be detected and eliminated in this way (29). These defects probably represent segments of recanalized thrombophlebitis. If undetected, they will cause graft failure because the narrowed lumen in such areas is crisscrossed with fibrous strands. These segments are detectable because palpation of the vein wall over the cannula reveals thickening or because the cannula’s passage is impeded by fibrous webs or strands (29). Once the vein is prepared, it is kept immersed in chilled Hanks’ solution until and, insofar as possible, during its implantation.

Technique for Occluding, Incising, and Suturing Small Arteries Although there are many techniques for accomplishing these objectives, the keynote for all is extreme care and delicacy. If techniques and instruments that are used on larger vessels are used on small arteries, injury may occur with untoward results, particularly when disease is present in the segment of vessel being occluded or sutured—a common occurrence in this group of patients. Arterial Occlusion Heparin (7500 IU) is administered intravenously before any arterial occlusion. Heparin (2500 IU) is then administered after every hour that an artery is occluded. To occlude these small arteries and render the lumen bloodless, simple gentle traction with single or double-looped Silastic vessel loops will often suffice (Fig. 44.7G). Minimal tension that prevents flow into the segment is all that should be used. This technique is particularly useful for soft, normal arteries. A second technique is to use microvascular spring-loaded clips (see Fig. 44.7G), which are also atraumatic. Occasionally these clips may also have to be placed on branches to obtain a dry field. If the vessel is thick-walled, atraumatic microclamps similar to those used on larger arteries, but smaller and gentler, are available. Care must be exercised to avoid twisting. If all these techniques fail, an intraluminal balloon catheter

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

(No. 2) may have to be used. However, passage of this or any other catheter into the lumen of these vessels carries considerable risk and should generally be avoided, particularly if the vessel is at all diseased. In the last 7 years we have used a tourniquet to obtain distal hemostasis and minimize arterial dissection. However, this technique may not be effective, particularly in patients with heavily calcified arteries. Arterial Incision To gain entrance to the lumen of small arteries, we use a new No. 15 scalpel blade (see Fig. 44.7G). Smaller (Beaver) blades are also available. If the artery is normal, microscissors (Fig. 44.7H-2) may be used. Generally, however, the artery is thick-walled or diseased, and use of any scissors will produce a jagged arteriotomy with overhanging or undercut intimal layers. We therefore carefully insert a microhemostat into the initial arteriotomy and complete the incision with a knife, cutting between the gently opened blades of the microhemostat (Fig. 44.7H1). In this way a clean, even incision of all layers is obtained (Fig. 44.7I-1). Suturing of the graft to the artery is performed under adequate (headlight) illumination, exercising extreme care to see every bite of graft and arterial wall, both from within and without. Double-armed running sutures are placed at the apex (toe) of the anastomosis and the heel. The apex suture is tied and carefully run along both sides of the anastomosis, catching equal small bites of graft and artery (Figs. 44.7I-1 and 44.7I-2). The heel suture is then tied and run similarly to both midpoints of the anastomosis, where it is tied. Frequent saline irrigations and optical (loop) magnification may be helpful in precise suture placement. One poor stitch at either end of the anastomosis can lead to failure. After the distal anastomosis is completed, the occlusion is released, and the graft and distal artery are flushed with heparinized saline. The graft is carefully passed through the previously made tunnels to avoid any twists. The proximal graft-to-artery anastomosis is then carried out with the same care, although larger clamps and slightly wider spaced suture bites may be used with the larger vessels. Calcified Arteries Even when calcification is extreme, as in some diabetics, arterial occlusion, incision, and suturing can be performed successfully (1,3). Our technique for dealing with these difficult arteries involves gentle crushing of the calcific deposits with a clamp. The resulting fractured fragments lie within an intact intimal envelope and rarely injure its continuity. If intimal tears occur, they can be repaired with U stitches carefully placed from within the lumen (3). After completion of all anastomoses, residual heparin is neutralized with protamine, and careful hemostasis is obtained. Intraoperative angiography or digital ciné fluo-

577

roscopy to visualize the graft, the distal anastomosis, and the outflow tract may be performed but may be misleading, with both false-positive and false-negative results. The wounds are closed carefully in layers using meticulous technique.

Foot Debridements and Minor Amputations If the ischemic foot contains necrotic tissue or undrained infection, the necrotic, infected material should be excised at the conclusion of the small-vessel bypass procedure, and the resulting wound left open. If limited gangrene of the heel or forefoot is present and there is no evidence of infection, the gangrene may be left alone, and it will slowly heal with the improved blood supply. Necrotic toes may have to be excised to achieve a healed foot. If infection is controlled, truly remarkable healing can occur after arterial reconstruction. On the other hand, infection may sometimes preclude healing even with uninterrupted arterial flow to the foot and despite all efforts at local drainage and debridement (1,9). The extent of infection and necrosis in the foot can often preclude salvage of all but a small remnant of the midfoot or hindfoot. Despite many opinions to the contrary, we have found such small foot remnants to be remarkably effective in maintaining bipedal ambulation and keeping patients out of nursing homes. Accordingly, we regard these foot remnants worthy of salvage, and almost uniformly the patients agree. Similarly, in many patients, a split-thickness skin graft may be required to obtain a healed foot wound. Even when placed on a weight-bearing surface, these grafts can function extremely well in helping to maintain a patient’s effective ambulation.

Results Mortality With improved anesthetic management and perioperative cardiac monitoring and intensive care, operative (1 month) mortality for these small-vessel bypasses has been low, in the 3% to 5% range, despite the facts that advanced coronary atherosclerosis and other diseases are present in most of the patients and that almost no patient was denied operation because of his or her medical risk status (1). Most of this mortality is due to perioperative cardiac events, chiefly myocardial infarction, and this event can occur even in patients presumed to be relatively good risks. In contrast to this low operative mortality, the late mortality from intercurrent coronary atherosclerosis in patients undergoing small-vessel bypass for limb salvage is very high. In 5 years, more than 50% of these patients will be dead from causes other than their infrainguinal arteriosclerosis or its treatment (1). This percentage underscores the facts that patients requiring operations are at

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Part VI Chronic Arterial Occlusions of the Lower Extremities

the end stage of their life and that the goal of surgical therapy should be palliation (1).

The morbidity of these operations stems chiefly from the protracted hospital stays that are often required to achieve a healed foot, particularly when gangrene and infection in the foot are extensive. In 7% of our limb-salvage patients, four to seven local operations and 2 to 4 months of hospitalization were required to achieve foot healing (1). Other factors contribute to this morbidity. Although wound infections involving the bypass are uncommon, occurring in less than 0.5% of our patients undergoing a primary distal bypass, wound problems involving the vein harvest site are common and increase the need for hospital care. These usually respond to conservative measures, although operative debridement and even skin grafting may occasionally be required.

Bypass Patency Primary patency is defined as the duration of bypass patency until the time of graft thrombosis or until the need for a secondary intervention to fix a problem with the arterial reconstruction. Figures for primary patency of bypasses to infrapopliteal arteries vary widely, depending on the graft used, the length of the vein graft (8,23), the criteria of operability, the operative techniques used, the outflow resistance (30), the number of patients observed after 2 years, the care during follow-up, and the methods used to determine patency. Although better results have been reported, a primary patency rate of approximately 50% in those patients surviving 5 years would be a reasonable expectation for small-vessel bypasses. Many of the bypasses considered “failures” can be rescued if the threatening lesion can be detected before thrombosis occurs (i.e., in the failing state), and be repaired (19,20,31). Furthermore, 15% to 30% of limb-salvage distal bypasses that thrombose do so without leading to a renewed threat to the limb, probably because the original lesion has been healed by virtue of the bypass and remains healed even after it fails (1). Patency and Graft Material Small-artery bypass primary patency has been reported from a large randomized prospective comparison of autogenous vein and PTFE grafts (32). Primary patency at 4 years with vein grafts was 49% ± 10% whereas with PTFE grafts it was 12% ± 7% (Fig. 44.11). The clear superiority of vein grafts for these operations is thereby established. Better patency and limb salvage results for PTFE distal bypasses have more recently been reported by our group (25). We therefore continue to perform PTFE bypasses to tibial and peroneal arteries without vein cuffs or patches, although many authors support their

Cumulative patency (%)

Morbidity

100 80 55 38

21

11

60

49%

40

39

20

ASV grafts (n = 106) PTFE grafts (n = 98)

0

22

16 12%

p⬍0.001 3

6

12

18

24

30

36

42

48

Time (months)

FIGURE 44.11 Cumulative life-table primary patency rate for all randomized bypasses to infrapopliteal arteries with autologous saphenous vein (ASV) and polytetrafluoroethylene (PTFE) grafts. Number with each point indicates number of grafts observed to be patent for that length of time. Standard error of each point is shown. (Reproduced by permission from Veith FJ, Gupta SK. et al. Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 1986,1:104.)

use. The value of such cuffs or patches remains uncertain (25).

Limb Salvage and Palliation Limb salvage is the parameter that is important to the patient. Limb-salvage rates consistently exceed primary bypass patency rates by 10% to 40% for a variety of reasons, even when the original bypass was performed for critical ischemia. Sustained healing after bypass failure has already been mentioned. The effectiveness of secondary interventions is probably of equal importance. Four-year limb salvage rates for distal bypasses in the cooperative study were 57% ± 10% for vein grafts and 61% ± 10% for PTFE grafts (Fig. 44.12) (32). Although these figures reflect the fate of the limb in patients who had surgery and survived 4 to 5 years, they do not tell the limb-salvage story in the larger fraction of patients who succumb within that period. The latter parameter is of importance in determining the value or merit of the operations from the patient’s perspective. Several years ago we showed that 81% to 95% of patients undergoing these operations and dying within 5 years kept their limb and used it effectively for walking until the time of their death (1). On the basis of all these data we concluded that limb-salvage small-vessel bypasses are generally worthwhile and provide better palliation than the alternative of a major above-knee or below-knee amputation. This is particularly true in light of the fact that more than 25% of our patients are so aged or infirm that they cannot learn to walk with a below-knee prosthesis (33).

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage 100 53

19

33

Limb salvage (%)

80

7 43

60

61% 57% 25

19

40

8 ASV grafts (n = 94) PTFE grafts (n = 87)

p ⬎ 9.5

20 0

6

12

18

24

30

36

42

48

Time (months)

FIGURE 44.12 Cumulative life-table limb salvage rates for patients with randomized autologous saphenous vein (ASV) and polytetrafluoroethylene (PTFE) grafts to infrapopliteal arteries. All operations represented here were performed to control critical ischemia. Number with each point indicates number of operated limbs observed to be intact for that length of time. Standard error of each point is shown. (Reproduced by permission from Veith FJ, Gupta SK. et al. Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 1986,1:104.)

Postoperative Follow-up and Reintervention Performance of a successful infrainguinal bypass of any sort does not preclude continuing progression of the atherosclerotic disease process. Moreover, in some patients, although fortunately not in all, the operation initiates the process of neointimal hyperplasia. This lesion can involve bypass inflow or outflow tracts if a prosthetic graft is used. If a vein graft is used, it can develop lumen-reducing hyperplastic lesions, which can be focal or diffuse. Any of these processes, as well as technical imperfections in the arterial reconstruction, can reduce its flow. This in turn can reduce the hemodynamic therapeutic effectiveness of the procedure and can lead to graft thrombosis. In light of all these processes, plus the advanced stage of the atherosclerosis in patients requiring limb-salvage bypasses to small infrapopliteal arteries, it is not surprising that up to 37% of these operations will, with time, fail (thrombose) or develop lesions that reduce their hemodynamic effectiveness (2).

Failing Graft Concept We and others have shown that, with frequent careful follow-up examinations by the surgeon and through noninvasive laboratory procedures, it is possible to detect hemodynamically significant lesions that threaten the patency of arterial reconstructions before they cause thrombosis (1,19,31,34–36). These lesions can be in or proximal or distal to the bypass graft. We have shown that

579

these lesions, if left untreated, will invariably result in graft thrombosis (19). Moreover, we have observed the failing state in arterial reconstructions performed with all types of vein grafts, as well as PTFE grafts, and we and others have been able to show that correction of the responsible lesions before they produce graft thrombosis is both simpler and more effective (19,20,31). Moreover, healthy segments of vein graft are not damaged by thrombosis and may continue to be useful. Because of these facts, it is extremely important to observe patients undergoing small-artery bypasses at frequent intervals. The surgeon should perform a careful pulse examination every 6 weeks for the first 6 months after operation. Thereafter the interval between examinations can be increased to 2 to 3 months. Ideally, noninvasive arterial tests should be performed with the same frequency. However, their cost may be prohibitive, and we have usually relied on the surgeon’s examination alone for most follow-up. With this modality alone, we have now been able to detect more than 150 failing grafts (37). When there is any change in a patient’s pulse examination in the involved extremity or if there is any return of symptoms, confirmatory noninvasive studies and arteriography are almost always performed on an urgent basis. If short stenotic lesions are found and they are inaccessible and can be treated by percutaneous balloon angioplasty, it is our preferred treatment. If the lesion is an occlusion or is not suitable for angioplasty or is easily accessible, a small operation is performed. Usually it takes the form of a veinpatch angioplasty, a short proximal or distal graft extension, or a short-vein bypass of a lesion in the original vein graft. Where vein is unavailable, PTFE may be substituted with surprisingly good results (38).

Failed or Thrombosed Distal Bypasses Early failure (within 30 days) of a distal bypass is usually associated with some technical imperfection, although rarely it may be due to poor selection of a distal outflow site and extremely high outflow resistance (30). Invariably if the original operation was for limb salvage, the limb with the failed graft will be threatened again, and urgent reoperation is indicated. The reconstruction is explored by opening the graft by a linear incision in its hood so that the thrombus can be removed with balloon catheters, the interior of the recipient artery can be carefully cleared of clot, and the anastomosis can be clearly visualized (39,40). Any defect is corrected. The proximal wound is reopened only if necessary. After closure of all arterial and graft openings with fine monofilament sutures, using techniques similar to those already described, intraoperative arteriography of the graft and outflow site is obtained. Any visualized defect is corrected. Distal graft pressure may be measured to rule out inflow gradients. Heparin is reversed. Hemostasis is obtained, and the wounds are closed. Perioperative antiplatelet agents, low-molecular-weight dextran, or dicumarol derivatives may be used, although there is no conclusive evidence of

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Part VI Chronic Arterial Occlusions of the Lower Extremities

their value and all these agents have potential risks and advantages. Late graft failure can occur at any time after 30 days. Failures occurring up to 18 months after operation are generally due to neointimal hyperplasia involving the graft or one anastomosis, usually the distal one (40). After that time, they are usually due to progression of atherosclerosis. Failures can occur in PTFE grafts to small arteries for no obvious reason, presumably because of this material’s greater thrombogenicity. If graft thrombosis occurs several months or years after a small-artery bypass, the patient’s foot may have healed and may remain so despite the decreased arterial flow. For that patient, repeat surgery is not indicated unless rest pain is truly intolerable even with analgesic medication. If, however, the limb is threatened again, full preoperative arteriography is performed in an attempt to determine the cause of the graft failure (e.g., an inflow lesion) but more importantly to determine what patent arterial segments exist for use in the performance of a new bypass (40). Almost always such segments are present at some level, and we have extensively used the distal deep femoral artery, the popliteal artery, and the same or other infrapopliteal arteries for such secondary short vein bypasses. The unusual approaches to these vessels discussed previously are particularly helpful in this regard. Usually, suitable short segments of a vein can also be found, but if not, PTFE grafts are a better option than a major amputation. Recently, lytic drugs and endovascular thrombectomy devices have also gained a place in the treatment of failed grafts, although they cannot displace the need for some open operations. Use of fluoroscopically assisted thromboembolectomy has also been reported by our group and is of great value (41).

Conclusion Bypasses to small infrapopliteal arteries in the leg or foot can, if performed properly, be useful operations that usually result in limb salvage and help to palliate patients threatened with loss of a lower limb. These operations must be based on accurate preoperative arteriography and should be conducted in centers with individuals who are committed not only to the operative details of the bypass operation but also to the preoperative, intraoperative, and postoperative intensive care required. Moreover, because of the nature of the disease process, ultimate failure of a sizable fraction of these operations is to be expected. Accordingly, diligent follow-up is essential to detect and correct significant lesions in the “failing state,” that is, before graft thrombosis occurs. Also important is the commitment to perform difficult repeat operations when failure with graft thrombosis occurs. With these provisos, gratifying results can be obtained in most patients requiring these operations.

Acknowledgments This work was supported in part by grants from the Manning Foundation, the Anna S. Brown Foundation, the New York Institute for Vascular Studies, and the William J. von Liebig Foundation.

References 1. Veith FJ, Gupta SR, et al. Progress in limb salvage by reconstructive arterial surgery combined with new or improved adjunctive procedures. Ann Surg 1981;194: 386. 2. Veith FJ, Gupta SK, et al. Changing arteriosclerotic disease patterns and management strategies in lower limb threatening ischemia. Ann Surg 1990;212:402. 3. Ascer E, Veith FJ, White-Flores S. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986;152:220. 4. Hall KV. The great saphenous vein used in situ as an arterial shunt after extirpation of the vein valves: a preliminary report. Surgery 1962;51:492. 5. Leather RP, Shah DM, et al. Infrapopliteal bypass for limb salvage: increased patency and utilization of the saphenous vein used “in situ.” Surgery 1981;90:1000. 6. Wengerter KR, Veith FJ, et al. Prospective randomized multicenter comparison of in situ and reversed vein infrapopliteal bypasses. J Vasc Surg 1991;12:189. 7. Veith FJ, Gupta SK, et al. Superficial femoral and popliteal arteries as inflow site for distal bypasses. Surgery 1981;90:980. 8. Veith FJ, Ascer F, et al. Tibiotibial vein bypass grafts: a new operation for limb salvage. J Vasc Surg 1985;2:552. 9. Veith FJ, Gupta SK, Daly V. Femoropopliteal bypass to the isolated popliteal segment: Is polytetrafluoroethylene graft acceptable? Surgery 1981;89:296. 10. Davis RC, Davies WT, Mannick JA. Bypass vein grafts in patients with distal popliteal artery occlusion. Am J Surg 1975;129:421. 11. Rivers SP, Veith FJ, et al. Successful conservative therapy of severe limb threatening ischemia: the value of nonsympathectomy. Surgery 1986;99:759. 12. Nunez A, Veith FJ, et al. Direct approach to the distal two portions of the deep femoral artery for origin or insertion of secondary bypasses. J Vasc Surg. 13. Veith FJ, Ascer E, et al. Unusual approaches to infrainguinal arteries. J Cardiovasc Surg 1987;28:58. 14. Veith FJ, Ascer E, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:119. 15. Veith FJ, Gupta SK. Femoral-distal artery bypasses. In: Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980:141. 16. Dardik H, Dardik I, Veith FJ. Exposure of the tibialperoneal arteries by a single lateral approach. Surgery 1974;75:337. 17. Veith FJ, Gupta SK, et al. Alternative approaches to the deep femoral, the popliteal and infrapopliteal arteries in the leg and foot. In: JJ Bergan, JST Yao, eds. Techniques in arterial surgery. Philadelphia: WB Saunders, 1990:145–156. 18. Szilagyi DE, Smith RF, et al. The biologic fate of auto-

Chapter 44 Small-artery Bypasses to the Tibial and Peroneal Arteries for Limb Salvage

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

genous vein implants as arterial substitutes: clinical, angiographic and histopathologic observations in femoropopliteal operations for atherosclerosis. Ann Surg 1973;178:232. Veith FJ, Weiser RK, et al. Diagnosis and management of failing lower extremity arterial reconstructions. J Cardiovasc Surg 1984;25:381. Ascer E, Collier P, et al. Reoperation for PTFE bypass failure: the importance of distal outflow site and operative technique in determining outcome. J Vasc Surg 1987;5:298. Wengerter KR, Veith FJ, et al. influence of vein size (diameter) on infrapopliteal reversed vein graft patency. J Vasc Surg 1990;11:525. Veith F, Moss CM, et al. Preoperative saphenous venography in arterial reconstructive surgery of the lower extremity. Surgery 1979;85:253. Ascer E, Veith FJ, et al. Short vein grafts: a superior option for arterial reconstructions to poor or compromised outflow tracts. J Vasc Surg 1988;7:370. Hobson RW II, Lynch TG, et al. Results of revascularization and amputation in severe lower extremity ischemia: a 5-year clinical experience. J Vasc Surg 1985;2: 174. Parsons RE, Suggs WD, Veith FJ, et al. Polytetrafluoroethylene bypasses to infrapopliteal arteries without cuffs or patches: a better option than amputation in patients without autologous vein. J Vasc Surg 1996;23:347. Dardik H, Baier RE, et al. Morphologic biophysical assessment of long-term human umbilical cord vein implants used as vascular conduits. Surg Gynecol Obstet 1982;154:17. Karkow WS, Cranley JJ, et al. Extended study of aneurysm formation in umbilical grafts. J Vasc Surg 1986;4:486. Hasson JE, Newton WD, et al. Mural degeneration in the glutaraldehyde tanned umbilical vein graft: incidence and implications. J Vasc Surg 1986;4:243. Panetta TF, Marin ML, et al. Unsuspected pre-existing saphenous vein disease: an unrecognized cause of vein bypass failure. J Vasc Surg 1992;15:102. Ascer E, Veith FJ, et al. Intraoperative outflow resistance

31. 32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

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as a predictor of late patency of femoropopliteal and infrapopliteal arterial bypasses. J Vasc Surg 1987;5: 820. Whittemore AD, Clowes AW, et al. Secondary femoropopliteal reconstruction. Ann Surg 1981;193:35. Veith FJ, Gupta SR, et al. Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 1986; J:104. Gupta SK, Veith FJ, et al. Cost analysis of operations for infrainguinal arteriosclerosis. Circulation 1982;66:(Suppl 2):9. O’Mara CS, Flinn WR, et al. Recognition and surgical management of patent hut hemodynamically failed arterial grafts. Ann Surg 1981;193:467. Ring EJ, Alpert JR, et al. Early experience with percutaneous transluminal angioplasty using a vinyl balloon catheter. Ann Surg 1980;191:438. Smith CR, Green RM, DeWeese JA. Pseudoocclusion of femoropopliteal bypass grafts. Circulation 1983;68(Suppl 2):88. Sanchez L, Gupta SK, et al. A ten-year experience with one hundred fifty failing or threatened vein and polytetrafluoroethylene arterial bypass grafts. J Vasc Surg 1991;14:729. Sanchez LA, Suggs WD, Veith FJ, et al. The merit of polytetrafluoroethylene extensions and interposition grafts to salvage failing infrainguinal vein bypasses. J Vasc Surg 1996;23:329. Veith FJ, Gupta SK, Daly V. Management of early and late thrombosis of expanded polytetrafluoroethylene (PTFE) femoropopliteal bypass grafts: favorable prognosis with appropriate reoperation. Surgery 1980;87:581. Veith FJ, Gupta SK, et al. Improved strategies for secondary operations on infrainguinal arteries. Ann Vasc Surg 1990;4:85. Parsons RE, Marin ML, Veith FJ, et al. Fluroscopically assisted thrombembolectomy: an improved method for treating acute arterial occlusions. Ann Vasc Surg 1996;10:201.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 45 Bypasses to Plantar Arteries and Other Branches of Tibial Arteries Enrico Ascher and William R. Yorkovich

More than half a century has elapsed since Jean Kunlin’s landmark publication described his clinical experience with a new type of arterial reconstruction to avert a major amputation in patients with severe occlusive disease of the superficial femoral artery (1). The efficacy and durability of femoropopliteal bypasses using reversed saphenous vein was confirmed by other investigators and has since become the procedure of choice over lumbar sympathectomy and endarterectomy (2–5). Subsequently, other surgeons extended the bypass of occluded arterial segments in the lower extremity to the major branches of the popliteal artery (6,7). Yet, although the majority of patients with lower extremity atherosclerotic occlusive disease involving, or threatening, tissue loss have a disease pattern amenable to arterial reconstruction above or below the knee (8), a small, but significant, number will require bypass to inframalleolar vessels. These bypasses to branches of tibial arteries in the foot have proved to be an acceptable alternative and are preferable to major amputation, especially in the elderly, diabetic population with limited rehabilitation potential in which this clinical presentation occurs most frequently (9–12). The following discussion will focus on the management of these patients, including a review of the anatomic relations important for vessel exposure, and the reported results. The indications for surgery remain tissue loss or rest pain. Preoperative evaluation with noninvasive segmental blood pressure measurements and pulse–volume recordings are useful not only to document and confirm clinical

582

impressions, but as a comparison for postoperative surveillance. Angiography is required to demonstrate both inflow and outflow sites for the bypass. Usually, the most distally available inflow site is preferentially utilized to shorten the length of the vein graft. Identification of a distal outflow vessel occasionally requires biplanar views to differentiate a “blind” dorsalis pedis artery from a lateral tarsal or the medial from the plantar arteries. Timedelayed imaging may be required to visualize the foot arteries because of the reduced flow. More recently, the use of magnetic resonance angiography has proved to be of benefit in identifying patent lower extremity arteries not demonstrated by conventional arteriographic techniques (13).

Anatomic Exposure and Techniques Plantar Arteries A thorough knowledge of the topographic anatomy of the foot is necessary to facilitate the exposure of these vessels. The posterior tibial artery bifurcates a short distance inferior to the medial malleolus into two major branches: the lateral and medial plantar arteries (Fig. 45.1). Exposure of the medial or lateral plantar arteries is facilitated by initially dissecting the retro-malleolar posterior tibial artery lying deep to the lacinate ligament (flexor retinaculum) (Fig. 45.2). Extension of the incision into the sole of

Chapter 45 Bypasses to Plantar Arteries and Other Branches of Tibial Arteries

FIGURE 45.1 The two major branches of the posterior tibial artery. The lateral plantar artery is usually the larger and forms the deep pedal arch, while the medial plantar supplies the intrinsic muscles of the first, second, and third digits.

FIGURE 45.2 The relation of the posterior tibial artery to the lacinate ligament and the abductor hallucis muscle is shown. Adequate exposure of the plantar arteries usually requires incision into the muscle.

the foot will ultimately expose the two main branches of the posterior tibial artery (Fig. 45.3). Although anatomic variation is not rare (14), the lateral plantar artery usually forms the main plantar arch and is larger than its medial counterpart. The smaller medial plantar artery supplies, via small collateral vessels, the intrinsic muscles of the first, second and third toes (Fig. 45.1). If the lateral plantar branch is occluded, then the medial plantar artery may enlarge and supply the arch via collaterals. We do not advocate a direct approach to these vessels for several reasons. Because the skin of the sole of the foot is thick and not easily retractable, adequate exposure is difficult unless the incision exactly follows the course of the vessel. Second, the small diameter of these vessels, coupled with their relatively deep location within the foot, makes their localization difficult when approached directly. Finally, because

583

FIGURE 45.3 Exposure of the distal portion of the posterior tibial artery and the lateral and medial plantar branches. This can be accomplished by incision of the flexor retinaculum and the abductor hallucis muscle. The larger lateral plantar branch is usually inferior to the medial plantar branch when the foot is externally rotated in the supine position.

FIGURE 45.4 The deep plantar arch is the main terminal branch of the dorsalis pedis artery. The inset highlights the origin of the deep plantar branch and its downward course between the base of the first and second metatarsal bones. This exposure is facilitated by the lateral retraction of the extensor hallucis brevis muscle.

the lateral plantar artery is usually larger and inferiorly located when the foot is externally rotated, its exposure and isolation is facilitated by observing the branch point from the posterior tibial artery. Once either of the vessels is identified and isolated, further exposure can be accomplished by incising the lacinate ligament along with transection of the abductor hallucis muscle. More distal exposure can be obtained by division of the medial border of the plantar aponeurosis and the flexor digitorum brevis muscle.

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 45.5 (A) The entire exposure of the deep plantar arch branch after partial resection of the second metatarsal bone. (B) Placement of the distal anastomosis can be easily accomplished through this exposure.

A B

Deep Plantar Artery The deep plantar arch branch of the dorsalis pedis artery is located by extending the initial incision used to identify the dorsalis pedis artery distally to the metatarsal bone level. The deep plantar branch originates at this point and courses through a foramen bounded proximally by the dorsal metatarsal ligament, distally by the dorsal interosseous muscle ring, and medially and laterally by the base of the first and second metatarsal bones (Fig. 45.4). Deep to the foramen, the plantar arch joins with the lateral plantar artery to form the deep pedal arch. Exposure of the artery within the foramen is improved by retracting or transecting the extensor hallucis brevis muscle along with elevating the periosteum of the proximal portion of the second metatarsal bone. This part of the bone is then excised using a rongeur, allowing ample exposure of the underlying deep plantar artery (Fig. 45.5).

Lateral Tarsal Artery One of the terminal branches of the dorsalis pedal artery, the lateral tarsal artery, is approached by identifying the patent artery at the junction of the ankle and the dorsum of the foot (Fig. 45.4). Using a curvilinear incision centered over the dorsum of the foot, the dorsalis pedis artery is dissected by dividing the extensor retinaculum. More distal dissection to the level of the navicular bone will reveal the origin of the lateral tarsal branch where it runs laterally toward the fifth metatarsal bone and then under the extensor digitorum brevis muscle. If more distal exposure of the artery is required, lateral retraction of the extensor digitorum longus tendon and partial excision of extensor hallucis brevis muscle can provide additional mobilization. This branch can be an important blood supply source to the dorsal aspect of the foot via its anastomosis with the arcuate artery. The technical aspects of the surgery are no different from those required for bypasses to more proximal arteries. Gentle handling of vessels, using a headlight for adequate illumination of the surgical field, fracturing of calcified

A

B

FIGURE 45.6 Positioning of the distal anastomosis for bypasses to branches of tibial arteries. (A) Limiting the anastomosis to a short tibial segment may give rise to turbulence with subsequent graft thrombosis. (B) Preferred technique of placing the distal anastomosis directly into the patent recipient branch.

arteries, placement of tacking sutures where necessary (15), and performance of completion angiography are all technical components useful for prolonging graft patency. When the recipient artery branch is patent in continuity with a short isolated tibial segment, the distal anastomosis should be placed directly across its origin (Fig. 45.6). The mandatory utilization of a vein as conduit is perhaps the single most important factor determining the long-term patency of these bypasses. Every effort, including the preparation of arm vein, must be made to procure an adequate length to complete the bypass.

Results Our experience over a 4-year period comprised 20 bypasses to named branches in the foot, performed with a 2-

Chapter 45 Bypasses to Plantar Arteries and Other Branches of Tibial Arteries

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FIGURE 45.7 Cumulative life-table primary graft patency rates for the 20 bypasses to foot branches. Number of patients at risk and standard error are shown at each interval.

FIGURE 45.9 Angiogram of a popliteal to medial plantar artery with reversed saphenous vein. Note the excellent size and ramification of the medial plantar artery when the origin of the lateral plantar artery is occluded. Graft patency and limb salvage were achieved in this diabetic patient for over 3 years.

FIGURE 45.8 Completion angiogram of a very short (6-cm) vein bypass from the distal posterior tibial artery to the lateral plantar artery. This bypass remained patent for over 2 years.

year patency of 81% as calculated by life-table analysis (9) (Fig. 45.7). No perioperative death occurred, although two patients died during the follow-up period from myocardial infarction. Limb salvage at 2 years was 85%. Wound complications occurred infrequently, with only two superficial wound infections noted at the vein harvest site. Acceptable results with bypass to plantar arteries were later reported by others, with 2-year patency rates ranging from 66% to 73% (10,11) and 2-year limb salvage of 89% (11). We have also reviewed our experience with plantar artery bypasses at Maimonides Medical Center from 1989 to 1994. Eleven patients with limb-threatening ischemia underwent unilateral bypasses to the plantar arteries (seven lateral plantar and four medial plantar). Ten of these bypasses remained patent from 6 months to 4 years (mean 18 months) (Figs. 45.8 and 45.9). The remaining bypass failed 2 years following implantation and led to a below-knee amputation. The results of these bypasses justified the intense effort required for their completion.

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These excellent patency results were obtained despite the relatively high outflow resistance measured intraoperatively. Previous reports have documented the correlation between elevated outflow resistance and graft patency (16). Perhaps negating the effect of elevated outflow resistance is the benefit obtained by using shorter-vein bypasses via the utilization of the most distally patent inflow source. We, and others, have noted improved patency rates in distal bypasses to vessels with compromised outflow tracts when the length of the graft is reduced to 40 cm or less (17,18). Whether this is a consequence of reduced incidence of fibrotic stenosis or less intimal injury remains speculative. Yet, these and other potential benefits, such as higher vein utilization rates, minimizing vein-harvest wound complications and avoiding excessively scarred or obese groins appear to be real advantages offered by use of the short-vein bypass.

Conclusion When intervening arterial segments are severely diseased, bypasses to branches of the tibial arteries in the foot are an acceptable means of obtaining limb salvage in patients otherwise facing major amputation. Use of autologous vein and minimizing the length of the graft by using the most distal acceptable inflow source appear to be the major factors predicting graft patency, despite the presence of poor or compromised outflow tracts represented by the absence of a pedal arch. In at least one report, there was an increased perioperative mortality associated with these most distal bypasses. However, when compared with those more proximal (19), the long-term survival rates were similar. This finding underscores that the preservation of limb in these patients is worthwhile and that perioperative evaluation and care must be meticulous. This extended approach to limb salvage should be included in the armamentarium of the vascular surgeon.

References 1. Kunlin J. Le traitment de l’arterite obliterante apr la greffe veineuse. Arch Mal Coeur 1949; 42: 371–375. 2. Julian OC, Dye WS, et al. Direct surgery of arteriosclerosis. Ann Surg 1952; 135: 459–474.

3. Pratt GH, Krahl E. Surgical therapy for the occluded artery. Am J Surg 1954; 87: 722–729. 4. Shaw RS, Wheelock F. Blood vessel grafts in the treatment of chronic occlusive disease in the femoral artery. Surgery 1955; 37: 94–104. 5. Dye WS, Grove WJ, et al. Two and four year behavior of vein grafts in the lower extremities. AMA Arch Surg 1956; 72: 164. 6. Morris GC, DeBakey ME, et al. Arterial bypass below the knee. Surg Gynecol Obstet 1956; 108: 321. 7. McCaughan JJ. Successful arterial grafts to the anterior tibial, posterior tibial (below the peroneal) and peroneal arteries. Angiology 1961; 12: 91–94. 8. Veith FJ, Gupta SK, et al. Changing arteriosclerotic disease patterns and management strategies in lowerlimb-threatening ischemia. Ann Surg 1990; 212: 402–414. 9. Ascer E, Veith FJ, Gupta SK. Bypasses of plantar arteries and other tibial branches: an extended approach to limb salvage. J Vasc Surg 1988; 8: 434–441. 10. Quinone-Baldrich WJ, Colburn MD, et al. Very distal for bypass for salvage of the very ischemic extremity. Am J Surg 1993; 166: 117–123. 11 Andros G, Harris RW, et al. Lateral plantar artery bypass grafting: defining the limits of foot revascularization. J Vasc Surg 1989; 10: 511–521. 12. Connors JP, Walsh DB, et al. Pedal branch artery bypass: a viable limb salvage option. J Vasc Surg 2000; 6: 1071–1079. 13. Carpenter JP, Owen RS, et al. Magnetic resonance angiography of peripheral runoff vessels. J Vasc Surg 1992; 16: 807–815. 14. Yamado T, Gloviczki P, et al. Variations of the arterial anatomy of the foot. Am J Surg 1993; 166: 130–135. 15. Ascer E, Veith FJ, White-Flores SA. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986; 152: 220–223. 16. Ascer E, Veith FJ, et al. Components of outflow resistance and their correlation with graft patency in lower extremity arterial reconstructions. J Vasc Surg 1984; 1: 817–828. 17. Ascer E, Veith FJ, et al. Short vein grafts: a superior option for arterial reconstructions to poor or compromised outflow tracts? J Vasc Surg 1988; 7: 370–378. 18. Andros G, Harris RW, et al. Bypass grafts to the ankle and foot. J Vasc Surg 1988; 7: 785–794. 19. Schneider JR, Walsh DB, et al. Pedal bypass versus tibial bypass with autogenous vein: a comparison of outcome and hemodynamic results. J Vasc Surg 1993; 17: 1029–1040.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 46 Extended Techniques for Limb Salvage Using Free Flaps David L. Feldman and L. Scott Levin

Autologous transplantation of composite tissue is a procedure widely used for the reconstruction of traumatic, congenital, and neoplastic deformities. This application of microsurgical technique has enabled reconstructive surgeons to heal complex wounds, restore disfiguring deformities, and salvage extremities threatened with amputation. A microvascular free flap is most often a one-stage transfer of a composite segment of muscle or skin and subcutaneous tissue made possible by the anastomosis of a single artery and one or two veins in the flap to an artery and vein or veins at the recipient site. Recent anatomic studies have enabled reconstructive surgeons to incorporate a variety of other tissues such as bone, nerve, and tendon into free flaps, and such studies have also made possible the tailoring of free flaps to meet specific needs of recipient wounds. The early twentieth-century work of Carrel and Guthrie included the establishment of the triangulation method, the use of the interposition vein graft, and the end-to-side anastomosis—techniques critical to the performance of modern microvascular surgery. In 1907 Carrel documented the first successful canine limb replantation in his historic manuscript “The Surgery of Blood Vessels” published in the Johns Hopkins Hospital Bulletin. In the early 1960s Jacobson and Suarez (1) and then Buncke and Buncke (2) pioneered the use of the operating microscope, which paved the way for successful replantation and transplantation of severed digits in monkeys. Soon to follow were developments in the study of cuta-

neous vascularization that helped identify territories of skin supplied by a solitary arterial and venous pedicle, the axial pattern flap. The first of these were the deltopectoral flap described by Bakamjian (3) and the groin flap described by McGregor and Jackson (4). An anatomic classification of muscle blood supply by Mathes and Nahai aided in the identification of those muscles best suited for free tissue transfer (5). Recent studies in microphysiology have tried to explain the no-reflow phenomenon whereby reconstitution of blood flow is associated with damage to the microvascular system. The application of microsurgery to salvage of limbs is currently in widespread use for traumatic defects as well as those found in the presence of chronic vascular insufficiency.

Indications Wound coverage can be achieved with a multitude of techniques ranging from simple closure to free tissue transfer. The “reconstructive ladder” (Fig. 46.1) provides a general approach to wound closure and a framework in which to view reconstructive procedures. Therefore, in considering appropriate indications for a microvascular flap, the surgeon must first examine simpler techniques available. Occasionally, primary wound closure or skin grafting can be used to heal extremity wounds. More sophisticated local flaps such as the reversed fasciosubcutaneous flap (6), medial plantar foot flap (7), and pedicled island flaps

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FIGURE 46.1 The reconstructive ladder.

(8) have been used to achieve wound closure in the lower extremity. Local flaps provide more stable coverage in areas such as the heel. Despite the fact that these options are considered “local” procedures, they require vascular inflow, so a full vascular workup of the affected extremity should be obtained prior to plastic surgery intervention in these patients. Select patients may require angioplasty or bypass to improve inflow. In general, a free microvascular flap is indicated for those wounds not amenable to simple closure, skin grafting, or local flaps—a relatively common situation in the distal lower extremity. The paucity of skin and subcutaneous tissue excess prevents primary closure and limits the size and mobility of local flaps. Skin grafts, both partial and full-thickness, provide mediocre coverage of lower extremity wounds with respect to long-term durability, especially in the foot. Skin grafting is not possible in patients with exposed tendon or bone. Prior to the use of free tissue transfer, distant pedicled flaps such as the cross-leg flap were used to help close such wounds. By definition, a pedicled flap from another region of the body must be delayed, thus requiring at least two and often three or more surgical procedures to complete the wound closure. (Free flap procedures are most often performed at one sitting.) Distant pedicled flaps require the immobilization of one or more extremities for a con-

siderable period of time. These positions can be difficult if not impossible in elderly patients or in patients with stiff joints (9). Free flaps in the extremity will require elevation, but there is rarely joint immobilization for an extended period of time. A cross-leg flap creates a wound on the other leg: a potential disaster in the vasculopathic patient. Perhaps most importantly, cross-leg flaps are parasitic to the recipient wound, whereas free flaps provide improved blood supply to an already compromised wound. Only in selected patients who are unsuitable for microvascular free tissue transfer (see below) is a cross-leg flap considered for lower extremity limb salvage. Free tissue transfer can provide stable coverage to large wounds, in virtually any location, as long as an adequate inflow vessel can be established. The wide variety of flaps currently available allows for tailor-made coverage of these wounds. The procedure is multifaceted, requiring dissection of both the donor flap and the recipient vessels, microsurgical anastomoses, insetting of the flap, and very often skin grafting. When one adds anesthesia preparation and positioning of the patient at the start of the case, and the dressing and splinting at the end of the case, the procedure can take from 4 to 6 hours. Thus appropriate preoperative medical evaluation is mandatory for even the healthiest patients. When considering free tissue transfer for limb salvage, as with contemplation of any other major procedure, the surgeon and patient must carefully weigh the risks and potential benefits of the procedure with its alternative —in this case amputation. Although the vascular surgery literature has documented a clear advantage (with respect to morbidity and mortality rates) for bypass procedures in limb salvage, no similar data exist confirming an advantage in the use of free tissue transfer in patients with “vasculitic ulcers” (10). Pederson refers to three potential contraindications to limb salvage with free tissue transfer: 1. 2. 3.

the presence of peripheral neuropathy (e.g., in diabetic patients); gait problems caused by Charcot joints or arthritic conditions; and poor general health (10).

Another consideration that should be addressed prior to free flap surgery is the patient’s ability to cooperate with the postoperative treatment regimen and rehabilitation program. All lower extremity free flaps require strict bedrest with elevation for at least 3 weeks, followed by intensive physical therapy. This involves training the flap to establish additional venous outflow channels and lifelong recognition of the devastating effects of prolonged dependency. Patients with advanced dementia, for example, would not be good candidates for limb salvage with free tissue transfer. Conversely, many of these same patients will have difficulty adapting to artificial limbs and complying with their requisite rehabilitation programs (11).

Chapter 46 Extended Techniques for Limb Salvage Using Free Flaps

Finally, the surgical team as well as the patient and his or her family must fully understand the commitment that needs to be made before undertaking this procedure. In addition to the long initial operating time, potential complications, both major and minor, need to be explained and understood. Lengthy postoperative recovery, often involving 1 to 2 months of acute-care hospitalization followed by an additional 6 to 8 weeks of rehabilitation at home or in a skilled-care facility, is another factor. A number of reports in the plastic surgery literature document successful free tissue transfer in elderly patients (12–14), suggesting that advanced age alone should not be a strict contraindication for this procedure. In our institution we have performed successful free flap surgery in selected elderly patients. Diabetic patients make up a significant proportion of the patients with lower extremity occlusive disease who have open wounds that place them in a limb-salvage situation. In a review of nine selected diabetic patients with infected foot ulcers, free gracilis muscle flaps were used for successful limb salvage in all patients, with an overall morbidity of 22% (15). Oishi et al. reviewed limb salvage with free flaps in 19 diabetic patients with peripheral vascular disease. They found a 47% morbidity at the recipient site, 5% flap loss (one patient), and an overall limb salvage rate of 72% during a follow-up period of 22 months (16). Although they conclude that these procedures can be done safely with short-term efficacy, they admit that during the time of their study “at least twice as many patients referred to [their] service were…refused microsurgical reconstruction as those undergoing reconstruction” (16). In a similar study involving 65 patients, Illig et al. found a 57% limb salvage rate at 5 years, but noted that the combination of diabetes and dialysis-dependent renal failure was the strongest predictor of overall limb loss, and diabetes the strongest predictor of death (28). Patients being considered for free flap limb salvage should undergo noninvasive vascular studies. A palpable pulse is usually evidence of adequate inflow, but arteriography should be performed to obtain an accurate anatomic guide to the recipient extremity. In those patients with questionable inflow status, arteriograms will delineate the areas suitable for angioplasty or bypass. Multiple authors have demonstrated successful application of a procedure combining bypass and free tissue transfer as a way to expedite wound coverage (27–33,35). Although a simultaneous procedure has advantages there should be no question of the patency of vascular inflow at the time of flap anastomoses. Confirming the patency of the bypass or angioplasty for 2 to 3 weeks before free tissue transfer is an acceptable alternative. In deciding on an appropriate recipient vessel, location and flow are critical factors. Selection of a flap with a longer pedicle (e.g., radial forearm flap), or use of vein grafts can help overcome these problems. End-to-side anastomoses are performed in most situations, especially

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when the recipient vessel is the only patent vessel in the affected extremity. In many cases, anastomosis into the bypass is desirable.

Selection of Free Flap The availability of a multitude of tissues suitable for free transfer has made it possible for the plastic surgeon to be highly selective in choosing a well-suited flap for a given situation. Flap characteristics such as size, texture, thickness, color, innervation, fingerprinted or hair-bearing skin, and compound tissue transfers involving skin, bone, tendon, and muscle can all be incorporated into the decision of which free flap to use. In general, either muscle, musculocutaneous, or cutaneous flaps are used for lower extremity coverage (Table 46.1). Muscle flaps offer the advantage of a large surface area, whereas cutaneous flaps can provide superior contour. This may be especially important in reconstruction of the foot and the subsequent wearing of shoes. With regard to long-term durability, however, there is no current evidence that demonstrates any advantage to cutaneous flaps over muscle flaps (17). Neither is there consensus on whether the use of neurotized flaps contributes to better long-term results (17). Free omental flaps have also been used for limb salvage (30,34,35). In the osteomyelitic wound, muscle flaps (after debridement) have proved to be beneficial in achieving wound closure (18). Free muscle flaps offer the advantages of maximal flexibility and transfer of undamaged tissue from outside the zone of injury (19). Gayle et al. reviewed seven series, including their own, of microvascular tissue transfer for treatment of chronic osteomyelitis and found an average success rate of 91% (19). The donor areas from which free flaps are taken can often be closed with cosmetically acceptable results and little functional deficit.

Postoperative Management In the first 24 hours after free flap surgery, patients will require an intensive care unit setting for general surgical care as well as monitoring of the flap. Antibiotic therapy is continued for at least 5 to 7 days, depending on the status of the wound at the time of flap transfer. With regard to

TABLE 46.1 Commonly used free flaps for lower extremity limb salvage Muscle With or Without Skin Latissimus dorsi Rectus abdominis Gracilis Serratus

Cutaneous Scapular Radial forearm Lateral arm Anterolateral thigh flap

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TABLE 46.2 Studies of free tissue transfer for lower extremity limb salvage Series (ref.) Chowdary et al. 1991(25) Oishi et al. 1993 (16) Serletti et al. 1993 (35) Lepantalo et al. 1996 (32) McCarthy et al. 1999 (30) Quinones-Baldrich et al. 2000 (31) Vermassen et al. 2000 (29) Tukiainen et al. 2000 (27) Illig et al. 2001 (28)

Patients/Flaps

C/D*

Success† (%)

Ambulation‡ (%)

DM§ (%)

8/8 19/19 20/20 15/15 21/21 15/15 45/47 29/30 65/65

1/7 NA 10/10 6/9 21/0 15/0 39/8 24/6 49/16

75 95 90 87 90 80 89 82 92

63 66 90 80 86 67 71 82 65

88 10 65 53 86 80 10 83 NA0

*C, free flap and revascularization procedure done simultaneously; D, staged. †Success rate of flaps. ‡

Ambulation rate of patients.

§Presence of diabetes mellitus, type I or II.

NA, information not available.

anticoagulants, there is little consensus on the use of heparin, low-molecular-weight dextran, aspirin, fibrinolytic agents, and other antithrombotic agents. The reader is referred to Johnson and Barker’s excellent review regarding use of these agents (20). In our institution, we begin administration of dextran at the time of flap elevation and continue its use for 5 days after surgery. Heparin is given just prior to pedicle division and used subsequently only if there is a problem with an anastomoses such as that requiring a return to the operating room. Flap viability must be assessed by an experienced surgeon every hour for the first 2 to 3 hours, and then every 4 to 6 hours for the next 12 hours (10). Flap color, turgor, and quality of bleeding when stuck are some of the parameters used to determine whether or not a flap is alive. In addition to physician observation, monitoring devices have been used in an effort to improve both the accuracy and efficiency of postoperative flap assessment. Commonly used monitoring techniques for free tissue transfer are clinical observation, transcutaneous or implantable Doppler ultrasound, temperature probe, photoplethysmography, laser Doppler flowmetry, and transcutaneous PO2 monitoring. Although there is no consensus regarding the ideal monitoring system, at our institution the laser Doppler is currently used to monitor free flaps. This device utilizes a surface probe that calculates blood flow 1 to 2 mm deep in tissue by measuring the relative motion between blood cells and the probe, using the frequency shift of light. Others have found that using this device for monitoring of free flaps has increased the salvage rate of compromised tissue from 50% to 83% (21). Patients in whom extremity free flaps are used for limb salvage require strict bedrest with elevation for 3 weeks. The leg is then allowed to be dependent for slowly increasing periods of time, along with progressive weight bearing and ambulation under the direction of an experienced therapist. Compression stockings can be helpful in

the long term to prevent venous congestion, but should be used with care.

Results Overall success rates for free tissue transfer are in excess of 90% at present. This statistic includes flaps used in patients of all ages, and those used to reconstruct defects of the head and neck, trunk, and upper and lower extremities. Thus results in the population of patients in whom free flaps are used for limb salvage in the setting of lower extremity vascular disease are likely to be slightly worse. This is due to the quality of the recipient vessels, status of the recipient wound, and the overall condition of the patient. Multiple series in the literature have described free tissue transfer in association with vascular procedures for limb salvage (Table 46.2). These series include patients who have had vascular and reconstructive procedures done simultaneously. Results have been quite good, with 75% to 95% success rates being reported. When evaluating the results of these procedures, one must examine not only tissue survival, but also the overall functional result for the patient. Table 46.2 also lists ambulatory status rates for patients undergoing free tissue transfer for limb salvage. In certain situations, free tissue transfer has been used for amputation stumps with good results. Flaps in this setting can aid in the fitting of a prosthesis and increase the durability of stump coverage.

The Future With increasing advances in immunology, the use of homologous tissues may enable plastic surgeons to use cadaveric “spare parts” in their reconstructive armamentarium (22). The resultant decrease in operating time and

Chapter 46 Extended Techniques for Limb Salvage Using Free Flaps

complexity may allow more widespread use of free tissue transfer techniques for limb salvage.

References 1. Jacobson JR, Suarez EL. Microsurgery in anastomosis of small vessels. Surg Forum 1960; 11: 243. 2. Buneke HJ, Buneke CM, Schulz WP. Immediate nicoladoni procedure in the rhesus monkey, or hallux-tohand transplantation utilizing microminiature vascular anastomoses. Br J Plast Surg 1966; 19: 332–337. 3. Bakamjian VY. A two-stage method for pharyngoesophageal reconstruction with a primary pectoral skin flap. Plast Reconstr Surg 1965; 36: 173–184. 4. McGregor IA, Morgan G. Axial and random pattern flaps. Br J Plast Surg 1963; 26: 202–213. 5. Mathes SJ, Nahai E Clinical atlas of muscle and musculocutaneous flaps. St Louis: CV Mosby, 1979. 6. Gumener R, Zbrodowki A, Montandon D. The reversed fasciosubeutaneous flap in the leg. Plast Reconstr Surg 1991; 88: 1034–1041. 7. Shaw WW, Hidalgo DA. Anatomic basis of plantar flap design: clinical applications. Plast Reconstr Surg 1986; 78: 637–649. 8. Leitner DW, Gordon L, Buncke HJ. The extensor digitoruin brevis as a muscle island flap. Plast Reconstr Surg 1985; 76: 777–780. 9. O’Brien BM, Morrison WA, Gumley GJ. Principles and techniques of microvascular surgery. In: McCarthy JG, ed. Plastic surgery, vol 1. New York: WB Saunders, 1990: 412–473. 10. Pederson WC. Limb salvage. Prob Plast Reconstr Surg 1991; 1: 125–156. 11. Byrd HS. Lower extremity reconstruction. In: Selected readings in plastic surgery, vol 5. Dallas: Baylor University Medical Center, 1990: 1–26. 12. Chick LR, Walton RL, et al. Free flaps in the elderly. Plast Reconstr Surg 1992; 90: 87–94. 13. Shestak KC, Jones NE Microsurgical free-tissue transfer in the eldeth’ patient. Plast Reconstr Surg 1991; 88: 259–263. 14. Dabb RW, Davis RM. Latissimus dorsi free flaps in the elderly: an alternative to below-knee amputation. Plast Reconstr Surg 1984; 73: 633–640 15. Lao CS, Lin SD, et al. Limb salvage of infected diabetic foot ulcers with microsurgical free-muscle transfer. Ann Plast Surg 1991; 26: 212–220. 16. Oishi SN, Levin LS, Pederson WC. Microsurgical management of extremity wounds in diabetics with peripheral vascular disease. Plast Reconstr Surg 1993; 92: 485–492. 17. Levin LS, Serafin D. Plantar skin coverage. Probl Plast Reconstr Surg 1991; 1: 156–184. 18. Kelly PJ, Fitzgerald RH, et al. Results of treatment of tibial and femoral osteomyelitis in adults. Clin Orthop Rel Res 1990; 259: 295–303. 19. Gayle LB, Lineaweaver WC, et al. Treatment of chronic osteomyelitis of the lower extremities with debridement

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

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and microvascular muscle transfer. Clin Plast Surg 1992; 19: 895–903. Johnson PC, Barker JR. Thrombosis and antithrombotic therapy in microvascular surgery. Clin Plast Surg 1992; 19: 799807. Goldberg J, Sepka RS, et al. Laser Doppler blood flow measurements of common cutaneous donor sites for reconstructive surgery. Plast Reconstr Surg 1990; 85: 581–586. Briggs SE, Banis JC, et al. Distal revascularization and microvascular free tissue transfer: an alternative to amputation in ischemic lesions of the lower extremity. J Vasc Surg 1985; 2: 806–811. Colen LB. Limb salvage in the patient with severe peripheral vascular disease: the role of microsurgical free-tissue transfer. Plast Reconstr Surg 1987; 79: 389–395. Cronenwett JL, McDaniel MD, et al. Limb salvage despite extensive tissue loss. Arch Surg 1989; 124: 609–615. Chowdary RE, Celani VJ, et al. Free-tissue transfers for limb salvage utilizing in situ saphenous vein bypass conduit as the inflow. Plast Reconstr Surg 1991; 87: 529–535. Serafin D. Basic principles of microsurgery. In: Georgiade N, Georgiade G, et al., eds. Essentials of plastic, maxillofacial, and reconstructive surgery. Baltimore: Williams and Wilkins, 1987: 817–834. Tukiainen E, Biancari F, Lepantalo M. Lower limb revascularization and free flap transfer for major ischemic tissue loss. World J Surg 2000; 24: 1531–1536. Illig KA, Moran S, et al. Combined free tissue transfer and infrainguinal bypass graft: an alternative to major amputation in selected patients. J Vasc Surg 2001; 33: 17–23. Vermassen FE, van Landuyt K. Combined vascular reconstruction and free flap transfer in diabetic arterial disease. Diabetes Metab Res Rev 2000; 16Journal Article: S33-S36. McCarthy WJ 3rd, Matsumura JS, et al. Combined arterial reconstruction and free tissue transfer for limb salvage. J Vasc Surg 1999; 29: 814–818. Quinones-Baldrich WJ, Kashyap VS, et al. Combined revascularization and microvascular free tissue transfer for limb salvage: a six-year experience. Ann Vasc Surg 2000; 14: 99–104. Lepantalo M, Tukiainen E. Combined vascular reconstruction and microvascular muscle flap transfer for salvage of ischaemic legs with major tissue loss and wound complications. Eur J Vasc Endovasc Surg 1996; 12: 65–69. Serletti JM, Deuber MA, et al. Atherosclerosis of the lower extremity and free-tissue reconstruction for limb salvage. Plast Reconstr Surg 1995; 96: 1136–1144. Piano G, Massad MG, et al. Omental transfer for salvage of the moribund lower extremity. Am Surg 1998; 64: 424–427. Serletti JM, Hurwitz SR, et al. Extension of limb salvage by combined vascular reconstruction and adjunctive free-tissue transfer. J Vasc Surg 1993; 18: 972–978.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 47 Extended Techniques for Limb Salvage Using Complementary Fistulas, Combined with Deep Vein Interposition Enrico Ascher

The management of threatened ischemic limbs in the absence of an adequate autogenous vein in patients requiring a small-vessel bypass is one of the greatest challenges to vascular surgeons. Despite improvements in vascular surgical and angiographic techniques in infrapopliteal reconstructions that are due to immediate and chronic anticoagulation, the overall results have been poor enough to warrant further investigations, particularly when these bypasses are performed on tracts with limited outflow. Thus, it is evident that if limb salvage is to be attained in some of these patients, then a nonstandard option must be evaluated. The use of a complementary or adjunctive arteriovenous fistula to increase flow in prosthetic grafts in an attempt to improve the chances of prolonged patency and limb salvage is one such technique. Surgeons would not increase the complexity of a distal arterial bypass operation by adding another procedure to it unless they thought that such an operation alone had little or no chance of success. Exceedingly high outflow resistance is a relatively common cause of prosthetic graft failure. A simple way to decrease the outflow resistance and effectively increase the blood flow through the graft is by creating an arteriovenous fistula at the distal anastomosis, thereby preventing stasis and thrombosis in the graft (1).

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This type of adjunctive procedure may be technically demanding and time-consuming, and may distort or compromise an already precarious arterial outflow. It may also decrease the blood flow into the distal arterial circulation by shunting or “stealing” the arterial inflow into the venous system. Flow could even be diverted from the distal arterial bed into the venous system, producing the ultimate “steal.” Congestive heart failure may be precipitated by increasing the work of the right ventricle. Lastly, it may not have a significant beneficial effect on patency because many factors other than flow can lead to bypass failure.

Experimental Data Dean and Read were the first to use an arteriovenous fistula (AVF) to help prevent prosthetic graft thrombosis in a well-designed canine model. Construction of a distal adjunctive AVF significantly improved graft patency rates (2). Blaisdell and associates further contributed to this subject by angiographically demonstrating that a steal need not occur distal to an adjunctive arteriovenous fistula and that controlling the size of the venous component of the fistula may also be of critical importance to prevent adverse cardiac effects. They, too, confirmed that patency

Chapter 47 Extended Techniques for Limb Salvage Using Complementary Fistulas

rates of aortofemoral Dacron grafts in dogs were improved when a distal fistula was added (3). Comparison of control graft and fistula patency rates in two different sets of animals, despite the documented wide variability of thrombogenic potential in dogs, is the major flaw in both of these studies (4). We controlled this variable in our experimental study by performing both types of procedure in the same animal, using an iliofemoral polytetrafluoroethylene (PTFE) bypass model to compare the patency results of PTFE grafts alone with that of PTFE grafts plus an adjunctive distal AV fistula (DAVF). The group with a DAVF had almost twice the patency rate (42% vs. 24%) when compared with the control group after 12 months. This difference did not reach statistical significance, probably because of the limited number of animals in the study. Interestingly, using serial arteriographic examinations in this study, we also demonstrated persistent flow into the distal arterial tree despite the presence of a patent fistula in all experimental animals (5). Furthermore, we failed to document any significant pressure gradient in the recipient artery distal to the fistula. It is important to note that our fistulas were constructed with the saphenous vein, which averaged 2 mm in diameter, while the femoral artery averaged 5 mm. In earlier work, Holman and Taylor had recommended that the size of the fistula should be less than or equal to the diameter of the artery or vein involved to avoid a steal phenomenon (6). Kismer subsequently reported that the fistula anastomosis must be less than 60% of the diameter of the proximal artery to prevent impairment of the distal arterial circulation (7). However, Schenk and collaborators were unable to detect any decrease in distal arterial flow following a 1- to 1.5-cm anastomosis between the femoral artery and vein in dogs followed up to 1 year after fistula formation (8). Campbell and associates have demonstrated in an in vitro femorotibial bypass model that an adjunctive distal fistula causes a steal only in the presence of an inflow stenosis (9). Holman had also previously demonstrated that the cardiac hemodynamic effects of an AVF depend upon its size as well as on the diameter of the inflow and the outflow vessels. In all his dog experiments, animals subjected to the creation of a 1.5- to 2-cm anastomosis between the aorta and vena cava died from heart failure, while a 2-cm fistula between the femoral vessel was well tolerated (10). To date, there has been no clinical or experimental evidence of cardiac failure being caused or worsened by the creation of an adjunctive DAVF along with a distal extremity bypass. This probably results from the small size of the infrapopliteal vessels (11).

Clinical Experience The realization that bypass patency rates were directly proportional to the size of the recipient artery as well as to the arteriographic quality of the outflow led Blaisdell and

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his colleagues in 1966 to insert an AV graft from the popliteal artery to the superficial femoral vein as an adjunctive technique for popliteal bypasses with poor runoff. Early patency and limb-salvage results were not clearly improved, and Blaisdell recommended that the procedure not be generally used (12). In 1976, Gyurko and Posze described a patient in whom a femoral-to-popliteal bypass was performed in conjunction with a DAVF created between the distal segment of the saphenous vein and the popliteal artery. No attempt was made to lyse the vein valves to facilitate retrograde flow and this fistula thrombosed less than 2 months after the operation (13). A few years later Kusaba et al. reported acceptable salvage results in 63 limbs subjected to extensive endarterectomy of the superficial femoral and popliteal arteries, a short proximal PTFE graft extension to the common femoral artery, and construction of an AVF between the tibioperoneal trunk and the adjacent vein. The “long-term” limb-salvage rate was reported to be 57% (14). In the nearly three decades since, better prosthetic graft materials and more attention to surgical techniques have greatly improved primary and secondary patency rates of femoropopliteal bypasses, thus lessening earlier enthusiasm for adjunctive procedures such as an AVF. However, progress has not been sufficient to improve the poor graft patency results obtained with prosthetic bypasses to infrapopliteal arteries. Consequently, some surgeons have reexplored the use of adjunctive AVFs with prosthetic or nonautogenous biological graft bypasses to infrapopliteal arteries for critical ischemia.

Types of Arteriovenous Fistulas for Infrapopliteal Bypasses Common Ostium Arteriovenous Fistula In 1980 Dardik and his group began clinical attempts to use adjunctive DAVFs in an effort to enhance patency results of glutaraldehyde-tanned human umbilical vein grafts inserted below the popliteal artery. These fistulas were constructed by joining the common wall of the opened adjacent artery and vein and then suturing the graft end-to-side to the resulting common ostium. Although their initial experience was limited to patients with disadvantaged outflow tracts, they subsequently liberalized their indications to include all nonautogenous vein bypasses (15). Dardik’s group has also published a 10-year experience with 210 adjunctive AVFs demonstrating 2-year graft patency rates that varied from 18% for bypasses constructed during the first 4 years of the study to 44% for the ones performed in the last 3 years (16). It is worth noting that the latter results are quite similar to the 45% 2-year infrapopliteal PTFE bypass patency rate achieved by Flinn and his associates utilizing continuous systemic anticoagulation without an adjunctive AVF

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(17). However, this type of comparison may be misleading. Both studies were retrospective in nature, the exact location of the distal anastomosis and the quality of the angiographic runoff and the measurement of the outflow resistance have not been reported by either group, and differences in nonautogenous graft material used in these studies may have also influenced the results. Interest in and controversies over the use of adjunctive AV fistulas have also been fueled by the work and opinions of other authors. Harris and Campbell supported the use of AVFs by reporting a 47% 1-year graft patency in high-risk reconstructions (18). Similarly, Hinshaw and co-authors published good results with this technique. In a relatively short follow-up of 4 to 24 months, only 6 (16%) of their 37 grafts occluded, resulting in a limb salvage rate of 75% (19). Similarly, Sommoggy, Maurer, and associates reported a 5-year patency rate of 38% and a 5-year limb-salvage rate of 41% with 82 patients in whom PTFE crural bypasses were performed with adjunctive AVFs (20). Despite these results, Maurer’s group believed the value of the fistula in improving short- and long-term patency remained unproved. Moreover, Snyder and his colleagues found a high rate of 8-month fistula failure (70%) and limb loss (37%) in 30 common ostium AV fistulas constructed in 27 patients. They also reported excessive limb edema in 27% of their patients and serious wound healing problems in 12% (21), and recommended that the procedure be abandoned. In our own experience with seven of these AV fistulas, we found that only two of these reconstructions remained patent for more than 1 year. We speculate that a prosthetic bypass without an AVF could have had equal patency. As the same speculation could apply to the other clinical results, the value of this sort of fistula in improving patency must be considered unproved.

Remote Arteriovenous Fistula Introduced by Paty, Shah, and their collaborators, a newer technique consisted of creating an AV fistula at the most distal extent of the recipient artery several centimeters below the distal arterial anastomosis (22). These authors suggest that the proposed technique is superior to the common ostium AVF because it produces high flow rates not only in the prosthetic graft (average 264 mL/min) but also in the intervening arterial segment between the graft anastomosis and the remote AVF (average 170 mL/min). However, the average flow rate measured at the arterial segment distal to the fistula was only 19 mL/min or 11% of the arterial flow proximal to the fistula, despite the fact that the fistula size was limited to 5 mm. This observation raises the question as to whether or not this low flow rate may potentially impair healing of ischemic lesions located far distal to the AVF. Moreover, the authors did not report whether the arterial pressure distal to the AVF was increased, decreased, or unchanged by the creation of the fistula. In addition,

their hypothesis that distal perfusion is increased via collaterals from the intervening artery lacks objective documentation. In the worst-case scenario, the intervening artery could be the source of collateral flow away from the distal arterial bed into the low-resistance fistula. Some clear disadvantages to this technique also include the need to construct an additional small-vessel anastomosis and the fact that it is not applicable for perimalleolar and pedal reconstructions because of the short length of the available distal arterial segment. Nevertheless, Shah’s group described a clinical experience that appears promising, as 11 of the 16 infrapopliteal PTFE bypasses constructed with a remote AVF were patent with an average follow-up of 9 months, and 1-year limb salvage was excellent (75%) after these complex operations.

Saphenous Turndown Arteriovenous Fistula The use of the distal superficial venous system as an additional outflow site for high-risk perimalleolar bypasses has not yet been reported. Our experience with this technique consists of 20 patients who presented with a very limited distal runoff and in whom no autogenous vein or vein segments of sufficient length for bypass grafting were available (Fig. 47.1). In addition, neither a common ostium nor a remote AVF would have been feasible in these patients because of the small size of the veins accompanying the arterial outflow segment. Adjunctive AVFs were constructed with the greater saphenous vein in 15 patients and with the lesser saphenous vein in five patients. The recipient arteries were the distal posterior tibia in seven cases, the anterior tibial or dorsalis pedis in seven cases, plantar branches in five cases, and the peroneal in one case. The donor arteries were the external iliac in three cases, the common femoral in 13 cases, and the superficial femoral in four cases. The saphenous turndown technique includes: 1. 2. 3. 4. 5. 6.

transection of the greater or lesser saphenous vein in the lower leg; circumferential mobilization of the vein down to the level of the ankle; ablation of the distal valves with an antegrade valvulotome under direct vision; subcutaneous tunneling of the free portion of the vein in a gentle arc toward the perimalleolar artery; anastomosis of the peripheral end of the vein to the side of the artery; and anastomosis of the distal end of a 6-mm PTFE ringed graft to the vein at or near its anastomosis to the artery.

Of the 20 cases with a PTFE bypass (Fig. 47.2) and a saphenous turndown AVF 13 were patent from 6 to 24 months (mean 14 months), and five patients have had patent grafts and fistula for more than 2 years. Limb salvage was achieved in 14 (70%) of these “hopeless”

Chapter 47 Extended Techniques for Limb Salvage Using Complementary Fistulas

FIGURE 47.1 A completion angiogram of a saphenous turndown arteriovenous fistula. The anastomosis (arrow) is between the greater saphenous vein, the posterior tibial artery below the ankle, and the 6-mm PTFE graft. A gentle arc is created with the saphenous vein to avert the possibility of kinking. Retrograde flow into the distal venous system is clearly demonstrated. (Reproduced by permission from Ascer E, Veith FJ. Prospectives in vascular surgery 1993; 6: 79.)

cases from 3 to 24 months (mean 12 months). All successful AVFs had considerable pedal edema but with no impairment in their ability to ambulate, and one patient developed mild superficial forefoot ulcerations, probably caused by venous stasis. The potential advantages of this technique over common ostium AVFs are: 1.

2.

3.

less compliance mismatch at the distal anastomosis because a segment of vein is interposed between the artery and the prosthetic graft; avoidance of a flow divider created by a side-to-side AV fistula that may lead to turbulent flow and thrombosis; and possible retrograde nutritive perfusion via the distal venous system.

Clearly, the results of complementary or adjunctive AVFs are better than those achievable with prosthetic

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FIGURE 47.2 Angiogram depicting a PTFE bypass from the distal portion of an external iliac artery to the dorsalis pedis artery with an adjunctive AV fistula. The lesser saphenous vein was turned down and anastomosed to the dorsalis pedis artery after ablation of the distal vein valves. The distal end of a PTFE graft (arrow) was inserted into the hood of the arteriovenous anastomosis. (Reproduced by permission from DE Strandness Jr. and A Van Breda, eds. Vascular Diseases: Surgical and Interventional Therapy, New York: Churchill Livingstone 1993: figure 30-3.)

bypasses alone, in terms of both graft patency and limb salvage.

Complementary Distal Arteriovenous Fistula and Deep Vein Interposition The continued evolution of vascular surgery techniques in the past decade, combined with the availability of an adequate venous conduit, has permitted a liberal and aggressive approach to salvage ischemic limbs caused by advanced atherosclerosis. This approach is epitomized by the construction of arterial bypasses to the terminal branches of tibial vessels (23). However, significant numbers of patients will continue to face the threat of a major amputation because of insufficient vein necessary to perform a totally autogenous bypass to one of the in-

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frapopliteal arteries. In these instances, less durable grafts made of prosthetic material must be used if limb salvage is to be attempted. Accordingly, several adjunctive techniques have been designed in an attempt to improve the poor patency results achieved with prosthetic bypasses. These include the administration of immediate and chronic anticoagulants (24), the construction of a vein patch or cuff at the distal anastomosis to prevent occlusion by intimal hyperplasia (25,26) and the creation of a distal arteriovenous fistula to increase graft blood flow in high outflow resistance systems (27,28). Still, none of these adjunctive techniques have generated sufficiently adequate results. For that reason, we have developed a simple technique (29) that combines some of the previously described principles. We utilize a PTFE graft in combination with a DAVF as well as a deep vein interposition (DVI) at the distal anastomosis in a single technique in patients presenting with critical lower limb ischemia and in whom a standard infrapopliteal vein bypass is not feasible. Our combined DAVF/DVI technique attempts to correct the two main causes of infrapopliteal PTFE graft failure— limited runoff and intimal hyperplasia.

General Considerations Indications for surgery are restricted to ischemic ulcers, gangrene or rest pain. Preoperative evaluation with noninvasive segmental blood pressure measurements and pulse volume recordings are useful, not only to document and confirm clinical impressions but also as a comparison for postoperative surveillance. Angiography may be used to visualize both inflow and outflow sites. In general, the most distal available inflow site is utilized to shorten the length of the graft. Time-delayed imaging may be required to visualize the foot arteries because of reduced flow. The use of magnetic resonance angiography has proven to be beneficial of late in identifying patent lower extremity arteries not visualized by conventional arteriographic techniques, particularly in view of the recent advances in imaging technology (30). Finally, high-resolution duplex imaging has now become a viable alternative for visualization of inflow and outflow sites with the added advantages of cost reduction, fewer complications associated with angiography and the ability to identify the least calcified artery segment (31,32).

Surgical Technique Basic surgical principles involved in creating a complementary distal DAVF/DVI are the same as for any infrapopliteal bypass. Crucial elements for the success of these reconstructions are meticulous technique, excellent illumination, fine instrumentation and, most importantly, commitments of time and effort. Additional strategies to deal with intraoperative problems are applied whenever indicated either to facilitate the operation or to improve

distal runoff. We use a previously described fracture technique in heavily calcified arteries to overcome the rigidity of the arterial wall, rendering it suitable for occlusion, incision, and suture placement (33). A short stenotic arterial segment may be used as an outflow site, widening the vein interposition portion of the bypass and thereby decreasing the total outflow resistance via graft angioplasty (34). Adequate exposure of the recipient artery and its adjacent deep veins is achieved by using standard approaches. Once the better of the two deep veins is selected, extreme care and patience are required during dissection of both the artery and vein. Every attempt should be made to avoid injury to the vein wall during dissection since control of bleeding may be difficult without further compromising vein integrity. All vein branches are carefully isolated, doubly ligated with 5–0 silk and divided. Severe inflammatory reaction of the surrounding tissue may be encountered that causes the vein and the artery to firmly adhere to each other. This should not discourage proceeding with the operation but rather encourage more precise dissection. Extensive mobilization of the vein is demanded by this technique to permit transposition onto the artery without undue tension. At least 2 cm proximal and 1 cm distal to the length of the arteriotomy is usually necessary to accomplish this goal. Next, the recipient artery is mobilized and secured with Silastic vessel loops. After dissection of the inflow artery, an appropriate tunnel is constructed and a 6-mm ringed PTFE graft is placed into the tunnel. After accomplishing these steps, intravenous heparin is initiated. An arteriotomy ranging in length from 1.3 to 2 cm is performed in the recipient vessel and the adjacent deep vein is ligated and transected at a level anywhere from 0.5 to 1 cm distal to the endpoint of the arteriotomy (Fig. 47.3A and B). This is an important technical detail since both ends of the vein will retract upon transection and the proximal end may be too short to reach the toe of the anastomosis. The open end of the central portion of the vein is then fashioned and anastomosed to the adjacent artery with continuous monofilament 7–0 sutures in a four-quadrant technique where every stitch is applied under direct vision (Fig. 47.4A). This is followed by a venotomy that is initiated over the hood of the anastomosis and is extended proximally beyond the level of the heel of the arteriovenous anastomosis to prevent potential stricture of the vein (Fig. 47.4B). Next, an endto-side anastomosis is accomplished between the distal end of the PTFE graft and the vein utilizing similar techniques (Fig. 47.4C). Configuration of the complementary DAVF/DVI technique in now complete (Fig. 47.4D). Routine intraoperative measurements of arterial bypass pressures are recorded in all cases by inserting a 23-gauge butterfly needle into the graft at the distal anastomosis. A short sleeve of PTFE is wrapped around the vein proximal to the distal anastomosis or placed before the construction of the fistula (Fig. 47.5A, B). This will narrow the vein in those cases where a gradient over 30 mmHg was detected between the bypass and the radial

Chapter 47 Extended Techniques for Limb Salvage Using Complementary Fistulas

systolic pressures or when the absolute graft systolic pressure was less than 100 mmHg. This pressure will provide sufficient blood flow to heal a foot lesion. The amount of banding necessary to produce this pressure or to decrease a significant gradient is guided by a continuous and simultaneous monitoring of intragraft and radial artery pressures. Measuring intragraft pressures and banding the graft when indicated is an important step that may prevent bypass failure by avoiding the “steal” phenomenon. The same needle is then used to perform a completion arteriogram (in all cases) to evaluate the adequacy of the technique (Fig. 47.6). After the proximal anastomosis is

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completed in a standard manner, the clamps are released and hemostasis is achieved by reversing the effects of heparin with protamine sulphate.

Complications The usual vascular operative complications must be anticipated and managed accordingly. These complications include inadequate wound healing, groin lymphorrhea and graft infection. Full thickness skin necrosis over the distal portion of the graft may also ensue. This can be avoided by careful technique. Anticoagulation therapy may produce significant hemorrhage and may necessitate temporary cessation of anticoagulation. Postoperative swelling of the lower extremity has not been a major factor in limiting ambulation. We have observed a dramatic improvement in the amount of leg edema 3 to 4 weeks after the operation. In the event of severe initial swelling, bedrest and leg elevation for approximately 1 week postoperatively may be required.

Follow-up Graft and fistula patency are evaluated by physical examination (auscultation of a bruit over the distal anastomosis) and by noninvasive parameters including pulse–volume recording tracings and duplex scanning. Worsening of noninvasive vascular examination or recurrence of symptoms are indications for new arteriographic studies.

Conclusion A

B

FIGURE 47.3 (A) Preferred site of transection of the adjacent vein relative to the arteriotomy. (B) The vein prepared for an end-to-side anastomosis to an infrapopliteal artery.

Aggressive approaches to the salvage of ischemic limbs using autogenous tissues have demonstrated excellent results, but a significant number of patients still face major amputation due to the insufficient available vein with which to perform a totally autologous bypass procedure FIGURE 47.4 (A) Illustrates the technique for performing the distal arteriovenous fistula. (B) Location for venotomy for constructing graft to distal arteriovenous fistula anastomosis. (C) Technique for performing the distal arteriovenous fistula combined with deep vein interposition. (D) Completed bypass demonstrating the final configuration of the distal arteriovenous fistula combined with deep vein interposition.

A

B

C

D

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to one of the infrapopliteal arteries. Only after all potential autologous vein sources have been sought and exhausted should consideration then turn to a nonautologous conduit to attempt limb salvage (35).

References A

B FIGURE 47.5 (A) Lateral view of the distal arteriovenous fistula combined with deep vein interposition. (B) Illustration of the distal arteriovenous fistula combined with deep vein interposition and PTFE venous band in place.

FIGURE 47.6 Intraoperative completion arteriogram demonstrating a patent PTFE bypass to the distal anterior tibial artery and free flow into the vein portion of the fistula as well as into the distal circulation.

1. Ascer E, Veith FJ, et al. Intraoperative outflow resistance as a predictor of late patency of femoropopliteal and infrapopliteal arterial bypasses. J Vasc Surg1987; 5: 820–827. 2. Dean RE, Read RC. The influence of increased blood flow on thrombosis in prosthetic grafts. Surgery 1964; 55: 581–584. 3. Blaisdell FW, Lim RC, et al. Revascularization of severely ischemic extremities with an arteriovenous fistula. Am J Surg 1966; 112: 166–174. 4. Freeman MB, Sicard GA, et al. The association of in vitro arachidonic acid responsiveness and plasma thromboxane levels with early platelet deposition on the luminal surface of small-diameter grafts. J Vasc Surg 1988; 7: 554–561. 5. Calligaro KD, Ascer E, et al. The effect of adjunctive arteriovenous fistula on prosthetic graft patency: a controlled study in a canine model. J Cardiovasc Surg 1990; 31: 646–650. 6. Holman E, Taylor G. Problems in the dynamics of blood flow: II. Pressure relations at site of an arteriovenous fistula. Angiology 1952; 3: 415–418. 7. Kismer RL, Vermeulen WJ. Therapeutic arteriovenous fistula in management of severe ischemia of the extremities. Surg Clin North Am 1970; 50; 291–300. 8. Schenk WG, Martin JW, et al. The regional hemodynamics of chronic experimental arteriovenous fistulas. Surg Gynecol Obstet 1960; 108: 44–50. 9. Campbell H, How TV, Harris PL. Experimental evaluation of arterial steal in vitro models of femoro-tibial bypass with adjuvant arteriovenous shunt. Clin Phys Physiol Meas 1984; 5: 253–262. 10. Holman E. Problems in the dynamics of blood flow: Conditions controlling collateral circulation in the presence of an arteriovenous fistula and following the ligation of an artery. Surgery 1949; 25: 880. 11. Dardik H, Sussman B, et al. Distal arteriovenous fistula as an adjunct to maintain arterial and graft patency for limb salvage. Surgery 1983; 94: 478–486. 12. Blaisdell FW, Lim RC, et al. Revascularization of severely schemic extremities with an arteriovenous fistula. Am J Surg 1966; 112: 166–173. 13. Cyorko G, Posze J. Attempts at saving severely ischaemic limbs. Acta Chir Acad Scient Hung 1976; 17: 109417. 14. Kusaba A, Inokuchi K, et al. A new revascularization procedure for extensive arterial occlusions of lower extremity. A-V shunt procedure. J Cardiovasc Surg 1982; 23: 99–104. 15. Ibrahim IM, Sussinan B, et al. Adjunctive arteriovenous fistula with tibial and peroneal reconstruction for limb salvage. Am J Surg 1980; 140: 246–251. 16. Dardik H, Berry SM, et al. Infrapopliteal prosthetic graft patency by use of the distal adjunctive arteriovenous fistula. J Vasc Surg 1991; 13(5): 685–691.

Chapter 47 Extended Techniques for Limb Salvage Using Complementary Fistulas 17. Flinn WR, Rohrer MJ, et al. Improved long-term patency of infragenicular polytetrafluoroethylene grafts. J Vasc Surg 1988; 7: 685–690. 18. Harris PL, Campbell H. Adjuvant distal arteriovenous shunt with femorotibial bypass for critical ischemia. Br J Surg 1983; 70: 377–380. 19. Hinshaw DB, Schmidt CA, et al. Arteriovenous fistula in arterial reconstruction of the ischemic limb. Arch Surg 1983; 118: 589–592. 20. Sommoggy S, Maurer PC, et al. Femorodistal PTFE bypasses combined with distal arteriovenous fistula: a chance in critical limb ischemia. In: Veith FJ, ed. Current critical problems in vascular surgery, vol 2. St Louis: Quality Medical Publishing, 1990: 98–105. 21. Snyder SO, Wheeler JR, et al. Failure of arteriovenous fistulas at distal tibial bypass anastomotic sites. J Cardiovasc Surg 1985; 26: 137–142. 22. Paty PSK, Shah DM, et al. Remote distal arteriovenous fistula to improve infrapopliteal bypass patency. J Vasc Surg 1990; 1: 171–178. 23. Ascer E, Veith FJ, Gupta SK. Bypasses to plantar arteries and other tibial branches: An extended approach to limb salvage. J Vasc Surg 1988; 8: 434–441. 24. Flinn WR, Rohrer MJ, et al. Improved long-term patency of infravenicular polytetrafluoroethylene grafts. J Vasc Surg 1988; 7: 685–690. 25. Siegman FA. Use of the venous cuff for graft anastomosis. Surg Gynec Obstet 1979; 148: 930–931. 26. Miller JH, Foreman RK, et al. Interposition vein cuff for anastomosis of prosthesis to small artery. Aust NZJ Surg 1984; 54(3): 283–285.

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27. Dardik H, Sussman B, et al. Distal arteriovenous fistula as an adjunct to maintain arterial and graft patency for limb salvage. Surgery 1983; 94: 478–486. 28. Ascer E, Veith FJ, et al. Intraoperative outflow resistance as a predictor of late patency of femoropopliteal and infrapopliteal arterial bypasses. J Vasc Surg 1987; 5: 820–827. 29. Ascher E, Gennaro M, et al. Complementary distal arteriovenous fistula and deep interposition: a five-year experience with a new technique to improve infrapopliteal prosthetic bypass patency. J Vasc Surg 1996; 24: 134–143. 30. Carpenter JP, Owen RS, et al. Magnetic resonance angiography of peripheral runoff vessels. J Vasc Surg 1992; 16: 807–813. 31. Ascher E, Mazzariol F, et al. The use of duplex ultrasound arterial mapping as an alternative to conventional arteriography for primary and secondary infrapopliteal bypasses. Am J Surg 1999; 178(2): 162–5. 32. Mazzariol F, Ascher E, et al. Values and limitations of duplex ultrasonography as the sole imaging method of preoperative evaluation for popliteal and infrapopliteal bypasses. Ann Vasc Surg 1999; 13: 1–10. 33. Ascer E, Veith FJ, White-Flores SA. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986; 152: 220–222. 34. Ascer E, Calligaro KD, et al. Graft angioplasty: use of the stenotic lesion as an inflow or outflow site in lower extremity arterial bypasses. J Vasc Surg 1990; 11: 576–579. 35. Calligaro KD, Syrek JR, et al. Use of arm and lesser saphenous vein compared with prosthetic grafts for infrapopliteal arterial bypass: Are they worth the effort? J Vasc Surg 1997; 26: 919–924.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 48 Extended Techniques for Limb Salvage Using Vein Cuffs and Patches Robyn Macsata, Richard F. Neville, and Anton N. Sidawy

Autologous saphenous vein has long been accepted as the conduit of choice for infrapopliteal revascularization. Despite the use of duplex ultrasound techniques to improve the ability to locate acceptable greater saphenous vein, as many as 30% of patients requiring primary distal revascularization may lack suitable vein. This number increases to 50% in those patients requiring secondary procedures (1). The most common reasons for lack of vein include previous vein harvest for coronary or peripheral bypass grafts, excision of varicose saphenous vein, or unsuitable saphenous vein due to size or phlebitic changes. This has led to the use of alternative conduits including lesser saphenous vein, superficial femoral vein, cryopreserved vein, human umbilical vein, and polytetrafluoroethylene (PTFE), all with varying degrees of success (2–7). Campbell et al. originally reported the use of PTFE for lower extremity bypass in 1976. This preliminary report described 15 patients undergoing lower extremity revascularization with PTFE, 9 of which were below the knee, with an 87% cumulative graft patency at 1–8 months (8). A follow-up report at 28 months showed a 75% cumulative patency rate in this same group of patients (9). In a similar preliminary report by Veith et al. in 1978, they reported a 76% graft patency rate in 29 infrapopliteal bypasses followed for 3–16 months (10). Although these initial reports stimulated the use of PTFE for infrainguinal bypasses, additional experience ques-

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tioned this practice as more mature data showed disappointing long-term patency results (2–7). In one of the first long-term follow-up studies completed in 1985, Hobson et al. reported on 547 lower extremity procedures including 375 revascularizations and 172 below-knee amputations, performed over 5 years. In this group, 91 femoral tibial bypasses were performed with autologous saphenous vein used preferentially in 50 cases (54%). Limb salvage rates at 2 and 5 years were 53% and 47%, respectively, for femoral tibial bypasses with vein, versus 20% and 15% for femoral tibial bypasses with PTFE. In addition, the perioperative mortality for patients undergoing revascularization was 3% compared to 13% for those patients undergoing primary amputation. They concluded that revascularization is preferable to primary amputation with the possible exception of those patients requiring distal reconstruction in the absence of adequate saphenous vein in whom primary amputation should be considered (3). This conclusion was supported by similar studies which reported 2-year patency rates between 30% and 45% (4–6) and 4-year patency rates between 12% and 37% for infrapopliteal bypasses using PTFE (4,5,7). In 1986, Veith et al. reported the results of a multicenter, prospective, randomized trial comparing saphenous vein to PTFE in infrainguinal arterial reconstructions. Overall 845 patients were entered, 485 underwent popliteal bypasses and 360 underwent infrapopliteal

Chapter 48 Extended Techniques for Limb Salvage Using Vein Cuffs and Patches

bypasses. Patients who were believed to have a usable ipsilateral autologous saphenous vein were randomized to either saphenous vein or PTFE for their conduits. Patency differences became apparent within one month of operation and increased progressively thereafter. Primary patency rates of 49% at 4 years for infrapopliteal bypasses with randomized autologous saphenous vein were significantly better than the 12% at 4 years for those undergoing infrapopliteal bypass randomized to PTFE. However, limb salvage rates at 3.5 years (57% for autologous saphenous vein and 61% for PTFE) were not significantly different. This could be explained because PTFE graft failure was not always associated with renewed limb-threatening ischemia, and when secondary vein bypass procedures were performed, they resulted in limb salvage. This study supported previous data of the poor patency of infrapopliteal PTFE grafts and revisited the question of the need for primary amputation in this population of patients (2).

Pathophysiology Intimal hyperplasia (IH) has been implicated as a cause of outflow stenosis with eventual PTFE graft thrombosis and failure (11). The hyperplastic lesion is thought to originate from the proliferation of smooth muscle cells in the media with subsequent migration into the intima. Progression to a hyperplastic occlusive lesion is an important cause of prosthetic graft failure (12,13). The exact mechanism leading to intimal hyperplasia at the arterial graft anastomosis remains incompletely understood, with possibilities ranging from hemodynamic factors to endothelial-derived growth factors (14). In order to alter this relationship between intimal hyperplasia and PTFE graft failure, investigators have proposed adjuvant techniques aiming to improve prosthetic bypass patency. The most prominent of these techniques are distal arteriovenous fistula (DAVF) and the interposition of minimal amount of venous tissue at the prosthetic graft–outflow artery distal anastomosis. The placement of DAVF aims to increase the flow rate in the graft in the hopes of decreasing the incidence of thrombosis. In this chapter we discuss the interposition of minimal venous tissue at the outflow anastomosis to improve patency of prosthetic grafts.

Mechanism of Action Although Siegman was first to describe a vein cuff at the outflow of prosthetic bypasses, he did so in the hopes of facilitating a graft anastomosis to a calcified artery. Miller et al. were first to report, in 1984, the use of a vein cuff to decrease intimal hyperplasia and improve patency (15). Quantitative inhibition of intimal hyperplasia formation at outflow anastomosis by vein cuff interposition between PTFE grafts and the carotid artery in a canine model has been demonstrated by Suggs et al. In this experiment, 12 dogs received interposition PTFE grafts in their carotid artery bilaterally. On one side, the prosthetic graft

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was anastomosed end-to-side to the carotid artery. On the other side, a vein cuff was interposed at the distal anastomosis between the graft and the carotid artery. At 3–12 weeks, the dogs were sacrificed and graft patency was assessed along with the luminal diameters, which were measured at three sites along the anastomosis and 1 mm distal to the toe of the anastomosis. Graft patency in the 11 longterm survivors was 36% (4 of 11) for PTFE grafts without cuffs and 64% (7 of 11) for PTFE grafts with a cuff. Regardless of graft thrombosis, antibody-positive cellular proliferation occurred mainly at the non-cuffed PTFE anastomosis. Luminal encroachment was mainly by cells highly reactive to smooth-muscle-derived antibody. The authors hypothesized that the decreased hyperplastic reaction with the cuffed grafts may be secondary to the positioning of an autogenous endothelial “buffer zone” or a range of hemodynamic factors such as increased compliance and surface area at the anastomotic site or a change in the angle of the cuffed anastomosis (16). In order to determine if mechanical factors diminished intimal hyperplasia at the vein cuff anastomosis, we studied two groups of dogs. Group A consisted of nine dogs who received a 4-mm PTFE graft with vein cuff on one side and a 4-mm PTFE graft with vein cuff that was encircled with a PTFE cuff to prevent expansibility of the cuff on the opposite side. Group B consisted of five dogs who received a PTFE graft at an acute angle as done commonly with hypasses on one side. On the opposite side a 1cm-long, 6-mm PTFE interposition segment was placed at a perpendicular angle between artery and graft. After 10 weeks the grafts were harvested and the thickness of the intimal hyperplasia was measured with an ocular micrometer. In group A, there was no statistically significant difference in the thickness of intimal hyperplasia at all levels of the anastomosis studied. This suggested that the expansibility (or compliance) of the cuff was not the protective factor proposed by Suggs. Analysis of group B bypasses revealed high incidence of thrombosis bilaterally, which indicated that the angle of the distal anastomosis did not play a role in protection from the hyperplastic process. These studies suggest that the protective effect of the vein cuff is not mechanical in origin. This leaves the possibility that the vein cuff acts as an autogenous endothelial “buffer zone” (14). Further analysis of the specimens revealed that the hyperplastic response moved from the graft–artery anastomosis (in traditional end-to-side configuration) to the graft–vein cuff interface (in the vein cuff interposition configuration). We now feel that since the graft–vein cuff anastomosis is wide, it takes longer time and larger hyperplastic mass to cause complete or hemodynamically significant stenosis of the lumen to result in graft thrombosis.

Cuffs, Collars, Boots Over the past two decades, multiple configurations of venous tissue interposition between prosthetic graft and

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artery have been proposed and used clinically. Each different configuration has benefits and drawbacks. In 1979, Siegman was the first to propose a vein cuff technique to ease the performance of a difficult anastomosis without predicting the possible effects it would have on intimal hyperplasia and graft patency. This was initially intended for use between any thickened artery or graft to a venous bypass. He described incising the artery or graft for an appropriate length and suturing a segment of split vein into the defect. His anastomosis began at the apex and traveled around the arteriotomy back to this corner. The terminal ends of the vein cuff were sutured together or beveled if necessary in order to fit the vein graft appropriately. The vein graft was then sutured to the remaining free edge (17). Miller et al. recognized that PTFE grafts for infrapopliteal bypasses consistently produced poor results and postulated that this may be due to technical difficulties with the anastomosis between a graft and a small artery, or to the different elastic properties of the prosthetic graft and the artery. Attempting to address both concerns, the Miller cuff used a similar configuration as described by Siegman et al. However, they described beginning the suture line in the middle of the posterior wall of the arteriotomy and the center of the vein graft and then running the suture toward the apices (Fig. 48.1). With this technique, this critical area could be well visualized and luminal narrowing could be avoided. From there, in a similar fashion to Siegman, the two cut ends of the vein were sutured together and the prosthetic graft was sutured to the vein cuff. Miller et al. reported on 114 infrainguinal bypass procedures performed with the cuff technique, 21 of which were femoral-tibial bypass grafts and were followed for 18 months. He reported patency rates of 90% for femoral-popliteal bypass grafts and 72% for femoraltibial bypass grafts (15). Using the Miller cuff, Pappas et al. obtained improved patency of all prosthetic grafts, femoral-popliteal and infrapopliteal, at various time intervals of 64%, 75%, and 62%, respectively, when compared with historical controls obtained at the same institution without vein cuffs of 35%, 46%, and 12%, respectively (18). Kreienberg et al. compared the results of infrapopliteal prosthetic grafts performed with the Miller cuff with those performed with distal arteriovenous fistula; they obtained 3-year limb salvage rates of 92% and

76% respectively (19). Even with these improved patency and limb salvage rates, other investigators were concerned that the perpendicular configuration of the Miller cuff, as well as the anastomotic reservoir, could theoretically increase turbulence and shear stress at the distal anastomosis. In addition, the silo effect of the Miller cuff makes it difficult to place in tight spaces such as in bypasses to the dorsalis pedis artery (1). This led to the development of alternative techniques. Taylor et al. used a different technique known as the “Taylor patch” (20). They commented on a group of patients that had a vein patch placed in the distal anastomosis at the time of graft thrombectomy for graft failure. They recognized that these patients had only minimal narrowing of the distal anastomosis on arteriogram performed up to 5 years later. They hypothesized that this protective effect was due either to reduction of compliance mismatch between graft and artery or to the inherent properties of the vein (20). Taylor et al. felt that using a vein patch at the distal anastomosis could obtain a more tapered funnel shape and theoretically decrease turbulence in this area. In addition, they felt that adding a vein patch at the proximal anastomosis may change the hemodynamics and prevent the development of intimal hyperplasia even at that location (20). They described making an arteriotomy 3–4 cm in length for the distal anastomosis, at least four to five times longer than the diameter of the PTFE conduit. The anastomosis was made end-to-side at a very sharp angle to ensure that the PTFE lay almost parallel to the artery. Next, the hood of the PTFE graft was incised in line with the arteriotomy to a point 2 cm proximal to the heel of the anastomosis. A vein patch varying from 5 to 6 cm was harvested to close the elliptical defect. The patch was begun distally with interrupted sutures and completed proximally with a running suture (Fig. 48.2). The proximal anastomosis was described as a conventional end-to-side anastomosis with a subsequent 3-cm longitudinal in the hood of the graft, which is closed with a vein patch. Using this technique, Taylor et al. reported on 256 grafts, 83 to the tibial arteries, with 1-, 3-, and 5-year patency rates of 74%, 58%, and 54% respectively (20). Theoretical disadvantages of the Taylor patch include the exposure of graft material directly to the artery for at least half the anastomosis, and the length of the artery and venous tissue required to accomplish the anastomosis. Tyrell et al. recognized the encouraging patency rates of both the Miller cuff and Taylor patch and reported 1year patency rates of 74% (n = 72) with use of the Taylor

FIGURE 48.1 Miller’s cuff.

FIGURE 48.2 Taylor’s patch.

Chapter 48 Extended Techniques for Limb Salvage Using Vein Cuffs and Patches

patch technique and 47% (n = 27) with use of the Miller collar technique. They recognized the theoretical disadvantages of both techniques; most notably, the large anastomotic reservoir and the perpendicular configuration of the Miller cuff and the need for direct suturing of graft directly to artery with the Taylor patch—both could increase the possibility of intimal hyperplasia. This led to the development of the St Mary’s boot, which describes a similar arteriotomy and venous harvest as the Miller cuff; however, the corner of the venous sheet is sutured to the apex of the arteriotomy to form the anastomotic toe. The remainder of the venous-arterial anastomosis is formed in a similar fashion to the Miller cuff. However, the redundant vein is excised obliquely and sutured to the longitudinal edge. Next, a segment of the posterior collar is incised to increase the size of the anastomosis between the graft and vein collar (Fig. 48.3). Overall the St Mary’s boot maintains a fully compliant venous collar, avoids any direct contact between artery and PTFE, and avoids the perpendicular angle of the vein cuff. Its main drawback is the technically demanding nature of the operation (21). Recognizing the theoretical disadvantages of the above, we fashioned a technique which used a standard vascular procedure (the Linton patch) allowing a lesser arteriotomy, thereby decreasing the amount of venous tissue required (1,22). A 2- to 3-cm segment of vein is required and can include saphenous remnants, arm vein harvested under local anesthesia, and rarely, superficial femoral vein. This vein segment is gently irrigated with prepared vein solution and opened longitudinally. Any valves are excised and the vein segment is briefly stored in vein solution. A 2- to 3-cm arteriotomy is then performed in the artery chosen for distal anastomosis. The venous segment is cut to the appropriate length in preparation for the patch. In most cases, the width is left unaltered to allow for a generous patch. A longitudinal venotomy is then made in the proximal two-thirds of the patch (Fig. 48.4A). An externally reinforced, 6 mm, thin-walled e-PTFE graft is then sutured to the vein patch using 6-0 Prolene in a continuous fashion, allowing a rim of venous tissue interposed between the PTFE graft and the arterial wall. As described above, more venous tissue is left interposed at the toe of the anastomosis than the heel of the anastomosis. Since the patch is left wide, it bulges under arterial flow, providing a cuff-like configuration (Fig. 48.4B). Figure 48.5 shows intraoperative photograph and an arteriogram illustrating PTFE bypass to the posterior tibial artery with vein patch interposition. A heparin infusion is started 4–6 hours postoperatively with coumadin admin-

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istered on the first postoperative day. Long-term anticoagulation with coumadin is continued with an INR of 2.0 as the goal. This technique was used in 79 patients with no autogenous vein available as the conduit (1). In these patients, the ipsilateral and contralateral greater saphenous veins were either not available, having been used for previous revascularization procedures, or were unsuitable due to inadequate length or quality. In all, 80 bypasses were performed in the 79 patients, with follow-up ranging from 30 days to 4 years. This group represented 16% of the total tibial bypass experience during this time period. There were 39 men and 40 women, with a mean age of 67 years. Risk factor analysis revealed 42 (53%) patients with diabetes mellitus, 16 (20%) patients with renal failure, and 48 (60%) patients with increased perioperative cardiac risk as assessed by Eagle’s criteria. Out of the 16 patients with renal failure, 12 were on dialysis and the remainder had a creatinine level greater than 2.5 mg/dl. The indication for revascularization was limb-threatening ischemia in all patients with rest pain in 39 (49%) limbs and gangrene or non-healing ulceration present in 41 (51%). Reasons for the lack of adequate saphenous vein included previous failed lower extremity bypass at an outside institution in 47 patients (59%), previous coronary bypass in 21 (26%), unsuitable vein quality due to size or thrombosis in 8 (10%), and absence of vein due to varicose vein stripping in 4 (5%). Bypass grafts originated from the common femoral artery in 40 cases (50%), the external iliac artery in 34 cases (43%), and the superficial femoral artery in 6 cases (8%). Recipient arteries included the peroneal artery in 35 cases (44%), the posterior tibial artery in 28 cases (35%), and the anterior tibial artery in 17 cases (21%). Two of the posterior tibial bypasses were to inframalleolar plantar branches.

A

B

FIGURE 48.3 St. Mary’s boot.

FIGURE 48.4 Technique of distal vein patch. (A) Venotomy location in the patch. (B) Final result of the patch, illustrating the cuff-like configuration after blood flow is allowed in the distal anastomosis.

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 48.5 Posterior tibial bypass with PTFE and dital vein patch. (A) Intraoperative photography. (B) Intraoperative arteriogram.

A

B

Graft patency and limb salvage rates were determined at follow-up intervals ranging from 6 to 48 months. Data were analyzed by life table method and reported as patency and limb salvage ± standard error (Fig. 48.6). Primary graft patency was 90% at 6 months, and 82%, 78%, 69%, and 62% at respective 12-month intervals to 48 months. Limb salvage was 93% at 6 months, and 88%, 83%, 79%, and 79% at 12-month intervals to 48 months. Of note, limb salvage and secondary patency were equivalent at all time intervals. Therefore, secodnary patency at 4-year follow-up was 79%. Beyond 48 months, six grafts remained at risk. Three grafts failed, resulting in three amputations. There was one perioperative death due to myocardial infarction (1.25%). Further analysis revealed that seven grafts failed in the immediate postoperative period, leading to five amputations. Four of the patients with failed grafts had an operative thrombectomy with no technical problem noted at the time of reoperation. Two of the thrombectomies were successful and these grafts were patent at 12 and 24 months. Two thrombectomies were not successful, resulting in amputation. Three patients went directly to amputation without an attempt to reestablish graft patency. There were three graft infections. Two were noted at the time graft thrombosis was diagnosed, resulting in graft excision and amputation. The remaining infection occurred in a known thrombosed graft, leading to amputation.

FIGURE 48.6 Graph depicting primary patency and limb salvage rates. The numbers on the graph represent grafts at risk at the beginning of specific time interval.

above suggest that the addition of venous tissue at the outflow anastomosis improves patency of prosthetic bypasses, it is difficult to make a conclusive statement to that effect. The final question of whether the addition of minimal venous tissue at the outflow anastomosis enhances the patency of lower extremity prosthetic bypasses would best be answered by a randomized prospective trial of obligatory prosthetic bypasses in patients with unavailable autogenous vein requiring infrapopliteal bypasses.

Conclusions Acceptable long-term patency and limb salvage can be achieved using PTFE with the interposition of venous tissue at the distal anastomosis to infrapopliteal arteries in patients with limb-threatening ischemia and unavailable autogenous venous tissue. Although the results presented

References 1. Neville RF, Tempesta B, Sidawy AN. Tibial bypass for limb salvage using polytetrafluoroethylene and a distal vein patch. J Vasc Surg 2001; 33:266–271.

Chapter 48 Extended Techniques for Limb Salvage Using Vein Cuffs and Patches 2. Veith FJ, Gupta SK, et al. Six-year prospective multicenter randomized comparison of autologous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 1986; 3:104–114. 3. Hobson RWI, Lynch TG, et al. Results of vascularization and amputation in severe lower extremity ischemia: a five-year clinical experience. J Vasc Surg 1985; 2:174–185. 4. Flinn WR, Rohrer MJ, et al. Improved long-term patency of infragenicular polytetrafluoroethylene grafts. J Vasc Surg 1988; 7:685–690. 5. Ascer E, Veith FJ, et al. Six-year experience with expanded polytetrafluoroethylene arterial grafts for limb salvage. J Cardiovasc Surg 1985; 26:468–472. 6. Veterans’ Administration Cooperative Study Group 141. Comparative evaluation of prosthetic, reversed, and insitu vein bypass grafts in distal popliteal and tibialperoneal revascularization. Arch Surg 1988; 123: 434–438. 7. Whittemore AD, Kent KC, et al. What is the proper role of polytetrafluoroethylene grafts in infrainguinal reconstruction? J Vasc Surg 1989; 10:299–305. 8. Campbell CD, Brooks DH, et al. Use of expanded microporous polytetrafluoroethylene for limb salvage: a preliminary report. Rev Surg 1977; 34:206–209. 9. Campbell CD, Brooks DH, et al. Expanded microporous polytetrafluoroethylene as a vascular substitute: a two year follow-up. Surgery 1979; 85:177–183. 10. Veith FJ, Moss CM, et al. Expanded polytetrafluoroethylene grafts in reconstructive arterial surgery: preliminary report of the first 110 consecutive cases for limb salvage. JAMA 1978; %20;240:1867–1869. 11. Chervu A, Moore W. An overview of intimal hyperplasia. Surg Gynecol Obstet 1990; 171:433–432. 12. Bassiouny H, White S, et al. Anastomotic intimal hyper-

13.

14.

15.

16.

17. 18.

19.

20.

21.

22.

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plasia: mechanical injury or flow induced. Surgery 1992; 15:708–717. Imparato AM, Braco A, et al. Intimal and neointimal fibrous proliferation causing failures of arterial reconstructions. Surgery 1972;1007–1014. Norberto JJ, Sidawy AN, et al. The protective effect of vein cuffed anastomoses is not mechanical in origin. J Vasc Surg 1995; 21:558–64; discussion 564–6. Miller JH, Foreman RK, et al. Interposition vein cuff for anastomosis of prosthesis to small artery. Aust N Z J Surg 1984; 54:283–285. Suggs WD, Henriques HF, DePalma RG. Vein cuff interposition prevents juxta-anastomotic neointimal hyperplasia. Ann Surg 1988; 207:717–723. Siegman FA. Use of venous cuffs for graft anastomosis. Surg Gynecol Obstet 1979; 148:930. Pappas PJ, Hobson RW, et al. Patency of infrainguinal polytetrafluoroethylene bypass grafts with distal interposition vein cuffs. Cardiovasc Surg 1998; 6:19–26. Kreienberg PB, Darling RC III, et al. Adjunctive techniques to improve patency of distal prosthetic bypass grafts: polytetrafluoroethylene with remote arteriovenous fistulae versus vein cuffs. J Vasc Surg 2000; 31:696–701. Taylor RS, Loh A, et al. Improved technique for polytetrafluoroethylene bypass grafting: long-term results using anastomotic vein patches. Br J Surg 1992; 79:348–354. Tyrrell MR, Wolfe HN. New prosthetic venous collar anastomotic technique: combining the best of other procedures. Br J Surg 1991; 78:1016–1017. Neville RF, Attinger C, Sidawy AN. Prosthetic bypass with a distal vein patch for limb salvage. Am J Surg 1997; 174:173–176.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 49 Intraoperative Assessment of Vascular Reconstruction Jonathan B. Towne

Intraoperative assessment of vascular reconstructive procedures is an integral part of vascular surgery and is necessary to ensure technical adequacy (1). Despite careful operative technique, residual lesions or surgical defects can occur that can adversely affect both the short-term and long-term outcomes of the surgical procedure. The ideal intraoperative test should be safe and inexpensive, provide functional as well as anatomic information, and should be reliable enough to permit operative revision. Currently there are three types of intraoperative assessment utilized: arteriography, pulsed or continuous wave Doppler ultrasound and duplex color imaging. The relative advantages of each are listed in Table 49.1. This chapter will examine each of these modalities, discussing their relative value in intraoperative assessment of vascular repair.

Operative Angiography Angiography was the first widely used modality for intraoperative evaluation of vascular repair. Traditionally it involves the injection of contrast material and obtaining a single anteroposterior view of the arterial reconstruction. The three principal areas in which it is used are carotid endarterectomy, visceral vessel reconstruction, and lower limb revascularization, each of which requires modification of the technique to adequately evaluate the repair because of the unique anatomic and physiologic characteristics of these widelv varying vascular beds. We will consider each separately.

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Carotid Endarterectomy Completion angiography is an excellent technique to evaluate carotid endarterectomy. A 19-gauge scalp vein needle is inserted into the common carotid artery proximal to the suture line following completion of the repair. A 20-mL syringe is filled with contrast material, with care taken to evacuate all residual air bubbles. The x-ray plate is placed beneath the patient’s head and neck. A single exposure is obtained after the injection of 6 to 8 mL of contrast material. Because of the speed of internal carotid flow, the filming must be quick to ensure that the contrast outlines the operative repair. Air emboli are a risk unique to carotid angiography, resulting in possible neurologic deficit. In a study of 260 carotid procedures, Rosental and his colleagues noted unacceptable defect problems in 8% of their patients (2). These included problems with the external carotid in 4%, common carotid in 1.2%, and internal carotid artery in 2.6%. The internal carotid was occluded in two patients (0.1%), and an intimal flap was identified in five (1.9%). Dardik et al. noted correctable lesions in 11.8% of carotid repairs (3). Donaldson et al. noted defects warranting correction in 16.1%, which included kinks in 32%, external carotid flap in 25%, common carotid plaque in 14%, thrombus in 14%, distal internal carotid plaque in 11%, and internal carotid occlusion and spasm in 1.4% each (4).

Lower Limb Bypass Completion angiography for the evaluation of lower limb bypass is the area where intraoperative arteriography has

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TABLE 49.1 Comparison of intraoperative methods of assessment

Safety Expense Functional information Anatomic information Basis for revision

Arteriography

Continuous Wave or Pulsed Doppler

Duplex Scanning/Color Flow

– – – + +

+ + + – –

+ + + + +

obtained its most widespread use. We use angiography to evaluate the distal anastomosis of both prosthetic and autogenous vein grafts to the popliteal and more distal vessels in order to determine that the technical repair is satisfactory. An angiogram is obtained following restoration of flow to lower extremities by inserting a 19-gauge scalp vein needle into the proximal portion of the bypass graft. The x-ray cassette is placed in a sterile plastic cover first and then positioned beneath the patient’s leg. The operating table is then lowered as much as possible to increase the distance from the tube to the x-ray cassette. Our technique is to clamp the vessel proximal to the insertion of the needle and to inject 20 to 25 mL of contrast material into the conduit. A single angiogram is obtained, focusing the x-ray tube on the distal anastomosis. There are now available in most operating rooms portable digital x-ray units which can obtain angiograms using digital subtraction techniques, which result in high-quality intraoperative studies. The incidence of technical problems requiring revision ranges from 8% to 25% (1,3). Detecting these technical errors, particularly when an autogenous vein is the graft conduit, avoids an unexpected occlusion in the perioperative period that could result in ischemic damage to the vein. Veins that have been removed from their vascular beds before implantation as an arterial conduit are especially susceptible to ischemic changes. The amount of ischemia is often sufficient to make the conduit unusable.

Mesenteric Revascularization Operative angiography has never gained widespread use in the evaluation of renal and mesenteric arterial repairs, primarily because of the difficulty in obtaining adequate images. Flow in these vessels is quite rapid, making it difficult to time the injections to obtain a quality angiogram. With the emergence of Doppler and duplex techniques, intra-abdominal completion angiography has been essentially abandoned in most medical centers. One of the problems common to completion angiography is the exposure of the surgeon to radiation. Use of a shield, usually constructed by placing a lead apron over an intravenous pole, then covering with a sterile gown, minimizes the exposure to radiation but certainly does not eliminate it. The other problem with completion angiography is the use of contrast material, which can be toxic to the kidneys, particularly in patients who have preexisting renal insufficiency and patients with diabetes mellitus. Al-

though the incidence of anuric renal failure is low, it can contribute to renal problems in the postoperative period.

Doppler Ultrasound A continuous wave Doppler ultrasound system can be used to quickly determine patency, and a major shift in audible Doppler frequency can indicate the presence of a stenotic or residual lesion in the carotid artery or a competent valve or patent side branch in an in situ graft. Audible interpretation is not quantitative and is very subjective. We have used a high-frequency (20-MHz) pulsed Doppler and fast Fourier transform (FFT) spectrum analyzer to evaluate flow signals immediately following such procedures as carotid endarterectomy, in situ saphenous vein bypass grafts, and visceral artery endarterectomy or bypass (5,6). This method is superior to continuous wave Doppler as it permits quantitative and qualitative interpretations of the Doppler signal obtained from a specific site, but arteriography is still needed for anatomic evaluation. Spectral analysis of Doppler flow signals can detect abnormalities of blood flow produced by lesions in the arterial system. This method is used clinically to determine the extent of occlusive disease or stenotic lesions based on changes in the spectral and temporal characteristics of the Doppler-derived velocity waveform. In an animal model, pulsed Doppler spectral analysis of midstream flow identified flow disturbances produced by lesions that were unassociated with a pressure gradient or a reduction in flow volume (7). The high-frequency pulsed Doppler and spectrum analyzer are used intraoperatively to identify flow abnormalities in the region of the endarterectomy and anastomotic sites following carotid endarterectomy or lower extremity bypass grafting. The detection of technical errors by pulsed Doppler spectral analysis is quite accurate (8–10). The arterial flow pattern is analyzed with a 20-MHz pulsed-wave direction-sensitive Doppler velocity detector. The Doppler probe consists of a small ultrasonic transducer mounted on a 16-gauge needle. The sample volume of the pulsed Doppler detector is approximately 0.2 mm3. By range-gating, the sample volume can be positioned at any point between 1.1 and 11.5 mm from the end of the probe. Two direction-sensitive quadrature signals

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from the pulsed Doppler system are processed by a realtime, PET spectrum analyzer and displayed on a video monitor for interpretation. A spectrum analyzer determines the amplitude of all frequencies present in a Doppler signal. The amplitude of a particular frequency is proportional to the number of red blood cells moving through the Doppler beam that produce that particular frequency shift at a point in time. Spectral information is presented graphically, with the frequency on the vertical axis, the time on the horizontal axis, and amplitude indicated by the intensity of the waveform. Real-time spectral analysis permits immediate assessment of the velocity waveform and selection of representative waveforms for tape recording or for self-developing prints photographed from the video monitor. The pulsed Doppler flow pattern is analyzed following completion of the arterial reconstruction and restoration of blood flow. The gas-sterilized Doppler probe is placed directly on the external surface of the artery and acoustically coupled with saline solution. The sample volume is located in the midstream of the flow by adjustment of the range control. The range is calculated from caliper measurements of the vessel diameter and the cosine of the Doppler angle. An angle of approximately 60° is maintained between the Doppler probe and the longitudinal axis of the artery. Midstream flow patterns are examined at multiple sample sites proximal to, in the center of, and immediately downstream of endarterectomized arterial segments or the graft anastomosis. Longitudinal scanning of the arterial reconstruction is required because the flow disruption produced by technical errors is maximal immediately downstream of the vascular defect. Special attention is directed to regions of the arterial reconstruction where technical errors are known to occur, such as the endarterectomy end point of the internal carotid artery. Regions requiring special attention in the lower extremity bypass graft include proximal and distal anastomoses, valve sites, and the distal outflow artery (6,11). Generally, the normal arterial flow pattern in the midstream of a vessel consists of laminar flow throughout systole and diastole. Under laminar flow conditions, all red blood cells encountering the pulsed Doppler beam in the region of the sample volume are moving at similar speeds and directions. This flow pattern is evident in the backscattered Doppler signal by a narrow range of frequencies (spectral width). When flow is disturbed, the velocities and direction of the red blood cells become more random, and the range of frequencies present in the Doppler signal is increased, which is commonly referred to as spectral broadening. The feasibility of using pulsed Doppler spectral analysis to detect vascular defects has been verified in an animal model. Technical errors (intimal flaps, intraluminal thrombus, and intimal defects) were constructed in a canine abdominal aorta (7,12). Large intimal flaps and thrombus produced midstream flow disruptions immediately downstream of the arterial defect. The

ability to detect a vascular defect was dependent on the severity of the flow disturbance produced. Minor defects such as intimal flaps or other intimal defects were not identified because they did not significantly disrupt midstream flow. If an arterial stricture is present, an increase in peak systolic velocity will occur, as well as spectral broadening. These spectral changes in the velocity waveform occur with diameter reductions as small as 15% (7). A diameter reduction of 50% or more, which is associated with a pressure gradient and flow volume reduction, results in a marked increase in both peak systolic velocity (Vp) and spectral broadening throughout systole and diastole. The midstream flow pattern in the arterial reconstruction is interpreted as normal or abnormal based on Vp and changes in the velocity waveform. The criterea an abnormal flow pattern is a localized increase in Vp associated with significant spectral broadening. These waveform values were assessed visually from the video monitor. Following this determination in animal models, Bandyk et al. compared pulsed Doppler spectral analysis of midstream flow with arteriography in 90 patients after carotid endarterectomy (n = 60) or lower extremity bypass grafting (n = 30) (11). Unsuspected technical error of the endarterectomy or anastomotic sites was detected in 12% of the patients. These errors were detected because of spectral changes in the velocity waveform, indicating turbulent flow. All were associated with anatomic defects not apparent with arteriography. The revision of major defects in six (7%) of the patients corrected the flow disturbance. The absence of flow disturbance in 88% of the patients predicted a technically satisfactory arterial reconstruction. Intraoperative assessment by pulsed Doppler spectral analysis is a noninvasive, rapid, and accurate method for detecting technical errors during arterial surgery. The high sensitivity of this test as determined in this study indicates the validity of this method for the intraoperative assessment of vascular reconstructions.

Duplex Scanning B-mode imaging has been used to assess completed arterial reconstructions, and intravascular defects can be detected by this method. Sigel et al. detected residual defects in more than 20% of patients having post-reconstruction B-mode scans (13). Like arteriography, however, this method can provide only anatomic information and is incapable of determining the hemodynamic consequences of a detected lesion. Advances in technology have provided instrumentation that combines the advantages of Doppler spectral analysis for hemodynamic assessment and B-mode imaging to determine vessel wall integrity. The further addition of color-coded imaging greatly facilitates vessel imaging, making this the ideal method for intraoperative evaluation of arterial reconstructions.

Chapter 49 Intraoperative Assessment of Vascular Reconstruction

Technique Duplex examinations use color coding to display velocity spectra within the B-mode image (5). Intraoperative techniques are identical whether employing gray-scale or color-coded imaging, although color allows for more rapid vessel identification and interrogation. This technique can be used for cerebrovascular, peripheral arterial, and visceral vessels and requires a high-frequency transducer, because it is applied directly to the reconstructed vessel. The duplex scan is performed and recorded on videotape after closure of the arteriotomy and restoration of blood flow. A sterile plastic sleeve is filled at one end with acoustic gel before placing the transducer inside. The cervical wound is filled with sterile saline, and the handheld transducer is positioned directly over the exposed vessels. The vascular technologist is present to make necessary adjustments in Doppler angle assignment, sample volume placement, and color parameters in order to obtain the optimal image and accurate spectral display.

Applications Carotid Artery Reconstruction Despite careful technique during carotid endarterectomy, residual abnormalities in the reconstructed artery may lead to perioperative or long-term complications. These defects include elevated intimal flaps (Fig. 49.1), stenosis of the repair, problems with the endarterectomy of the external carotid artery, and the occasional development of abnormal platelet aggregation along the suture line. The failure to detect and correct these problems can lead to thrombus formation with distal embolization or vessel thrombosis. Early carotid studies using ocular pneumoplethysmography in the recovery room in patients who had no intraoperative assessment identified early internal carotid artery (ICA) occlusions in 4% of patients (14). In a study in which Zierler et al. performed routine completion angiography, major defects in the internal carotid repair were detected in 5% of patients undergoing carotid endarterectomy (6). Other studies of completion angiography following carotid artery repairs report a 4% to 6% incidence of defects that require correction (1–3,8). Duplex scanning after carotid reconstruction was performed in both longitudinal and transverse planes. The common carotid artery (CCA) was examined first, noting any wall irregularity and obtaining spectral data from midstream flow. The proximal endarterectomy point was closely examined, and the spectral display was noted and recorded. The transducer was advanced cephalad to the bifurcation, and the proximal and distal ICA was examined. Any area of increased or decreased flow velocity or turbulent flow was examined closely by turning off the color and enlarging the B-mode image to detect the etiology of flow disturbance (Fig. 49.2). This is important, as color can mask subtle defects that may be more visible with gray-

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scale imaging. The external carotid artery (ECA) was examined in a similar fashion. Finally, transverse scanning was performed to obtain diameter measurements of the ICA and vein-patched segments. Classification of flow disturbance is described in Table 49.2. The entire endarterectomized segment must be visualized, particularly the distal end where residual plaques and intimal flaps can occur. The diagnostic algorithm used for decision-making regarding reexploration is described in Figure 49.3. If markedly abnormal findings are noted in the B-mode image, the vessel is immediately reexplored. Usually, however, a defect is first identified by observing an area with abrupt color change and a spectral display showing high Vp (>125 cm/s) and marked spectral broadening. If no corresponding defect can be identified in the B-mode image, an operative carotid angiogram is obtained to further evaluate the reconstruction. We determined the accuracy of intraoperative flow assessment in a study of 250 carotid endarterectomy sites in 235 patients who were assessed at operation by pulsed Doppler spectral analysis and arteriography (15). The degree of flow abnormality by pulsed Doppler spectral analysis correlated closely with operative arteriographic interpretation (Table 49.3). The presence of normal laminar flow or only mild flow disturbances was demonstrated in 182 of the 250 internal carotid arteries after endarterectomy, including six arteries revised at the primary operation, and correlated with a normal arteriogram and early patency. Minor anatomic abnormalities, ICA wall irregularity and angulation, and 10% to 30% diameter reduction were noted in 113 (45%) of the 251 angiograms suitable for interpretation and classification of residual disease. Severe flow disturbance was demonstrated in 20 (8%) of the ICAs, and in all cases was associated with minor or major anatomic abnormalities on arteriography. In 10 (4%) of the patients, the arteriograms were judged abnormal and the vessel was explored. Exploration identified stricture produced by the suture closure or vessel kinking at the arteriotomy end point (n = 4), intimal flaps (n = 3), or fibrin and platelet aggregates (n = 3). Initially, nine of the operative revisions had primary closure of the arteriotomy. After endarterectomy site revision and patch angioplasty, the velocity spectrum and arteriogram showed improvement. In eight (3%) of the patients, Doppler flow analysis demonstrated occlusion or severe flow disturbance involving the ECA. Seven patients had residual atherosclerotic plaque removed through a separate external carotid arteriotomy without interruption of ICA flow. Color flow imaging with pulsed Doppler spectral analysis has important advantages compared with arteriography in detecting problems that may lead to thrombosis formation or distal embolization resulting in perioperative stroke. The development of platelet aggregation in the endarterectomy site and the abnormal hemodynamics associated with distal ICA kinking or angulation with arteriotomy closure were reliably identified

610

Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 49.1 (A) Gray-scale image of intimal flap. (B) Normal flow velocity following revision.

by Doppler flow analysis and imaging. In contrast, the significance of these anatomic abnormalities was difficult to detect and assess by arteriography because of the unpredictable image resolution and vessel projection obtained with intraoperative studies. Operative arteriography was abnormal in only three of five patients demonstrated to have platelet aggregation at reoperation. All of these patients had severe flow disturbance identified in the ICA by Doppler flow analysis and a visible defect in the Bmode image. Unrecognized platelet aggregation may be a factor in the discrepancy between Doppler flow analysis and angiography. Duplex ultrasonography can be used to detect this complication in the early nonocclusive phase (Fig. 49.4).

A flow pattern of normal laminar flow or mild flow disturbance was seen in 73% of the ICAs in this study and correlated with a normal completion arteriogram, long-term patency of the endarterectomy, site, and low incidence of recurrent stenosis (12% at 3 years) (15). In contrast, occlusion and early stenosis (<3 months) of the endarterectomy site correlated with the presence of residual flow disturbance (turbulence) at operation. Endarterectomy sites with residual flow disturbance were associated with anatomic abnormalities on completion arteriography and an increased incidence of recurrent stenosis (21% at 3 years) compared with sites with normal flow patterns. No false-negative duplex studies occurred.

Chapter 49 Intraoperative Assessment of Vascular Reconstruction

The clinical implication of these data is that colorcoded imaging and Doppler flow analysis can be used with the same confidence as arteriography in defining the technical adequacy of carotid reconstruction. In addition, duplex scanning provides objective physiologic criteria for determining the hemodynamic significance of minor

611

anatomic imperfections of the endarterectomy shown by visual inspection of arteriography. The presence of severe residual flow disturbance should not be ignored. This flow pattern was associated with vascular defects that threatened patency and increased the incidence of recurrent stenosis. Only 20% of patients with this flow abnormality had a patent endarterectomy site free of stenosis during the follow-up interval. These results have prompted us to adopt a policy to explore all endarterectomy sites with severe residual flow disturbances.

Intraoperative Revisions In a subsequent prospective study of 443 patients having 461 carotid endarterectomies, we evaluated the validity of intraoperative assessment to detect technical error and to determine the incidence and type of intraoperative revisions (8). Intraoperative ultrasound studies were performed on 410 (89%) of the 461 carotid endarterectomies. Of the 461 carotid endarterectomy sites, 26 (5.6%) were revised based on intraoperative study results. Patch angioplasty was performed in nine of the eleven ICA revisions, one of eleven ECA revisions, and two of four CCA revisions. In 10 of 11 patients, ECA revision was accomplished by removing residual atherosclerotic plaque through a separate ECA arteriotomy without interrupting

FIGURE 49.2 Gray-scale image of small intimal flap.

FIGURE 49.3 Diagnostic algorithm for intraoperative duplex scanning following carotid endarterectomy.

TABLE 49.2 Categories of internal carotid artery stenosis Diameter Reduction (%) 0–15 16–49 50–75 76–99 Occlusion

Velocity Spectra Characteristics Systolic peak flow velocity <100 cm/s; no spectral broadening or only in deceleration phase of systole Systolic peak flow velocity to 125 cm/s; spectral broadening throughout pulse cycle Systolic peak flow velocity >125 cm/s; spectral broadening throughout pulse cycle End-diastolic flow velocity >125 cm/s; uniform spectral broadening throughout pulse cycle with simultaneous reversed flow components during systole No flow signal in imaged vessel; flow to zero in common carotid artery

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ICA flow. Residual ECA problems were usually evident by lack of flow or markedly abnormal velocity spectra. One perioperative stroke occurred in this subset of 26 patients. This stroke, caused by CCA thrombosis, occurred despite improvement in the spectrum after revision. The patient had extensive CCA atherosclerosis.

A total of 23 reconstructions were classified as normal by repeat intraoperative ultrasound examination after revision; of these, 20 remained normal on late follow-up. Recurrent stenosis was seen in three of 23 cases, one of which progressed to occlusion without stroke. Three reconstructions retained a moderate resid-

TABLE 49.3 Comparison of internal carotid artery (ICA) flow disturbance and operative arteriograph interpretation of 251 carotid endarterectomies Angiographic Disease Category

ICA Flow Disturbance None/mild Moderate Severe Total

Normal

Diameter Reduction <10%

Diameter Reduction 10–30%

115 13 10 128

54 18 10 72

7 24 20 41

Abnormal

Total

176 55 10

251

FIGURE 49.4 (A) Image and spectral waveform in internal carotid artery. “Shadowing” in vessel represents platelet aggregation. (B) Normal flow following revision.

Chapter 49 Intraoperative Assessment of Vascular Reconstruction

ual flow disturbance by intraoperative ultrasound examination after revision. Two of the three patients had recurrent stenosis on late follow-up and one patient underwent reoperation for a lesion with more than 80% diameter reduction in association with recurrent symptoms. In patients studied with intraoperative ultrasound, there was normal laminar flow in 337 ICAs after endarterectomy, and the perioperative stroke rate was 2.1%. Moderate flow disturbance was identified in 73 patients, and the perioperative stroke rate was 4.1% for this group. Duplex scanning performed within 3 months of surgery revealed more than 50% residual carotid stenosis in 11 (2.4%) of 461 patients. These 11 patients included 5 (9.8%) of 51 patients in whom intraoperative ultrasound studies had revealed a mild or moderate flow disturbance, and one (0.3%) of 337 patients in whom intraoperative ultrasound studies had revealed no flow disturbance. The incidence of residual stenosis was significantly lower in patients with no flow disturbance by intraoperative ultrasound studies than in patients with mild or moderate flow disturbance by intraoperative ultrasonography or in the patients in whom no intraoperative ultrasound studies had been performed.

Causes of Intraoperative Errors Duplex scanning has the ability to detect a wide range of lesions by providing a method of directly assessing the vessel wall anatomy and flow hemodynamics. There are, however, inherent possibilities for interpretation errors that could lead to unnecessary intraoperative revisions (Table 49.4). There are anatomic factors that may affect flow patterns, resulting in Doppler flow signals suggestive of stenosis even though no technical defect is present. Spasm of the carotid artery causes increased flow velocities due to decreased vessel diameter and is difficult to distinguish by imaging from true stenosis, which may produce the same flow velocities and spectral broadening. Spasm may be suspected when the Vp is increased but no abnormality can be visualized. The increased velocities and spectral broadening that are related to arterial spasm

TABLE 49.4 Causes of interpretation errors Cause of Error

Spectral Characteristics

Arterial spasm

Increased Vp with no visible defect Small-diameter vessel Generalized increased Vp (not focal) Optimal angle is 60° (45–60° acceptable) Acute angle = increased frequency shift Perpendicular angle = decreased frequency shift Increased Vp without significant spectral broadening Severe contralateral stenosis or occlusion Angiographic evidence of cross-filling

Doppler angle

Contralateral stenosis

Vp, peak systolic velocity.

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are not focal, have no associated wall irregularity, and are associated with small vessel diameter. Spasm is most often seen in the ICA, but it can occur in the CCA as well. Another possibility for interpretation error exists when the vessel is tortuous and the velocity is obtained with an erroneous Doppler beam angle. Recordings of flow from each vessel must be obtained by placing the Doppler sample volume in the center of the flow stream and adjusting the Doppler beam angle parallel to the axis of flow. An angle of 45° to 60° is acceptable when the optimum 60° cannot be obtained. An acute angle will cause an increased frequency shift, and a perpendicular angle will cause a decreased shift, resulting respectively in overestimated and underestimated peak systolic flow (9,10). FamiIiarity with the anatomy and hemodynamics of the intracranial and extracranial vasculature is essential for evaluating patients with carotid occlusive disease. The intracranial circulation is supplied by four major extracranial vessels, consisting of the carotid and vertebral arteries on each side of the neck. The extracranial carotid arteries terminate at the base of the brain to form the anterior portion of the circle of Willis. Posteriorly the circle is formed by the basilar and posterior cerebral arteries, which anastomose via the posterior communicating arteries. Of the patients in our study, 4% had an elevated Vp consistent with a 50% ICA stenosis at operation. Although the Vp would indicate a significant stenosis, only moderate spectral broadening was present and no visible defect was noted on the B-mode image. These patients also had severe (>75%) stenosis or occlusion of the contralateral ICA. In previous work, we identified increased Vp without spectral broadening in patients with severe contralateral carotid occlusive disease and angiographic evidence of cross-filling at the circle of Willis (16). Even though Vp was increased, spectral broadening was minimal and no technical defect could be visualized. We attributed the elevated velocities to increased blood flow in the ICA supplying both cerebral hemispheres. From follow-up examinations, these patients have all shown only moderate (<50%) stenosis. One patient who appeared to have a normal intraoperative duplex scan had abnormal findings at 1 month after surgery. Flow velocities consistent with a 50% stenosis as well as an area of wall irregularity were noted in the distal ICA in each of four consecutive postoperative duplex scans performed at 3-month intervals. Because this area is in the very distal portion of the ICA, it was probably inaccessible at operation. This is particularly important in patients who have high bifurcations or in patients with short necks in whom the angle of the mandible prevents the placement of the duplex probe over the area of the artery to be interrogated. This represents a limitation in intraoperative duplex scanning with the current transducers, which are large and wedge-shaped, limiting placement within the surgical wound. This could be eliminated with smaller transducers that are currently being developed. To evaluate our experience with intraoperative carotid evaluation in a recent series, we evaluated 100

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consecutive carotid operations in 96 patients (60 men and 36 women) from 1995 to 1998. Preoperative, intraoperative and 6-week follow-up duplex scan results were analyzed (18). The average time of the scan was 10.6 ± 1.1 minutes. There were 33 intraoperative duplex studies with abnormal findings. Seven involved the CCA and resulted in intraoperative revision in five. These presented as intimal fractures occurring at the site of the proximal clamp placement. Two patients with scans that showed abnormalities secondary to step-off in the size of the vessel at the endarterectomy breakpoint did not undergo revision. Eleven patients had external carotid artery flow disturbances, all of which were caused by elevated distal intimal flaps secondary to an incomplete eversion endarterectomy. These were repaired through arteriotomy in the external carotid artery, which did not require reclamping of the CCA or ICA. There were 15 abnormalities in the ICA. Five of these required revision of a patch or patching of a previously unpatched artery. Five studies had PSV in the 100 to 150 cm/s category, but had no defects on B-mode imaging and were observed without treatment. The arterial reconstruction was clearly visualized in its entirety and no stenosis, wall abnormalities, or technical defects were detected. The remaining five were felt to be false-positive studies owing to an increase in velocity flow due to occlusion or high-grade stenosis of the contralateral ICA, a small ICA, or arterial spasm. In these false-positive studies, a distinguishing characteristic was the absence of turbulent flow. At the 6-week postoperative duplex, four of the five repaired CCAs demonstrated normal flow and one had a mild residual stenosis. Ten of the eleven external carotid artery repairs were patent and one was occluded. Four of the five ICA repairs were normal and one had a mild residual stenosis. Of the ten abnormal ICAs that were observed, nine were normal on postoperative duplex and one had a mild residual stenosis. The importance of achieving a technically perfect repair cannot be overstated. Our institutional experience spans more than 10 years with this technique, and we have learned that there are three distinct anatomical sites to carefully scrutinize when performing intraoperative duplex studies. Most significant is the distal ICA endarterectomy end point because of its orientation in the flow stream. The proximal clamp may fracture the intima of the CCA and cause a flow disturbance which may be the source of emboli or the site of stricture and/or occlusion from intimal hyperplasia. We noted five intimal flaps occurring in the proximal CCA from application of a vascular clamp even when the jaws of the clamp were modified with protective material. After detecting this the first time, we started using clamps with soft jaws. We have continued to see this pattern of injury. Another possible cause would be the application of a Rummel tourniquet to secure the intraluminal shunt. Not all of these lesions would cause problems, but certainly an intimal flap has the po-

tential to elevate with arterial flow and obstruct the CCA. Clamp injury to the CCA has not been noted in other reports on intraoperative duplex imaging (19–22). The external carotid artery should not be neglected, as it can be a source of transient ischemic attack or may preserve ICA flow in the event of CCA occlusion. Intraoperative assessment of carotid repair results in more careful scrutiny of the technical reconstruction by the surgeon. Small defects are obvious because of the sensitivity of the technique. As a result, the incidence of patching carotid arteries has increased from less than 10% to 70%. While detected lesions will not all result in vessel occlusion and/or neurologic deficits, the surgical axiom “the better the operation the better the operative results” remains valid. For the best carotid artery reconstruction, early and late postoperative results begin with a technically perfect repair. Intraoperative duplex give the surgeon a timely and unique opportunity to achieve this goal.

In Situ Bypass Grafts A variety of lower extremity bypasses such as saphenous vein (in situ or reversed), nonreversed venous conduits, or concomitant endarterectomy procedures should be evaluated at operation to exclude technical error and confirm patency and adequate flow. Early graft failure (<3 months) has been attributed to unrecognized (or uncorrected) defects, which can result in thrombosis, distal embolization, or hemodynamic graft failure. Intraoperative assessment of bypass grafts has followed an evolution similar to carotid assessment, utilizing arteriography, continuous wave Doppler, spectral analysis, and finally color flow duplex scanning. Color duplex scanning provides a rapid, accurate means of graft assessment. As the transducer is advanced slowly along the entire length of the reconstruction, the surgeon observes the color image. Uniform color during diastole and an absence of anatomic defects in the B-mode image indicate normal flow. A residual lesion is diagnosed when a turbulent color pattern and a spectral waveform with increased Vp (>140 cm/s) and severe spectral broadening is visualized. Graft-threatening lesions and their identifying spectral characteristics are detailed in Table 49.5. Diagnostic

TABLE 49.5 Potential technical errors: in situ saphenous vein grafts Defect Anastomotic stricture Intact valve leaflet Residual arteriovenous fistula Inadequate graft flow Inadequate outflow

Duplex Characteristic ≠Vp, turbulent flow, visible narrowing ≠Vp, turbulent flow, visible valve (gray scale) ≠Vp, ≠Vd, turbulent flow, visible venous branch ØVp (<45 cm/s) in smallest diameter ØVp, ØVd, minimal turbulence

Vp, peak systolic velocity; Vd, end-diastolic velocity.

Chapter 49 Intraoperative Assessment of Vascular Reconstruction

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TABLE 49.6 Lower extremity arterial duplex ultrasonography: categories of arterial stenosis and velocity spectra characteristics Diameter Reduction (%) <20 20–49 50–75 >75

Peak Velocity (cm/s)

Velocity Increase Relative to Proximal Segment (%)

Spectral Broadening

<125 <125 >125 >125 Diastolic >100

<30 >30 >100 >100

Slight Throughout pulse cycle Severe Severe

criteria used for postoperative graft surveillance are also used for intraoperative assessment (Table 49.6).

Visceral Artery Reconstruction Intraoperative assessment of renal arterial repair utilizing some method other than arteriography is especially important because the contrast dose used in arteriography introduces additional risk to an already impaired kidney. Duplex ultrasonography has been used during surgery to assess renal blood flow before and after reconstruction. This technique is used to detect and localize renal artery stenosis and allows the surgeon to establish the location of the artery, which may be encapsulated in dense, fibrous tissue. Henderson et al. used intraoperative color duplex to identify renal arteries and transplant renal artery stenoses in three patients who required revision of previously transplanted kidneys (17). In our experience, visceral artery reconstructions were more difficult to image, primarily due to vessel tortuosity. Anastomotic sites including origins of graft from the abdomen aorta can be successfully imaged. Duplex scanning can confirm vessel patency following reimplantation of the celiac, superior mesenteric, and renal arteries as a part of thoracoabdominal aneurysm repair. Bypass grafts to the renal and superior mesenteric arteries can be imaged throughout their length, and normal graft flow hemodynamics can also be verified.

Conclusion Routine use of some intraoperative assessment techniques has been shown to result in the correction of technical errors that could lead to postoperative complications. Duplex scanning provides a safe, effective method for such assessment by combining a means for visualizing any surgical defect and the hemodynamics of such defects into one testing modality. Careful adherence to recognized interpretation criteria is necessary to avoid interpretation errors that could result from erroneous placement of the Doppler sample volume or inaccurate assignment of the Doppler beam angle. These components are all important in order to avoid misinterpreting the acquired velocity patterns. Attention to these details is essential for the precise assessment of any arterial segment. When the sample volume

deviates from center stream and approaches the vessel wall, where velocity gradients exist even in normal vessels, misclassification can occur because these gradients will be identified as abnormal flow. Duplex ultrasonography has become the standard test of choice for detecting atherosclerotic lesions in preoperative and postoperative patients. The development of color flow imaging has added a new dimension to this technique. Intraoperative ultrasonography has a low potential for complications and is an ideal test for confirming normal flow or detecting technical errors during vascular reconstructive surgery.

References 1. Bandyk DF, Govistis DM. Intraoperative color flow imaging of “difficult” arterial reconstructions. Video J Color Flow Imag 1991; 1: 13–20. 2. Rosental JJ, Gaspar MR, Movius HJ. Intraoperative arteriography in carotid thromboendarterectomy. Arch Surg 1973; 106: 806. 3. Dardik II, Ibrahim IM, et al. Routine intraoperative angiography. Arch Surg 1975; 110: 184. 4. Donaldson MC, Ivarsson BL, et al. Impact of completion angiography on operative conduct and results of carotid endarterectomy. Ann Surg 1993, 217: 682–687. 5. Cato RU, Bandyk DF, et al. Duplex scanning after carotid reconstruction: a comparison of intraoperative and postoperative results. J Vasc Tech 1991; 15: 61–65. 6. Zierler RE, Bandyk DF, et al. Carotid artery stenosis following endarterectomy. Arch Surg 1982; 117: 1408–1412. 7. Thiele BL, Hutchinson KJ, et al. Pulsed Doppler waveform patterns produced by smooth stenosis in the dog thoracic aorta. In: Taylor DEM, Stevens AL, eds. Blood flow theory and practice. New York: Academic Press 1983: 85–104. 8. Kinney EV, Seabrook GR, et al. The importance of intraoperative detection of residual flow abnormalities after carotid artery endarterectomy. J Vasc Surg 1993; 17: 912–923. 9. Kohler TR, Langlais Y, et at. Variability in measurement of specific parameters for carotid duplex examination. Ultrasound Med Biol 1987; 13.673–742. 10. Sumner DS. Evaluation of noninvasive testing procedures: data analysis and interpretation. In: Bergstein FF, ed. Noninvasive diagnostic techniques in vascular disease. St Louis: CV Mosby, 1985: 1861–1889.

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11. Bandyk DF, Zierler RE, Thiele BL. Detection of technical error during arterial surgery by pulsed Doppler spectral analysis. Arch Surg 1984; 119: 421–428. 12. Bandyk DF, Zierler RE, et al. Pulsed Doppler velocity patterns produced by arterial anastomoses. Ultrasound Med Biol 1983; 9: 79–87. 13. Sigel B, Coelho JC, et al. Ultrasonic imaging during vascular surgery. Arch Surg 1982; 117: 764–767. 14. Kremen JE, Gee W, et al. Restenosis or occlusion after carotid endarterectomy. Arch Surg 1979; 114: 608–610. 15. Bandyk DF, Kaebnick HW, et al. Turbulence occurring after carotid bifurcation endarterectomy: a harbinger of residual and recurrent carotid stenosis. J Vasc Surg 1988; 7: 261–274. 16. Bandyk DF, Moldenauer P, et al. Accuracy of duplex scanning in the detection of stenosis after carotid endarterectomy. J Vasc Surg 1988; 8: 696–702. 17. Henderson MC, Delahunt TA, van Bockel JH. Pre- and

18. 19.

20.

21.

22.

intraoperative role of color duplex ultrasound for the evaluation and diagnosis of transplant renal artery stenosis. J Vasc Tech 1993; 17: 27l-274. Mays BW, Towne JB, et al. Intraoperative carotid evaluation. Arch Surg 2000: 135: 525–529. Dykes JR, Bergamini TM, et al. Intraoperative duplex scanning reduces both residual stenosis and postoperative morbidity of carotid endarterectomy. Am Surgeon 1997; 63: 50–54. Seelig MH, Klinger PJ, et al. Use of intraoperative duplex ultrasonography and routine patch angioplasty in patients undergoing carotid endarterectomy. Mayo Clin Proc 1999; 74: 870–876. Steinmetz OK, MacKenzie K, et al. Intraoperative duplex scanning for carotid endarterectomy. Eur J Vasc Endovasc Surg 1998; 16: 153–158. Baker WH, Koustas G, et al. Intraoperative duplex scanning and late carotid stenosis. J Vasc Surg 1994; 19(5): 829.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 50 Postoperative Surveillance Jonathan B. Towne

The steady decline with time in the patency of vascular grafts mandates a protocol of postoperative surveillance to identify grafts at risk of thrombosis. The correction of lesions before graft thrombosis can have a significant impact on long-term patency. It is particularly important for vein grafts because most will not maintain patency after thrombectomy (1–3). Careful postoperative evaluation of patients with infrainguinal grafts over the past decade has clearly demonstrated that factors other than the skill of the surgeon and the completion of a satisfactory operative procedure will affect the long-term patency of vascular conduits. These factors vary depending on the interval in the follow-up period, demonstrating that the venous conduit has a unique biology that affects patency. Factors adversely affecting 30-day patency are primarily technical in nature and are related to surgical technique. Such factors are best prevented, and can often be identified by intraoperative evaluation using angiographic and physiologic assessment techniques. These factors include technical errors in constructing the anastomosis, problems with vein preparation (residual competent valves, arteriovenous fistulas), graft twist, and hyperthrombotic states. In the time period between 1 month and 24 months, fibrointimal hyperplasia, in a variety of forms, is the primary cause of graft failure. Beyond 24 months, the progression of atherosclerotic problems in both the inflow and outflow vessels becomes manifest. Similarly, as the autogenous conduits age, they are prone to degenerative changes. In addition, it has clearly been shown that prosthetic conduits, primarily knitted Dacron and polytetrafluoroethylene (PTFE), behave differently than autogenous conduits, of which the saphenous vein is most commonly used. This chapter will give the rationale for a prospective surveillance protocol that uses the autogenous vein graft as the model.

Much of what will be presented is applicable to prosthetic grafts; however, surveillance of prosthetic grafts is not as productive as that of autogenous vein grafts.

Techniques for Surveillance Physical Examination Until recently, the evaluation of lower limb arterial reconstructions was limited to physical examination. Physical examination has many inherent problems as a surveillance technique. A pulse can be felt in a vein graft and a distal pulse palpated, but impending graft failure can rarely be detected by physical examination alone. Detection of distal pulses and examination of the foot for evidence of capillary refill time are very gross measures that have little predictive value in assessing potential graft problems.

Doppler-derived Pressure Measurements The noninvasive vascular laboratory forms the cornerstone for the surveillance program because clinical diagnosis has low sensitivity in detecting lesions such as stenosis, anastomotic pseudoaneurysm, aneurysmal degeneration, and host vessel atherosclerosis, which can produce sudden graft occlusion. The majority of patients with graft stenosis are asymptomatic, and changes noted in physical examination, such as the quality of peripheral pulses, are incapable of reflecting the subtle signs of hemodynamically failing patent bypasses. The first techniques to be applied to graft evaluation were Doppler-derived systolic pressure measurements or plethysmographic

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Part VI Chronic Arterial Occlusions of the Lower Extremities

volume changes. These noninvasive tests selected those patients who might need angiography and subsequent surgery to correct anatomic lesions, such as stenosis or aneurysm, which could produce sudden thrombosis and its resulting ischemia. This diagnostic method has important limitations when used alone for postoperative surveillance. There are several specific instances in which these tests cannot be used. The incidence of diabetes mellitus in a series of patients with lower extremity bypass approaches 50% (3). In roughly one-third of these patients, calcification of tibial vessels, with the resulting incompressible vessels, makes the measurement of ankle pressures impossible. The measurement of ankle pressures can only determine that there is a problem with blood flow in some segment of the limb; however, it cannot localize hemodynamically abnormal arterial segments. In instances in which Doppler-derived pressure measurements can be obtained, a drop of 0.15 in the ankle–brachial index (ABI) of systolic pressure indicates a significant change in blood flow in the lower extremities and should be evaluated to determine its cause. The advantages of Doppler-derived pressure measurements and waveforms include the fact that they are easily obtainable and are relatively inexpensive. In some instances there is a lack of specificity; however, this may be offset by the ease of performing the test and the lack of expense.

Measurement of Blood Flow Velocity Both continuous wave and pulsed Doppler ultrasound flow detectors are used to measure blood flow velocity. After surgery a 5-MHz hand-held Doppler probe or a 5- to 10-MHz pulsed Doppler flow detector of a duplex scanner has been used to measure graft blood flow velocity (4,5). Use of the duplex scanner permits graft imaging and precise placement of the sample volume and accurate alignment of the Doppler beam angle. The sample volume of the pulsed Doppler flow detector is placed in the center stream of the lumen, and the Doppler angle is calculated by positioning a cursor parallel to the flow axis. Flow velocity measurements are made at a Doppler beam angle of approximately 60°. The Doppler direction-sensitive (quadrature) signals are processed by a real-time fast Fourier transform spectral analyzer with a frequency waveform displayed on a video monitor (5). Peak systolic and end-diastolic frequency are measured by an operator-controlled cursor. Blood flow velocity is calculated from the frequency spectral waveform measurements by means of the following Doppler equation (6): Flow velocity = C Fs/2Fo cos q (cm/s)

where C is the average speed of sound in tissue (1.54 ¥ 104 cm/s), Fs is the measured frequency of the Doppler shifted signal, Fo is the frequency of the incident Doppler beam (5 or 20 ¥ 106 Hz), and q is the angle between the incident Doppler beam and the blood velocity

vector (cos 60° = 0.5, cos 45° = 0.707). Velocity waveform parameters are measured in the distal segment of the in situ saphenous vein graft. A normal laminar arterial flow pattern without turbulence is uniformly found in this graft segment, the Doppler angle can be accurately measured, and the diameter does not usually vary over short distances. Postoperative measurements are made in the same graft segment with the recording site being a measured distance from the patella. Quantitative velocity waveform analyses are performed at the time of operation, the perioperative period, and then serially at 3-month intervals for the first 2 years and every 6 months thereafter.

Duplex Scanning A variety of instruments provide simultaneous color coding of Doppler flow information based on direction and velocity within a real-time B-mode image (7). The principal component of these instruments is the ability to assess tissue anatomy and blood flow physiology in a simultaneous or sequential manner, so that the location and extent of disease can be accurately evaluated. Most studies are performed with a 10-MHz linear array transducer, which permits visualization of superficially placed grafts such as in situ saphenous vein grafts. Graft assessment begins with the imaging system set for evaluation of a normal graft, and adjustments are made as necessary for imaging and Doppler assessment of stenotic lesions. The velocity range and pulse repetition frequency can be increased to prevent aliasing when a stenotic graft segment is found. A 3-MHz linear array transducer is the scan head of choice when evaluating a deeply placed graft or when visualizing the distal anastomosis. Time gain compensation controls are preset in the scanner used for our graft studies but are often adjusted to compensate for attenuation of the ultrasound as it passes through soft tissue. The duplex examination of the infrainguinal bypass graft is performed with the patient in a supine position. The limb to be examined is externally rotated and slightly bent with the knee resting on a small pillow. A tape measure is positioned along the limb and held in place with tape to facilitate documentation of recording sites. It is important to have the operative report and details of any previous studies available for comparison. Duplex mapping of the graft begins by visualizing the graft in the upper thigh, where it is easily imaged. The transducer is advanced cephalad to the proximal anastomosis. The graft is first imaged and assessed with the transducer in the longitudinal orientation. This orientation produces an image of a long segment of the graft for observation and for obtaining velocity spectral waveforms. Doppler spectral analysis is performed with the Doppler beam angle aligned to the long axis of the vessel, and the angle is maintained at less than 65° in order to obtain accurate velocity data. The transducer is then rotated so that graft diameter measurements may be obtained. The graft conduit is mapped for structural abnormalities,

Chapter 50 Postoperative Surveillance

stenosis, aneurysmal dilation, intraluminal defects, and sites of flow disturbance. Graft anastomoses to the belowknee popliteal artery are best imaged using a posterior approach with the patient in a prone position. The hemodynamics of graft blood flow and limb arterial circulation are characterized with Doppler-derived blood flow velocity analysis and limb blood pressure measurements. The blood flow velocity of peak systole and end-diastole is calculated from operator-controlled cursor measurements. Indications for angiography include low graft flow velocity (<45 cm/s) in the smallest-diameter segment, a decrease in graft velocity of 30 cm/s or greater, or a decrease of ABI of 0.15. It is also useful to perform a velocity ratio, defined as the velocity at the area of the stenosis divided by the velocity in the normal graft away from the stenosis. A ratio showing greater than 3.5 indicates a significant stenosis (8).

Rationale for Surveillance Surveillance is particularly pertinent when dealing with autogenous vein bypass grafts. The aspect of autogenous veins that makes them valuable as a conduit is that they are a living tissue. If thrombus is allowed to sit for a prolonged period in the vein, the vein will undergo either intimal or, on occasion, transmural necrosis. This changes a vein from a conduit that is able to keep blood liquid as it flows over a surface to a highly thrombogenic structure. There are many examples in the literature in which drastic differences in patency can be demonstrated between revisions done on patent grafts and those done on thrombosed grafts (1–3). In a prospective surveillance protocol, we noted a 93% 36-month patency on grafts that were revised before thrombosis, compared with 47% for those done on thrombosed grafts (3). Other investigators report even more dismal results for repair of thrombosed grafts (1, 2). In addition to the effects on the conduit, thrombosis of a bypass graft, when it occurs, can propagate distally and can occasionally go into the side branch vessels of the distal vascular tree. Even though the conduit and the main runoff vessels (e.g., tibial vessels) can be cleared with Fogarty catheters, clearing the side branches surgically is not as effective. Thrombolytic therapy has been proposed in such instances, but this requires time. The period of 18 to 24 hours that is often needed to clear the distal circulation with thrombolytic therapy is not available in patients with severe limb-threatening ischemia. Routine hemodynamic surveillance of in situ bypasses confirms that the most common mechanism of graft failure is the development of a low-flow state (low blood flow velocity), which increases the likelihood of unexpected graft thrombosis. Even though occlusive lesions in the vein conduit, anastomotic sites, and inflow or outflow vessels tend to develop without symptoms, bypass graft hemodynamics can be altered sufficiently that detection before graft thrombosis is possible. Further importance of

619

a routine surveillance follow-up is that less than onefourth of patients will have unequivocal evidence of graft stenosis based on decreased pedal graft pressure wave or recurrence of limb ischemia (9–11). The absence of symptoms in patients with graft stenosis was not surprising because lesions can be identified early. We have noted that pressure measurements were not good at identifying grafts that are prone to occlude. In a surveillance protocol using both duplex scanning and Doppler-derived pressure measurements to assess in situ vein bypasses, 8 (27%) of 30 graft stenoses were not apparent from serial measurements of resting ankle pressures, because the tibial arteries were incompressible, rendering pressure measurements unreliable (12). Justification for graft surveillance is based on the observed 20% to 30% incidence of lesions identified by surveillance protocols by use of either arteriography or noninvasive hemodynamic testing, and the superior graft patency when lesions that threaten patency are repaired before graft thrombosis. Moody et al. demonstrated, by means of intravenous digital subtraction angiography, a 27.5% stricture rate in asymptomatic patients after in situ and reverse saphenous vein infrainguinal bypass grafting (13). Although two-thirds of the strictures remained stable, a threefold risk of occlusion was documented when compared with normal grafts. In a similar study, Whittemore et al. reported 5-year patency rates in excess of 80% when lesions were prophylacticly corrected, but less than 40% when stenosis was repaired in conjunction with graft thrombectomy (14). Green et al. have presented convincing data in support of the concept of graft surveillance based on retrospective comparison techniques (15). These authors found that grafts harboring lesions that decreased the ABI by 10% or more and were associated with an abnormal duplex scan had a 66% incidence of thrombosis within 3 months, compared with a 14% risk of failure if the ABI was decreased but the duplex was normal, and 4% risk of failure if only the duplex scan was abnormal. Common to all reports dealing with management of postimplantation occlusive lesions was a caveat that the presence of symptomatic limb ischemia should not be the only requisite for graft revision. We have used noninvasive hemodynamic testing methods, not only to assess vein bypass for technical adequacy and identify acquired graft stenosis, but also as a basis for timing of the secondary procedure. After operation, duplex scanning will detect a variety of occlusive lesions ranging from the minor flow disturbance created by a venous valve or anastomotic site to severe flow and pressure-reducing stenosis. These latter lesions warrant correction, particularly when associated with a low-flow state in the graft. A moderate stenosis (<50% diameter reduction) can be safely followed for progression to stenosis of more than 50% diameter reduction by serial (3-month) examinations. The decision to revise a patent graft or bypass is straightforward when patients have recurrent symptoms of claudication, or ischemic lesions on the leg or foot de-

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Part VI Chronic Arterial Occlusions of the Lower Extremities

velop. Unfortunately, this scenario was present in only one-third of our patients despite conclusive vascular laboratory data indicating that the bypass graft had developed hemodynamic failure (16). Deterioration in graft or limb hemodynamics was typically detected through scheduled perioperative and outpatient evaluations, and although patients were carefully queried regarding limb symptomatology, no complaints of ischemia were listed for most patients. We feel that asymptomatic graft stenosis may occur more frequently in patients who undergo lower limb revascularization to correct critical limb ischemia than in patients in whom indication for revascularization is claudication or popliteal aneurysm. Whether patients admit to symptoms of claudication depends on their lifestyle, presence of concomitant medical problems, and the severity of atherosclerosis in the contralateral limb. When a correctable graft stenosis is detected in asymptomatic patients, revision is recommended if flow velocity in the distal graft has decreased to less than 45 cm/s, or if there has been a decrease in any graft segment of more than 30 cm/s combined with a decrease in ABI of more than 0.15 when compared with prior measurements. Severe stenosis identified by duplex scanning with velocity spectrum indicating more than 75% diameter reduction should always be repaired. These lesions reduce pressure and flow, and the time interval of progression to graft occlusion is unpredictable, particularly in the early postoperative period (within 6 months).

Postoperative Surveillance Protocol Vein bypass hemodynamics were evaluated by a combination of the following noninvasive vascular testing methods: 1.

2.

3.

measurement of resting limb arterial pressure (ABI) by the transcutaneous Doppler ultrasonographic flow detection technique; transcutaneous, continuous wave Doppler spectral analysis (5-MHz probe frequency, 45° Doppler angle to the skin, subcutaneous grafts only) of graft blood flow pattern with calculation of peak systolic blood flow velocity (Vp) in the mid and distal graft segments; and duplex ultrasonography or color Doppler flow imaging. Since 1987, duplex scanning has been used to map the entire bypass graft for flow abnormality before discharge of the patient from the hospital.

After discharge from the hospital, graft surveillance was performed at intervals of 3 to 6 months according to our previously described protocol. A decrease in ABI greater than 0.15 or Vp greater than 30 cm/s on serial examinations prompted diagnostic studies to locate a cor-

rectable occlusive lesion. This workup included duplex scanning of the entire bypass, including inflow and outflow arteries. If the duplex examination was normal, angiography was performed to assess the graft runoff for progression of atherosclerotic disease. Recommendation for graft revision was based on the following: 1.

2.

presence of symptomatic limb ischemia despite a patent bypass graft; hemodynamic deterioration in graft blood flow velocity (Vp) and ABI; or identification of a low flow state (Vp <45 cm/s) in the distal segment of the venous conduit, and documentation of a correctable occlusive lesion by either duplex scanning or arteriography.

After graft revision, ABI and Vp were measured on the first postoperative day and repeated within 1 week. Graft revision sites were serially assessed by duplex scanning to identify recurrent stenosis or occlusion of a sequentialjump graft.

Types of Graft-threatening Lesions In an attempt to evaluate the effectiveness of a graft surveillance program and determine the type of lesion that caused graft-threatening stenosis, we reviewed 370 patients with a total of 396 infrainguinal bypass grafts (in situ, 372; reversed saphenous vein, 24) and detected 83 lesions at a mean time interval of 11.5 ± 14 months with a range of 1 week to 65 months (16). Most recurrent graft stenoses corrected in this series were myointimal in nature and were located at either venous valve or anastomotic sites. Of note, only three of the 83 revised infrainguinal vein bypasses developed stenotic lesions at multiple sites. Most grafts developed only one stenosis, and if restenosis or occlusion developed, it involved the graft revision site. The variety and number of secondary procedures performed in this series permitted a relevant assessment of the outcome including incidence of restenosis and late graft failure. Bypass of both myointimal and atherosclerotic lesions located in graft runoff arteries was the least durable procedure. Graft extensions constructed of cephalic vein or saphenous vein remnants reliably restored hemodynamics in the limbs to normal and relieved ischemic symptoms, and blood flow velocity in the vein graft returned to levels measured following the primary operation. The ultimate failure of infrainguinal bypass grafts depends in part on the philosophy and aggressiveness of the vascular surgeon. We have found a combination of duplex scanning and ABI provides an accurate method of detecting occlusive lesions after implantation and aids in timing graft revisions. When a high-grade (>75%) diameter-reducing stenosis was identified, graft blood flow was found to be severely compromised (Vp < 40–45 cm/s). This study documents that the secondary procedure is safe, effective,

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Incidence of Postoperative Revisions During postoperative surveillance, 26% of the grafts subsequently required revision to maintain patency. Of the revisions, 14% were to ligate bypass fistulas, and 6% to lyse residual valves recognized within 30 days of operation

500 450 400 350 300 250 200 150 100 50 0

462

236

Abnormality free grafts at the beginning of each year of follow-up Grafts developing at least one abnormality at sometime during the remaining life of the graft

222

169 120 86

73

(51%) 0

(33%) 12

50 (30%) 24

60

29

22

14

(24%)

(26%) 48

(23%) 60

36 Months

36

7

(19%) 72

FIGURE 50.1 Percentage of saphenous vein in situ bypass grafts free of abnormality at the beginning of each year of follow-up that subsequently develop at least one significant abnormality during postoperative surveillance at sometime during remaining life of graft. (Reprinted with permission from Curtis A, Erickson CA, Towne JB, et al. Ongoing vascular laboratory surveillance is essential to maximize long-term in situ saphenous vein bypass patency. J Vasc Surg 1996; 23: 18–27.) 600

556

Primary patent grafts at the beginning of each year of follow-up Grafts excluded from primary patency at sometime during the remaining life of the graft

500 Number of grafts

and associated with excellent late graft patency (85% after 5 years of revision). More recently, studies have been conducted to determine if ongoing surveillance needs to be done for the life of the conduit. In long-term evaluation of 462 saphenous vein in situ bypass performed over a 13-year period, 30% of the grafts required at least one revision (18). Even grafts that have exhibited good hemodynamics for up to 24 months are at risk for developing abnormalities that could lead to graft failure. Of the initial graft revisions in this study, 18% occurred after 24 months. Because of the increasing incidence of atherosclerosis in the inflow and outflow vessels with long-term follow-up, a greater percentage of revisions involve inflow and outflow vessels as opposed to the conduit itself. Of the revisions performed after 24 months, 68% were to the conduit, compared with 85% in the earlier time period. As the follow-up becomes longer, degenerative changes can develop in the conduit itself. Previous work from our institution demonstrated that more than 50% of vein bypass conduits followed for at least 5 years demonstrated evidence of atherosclerotic degeneration (17). Often these changes represent areas of intimal thickening, but in a significant portion the disease has progressed to form focal point stenosis caused by atherosclerosis. The likelihood of developing graft-threatening lesions is even greater in conduits that have been previously revised or have hemodynamic abnormalities, but some conduits that have been free of abnormalities for the first 2 years will go on to require revision. Recognizing that conduits that have previously required revision are more prone to develop secondary degenerative processes allows surveillance of these conduits to be more focused. Other authors have suggested that if the conduit has normal hemodynamics in the early perioperative period the chance for problems are such that further surveillance may not be warranted (19). Our study reveals that of the 67 graft revisions performed after 24 months, 37 were to previously revised conduits, but 30 were to vein grafts that had required no previous revision (Figs. 50.1 and 50.2). Conduits that are hemodynamically normal beyond 2 years evolve lesions at a significant rate to warrant ongoing surveillance. The average incidence of primary graft failure was 10% of the number of grafts remaining patent at each yearly time interval beyond 24 months. If vascular surgeons want to optimize long-term graft patency, surveillance must be done for the life of the conduit. Other authors whose series consist of primarily reverse vein bypasses have reached similar conclusions (20).

Number of grafts

Chapter 50 Postoperative Surveillance

400 287

300

162 107

100 0

213

174

200

44

79

48

23

15

11

10

(10%)

(13%)

(10%)

60

72

(31%)

(15%)

(11%)

(9%)

0

12

24

36 Months

48

5

FIGURE 50.2 Percentage of primary patent saphenous vein in situ bypass grafts at beginning of each year of follow-up that subsequently fail at some time during the remaining life of the graft. (Reprinted with permission from Curtis A, Erickson CA, Towne JB, et al. Ongoing vascular laboratory surveillance is essential to maximize long-term in situ saphenous vein bypass patency. J Vasc Surg 1996; 23: 18–27.)

(3). A diseased inflow or outflow artery required correction in 15%, and anastomotic stenosis correction was required in 21%. The secondary patency at 4 years was significantly lower for bypasses undergoing revision (68%) than for nonrevised bypasses (88%). The decline in secondary patency for the revised bypasses was due primarily to poor patency of bypasses that were thrombosed at the time of revision (47%) compared with the patency of the bypasses patent at the time of revision (93%). The secondary patency for revision of the patent bypass was equivalent to the secondary patency for bypasses that never underwent revision. The two main disease processes that resulted in hemodynamically failing bypasses were progression of atherosclerotic disease of the inflow and outflow arteries and fibrointimal hyperplasia of the bypass conduit or anastomotic site. The long-term success of infrainguinal arterial

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Part VI Chronic Arterial Occlusions of the Lower Extremities

bypass was dependent on the recognition and correction of anatomic and hemodynamic abnormalities of anastomotic sites, the bypass conduit, and the inflow and outflow arteries before thrombosis. The second half of our series has shown a decreasing number of bypasses that thrombosed before revision due to a compulsive graft surveillance program (3). The unsurpassed 3-year patency of 142 bypasses never undergoing revision (97%) in the second half of our series is testimony to the efficacy of postoperative surveillance in the durability of the hemodynamically normal in situ bypass.

Effect of lntraoperative Modification on Long-term Results Modification of the in situ saphenous vein was performed because of a residual competent valve requiring venotomy for lysis, valvulotome injury, torsion of the bypass conduit, anastomotic stricture, the formation of platelet aggregates along the endothelial flow surface detected on completion angiography or intraoperative flow analysis that required venotomy for removal, a sclerotic vein segment requiring resection, insertion of venous interposition conduit, varicosity, and a vein segment previously removed (3). The intraoperative modification of the vein conduit was associated with a significant increase in the incidence of late-appearing bypass stenosis and revision and a significant decrease in primary and secondary patency. The occurrence and progression of fibrointimal hyperplasia was associated with the injurious effect of bypass modification to correct a poor-quality vein or technical error. As the number of technical errors decrease with increasing surgical experience, the quality of the vein has become the most important factor to determine the need for modification of the bypass conduit. We define a good-quality vein as a thin-walled vein, more than 2 mm in diameter, with or without a bifurcated segment, that has a glistening endothelial flow surface. When a technical error occurs, or if a poor-quality vein segment is identified, the short segment of normal vein can be modified with the maintenance of the in situ technique. The intraoperative modification of the in situ conduit can restore normal hemodynamics and result in early bypass patency. Long-term patency is dependent on careful postoperative hemodynamic surveillance to identify and correct a bypass-threatening stenosis before thrombosis.

Long-term Changes in Autogenous Grafts Autogenous grafts that are in place for a long time are vulnerable to the same atherosclerotic changes as the native

arteries, although in overall timing they take less time to develop. In a study of 72 lower extremity vein grafts that functioned and were patent from 4.6 to 21.6 years, the median being 6.6 years, we found that only 43% were normal (17). In addition, nearly one in five grafts harbored a lesion that was felt to pose a threat to continued graft patency. Atherosclerotic degeneration of saphenous vein grafts was first described in 1947 when a femoral interposition graft that had been in place for 22 years was removed and found to contain atheromatous plaques. In 1973 Szilagyi et al. reported their experience with a lower extremity saphenous vein graft that had been monitored with arteriography (21). They described eight different morphologic findings in grafts of varying ages. Several of these were related to surgical technique, including suture stenosis caused by tying side branches too closely, long venous side branch stumps, and traumatic stenosis caused by clamps. They also described the changes that occur including intimal thickening, myointimal hyperplasia at valve sites, atherosclerotic irregularity, and aneurysmal dilation. In our study, autogenous grafts were examined at least 4.6 years after construction. The early postoperative changes that Szilagyi et al. described were not detectable. However, we did find three distinct atherosclerotic abnormalities: wall plaque, aneurysmal dilation, and discrete stenosis. The most prevalent finding was wall plaque, which was present in all of the abnormal grafts, although this was frequently overshadowed with more impressive stenosis or aneurysms. Typically, plaques were several centimeters long, multicentric, echogenic, and slightly raised from the normal wall. These are mild forms of atherosclerotic degeneration. In the series of Szilagyi et al., atherosclerotic changes developed at approximately 45 months. Atkinson et al. looked at coronary artery saphenous vein grafts during autopsy and found atherosclerotic changes in 21% of the grafts that had been in place an average of 62 months (22). However, when DeWeese and Robb monitored long-term grafts with the use of arteriography, they noted atherosclerotic changes in only 3 of 18 patients studied after 5 years, and two grafts did not develop changes until after 10 years (23). We use color duplex ultrasonography to study the grafts and have been able to visualize changes in the arterial wall such as thickening and wall plaque that are not necessarily seen on contrast arteriography, which defines only the column of flowing blood. Aneurysmal degeneration in saphenous vein grafts is a more extreme late finding, although it is infrequent, with only 29 cases described in the literature. We found eight grafts that harbored 16 segments with aneurysmal change. Five (63%) of these grafts had occluded and had undergone either a thrombectomy or thrombolysis many months before diagnosis of the vein graft aneurysm (Fig. 50.3). Three grafts with aneurysms had no history of occlusion, and two of these were reverse saphenous vein grafts. We postulate that transmural ischemic injury oc-

Chapter 50 Postoperative Surveillance

FIGURE 50.3 Angiogram of distal graft aneurysm.

curs at the time of graft thrombosis or vein retrieval. This alters the integrity of the vein graft wall, which allows subsequent aneurysm formation. Vein graft aneurysms have been described as atherosclerotic in nature, but this may be the result of the ongoing reparative changes rather than the cause of the aneurysm. Another severe presentation of atherosclerosis in these grafts was graft-threatening stenoses. They were always very discrete, short lesions with what was apparently normal graft proximally and distally. Half of these stenoses were at the site of a previous defect, and other stenoses developed in the undisturbed segment de novo. The fact that some grafts developed stenosis can be attributed to hyperplastic reparative changes, but the cause of all of this is elusive. One of our patients has undergone nine different procedures in an attempt to correct the stenosis in the distal third of a femoral anterior tibial graft. Even when the stenosis plus 10 cm of normal graft on either side was replaced, a new stenosis developed in the mid-portion of the replacement graft within a few months. Why some grafts developed stenosis whereas others developed only wall plaque is unknown and cannot be determined from our study.

References 1. Wittemore AD, Clowes AW, et al. Secondary femoropopliteal reconstruction. Ann Surg 1981: 193: 35–42.

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2. Belkin M, Donaldson MC, et al. Observations on the use of thrombolytic agents for thrombotic occlusion of infrainguina] vein grafts. J Vasc Surg 1990: 11: 289–296. 3. Bergamini TM, Towne JB, et al. Experience with in situ saphenous vein bypasses during 1981 to 1989: determinant factors of long-term patency. J Vasc Surg 1991; 13: 137–147. 4. Bandyk DF, Zierler ER, Thiele BL. Detection of technical error during arterial surgery by pulsed Doppler spectral analysis. Arch Surg 1984; 119: 421–428. 5. Bandyk DF, Kaebnick HW, et al. Durability of the in situ saphenous vein arterial bypass: a comparison of primary and secondary patency. J Vasc Surg 1987: 5: 256–268. 6. Bandyk DF, Kaebnick HW, et al. Hemodynamics of in situ saphenous vein arterial bypass. Arch Surg 1988; 123: 477–482. 7. Bandyk DF. Monitoring functional patency of vascular grafts. Semin Vasc Surg 1988; 1: 40–50. 8. Grigg MJ, Nicolaides AN, Wolfe JHN. Detection and grading of femorodistal vein stenoses: duplex velocity measurements compared with angiography. J Vasc Surg 1988; 8: 661–666. 9. Berkowitz HD. Postoperative screening in peripheral vascular disease. In: Bernstein EF, ed. Noninvasive diagnostic techniques in vascular disease. St Louis: CV Mosby, 1985: 632–638. 10. Turnipseed WD, Acher CW. Postoperative surveillance: an effective means of detecting correctable lesions that threaten graft patency. Arch Surg 1985; 120: 324–328. 11. Bandyk DF, Seabrook GR, et al. Hemodynamics of vein graft stenosis. J Vasc Surg 1988; 8: 688–695. 12. Bandyk DF, Schmitt DD, et al. Monitoring functional patency of in situ saphenous vein bypasses: the impact of a surveillance protocol and elective revision. J Vasc Surg 1989; 9: 286–296. 13. Moody P, de Cossart LM, et al. Asymptomatic strictures in femoropopliteal vein grafts. Eur J Vasc Surg 1989; 3: 389–392. 14. Whittemore AD, Clowes AW, et al. Secondary femoropopliteal reconstruction. Ann Surg 1981; 193: 35–42. 15. Green RM, McNamara J, et al. Comparison of infrainguinal graft surveillance techniques. J Vasc Surg 1990; 11: 207–215. 16. Bandyk DF, Bergamini TM, et al. Durability of vein graft revision: the outcome of secondary procedures. J Vasc Surg 1991: 13: 200–210. 17. Reifsnyder T, Towne JB, et al. Biologic characteristics of long-term autogenous vein grafts: a dynamic evolution. J Vasc Surg 1993; 17: 207–217. 18. Erickson CA, Towne JB, et al. Ongoing vascular laboratory surveillance is essential to maximize long-term in situ saphenous vein bypass patency. J Vasc Surg 1996; 23: 18–27. 19. Mills JL, Bandyk DF, et al. The origin of infrainguinal vein graft stenosis: a prospective study based on duplex surveillance. J Vasc Surg 1995; 21: 16–25. 20. Passman MA, Manetta GL, et al. Do normal early colorflow duplex surveillance examination results of infrain-

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guinal vein grafts preclude the need for life graft revision? J Vasc Surg 1995; 22: 476–484. 21. Szilagyi DE, Elliott JP, et al. Biologic fate of autogenous vein implants as arterial substitutes. Ann Surg 1973; 178: 775–784.

22. Atkinson JB, Forman MB, et al. Morphologic changes in long-term saphenous vein bypass grafts. Chest 1985; 88: 341–348. 23. DeWeese JA, Robb CG. Autogenous venous grafts ten years later. Surgery 1977; 82: 775–784.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 51 Extra-anatomic Bypasses Enrico Ascher and Frank J. Veith

Extra-anatomic arterial reconstructions were devised to circumvent complex vascular problems when conventional anatomic procedures necessary for the relief of severe ischemia were deemed impossible or too hazardous to perform. Freeman and Leeds first applied this concept in 1949, just three years after Kunlin described the first anatomic femoropopliteal bypass. They used the superficial femoral artery as a donor to transport blood to the contralateral femoral artery through a subcutaneous, transabdominal pathway (1). A multitude of ingenious extra-anatomic procedures have been described since then and widely used with varying degrees of success, to restore an adequate blood supply to both the upper and lower extremities, the brain, and more recently the kidneys. These procedures have been predominately primary or secondary operations in patients considered at high risk for an abdominal or thoracic operation or in the management of anatomically placed infected grafts. Extra-anatomic bypasses such as carotid–subclavian, carotid–carotid, carotid–vertebral, and axilloaxillary have been successfully used for the treatment of brachiocephalic occlusive disease and are described in other chapters. Interest in anticoagulant therapies utilized in conjunction with extra-anatomic bypasses has resulted in several recent studies in which such a regimen may favorably affect the outcome of axillofemoral bypasses has been postulated. One of the earliest studies in which anticoagulation therapy (aspirin or warfarin) was evaluated in extra-anatomic bypasses reported primary and secondary patencies of 80% and 89% at 3 years, respectively (2). Although perioperative anticoagulation with

heparin increases the rate of wound hematomas, therapy with warfarin improves the patency and limb salvage rates for patients with autogenous vein bypass grafts who are at high risk for graft failure (3). Substantially improved results have also been reported for bypass grafts for limb salvage with cryopreserved saphenous vein allograft in the absence of autogenous vein. A treatment protocol substantially improved allograft patency and limb salvage, when compared with currently published data (4). In one of the earliest important ppers to specifically compare the outcome of axillofemoral versus aortofemoral bypasses, Porter’s group concluded that the patency and limb salvage results, for patients with limited life expectancy, of axillofemoral bypasses were equivalent to those of aortofemoral bypasses (5). Long-term patency rates of axillofemoral grafts approach those of aortofemoral bypass and offer a viable option for patients at prohibitive risk for direct aortic reconstruction (6). It has been further suggested that axillofemoral bypasses equal, or exceed, those results reported with alternative operations, including femoral vein grafts or aortic allografts (7) with primary patency rates of 86%, 72%, and 63% at 1, 3, and 5 years. Primary and secondary patencies at 75% and 100% for 41-month duration have also been reported (8). In this chapter, we focus on conventional extra-anatomic reconstructions designed to improve lower-limb ischemia, including axillofemoral and femorofemoral bypasses as well as extended extraanatomic bypasses, such as axillopopliteal and crossover femoropopliteal.

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Conventional Extra-anatomic Bypasses Axillofemoral Bypasses Lewis made an important contribution to vascular surgery in 1959 by demonstrating that the subclavian artery could adapt itself to deliver an adequate blood supply to the lower half of the body without shunting blood away from the ipsilateral arm or cerebral circulation (9). Blaisdell and Hall in the United States (10) and Louw in South Africa (11) combined this principle with the idea of performing a simpler, quicker, and less risky operation to save ischemic lower limbs in patients too sick to undergo standard aortofemoral procedures. Almost simultaneously, they performed extra-cavitary bypasses from the axillary artery to the common femoral artery using synthetic graft material. In 1966, Sauvage and Wood modified this procedure by adding a crossover femoral limb to the axillofemoral graft for the treatment of bilateral lower-limb ischemia, thereby sparing the contralateral axillary artery (12). One other potential benefit of this crossover graft is that the flow through the long, vertical portion of the bypass is increased. Whether this configuration minimizes graft thrombosis by the augmentation of blood flow rates remains controversial. Indications Axillofemoral bypasses rapidly became an integral part of the overall approach to the management of infected aortic grafts and aortoduodenal fistula complicated by in situ infection. Other local factors known to discourage the use of the aorta as an inflow source in favor of the axillary artery include multiple previous abdominal operations, colostomies and ileostomies, inoperable intra-abdominal malignancies, abdominal or pelvic irradiation, and morbid obesity. Systemic factors, as well, play an important role in the decision to preferentially perform an extra-anatomic reconstruction. There is little doubt that a history of recent myocardial infarction, congestive heart failure, inoperable unstable coronary angina, chronic renal failure, advanced malignancy, advanced chronic obstructive pulmonary disease, or any other severely debilitating illnesses in patients with threatened, ischemic lower limbs also calls for less invasive procedures. Acute aortic occlusion in high-risk patients is one other common indication for axillofemoral bypasses. Less commonly, axillofemoral bypasses have been used as adjunctive procedures in the nonresective treatment of abdominal aortic aneurysms and in symptomatic iliofemoral occlusion caused by acute aortic dissections. The safety and ease with which these extra-anatomic operations are performed, coupled with earlier optimistic reports regarding their long-term graft-patency results, encouraged a more lenient attitude toward performing these procedures that included performing them on lowerrisk patients and individuals with claudication. However,

the original reports did not differentiate the results obtained with a single operation (primary patency) from those obtained when one or more repeat operations were necessary for continued graft patency (secondary patency) (13,14). They also did not emphasize the frequency, complexity, and number of complications associated with secondary procedures. A review of our own experience revealed that the cumulative primary patency rate for axillofemoral bypasses was only 47% at 5 years with more than one-third of them requiring one or more repeat operations to achieve continued limb salvage (15). These findings are clearly worse than the ones reported for aortofemoral procedures. Considering that many patients who carry a prohibitive surgical risk for an abdominal procedure may already have limited ambulation resulting from restricted cardiac or pulmonary capacity, improving their circulation for increasing their walking distance would be futile. Therefore, we believe that axillofemoral bypasses should be reserved for high-risk patients with severe lower-limb ischemia. Preoperative Evaluation Clinical examination of the lower extremities, by noninvasive evaluation of the degree of distal ischemia, and angiographic visualization of the outflow tract are no longer sufficient diagnostic measures to ensure completeness of the preoperative workup. The inflow tract may harbor hemodynamically significant lesions that escape detection even by a skilled examiner when listening for a supraclavicular bruit or when measuring and comparing upper-extremity blood pressures, and occlusive disease of the subclavian or axillary artery can be a cause of axillofemoral bypass failure (9). We prospectively evaluated the incidence of unsuspected inflow disease in candidates for axillofemoral operations. Forty patients underwent angiographic studies of the aortic arch and its branches before axillofemoral bypasses. This study revealed that the incidence of significant inflow disease (more than 50% stenosis) was 25%. The consensus that these lesions are more often located on the left side was confirmed, but a significant number were detected on the right (42% of all lesions). As a result, angiographic assessment of the inflow and outflow tracts should be included as an important component of the preoperative workup (16). A Swan-Ganz balloon-tipped catheter inserted to monitor left ventricular function has been helpful in the perioperative management of these patients. Technique Although the basic technical principles involved in the construction of an axillofemoral bypass have remained unchanged since the original report by Blaisdell and Hall (4), we have added some modifications that we believe are worth describing. This procedure can be entirely performed with the patient under local anesthesia; however, most high-risk patients will tolerate light general endotracheal anesthesia without untoward effects. We prefer the

Chapter 51 Extra-anatomic Bypasses

latter method of anesthesia because it provides a comfortable environment in which the surgeon can perform careful dissections, tunnelings, and meticulous anastomoses, and it gives the anesthesiologist optimal control for monitoring the patient’s blood pressure and respiratory function. Axillounifemoral Bypass With the patient in the supine position, the donor upper extremity is abducted to 90°, and a cannula is routinely inserted in the contralateral radial artery for continuous blood pressure monitoring. The infraclavicular incision starts approximately 2 cm lateral to the costoclavicular joint and is extended toward the deltopectoral groove for approximately 5 to 6 cm, forming a 35° angle with the clavicle (Fig. 51.1). The incision is then deepened through the pectoral fascia, displaying the pectoralis major muscle fibers, which are split horizontally along the entire length of the incision. At this point, placing a self-retaining retractor gives adequate exposure for incising the clavipectoral fascia. After this procedure is accomplished, the pectoralis minor muscle can be readily identified, and then isolated by blunt dissection. Although the operation may proceed by laterally retracting this muscle, exposure of the second portion of the axillary artery is facilitated by division of the pectoralis minor muscle at the coracoid process. The axillary artery is best localized by palpation of a strong pulse underneath the deep clavipectoral fascia. Awareness of the surrounding structures in this anatomic plane is of the utmost importance to prevent potentially disastrous complications. At this level, the axillary artery is guarded superiorly by the brachial plexus and inferiorly and slight-

FIGURE 51.1 Inset illustrates position of the shoulder and the line of incision for exposure of the axillary artery. Note the angle formed by the incision and the lower border of the clavicle. Larger diagram shows the topographic anatomy of the axillary artery and surrounding structures after transection of pectoralis minor muscle.

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ly anteriorly by the axillary vein (see Fig. 51.1). Mobilization of the artery from the loose periadventitial attachments is initiated at the junction of its first and second portions at the medial border of the pectoralis minor muscle. The axillary artery is encircled with a Silastic sling and gently lifted from its bed to facilitate its circumferential dissection and to isolate its branches. Proximally, the axillary dissection is carried 1 to 2 cm past the origin of the thoracoacromial trunk, and distally dissected to the point where the crossing neural branches form the median nerve. After completion of the axillary dissection, attention is now focused on the outflow tract. Selection of the anastomotic outflow site is primarily based on preoperative angiograms. When the runoff from the common femoral artery is unimpeded, this vessel is approached using the standard vertical groin incision, with care taken to leave the deep femoral artery undisturbed for possible future use. However, if the origin of the deep femoral artery is stenosed, the dissection is extended to include its proximal portion. Here, it is necessary to ligate and transect a crossing tributary of the deep femoral vein, thus allowing the placement of the distal anastomosis across the stenotic segment of the deep femoral artery. Whenever possible, rather than performing a local endarterectomy, we prefer to fashion the distal end of the graft into a patch to widen the narrowed segment. This technique avoids the problem of dealing with the distal end of an endarterectomized segment, which can be a factor leading to turbulence and graft thrombosis, particularly when the occlusive process is extensive. Troublesome areas, such as groin infection, multiple previous groin dissections, or significant disease of the proximal arteries may be avoided by selecting a direct approach to the distal two-thirds of the deep femoral artery through an incision in the mid-thigh along the medial border of the sartorius muscle. After both arterial dissections are completed, the connecting tunnel is initiated at each end by finger dissection. The upper end of the tunnel is paved under the pectoralis major muscle and between the transected portions of the pectoralis minor muscle and then subcutaneously toward the posterior axillary line. The lower end of the tunnel begins subcutaneously at the superior edge of the incision and moves upward and lateral in the direction of the posterior axillary line, staying medial to the anterosuperior iliac spine. A slightly curved, hollow tunneler is passed from the lower to the upper incision to bridge the remaining distance and is kept in place to transport the graft after the proximal anastomosis is completed. Efforts should be made to avoid making counterincisions when constructing the tunnel because they have been identified as possible culprits for graft infection. Because the axillary anastomosis and the positioning of the proximal portion of the graft are usually more demanding than the distal anastomosis, we elect to perform this part first to have the freedom to maneuver the graft. Systemic heparinization is accomplished before crossclamping. Proximal and distal control of the axillary

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A'

A

B

artery flow is obtained through the use of atraumatic vascular clamps rather than by pulling on double-looped Silastic slings. Undue tension on the donor artery, which can cause severe spasm with diminished flow to the upper extremity, is thereby minimized. A longitudinal incision, 1.8 to 2 cm long, is performed in the anteroinferior border of the second portion of the axillary artery. We select 6-mm polytetrafluoroethylene (PTFE) grafts for most bypasses. The proximal end of the graft is cut sharply with scissors and is measured to fit the arteriotomy exactly. A running, four-quadrant suture technique, beginning at the toe of the end-to-side anastomosis, is then performed using monofilament No. 6-0 sutures. To avoid mechanical obstruction of the artery due to shoulder motion (Fig. 51.2A and A¢), this long, oblique anastomosis allows for an intentional slight redundancy of the axillofemoral graft (Fig. 51.2B and B¢). After this procedure, the graft is filled with a crystalloid solution to test the integrity of the proximal anastomosis and to assist in passing it through the tunneler to avoid torsion, kinking, or excessive tension. Attention is then turned to the recipient artery. After gaining proximal and distal control with atraumatic vascular clamps, a 1.7- to 2.0-cm arteriotomy is performed at the appropriate site. The distal end of the graft is tailored to fit this opening, and the anastomosis is likewise performed with a four-quadrant running suture technique beginning at the heel of the anastomosis. At the completion of the bypass, the heparin is reversed with protamine sulfate according to the activated clotting time.

Axillobifemoral Bypass In addition to the technical details previously mentioned for axillounifemoral bypass, dissection of the contralateral femoral artery and creation of a subcutaneous, suprapubic tunnel are necessary for performing the crossover extension. The suprapubic communication between the two groin incisions should be accomplished by careful fin-

FIGURE 51.2 (A and B) Two techniques for performing the axillary anastomosis. The beveled anastomosis (B) allows for an intentional slight redundancy of the axillofemoral graft (B¢) to avoid mechanical obstruction of the artery due to shoulder motion (A¢).

B'

FIGURE 51.3 Crossover portion of axillobifemoral procedure is placed directly over the first femoral anastomosis. (Reproduced by permission from Ascer E, Collier P, et al. Reoperation for polytetrafluoroethylene bypass failure: the importance of distal outflow site and operative technique in determining outcome. J Vasc Surg 1957;5:300.)

ger dissection, rather than by using long clamps, to avoid inadvertent penetration into either the abdominal cavity or the bladder. After completion of the vertical limb of the bypass, the contralateral femoral anastomosis is made using a 6mm PTFE graft with similarly described techniques. The crossover limb is then filled with crystalloid solution and passed through the tunnel with care taken to avoid torsion or kinking of the graft, particularly at both curvatures. Next, the vascular clamps are removed from the femoral artery and are placed on the graft just past the anastomosis, allowing return of blood flow into the femoral artery In this manner, platelet aggregates plug the suture holes in the graft, thus decreasing the blood loss when all clamps are released and the anastomosis is subjected to higher blood pressures. Lastly, the proximal end of the graft is beveled and placed directly over the first femoral anastomosis (Fig. 51.3).

Chapter 51 Extra-anatomic Bypasses

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Completion Angiograms We no longer obtain completion angiograms routinely with axillofemoral bypasses. Rather, we limit our indications to the following situations: 1. 2. 3. 4.

the surgeon has doubt that the surgical technique was flawless; the preoperative angiogram failed to demonstrate a more distal artery that can serve as an outflow site; thrombectomy or embolectomy of the femoral arteries was part of the procedure; and after all repeat operations.

Two-team Approach A well-coordinated two-team approach to some vascular operations, particularly those that entail more than two anastomoses, can significantly shorten the operation time, a decisive factor in high-risk patients. Axillobifemoral bypasses are particularly well suited for this approach since the operative sites are far enough apart to allow both teams to work simultaneously without obstructing each other. This two-team approach works most efficiently when team A exposes the axillary artery while team B dissects both femoral arteries. Creation of the longitudinal and horizontal tunnelings and passage of the grafts across the tunnels are performed by both teams simultaneously. Then teams A and B, respectively, perform the axillary and the ipsilateral femoral anastomoses concomitantly. Lastly, team B constructs the contralateral femoral anastomosis while team A works on the graft-tograft anastomosis in the groin.

FIGURE 51.4 Distal incision over the graft-to-graft anastomosis of an axillobifemoral bypass provides excellent exposure of the interior of the femoral anastomosis.

Management of Failed Axillofemoral Grafts Important additional periods of graft patency and limb salvage can be obtained by an appropriate aggressive approach during repeat surgery after axillofemoral graft failure (15). If the graft fails within the first postoperative month, the patient is immediately placed on continuous intravenous heparin, and surgery is performed as soon as possible. If late graft failure occurs (>1 month), the management should also include preoperative angiography to visualize the inflow and outflow arteries. A crucial operative element in this technique is approaching the failed graft at its distal anastomotic end rather than in the midportion. A single distal graft incision over the graft-tograft anastomosis of an axillobifemoral graft provides ample visualization of the interior of the ipsilateral femoral anastomosis (Fig. 51.4), facilitating corrective revisions and permitting safe removal of adherent clot at the distal anastomosis. This technical modification offers several advantages in cases of early or late graft failure. In cases of early failure, intimal flaps, anastomotic strictures, and unrecognized distal disease are ruled out by inspection and intraoperative angiography after the passage of an embolectomy catheter into both the vertical and crossover limbs of the graft (Fig. 51.5B), whereas in late graft failures intimal hyperplasia and progression of

A D

B C

FIGURE 51.5 (A) Our axillobifemoral bypass configuration has several advantages in the management of occluded grafts. (B) A single opening over the graft-to-graft anastomosis allows thrombectomy of both limbs of the bypass. (C) It can be used as an inflow site for a distal extension. (D) Or it can be carried across the stenotic outflow and repaired with a patch.

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atherosclerotic disease are identified if present. When progression of disease is the reason for graft failure, a graft extension to the most proximal patent and adequate arterial segment is performed using the graftotomy as an inflow site (Fig. 51.5C). Anastomotic intimal hyperplasia is best treated by extending the incision into the recipient artery past the stenotic area. A patch of synthetic or autogenous material is used to widen the lumen (Fig. 51.5D). Axillounifemoral versus Axillobifemoral Bypasses Some clinicians have advocated the routine use of axillobifemoral bypasses rather than the unilateral procedure even when the contralateral lower extremity is not threatened (13,14). This rationale was based on the higher flow rates obtained in the long, vertical limb of the bypass graft when a second outflow site was added. However, these investigators failed to demonstrate a statistically significant difference in primary patency results between the two types of bypass. Moreover, despite the presence of significant bilateral iliac disease in most patients, only 5 (15%) of 34 patients from our series of axillounifemoral bypasses eventually required an operation to salvage the contralateral limb (15). This approach not only shortens the operative time in these high-risk patients, but it also avoids placing the asymptomatic limb in jeopardy because of early or late failure of what would amount to a prophylactic portion of a bilateral procedure. Results Our 30-day operative mortality has been low, considering the poor general status of these patients. In a series of 56 patients, it was 5.3%, and all deaths were caused by myocardial infarctions. The severity of the underlying diseases was clearly reflected in the 5-year cumulative survival rate of only 43% (15). The most common cause of axillofemoral graft failure is “spontaneous thrombosis,” which occurs most frequently in the first year of graft implantation. It remains controversial whether external compression (e.g., tight belts, sleeping on the side of the graft) contributes to graft thrombosis. When no obvious cause of graft failure has been identified, these bypasses respond favorably to repeated attempts at simple thrombectomy. Progression of distal disease followed by progression of inflow disease is another important cause of graft failure, whereas intimal hyperplasia has been a rare finding during repeat surgery. The reported cumulative patency rates for axillofemoral bypasses have varied from approximately 35% to 76% at 5 years (17,18). This wide variation could point out the lack of standardization in the reporting of results. The former figure indicates the results obtained with a single operation, whereas the latter reflects the multiple repeat operations needed to maintain graft patency. We were first to call attention to this notable issue by distinguishing primary from secondary patency rates for axillounifemoral and axillobifemoral bypasses. In our experience, the 4-year primary patency rate for the

unifemoral procedure was 44%, and it was 50% for the bifemoral (not statistically significant). An aggressive approach during repeat operations improved the results to 71% and 77%, respectively. Comparable limb salvage rates were 73% and 89%, respectively (15). Improved primary patency results (78% at 5 years) have been reported by Sauvage and coleagues using 8-mm externally supported Dacron grafts (19). Similar results have been reported by the University of Oregon using PTFE ringed grafts (85% at 4 years) (20). Failed Versus Failing Grafts Contrary to general belief, detection of hemodynamically compromised PTFE grafts due to an inflow or outflow stenosis before actual graft thrombosis is possible and preferable because it allows precise identification of the causative lesion (21). Thus far, we have detected and treated 13 failing axillofemoral bypasses by percutaneous transluminal angioplasty (five cases), a graft extension (six cases), or a simple patch (two cases). These procedures were easier to perform than repeat operations on thrombosed grafts because there was no propagation of clot into the patient’s own arteries. More importantly, our patency results for failing PTFE grafts after a single intervention are strikingly superior to those obtained with repeat operations on grafts that had already thrombosed (81% vs. 33% at 2 years). Therefore, the reappearance of ischemic manifestations, diminished or absent graft pulse, or deterioration of noninvasive parameters is a signal that should alert one to obtain angiographic studies to detect a failing graft. The addition of duplex scanning as an integral part of postoperative graft surveillance has increased our ability to diagnose failing grafts and, in many cases, to distinguish a failing from an occluded graft. This differentiation is particularly useful in patients whose limbs are not threatened. Angiography may be avoided if the graft has failed and the limb is unthreatened, in which case repeat operation should not be undertaken. However, angiography is mandatory if the presence of a still-patent but failing graft is confirmed because treatment will be greatly simplified and far more effective if carried out before graft thrombosis occurs. Complications Axillofemoral bypasses have not been spared from any complication occurring with other prosthetic bypasses such as hematoma, seroma, and false aneurysm. Fortunately, these problems are rare (1% to 2%). The graft infection rate is approximately 1.5%, increasing to 2.7% after multiple repeat operations (22). Injury to the brachial plexus, due either to direct trauma during exposure of the axillary artery or to excessive abduction of the arm, is also a rare occurrence.

Femorofemoral Bypasses Although Freeman and Leeds first described the crossover femorofemoral bypass for unilateral iliac occlusive disease (1), it was Vetto, in 1962, who popularized this concept by performing subcutaneous crossover femoro-

Chapter 51 Extra-anatomic Bypasses

femoral grafts in 10 patients with acceptable limb salvage results (23). This short, suprapubic graft rapidly emerged as the least controversial of all extra-anatomic bypasses, and several clinicians have since confirmed its long-term durability. Indications The long-term primary patency rates for crossover femorofemoral grafts are superior to those obtained with axillounifemoral reconstructions. Thus, high-risk patients who are initially seen with unilateral, limb-threatening ischemia due to iliofemoral occlusive disease should be preferentially treated by using the former procedure if the adequacy of the contralateral inflow system is confirmed by angiographic and hemodynamic criteria. For this reason, one can broaden the indications for this operation by including better-risk techniques and patients in whom the ischemic process results in disabling claudication alone. Femorofemoral bypasses are a satisfactory option for patients who develop severe leg ischemia after transfemoral placement of an intra-aortic counter-pulsation balloon but who are too unstable to have it removed (24). Simple crossover extension grafts can also be successfully performed in patients already subjected to unilateral aortofemoral or axillofemoral procedures who have become symptomatic in the contralateral limb. Failed attempts at thrombectomy of a unilaterally occluded aortobifemoral graft also warrant placement of a crossover femoral graft to avoid a difficult abdominal repeat operation. Inflow Arteries Concern has been raised regarding the possibility of impaired distal perfusion in the donor limb after placement of a femorofemoral bypass. However, experimental data published by Ehrenfeld and his colleagues demonstrated that a normal donor artery, when challenged with an arteriovenous (AV) fistula, can deliver up to 10 times its resting flow rates without diverting blood away from the distal arterial segment (“steal” phenomenon) (25). This physiologic adaptive response to an increased flow demand may be impaired in the presence of a narrowed inflow vessel. Therefore complete preoperative angiographic studies of the inflow and outflow tracts with biplane films are important to rule out obstructing lesions. In cases in which the donor artery is diffusely narrowed, or if it harbors a stenosis more than 25% in diameter, the hemodynamic significance of these lesions should be assessed during angiography by measuring pressures across the lesion. Pressure gradients higher than 10 to 15 mmHg indicate that it is a critical stenosis. When no pressure gradient is elicited at rest, yet the stenosis appears suspicious, an intra-arterial injection of a peripheral vasodilator is warranted. It will challenge the stenosis by decreasing the outflow resistance and increasing flow rates. However, markedly diseased outflow vessels may mask the hemodynamic significance of an inflow lesion even when vasodilators are used. Therefore, it is good practice to measure

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intraoperative pressures after the graft is in place and to be prepared to use an alternative inflow site when unacceptably high gradients are identified. In some high-risk patients in whom critical stenoses of the inflow tract were detected (with or without pharmacologic manipulation), we have staged the performance of a percutaneous transluminal angioplasty followed by a crossover femoral graft in preference to an axillounifemoral bypass. Our experience with 35 of these tandem procedures is promising, yielding a 4-year graft patency rate of 68%. Techniques Although the crossover femorofemoral bypass graft can be performed entirely with the patient under local anesthesia, we prefer to use light general anesthesia for the reasons previously described. The operative technique for this procedure has not changed significantly since its description by Vetto (23). We too prefer the inverted C configuration for a primary crossover graft since we often extend the anastomosis into the deep femoral artery. In all our cases 6-mm PTFE grafts have been used, although it has been reported that Dacron grafts function equally well. Both femoral arteries are exposed through standard longitudinal groin incisions and are connected via a suprapubic subcutaneous tunnel. Digital dissection should be used when creating the tunnel to prevent inadvertent penetration into the abdominal cavity or the bladder. It is important that the anastomosis of the graft to the low-pressure recipient femoral artery be carried out before its anastomosis to the donor artery. This preference is based on the observation that suture leakage in the graft may be significant under normal arterial pressure and anticoagulation. In this manner, not only is blood loss diminished, but also the period of occlusion of the donor artery is minimized. Generally, this operation is simple and can be expeditiously performed. At times, however, the femoral arteries may harbor a thick anterior plaque or may be heavily calcified. Because these two factors can significantly add to the complexity of the procedure, judicious technique should be used to ensure turbulence-free circulation into the outflow vessels. In these circumstances, ample exposure of the femoral artery and its bifurcation is necessary to permit adequate reconstruction of a possibly damaged lumen. Excessive tension should not be applied to the side branches because it may induce separation of the thickened plaque from the arterial wall. In addition, one should not be tempted to perform a femoral endarterectomy because the disease process may extend well into the deep femoral artery, making appropriate repair difficult to accomplish. Instead, the edges of the plaque should be anchored to the arterial wall with interrupted U stitches, and the distal end of the graft should be tailored as a patch over this repair. We have previously described our technique for overcoming circumferentially calcified arteries that cannot be

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Part VI Chronic Arterial Occlusions of the Lower Extremities

occluded or entered with either an ordinary scalpel or Potts scissors (26). By partially fracturing the calcified artery with a hemostat clamp at 3- to 4-mm intervals, the artery is rendered suitable for occlusion, incision, and suture placement (Fig. 51.6). Intimal damage can occur in approximately 30% of the cases subjected to the fracture technique; however, adventitial perforation is uncommon. When careful repair of any existing intimal flap is undertaken, as shown in Figure 51.7, acceptable short-

term and long-term results can be expected despite this seemingly traumatic approach. If any question remains about the technical perfection of the bypass or if the preoperative angiogram has failed to demonstrate the runoff vessels at least to the knee level, a completion angiogram must be obtained. Intraoperative duplex scanning may also be helpful in ruling out technical defects, although at this point the angiogram continues to be the gold standard. Results

FIGURE 51.6 Fracture technique used with a calcified artery. The artery is partially fractured at intervals of 3 to 4 mm with a hemostat clamp, allowing for occlusion, incision, and suture placement. (Reproduced by permission from Ascer E, Veith FJ, White Flores SA. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986;152:221.)

Reports of operative mortality ranging from 2% to 15% reflect differences in patient populations rather than the complexity of the procedure (17,27). Similarly, long-term patient survival has varied from 42% to 80% at 5 years (17,27). Although the graft patency results published to date have not distinguished primary from secondary results, it is widely accepted that these operations are less likely to require multiple thrombectomies than axillofemoral bypasses. Our published 5-year graft-patency rate for femorofemoral bypasses is 83% (28). However, others have found somewhat lower patency rates (70%) (27). Several factors could have influenced these differing results, including the indications for surgery (claudication vs. limb salvage), the morphology of the runoff vessels, the type and diameter of the graft, and the surgeon’s philosophy toward an aggressive repeat operation. Nevertheless, femorofemoral bypasses are now established procedures for limb salvage and disabling claudication.

Extended Extra-anatomic Bypasses The idea of crossing multiple joints with synthetic conduits crystallized with the reports of Smith and his colleagues in 1977 (29) and by Veith and his associates in 1978 (30). Until then the concept of extended extraanatomic bypasses was not applied, even though many patients with threatened limbs would not have been able to ambulate with a prosthesis after major primary or secondary amputations. The latter report demonstrated satisfactory early graft patency and limb salvage results with axillopopliteal, crossover axillopopliteal, and crossover femoropopliteal bypasses that supported their continued use (31). Clearly, the advent of the PTFE graft played an important role in the successful outcome of these types of bypasses as its thrombotic threshold is higher than that of Dacron grafts. More recently, other groups have confirmed the efficacy and durability of axillopopliteal bypasses (32,33).

FIGURE 51.7 Placement of interrupted U stitches to tack down the intimal flap. (Reproduced by permission from Ascer E, Veith F, White Flores SA. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1985;152:221.)

Axillopopliteal Bypasses The limb salvage results obtained from using the axillary artery as an inflow site for standard extra-anatomic bypasses in poor-risk patients were sufficiently good to mo-

Chapter 51 Extra-anatomic Bypasses

tivate us to extend these procedures further-to the level of the knee or beyond (30. We have performed more than 60 straight axillopopliteal or sequential axillofemoral-popliteal bypasses using 6-mm PTFE grafts. A number of different bypass configurations were used to overcome the various complexities often encountered in these patients such as scarring due to multiple repeat operations, local infection, or marked arterial occlusive disease. We have not hesitated to perform crossover bypasses or to use unusual approaches to the infrainguinal arteries. Often, it has been necessary to expose either the above-knee or the belowknee popliteal arteries through a lateral, virginal approach to allow or facilitate the performance of an axillopopliteal bypass (34). Furthermore, we have ventured to use, in six instances, one of the infrapopliteal vessels as a sequential bypass when the outflow from the popliteal artery was compromised by extensive disease. Selection Criteria Thus far, our criteria for selecting high-risk patients for axillopopliteal bypasses have included the following: 1. 2. 3. 4.

severe atherosclerotic occlusive disease of the common, superficial, and deep femoral arteries; failed aortofemoral bypass with disease progression into the deep femoral artery; insufficient hemodynamic and clinical improvement after an axillofemoral bypass; and groin sepsis from a previously infected graft in patients in whom a standard obturator canal bypass was not possible because of multiple cardiac risk factors or morbid obesity. These procedures were limited to patients with limb-threatening ischemia.

Preoperative Evaluation The same clinical and diagnostic protocol described previously for conventional extra-anatomic bypasses is followed to prepare patients for the extended procedures. Techniques The basic principles regarding positioning of the patient on the operating table, type of anesthesia, exposure of the axillary artery, performance of the proximal anastomosis, and creation of the tunnel from the infraclavicular region to the lower abdomen remain similar to those described for axillofemoral bypasses. The choice of the surgical access to the recipient arteries and the corresponding tunnelings depends on the presence or absence of infection or scar tissue. In primary, uncomplicated cases, the above-knee or below-knee popliteal arteries are exposed through standard medial approaches, and the tunnels follow an anatomic, subsartorial route. When the ischemic limb is opposite to the axillary inflow site, a crossover bypass operation is necessary. The graft should not be tunneled across the chest or the mid-

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abdomen because this route may complicate unanticipated abdominal or chest operations. Rather, the tunnel is formed from the axillary artery to the ipsilateral groin and is brought to the contralateral groin through a subcutaneous, suprapubic approach. In cases of densely scarred or infected groins, the tunnel is created away from the area in question, even as far as lateral to the anterosuperior iliac spine, and then is carried subcutaneously, straight down to the level of the midthigh, where it is gradually curved toward the medial aspect of the lower thigh. At this level, the popliteal fossa is entered and the tunnel follows the anatomic route of the popliteal artery to the elected site of graft insertion. When infection or previous multiple repeat operations make the standard medial approach to the popliteal artery not feasible, the popliteal artery can be safely reached through a lateral approach. This approach consists of a lateral skin incision of 7 to 10 cm along the groove formed by the iliotibial tract muscle and the biceps femoris muscle at the lower third of the thigh (Fig. 51.8). This incision is deepened through the lateral intermuscular septum to allow entry into the popliteal space and isolation of the popliteal artery. Caution should be used not to injure the common peroneal nerve and adjacent veins (Fig. 51.9). Lateral exposure of the below-knee popliteal artery is somewhat more complex than for the above-knee popliteal artery. A skin incision of 10 to 12 cm is made over the lower border of the upper fibula (see Fig. 51.8). This incision is deepened through the subcutaneous tissue and superficial muscle attachments to the fibula, allowing identification of the common peroneal nerve as it traverses the neck of this bone (Fig. 51.10). Then the nerve is dissected free so it can be retracted and protected from harm, and the biceps femoris tendon is divided. The ligamentous attachments of the fibula head are incised, and the upper fourth of the fibula is bluntly freed from its muscular and ligamentous attachments, staying as close to the bone as possible. A retractor is placed deep to the fibula to protect underlying structures, and one or two holes are drilled in the bone at the selected site of transection. Through these holes, a rib shears can cleanly transect the bone without leaving sharp edges. With the upper fibula removed, the entire belowknee popliteal artery, tibioperoneal trunk, anterior tibial artery, and the origins of the peroneal and posterior tibial arteries lie just deep to the excised bone and can easily be dissected from their adjacent veins (Fig. 51.11). Tunnelings for bypasses performed through the lateral approach are preferentially constructed in a subcutaneous plane. We now prefer to use externally supported prosthetic grafts for all our extended bypasses, particularly when the pathway of the graft is tortuous or is through scarred tissue. Results Operative Mortality Despite a multitude of risk factors, the operative mortality (1 month) was only 6% in our reported series.

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Part VI Chronic Arterial Occlusions of the Lower Extremities FIGURE 51.8 Incisions in lateral aspect of thigh and calf to gain access to above-knee and below-knee popliteal artery. (Reproduced by permission from Veith FJ, Ascer E, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:120.)

FIGURE 51.10 Lateral exposure of upper fourth of fibula before its resection. Note position of common peroneal nerve, which must be protected from injury. FIGURE 51.9 Lateral exposure of the above-knee popliteal artery. (Reproduced by permission from Veith FJ, Ascer E, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:121.)

Patency and Limb salvage The cumulative patency rates for our initial 34 PTFE axillopopliteal bypasses were 77% at 1 year, 51% at 3 years, and 45% at 5 years. Comparable limb salvage rates were 86%, 57%, and 57%, respectively. It is of interest that the cumulative patient survival rate was approximately 50% at 3 years and that more than 80% of the patients who died during the remote postoperative period had intact limbs at the time of death. Complications Of the 34 limbs revascularized by axillopopliteal bypass, 10 required major amputation after graft thrombosis. In seven instances, this amputation was

(Reproduced by permission from Veith FJ, Ascer E, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:122.)

at the above-knee level, and in three instances, at the below-knee level. Six of these patients were not deemed candidates for prosthetic rehabilitation and have been confined to a wheelchair. No graft infection or any other major complication occurred in this series of cases.

Crossover Femoropopliteal Bypasses The contralateral femoral artery may be a suitable alternative for an inflow site whenever the ipsilateral femoral artery cannot be used because of severe occlusive disease or groin infection. Crossover femoropopliteal or distal

Chapter 51 Extra-anatomic Bypasses

FIGURE 51.11 Lateral exposure of below-knee popliteal artery and its distal branches after removal of upper portion of fibula. (Reproduced by permission from Veith FJ, Ascer E, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:122.)

FIGURE 51.12 Crossover femoropopliteal bypass in a high-risk patient in whom a standard procedure was not feasible because of extensive ipsilateral iliofemoral occlusive disease.

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bypasses are appropriate options for the high-risk patient with threatened ischemic limbs in whom an aortic procedure is technically difficult or carries too high a morbidity or mortality rate. Since our preliminary report describing our experience with this newer approach, we have preferentially used it rather than an axillopopliteal bypass. This rationale is based on the superior patency results generated by grafts originating from the femoral artery (femorofemoral bypasses) as compared with those from the axillary artery (axillofemoral bypasses). Thus far, we have performed 28 crossover femoropopliteal bypasses (Fig. 51.12), including seven extensions to infrapopliteal vessels. The 5-year cumulative patency rate for the entire series is 52%, with a similar limb salvage rate of 68%. The complication rate is small, and continued use of this type of extended approach to limb salvage is justified.

References 1. Freeman NE, Leeds FH. Operations on large arteries. Calif Med 1952;77:229. 2. Mohan CR, Sharp WJ, et al. A comparative evaluation of externally supported polytetrafluoroethylene axillobifemoral and axillounifemoral bypass grafts. J Vasc Surg 1995;21:801. 3. Sarac TP, Huber TS, et al. Warfarin improves the outcome of infrainguinal bypass grafting at high risk for failure. J Vasc Surg 1998;28:446. 4. Buckley CJ, Abernathy S, et al. Suggested treatment protocol for improving patency of femoral-infrapopliteal cryopreserved saphenous vein allografts. J Vasc Surg 2000;32:731. 5. Passman MA, Taylor LM, et al. Comparison of axillofemoral and aortofemoral bypass for aortoiliac occlusive disease. J Vasc Surg 1996;23:263. 6. Martin D, Katz SG. Axillofemoral bypass for aortoiliac occlusive disease. Am J Surg 2000;180:100. 7. Yeager RA, Taylor LM, et al. Improved results with conventional management of infrarenal aortic infection. J Vasc Surg 1999;30:76. 8. Seeger JM, Pretus HA, et al. Long-term outcome after treatment of aortic graft infection with staged extraanatomic bypass grafting and aortic graft removal. J Vasc Surg 2000;32:451. 9. Lewis CD. A subclavian artery as a means of blood supply to the lower half of the body. Br J Surg 1961;48: 574. 10. Blaisdell FW, Hall AD. Axillary-femoral artery bypass for lower extremity ischemia. Surgery 1963;54:563. 11. Louw JR. The treatment of combined aorto-iliac and femoropopliteal occlusive disease by spleno-femoral and axillo-femoral bypass grafts. Surgery 1964;55:387. 12. Sauvage LR, Wood SJ. Unilateral axillary bilateral femoral bifurcation graft: a procedure for the poor risk patient with aortoiliac disease. Surgery 1966;60:573. 13. Ray LI, O’Connor JB, et al. Axillofemoral bypass: a critical reappraisal of its role in the management of aortoiliac occlusive disease. Am J Surg 1979;138:117.

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14. Logerfo FW, Johnson WC, et al. A comparison of the late patency rates of axillo-bilateral femoral and axillounilateral femoral grafts. Surgery 1977;81:33. 15. Ascer E, Veith FJ, et al. Comparison of axillounifemoral and axillobifemoral bypass operations. Surgery 1985;97:169. 16. Calligaro KD, Ascer E, et al. Unsuspected inflow disease in candidates for axillofemoral bypass operations: a prospective study. J Vasc Surg 1990;11(6):832. 17. Eugene J, Goldstone J, Moore WS. Fifteen year experience with subcutaneous bypass grafts for lower extremity ischemia. Ann Surg 1977;186:177. 18. Johnson WC, Logerfo FW, et al. Is axillo-bilateral femoral graft an effective substitute for aortic-bilateral iliac/femoral graft? Ann Surg 1977:186:123. 19. El-Massry S, Saad E, et al. Axillofemoral bypass with externally supported, knitted Dacron grafts: a followup through twelve years. J Vasc Surg 1993;17(1): 107. 20. Harris EJ Jr, Taylor LM Jr, et al. Clinical results of axillobifemoral bypass using externally supported polytetrafluoroethylene. J Vasc Surg 1990;12(4):416. 21. Veith FJ, Weiser RK, et al. Diagnosis and management of failing lower extremity arterial reconstructions prior to graft occlusion. J Cardiovasc Surg 1984;25:381. 22. Ascer E, Collier P, et al. Reoperation for polytetrafluoroethylene bypass failure: the importance of distal outflow site and operative technique in determining outcome. J Vasc Surg 1987;5:298. 23. Vetto RM. The treatment of unilateral iliac artery obstruction with a transabdominal, subcutaneous, femorofemoral graft. Surgery 1962:52:342. 24. Alpert J, Goldenkranz R, et al. Limb ischemia during

25.

26.

27.

28.

29.

30.

31.

32.

33. 34.

intra-aortic balloon pumping: indication for femorofemoral crossover graft. J Thorac Cardiovasc Surg 1980;79:729. Ehrenfeld WK, Harris JD, Wylie EJ. Vascular “steal” phenomenon: an experimental study. Am J Surg 1968:116:192. Ascer E, Veith FJ, White Flores SA. Infrapopliteal bypasses to heavily calcified rock-like arteries: management and results. Am J Surg 1986;152: 220. Brief DK, Brener J. Extraanatomic bypasses. In: Wilson S, Veith FJ, et al., eds. Vascular surgery: principles and practice. New York: McGraw-Hill, 1987:414. Ascer E, Veith FJ, et al. Six year experience with expanded polytetrafluoroethylene arterial grafts for limb salvage. J Cardiovasc Surg 1985;26:468. Smith RB, Perdue GD, et al. Management of the infected aortofemoral prosthesis including use of an axillopopliteal bypass. Am Surg 1977:43:65. Veith FJ, Moss CM, et al. New approaches to limb salvage by extended extra-anatomic bypasses and prosthetic reconstructions to foot arteries. Surgery 1978;84: 764. Ascer E, Veith FJ, et al. Axillopopliteal bypasses: indications, late results and determinants of long-term patency. Vasc Surg 1989;10:285. MacCarthy WJ, McGee GS, et al. Axillary-popliteal artery bypass provides successful limb salvage after removal of infected aortofemoral grafts. Arch Surg 1992;127(8):974. Keller MP, Hoch JR, et al. Axillopopliteal bypass for limb salvage. J Vasc Surg 1992:15(5):817. Veith FJ, Ascer F, et al. Lateral approach to the popliteal artery. J Vasc Surg 1987;6:119.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 52 Popliteal Entrapment and Chronic Compartment Syndrome: Unusual Causes for Claudication in Young Adults William Turnipseed

Intermittent claudication is commonly associated with elderly persons and is rarely diagnosed in young healthy adults with chronic leg pain. Claudication can occur in these individuals, without clinical evidence of venous insufficiency or arterial occlusive disease, because of extrinsic arterial compression caused by popliteal artery entrapment or chronic compartment syndrome (CCS). This chapter describes the diagnosis and management of claudication associated with these conditions.

Popliteal Entrapment The term popliteal entrapment was coined by Love and Whelan in 1965, but the condition was first described by Stuart in 1879 (1,2). The original concept of popliteal entrapment was based on the discovery of abnormal anatomic relations between the popliteal artery and the medial head of the gastrocnemius muscle. Numerous congenital abnormalities have subsequently been associated with this condition. In 1970, Insua classified the most common anatomic variations of popliteal entrapment. They are: Type I

Medial deviation of the popliteal artery around the medial head of the gastrocnemius muscle.

Type II

Type III

Type IV

Abnormal attachments of the medial head of the gastrocnemius muscle with the popliteal artery passing medially but with less deviation than the type I entrapment. Aberrant slips of muscle from the medial head of the gastrocnemius muscle that entrap the popliteal artery. Entrapment with fibrous bands originating from the popliteus muscle (3).

Rich and associates have described a less common variant of the entrapment syndrome, in which the artery and vein follow a deviant course around the medial head of the gastrocnemius muscle as well (4). The classic and commonly held perception of popliteal entrapment syndrome is that the constellation of neuromuscular and ischemic symptoms result from pathologic impingement by anomalous musculotendinous structures behind the knee. In 1985, Rignault suggested that popliteal impingement may occur in the absence of such musculotendinous anomalies. He described the development of claudication and plantar paresthesias in military personnel and athletes, concluding that the onset of symptoms was associated with repetitive overuse or orthopedic injury. Surgical exploration demonstrated no evidence of musculotendinous anomaly and none of these patients showed evidence of lower ex-

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tremity ischemia, leading him to conclude that symptoms were neuromuscular in origin (5). Over the last 15 years, we have treated only six patients with the anatomic form of popliteal entrapment. The majority were male who developed claudication symptoms before the age of 40, and 60% had angiographic confirmation of occlusion, stenosis, or aneurysm limited to the popliteal artery segment. Differential diagnosis in young patients with claudication must exclude conditions such as: premature atherosclerosis associated with hyperlipidemia or type I diabetes; medial cystic occlusive disease; and vasculitis associated with underlying collagen vascular disorders. A history and physical examination may help to distinguish individuals that have popliteal entrapment or chronic compartment syndrome from those who have other unusual causes of claudication. Patients with symptomatic anatomic popliteal entrapment often notice that the claudication is aggravated by walking, but ironically not always by running. On physical examination, normal resting tibial pulses may fade or disappear with the knee extended and the foot placed in forced plantar or dorsiflexion positions. Over the same 15-year period, we have identified and treated 30 patients with the functional form of popliteal entrapment. This condition tends to occur in healthy young adults, particularly in well-conditioned athletes participating in sports such as cross country, basketball, and volleyball. Symptoms are most predictably aggravated by running up inclines or by repetitive jumping and are characterized by deep calf soleal muscle cramping, rapid limb fatigue, and plantar paresthesias. Unlike the anatomic form of popliteal entrapment, women are more commonly affected and there appears to be a strong correlation with other chronic overuse injuries such as compartment syndrome and/or shin splints.

Diagnosis The diagnosis of extrinsic popliteal artery compression or entrapment can be confirmed by noninvasive screening tests. We most commonly use the PVR technique to monitor plethysmographic change in the posterior and anterior tibial arteries with the foot in neutral, forced plantar flexion, and dorsiflexion positions. This test is performed while the patient is supine with the knee in full extension. The test is considered positive if there is blunting of the plethysmographic wave forms and/or more than a 25% depression in the ankle brachial index with positional stress (Fig. 52.1). This test is more reproducible if a footboard is used to maximize the effect of plantar flexion. In our early experience, we routinely performed duplex scanning on all symptomatic patients that had positive plethysmographic stress tests. We no longer consider this an essential diagnostic test, even though duplex scanning makes it possible to visualize dynamic compression of the popliteal artery or vein and to identify the rare aneurysmal change sometimes associated with this condition. To perform the duplex examination, the patient must be placed in the prone position, making it more difficult to reproduce the stress forces in dorsi- and plantarflexion required for accurate detection of impingement (Fig. 52.2). The major shortcoming of both noninvasive tests is the inability to distinguish between anatomic and functional forms of neurovascular compression. Computed tomography (CT) with contrast enhancement or magnetic resonance imaging (MRI) are the best methods for characterizing popliteal entrapment. We prefer the use of MRI because contrast agents are not required and because more detailed analysis of musculotendinous structures and their relationship to the popliteal vessels can be acquired. Magnetic resonance arteriography allows for accurate distinction between intrinsic arterial occlusive disease and

FIGURE 52.1 This PVR test demonstrates bilateral popliteal artery compression with dorsiflexion and plantarflexion of the foot, suggesting popliteal entrapment syndrome.

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FIGURE 52.2 (A) Duplex imaging demonstrates a widely patent popliteal artery with the foot in neutral position. (B) The popliteal artery in the same patient occludes because of extrinsic compression when the foot is placed in forced plantarflexion.

A

B

extrinsic compression and makes it possible to correlate popliteal impingement with the presence or absence of abnormal musculotendinous structures (Fig. 52.3). Patients with the anatomic form of popliteal impingement most commonly develop ischemic symptoms because of malposition of the popliteal artery or because of mechanical compression by aberrant muscle fibers which cause sclerotic or aneurysmal arterial wall changes that lead to thromboembolism. Patients with functional popliteal entrapment have no identifiable musculotendinous anomalies in the popliteal fossa, have no evidence of intrinsic arterial disease and most commonly develop neuromuscular symptoms associated with repetitive overuse or orthopedic injury. Aberrant positioning or intrinsic vessel wall change cannot be documented in any of these patients. With forced plantarflexion, it appears that the neurovascular bundle at the level of the popliteal fossa is forced laterally against the femoral condyle proximally and against the lateral angle of the fibrous soleal muscle band distally by simultaneous contractions of the medial head of the gastrocnemius and plantaris muscles (Fig.

52.4). Lateral compression of the neurovascular bundle rarely occurs in patients that have anatomic entrapment. Unlike in patients with anatomic impingement, we have not been able to document the presence of intrinsic stenosis, thrombosis, or aneurysmal dilation in any patient with claudication symptoms associated with functional entrapment. Furthermore, we have been unable to document abnormal muscle attachments or fibrous bands when MRI or CT studies are used to evaluate these patients. Neural structures are the most laterally placed components of popliteal neurovascular bundle. When lateral impingement is forceful enough to cause arterial venous compression, significant trauma to the popliteal nerve may occur, causing neuromuscular claudication. This can explain the strong prevalence of paresthesias commonly associated with functional entrapment (Table 52.1). Similarities between popliteal entrapment and thoracic outlet syndromes are quite striking and provide an alternative means of explaining the difference between anatomic and functional entrapment. Noninvasive

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A

FIGURE 52.4 Intravenous digital subtraction angiography demonstrates normal arterial positioning on the right side with the foot in neutral position. On the left side, lateral displacement of the popliteal artery from the midline position is demonstrated, with subsequent compression of the popliteal artery against the lateral condyle of the femur (arrow).

TABLE 52.1 Popliteal entrapment syndromes: demographics

Male Female Age (years) Athletic

B

FIGURE 52.3 (A) This sagittal MRI of the popliteal fossa demonstrates arterial patency with the foot in neutral position. (B) Sagittal MRI demonstrates extrinsic compression of the popliteal artery with occlusion when the foot is placed in forced plantarflexion.

screening studies have documented the occurrence of asymptomatic neurovascular impingement at the level of thoracic outlet and at the level of the popliteal fossa in approximately 25% of any population group tested. Despite the prevalence of detectable impingement, very few individuals develop symptoms associated with these findings. Vascular complications such as embolization or thrombo-

Symptoms Claudication Skin ischemia Paresthesia Associated compartment syndrome Unilateral

Anatomic

Functional

4 2 38.6 1 patient = 17%

10 20 24 25 patients = 83%

4 = 66% 2 = 33% 1 = 17% 0%

3 = 100% 0% 18 = 60% 14 = 47%

6 = 100%

23 = 77%

sis almost never occur at the thoracic outlet in the absence of structural abnormalities such as a prominent cervical rib or aberrant musculotendinous bands. Neuromuscular symptoms are much more common and appear to be related to repetitive upper extremity maneuvers or physical injury. In just the same fashion, vascular complications associated with popliteal impingement are almost always associated with the presence of aberrant musculotendinous fibers which cause extrinsic compression, resulting in focal hyperplasia, atherosclerosis, or aneurysmal degeneration. As in the case of thoracic outlet syndrome, neuromuscular symptoms associated with functional entrapment commonly develop as a result of repetitive stress

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or orthopedic injury. Individuals most commonly afflicted by the functional entrapment syndrome are highly trained athletes involved in running sports.

Treatment Surgery is the only effective method of treating patients with claudication symptoms caused by anatomic or functional forms of popliteal entrapment. The surgical approach and technique for treatment are significantly different, however. Patients with intrinsic arterial disease associated with anatomic impingement should be treated with the posterior approach to the popliteal fossa, enabling the surgeon to identify and excise abnormal musculotendinous bands and to reconstruct stenotic or aneurysmal vessels when necessary. The medial approach is usually restricted to treatment of patients with complete popliteal artery occlusions that require bypass grafting. In patients with asymptomatic contralateral anatomic popliteal entrapment, surgical correction should be electively performed in order to prevent secondary vascular complications. In general, long-term results are better when muscular resection is performed before development of vascular disease. The surgical treatment of patients with functional entrapment syndrome is considerably different. The main objective in this operation is to alleviate neuromuscular compression. Vascular repair is not an issue. Since many patients are professional or student athletes, surgical release procedures should be designed to allow maximum recovery of function and minimal rehabilitation requirements. The medial approach to the popliteal fossa allows access to the muscular structures causing impingement at the distal border of the popliteal fossa. The incision is made medially just below the knee, leaving the insertions of the sartorius, gracilis, semimembranosus, and semitendinosus muscles intact. Most of these patients have an overdeveloped soleus muscle with a dense fibrofascial band that arcs around the neurovascular bundle at the entrance of the soleal canal. With plantarflexion, the medial head of the gastrocnemius muscle, in conjunction with the plantaris muscle, compresses the neurovascular bundle laterally against this fibrous band of fascia, which acts as a compression point much like the first rib in the thoracic outlet syndrome. Treatment requires resection of this fascial band. This is performed by taking down the medial attachments of the soleus muscle from the posterior medial surface of the tibia and sharply resecting the anterior facial band as it crosses laterally and attaches to the proximal fibula. The posterior fascia of the popliteus muscles may also be excised so that opposing surfaces of the popliteus and soleus muscles are less likely to scar against rigid surfaces re-entrapping the neurovascular bundle. Once the soleus release is completed, the plantaris muscle tendon is resected and the fascia overlying the medial head of the gastrocnemius muscle is resected as well (Fig. 52.5). This operation has been extremely successful in the treatment of patients with functional entrapment. Over 90%

FIGURE 52.5 Surgical treatment for the “functional” entrapment syndrome requires detachment of the medial insertions of the soleus muscle to the tibia and resection of the dense anterior fascial sling of the soleus laterally to its fibular attachments. The plantaris muscle and tendon is also resected. These maneuvers prevent lateral compression of the neurovascular bundle against the soleal sling.

of patients with functional entrapment release have returned to fully active lifestyles. Follow-up noninvasive testing has shown no evidence of recurrence with up to 5 years of follow up. Those patients who did not return to an active lifestyle made the decision based on other athletic injuries such as Achilles tendon rupture or tendinitis, chronic recurrent shin splints, or the development of chronic compartment syndromes in other muscle groups.

Summary In summary, the surgeon must be aware that there are several causes for popliteal entrapment. The decision to operate, the kind of operation, and the surgical approach should be tailored to information derived from clinical history and preoperative testing. The posterior approach with muscle resection and artery repair when necessary may be quite appropriate in patients with threatened limbs resulting from anatomic entrapment. However, the medial approach with resection of the plantaris muscles, excision of the soleal band and gastrocnemius fascia is effective for treating functional forms of the disease and minimizes rehabilitation efforts, particularly in the competitive athlete. Our experience suggests that functional popliteal entrapment is more prevalent than the anatomic form of disease and that symptoms associated with functional entrapment are generally uncommon and tend to be the product of specific repetitive physical activity in sports such as cross-country, basketball, and volleyball. Surgical

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release is indicated for symptomatic patients when anatomic or functional forms of entrapment occur. Prophylactic correction of anatomic entrapment in asymptomatic patients should be seriously considered because of the risk for secondary vascular complications. Prophylactic surgery is not indicated in asymptomatic patients with functional impingement.

Chronic Compartment Syndrome Chronic compartment syndrome is another unusual cause for claudication in young adults (7–9). This condition is usually caused by overuse injury in well-conditioned athletes, particularly runners. Other common etiologies include blunt trauma, venous insufficiency, and soft tissue tumors. Unlike other forms of overuse injury such as tendinitis or stress fractures, CCS does not respond readily to rest, anti-inflammatory medications, or physical therapy. Symptoms frequently associated with CCS are severe muscle cramping and occasional paraesthesias that can seriously affect athletic levels of performance and in some circumstances progress to acute neuromuscular injury. Awareness of this condition is not widespread. The diagnosis is rarely considered by trainers and coaches who first encounter the problem, or by family physicians who are asked to evaluate the patients when rest and rehabilitation fail to resolve the problem. Patients affected with CCS, for the most part, are young (mean age 22 years) with longstanding symptoms (mean 24 months) that abate or disappear after extended rest, only to reappear again when exercise is resumed. Males and females seem to be equally susceptible to this problem. Attempts at medical management commonly fail, and the severity of symptoms cannot be controlled until physical activity is restricted. The diagnosis of this condition is made by taking a detailed clinical history and is confirmed by measuring compartment pressures (10). In our experience, normal resting compartment pressures in the lower leg are less than 15 mmHg. Borderline pressures are between 16 and 20 mmHg, and pressures above 25 mmHg at rest are abnormal and uniformly consistent with CCS. Although resting compartment pressures are elevated in most patients with this condition (85%), some may have borderline pressure elevations. They should be stressed by running until they become symptomatic, and then their compartment pressures should be measured again. Compartment pressure in normal patients will increase to three or four times the baseline but will return to normal within a few minutes. Patients with latent CCS will show marked postexercise increases in compartment pressure and a prolonged return to baseline (>10 minutes). Most of our patients are athletes (90%); the rest have a history of blunt lower extremity trauma (6%), venous insufficiency (3%), or soft tissue tumor (1%). The most

common symptoms are claudication (90%), isolated muscle swelling and tightness (60%), and paraesthesias (25%). Symptoms most commonly affect the anteriorlateral and deep posterior compartments (48% and 40%), and least commonly involve the posterior superficial compartment (12%). Paraesthesias are most frequently associated with the deep posterior compartment. Symptoms of CCS appear to be related to local neuromuscular compression and ischemia. Increased compartment pressure can be caused by a number of different factors including muscle hypertrophy, altered fascial compliance associated with changes in thickness and elasticity, myofascial scarring, venous hypertension, and posttraumatic soft tissue inflammation.

Treatment The only effective treatment for this condition is surgical compartment release (11). The objective of surgical treatment is to reduce intracompartmental pressure. The most common indications for surgery are a failure to respond to medical management, progression of claudication to the point of adversely affecting routine activities, or the onset of paresthesias associated with resting pressures greater than 25 mmHg. Recreational and nonscholarship student athletes who develop CCS symptoms are encouraged to change sports or at least to modify the intensity and duration of their workouts as an alternative to surgery. In our experience, most individuals seriously involved in competitive athletics are unwilling or unable to accept behavior or training modification as a permanent means of controlling their symptoms. Perhaps the most commonly performed operation for CCS is subcutaneous fasciotomy (12). Our experience suggests that open fasciectomy is a safer and more effective treatment. Open fasciectomy has fewer postoperative complications and fewer recurrences than subcutaneous fasciotomy. Fasciectomy is done through a skin incision made parallel to the long axis of the muscle compartment. This incision improves exposure, makes identification of anatomic structures more precise, allows for direct control of bleeding points, and makes it easier to perform a fasciectomy and extended subcutaneous fasciotomy under direct visualization. Better exposure reduces the hazards of intraoperative trauma to neurovascular structures. Fasciectomy combined with extended subcutaneous fasciotomy allows for complete decompression of the muscle compartment and greatly reduces the possibility of recurrent compartment syndrome secondary to postoperative scarring (Figs. 52.6 and 52.7). Although fasciectomy is a more extensive procedure than fasciotomy, early complication rates and late recurrences have been significantly reduced with little or no effect on the time required for rehabilitation. We have not been able to document any reduction of strength or endurance a s result of fasciectomy.

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Summary In summary, although uncommon, CCS is probably underdiagnosed and should be considered in young persons with claudication who have normal vascular studies. This condition will not improve without surgery. The best results tend to occur in those individuals who develop the problem because of overuse injury, not in patients who have developed the condition because of trauma, venous hypertension, or soft tissue tumors. Open fasciectomy causes fewer complications and fewer recurrences than closed subcutaneous fasciotomy and should be considered as the preferred surgical procedure for managing this condition.

FIGURE 52.6 Surgical release of the anterior and lateral compartments can be performed using subcutaneous fasciotomy (left) or open fasciectomy (right). Both procedures can be done using local anesthesia. Subcutaneous fasciotomy is performed using transverse skin incisions placed proximal and distal over the symptomatic compartment. The fascia is incised by subcutaneously passing scissors between the skin incisions. Open fasciectomy is performed using a linear incision over the medial one-third of the anterial lateral surface of the leg. An ellipse of fascia approximately 6 cm long and 2 cm wide is removed from the anterior and lateral compartments, leaving a strip of fascia over the intermuscular septum. This strip protects the superficial peroneal nerve from injury or scar adherence. Extended compartment release can be achieved by proximal and distal subcutaneous fasciotomy performed under direct vision.

FIGURE 52.7 Cross-section of the distal lower extremity muscle compartments (L, lateral comparent; A, anterior compartment; DP, deep posterior compartment; SP, superficial posterior compartment) demonstrating location of fascial excision required for release of the posterior compartments. The medial approach is used for posterior compartment releases. Skin incision should be placed posterior to the saphenous nerve and vein, and dissection around these structures should be avoided to reduce the probability of intraoperative trauma or postoperative scar entrapment.

References 1. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg 1965;109:620. 2. Stuart TPA. Note on a variation in the course of the popliteal artery. J Anat Physiol 1879;13:162. 3. Insua JA, Young JR, Humphries AW. Popliteal artery entrapment syndrome. Arch Surg 1970;101:771–775. 4. Rich NM, Collins GJ, et al. Popliteal vascular entrapment: its increasing interest. Arch Surg 1979;114:1377–1384. 5. Rignault DP, Pailler JL, Lunel F. The “functional” popliteal entrapment syndrome. Int Angiol 1985;4:341–343. 6. Turnipseed WD, Posniak M. Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles. J Vasc Surg 1992;15:285–294. 7. Williams LR, Flinn WR, et al. Popliteal artery entrapment: diagnosis by computed tomography. J Vasc Surg 1986;3:360–363. 8. Turnipseed WD, Detmer DE, Girdley F. Chronic compartment syndrome: an unusual cause for claudication. Ann Surg 1989;210:557–563. 9. Detmer DE, Sharpe K, et al. Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med 1985;13:162–170. 10. Veith RG, Matsen FA III, Newell SG. Recurrent anterior compartmental syndromes. Physician Sports Med 1980;8:8–88. 11. Whitesides E Jr, Haney TC, et al. A simple method for tissue pressure determination. Arch Surg 1975;110:1311–1313. 12. Detmer DE. Diagnosis and management of chronic compartment syndrome of the leg. Semin Orthop 1988;3:223–233. 13. Murbarak SJ, Owen C. Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg 1977;59A:184–187.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 53 Infected Extracavitary Prosthetic Grafts Sean V. Ryan, Keith D. Calligaro, and Matthew J. Dougherty

Infection of a vascular graft is a challenging complication for vascular surgeons. Occurring with a frequency of only 2% to 6% of cases, graft infection is one of the most serious complication a vascular surgeon will face and frequently leads to significant morbidity and mortality (1–3). The traditional approach has been to completely excise all infected grafts to prevent nonhealing wounds, anastomotic hemorrhage, and generalized sepsis. This is the “gold standard” to which all other approaches should be compared (4). In rare instances, removal of an infected arterial graft is straightforward and does not require major revascularization or amputation. More often, total graft excision is associated with a lengthy operation and the potential for amputation. As a result, graft preservation techniques have evolved to avoid extensive dissection of incorporated portions of infected grafts, to preserve graft function and to potentially salvage threatened limbs (5). Various strategies of graft excision, partial preservation or total preservation require careful selection of patients, an understanding of the pathogens involved, and close postoperative surveillance. This chapter will focus on the presentation, diagnosis and management of infected prosthetic arterial grafts, the indications for selective graft preservation, and newer approaches to treat these complications including cryopreserved cadaveric grafts.

Presentation and Diagnosis Graft infections can occur at any time after surgery, even years after original placement (6,7). Potential risk factors

644

for infection include grafts placed for emergency procedures, subcutaneously tunneled grafts, remote perioperative infections, prolonged preoperative stay, concurrent biliary, bowel, or urologic procedure, postoperative wound hematoma, grafts anastomosed to the femoral artery (i.e., groin incisions), and grafts requiring revision or “re-do” surgery (6,8). Ipsilateral pedal infection has been thought to be a major risk factor, but recent evidence has shown that this may not predispose to wound infections if perioperative antibiotics are given (9). Presentation varies depending on the location of the infected graft. Peripheral graft infections or isolated infections of the extracavitary portion of aortobifemoral grafts frequently present with obvious clinical features (Fig. 53.1). These include erythema, hemorrhage, tenderness, a swollen pulsatile mass, exposed graft, or a persistently draining sinus tract. Intracavitary grafts, however, can present with more indolent and nonspecific features such as anorexia, malaise, weight loss, and abdominal or back pain. A patient presenting with upper gastrointestinal bleeding with a history of aortic surgery should be considered to have an enteric fistula until proven otherwise (10). Laboratory studies typically show an elevated white blood cell count with a left shift in the differential, but may be normal if the organism is indolent. Cultures of draining wounds, blood and urine should be sent as a routine part of management. Imaging studies are useful to diagnose graft infection as well as the extent of graft involvement. The particular choice of study will depend on institutional availability and reliability, clinical circumstances, and surgeon prefer-

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B

A

FIGURE 53.1 (A) Isolated infection of the right limb of an aortobifemoral graft showing exposed graft and pus surrounding the graft. (B) Contrast-enhanced CT scan shows perigraft inflammation and fluid.

ence. Numerous diagnostic studies are available to confirm the diagnosis of an infected arterial graft. These include duplex imaging, contrast-enhanced computed tomography (CT), magnetic resonance imaging (MRI), radiolabeled white cell scintigraphy, and angiography. Contrast-enhanced CT scan or MRI is most often used in the diagnosis of intracavitary graft infections. Fluid collections, perigraft inflammation, loss of tissue planes, unexplained hydronephrosis, perigraft air, or anastomotic pseudoaneurysm suggest graft infection. Although CT scan is used more frequently, MRI offers the additional advantage of T2-weighted images that can better define soft tissue inflamation and may be more sensitive in identifying smaller fluid collections (11,12). Perigraft fluid collections, inflammation, and air noted on CT scan or MRI within the first 3 months after graft placement may represent a normal finding and should be interpreted with caution (12). Neither MRI nor CT scan differentiates between a sterile versus an infected fluid collection. In a case where this is a question, tagged WBC scans using indium111 or gallium-67 may be helpful. These are highly sensitive, but in the absence of clinical suspicion, specificity is only about 50% (13). The positive predictive value of labeled WBC scans is particularly low in the early postoperative period (<3 months), but may improve with later appearing infections (14). In the case of presumed isolated infection in the groin of an aortobifemoral graft, it is our practice to obtain a contrast-enhanced CT scan to evaluate the possibility of infection of the intra-abdominal portion of the graft. Additionally, an arteriography is obtained to evaluate the neck of the aorta and the distal vessels for revascularization after excision of the graft. Ultrasound is useful for the evaluation of suspected in-

frainguinal bypass graft infections. One can readily evaluate the graft for fluid collections, pseudoaneurysm formation, or thrombosis. Despite the various studies available to confirm the diagnosis of graft infection, operative exploration remains the most sensitive and specific method of diagnosing graft infection.

Microbiology Identifying the causative organism(s) involved in prosthetic graft infection is extremely important. The majority of infections are caused by contamination at the time of surgery or in the perioperative period. Not surprisingly, more than 50% of graft infections are caused by staphylococcal species, classically S. aureus and S. epidermidis (7,15). Staphylococcal species are more likely to be the offending organism as a result of being a dominant inhabitant of skin flora, especially in the perineum. Additionally, staphylococcal organisms have unique properties, allowing evasion of host defenses and proliferation within the perigraft microenvironment. The cell wall of S. aureus contains surface receptors and peptidoglycans which promote binding to cell surface components and foreign material. In addition, S. aureus secretes exotoxins and proteolytic enzymes that enhance its ability to invade surrounding tissue and overcome host defenses. S. epidermidis, in addition to secreting enzymes and toxins, produces a mucin capsule which allows protection from immune cells and provides a microenvironment for replication. Mucinproducing S. epidermidis binds to prosthetic grafts more avidly than other non-mucin-secreting bacteria (16). Gram-negative organisms, particularly Pseudomonas auruginosa, Proteus mirabilis, and Escherichia coli,

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also account for a significant percentage of graft infections (17). Pseudomonas is a particularly virulent organism because of its relative resistance to antibiotics. It produces extracellular products such as elastase and alkaline protease that inhibit phagocytosis and degrade elastin, collagen, and fibrin, which can lead to vascular disruption. Additionally, the endotoxin produced by Pseudomonas species mediates septic shock, particularly through the release of tumor necrosis factor (18,19). The prosthetic perigraft enviroment is characterized by poor blood supply, low oxygen tension, and relative acidity. This contrasts to autogenous grafts, which develop rich perivascular lymphatic networks and microvascular blood supply. The graft material elicits a host versus graft inflammatory response resulting in the development of a fibrous capsule around the graft providing a “safe haven” from immune clearance of contaminating bacteria. Once isolated in this perigraft environment, bacteria are more likely to thrive. The implication is that even a small inoculum can ultimately progress to overt graft infection. Indeed, experimental studies have shown that larger inoculums will produce clinical symptoms sooner and a threshold level of bacterial load exists beyond which bacterial invasion of the graft and tissues will occur (20–22). This may be the reason for the variable time of presentation of graft infections. Bacteria may grow unimpeded in the avascular periprosthetic environment. Bacterial invasion of the graft and surrounding tissue elicits an immune response, resulting in the development of clinical symptoms. Organism virulence, the size of bacterial inoculum and host immune capacity will determine the clinical picture. Preoperative antibiotics and strict attention to sterile technique are the best ways to prevent graft infection.

to successful preservation of infected peripheral prosthetic grafts is repeated, aggressive wound debridement. This is not possible when the infection involves the intracavitary portion of an aortic graft. If the infection if confined to the distal limb of the graft, however, complete or partial preservation may be attempted. Total graft excision is required when infection is responsible for systemic sepsis. When a patient with a graft infection presents with signs of sepsis, including hypotension, tachycardia, a markedly elevated white blood cell count, and a high fever, the graft is almost certainly irreversibly seeded with bacteria if no other source of infection can be found. In these cases, a prolonged course of intravenous antibiotics will not rid the patient of the infection unless the graft is excised (23–25). On the other hand, when a patient presents with an infected peripheral patent prosthetic graft and 1) stable hemodynamic parameters, 2) a mildly elevated or normal white blood cell count, and 3) low-grade or absent fever, graft preservation may be considered. Positive blood cultures without other signs of sepsis do not necessarily dictate graft removal.

Indications for Partial Preservation There are two circumstances in which preserving a portion of an infected graft offers several advantages over total graft excision. The first is the case of an occluded peripheral prosthetic graft where almost all of the graft is excised except for a small cuff on the artery. The second is the case of anastomotic disruption where the infected segment of the graft is removed but the remaining uninfected majority of the graft can be preserved. This technique can be applied only when the infection is confined to one part of the graft. Occluded Peripheral Prosthetic Graft

Management Once a graft infection is diagnosed, the extent of the infection defined and the underlying anatomy delineated, the physician must decide if the graft must be excised or if selective graft preservation techniques can be employed.

Total Graft Excision Despite efforts to preserve grafts, there are three conditions that require strict adherence to the dictum to remove infected extracavitary grafts: 1. 2. 3.

when the anastomosis is disrupted; when the patient exhibits signs of systemic sepsis; and when the graft is occluded.

A patient presenting with infection involving the distal limb of an aortofemoral graft should be treated by total graft excision when further investigation including CT scan or intraoperative findings document infection of the stem of the graft. As will be discussed, an essential adjunct

If a patient presents with infection involving an occluded peripheral prosthetic graft, the majority or all of the graft should be excised. Since thrombosis of the lumen of the graft will indefinitely harbor bacteria regardless of prolonged administration of intravenous antibiotics, and since the graft is nonfunctional, there is no reason to attempt complete graft preservation in this circumstance. Removal of the graft requires dealing with the resultant defect at the arterial anastomosis of an artery often critical for limb salvage, such as a patent common femoral artery with runoff into the deep femoral artery. Ligation of the artery is the safest method to prevent subsequent arterial hemorrhage after graft excision. A revascularization procedure to prevent limb loss may be extremely challenging or impossible because of lack of a suitable outflow vessel or inability to place a new graft in a sterile field. In these cases, maintaining patency of the artery involved with the infection may prove critical to provide adequate circulation to avoid limb loss or at least heal a more proximal amputation. Oversewing the artery may lead to stenosis or occlusion of the vessel. Other options include placement of a patch of autologous tissue to prevent narrowing

Chapter 53 Infected Extracavitary Prosthetic Grafts

of the artery. We have been disappointed with placing autologous tissue in an infected field and have noted several instances of anastomotic disruption from recurrent infection, possibly because these manipulations may weaken the arterial wall and still carry the risk of reinfection and disruption (23,24). We also do not favor performing a patch angioplasty with new prosthetic material since the new prosthetic material will invariably become infected. Instead, if the anastomosis is intact, we frequently oversew a 2- to 3-mm cuff of the original prosthetic graft on the underlying artery after excising the remainder of the graft (23,24) (Fig. 53.2). Leaving a small remnant of the original graft avoids the need for placing a new patch and avoids dissecting an artery encased in scar tissue. An example illustrating the advantages of this technique is subtotal excision of an infected occluded common femoral artery to distal artery prosthetic bypass. Leaving an oversewn cuff on the common femoral artery to maintain perfusion of a patent deep femoral artery may achieve limb salvage without the need to perform a secondary revascularization procedure (23,26). Aggressive operative debridement of the wound and frequent dressing changes are mandatory for promoting granulation tissue to incorporate the oversewn prosthetic patch and ensure successful wound healing. This strategy is successful in approximately three-quarters of cases. Unsuccessful cases almost always present as nonhealing wounds or recurrent infected sinus tracts and almost never as frank hemorrhage. In addition to maintaining patency of the underlying artery, a second advantage of subtotal graft excision to treat an infected occluded prosthetic graft is that dissection in the scarred wound is much easier and less time consuming. A clamp can often be placed across the most proximal aspect of the graft at the intact anastomosis without dissecting the underlying artery. The graft can

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then be transected above the clamp, leaving a cuff of graft to be oversewn. Dissection of the underlying artery, which may be encased in dense scar tissue, can often be avoided. Anastomotic Disruption Patent peripheral prosthetic grafts presenting with an infected disrupted anastomosis either as frank hemorrhage or infected pseudoaneurysm can also be treated by subtotal graft excision. The infected part of the graft involving the disrupted anastomosis must be excised. Infection causing a suture line disruption manifested by an infected pseudoaneurysm or frank hemorrhage represents an extremely virulent form of infection. Attempting to oversew the anastomosis will result in recurrent bleeding. The involved artery should be oversewn or ligated, and frequently a secondary bypass will be necessary to prevent limb loss. In these cases, instead of removing the entire graft, a segment of the original patent graft distant from the infected site may be left in place to make a revascularization procedure simpler. This technique using partial graft preservation avoids the need to excise the remainder of the original graft, which if noninfected may be densely incorporated, and avoids a second arterial anastomosis. Ideally, the revascularization part of the procedure is performed first, followed by excision of the infected portion of the graft. For example, a patient with an infected pseudoaneurysm involving the proximal anastomosis of a common femoral artery to tibial artery prosthetic bypass may be managed in the following manner. If the infection is isolated to the groin and the proximal part of the graft, a new bypass can be placed from the proximal uninvolved external iliac artery. The new graft is then tunneled lateral to the infected wound deep to the inguinal ligament, subcutaneously down the thigh, and carried to the middle, uninfected segment of the original graft. Once the secondary bypass has been completed, and the incisions closed and

FIGURE 53.2 (A) Schematic of an occluded infected prosthetic groin graft shown with pus covering an intact anastomosis of the common femoral artery with surrounding necrotic tissue. (B) Schematic of the infected groin after subtotal excision of the occluded prosthetic graft with a 2- to 3-mm oversewn graft remnant on the common femoral artery. This technique maintains patency of the underlying artery that is critical to limb survival and potentially avoids the need for complex revascularization procedures. Another essential adjunct is wide, repeated, operative debridement of all infected, necrotic soft tissue and debris.

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isolated, the infected proximal part of the original graft is excised and the common femoral artery oversewn or ligated. This technique avoids the need to excise the entire graft and perform a new tibial artery anastomosis. This method can be applied only if the infection is confined to one part of the graft. If the patient presents with frank hemorrhage, then stopping the bleeding takes first priority. After excising the infected segment of graft and oversewing or ligating the underlying artery, the patient can be heparinized, re-prepared and draped, and secondary revascularization performed through a sterile field. In summary, partial graft preservation can be attempted in the case of an occluded graft or anastamotic hemorrhage. Oversewing a cuff of the original graft at the proximal anastomosis in the case of graft thrombosis minimizes dissection and allows patency of the underlying vessel. Bypassing from uninfected artery to healthy graft around an infected portion of a patent prosthetic graft via clean tissue allows continued patency of the graft and control of infection. As long as systemic sepsis is not evident, these techniques can be utilized to minimize surgical morbidity and potentially prevent amputation. These techniques are particularly useful when there is limited autologous vein available for a complete new bypass or when there are limited or no other suitable outflow tracts available.

Indications for Complete Preservation Complete preservation of an infected prosthetic graft involving a peripheral artery is indicated only when the following three conditions are present: 1. 2. 3.

the graft is patent; the anastomosis is intact, and the patient is not systemically septic (23–25,27,28).

This strategy is very controversial and must be thoroughly understood before it is attempted since application in unsuitable conditions is fraught with hazards. This approach is particularly useful when graft excision would almost certainly be associated with amputation. Essential adjuncts to achieve successful complete graft preservation include repeated and aggressive operative wound debridements, frequent wet to dry dressing changes, and prolonged administration of appropriate antibiotics. Each of these measures deserves special attention. The first wound debridement should always be performed in the operating room where proper lighting and instrument are available. Usually general or regional anesthesia is necessary to widely debride these wounds and avoid severe patient discomfort. All infected necrotic tissue must be excised, especially any exudative material on the graft or anastomosis. If this tissue is not completely debrided, infection will persist and graft preservation will not be successful. The patient should be returned to the

operating room for subsequent major debridements as dictated by the appearance of the wound. Frequent daily bedside wound debridements may also be necessary. Wet-to-dry dressings should be performed three times a day. Initially the dressings should be changed by the surgical house staff in the intensive care unit since careful packing of a wound near an anastomosis may be required. After the anastomosis is covered with granulation tissue or a rotational muscle flap, the patient can be transferred out of the intensive care unit to the ward. Since a recent review of our patients with peripheral graft infections has documented that Gram’s stains correlate with final wound cultures in less than half the cases (29), we initially administer intravenous antibiotics that are highly efficacious against both Staphylococcus aureus and Pseudomonas aeruginosa. These are two of the more common, virulent, and resistant organisms responsible for graft infections. For this reason we recommend vancomycin and a third-generation cephalosporin, or another appropriate antibiotic, with excellent antipseudomonal activity, be given initially. When final wound and blood cultures return, appropriate changes can be made in the antibiotics. Intravenous antibiotics should be given for at least 6 weeks when complete graft preservation is attempted. This suggestion is based on the recommended duration of antibiotic treatment for any endovascular infection (30). This usually requires placement of an indwelling catheter. We do not usually give oral antibiotics for an additional 6 weeks or for life, as others have suggested. When complete graft preservation is attempted, the choice of antibiotic obviously cannot be based on graft or arterial wall cultures since graft or artery wall specimens are not obtained (31). Thus, our final choice of antibiotics in patients treated by complete graft preservation is based on wound and blood cultures. In a recent review of our experience over a 20-year period, complete graft preservation was attempted in 51 out of 120 patients involving a peripheral artery who fulfilled the above three criteria at Pennsylvania Hospital in Philadelphia and Montefiore Medical Center in New York. In our series, aerobic and anaerobic wound cultures were obtained in all patients. Blood cultures were obtained selectively based on the patient’s clinical presentation. Gross purulent material bathed the anastomosis or body of the graft in all cases. S. aureus was the most common organism cultured. Amputation was required in only 2 of these 51 patients and long-term graft preservation was successful in 71% of cases. This represents a significant improvement in limb salvage compared with other series of infected extracavitary grafts treated by routine graft excision (32–35). The most common reason for unsuccessful complete graft preservation in this series was a nonhealing wound, most commonly associated with the presence of Pseudomonas. Despite the common misconception that Gram-negative organisms are more virulent, the only Gram-negative bacteria that predicted a poor outcome was Pseudomonas (17). When grafts infected

Chapter 53 Infected Extracavitary Prosthetic Grafts

with Pseudomonas are excluded from the analysis, wound healing and successful graft preservation was accomplished in over 90% of the wounds which grew Gram-negative organisms. Although our hospital mortality rate was 12%, this compares favorably to other series of infected peripheral grafts (9–36%) (32–36). In summary, important prerequisites for complete graft preservation include a patent graft without evidence of anastomotic disruption in a clinically hemodynamically stable patient. Critical adjuncts include aggressive, repeated wound debridement and frequent dressing changes. Initial antibiotics should be broad spectrum. Subsequent culture results should narrow therapy based on organism sensitivities. The presence of Pseudomonas usually predicts failure and should mandate more traditional approaches to infected grafts. In most cases, unsuccessful graft preservation is manifested by graft thrombosis, failure to develop granulation tissue within the wound bed, anastomotic hemorrhage, or development of clinical sepsis. Of note, frank hemorrhage rarely occurred when graft preservation was attempted and proved unsuccessful.

The Emerging Role of Cryopreserved Cadaveric Homografts Prior to the development of synthetic grafts, fresh allografts were used as alternate conduits. This early experience, however, was abandoned to an unacceptably high percentage of graft deterioration, dilation, or thrombosis (37). Further studies showed that post explantation processing and cryopreservation at 4 °C may improve the durability of these grafts, presumably by removing cellular antigens that elicit a host immune response (38). The concept of cadaveric grafts subsequently reemerged as alternate conduits for infected grafts based on the poor results associated with traditional treatments and the results of longer-term durability of these grafts in the thoracic aorta and aortic valve. The use of these grafts theoretically lowers the rate of reinfection by allowing ingrowth of lymphatics and capillaries that help clear infection and deliver immune cells. Indeed, reinfection rates after aortic valve replacement for bacterial endocarditis with a homograft are very low (39–41). Cryografts are now used with increasing frequency as in situ replacement of infected abdominal aortic grafts. In situ replacement with a cadaveric homograft may prove to be superior to extra-anatomic bypass because initial studies have shown that patency rates are reasonable and reinfection rates are low. Durability of these grafts, however, remains an unanswered question (42–44). The use of cryopreserved grafts in the infrainguinal position for limb salvage may be a viable option when autologous vein is not available and a prosthetic graft is contraindicated due to infection. Patency rates, however, have been uniformly poor (45). As such, allografts are not recommended for lower extremity bypass.

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Conclusions Vascular graft infections remain a significant operative and management challenge for the vascular surgeon. Although early mortality has not changed dramatically in recent years, management options have evolved significantly. Diagnosis and management require an understanding of the pathophysiology of graft infection and identification of the offending organism(s). Partial and complete graft preservation techniques are acceptable alternatives when the patient is not systemically septic and infection is extracavitary. These techniques minimize morbidity and improve limb salvage. Pseudomonas is a particularly virulent organism that generally predicts failure of graft preservation techniques. Cryopreserved allografts show promise as alternate conduits for in situ replacement of infected aortic grafts, but have only a temporizing role for extracavitary infections.

References 1. Kikta MJ, et al. Mortality and limb loss with infected infrainguinal bypass grafts. J Vasc Surg 1987;5(4): 566–571. 2. DeRose G, Provan, JL. Infected arterial grafts: clinical manifestations and surgical management. J Cardiovasc Surg (Torino) 1984;25(1):51–57. 3. Goldstone J, Moore, WS. Infection in vascular prostheses: clinical manifestations and surgical management. Am J Surg 1974;128(2):225–233. 4. Shaw RS, Baue AE. Management of sepsis complicating arterial reconstructive surgery. Surgery 1963;53:75–79. 5. Calligaro KD, Veith FJ. Selective prosthetic graft preservation. In: Management of Infected Arterial Grafts. Calligaro KD, Veith FJ, eds. St. Louis, MO: Quality Medical Publishing, Inc., 1994;202–211. 6. O’Hara PJ, et al. Surgical management of infected abdominal aortic grafts: review of a 25-year experience. J Vasc Surg 1986;3(5):725–731. 7. Calligaro KD, et al. Are gram-negative bacteria a contraindication to selective preservation of infected prosthetic arterial grafts? J Vasc Surg 1992;16(3):337–345; discussion 345–346. 8. Schellack J, et al. Infected aortobifemoral prosthesis: a dreaded complication. Am Surg 1988;54(3): 137–141. 9. Tannenbaum GA, et al. Safety of vein bypass grafting to the dorsal pedal artery in diabetic patients with foot infections. J Vasc Surg 1992;15(6):982–988; discussion 989–990. 10. Reilly LM, et al. Improved management of aortic graft infection: the influence of operation sequence and staging. J Vasc Surg 1987;5(3):421–431. 11. Schubart P, et al. The significance of hydronephrosis after aortofemoral reconstruction. Arch Surg 1985;120(3):377–381. 12. Modrall JG, Clagett GP. The role of imaging techniques in evaluating possible graft infections. Semin Vasc Surg 1999;12(4):339–347.

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13. Sedwitz MM, et al. Indium 111-labeled white blood cell scans after vascular prosthetic reconstruction. J Vasc Surg 1987;6(5):476–481. 14. Williamson MR, Boyd CM, Shah HR. Prosthetic vascular graft infections: diagnosis and treatment. Crit Rev Diagn Imaging 1989;29(2):181–213. 15. Bandyk DF, Berni GA, et al. Aortofemoral graft infection due to Staphylococcus epidermidis. Arch Surg 1984;119:102–108. 16. Muller E, Takeda S, et al. Blood proteins do not promote adherence of coagulase-negative staphylococci to biomaterials. Infect Immun 1991;59:3323–3326. 17. Calligaro KD, et al. Selective preservation of infected prosthetic arterial grafts: analysis of a 20-year experience with 120 extracavitary-infected grafts. Ann Surg 1994;220(4):461–469; discussion 469–471. 18. Bandyk DF, et al. In situ replacement of vascular prostheses infected by bacterial biofilms. J Vasc Surg 1991;13(5):575–583. 19. Geary KJ, et al. Differential effects of a gram-negative and a gram-positive infection on autogenous and prosthetic grafts. J Vasc Surg 1990;11(2):339–345; discussion 346–347. 20. Bennion RS, Williams RA, Wilson SE. Comparison of infectibility of vascular prosthetic materials by quantitation of median infective dose. Surgery 1984;95:22–26. 21. Rosenman JE, Kempczinski RF, et al. Bacterial adherence to endothelial-seeded polytetrafluoroethylene grafts. Surgery 1985;98:816–823. 22. Birinyi LK, Douville EC, et al. Increased resistance to bacteremic graft infection after endothelial seeding. J Vasc Surg 1987;5:193–197. 23. Calligaro KD, et al. A modified method for management of prosthetic graft infections involving an anastomosis to the common femoral artery. J Vasc Surg 1990;11(4):485–492. 24. Samson RH, et al. A modified classification and approach to the management of infections involving peripheral arterial prosthetic grafts. J Vasc Surg 1988;8(2):147–153. 25. Calligaro KD, DeLaurentis DA, Veith, FJ. An overview of the treatment of infected prosthetic vascular grafts. Adv Surg 1996;29:3–16. 26. Calligaro KD, et al. Prosthetic patch remnants to treat infected arterial grafts. J Vasc Surg 2000;31(2): 245–252. 27. Calligaro KD, Veith, FJ. Graft preserving methods for managing aortofemoral prosthetic graft infection. Eur J Vasc Endovasc Surg 1997;14 Suppl A:38–42. 28. Piano G. Infections in lower extremity vascular grafts. Surg Clin North Am 1995;75(4):799–809.

29. Calligaro KD, et al. Management and outcome of infrapopliteal arterial graft infections with distal graft involvement. Am J Surg 1996;172(2):178–180. 30. Threlkeld MG, Cobbs CG. Infectious disorders of prosthetic valves and intravascular devices. In: Principles and Practice of Infectious Disease. New York: Churchill Livingstone, 1990;706–715. 31. Malone JM, et al. The necessity for long-term antibiotic therapy with positive arterial wall cultures. J Vasc Surg 1988;8(3):262–267. 32. Szilagyi DE, et al. Infection in arterial reconstruction with synthetic grafts. Ann Surg 1972;176(3):321–333. 33. Bunt TJ. Synthetic vascular graft infections. I. Graft infections. Surgery 1983;93(6):733–746. 34. Yeager RA, et al. Aortic and peripheral prosthetic graft infection: differential management and causes of mortality. Am J Surg 1985;150(1):36–43. 35. Veith FJ, Hartsuck JM, Crane C. Management of aortoiliac reconstruction complicated by sepsis and hemorrhage. New Engl J Med 1963;270:1389–1392. 36. Ehrenfeld WK, et al. Autogenous tissue reconstruction in the management of infected prosthetic grafts. Surgery 1979;85(1):82–92. 37. Szilagyi DE, et al. Late fate of arterial allografts: observations 6 to 15 years after implantation. Arch Surg 1970;101(6):721–733. 38. Schmitz-Rixen T, et al. Immunosuppressive treatment of aortic allografts. J Vasc Surg 1988;7(1):82–92. 39. Donaldson RM, Ross DM. Homograft aortic root replacement for complicated prosthetic valve endocarditis. Circulation 1984;70(suppl 1):178–181. 40. Tuna IL, Orszulak TA, Schaff HV, Danielson GK. Results of homograft aortic valve replacement for active endocarditis. Ann Thorac Surg 1990;49:619–624. 41. Zwischenberger JB, Shalaby TZ, Conti VR. Viable cryopreserved aortic homograft for aortic valve endocarditis and annular abscesses. Ann Thorac Surg 1989;48:365–370. 42. Vogt PR, et al. Cryopreserved arterial allografts in the treatment of major vascular infection: a comparison with conventional surgical techniques. J Thorac Cardiovasc Surg 1998;116(6):965–972. 43. Kieffer E, et al. In situ allograft replacement of infected infrarenal aortic prosthetic grafts: results in forty-three patients. J Vasc Surg 1993;17(2):349–355; discussion 355–356. 44. Verhelst R, et al. Use of cryopreserved arterial homografts for management of infected prosthetic grafts: a multicentric study. Ann Vasc Surg 2000;14(6):602–607. 45. Albertini JN, et al. Long-term results of arterial allograft below-knee bypass grafts for limb salvage: a retrospective multicenter study. J Vasc Surg 2000;31(3):426–435.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 54 Lumbar Sympathectomy: Conventional Technique Henry Haimovici

Introduced many decades ago as a method of treatment for ischemic and painful disorders of the lower extremity, much controversy still persists over the physiologic effects, clinical indications, and long-term results of lumbar sympathectomy. The first lumbar sympathectomy for arterial occlusive disease of the lower extremity was performed in 1924 by Julio Diez of Buenos Aires (1). From this point on, the history of lumbar sympathectomy has been one of mixed fortunes. Its place in the management of vascular disorders underwent periodic reappraisals because of uneven clinical results. This became especially relevant after the advent of reconstructive arterial surgery.

Neuroanatomy of the Lumbar Sympathetic Trunk The standard anatomy textbooks indicate that, as a rule, the lumbar sympathetic trunk contains four or five ganglia (2–4). Ganglion L1 is described as lying anterior to the body of vertebra L1, over the second lumbar vertebra or anterior to the intervertebral disk. The second ganglion (L2) has been described as lying anterior to the body of the second lumbar vertebra. Ganglia below the second are common; the second and the fourth are the more constant ones. The latter is usually located behind the origin of the iliac vessels. Rami of the first ganglion have a cephalic direction, the second has a transverse direction, and the third and forth ganglia have a transverse or caudal direction.

Distribution of Sympathetic Innervation of the Lower Extremity Completeness of anatomic denervation is important for achieving adequate sympathectomy of a given segment of an extremity. Excision of the chain from L2 to L4, sometimes including L1, offers satisfactory results. Removal of a lesser portion of the sympathetic chain may, however, prove to be inadequate. The source of sympathetic fibers as related to the lumbar ganglia may be helpful in determining the extent of the sympathectomy. Thus the first lumbar ganglion supplies the sympathectic innervation of the thigh and parts of the leg. The ablation of the second and third lumbar ganglia denervates the posterior aspect of the thigh, the leg, and the foot.

Criteria for Completeness of Sympathetic Denervation Evaluation of the degree of denervation following a lumbar sympathectomy relies upon two main physiologic effects: 1. 2.

vasomotor responses as determined by skin thermometry; and cessation of the secretory activity of the sweat glands (5,6).

Indications Indications for lumbar sympathectomy are limited essentially to patients with nonreconstructible arterial disease

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or vasospastic conditions of the leg and foot. Predicting the effects of a sympathectomy upon the circulation of the lower extremity, especially the foot and toes, is essential for determining the operative indications. Essentially, one has to evaluate properly: 1. 2. 3.

the collateral circulation or its potential availability, the vasomotor activity of the extremity, and clinical findings,

all of which may provide in most instances a fairly accurate prediction of the operative results (7). The physiologic effects of a lumbar sympathectomy still remain ill-defined, as attested by a number of reports. Interpretation of the blood flow increase effect has been called into question. Indeed, investigations of arteriovenous (AV) shunting following lumbar sympathectomy have raised the question of the therapeutic value of its nutritive blood flow to the denervated tissue, especially to

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the skin. It should be noted that such data were obtained primarily in acute animal experiments, which disclosed that after sympathectomy there is an increased AV flow with no change in total capillary nutritive flow, to both skin and muscle (8). Other investigations, however, are at variance with these results. One of the reasons invoked is the experimental model, and the other is the possible lack of correlation with the arteriosclerotic human extremity. Thus, while in the above-mentioned experimental model the arterial tree was undisturbed, by contrast, when the femoral arteries were ligated so as to mimic ischemic clinical conditions, significant increase in tissue blood flow was obtained following sympathectomy (9). The failure of sympathectomy to relieve intermittent claudication in the majority of cases has been interpreted as a lack of sympathetic innervation of those vessels of skeletal muscle. In the presence of advanced arterial disease due to diffuse lesions not lending themselves to reconstructive vas-

FIGURE 54.1 Right lumbar sympathectomy. (A) Position of patient on the operating table with a bolster placed under the thoracolumbar region. Heavy, broken line indicates the site of the skin incision. (B) Incision of the external oblique muscle and of its aponeurosis along their fibers. (C) Retraction of the external oblique muscle and divided internal oblique muscle along its fibers. (D) Transverse muscle divided along its fibers, exposing the retroperitoneal space. (E) Retroperitoneal space enlarged, showing the peritoneum and lumbar adipose tissue.

Chapter 54 Lumbar Sympathectomy: Conventional Technique

cular surgery, sympathectomy may be the only measure of limb revascularization. In these cases, its role and greatest effectiveness reside in the physiologic ability to increase the collateral system for improving and preserving the viability of the skin. Based on our experience and that of others, relief of rest pain and prevention of major amputations in a significant percentage of patients attest to the effectiveness of this procedure, even in patients with advanced ischemic changes (7,9–11). It should be pointed out that, during the critical postoperative period, meticulous care of the foot lesions, cessation of smoking, and avoidance of any other vasoconstrictor influence may greatly enhance the effectiveness of the sympathectomy. The role of diabetes mellitus is generally recognized as an accelerating and aggravating factor in limb and life prognosis. Indications of lumbar sympathectomy in patients with diabetes are questionable because of the frequency of “autosympathectomy” in such patients. The diffuse nature of the arteriosclerotic process may account primarily for the greater severity of isehemic changes in diabetic as compared with nondiabetic patients. This is substantiated by arteriographic studies of the lower extremity (12). As shown by our own findings, occlusion of the distal arterial tree (popliteal, tibials), poor or absent runoff, and inefficient collaterals are more prevalent among diabetic patients (8,13).

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In a number of reports, and in our own study, it is apparent that sympathectomy in a certain number of cases may have only a delaying action, as it does not arrest the downgrade progression of the atherosclerotic process. Contraindications to lumbar sympathectomy are rapidly progressing ischemic lesions and poor general condition of the patient. Unsatisfactory results may be avoided by adhering to the criteria for selection of patients as outlined above. Lumbar sympathectomy alone or in combination with reconstructive arterial surgery, however, may be a valuable procedure in selected patients with advanced arterial insufficiency (8). The method of choice for either unilateral or bilateral lumbar sympathectomy is by the extraperitoneal exposure. Two approaches are most convenient and simple: 1) anterior transverse and 2) anterolateral. The former is the most commonly used. The latter is employed in conjunction with exposure of an iliac vessel.

Anterior Transverse Exposure For right lumbar sympathectomy (see Figs. 54.1 and 54.2), general endotracheal anesthesia is preferred, although epidural or spinal anesthesia is often used in certain patients. FIGURE 54.2 (A) Abdominal contents retracted medially, thus exposing the ureter. Note the ilioinguinal and genitofemoral nerves lying on the psoas. (B) Further retraction of the abdominal contents, exposing the inferior vena cava and right iliac vein, lumbar sympathetic trunk, and lumbar vessels. (C) Mobilization of the sympathetic trunk lifted by a nerve hook. (D) Excision of the sympathetic trunk.

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FIGURE 54.5 Left lumbar sympathectomy. (A) Position of the patient on the operating table and the line of the skin incision. (B) Exposure of the lumbar sympathetic trunk and application of clips on the chain and its rami. Note the presence of lumbar vessels anterior to the sympathetic trunk.

FIGURE 54.3 Specimen of sympathetic trunk removed between L1 and L4. FIGURE 54.4 Steps of layer closure of the abdominal incision.

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Chapter 54 Lumbar Sympathectomy: Conventional Technique

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The number and location of the ganglia are variable. From a practical point of view, the chain should be removed between a point of emergence near the diaphragmatic crura and the point of disappearance beneath the common iliac vessels. This segment usually comprises the essential L2, L3, and L4 ganglia. For denervation of the anterior surface of the thigh, L1 should also be included (Fig. 54.3). In some instances the crus of the diaphragm may have to be divided in order to reach L1. In some patients, the sympathetic trunk may be obscured by overlying fibrous bands. When invisible, the trunk may be located by digital palpation over the vertebrae. Incision of the fibrous layer is then necessary before the chain is exposed and isolated. On the right side, the inferior vena cava covers the sympathetic trunk and hides it completely from view before its retraction. The left sympathetic chain is always more readily exposed when the adipose and lymphatic tissue masses are reflected medially toward the aorta. The transversalis fascia and the peritoneum are often inseparably adherent anteriorly and separated laterally by the properitoneal fat. If inadvertently incised or opened during the separation, the peritoneal rent should be promptly closed. The peritoneum should be reflected toward the midline before reaching the anterior surface of the psoas. Otherwise, the dissecting fingers may stray into the gutter between the quadratus lumborum and psoas muscles. The ureter with the genital vessels is incorporated in and retracted with the parietal peritoneal leaf. These structures are easily demonstrable and should not be confused with the lumbar sympathectomy chain. The operative techniques are summarized in Figures 54.4, 54.5, and 54.6.

Operative Pitfalls Injury to the structures adjacent to the sympathetic chain, if minor and consisting of bleeding from lumbar vessels, should be treated by temporary compression with gentle packing, to be followed immediately by the use of clips. Inadvertent rupture of a lumbar artery may be more difficult to control and may necessitate temporary occlusion of the aorta in order to secure the stump of the ruptured lumbar vessel. A tear in the inferior vena cava or abdominal aorta or iliac vessels is by far a more serious complication because of potentially significant loss of blood. Compression or clamping of the aorta or compression of the inferior vena cava is necessary for control of bleeding before repair of the vessels is carried out. Likewise, injury to the ureter should be recognized promptly in order to repair any rent. Removal of the genitofemoral nerve or iliolumbar nerve, mistaken for the sympathetic trunk, may cause less tragic consequences but may be responsible for some neuritic pain and, obviously, results in failure of the desired sympathetic denervation.

FIGURE 54.6 Anterolateral exposure of the right lumbar sympathetic trunk. (A) Position of the patient and the line of skin incision extending from the 11th rib to the lateral border of the rectus abdominis muscle. Note the skin incision is oblique. (B) Line of incision of the external oblique muscle extending proximally to the tip of the 11th rib. Except for the latter muscle, the internal oblique and transversus muscles are transected along the oblique incision of the skin. (C) Exposure of the sympathetic trunk, inferior vena cava, and right iliac vein. Note also exposure of the crus of the diaphragm.

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Postoperative Care As a rule, after a successful sympathectomy, the extremity becomes warm and dry within a matter of hours. Painful ulcers or rest pain usually subside in the majority of cases. Postoperative abdominal distention due to a paralytic ileus may be a source of discomfort to the patient for 2 to 3 days. In such instances, administration of 250 or 500 mg of neostigmine (Prostigmin) every 6 hours, combined with intermittent use of a rectal tube, may promptly alleviate the discomfort.

Knowledge and understanding of the therapeutic limitations of the sympathectomy may help to dispel much of the controversy regarding its effectiveness. The procedure neither alters the basic arterial lesion nor prevents its progression. The operative technique is usually simple and safe, with a low mortality rate. Although varied, the postoperative complications are mostly related to sympathetic denervation. Understanding of their mechanisms will facilitate both prevention and subsequent management.

References Complications Postsympathectomy Neuralgia It is important to reassure the patient that postsympathectomy neuralgia does not reflect aggravation of the disease and that the process is self-limited and will subside within a reasonable period of time.

Sympathetic Regeneration The concept of sympathetic regeneration to account for a return of sympathectomy activity in humans may have been overstated. To prevent regeneration, a considerable length of the sympathetic trunk must be removed and this may not always be certain, as we have presented evidence for regeneration even after removal of the entire sympathetic chain on both sides (14). Another possibility is progression of the disease, which may at a later stage nullify partially or completely the beneficial effects of a sympathectomy. The arterial process should be reevaluated to ascertain the cause of sympathectomy failure.

Conclusion Lumbar sympathectomy may represent an important adjunct in the management of occlusive arterial disease provided that: 1. 2. 3. 4.

patients are properly selected; removal of the sympathetic trunk is adequate; postoperative care of the foot lesions is meticulous; and use of tobacco is rigorously eliminated.

1. Diez J. Un nuevo metodo de simpatectomia periferica para el tratamiento de los afecciones troficas y gangrenosas de los miembros: la disociacion fascicular. Bol Soc Cir B Aires 1924;8:792. 2. Yeager GH, Cowley RA. Anatomical observations on the lumbar sympathetics with evaluation of sympathectomies in organic peripheral vascular disease. Ann Surg 1948;127:953. 3. Lowenberg RI, Morton DE. The anatomic and surgical significance of the lumbar sympathetic nervous system. Ann Surg 1951;133:525. 4. Edwards EA. Operative anatomy of the lumbar sympathetic chain. Angiology 1951;2:184. 5. Haimovici H. Criteria for completeness of sympathetic denervation [Editorial]. Angiology 1951;2:423. 6. Haimovici H. Evidence for adrenergic sweating in man. J Appl Physiol 1950;2:512. 7. Haimovici H, Steinman C, Karson IH. Evaluation of lumbar sympathectomy: advanced occlusive arterial disease. Arch Surg 1964;89:1089. 8. Terry HJ, Allan JS, Taylor GW. The effect of adding lumbar sympathectomy to reconstructive arterial surgery in the lower limb. Br J Surg 1970;57:51. 9. Smithwick RH. Lumbar sympathectomy in treatment of obliterative vascular disease of lower extremities. Surgery 1957;42:415, 567. 10. Dc Takats G. Place of sympathectomy in treatment of occlusive arterial disease. Arch Surg 1958;77:655. 11. Gillespie JA. Future place of lumbar sympathectomy in obliterative vascular disease of lower limbs. Br Med J 1964;2:1640. 12. Haimovici H. Patterns of arteriosclerotic lesions of the lower extremity. Arch Surg 1967;95:918. 13. Haimovici H. Peripheral arterial disease in diabetes. NY State J Med 61:2988, 1961; in Ellenberg M, Rifkin H, eds. Diabetes mellitus: theory and practice. New York: McGraw-Hill, 1970:890. 14. Haimovici H, Hodes R. Preganglionic nerve regeneration in completely sympathectomized cats. Am J Physiol 1940;128:463.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 55

Laparoscopic Lumbar Sympathectomy Armando Sardi and Larry H. Hollier

Lumbar sympathectomy has a place in the management of peripheral vascular disease of the lower extremities in patients who, after clinical, hemodynamic, and angiographic studies, are found to be unsuitable for arterial reconstruction. Several studies have demonstrated its benefit for limb salvage (1), and it has been considered valuable in the management of patients with rest pain, with early success rates of 50% to 70% (2). It has also demonstrated satisfactory results in patients with causalgia (3) or reflex sympathetic dystrophy (4). Lumbar sympathectomy is traditionally performed through bilateral flank incisions using a retroperitoneal approach. Similar results have been described using chemical sympathectomy (5,6); however, this technique, although claimed to reduce operative morbidity and mortality (7), has been questioned by some with regard to its completeness (8) and its permanency (7). Laparoscopic techniques have altered our approach to surgery. As better instrumentation is developed, more complicated surgical procedures are being performed. Following the techniques of minimally invasive surgery, thoracoscopic transthoracic dorsal sympathectomy has been performed rapidly and safely in patients with hyperhidrosis and reflex sympathetic dystrophy (9,10). We describe below a technique that can be used to perform bilateral lumbar sympathectomy.

Surgical Technique After the administration of general anaesthesia, five 10-mm trocars are placed in the abdomen: one in the umbilicus; two in the lower quadrants of the abdomen, later-

al to the rectus abdominis muscle; and two more in the upper quadrants, two fingerbreadths beneath the costal margin at the level of the anterior axillary line (Fig. 55.1). The patient is placed in the right lateral Trendelenburg position. The small bowel is retracted superiorly and to the right using fan retractors. An incision is made in the peritoneum to the left of the aorta and superior to the inferior mesenteric artery; the sympathetic trunk is identified, and the appropriate ganglia are resected (Fig. 55.2). The right side is then approached, again incising the peritoneum superior and lateral to the bifurcation of the inferior vena cava. The vena cava is retracted toward the left, and the sympathetic trunk is identified, again resecting two to three ganglia (Fig. 55.3). After histologic confirmation of the ganglia and obtaining appropriate hemostasis, the procedure is completed. All trocars are removed under direct visualization, and the muscle in the umbilical port is approximated with No. 1 polyglycolic acid suture. In all other trocar sites only the skin is closed using No. 4–0 polyglycolic acid sutures placed in a subcuticular fashion. The operative time is usually under 2 hours. The patients are allowed a regular diet on the day of surgery and are ready for discharge on the first postoperative day. There are some technical points that need to be taken into consideration: 1. With the exception of the umbilical port, all trocars are placed laterally, allowing appropriate placement of instruments. 2. All trocars should be 10 mm in size to allow instruments to be placed from different angles depending on the desired exposure.

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FIGURE 55.1 Trocar placement. All trocars should be 10 mm in size to allow instruments to be placed from different angles depending on the desired exposure.

FIGURE 55.3 Right-side sympathectomy. The peritoneum has been entered superior to the bifurcation of the inferior vena cava (IVC). A single arm blunt retractor is used to displace the IVC to the left. A right angle hook facilitates the dissection of the trunk (S). Ao, aorta; U, ureter; Ov A., V., ovarian artery and vein.

FIGURE 55.2 Left-side sympathectomy. The peritoneum has been entered superior to the inferior mesenteric artery. The sympathetic trunk(S) is identified and a ganglion removed. Duo, duodenum; RV, left renal vein; IVC, inferior vena cava; Ao, aorta; IMV, inferior mesenteric vein.

3. Appropriate rotation of the operating table allows gravity to help obtain good exposure. 4. Fan retractors are useful in displacing the bowel toward the upper abdomen, exposing the retroperitoneal structures. 5. Blunt and sharp dissection with the use of coagulating scissors are required. 6. Operative blood loss is minimal. The lumbar vessels are usually posterior to the sympathetic trunks. Occasionally a lumbar vein may be anterior to it (11). This can be dealt with by the use of hemoclips. 7. Retraction to the aorta should be limited and carefully performed to avoid emboli to lower extremities. 8. The sympathetic trunk on the right side is posterior to the inferior vena cava. It is necessary to use a singlearm blunt retractor to displace the inferior vena cava to the left and expose the trunk. 9. Mobilization and traction of the trunk can be easily and rapidly performed using a hook. Hemoclips are used before transection. 10. No special instruments are required for the safe performance of this procedure. The basic laparoscopic cholecystectomy tray will have all the required instruments.

Chapter 55 Laparoscopic Lumbar Sympathectomy

Discussion Surgical techniques learned from other intra-abdominal procedures have expanded our applications in surgery. Our previous experience with advanced laparoscopic approaches such as splenectomy, staging laparotomy, and adrenalectomy (12,13) encouraged us to perform laparoscopic lumbar sympathectomy. Patients who are candidates for lumbar sympathectomy usually have complicated medical problems such as diabetes, renal failure, and severe cardiovascular disease and hence benefit from minimally invasive surgery. Following laparoscopic sympathectomy, the patients are allowed a regular diet and are ready for discharge on the first postoperative day. Although the described techniques vary in detail, the common features are simplicity, expedience, minimal surgical trauma, few complications, and a low cost compared with standard methods of open surgery (10,14–16). Laparoscopic lumbar sympathectomy has these same benefits. Currently there are no published series on laparoscopic lumbar sympathectomy. Our limited experience with this procedure has been very rewarding. No perioperative complications have developed, and all patients have been able to tolerate a normal diet on the day of surgery. They are ready to be discharged on the first postoperative day, providing that the underlying disease does not demand a longer hospital stay. It is important to have the collaboration of a vascular surgeon experienced with the open technique and a laparoscopic surgeon who has the manual dexterity required for the safe performance of the procedure. This collaboration ensures that if there are technical problems with the procedure, we can rapidly and safely convert to an open procedure. This collaboration will also ensure good patient selection. We believe that bilateral laparoscopic lumbar sympathectomy can be performed safely and expeditiously and will become the method of choice for patients requiring sympathectomy.

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References 1. Lee BY, Madden JL, et al. Lumbar sympathectomy for toe gangrene: long term follow-up. Am J Surg 1983; 145:398–401. 2. Norman PE, House AK. The early use of operative lumbar sympathectomy in peripheral vascular disease. J Cardiovasc Surg 1988;29;717–722. 3. Mockus MB, Rutherford RB, et al. Sympathectomy for causalgia: patient selection and long term results. Arch Surg 1987;122:668–672. 4. Olcott C, Eltherington LG, et al. Reflex sympathetic dystrophy: the surgeon’s role in management. J Vasc Surg 1991;14:488–492. 5. Walker PM, Key JA, et al. Phenol sympathectomy for vascular occlusive disease. Surg Gynecol Obstet 1978; 146:741–744. 6. Walker PM, Johnston KW. Predicting the success of a sympathectomy: a prospective study using discriminant function and multiple regression analysis. Surgery 1980;87:216–221. 7. Cotton LT, Cross FW. Lumbar sympathectomy for arterial disease. Br J Surg 1985;72:678–683. 8. Lemberger R, Hopkinson BR, Makin GS. An assessment of the completeness of phenol lumbar sympathectomy. In: Pollock JC ed. Topical reviews in vascular surgery, vol 1. Bristol, UK: Wright PSG, 1982;188–210. 9. Pace RI, Brown PM, Gutelius JR. Thoracoscopic transthoracic dorsal sympathectomy. JCC 1992;35:509–511. 10. Williams PL, Warnick R. Gray’s anatomy. Neurology. New York: Churchill Livingstone, 1980;801–1226. 11. Sardi A, McKinnon WP. Laparoscopic adrenalectomy for primary aldosteronism. JAMA 1993;269(8):989–990. 12. Sardi A. Laparoscopic splenectomy for patients with idiopathic thrombocytopenic purpura. Surg Laparosc Endosc 1994;4:316–319. 13. Kux M. Thoracic endoscopic sympathectomy in palmar and axillary hyperhidrosis. Arch Surg 1978;113: 264–266. 14. Horgan K, O’Flanagan S, et al. Palmar and axillary hyperhidrosis treated with sympathectomy by transthoracic endoscopic electrocoagulation. Br J Surg 1984; 71:1002. 15. Alone P, Cameron A, Rennie J. The surgical treatment of upper limb hyperhidrosis. Br J Dermatol 1986; 115:81–84.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART VII Aortic and Peripheral Aneurysms

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 56 Thoracic Aortic Aneurysms Joseph S. Coselli

The large volume of blood that flows through the thoracic aorta at high pressure is unparalleled by any other vascular structure. For this reason, any condition that disrupts the integrity of the thoracic aorta, such as aortic dissection, rupture, and traumatic injury, will have catastrophic consequences. Aortic aneurysm is defined as a permanent localized dilation resulting in at least a 50% increase in diameter compared with the normal expected aortic diameter at the same anatomic level. Thoracic aortic aneurysms have several causes: degenerative disease of aortic wall, aortic dissection, aortitis, infection, and trauma. Poststenotic dilation with aneurysm formation may occur in patients with coarctation or aortic valvular stenosis. The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and aortic segment involved. Aneurysms of the thoracic aorta consistently increase in size and progress to serious complications including rupture, which is usually a fatal event. Therefore, aggressive treatment is indicated in all but the poorest surgical candidates. Small asymptomatic thoracic aortic aneurysms can be followed, especially in poor-risk patients, and later treated surgically if the patient develops symptoms or complications, or if progressive enlargement occurs. Meticulous control of hypertension is the primary medical treatment. Elective resection with graft replacement is indicated in asymptomatic patients with an aortic diameter of at least twice the normal diameter for the involved segment (5 to 6 cm in most thoracic segments). Contraindications to elective repair are extreme operative risk because of severe coexisting cardiac or pulmonary disease, or a limited life expectancy due to other conditions, such as malignancy.

An emergency operation is required for any patient in whom a ruptured aneurysm is suspected. Patients with thoracic aortic aneurysm often have coexisting aneurysms of other aortic segments. A common cause of death following repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic segments is often necessary. As with any major operative procedure, careful preoperative evaluation regarding coexisting disease and subsequent medical optimization are essential for successful surgical treatment.

Methods of Clinical Evaluation Physical examination rarely provides direct evidence of a thoracic aortic aneurysm. A pulsatile abdominal mass may be present in a patient with a thoracoabdominal aortic aneurysm, and tenderness of such a mass signifies impending rupture. Most physical findings are nonspecific and are usually related to complications and cardiovascular disease. A diastolic cardiac murmur is present in patients with aortic insufficiency. An ascending aortic aneurysm may compress the superior vena cava, producing jugular venous distension and upper extremity edema. Findings secondary to associated cerebrovascular or peripheral arterial occlusive disease are common. Patients with thoracic aortic aneurysms are usually asymptomatic at the time of diagnosis. The aneurysm is frequently discovered serendipitously during either routine examination or evaluation for an unrelated problem. A patient presenting with pain related to a thoracic aortic aneurysm should be considered to have actual or impending rupture, an indication for emergency surgery. Anterior

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chest pain suggests an ascending aortic aneurysm, whereas back pain is suggestive of descending thoracic aortic aneurysm, and abdominal pain may signify and be caused by a rupturing thoracoabdominal aortic aneurysm. Compression of the trachea may cause cough, dyspnea or stridor, whereas rupture in to the tracheobronchial tree produces massive hemoptysis. Involvement of the gastrointestinal tract can include compression of the esophagus, resulting in dysphagia, or erosion into the viscera, leading to either hematemesis or hematochezia. Neurologic symptoms include a hoarse voice due to pressure on the left recurrent laryngeal nerve. Symptoms characteristic of associated conditions, such as aortic valvular insufficiency and congestive heart failure, are commonly present in patients with thoracic aneurysms. Because history and physical examination are imprecise in the diagnosis of thoracic aortic aneurysms, various imaging studies play a critical role in detection and follow-up. In many cases, the initial suspicion of a thoracic aortic aneurysm is raised by findings on a chest radiograph. The presence of a mediastinal mass or generalized mediastinal widening is suggestive of an aneurysm. Ascending aortic aneurysms tend to produce convexity of the right heart border. A prominent aortic knob is consistent with an aneurysm involving the transverse aortic arch. The trachea or left mainstream bronchus may be displaced or compressed. Descending thoracic aortic aneurysms often manifest as posterior or left lateral thoracic masses. Although a chest radiograph is helpful: 1. 2. 3.

It cannot precisely define the extent of aortic involvement. It cannot always differentiate between an aneurysm and simply aortic tortuosity. It cannot identify an aneurysm of the sinus segment that is hidden within the cardiac silhouette.

A plain chest x-ray, of course, cannot be used to diagnose aortic dissection and usually will not show an aneurysm of the sinus segment hidden within the cardiac silhouette, such as often occurs in patients with Marfan syndrome (1,2). Other radiographic studies can occasionally show signs of aortic aneurysmal disease. In the presence of a radiopaque, calcified aortic wall, radiographs of the abdomen may demonstrate a thoracoabdominal aortic aneurysm. Barium studies of the upper gastrointestinal tract may reveal displacement or obstruction of the esophagus. Transthoracic echocardiography is useful in diagnosing ascending aortic aneurysms and in evaluating cardiac valve function. Unfortunately, transthoracic echocardiography cannot be used to evaluate the entire aorta. Preoperative ultrasound evaluation of the thoracic aorta is far better with transesophageal echocardiography (TEE), which produces high-resolution images of the car-

diac structures, entire thoracic aorta, and other great vessels. Transesophageal echocardiography is highly accurate in the detection of intraluminal thrombus, fistulization, aortic valvular insufficiency, and pericardial effusion or tamponade. This method is also useful for intraoperative cardiac monitoring. It can evaluate left ventricular volume and compliance to help refine anesthetic management and can confirm the surgical correction of aortic valvular insufficiency. Like transthoracic echocardiography, TEE provides no information concerning coronary artery patency and its usefulness depends on the skill of the operator. TEE has proved to be a superior technique in making the diagnosis of aortic dissection and demonstrating both the site of the aortic tear and reentry sites between the true and false lumina within the thoracic aorta (2,3). These two methods share the advantage of being able to be performed at the bedside or in the operating room. Computed tomography (CT) is highly accurate for determining the aortic diameter, the extent of aneurysmal disease, and the presence of intraluminal thrombus (2,4). CT images can identify aortic rupture contained by perioaortic tissues, a pulmonary lesion, a nonfunctioning atretic kidney, and a horseshoe kidney — conditions that affect operative strategy (5). Dynamic scanning with intravenous contrast material provides flow dynamics and opacification of two or more lumina as evidence for aortic dissection. When dissection is present, absence of flow within the false lumen secondary to thrombosis can also be confirmed. Additional advantages of CT are standardization of scale and resolution, near-ubiquitous availability, nonoperator dependence, speed of performance and relative cost-effectiveness. CT scans are not helpful in evaluating cardiac function or major branch vessel patency and are also limited in the amount of information provided regarding patency of major branch vessels of the aorta, which frequently is a necessary component of operative planning (2,6). With CT, a risk of renal dysfunction exists secondary to the administration of intravenous contrast and we frequently use simple CT scanning without the infusion of contrast material in patients with impaired renal function. Magnetic resonance imaging (MRI) is also effective in evaluating the entire aorta and allows visualization in the transverse, sagittal, and coronal planes. MRI provides information regarding the thoracic aorta that is frequently not dissimilar from that provided by CT scanning. The acuity of the aortic structures as delineated by MRI has been less than by CT scanning because of the physiologic motion that occurs in the chest (7). MRI has the capability of displaying blood flow characteristics within the aorta, including the presence of an intimal flap and two or more lumina, as occurs in aortic dissection, without the use of intravenous infusion of contrast material (2,7). Specialized magnetic resonance angiography (MRA) techniques greatly enhance the imaging of the aorta. Gated scans offer semiquantification of aortic valvular insufficiency

Chapter 56 Thoracic Aortic Aneurysms

and left ventricular function. MRI shares with CT the disadvantage of being performed in a nonintensive care area of the hospital. Monitoring equipment and ventilators required for critically ill patients are generally not compatible with the magnetic environment. The high cost, limited availability and great time requirements are further disadvantages of MRI. Although not absolutely essential for the planning of an operation, aortography is the single most informative method of evaluating the thoracic aorta. It precisely defines aortic anatomy and is the superior method of evaluating all the major branch vessels for patency and anatomic anomalies. This capability cannot be underemphasized in light of the common occurrence of concomitant branch vessel occlusive disease and its impact on the operative plan. For example, in 1509 patients who underwent thoracoabdominal aortic aneurysm repair, 271 (14%) had celiac, superior mesenteric, or renal artery occlusive disease and required either endarterectomy or bypass (8). Evaluation of the brachiocephalic vessels is critical in patients with transverse aortic arch aneurysms to detect arterial aneurysms, anomalies or occlusive disease that require special intraoperative attention. Aortography may underestimate the diameter of an aneurysm because of the nonopacification of luminal thrombus. Thoracic aortography can be performed as part of cardiac catheterization in patients with known or suspected coronary artery occlusive disease. In addition to having an understanding of the etiology, extent of disease, location and degree of branch involvement, special emphasis must be given to the preoperative evaluation of cardiac, pulmonary, and renal function. The frequent and concomitant presence of peripheral vascular occlusive disease resulting in claudication and hemodynamic fluctuations associated with treadmill stress testing has prompted us to screen patients with thoracic aortic aneurysms using transthoracic echocardiography to initially evaluate cardiac status. With transthoracic echocardiography, assessment of left ventricular systolic function, estimation of ejection fraction, and evaluation of regional wall motion may be obtained. Concomitantly, a thorough evaluation of cardiac valvular structures for stenosis and insufficiency may be obtained (9). Based upon the presence of prevailing symptoms and noninvasive testing, including both echocardiography and persantine thallium radioisotope scanning, a decision is made as to whether to proceed with cardiac catheterization and coronary artery arteriography preoperatively. Respiratory complications remain a significant source of morbidity and mortality following surgical treatment of thoracic aortic aneurysmal disease. In addition to clinical and radiographic evaluations, we routinely perform screening spirometry testing and arterial blood gas analysis to evaluate pulmonary function and estimate risk. In those patients with bronchospasm, an estimation

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of response to bronchodialators may be valuable in the perioperative period. Cessasion of smoking before elective surgery is as important as it is difficult to achieve. However, operation is not withheld in patients with symptomatic aortic aneurysms and poor pulmonary function. In such patients, preservation of the left recurrent laryngeal nerve, phrenic nerve, and diaphragmatic function is particularly important. Renal function is assessed preoperatively by serum electrolytes, blood urea nitrogen (BUN), and creatinine measurements. Renal size may be determined from a CT scan, by ultrasound, or from the nephrogram obtained during aortography. Renal artery patency can be confirmed by arteriography. Patients are not rejected as surgical candidates based on renal function. Patients with preoperative renal failure and an established hemodialysis program do not have significantly greater morbidity than patients with normal renal function. Patients with severely impaired renal function who are not on chronic hemodialysis frequently require transient temporary hemodialysis early after operation. Additionally, patients with poor renal function secondary to severe proximal renal occlusive disease are revascularized at operation by either renal arterial endarterectomy or bypass grafting with the expectation that renal function will stabilize or improve.

Aortitis Two unusual causes for aneurysms of the aorta are giant cell arteritis (temporal arteritis) and Takayasu’s arteritis. In either case, any or all segments of the aorta may be involved, with both true thoracic aortic aneurysms and dissecting aneurysms occurring. Giant cell arteritis is a systemic autoimmune disorder of unknown cause that affects the aorta and its branches. It typically occurs in patients over 50 years of age, with female to male ratio of about 3:1 (10). Granulomatous inflammation of the entire thickness of the vessel wall leads to intimal thickening and medial destruction. Vessel occlusion and aneurysm formation are the respective sequelae, and dissections may be superimposed. These lesions can be successfully treated surgically (11). Takayasu’s arteritis is a systemic autoimmune disorder that primarily affects the aorta, its branches, and the pulmonary artery. It is characterized by an acute inflammatory reaction with degeneration of the elastic tissue and proliferation of the connective tissue. This results in thickening of the intima and necrosis with fibrosis involving both the medial and adventitial layers. When the intimal thickening is the predominant manifestation, occlusion of the aorta and its branches results. Aortic dissection may occur as a superimposed process. Takayasu’s arteritis typically involves women, but in a younger age group, usually teenagers and young adults (12). Takaya-

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su’s disease is noted for the frequent presence of aneurysms of the coronary, internal mammary, vertebral, carotid and axillary arteries, as well as of the thoracic and abdominal aorta (13). The pulmonary artery is involved in 50% of cases. Within 10 years after diagnosis, nearly 40% of patients suffer cardiovascular complications such as stroke, aortic valvular insufficiency, myocardial infarction, cardiac failure, and ruptured aneurysm (14). Although the role for operation of the cerebral vascular component of this disease is not well defined, the aneurysmal manifestations carry the same risks as those of medical degeneration and atherosclerotic lesions and should be treated surgically based on their own merit to prevent rupture and dissection. Surgical management is by graft replacement with techniques appropriate for the involved segment (15). The surgical treatment of aortitis has an early survival rate exceeding 90% in centers experienced in aortic surgery. Long-term survival rates are also excellent. Because of their propensity for the development of further cardiovascular complications, these patients require lifelong follow-up.

Infection The term mycotic aneurysm is commonly used to describe aneurysm formation resulting from infectious destruction of an arterial wall and includes both bacterial and fungal infections. Syphilitic aneurysms are rare because of the effectiveness of antibiotic therapy administered in the early stages of the disease; however, when present, they generally arise in the ascending aorta and tend to be saccular in nature, with a peculiar propensity to erode bone. Aneurysms that are caused by pyogenic infection result from infection of the aortic wall and destruction of the aortic tissue. They are the result of direct extension of a perioaortic infection or from embolic seeding from bacterial endocarditis or septicemia to previously normal aortic intima, to areas of atherosclerosis, or to an established aortic aneurysm with or without superimposed atherosclerosis. Previously placed prosthetic aortic grafts can also become infected; this serious complication occurs in less than 2% of all aortic graft replacement operations. Infected grafts result from intraoperative contamination, wound and venous catheter infections, postoperative bacteremia, and erosion of the graft into the gastrointestinal tract (16). The clinical manifestations of mycotic aortic aneurysms include pain, fever, hoarseness, and a history of previous febrile illness. Organisms that are frequently identified include Staphylococcus species, Streptococcus species, Salmonella, Escherichia coli, and others (17). The most common sites for mycotic aneurysms are the lesser curvature of the transverse aortic arch and the thoracoabdominal aorta in and about the diaphragm and immediately below in the region posterior to the origin of the visceral vessels. Successful treatment involves early diagnosis, aggressive surgical intervention and management,

and sufficient perioperative and long-term antibiotic administration (18,19). The surgical management of patients with mycotic aneurysms is dependent upon location, extent of involvement, prior surgery, and infective organism. General principles include wide surgical debridement and restoration of arterial continuity. In the thoracic aorta, unlike peripheral locations, extra-anatomic bypass is generally not feasible; in situ Dacron graft replacement after wide excision and debridement has provided satisfactory clinical results (20). An important feature in the surgical treatment of patients with mycotic aneurysm and in situ graft replacement is filling of the periaortic dead space and wrapping of the prosthetic graft material with viable tissue using either the intra-abdominal omentum or a viable muscular flap (pectoralis major, rectus abdominis, latissimus dorsi, or serratus). To reduce the risk of prosthetic graft reinfection, the use of a tissue homograft to replace the involved segment has also been advocated. Postoperatively, patients with thoracic aortic infection are treated with high-dose intravenous antibiotics for 4 to 6 weeks, based on results of blood or aortic wall cultures. Resected aortic or graft tissue cultures are often negative because of intensive antibiotic treatment. Lifelong oral suppressive antibiotic therapy is mandatory to prevent recurrence.

Aneurysm and Coarctation of the Aorta Although various theories exist regarding causation, the etiology of typical coarctation of the aorta is considered congenital. The most common site for coarctation is at the level of attachment of the obliterated ductus; however, in rare instances, it may be either above or below the patent ductus arteriosus. In the “preductal” configuration and occasionally in the other forms, intractable cardiac failure develops early in infancy and results in death unless emergency repair is undertaken. Balloon dilation angioplasty may also have a role in early stabilization, buying time for the very sick infant, but should be followed by surgical intervention before restenosis or aneurysmal dilation (21). Rarely, fusiform aneurysms of the descending thoracic aorta are associated with coarctation (22). The majority of fusiform aneurysms are located distal to the coarctation and are considered poststenotic in origin (Fig. 56.1). In rare instances, the aneurysm occurs proximal to the coarctation, and in such cases, it has a propensity to involve the distal transverse aortic arch. Both of these lesions are considered to be due to medial degenerative changes within the aortic wall. In either event, treatment is graft replacement, replacing the aneurysm and relieving the coarctation. Another complication of aortic coarctation is aortic dissection; this is usually a late complication in the

Chapter 56 Thoracic Aortic Aneurysms

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Aneurysms of the Sinus of Valsalva

A

B FIGURE 56.1 Example of treatment of patient with poststenotic (coarctation) aneurysm of the proximal descending thoracic aorta. (A) Location of coarctation and distal aortic dilation. (B) Replacement by Dacron tube graft.

Aneurysms of the sinus of Valsalva are rare and usually of congenital origin. These result from lack of fusion of the aortic tissues above with the aortic valve annular tissue below because there is a structural defect in the tissues that bridge the two — that is, a congenital absence of fibroelastic tissue. This permits gradual dilation and aneurysm formation that has the capability of slowly burrowing within the wall of the heart (23,24). These lesions have a high incidence in males. The aneurysms formed are initially of little physiologic significance and produce no symptoms early in their course, with the diagnosis often made in this early stage by aortography performed in the study of other conditions. Late in their course, as in all forms of aortic aneurysm, rupture eventually occurs (25). Typically this complication develops in a patient’s early thirties. Depending on the location of the aneurysm, rupture occurs into one of the heart chambers, usually on the right side into the atrium or ventricle, producing a left-to-right shunt. When this occurs, heart failure rapidly ensues; unless successfully treated by operation, the condition leads to death within 1 year. The right coronary sinus is involved in 20% of cases and rupture is usually into the right atrium. Involvement of the left coronary sinus with rupture into the left atrium is rare (26).

Clinical Manifestations The symptoms produced by this condition are typically those of acute congestive heart failure suddenly occurring in a young adult who was previously healthy. Physical findings include an enlarged heart, parasternal murmurs, heart failure, a left-to-right shunt by cardiac catheterization, and the characteristic aortographic findings of sinus aneurysm with fistulous connection to either the right ventricle or the right atrium (Fig. 56.2) (27,28).

Treatment older patient (22). In most instances, the dissection arises proximal to the congenital defect and progresses in an antegrade fashion. In a minority of cases, the dissection originates distal to the congenital defect and extends distally. The presence of medial degeneration and long-term hypertension probably contribute to the occurrence of this complication. In general, the dissection does not pass through the fibrotic changes at the site of coarctation. Treatment required for dissection is based on the segment of aorta involved, with the essential features described elsewhere in this chapter, but complicated by the necessity for concomitant treatment of the coarctation. Dissection is less common currently because of the popularity of early surgical correction of coarctation.

Treatment, which is curative in nature, is early operation. Various procedures have been used; however, the method currently used is that first reported by Shumacker in 1965 (27). This procedure consist of exposing the aortic defect through an incision made in the proximal ascending aorta via a median sternotomy and using cardiopulmonary bypass. Once exposed, the defect can be closed without injury to the aortic valve. Closure may be accomplished either by direct suture or by insertion of a Dacron patch, depending on the size and the need to avoid deformity of the aortic valve. Associated ventricular septal defects are common, and these are repaired during the same operation. The results of treatment are good, with survival and permanent correction of abnormalities achieved in most cases (25,26).

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primary etiology for aneurysms of the proximal aorta (28).

Medial Degeneration

A

B

FIGURE 56.2 (A) Rupture of aortic sinus aneurysm into the right ventricle 5 years after graft replacement of ascending aorta and separate aortic valve replacement. (B) Treatment consisted of composite valve graft replacement.

Aneurysms of the Ascending Aorta Aneurysmal involvement of the ascending aorta is due to medial degeneration or dissection in over 95% of cases. Dissection is frequently a superimposed process in an aortic wall compromised by medial degenerative changes. Although atherosclerotic intimal disease may be superimposed upon either of these entities, it is only rarely the

In medial degenerative disease, the smooth muscle cells and elastic laminae in the aortic media are replaced by cystic spaces filled with mucoid material. The disease, frequently involving multiple segments of the aorta, produces progressive weakening and dilation of the aortic wall, with eventual aneurysm formation and subsequent complications including aortic valvular insufficiency, intimal laceration with dissection, and rupture. Medial degenerative disease is also responsible for thoracic aortic aneurysms in patients with Marfan syndrome, an autosomal dominant connective tissue disorder with associated cardiovascular, skeletal, and ocular abnormalities. Marfan syndrome is caused by a mutation involving a gene located on the 15th chromosome that codes for the microfibrillar protein, fibrillin. The resulting connective tissue defect weakens the aortic wall. The ascending aorta is most commonly affected with the development of generalized aortic root dilation (annuloaortic ectasia) and aortic valvular insufficiency. Cardiovascular complications, especially thoracic aortic aneurysms, are primarily responsible for the reduced life expectancy in patients with Marfan syndrome; without surgical treatment, patients die at an average age of 32 years (29). Patients with Marfan syndrome frequently have involvement of multiple segments of the aorta and over time may require numerous operations for replacement. Consequently, it is recommended that patients with Marfan syndrome undergo lifelong surveillance of their aortic and related cardiovascular manifestations of the disease. Aneurysms of the ascending aorta resulting from medial degeneration may involve only the tubular ascending segment, the portion between the coronary sinuses and the transverse aortic arch. Alternatively, dilation my occur in conjunction with involvement of the entire aortic root with similar pathological changes found throughout the aortic wall, aortic valve annulus, aortic valve leaflets, and the coronary sinus segment. Progressive weakening and dilation causes, in addition to aneurysmal formation, aortic valvular insufficiency with heart failure, intimal laceration and dissection, and rupture (30). The ultimate complication of aneurysmal disease is that the aortic root is ruptured. Rupture into the pericardial sac generally results in immediate cardiac tamponade and death. Alternatively, rupture may occur into an adjacent cardiac structure, i.e., the right ventricle, right atrium, or right pulmonary artery, resulting in a large left-to-right shunt and frequently producing severe congestive heart failure followed by death.

Treatment Operation is the treatment of choice for medial degeneration. Historically, a variety of techniques have been used

Chapter 56 Thoracic Aortic Aneurysms

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FIGURE 56.3 Technique for tubular graft replacement for ascending aortic aneurysm (A–D) using Dacron tube graft. In the presence of aortic valve disease, prosthetic replacement (E) is performed concomitantly.

A

B

C D

E

including valvuloplasty, aortoplasty, wrapping of the aorta, and prosthetic graft replacement with and without valve replacement. Aortoplasty and valvuloplasty fell into early disfavor because of the high frequency of early and late recurrence. Separate replacement of the ascending aorta and aortic valve without treatment of coronary artery sinus involvement consistently leads to progression and complications from the untreated segment (31,32). Improved treatment for aneurysm of the ascending aorta with involvement of the sinus portion was introduced in 1968 by Bentall and DeBono with a technique that consisted of direct reattachment of the coronary artery origins to a composite valve graft (33). This technique offered complete treatment and has been adopted widely with good early and late results (34–36). Disadvantages of this approach have included bleeding at operation, often necessitating aneurysm wall wrapping of the graft for hemostasis, and the late development of false aneurysms at the suture lines, particularly the coronary artery anastomoses. Recent modifications have remedied some of the problems associated with composite valve graft replacement (37). Operation for ascending aortic aneurysm is performed through a midsternal incision using cardiopulmonary bypass. We prefer to use bicaval cannulation with pump return via cannulation of a common femoral artery. The left ventricle is depressed through a sump placed

through the right superior pulmonary vein. Moderate hypothermia, cold blood cardioplegia, and topical cooling are employed for myocardial preservation. The technique of aortic replacement varies according to the extent of the aneurysm and the condition of the aortic valve. Simple Dacron graft replacement of the tubular portion is indicated when the sinus segment is normal and the aortic valve is competent (Fig. 56.3). When aortic valvular disease is present and the sinus segment is normal, separate replacement of the aortic valve and tubular ascending aorta is carried out. In patients with Marfan syndrome, separate replacement of the aortic valve and ascending aorta without replacement of the sinus segment consistently leads to progressive dilation of the sinus segment and subsequent complications. Therefore, a composite valve graft is always used in patients with Marfan syndrome. Composite valve grafts are also used to replace the entire aortic root in patients with aortic valvular dysfunction and an aneurysmal sinus segment (annuloaortic ectasia). Our preferred technique in patients undergoing primary operation involves complete resection of the ascending aortic aneurysms down to within 1 to 2 mm of the aortic valve annulus, leaving Carrel-type “buttons” of aortic wall around each of the coronary artery origins (Fig. 56.4) (37,38). The coronary arteries are mobilized for a sufficient length to allow tension-free attachment to

FIGURE 56.4 (A) Aortic root aneurysm in a patient with aortic valvular insufficiency. (B) Following cardiopulmonary bypass and cardioplegia, the aortic root aneurysm is excised, leaving “buttons” of aortic tissue around the coronary artery ostia. (C) Prefabricated composite valve graft is coated with albumin and sutured to the aortic valve annulus. (D) The left main coronary artery ostia is anastomosed to the composite graft. (E) Distal anastomosis is performed end-to-end. (F) Right coronary artery is attached to the anterior portion of the graft. (G) Following composite valve graft replacement, coronary arteries are widely patent.

A

B

C

E D

F

Chapter 56 Thoracic Aortic Aneurysms

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FIGURE 56.4 (continued)

the composite valve graft. Following insertion of the valve portion of the composite valve graft, openings are made for direct reattachment of the aortic buttons containing the origins of the coronary arteries. The suture line may be reinforced with Teflon felt and examined for hemostasis immediately after completion. All suture lines are accessible for placement of additional sutures to achieve hemostasis.

Dissection Aortic dissection begins as an intimal tear and extends as a longitudinal splitting through the media, creating a false channel. In general, the greater portion of a dissection progresses distally, but varying amounts of proximal extension occur in most patients. The intimal tear originates in the ascending aorta (usually 2 to 4 cm beyond the origin of the coronary arteries) in 62% of patients, the arch in 9%, the upper descending thoracic aorta in 26% and in the abdominal aorta in 3% of patients (28). Patients with involvement of the ascending aorta, arch, and descending thoracic aorta are classified as DeBakey type I (Stanford A, proximal); patients with involvement only of the ascending aorta are classified as DeBakey type II (Stanford A, proximal); and patients with dissection involving the aorta distal to the left subclavian artery are referred to as DeBakey type III (Stanford B, distal) (39,40). It is generally agreed that most patients with involvement of the ascending aorta succumb from complications in the acute phase within 2 weeks, if left untreated (41). Acute complications of proximal aortic involvement include rupture

into the pericardium, aortic valve insufficiency, coronary artery occlusion, or rupture into the right atrium or right ventricle with a left-to-right shunt. Distal complications include branch vessel occlusion resulting in stroke, visceral or extremity ischemia, and distal aortic rupture, usually into the left chest, although abdominal aortic rupture can occur later. Late complications include aneurysm formation from false lumen dilation, aortic valvular insufficiency, and rupture of the false lumen. A combination of computed tomography scanning, echocardiography (transthoracic and transesophageal), and aortography may be required for precise diagnosis and delineation of the full extent of aortic involvement. The chronicity of dissection is an important factor in determining appropriate management. Acute aortic dissections are arbitrarily defined as those presenting within 14 days of the initial dissection. After 14 days, dissections are considered chronic. Emergency operative intervention is undertaken at the time of diagnosis when the ascending aorta is found to be involved in the dissection process (DeBakey type I or II or Stanford A). Patients are initially stabilized in an intensive care unit where arterial pressure, hemodynamic parameters, urine output, peripheral pulses, and neurologic status are meticulously monitored. Therapeutic goals include Dacron graft replacement of the ascending aorta, which is frequently the site of the intimal tear and is consequently the weakest portion, and prevention of further proximal extension of the dissection with its deleterious effect upon the coronary artery origins and the aortic valve, and the treatment of aortic valve or coronary artery occlusive disease.

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Uncomplicated DeBakey type III (Stanford B) dissections without significant aortic dilation are treated medically with beta-blockers and antihypertensives. Without treatment, chronic distal aortic dissection carries a yearly mortality rate of 20%. Progressive aortic dilation reaching 6 cm and the development of complications related to the dissecting aortic aneurysm are indications for operative repair. At least one-third of patients with chronic distal aortic dissection require surgical treatment within 5 years of diagnosis (42). Following stabilization in the intensive care unit, patients with an acute DeBakey type I or II aortic dissection must undergo urgent graft replacement of the ascending aorta. The dissection usually progresses distally to involve at least the proximal transverse arch; therefore, placement of a cross-clamp across the distal ascending aorta can cause laceration of the friable intimal flap, creating a new entry into the false lumen distal to the proposed graft. Use of profound hypothermic circulatory arrest obviates the need for such a cross-clamp. In acute dissection, the distal anastomotic suture line between the graft and the aorta is placed so that the false lumen is obliterated and all blood flow is directed into the true lumen, potentially minimizing the distal progression of dissection. If the sinus segment and aortic valve are not involved, and the proximal aorta was previously normal, simple graft replacement of the tubular segment is performed. In most patients, this aortic resection includes the site of the original intimal tear. If there is calcific aortic valve disease with significant stenosis and a normal sinus segment, concomitant separate aortic valve replacement is performed. Aortic valve resuspension, rather than replacement, is attempted when aortic valvular insufficiency is secondary to dehiscence of one or more commissures from the aortic wall (43). In patients with annuloaortic ectasia and in all patients with Marfan syndrome, a composite valve graft is inserted. Concomitant coronary artery bypass is performed if the dissection extends into a coronary artery. In DeBakey type I (Stanford A) dissections, the entire transverse arch is involved. The mortality rate of transverse aortic arch replacement in acute dissections is 15.8%, contrasted to 3.5% mortality for the same repair in chronic dissections. Therefore, in the acute setting the transverse arch is addressed through a “hemi-arch” replacement, which is fashioned by beveling the distal anastomosis under the brachiocephalic vessels; the entire arch is replaced only if the transverse aortic arch is ruptured, contains the initiating intimal tear, or is severely dilated (44). Surgery is indicated for patients with acute DeBakey type III (Stanford B) dissections only when complications develop or medical management is unsatisfactory. Distal aortic repair in the presence of dissection is more complicated than in cases of fusiform degenerative aneurysms, and thus requires longer aortic clamp times and carries a higher risk of paraplegia and paraparesis. Therefore, left heart bypass is often used; this provides visceral and renal protection and may reduce spinal cord ischemia.

Graft replacement of the dissecting aneurysm includes resection of the weakest aortic segment, i.e., the site of the intimal tear, and the obliteration of the false lumen at the distal suture line. The resulting decompression of the false lumen frequently relieves arterial branch obstruction and prevents progression of the dissection. A thoracoabdominal aortic replacement, with reattachment of intercostal, lumbar, visceral, and renal vessels may be necessary, particularly if dissection is superimposed on a previously existing fusiform thoracoabdominal aortic aneurysm. Graft replacement of chronic DeBakey type III (Stanford B) dissections is performed when complications develop or when the false lumen expands to a diameter of 6 cm (5.5 cm in patients with Marfan syndrome). Because major arteries may branch off the false lumen, the distal anastomosis must direct blood flow into both lumina — otherwise, ischemic complications may result.

Transverse Aortic Arch Aneurysm The transverse aortic arch is the segment from which the brachiocephalic arteries arise; aneurysmal involvement of this segment is variable. Fusiform aneurysms of the ascending aorta can have limited involvement of the aortic arch in the region of the innominate artery, and those of the descending thoracic aorta can have aneurysmal involvement of the distal transverse arch including the left subclavian artery. In some cases, a saccular aneurysm develops opposite the origin of the brachiocephalic arteries off the lesser curvature of the arch; in other cases, there is a fusiform aneurysm of the entire aortic arch, sparing the ascending and descending aorta in some, while the entire aorta is diffusely aneurysmal (“mega-aorta”) in others. Although few dissections originate in the arch, the transverse aortic arch is commonly involved in dissections beginning in the ascending aorta and occasionally as proximal extension from distal dissections (45). Aneurysms in this region are usually medial degenerative in origin when fusiform, and atherosclerotic when saccular (46–48). Complications from aneurysms at this level are generally serious and result from compression of surrounding structure, rupture, or associated disease. The trachea and bronchi, pulmonary artery, and great veins are commonly compressed. Hoarseness from compression of the left recurrent laryngeal nerve is a common first symptom. Rupture occurs into the pericardium with tamponade, in the mediastinum or pleural cavity with fatal hemorrhage, or into the trachobronchial tree causing drowning. As in other segments, CT scanning and arteriography are the mainstays of diagnosis and evaluation of the extent of aneurysm involvement. Treatment is graft replacement undertaken electively following diagnosis to avoid the development of complications. The surgical approach depends on the extent of involvement and the need for cardiac and

Chapter 56 Thoracic Aortic Aneurysms

cerebral protection. Patients with distal involvement (the level of the left common carotid or left subclavian arteries and beyond) are approached through the left chest (49). Proximal aortic control is by simple cross-clamp while cardiovascular hemodynamics are controlled with sodium nitroprusside or nitroglycerin infusion. A doublelumen endotracheal tube is used for selective collapse of the left lung. Saccular aneurysms arising from the lesser curvature of the distal transverse arch that encompass less than 50% of the aortic circum-ference are treated by Dacron patch graft aortoplasty. Fusiform aneurysms are replaced with tube grafts to which separate side grafts are attached for reconstruction of the left subclavian or left common carotid artery as needed (50). When the vital aortic segment from which the innominate and left common carotid arteries arise is involved, technique must be used to protect critical organs, particularly the brain and heart, during the reconstruction period. For such cases we prefer to use circulatory arrest, which provides a dry, quiet surgical field unencumbered by clamps, bypass grafts, and tubes and reduces blood loss (51–53). Protection is provided by hypothermia achieved by cardiopulmonary bypass. Temperature is monitored in the nasopharynx, rectum, and esophagus; the cerebral electrical activity is continuously monitored with a 10lead surface electroencephalogram (EEG). We do not initiate circulatory arrest until the EEG is isoelectric (when the brain temperature is 20–21°C) (54). During circulatory arrest, we concomitantly utilize reversed cerebral perfusion via the superior vena caval cannula (55). Aortic arch aneurysms are preferentially approached through median sternotomy. However, when multiple previous median sternotomies have been performed in the same patient or large descending aneurysm pre-cludes staged repair, arch replacement can be accomplished through the left chest (49,56). Hypothermia is obtained with cardiopulmonary bypass by cannulating a femoral artery in the groin and both vena cavae in the chest. In selected cases of reoperation in which safe sternal reentry is not possible, cardiopulmonary bypass is established with the chest closed using femoral vein–femoral artery cannulation. Median sternotomy is then undertaken only after an appropriate safe level of hypothermia has been achieved and circulatory arrest initiated (53,57). Following exposure, hypothermia, and circulatory arrest, the patient is placed in a steep Trendelenburg position before the aneurysm is opened. This position prevents cerebral air embolism and eliminates unnecessary dissection and clamping of the brachiocephalic vessels. Sacciform aneurysms arising from the transverse arch that involve less than 50% of the aortic circumference are treated by patch aortoplasty using a Dacron patch that is either collagen-impregnated or treated with albumin. Fusiform aneurysms are treated with tube graft replacement with the distal anastomosis performed first end-toend to the proximal descending thoracic aorta. The brachiocephalic vessels are reattached to one or more openings made in the graft or are replaced with separate smaller grafts if they, too, are aneurysmsal. The graft is

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flushed of air and debris and clamped just proximal to the innominate artery as cardiopulmonary bypass and rewarming are resumed. The repair is completed with anastomosis to the proximal uninvolved ascending aorta, or proximal repair is undertaken based on principles previously outlined for the aortic root disease.

Aneurysm of the Descending Thoracic Aorta Aneurysms of this segment are most commonly secondary to medial degenerative changes, atherosclerosis, and aortic dissection. Other causes include trauma, aortitis, infection, and prosthetic dilation with coarctation. Aneurysms caused by medial degeneration tend to be fusiform and vary in length, and frequently have atherosclerosis superimposed. The abdominal aortic segment is involved separately in 25% of cases (48). Less commonly saccular aneurysms occur that tend to be more purely atherosclerotic in origin, with a propensity for development in the lower descending thoracic aorta. The left pleural cavity has the capacity to allow asymptomatic aneurysm expansion for variable periods of time, but eventually these lesions produce pain, dysphagia, hoarseness, hematemesis, or hemoptysis. Death occurs from rupture into the mediastinum, pleural cavity, esophagus, trachea, or bronchus in more than 80% of cases within 5 years of diagnosis (58,59). All patients are evaluated preoperatively for concurrent cardiac, renal, and pulmonary disease. Optimal medical management is achieved before surgical intervention. Patients are well hydrated prior to aortography, and operation is delayed for 24 to 48 h following dye studies in the asymptomatic patient. Operative treatment is recommended for all symptomatic patients and for all asymptomatic lesions that are twice the size of the normal adjacent aorta. The aorta is approached through a left posterior lateral thoracotomy, usually with resection of the fifth or sixth rib. Doublelumen tracheal intubation allows selective collapse of the left lung for improved expo-sure and reduces both pulmonary trauma from retraction and cardiac compression. The aneurysm is isolated between clamps and, as at other sites, saccular aneurysms are treated with patch grafts; fusiform lesions are treated with tube graft replacement using inclusion techniques (Fig. 56.5). Sodium nitroprusside and nitroglycerin infusions are used to maintain normal cardiac hemodynamics. Shed blood from the field is retrieved with an autotransfusion device that provides rapid cell washing and reinfusion.

Dissection The descending thoracic aorta is involved in most cases of aortic dissection (60,61). The origin of dissection is in the proximal descending thoracic aorta in about 26% of cases. When the origin of dissection is in the ascending aorta (62% of patients with dissection), distal extension

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B

FIGURE 56.5 Inclusion technique for graft replacement of descending thoracic aortic aneurysm using simple crossclamping and Dacron tube graft.

C

A D

F G E

A

B

C

FIGURE 56.6 (A) Type Ill aortic dissection and dilation of the false lumen. (B, C) Repair that includes preservation of distal intercostal arteries by beveling the graft and redirection of flow into the true lumen distally.

usually involves this segment. Ascending aortic involvement requires emergent surgical intervention, hut most cases arising in the proximal descending thoracic aorta can be initially treated medically with careful monitoring and blood pressure control as described by Wheat (60,62,63). Patients who do not respond to this type of

therapy — that is, who have continued pain, evidence of expansion of the false lumen, symptoms of arterial occlusion, or evidence of leak or rupture — are treated by immediate operation (Fig. 56.6). Surgical treatment is by graft replacement of the weakest aortic segment (i.e., the site of intimal tear, usually the very proximal descending

Chapter 56 Thoracic Aortic Aneurysms

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FIGURE 56.7 Technique for repair of aortic dissection involving the descending thoracic aorta using Dacron tube graft, proximal and distal clamping, and inclusion technique.

B

A

C

thoracic aorta) with restoration of flow back into the true lumen (Fig. 56.7). This is accomplished by sandwiching the two walls at the anatomic site with strips of Teflon felt. The latter decompresses the false lumen, which can relieve arterial branch obstruction and prevent progression of dissection. In the acute setting, extensive aortic replacement is often not required, which has the added benefit of maintaining normal flow through a maximum number of intercostal arteries. Patients who do respond to initial nonoperative management must continue meticulous control of blood pressure with medications that should include beta-blockers. In addition, they should be followed on a regular basis with CT surveillance for dilation of the false lumen. Over a period of 5 years, at least onethird will require surgical intervention. Surgical treatment in these cases is directed toward replacement of fusiform dilation of the outer lumen of the false channel. When required, operative treatment entails graft replacement of the dilated segment, which may include all or part of the descending aorta or abdominal aorta. In the chronic state, less attention needs to be directed toward reestablishing a single distal channel. The outer wall of the false lumen in the chronic phase may be strong enough to secure sutures, the walls are frequently too stiff to reapproximate, and the two lumina are often well established. In such instances a wedge of the partition between the two channels is removed distally before constructing the distal anastomosis so that flow may be directed down both lumina.

Aneurysms of the Thoracoabdominal Aorta Thoracoabdominal aortic aneurysms generally involve varying portions of both the descending thoracic and abdominal aortic segments, as demonstrated by Stanley Crawford’s classification based on extent (Fig. 56.8) (64). Although extent IV aneurysms — occasionally referred to as total abdominal aortic aneurysms — do not extend above the diaphragm, their repair requires access to the descending thoracic aorta to achieve proximal vascular control. Therefore, thoracoabdominal aortic aneurysms are best characterized by involvement of the aorta at the level of the diaphragmatic hiatus and the resulting need to clamp the thoracic aorta during repair. Accurate classification is important because the operative strategies, risks, and results are each dependent upon the extent of aortic replacement. Despite recent advances in endovascular approaches to the descending thoracic and abdominal aorta, conventional graft repair remains the treatment of choice for the more complex and extensive thoracoabdominal aortic aneurysms. Signs of impending or actual rupture, such as acute pain and hypotension, are clear indications for emergent repair. Hemoptysis and hematemesis may indicate rupture of the aneurysm into an adjacent pulmonary or gastrointestinal structure, respectively. In order to avoid the high mortality associated with rupture, thoracoabdominal aortic aneurysms — regardless of cause — are ideally repaired in the elective setting. Although we currently recommend elective repair once

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FIGURE 56.8 The Crawford classification of thoracoabdominal aortic aneurysms based on the extent of aortic involvement. Extent I thoracoabdominal aortic aneurysms begin near the left subclavian artery and extend down to encompass the aorta at the origins of the celiac axis and superior mesenteric arteries; the renal arteries may also be involved. Extent II aneurysms arise near the left subclavian artery and extend distally to the level of the aortic bifurcation. Extent III aneurysms involve the distal half of the descending thoracic aorta and the entire abdominal aorta. Extent IV aneurysms generally involve the entire abdominal aorta from the level of the diaphragm to the bifurcation. In patients with extent II, III and IV aneurysms, iliac artery aneurysms may exist in continuity with the abdominal component.

the aneurysm diameter exceeds 5.5 to 6.0 cm, applying such a specific size-based criterion to all patients has clear limitations. In an effort to better assess the risk of rupture in the individual patient, Juvonen et al. (65) recently developed a predictive model based on five risk factors: increasing age, diameter of the descending thoracic aorta, diameter of the abdominal aorta, chronic obstructive pulmonary disease, and the presence of symptoms. It is noteworthy that the symptoms found to be associated with an increased risk of rupture were characterized by experienced surgeons as being unrelated to the aneurysm. Therefore, the development of any symptoms — no matter how mild or uncharacteristic — in a patient with a thoracoabdominal aortic aneurysm demands immediate evaluation; the aneurysm must be considered the cause until proven otherwise. If the source of the problem remains unexplained, aneurysm repair should be considered. In patients with acute aortic dissection involving only the thoracoabdominal aorta (DeBakey type III), a nonoperative management strategy focuses on reducing the force of left ventricular ejection (dP/dT) (66,67). Similarly, following surgical repair of the ascending aorta in patients with DeBakey type I dissections, the distal dissection continues to be a threat and is therefore managed with aggressive dP/dT reduction. Classically, with appropriate medical therapy, only one-third of patients will ultimately require surgical intervention for distal aortic dissection. Indications for operation, in both the acute and chronic settings, include suspected rupture, con-

tinued pain despite intensive medical therapy, and evolving ischemic complications involving the kidneys, spinal cord, bowel, or legs. In patients with preexisting thoracoabdominal aortic aneurysms, superimposed acute dissection can produce pain that is impossible to distinguish from impending rupture and therefore warrants operative intervention. Nearly 25% of patients presenting with a thoracoabdominal aortic aneurysm have undergone previous thoracic aortic repairs (68). Data suggesting that sequential aortic operations carry increasing mortality rates have raised concerns regarding the appropriate management of such patients (69). A recent retrospective analysis demonstrated that previous thoracic aortic operations did not adversely affect the outcome of subsequent thoracoabdominal aortic aneurysm repair (68). Conversely, the group of 179 patients who had had prior thoracic aortic aneurysm repairs exhibited a trend toward lower mortality and fewer complications when compared with 544 patients without previous thoracic aortic repair. Prior thoracic aortic surgery, therefore, should not be considered a contraindication to thoracoabdominal aortic aneurysm surgery. An adequate preoperative assessment of physiologic reserve is critical in evaluating a patient’s operative risk and determining candidacy for surgery. Therefore, the cardiac, pulmonary, and renal systems are routinely thoroughly evaluated and optimized in all patients without acutely symptomatic aneurysms. Whenever possible, significant coronary artery disease is addressed by angio-

Chapter 56 Thoracic Aortic Aneurysms

plasty or operative revascularization prior to proceeding with aneurysm repair. In patients who have had a coronary artery bypass performed with the left internal mammary artery, a left carotid subclavian bypass is often required prior to thoracoabdominal aortic aneurysm repair in order to avoid cardiac ischemia upon crossclamping the transverse arch between the left common carotid artery and the left subclavian artery; alternatively, a subclavian to carotid transfer can be performed. In preparation for surgery, all patients undergo placement of a right radial arterial line for continuous pressure monitoring and access for blood sampling. A pulmonary artery catheter is placed via the right internal jugular vein and a second large-bore central venous access catheter is inserted for purposes of rapid fluid administration. A double-lumen endobronchial tube is positioned for selective right lung ventilation and left lung deflation. The patient is placed in a right lateral decubitus position with the shoulders at 60º and the hips rotated back to 30º; a beanbag underneath the patient is used to maintain this position. Preparing and draping ensures exposure of the left chest and abdomen from above the nipples to the midthigh and from the mid-back to the right anterior axillary line. Both inguinal areas should also be accessible. Our strategy for spinal cord protection — as described below in detail — involves moderate heparinization, selective left heart bypass, and aggressive reattachment of critical intercostal arteries. Mild hypothermia is also considered beneficial, therefore, no attempt is made to maintain normothermia during the repair; instead, the patient’s rectal temperature is allowed to drift down to between 32 and 33 ºC. We have not used naloxone, steroids, selective spinal cord cooling, or intrathecal papaverine. Cerebrospinal fluid drainage catheters are not used routinely. A cell-saving device is used throughout the case to salvage all shed blood from the operative field. If necessary, during periods of substantial blood loss, the device allows direct reinfusion of unwashed blood from the reservoir. It has been our preference to use citrate rather than heparin in the autotransfusion device; consequently, intermittent monitoring of the serum calcium level is important. In patients with aneurysms extending into the superior aspect of the thorax (extents I and II), the upper aspect of the thoracoabdominal incision is either through the sixth intercostal space or the bed of the resected sixth rib. An intermediate amount of exposure can be obtained by dividing the sixth rib posteriorly. With more distal aortic involvement (extents III and IV), incisions through the seventh through ninth interspaces are used. When the aneurysm extends only from the diaphragm to the aortic bifurcation (extent IV), a straight transverse incision through the ninth or tenth interspace is used. In all other extents, a gentle curve is required as the incision crosses the costal margin, in order to reduce the risk of tissue necrosis in this area. After entering the chest, the left lung is deflated and single lung ventilation is initiated. The diaphragm is

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divided in a circular fashion, protecting the phrenic nerve and preserving as much of the diaphragm muscle as possible. A 1- to 1.5-cm rim of diaphragmatic tissue is left intact laterally on the chest wall to allow secure closure at the completion of operative repair. Stable and consistent exposure is maintained with an assortment of self-retaining blades attached to a retractor arm that is secured to the operating table. The inferior costal margin and left lateral abdominal wall are reflected inferolaterally, while the upper chest wall is retracted toward the head. Abdominal aortic exposure is obtained using a transperitoneal approach. After entering the retroperitoneum lateral to the left colon, a dissection plane is developed in the retroperitoneum anterior to the psoas muscle and posterior to the left kidney. This dissection is carried directly to the left posterolateral aspect of the abdominal aorta and extends from the diaphragm to the aortic bifurcation. The plane of dissection from the lateral reflection of the peritoneum to the aorta is primarily avascular. The ureter is identified and carefully protected. The descending colon, spleen, left kidney, and tail of the pancreas are retracted anteriorly and to the right across the midline. An open abdominal approach allows for direct inspection of the abdominal viscera (particularly the spleen and the bowel) and their blood supply following completion of the aortic reconstruction. If necessary, the right kidney and its vasculature can easily be palpated and assessed. An entirely retroperitoneal approach is used in patients with a so-called “hostile” abdomen, e.g. multiple prior abdominal surgeries or a history of extensive adhesions and/or peritonitis. We have not encountered differences in fluid requirements, postoperative pulmonary function, or return of bowel function in patients who have undergone transperitoneal versus retroperitoneal exposures. In patients who have had prior abdominal aortic aneurysm repair, the left ureter may be incorporated in scar tissue along the old graft and particular care must be taken to preserve its integrity. In this setting, placement of a ureteral stent prior to operation may assist in its identification. After dividing the crus of the diaphragm, the left renal, superior mesenteric, and celiac arteries are identified; these vessels are not circumferentially dissected or encircled with tapes. A large lumbar branch of the left renal vein commonly courses posteriorly around the aorta and may be ligated and divided as needed. If a retroaortic left renal vein is encountered and the aortic repair will extend through the region, the vein is divided between vascular clamps. Direct reanastomosis or interposition graft repair of the retroaortic renal vein is necessary if left renal congestion occurs and distended testicular, ovarian, and adrenal collateral vessels develop. Heparin is administered intravenously (1 mg/kg) prior to placing the aortic cross-clamp or initiating left heart bypass. Potential benefits of heparinization include preservation of the microcirculation and prevention of embolization; we have not encountered increased bleeding or other morbidity related to the heparin. Following

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FIGURE 56.9 Preoperative drawing and aortogram demonstrating a Crawford extent II thoracoabdominal aortic aneurysm resulting from chronic aortic dissection. The patient has undergone composite valve graft replacement of the aortic root in the past.

this low heparin dose, the activated clotting time generally ranges from 220 to 270 seconds. Those patients with extensive thoracoabdominal aortic aneurysms (Crawford extents I and II, Fig. 56.9) are at greatest risk for the development of postoperative neurological deficits, i.e., paraplegia and paraparesis, resulting from intraoperative spinal cord ischemia. In these patients, therefore, we use left heart bypass to provide distal perfusion during the proximal portion of the repair, as advocated by several other authors (70–78). This is achieved by employing temporary bypass from the left atrium to either the femoral artery (most commonly the left) or the distal descending thoracic aorta with a closed circuit in-line centrifugal pump (Biomedicus, Medtronic, Inc., Eden-Prairie, MN). When the pericardium has been previously entered for coronary artery bypass grafting or valve replacement, access to the left atrium is obtained by cannulating the superior or inferior pulmonary vein. Cannulation of the distal descending thoracic aorta (usually at the level of the diaphragm) was initially used solely as an alternative to femoral artery cannulation in patients with

femoral or iliac arterial occlusive disease. Owing to the lack of complications using this technique and the elimination of femoral artery exposure and repair, distal aortic cannulation has become our preferred approach. Careful examination of the preoperative CT or MRI scan assists in the selection of an appropriate site for direct aortic cannulation, thereby avoiding areas with intraluminal thrombus that might embolize distally. Bypass flows are adjusted to maintain distal arterial pressures of 70 mmHg while maintaining normal proximal arterial pressure and normal venous filling pressures. Flows between 1500 and 2500 ml/min are generally adequate. Left heart bypass flows are targeted towards two-thirds of the baseline cardiac output, which is routinely measured shortly after induction. Additionally, the use of left heart bypass facilitates rapid adjustments in proximal arterial pressure and cardiac preload, thereby reducing the need for pharmacological intervention. In patients with primarily distal aortic aneurysms (extents III and IV), atrio-distal aortic bypass may be supplanted with atrio-visceral/renal bypass, which provides similar benefits: cardiac preload reduction, renal parenchymal protection, reduced post-clamp acidosis, and reduced bowel ischemia. The distal aortic arch is gently mobilized by dividing the remnant of the ductus arteriosus. The vagus and recurrent laryngeal nerves are identified. The vagus nerve may be divided distal to the take-off of the recurrent laryngeal nerve; this maneuver provides additional mobility to the latter nerve, consequently protecting it from injury. Preservation of the recurrent laryngeal nerve is particularly important in patients with chronic obstructive pulmonary disease and reduced pulmonary function. In these patients, injury to the nerve can impair the ability to cough effectively and may potentiate pulmonary complications. Vocal cord paralysis should be suspected in patients with postoperative hoarseness and confirmed by direct examination. Effective treatment can be provided by direct cord medialization (type I thyroplasty), or, in higher risk patients, Teflon injection (79). Careful circumferential dissection of the distal transverse aortic arch separates it from the adjacent pulmonary artery and esophagus. If cross-clamping proximal to the left subclavian artery is anticipated, the left subclavian artery is also mobilized circumferentially. As with all branch vessels, dissection is minimized and encircling tapes are avoided. For extent I and II thoracoabdominal aortic aneurysms, the proximal portion of the aneurysm is isolated between the proximal clamps and a distal clamp placed between T4 and T7 (Fig. 56.10). Distal aortic perfusion from the left heart bypass circuit provides arterial flow to the viscera, kidneys, lower extremities, and lower intercostal and lumbar arteries. The latter vessels provide flow to the spinal cord when the anterior spinal artery is not intact. The aneurysm is opened (Fig. 56.11) and prepared for the proximal anastomosis (Fig. 56.12). In cases of aortic dissection, the dissecting membrane is excised. The aorta is transected 1 cm distal to the proximal clamp

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FIGURE 56.10 After initiating left heart bypass, the proximal portion of the aneurysm is isolated by placing clamps (1) on the left subclavian artery, (2) between the left common carotid and left subclavian arteries, and (3) across the upper mid-descending thoracic aorta.

FIGURE 56.11 The isolated segment of aorta is opened using electrocautery.

and separated from the esophagus in order to allow full thickness suturing of the aortic wall while minimizing the risk of esophageal injury. Bleeding intercostal arteries at this level are ligated. A collagen-impregnated woven Dacron graft (Meadox Medical Inc., Oakland, NJ) is selected; 22- to 24-mm grafts are used in most patients. This and all remaining anastomoses are carried out using running 3–0 polypropylene suture (Fig. 56.13). Alternatively,

FIGURE 56.12 The dissecting membrane is excised and bleeding intercostal arteries are oversewn. The aorta is prepared for the proximal anastomosis by transecting it 1 cm distal to the proximal clamp and separating this portion from the esophagus.

4–0 polypropylene suture is used in patients with particularly fragile aortic tissues, such as patients with Marfan syndrome. Teflon felt strips are generally not used to reinforce the suture lines. As replacement of the aorta proceeds from proximal to distal, the distal aortic clamp may be sequentially

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moved to lower positions on the aorta in order to maintain the distal perfusion and restore proximal blood flow. Maintenance of distal perfusion reduces the severity of post-clamp acidosis and hyperkalemia. Sequential distal clamping, however, is often not feasible due to a variety of factors related to the severity of the aortic disease, includ-

FIGURE 56.13 The proximal anastomosis between the aorta and an appropriately sized Dacron graft is completed using continuous polypropylene suture.

ing aneurysm size and tortuosity, mural calcification, and intraluminal thrombus. Alternatively, left heart bypass may be discontinued following completion of the proximal anastomosis. The aneurysm is then opened longitudinally posterior to the left renal artery, to its distal extent (Fig. 56.14). A distal clamp is not used. With chronic dissection, careful yet complete removal of the dissecting mem-brane that separates the true and false lumina is necessary (Fig. 56.15). A Y-line off the arterial return tubing is attached to balloon perfusion catheters positioned within the origins of the celiac, superior mesenteric, and renal arteries (Fig. 56.16). This allows continued delivery of oxygenated blood from the pump circuit to the abdominal viscera and kidneys. With this technique, the total renal and visceral ischemic time can be reduced to just a few brief minutes during even the most complex aortic reconstructions. The potential benefits of reducing hepatic and bowel ischemia include decreased risks of postoperative coagulopathy and bacterial translocation respectively. One or more openings are made in the aortic graft and all patent intercostal arteries from T7 to L2 are reattached using continuous 3–0 monofilament suture (Fig. 56.16). The clamp may then be moved down on the graft to a position below the reattached intercostal arteries. If the visceral arteries are too close to the intercostal suture line to allow for proper positioning of the clamp between them, flow is restored temporarily to the intercostal arteries to allow spinal cord perfusion for a brief period of 3 to 5 minutes. The origins of the visceral arteries are then inspected. Visceral or renal arterial stenosis, which is encountered in at least 25% of cases, is addressed by either endarterectomy (if anatomically suitable) or interposition bypass grafting. In extent I repairs, the reattachment of the visceral arteries is often incorporated into the beveled distal anastomosis. In extent II and III repairs, however, the visceral and renal artery origins are reattached to one or more oval openings in the graft (Fig. 56.17). After completing this suture line,

FIGURE 56.14 After stopping the left heart bypass and removing the distal aortic cannula, the proximal clamp is repositioned onto the graft and the remainder of the aneurysm is opened.

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FIGURE 56.15 The rest of the dissecting membrane is excised and the openings to the celiac, renal, and superior mesenteric arteries are identified.

FIGURE 56.16 Selective visceral perfusion with oxygenated blood from the bypass circuit is delivered through balloon perfusion catheters placed in the celiac, renal, and superior mesenteric arterial ostea. The critical intercostal arteries are reattached to an opening cut in the graft.

FIGURE 56.17 In order to minimize spinal cord ischemia, the proximal clamp is repositioned distal to the intercostal reattachment site. A second oval opening is fashioned in the graft adjacent to the visceral vessels. Selective perfusion of the visceral arteries continues during their reattachment to the graft. A separate anastomosis is often required to reattach the left renal artery.

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Part VII Aortic and Peripheral Aneurysms FIGURE 56.18 After completing the visceral anastomosis, the balloon perfusion catheters are removed and the clamp is again moved distally, restoring flow to the celiac, renal, and superior mesenteric arteries. The final anastomosis is created between the graft and the distal aorta.

the balloon catheters are removed, the clamp is moved distally if possible, and the distal anastomosis is performed (Fig. 56.18). After completing the aortic repair, an inline heat exchanger in the bypass circuit may be employed to rewarm the patient and reduce the risk of arrhythmias or coagulopathy. In our experience, however, this has generally not been necessary. Alternatively, warm water may be used to irrigate the operative field, thereby reversing the downward temperature drift and initiating rewarming of the patient. Following completion of aortic repair (Fig. 56.19), protamine sulfate is administered to reverse the heparin. Bypass cannulae are then removed. It is imperative that adequate hemostasis is achieved and secured at all suture lines and cannulation sites. Renal, visceral, and peripheral perfusion is assessed. The remaining aneurysm wall is then loosely wrapped around the aortic graft and secured with a running suture. Bleeding through the interstices of modern collagen-sealed Dacron grafts, even in the presence of heparinization, is virtually nonexistent. Two thoracic drainage tubes are positioned posteriorly and a closed suction drain is placed in the retroperitoneum. The diaphragm is closed with running nonabsorbable suture (e.g. No. 1 polypropylene); postoperative diaphragmatic disruption is exceedingly rare. To stimulate and maintain renal function, a low-dose dopamine drip (2 to 3 mg per kg per min) is initiated and continued for 24 to 48 h. Patients are generally weaned from the respirator overnight and extubated the following morning. All drains are removed and antibiotics discontinued 36 to 48 h postoperatively. Ambulation is started on the second postoperative day. Mortality following surgical treatment of thoracoabdominal aortic aneurysms averages 13% for elective procedures and 47% for emergent operations. Intraoperative mortality is 4% to 5%, 30-day mortality 10% to 12%, and in-hospital mortality 12% to 15% (80–82). The incidence of postoperative renal dysfunction, defined as a

FIGURE 56.19 Drawing and aortogram demonstrating the completed graft repair of the thoracoabdominal aorta.

Chapter 56 Thoracic Aortic Aneurysms

significant increase in postoperative creatinine, averages 20% in reported series and ranges from 4% to 37% (81,82). A figure of 7% to 9% of patients required postoperative new onset hemodialysis. Prolonged ischemic times, extent of aorta replaced, and preoperative renal dysfunction with elevated creatinine are the primary variables associated with an increased risk of postoperative renal failure. During the period between January 11, 1986, and December 31, 2001, the author operated on a consecutive series of 1773 patients for treatment of aneurysm of the thoracoabdominal aorta. There were 1034 men (58.3%) and 739 women (41.7%). Mean age was 65.5 years (median 68 years) with a range of 18 to 88 years. A total of 1300 patients (73.3%) were treated for medial degenerative fusiform aneurysms or others of nondissection etiology. Acute dissection was present in 66 patients (3.7%) and chronic dissection occurred in 407 patients (23.0%). There were 126 patients (7.1%) with Marfan syndrome, and 109 patients (6.1%) presented with rupture. The extent of aortic replacement based on the Crawford classification included 580 with extent I (32.7%), 573 patients with extent II (32.3%), 291 patients with extent III (16.4%), and 329 patients with extent IV (18.6%). The 30-day overall survival was 94.3% and in-hospital survival was 92.9%. There were six (0.3%) intraoperative deaths. The overall incidence of paraplegia or paraparesis was 4.5% (79 patients). CSF drainage was not used in 173 (9.8%) patients. The incidence of paraplegia and paraparesis was evenly divided. Postoperative renal failure requiring hemodialysis occurred in 105 patients (5.9%); in 26 (24.8%), failure was temporary; and 29 patients (1.6%) suffered perioperative stroke. A total of 686 patients (38.7%) were operated on with the use of left heart bypass, i.e., atriofemoral bypass or femorofemoral bypass. In 573 patients with extent II aneurysms, the incidence of neurological deficit was 7.8% (44 patients). In patients with chronic aortic dissection, paraplegia and paraparesis developed in 3.4% versus 4.6% for patients with chronic fusiform medial degenerative disease. Consequently, the presence of chronic dissection is no longer a variable associated with the development of postoperative neurological deficits. However, in patients with acute dissection the incidence of spinal cord, ischemic sequelae remain high (5/66, 7.6%). Reattachment of intercostal arteries was accomplished in 61.0% of the entire group of patients, but, as a result of anatomic availability, was achieved as part of the repair in 79.9% of patients with extent I and II aneurysms. Preoperative, operative, and postoperative variables for this series were analyzed for development of postoperative neurological deficits and early (30-day) mortality. Multivariate analysis revealed that age, rupture, symptomatic aneurysm, preoperative renal insufficiency, and total clamp time were variables predictive of early mortality, whereas rupture,

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diabetes, and extent II were variables predictive of paraplegia or paraparesis. In this series of 1773 patients, left heart bypass and aggressive reattachment of lower intercostal and upper lumbar arteries substantially reduced postoperative paraplegia and paraparesis. The incidence of postoperative renal dysfunction remains a challenge. We recently reported on a group of patients undergoing Crawford extent II thoracoabdominal aortic aneurysm repair with left heart bypass randomized to renal artery perfusion of 4 °C lactated Ringer’s solution for renal cooling or normothermic blood perfusion from the left heart bypass circuit. Multivariate analysis confirmed that the use of cold crystalloid perfusion was independently protective against acute renal dysfunction (83). Ischemic spinal cord injury following repair remains a devastating complication. A total of 145 patients undergoing extent I or II thoracoabdominal repair with a consistent strategy of moderate heparinization, permissive mild hypothermia, left heart bypass, and reattachment of intercostals arteries were randomized to cerebrospinal fluid (CSF) drainage versus no CSF drainage. In that evaluation, nine patients (13%) in the control group developed either paraplegia or paraparesis while only two patients (2.6%) in the CSF drainage group developed deficits (84). A guiding principle for all patient management decisions involves determining whether the risk of the disease’s natural history outweighs the risk of its treatment. In the case of thoracoabdominal aortic aneurysm repair, this must be based on each individual’s risk of rupture without operation versus their risk of death or paraplegia with operation. A risk factor analysis of mortality and paraplegia after thoracoabdominal aortic aneurysm repair identified predictors of operative mortality to include preoperative renal insufficiency, increasing age, symptomatic aneurysm, and extent II aneurysms, while extent II aneurysms and diabetes were predictors of paraplegia. For patients who are acceptable candidates, contemporary surgical management provides favorable results.

References 1. Chen JT. Plain radiographic evaluation of the aorta. J Thorac Imaging 1990;5:1–17. 2. Petasnick JP. Radiologic evaluation of aortic dissection. Radiology 1991;180:297–305. 3. Engberding R, Bender F, et al. Identification of dissection or aneurysm of the descending thoracic aorta by conventional and transesophageal two-dimensional echocardiography. Am J Cardiol 1987;59:717–719. 4. Egen TJ, Neiman HL, et al. Computed tomography in the diagnosis of aortic aneurysm, dissection or traumatic injury. Radiology 1980;136:141–146. 5. Crawford ES, Coselli JS, et al. The impact of renal fusion and ectopia on aortic surgery. J Vasc Surg 1988;8:375–383.

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6. Godwin JD, Breiman RS, Speckman JM. Problems and pitfalls in the evaluation of thoracic aortic dissection by computed tomography. J Comput Assist Tomogr 1982;6:750–756. 7. Akins EW, Carmichael MJ, et al. Preoperative evaluation of the thoracic aorta using MRI and angiography. Ann Thorac Surg 1987;44:499–507. 8. Svensson LG, Crawford ES, et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357–370. 9. Bommer W, Miller L. Real time two-dimensional color flow Doppler: enhanced Doppler flow imaging in the diagnosis of cardiovascular disease. Am J Cardiol 1982;49:944. 10. Huston KA, Hunder GG, et al. Temporal arteritis: a 25year epidemiologic, clinical, and pathologic study. Ann Intern Med 1978:88:162–167. 11. Austen WG, Blennerhassett JR. Giant-cell aortitis causing aneurysm of the ascending aorta and aortic regurgitation. N Engl J Med 1965;272:80–83. 12. Lupi-Herrera E, Sancher-Torres G, et al. Takayasu’s arteritis: clinical study of 107 cases. Am Heart J 1977; 93:94–103. 13. Ishikawa K. Natural history and classification of occlusive thromboaortopathy, Takayasu’s disease. Circulation 1978;57:27–35. 14. Nasu T. Pathology of pulseless disease, a systematic study and critical review of twenty-one autopsy cases reported in Japan. Angiology 1962:14:225–242. 15. Robbs JV, Human RR, Rajaruthnam P. Operative treatment of nonspecific aortitis (Takayasu’s arteritis). J Vasc Surg 1986:3:605–616. 16. Johansen K, Devin J. Mycotic aortic aneurysms. Arch Surg 1983;118:583. 17. Brow SL, Busuttel RW, et al. Bacteriologic and surgical determinants of survival in patients with mycotic aneurysms. J Vasc Surg 1984;1:541–547. 18. Johansen K, Devin J. Mycotic aortic aneurysms. Arch Surg 1983;118:583–588. 19. Chan FY, Crawford ES, et al. In-situ prosthetic graft replacement for mycotic aneurysm of the aorta. Ann Thorac Surg 1989;47:193–203. 20. James EC, Gillespie JT. Aortic mycotic abdominal aneurysm involving all visceral branches: excision and Dacron graft replacement. J Cardiovasc Surg 1977;18:353–356. 21. Brandt B, Marvin WJ Jr, et al. Surgical treatment of coarctation of the aorta after balloon angioplasty. Thorac Cardiovasc Surg 1987;94:715–719. 22. Abbot ME, Hamilton WE. Coarctation of the aorta of the adult type: a statistical study and historical retrospect of 200 recorded cases with autopsy of stenosis or obliteration of the descending aortic arch in subjectsabove the age of two years. Am Heart J 1928:3:381–421. 23. Edwards JE, Burchell HR. The pathological anatomy of deficiencies between the aortic root and the heart, including aortic sinus aneurysms. Thorax 1957:12:125–139. 24. Sawyers JL, Adams JE, Scott HW Jr. Surgical treatment for aneurysms of the aortic sinuses with aorticoatrial fistula. Surgery 1957:41:26–42. 25. Nowicki ER, Aberdeen E, et al. Congenital left aortic sinuses, left ventricle fistula and review of aorto-cardiac fistulas. Ann Thorac Surg 1977;23:378–388.

26. Meyer J, Wukasch DC, et al. Aneurysm and fistula of the sinus of Valsalva: clinical considerations and surgical treatment in 45 patients. Ann Thorac Surg 1975:19:170–179. 27. Shumacker HE, King H, Waldhausen JA. Transthoracic approach for the repair of ruptured aneurysms of the sinus of Valsalva. Ann Surg 1965;161:946–954. 28. Roberts WC. Aortic dissection: anatomy, consequence and causes. Am Heart J 1981;101:195–214. 29. Gerry JL Jr, Morris L, Pyeritz RE. Clinical management of the cardiovascular complications of the Marfan syndrome. J LA State Med Soc 1991;143:43. 30. Moreno-Cabral CE, Miller DC, et al. Degenerative and atherosclerotic aneurysms of the thoracic aorta. Determinants of early and late surgical outcome. J Thorac Cardiovasc Surg 1984;88:1020–1032. 31. McCready RA, Pluth JR. Surgical treatment of ascending aortic aneurysms associated with aortic valve insufficiency. Ann Thorac Surg 1979;28:307–316. 32. Symbas TN, Rauner AE, et al. Aneurysms of all sinuses of Valsalva in patients with Marfan’s syndrome. Ann Surg 1971:174:902–907. 33. Bentall H, DeBono A. A technique for complete replacement of the ascending aorta. Thorax 1968;23:338–339. 34. Meyer JE Jr, Lindsay WG, et al. Composite replacement of the aortic valve and ascending aorta. J Thorac Cardiovasc Surg 1978;76:816–823. 35. Kouchoukos NT, Marshall WG Jr, Wedige-Stecher TA. Eleven-year experience with composite valve graft replacement of the ascending aorta and aortic valve. J Thorac Cardiovasc Surg 1986;92:691–705. 36. Helseth HK, Haglin JJ, et al. Results of composite graft replacement for aortic root aneurysm. J Thorac Cardiovasc Surg 1980:80:754–759. 37. Svensson LG, Crawford ES, et al. Composite valve graft replacement of the proximal aorta: comparison of techniques in 348 patients. Ann Thorac Surg 1992;54:427–439. 38. Coselli JS, Crawford ES. Technical Mini-Symposium: composite AVR and graft replacement of the ascending aorta plus coronary ostial reimplantation: how I do it. Semin Thorac Cardiovasc Surg 1993;5:55–62. 39. DeBakey ME, Henley WS, et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:130–149. 40. Daily PO, Trueblood HN, et al. Management of acute aortic dissection. Ann Thorac Surg 1970;10:237– 247. 41. Mist AE Jr, Johns VL Jr, Kime SW Jr. Dissecting aneurysm at the aorta: a review of 505 cases. Medicine 1958;37:217–279. 42. Crawford ES, Svensson LG, et al. Aortic dissection and dissecting aortic aneurysms. Ann Surg 1988; 208:254. 43. Koster JK, Cohn LM, et al. Late results of operation for acute aortic dissection producing aortic insufficiency. Ann Thorac Surg 1978;26:461–467. 44. Crawford ES, et al. Surgery for acute ascending aortic dissection: Should the arch be included? J Thorac Cardiovasc Surg 1992;104:46. 45. Tharion J, Johnson DC, et al. Profound hypothermia with circulatory arrest: nine years clinical experience. J Thorac Cardiovasc Surg 1982;84:66–72.

Chapter 56 Thoracic Aortic Aneurysms 46. Crawford ES, Stowe CL, et al. Aortic arch aneurysm, a sentinel of extensive aortic disease requiring subtotal and total aortic replacement. Ann Surg 1984;199:742– 752. 47. Crawford ES, Saleh SA, Schuessler JS. Treatment of aneurysm of transverse aortic arch. J Thorac Cardiovasc Surg 1979;78:383–393. 48. Crawford ES, Cohen ES. Aortic aneurysm: a multifocal disease. Arch Surg 1982:117:1393–1400. 49. Crawford ES, Coselli JS, Safi HJ. Partial cardiopulmonary bypass, hypothermic circulatory arrest, and posterolateral exposure for thoracic aortic aneurysm operation. J Thorac Cardiovasc Surg 1987;94:824– 827. 50. Crawford ES, Coselli JS. Replacement of the aortic arch. Semin Thorac Cardiovase Surg 1991;3:194– 202. 51. Griepp RB, Stinson ER, et al. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg 1975;70:1051–1063. 52. Crawford ES, Snyder DM. Treatment of aneurysms of the aortic arch: a progress report. J Thorac Cardiovasc Surg 1983;85:237–246. 53. Lillehei CW, Todd DR Jr, et al. Partial cardiopulmonary bypass, hypothermia, and total circulatory arrest. J Thorac Cardiovasc Surg 1969:58:530–544. 54. Coselli JS, Crawtord ES, et al. Determination of brain temperatures for safe circulatory arrest during cardiovascular operation. Ann Thorac Surg 1988;45:638 642. 55. Ueda Y, Miki S, et al. Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovase Surg 1990;31:553–558. 56. Massimo CG, Poma AG, et al. Simultaneous total aortic replacement from arch to bifurcation: experience with six cases. Tex Heart Inst J 1986;13:147–151. 57. Crawford ES, Crawford JL, et al. Redo operations for recurrent aneurysmal disease of the ascending aorta and transverse aortic arch. Ann Thorac Surg 1985;40:439–455. 58. Bickerstaff LK, Pairolero PC, et al. Thoracic aortic aneurysms: a population-based study. Surgery 1982;92:1103–1108. 59. McNamara JJ, Pressle VM. Natural history of atherosclerotic thoracic aortic aneurysms. Ann Thorac Surg 1978;26:468–473. 60. Wheat MW Jr. Acute dissecting aneurysms of the aorta: diagnosis and treatment. Am Heart J 1980;99:373– 387. 61. Svensson LG, Crawford ES, et al. Dissection of the aorta and dissecting aortic aneurysm: improving early and long-term surgical results. Circulation 1990;82:IV24–IV-38. 62. Wheat MW Jr. Acute dissecting aneurysm of the aorta: medical therapy current status. World J Surg 1980;4:563–569. 63. Glover DD, Fann JL, et al. Comparison of medical and surgical therapy for uncomplicated descending aortic dissection. Circulation 1990;82 (Suppl IV):IV-39– IV-50. 64. Crawford ES, Crawford JL, Safi HJ, et al. Thoracoabdominal aortic aneurysms: preoperative and intra-

65.

66.

67. 68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

81.

82.

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operative factors determining immediate and long-term results of operation in 605 patients. J Vasc Surg 1986;3:389. Juvonen T, Ergin MA, et al. Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 1997;63:1533. Fuster V, Ip JH. Medical aspects of acute aortic dissection. Semin Thorac Cardiovasc Surg 1991;3: 219. Hogan PJ. Medical management of dissecting thoracic aneurysms. Tex Heart Inst J 1990;17:281. Coselli JS, Poli de Figueiredo LF, LeMaire SA. Impact of previous thoracic aneurysm repair on thoracoabdominal aortic aneurysm management. Ann Thorac Surg 1997;64:639. Gloviczki P, Pairolero P, et al. Multiple aortic aneurysms: the results of surgical management. J Vasc Surg 1990;11:19. Bavaria JE, Woo YJ, et al. Retrograde cerebral and distal aortic perfusion during ascending and thoracoabdominal aortic operations. Ann Thorac Surg 1995;60:345. Frank SM, Parker SD, et al. Moderate hypothermia, with partial bypass and segmental sequential repair for thoracoabdominal aortic aneurysm. J Vasc Surg 1994;19:687. Griepp RB, Ergin MA, et al. Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabominal aorta. J Thorac Cardiovasc Surg 1996;112:1202. Hessmann M, Dossche K, et al. Surgical treatment of thoracic aneurysm: a 5-year experience. Cardiovasc Surg 1995;3:19. Jacobs MJHM, de Mol BAJM, et al. Retrograde aortic and selective organ perfusion during thoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 1997;14:360. Kitamura M, Hashimoto A, et al. Operation for type B aortic dissection: introduction of left heart bypass. Ann Thorac Surg 1995;59:1200. Morishita K, Inoue S, et al. Our distal aortic perfusion system in descending thoracic and thoracoabdominal aortic aneurysm repairs. Artif Organs 1997;21:822. Safi HJ, Campbell MP, et al. Cerebral spinal fluid drainage and distal aortic perfusion decrease the incidence of neurological deficit: the results of 343 descending and thoracoabdominal aortic aneurysm repairs. Eur J Vasc Endovasc Surg 1997;14:118. Schepens MA, Defauw JJ, et al. Use of left heart bypass in the surgical repair of thoracoabdominal aortic aneurysms. Ann Vasc Surg 1995;9:327. Rosingh HJ, Dikkers FG. Thyroplasty to improve the voice in patients with a unilateral vocal cord paralysis. Clin Otolaryngol 1995;20:124. Svensson LG, Crawford ES, et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357. Panneton JM, Hollier LH. Basic data underlying clinical decision making. Section ed. Lloyd M. Taylor Jr. Ann Vasc Surg 1995;9:503. Coselli JS. Thoracoabdominal aortic aneurysms: experience with 372 patients. J Card Surg 1994; 9:638.

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83. Koksoy C, LeMaire SA, et al. Renal perfusion during thoracoabdominal aortic operations: cold crystalloid is superior to normothermic blood. Ann Thorac Surg 2002;73:730.

84. Coselli JS, LeMaire SA, et al. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg 2002; 35:631.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 57 Endovascular Repair of Thoracic Aortic Aneurysms and Dissections Frank R. Arko and Christopher K. Zarins

The incidence of thoracic aortic aneurysms has increased since the early 1970s. Most patients with thoracic aneurysms have additional serious medical comorbidities that make them high-risk surgical candidates. The results of endovascular repair of abdominal aortic aneurysms indicate that stent–graft techniques, compared with conventional open repair, are associated with decreased morbidity, shorter hospitalizations, and a more rapid and less painful recovery from surgery (1–2). Thoracotomy for repair of thoracic aortic aneurysms is associated with an even higher risk of morbidity and mortality than conventional repair of abdominal aortic aneurysms. This is particularly true in patients with significant cardiopulmonary disease. The adaptation of stent–graft technology to the treatment of thoracic aneurysms is limited because most aneurysms that involve the descending thoracic aorta extend into the visceral segment of the aorta. However, in select patients whose aneurysm ends above the celiac axis, endovascular repair of thoracic aortic aneurysms offers the possibility of reducing morbidity and mortality by avoiding thoracotomy. In less than a decade, endovascular stent–graft therapy of abdominal aortic aneurysms has progressed from the placement of custom-crafted, home-made devices to an established therapy with commercially manufactured stent–grafts. Similar technology has been applied to thoracic aortic aneurysms and dissections but no devices approved by the US Food and Drug Administration

(FDA) are available at the present time. Endovascular stent–grafts of thoracic aneurysms and dissections offer an attractive alternative to open surgical repair that may potentially reduce the operative risk, hospital stay, and procedural cost in selected patients. Current clinical trials of commercially manufactured devices have been initiated to treat patients with descending thoracic aortic aneurysms. Results will be compared with those achieved in an enrolled group of contemporary surgical controls to better determine the effectiveness of stent–graft therapy and quantitate any benefits. However, the results of these studies are currently not available. This chapter outlines the indications for endovascular repair of thoracic aneurysms, patient selection, preoperative assessment, device selection, operative approaches, and postoperative considerations. Furthermore, we will address the use of endovascular stent grafts in the treatment of aortic dissection. Early results of endovascular repair, current trends, and future perspectives are also considered.

Natural History of Descending Thoracic Aortic Aneurysms Aneurysms of the descending thoracic aorta are typically associated with atherosclerosis and degenerative changes in the aortic wall. These aneurysms are typically fusiform

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in nature. However, saccular aneurysms may result from penetrating atherosclerotic ulcers or other causes of localized aortic wall compromise. Trauma, infection, dissection of the aortic wall, and autoimmune inflammatory arteritis can all cause aneurysmal degeneration of the thoracic aorta. The natural history of descending thoracic aortic aneurysms is progressive enlargement and rupture. Mural thrombus and calcification do not protect against rupture (3). Descending thoracic aortic aneurysms are typically asymptomatic and are typically detected incidentally on routine chest radiographs or other diagnostic imaging studies. Occasionally they can be symptomatic if mechanical compression of adjacent structures is present or distal embolization from the aneurysm occurs. Pain located in the chest, abdomen, flank, or back is the most common complaint. Compression of the trachea or bronchus may produce wheezing, cough, and pneumonitis distal to the area of obstruction. Erosion into the pulmonary parenchyma or airway may result in hemoptysis. Similarly, compression or erosion of the esophagus may produce dysphagia or hematemesis. Verterbral body erosion may be present and cause back pain, and, in some of these patients, neurologic deficits may occur spontaneously from spinal cord compression. Unless elective repair is performed for these patients, the long-term outlook is poor. The actuarial 5-year survival rate for patients with untreated thoracic aortic aneurysms is 9% to 13% (3–5).

Conventional Open Surgical Repair Operative repair is the treatment of choice in the patient with a descending thoracic aorta measuring 6 cm or more in diameter, or twice the diameter of the adjacent normal aorta. This requires a thoracotomy, excision of the aneurysm, and graft replacement. If the aneurysm extends into the visceral segment of the aorta, then visceral artery reconstruction is required as well. Complications of operative repair may vary depending on multiple factors, including the extent of aneurysmal disease and patient comorbidities. The mortality rate for elective repair of descending thoracic aortic aneurysms was 12% in a large single institutional study (5). The mortality rate for emergent repair of ruptured descending thoracic aortic aneurysms is 50% for patients who survive the acute event and do not die in an emergency room (3–5). Other significant complications of direct surgical repair include stroke, paraplegia, and renal, cardiac, and pulmonary failure.

Endovascular Stent–Graft Repair Endovascular repair of descending thoracic aortic aneurysms offers the advantages of reduced procedurerelated complications and mortality rates, decreased

length of hospital stay, and less expensive treatment than conventional operative repair. The first series of patients to undergo endovascular treatment of thoracic aneurysms was reported by Dake and colleagues in 1994 (4). Thirteen consecutive patients were treated for atherosclerotic, anastomotic, and post-traumatic aneurysms and for aortic dissections. Custom-made stent–grafts were made from self-expanding stainless steel stents and woven Dacron grafts. Device placement was successful in all 13 patients. No deaths or instances of paraplegia, distal embolization, or infection occurred during a mean follow-up of 12 months. Stent–grafts have been used successfully to treat acute ruptures of the descending thoracic aorta and posttraumatic aneurysms (7–12). Eleven patients had acute descending thoracic aortic ruptures treated with endoluminal stent–grafts. Eight patients (73%) had ruptures from aneurysms, and three (27%) had ruptures from trauma. There were no perigraft leaks, stent migrations, paraplegia, or intraoperative deaths. Two deaths occurred during the follow-up period, neither of which was related to the aneurysm or stent–graft procedure (7).

Patient Selection and Preoperative Assessment Indications for endoluminal stent–graft repair include aneurysms, penetrating ulcers, and dissections of the descending thoracic aorta. Most patients with aneurysms of the descending thoracic aorta typically have multiple severe comorbidities including severe chronic obstructive pulmonary disease, cardiomyopathy, congestive heart failure, renal disease, and/or advanced age. Endoluminal repair of thoracic aneurysms are currently performed at relatively few research centers through clinical trials approved by institutional review boards or the FDA. Patients who do not meet the criteria for enrollment in clinical trials, and who are high-risk surgical candidates, precluding open surgical repair, may have approval for compassionate use of devices granted by institutional review boards, the FDA, and the medical device industry. Successful treatment of descending thoracic aneurysms requires accurate preoperative assessment of the proximal and distal aortic neck as well as the morphology and dimensions of the aneurysm. Measurements needed to select or construct a stent–graft of appropriate dimensions for a given aneurysm include the proximal neck length below the left subclavian artery, aneurysm length, distal neck length above the celiac axis, and proximal and distal neck diameters. To be eligible as a candidate for endoluminal repair, a patient must have an adequate proximal and distal aneurysm neck, each at least 20 mm long and no more than 40 mm in diameter, for device fixation. Imaging of the entire aorta from the ascending arch to the femoral bifurcation is necessary. This rules

Chapter 57 Endovascular Repair of Thoracic Aortic Aneurysms and Dissections

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B

FIGURE 57.1 Computed tomography demonstrating a distal descending thoracic aneurysm (A) before and (B) after stent–graft repair. Post-procedure the aneurysm is completely excluded without evidence of endoleak.

out the possibility of other aneurysms as well as imaging the access vessels. About 20% to 30% of thoracic aortic aneurysms have associated abdominal aortic aneurysms (13). Severely diseased or noncompliant iliac arteries may preclude a femoral artery approach to the aorta. Most devices are delivered through 24 Fr. to 27 Fr. catheters. Thus, external iliac arteries should be at least 8 mm in diameter. If the access vessels are small, then a conduit to the common iliac artery or aorta may be required.

Imaging Studies Imaging studies helpful for assessing descending thoracic aortic aneurysms include spiral computed angiography, magnetic resonance angiography, standard aortography, transesophageal ultrasonography, and intravascular ultrasound. Volumetric spiral CT and MRA data can be used to study endoluminal surface detail and measure center-of-flow aortic length, accurate cross-sectional diameters of proximal and distal aortic necks, and aneurysm volume and angulation (Fig. 57.1). Aortography with digital subtraction provides excellent images for evaluating the left subclavian artery position relative to the proximal aneurysm neck. Length measurements during aortography can be performed

using a pigtail marker catheter. Furthermore, it delineates the contours of the endoluminal aortic surface, defines tortuosity, and identifies patent intercostal arteries. If a dominant intercostal artery is present in the lower thoracic aorta near the hiatus of the diaphragm, the artery should be preserved if possible. This is in an attempt to avoid anterior spinal cord ischemia and paraplegia. Magnetic resonance angiography utilizes gadolinium, which is not nephrotoxic. Patients with renal insuffiency, and a creatinine greater than 1.5 mg/dl should be considered for MRA over CT angiography. This will avoid the use of iodinated contrast that is given with CT.

Device Selection Devices are selected on the basis of the preoperative and intraoperative measurements, availability, and any access limitations imposed by the iliac arteries. A number of graft types have been tested. Basic designs include graft with an internal stent at each end, without columnar support, graft with internal tandem stents, graft with metallic endoskeleton, and graft with metallic exoskeleton. Both polyester and polytetrafluoroethylene (PTFE) graft materials have been used extensively. Self-expanding and balloon-expandable stainless-steel and nitinol stents have

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been used. No long-term data have proved the superiority of one device over another. Current devices in clinical trials include the AneuRx (Medtonic, Santa Rosa, CA), Talent (Medtronic/World Medical, Sunrise, FL) and Gore (Phoenix, AZ). Currently none of the devices is FDA approved for commercial use. Device delivery systems vary among the various stent–grafts. The most common delivery mechanism is the delivery sheath. The larger diameter device requires a larger sheath. Sheaths up to 28 Fr. are required for stents grafts of 46 mm diameter.

Operative Approaches and Technical Considerations Endovascular repair of thoracic aneurysms can be performed either in the interventional suite or the operating room. The operating room may be advantageous if immediate operative intervention is required should the aneurysm rupture during device manipulation. A C-arm fluoroscope with digital subtraction capability is the minimum system required for adequate imaging. Transesophageal echocardiography is also used for cardiac monitoring and to confirm proximal and distal aneurysm necks. Patients are positioned appropriately as for a thoracotomy or thoracoabdominal exposure. The right chest and upper torso is elevated 70° and 90° and the hips and pelvis are left as flat as possible. A right axillary roll is used for protection as well. The patient is prepared from the chest to the knees. The most commonly used approach for placing thoracic aortic endografts is through the femoral artery. A transverse incision in the groin is typically used and made just below the inguinal ligament. The artery is mobilized and controlled proximally and is punctured with a 0.035inch guidewire that is advanced into the thoracic aorta. An introducer sheath is advanced over the guidewire into the iliac system. The contralateral femoral artery is punctured percutaneously and a 0.035-inch guidewire is advanced and a 5-Fr. sheath placed. A marker pigtail catheter is then advanced into the thoracic aorta and an aortogram is obtained to image the proximal aortic neck distal to the left subclavian artery and distal aortic neck proximal from the celiac axis. Intravascular ultrasound may be used if additional aortic diameter measurements are needed, as well as to limit the amount of contrast required during the placement of the device. An appropriate-sized device is selected and advanced into the thoracic aorta over a stiff guidewire. For those devices without a tapered tip it is often safer to deliver the device through a delivery sheath. The stent–graft is then positioned under fluoroscopy. The use of road-mapping, transesophageal echocardiography, and bony landmarks can be helpful for reference. The device is deployed such that the proximal and distal fixation between the device

FIGURE 57.2 Three-dimensional reconstruction of CT angiogram in a patient with a distal descending thoracic aortic aneurysm that underwent endovascular stent–graft repair. Patient was a prohibitive operative risk secondary to coronary artery disease with a 15% ejection fraction and severe chronic obstructive pulmonary disease.

and the aorta is maximized (Figs. 57.2 and 57.3). Following successful deployment, a completion angiogram is performed to ensure adequate device position and patency. The presence or absence of endoleaks is also evaluated at this time. If preoperative assessment determines that the iliac or femoral arteries are too small, diseased, or tortuous for a femoral approach, an external iliac or common iliac artery can be used for aortic access. This involves making an incision proximal to the inguinal ligament for mobilization and control of the common, external, and internal iliac arteries. The external iliac artery is punctured as described above for the femoral approach. If the external iliac artery is too small, the common iliac artery can be used for access. This typically requires the placement of 10-mm tube graft sewn in an end-to-side fashion to the common iliac artery. This maneuver usually facilitates passage of the delivery sheath. Femoral and iliac artery access sites are generally repaired primarily. Side-limb grafts sewn to a common iliac artery are removed, and the iliac artery is repaired with a patch angioplasty. If an intimal flap is created during dilation of the femoral or iliac artery, endarterectomy and patch angioplasty may be required. In rare instances, significant arterial injury may require an interposition graft to restore flow to the limb. Some patients may have a combination of aneurysms involving both the descending thoracic aorta as well as the infrarenal aorta. If these patients are not candidates for endovascular abdominal aortic aneurysm repair, then replacement of the infrarenal aortic segment can be

Chapter 57 Endovascular Repair of Thoracic Aortic Aneurysms and Dissections

FIGURE 57.3 Three-dimensional reconstruction of CT angiogram post-procedure in the above patient following endovascular stent–graft repair with an AneuRx (Medtronic, AVE) stent–graft. There is excellent proximal and distal fixation of the stent–graft without evidence of endoleak. Access was obtained from the left common iliac artery. The patient tolerated the procedure well and was discharged on the second postoperative day.

A

691

performed through a retroperitoneal approach with placement of 10-mm graft sewn in an end-to-side fashion to the aortic graft. The end of the 10-mm graft is oversewn and then tunneled through the abdominal musculature. After recovery from the infrarenal abdominal aortic aneurysm repair, the 10-mm graft can be isolated under local anesthesia, an embolectomy of the graft is then performed, and the limb is used to access the thoracic aorta. After insertion of the thoracic graft the side-limb is oversewn and buried below the abdominal musculature. The best strategy is to approach the aorta through the smallest artery that can accommodate the device delivery system. If the external iliac artery is heavily calcified, tortuous, or small, initial exposure of the common iliac artery for access is the wisest approach and may markedly simplify the procedure and avoid unnecessary blood loss. If the proximal aneurysm neck arises less than 15 mm from the origin of the left subclavian artery, surgical transposition of the artery is necessary for adequate proximal neck fixation. Left subclavian to common carotid artery transposition can be performed to allow the proximal end of the graft to cover the left subclavian orifice for better proximal fixation (Fig. 57.4). Following thoracic aortic endograft repair through the femoral arteries, patients are managed in a monitored setting overnight. An oral diet is typically started the evening of surgery. Patients are encouraged to begin walking on the first postoperative day and are discharged home

B

FIGURE 57.4 Repair of thoracic aneurysm using endovascular stent–graft. (A) Preoperatively, the proximal neck fixation was increased by transposition of the left subclavian artery to the left common carotid artery. (B) Completion arteriogram demonstrates patent left subclavian transposition and complete exclusion of the thoracic aneurysm with an endovascular stent graft.

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on the second postoperative day. A chest radiograph and CT angiogram are obtained before hospital discharge to document the position of the device and the presence or absence of endoleaks. Clinic visits and CT angiograms are secheduled at 1, 3, 6, and 12 months after operation to assess the patient’s progress and device function.

Thoracic Aortic Dissections One of the other applications for thoracic aortic stent–grafts is the treatment of patients with aortic dissections. This is especially true in the setting of acute type B dissections as well as for chronic dissections with coexisting descending aortic false lumen aneurysms (14–16). For both cases, a successful outcome is dependent on obliteration of the primary entry tear of the dissection by placement of the prosthesis within the true lumen across the entry tear. Stent–graft coverage of the entry site closes the primary communication to the false lumen and its flow is diminished or obliterated. In acute type B dissection, the true lumen immediately increases in diameter without a corresponding incremental change in the overall aortic diameter. Distally, any branch vessel involvement of abdominal aortic true lumen arteries compromised by the dissection is reversed after stent–graft placement. For both acute and chronic dissections, stagnant blood in the thoracic aortic false lumen clots and, in the majority of patients, progressive thrombosis of the false lumen proceeds from the proximal aspect of the involved thoracic aorta distally. The overall rate of this process is variable and is based on the size of the false lumen, branch vessel distribution, and the amount of residual thoracic aortic false lumen flow via uncovered additional tears in the thoracic dissection flap. In terms of the procedure, there are some technical challenges related specifically to the aortic dissection when stent–graft therapy is considered. Specifically, the diameter and length of the prosthesis is a common issue. Since the true lumen is only a fraction of the overall aortic diameter, accurate diameter measurements can be difficult. The diameter of the nondissected aorta immediately proximal to the entry tear is a good estimate of the original size of the proximal involved segment prior to dissection. This measurement plus an oversize of 10% to 20% to ensure secure fixation is the approximation of device size most frequently used in practice. Regarding device length, most investigators implant devices that are longer than the entry tear. Most devices range between 10 and 15 cm long. This added length confers an appearance that is anatomically correct and promotes a rapid formation of thrombus within the false lumen. However, extension of the device into the distal one-third of the thoracic aorta should be avoided, to decrease the risk of spinal cord ischemia. In those cases of aortic dissection when the primary entry site is within 10 mm of the left subclavian artery, a device with a proximal segment consisiting of a bare stent

can be placed across the left subclavian artery to effectively maximize the length of graft fixation with the aortic wall. However, if there is retrograde proximal extension of the dissection from the tear to the subclavian artery, it may be necessary to place the graft over the branch with its leading margin between the left carotid and subclavian arteries. After the procedure, it is important to carefully monitor the patient for the presence of ischemic symptoms of the arm and to image the thoracic aorta to exclude persistent perfusion of the false lumen via retrograde subclavian flow around the device into the arch. Similar to acute type B dissection is the management of chronic aortic dissection as an alternative to open surgical repair in patients with false lumen aneurysm. In this regard, multiple reports describe aneurysm thrombosis, and false lumen shrinkage that mirror the results recorded in series of acute dissection (17–20). One controlled investigation that compared stent–graft therapy with open surgery in matched groups of patients with chronic type B dissection reported improved survival and decreased neurologic complications with the less invasive procedure (18).

Results of Stent–Graft Repair In 1997, Mitchell et al. reported the cumulative results of 108 patients treated with thoracic aortic stent–grafts at Stanford University Medical Center. The mean aneurysm diameter was 6.3 cm. Vascular access was obtained through the femoral artery in 64 patients (59%). The abdominal aorta, native or graft, an iliac artery, or the ascending aorta was used for access in 44 patients. In 22 patients (20%) stent–grafts were placed in conjunction with abdominal aortic aneurysm repair (21). Ehrlich and colleagues prospectively studied stent–graft repair versus direct repair of descending thoracic aortic aneurysms at the University of Vienna in Austria and reported their results in 1998. A total of 68 patients were deemed good candidates for stent–graft repair. Because of limited device availability, only 10 patients (15%) had stent–graft repair, and 58 (85%) had conventional open repair. The mean procedure time was 320 minutes in the conventional group and 150 minutes in the stent–graft group. Five patients (12%) in the open surgical group developed paraplegia, whereas no patient in the stent–graft group developed any neurologic sequelae. The mean length of hospital stay for the surgical group was 26 days versus 10 days for the stent–graft group. Five patients (50%) required transposition of the left subclavian artery onto the left common carotid artery to increase the length of the proximal fixation site. Stent–grafts were placed through a femoral artery in eight cases (80%) and the aorta in two (20%) (20). In the Stanford series of 108 patients treated with thoracic endografts, 10 (9%) patients died within 30 days from the time of stent–graft placement, and four deaths (4%) were directly attributable to the procedure (21). In

Chapter 57 Endovascular Repair of Thoracic Aortic Aneurysms and Dissections

the Austrian comparative study of stent–graft treatment versus conventional surgery, the 30-day mortality was 30% with conventional surgery and 10% with endovascular thoracic stent–graft repair (20). In a series of more than 40 patients (range 40–260) with non-dissection associated thoracic aneurysm presented in March 2001, at the First International Summit on Thoracic Aortic Endografting, operative mortalities were between 0% and 4%, technically successful device deployment occurred in 98% to 100% of cases, and immediate aneurysm thrombosis was achieved in 90% to 100% (16). The risk of paraplegia during operative repair increases with the sacrifice of intercostal arteries. In the Stanford series of 108 patients with descending thoracic aortic aneurysms, four patients (4%) had postoperative paraplegia and four had strokes. Paraplegia occurred in two patients who underwent repair of suprarenal abdominal aortic aneurysms immediately followed by thoracic aortic stent–graft placement and in two patients who had thoracic aortic stent–grafts placed across the orifices of intercostals arteries at the T10 level. One of the last two patients had also undergone a previous abdominal aortic aneurysm repair (21). In an effort to prevent this devastating complication, Ishimaru et al. described a retrievable stent–graft that can be used in conjunction with somatosensory-evoked potentials to test for spinal cord ischemia prior to the permanent deployment of a thoracic aortic stent–graft. Seventeen aneurysms were excluded using this technique, and no patient had postoperative paraplegia (22). Again, in those patients with nondissecting thoracic aneurysms reported at the First International Summit on Thoracic Aortic Endografting, paraplegia was a complication in 0% to 1.6%, and stroke occurred in 0% to 4% of cases (16). Perigraft flow or endoleak is a condition that exists when there is blood flow within the aneurysm and outside the lumen of the endograft. Helical CT scanning has been shown to be more sensitive than angiography for detecting endoleaks following placement of aortic endografts (23,24). There are distinct differences between the relative frequencies, types, and fates of endoleaks identified after stent–graft repair of thoracic aneurysms. Endoleaks can occur at the proximal and distal fixation sites (type 1), through the graft material itself (transgraft), or through patent branch vessels (type 2). Typically, endoleaks following endovascular thoracic aneurysm repair occur more commonly at proximal or distal attachment sites (type 1) due to a poor seal between the graft and normal aorta. Although type 2 endoleaks via intercostals or bronchial arteries have been reported after endovascular thoracic aneurysm repair, the incidence is very low. The reason for this difference is currently unclear. It is generally accepted that the prognosis for type 1 endoleaks is more serious than the natural history of type 2 endoleaks. The effects from the force of aortic arterial pressure transmitted directly to a thoracic aneurysm after stent–graft placement are potentially lethal, with multiple isolated reports of early rupture occurring in this setting.

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Endoleaks identified at proximal or distal fixation sites can often be treated by placing a short extender cuff directly over the source. In the Stanford series of 108 patients, five patients (4.6%) did not have complete aneurysm thrombosis after stent–graft placement. Of five late deaths, occurring more than 30 days after stent–graft placement, one was caused by exsanguinations from an aortoesophageal fistula in a patient with a persistent perigraft leak. Two additional late deaths may have resulted from graft failure and aneurysm rupture (21). Consequently, aggressive endovascular or surgical intervention is recommended if feasible, when type 1 endoleaks are documented more than 2 to 4 weeks after the implantation procedure.

Conclusions The recent development of endovascular stent–graft technology and its application as an alternative treatment to open surgical repair of thoracic aneurysms is an exciting and significant advance. However, many challenges lie ahead for evolving aortic endografting technology. The durability of devices beyond a few years and the natural history of small endoleaks remain unknown. Objectively determining the benefits, risks, and complications of thoracic stent–grafts through rigorous, prospective controlled investigations is necessary to allow physicians to confidently counsel patients with accurate information regarding their treatment options.

References 1. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5:491–499. 2. Blum U, Langer M, et al. Abdominal aortic aneurysms: preliminary technical and clinical results with transfemoral placement of endovascular self-expanding stent–grafts. Radiology 1996;198:25–31. 3. Coselli JS, de Figueiredo LF. Natural history of descending and thoracoabdominal aortic aneurysms. J Card Surg 1997;12(suppl):285–289. 4. Dake MD, Miller DC, et al. Transluminal placement of endovascular stent–grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994;331:1729–1734. 5. Moreno-Cabral CE, Miller DC, et al. Degenerative and atherosclerotic aneurysms of the thoracic aorta: determinants of early and late surgical outcome. J Thorac Cardiovasc Surg 1984;88:1020–1032. 6. Semba CP, Mitchell RS, et al. Thoracic aortic aneurysm repair with endovascular stent–grafts. Vasc Med 1997;2:25–30. 7. Semba CP, Kato N, et al. Acute rupture of the descending thoracic aorta: repair with use of endovascular stent– grafts. J Vasc Intervent Radiol 1997;8:337–342. 8. Kato N, Dake MD, et al. Traumatic thoracic aortic

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11.

12.

13.

14.

15.

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Part VII Aortic and Peripheral Aneurysms aneurysm: treatment with endovascular stent–grafts. Radiology 1997;205:657–662. Scharrer-Pamler R, Gorich J, et al. Emergent endoluminal repair of delayed abdominal aortic rupture after blunt trauma. J Endovasc Surg 1998;5:134–137. Deshpande A, Mossop P, et al. Treatment of traumatic false aneurysm of the thoracic aorta with endoluminal grafts. J Endovasc Surg 1998;5:120–125. Desgranges P, Mialhe C, et al. Endovascular repair of posttraumatic thoracic pseudoaneurysmwith a stent graft. Am J Roentgenol 1997;169:1743–1745. Semba CP, Sakai T, et al. Mycotic aneurysms of the thoracic aorta: repair with use of endovascular stent–grafts. J Vasc Intervent Radiol 1998;9:33–40. Moon MR, Mitchell RS, et al. Simultaneous abdominal aortic replacement and thoracic stent–graft placement for multi-level aortic disease. J Vasc Surg 1997;25:332–340. Kato N, Semba CP, Dake MD. Embolization of perigraft leaks after endovascular stent–graft treatment of aortic aneurysms. J Vasc Intervent Radiol 1996;7:805–811. Dake MD, Kato N, et al. Endovascular stent–graft placement for the treatment of acute aortic dissection. N Engl J Med 1999;340:1546–1552. Dake MD. Endovascular stent–graft management of thoracic aortic diseases. Eur J Radiol 2001;39:42–29.

17. Dake MD, Semba CP, et al. Endovascular procedures for the treatment of acute aortic dissection: techniques and results. J Cardiovasc Surg 1998;39:45–52. 18. Nienaber CA, Fattori R, et al. Non-surgical reconstruction of thoracic aortic dissection by stent–graft ploacement. N Engl J Med 1999;340:1539–1545. 19. Sakai T, Dake MD, et al. Descending thoracic aortic aneurysm: thoracic CT findings after endovascular stent–graft placement. Radiology 1999;212:169–174. 20. Ehrlich M, Grabenwoeger M, et al. Endovascular stent–graft repair for aneurysms of the descending thoracic aorta. Ann Thorac Surg 1998;66:19–24. 21. Mitchell RS, Miller DC, Dake MD. Stent–graft repair of thoracic aortic aneurysms. Semin Vasc Surg 1997;10:257–271. 22. Ishimaru S, Kawaguchi S, et al. Preliminary report on prediction of spinal cord ischemia in endovascular stent graft repair of thoracic aortic aneurysm by retrievable stent graft. J Thorac Surg 1998;115:811–818. 23. Golzarian J, Dussaussois L, et al. Helical CT of aorta after endoluminal stent–graft therapy: value of biphasic acquisition. Am J Roentgenol 1998;171:329–331. 24. Rozenblit A, Marin ML, et al. Endovascular repair of abdominal aortic aneurysm: value of postoperative follow-up with helical CT. Am J Roentgenol 1995;165:1473–1479.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 58 Thoracoabdominal Aortic Aneurysms Nicholas J. Morrissey and Larry H. Hollier

Aneurysms involving both the thoracic and abdominal aorta pose a major challenge to vascular clinicians. Due to the extensive nature of the disease process, the significant comorbidities and advanced age of the affected population, the morbidity associated with repair of these lesions remains high. Since the first repair of a thoracoabdominal aortic aneurysm (TAAA) reported by Etheredge in 1955 (1), numerous advances in surgical technique, anesthetic management, and critical care medicine have greatly improved outcomes. The incidence of major complications has been reduced sufficiently to permit many patients to undergo open repair of TAAAs. The combination of advanced age, cardiac, pulmonary, and renal comorbidities, and a massive two-cavity incision makes TAAA repair a most challenging undertaking.

Epidemiology An aneurysm is defined as a localized dilation of an artery that is at least one-half the size greater than is expected for that artery (2). Table 58.1 describes expected sizes of the aorta at various points along its course. The median age of patients with TAAA is 65 years, which is older than their counterparts with abdominal aortic aneurysms. TAAAs tend to occur in approximately 1 per 100,000 population, compared with the AAA incidence of 1% to 3% (3). Patients with TAAA have a high incidence of medical comorbidities, as is shown in Table 58.2. Factors such as advanced age and severity of comorbidities need to be considered when evaluating patients for TAAA repair.

Etiology The cause of thoracoabdominal aneurysms is not completely known. The end result of the pathophysiology is degeneration of the aortic wall, similar to that seen in AAAs. In AAA, degradation of the elastic fibers in the adventitia seems to be the structural pathway that leads to aneurysm formation. The majority of thoracoabdominal aortic aneurysms (82%) are classified as atherosclerotic or nonspecific. In these cases, degeneration of the aortic wall may be the end result of the atherosclerotic process. In approximately 17% of cases, TAAAs result from degeneration of a previous aortic dissection. The remaining lesions result from connective tissue disorders such as Marfan syndrome and Ehlers–Danlos type IV, trauma, infection, and Takayasu’s arteritis (5). Crawford classified TAAAs based on the anatomic extent of disease. His classification system has proven quite useful in predicting outcomes after TAAA repair (Fig. 58.1).

Natural History The most feared complication of TAAA is rupture. Because rupture results in high morbidity and mortality rates, it is beneficial to identify patients who will be able to undergo safe elective repair of TAAA. Crawford and DeNatale followed 94 patients with TAAA nonoperatively (6). At 2 years, survival was 24%, with half of the deaths being due to rupture. After 5 years, survival had decreased to 19%. In this series, rupture was the cause of death in 69% of patients with dissection but in only 46%

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FIGURE 58.1 Classification of types I–IV of thoracoabdominal aortic aneurysms.

TABLE 58.1 Diameters of normal adult aortas (reproduced by permission from reference 2) Level Thoracic aorta Mid-descending Thoracic aorta Diaphragmatic Abdominal aorta Supraceliac Abdominal aorta Suprarenal Abdominal aorta Proximal infrarenal Abdominal aorta Distal infrarenal

Range of Mean (cm)

Range of Standard Deviation (cm)

Sex

2.45–2.64 2.39–2.98 2.40–2.44 2.43–2.69 2.10–2.31 2.50–2.72 1.86–1.88 1.98–2.27 1.66–2.16 1.99–2.39 1.19–1.87 1.41–2.05

0.31 0.31 0.27–0.32 0.27–0.40 0.27 0.24–0.35 0.09–0.2 0.19–0.23 0.22–0.32 0.30–0.39 0.09–0.34 0.04–0.37

F M F M F M F M F M F M

TABLE 58.2 Risk factors in patients with thoracoabdonimal aortic aneurysm (reproduced by permission from reference 4) Factor Coronary artery disease Strokes/transient ischemic attacks Chronic lung disease Renal insufficiency Diabetes mellitus Smoking history

Incidence (%) 67 12 42 38 6 90

without dissection. Bickerstaff and colleagues reported 29% actuarial 2-year survival in patients with thoracic and thoracoabdominal aneurysms followed nonoperatively (3). Cambria and associates followed 57 patients with nondissecting TAAAs nonoperatively (7). The risk of rupture was 12% at 2 years and 32% at 4 years. For TAAA greater than 5 cm in diameter, the rupture risk was 18% at 2 years. No aneurysms under 5 cm ruptured. A number of the patients in this study underwent elective repair during the study; thus, these rupture estimates are

probably low. The leading cause of death in this series, as in others, was cardiac disease. In a series of ruptured TAAAs, Crawford found that 80% of ruptured aneurysms were less than 10 cm in diameter; 13% of ruptures occurred in TAAA less than 6 cm in diameter. Acute dissection seemed to increase the risk of rupture in smaller aneurysms, as did a rapid expansion rate (8). Most authors recommend elective repair of TAAAs over 6 cm diameter in patients who are acceptable risk. This recommendation is based on rupture risk determined from series as described above. Surgical repair in Crawford’s series of 605 patients resulted in a 5-year survival rate 60% (9).

Diagnosis Symptoms are present in more than half of patients with TAAAs (9,10). Back or abdominal pain is the most common symptom. The aneurysm may compress the esophagus, bronchus, or recurrent laryngeal nerve resulting in dysphagia, dyspnea, pneumonia, or hoarseness. Aneurysm erosion into the aerodigestive tract may cause hemoptysis or hematemesis while aortacaval fistula

Chapter 58 Thoracoabdominal Aortic Aneurysms

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FIGURE 58.3 Computed tomographic scan of a patient with a type I thoracoabdominal aneurysm.

FIGURE 58.2 Chest radiograph of a patient with a thoracoabdominal aneurysm. Note the mediastinal widening.

may cause congestive heart failure. Embolization of thrombus from within the aneurysm sac can cause renal or intestinal ischemia or the blue toe syndrome if the emboli lodge in the small digital arterioles. Frequently, a routine chest radiograph may suggest the presence of a calcified TAAA (Fig. 58.2). With CT scans of the chest and abdomen being used with ever greater frequency, aneurysms of the thoracic and abdominal aorta may be detected more often. The diagnostic imaging modalities used to define TAAA anatomy are used to plan operative therapy. Thin-slice helical CT scans provide excellent anatomic definition and can be used to reconstruct three-dimensional images useful in surgical planning (Figs. 58.3 and 58.4). Magnetic resonance angiography (MRA) techniques using less nephrotoxic contrast agents such as gadolinium have also been refined to provide excellent resolution. Contrast arteriography is often unnecessary if the previous modalities can define the anatomy of the thoracoabdominal aorta and its branches. Standard angiography may be needed if endovascular repair of a TAAA is planned since these images can be used to provide necessary measurements for designing devices. Contrast arteriography or MRA can be used to define the spinal cord circulation, specifically the arteria radicularis magna, which may help in planning for the reimplantation of crucial intercostal arteries (11,12).

FIGURE 58.4 Magnetic resonance image of a patient with a dissecting thoracoabdominal aortic aneurysm.

Preoperative Evaluation Many patients with TAAA have significant comorbidities, as shown in Table 58.2. In patients with severe cardiopulmonary comorbidities, thought should be given to the possibility of a combined open and endovascular procedure. Such an approach may be less invasive with the open portion limited to either the thorax or the abdomen, but not both. All patients undergoing TAAA repair must be evaluated by routine blood chemistries, coagulation studies, and complete blood count. Coexistent cardiac disease must be ruled out with ECG and pharmacologic stress scintigraphy. Newly diagnosed coronary artery disease should be treated appropriately prior to elective TAAA repair. Echocardiography should be done to rule out significant aortic insufficiency which can be

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exacerbated with proximal aortic cross-clamping. Carotid artery duplex studies should be performed to rule out hemodynamically significant lesions. Pulmonary function tests should be performed in patients with a history suggestive of pulmonary disease. Chronic obstructive pulmonary disease (COPD) has been shown to be a risk factor for TAAA rupture, perhaps due to the presence of elastase which can result in aortic wall degeneration (13). The presence of renal insufficiency complicates approximately 15% of cases, and has been associated with a higher morbidity and mortality rate. It is therefore prudent to use significant renal insufficiency as a factor in determining suitability for surgical repair.

Perioperative Care Once it is determined that the patient is suitable for surgical repair of their aneurysm, a number of perioperative maneuvers may be helpful to optimize the outcome for the patient. In patients with pulmonary disease, optimization of lung function with bronchodilators should be achieved preoperatively. It has recently been shown that administration of beta-blockers in the perioperative period results in fewer cardiac complications in patients undergoing major vascular surgical procedures (14).

Operative Management In the operating room, general anesthesia is induced and the airway controlled with a double-lumen tube. This allows for collapse of the left lung and ventilation of the right lung during the thoracic part of the procedure. An arterial pressure line and a Swan–Ganz catheter are placed. A spinal drain is placed in the third or fourth lumbar space in order to drain cerebrospinal fluid (CSF) (Fig. 58.5). The CSF is drained during the procedure in order to keep the pressure below 10 mmHg pressure. The patient is positioned in a left thoracotomy position with the pelvis tilted so the lower body is nearly parallel to the table. We

use a cell-saver system to return shed blood to the patient during the procedure. The level of the thoracic incision is determined by the extent of the aneurysm (15). Frequently, a rib must be removed in order to obtain adequate exposure of the proximal thoracic aorta. Less commonly, a double thoracic incision is needed to obtain proximal control and exposure of the distal thoracic aorta. The diaphragm and the crus are divided and the retroperitoneal aorta is widely exposed. The left kidney may be elevated but, if left renal artery bypass is needed, keeping the left kidney down may be preferred. Exposure of both common iliac arteries is possible with this approach. Care is taken to avoid injury to the ureters and renal and iliac veins. Distal aortic perfusion and maintenance of visceral perfusion during the procedure can help prevent complications of TAAA repair (16,17). A number of techniques for achieving distal aortic perfusion have been used. Left heart bypass as well as axillary–femoral grafts have been used to relieve the strain on the heart and to provide circulation to the lower aorta and its branches during the proximal reconstruction. Based on evidence that prolonged periods of mesenteric ischemia can result in higher rates of pulmonary, hematologic, and neurologic complications, we have attempted to minimize the duration of mesenteric and renal ischemia during TAAA repair. We construct a graft consisting of 28-mm tube graft with a 22 mm by 11 mm bifurcated graft sewn to its side near the proximal end. After exposure of the thoracic and abdominal aorta as well as the left iliac artery, one of the branches of the bifurcated graft is sewn end-to-side to the left iliac artery. The proximal anastomosis to the thoracic aorta is performed and the proximal clamp is moved down the graft below the takeoff of the bifurcated graft. This results in perfusion of the lower aorta and visceral segment via the iliac limb. After patent intercostal arteries are reimplanted, the clamps are moved down and the visceral segment of the aorta is opened. A catheter with four individual cannulae is positioned within the second limb of the bifurcated graft. The individual cannulae are inserted into the celiac, superior mesenteric artery, and both renal arteries. This allows perfusion of the viscera and kidneys during the reconstruction of this segment. The remainder of the reconstruction proceeds with anastomosis to the distal aorta or the iliac arteries as dictated by the quality of the aorta.

Complications and Their Prevention A list of common postoperative complications and their incidence in one large series are shown in Tables 58.3 and 58.4.

FIGURE 58.5 Operative photograph of intrathecal catheter placed for monitoring and withdrawal of cerebrospinal fluid.

Spinal Cord Ischemia Spinal cord ischemia may result in paraplegia or paraparesis. The incidence of this devastating complication

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Chapter 58 Thoracoabdominal Aortic Aneurysms TABLE 58.3 Complications with repair of thoracoabdominal aortic aneurysms Early

Late

Paraplegia/paraparesis Renal failure Coagulopathy

Graft thrombosis Graft infection True aneurysm of unreplaced segment Anastomotic false aneurysm Aortoenteric fistula Aortocaval fistula Erosion of graft into lung

TABLE 58.4 Major complications in 150 consecutive thoracoabdominal aortic aneurysm repairs (reproduced by permission from reference 34) Complication

Myocardial infarction Pulmonary insufficiency Cerebrovascular accident Sepsis Embolization/thrombosis distally Visceral ischemia Sexual dysfunction Splenic trauma Wound problems Arrythmias Urinary tract infection Neurogenic bladder Recurrent laryngeal nerve damage Pneumonia

was once reported to occur in up to 16% of TAAA repairs (9,10). With the evolution of techniques to protect the spinal cord, the rate of spinal cord dysfunction has been reduced to 3% to 10%. Anatomically, the spinal cord blood supply derives from the anterior spinal artery and the smaller, paired posterior spinal arteries. Segmental radicular arteries feed the spinal arteries. The largest radicular artery, the artery radicularis magna or artery of Adamkiewicz, arises from the T8–L1 aortic level in 85% of cases. The importance and location of the artery radicularis magna in humans is debatable; however, it is clear that a great part of the spinal cord circulation arises from the radicular arteries. Other sources of spinal cord blood flow include branches from the internal iliac arteries, the vertebral and subclavian arteries. These collateral pathways may become more important following TAAA repair and ligation of intercostal vessels. Factors which increase the risk of spinal cord complications include longer aortic cross-clamp times and more extensive aneurysms (10,16). Based on Crawford’s original work, paraplegia was more common in patients with type I and II TAAA (9). Longer periods of aortic clamping with interruption of the blood supply to the cord would obviously increase the risk of clinically significant spinal cord injury. Hypotension in the perioperative period has also been shown to increase the risk of neurologic dysfunction (9). Recently, clinical evidence links longer visceral ischemia times to higher rates of postoperative paraplegia (18,19). The presence of aortic dissection has classically been associated with higher rates of neurologic dysfunction following TAAA repair (9). More recent data from Coselli and colleagues suggest that acute but not chronic dissection increases the risk of paraplegia following thoracoabdominal aneurysm repair. In their series,

Pulmonary insufficiency Myocardial infarction Creatinine elevation to twice preoperative level Stroke Sepsis Dialysis (chronic) Bleeding (reoperation) Paraplegia/paraparesis*

Incidence (%) 23 9 9 7 5 4 4 4

*Since introduction of a multimodaility perioperative protocol, incidence is 0 in 42 patients.

paraplegia rates were 5% in patients without dissection and 5.5% in patients with dissection. In patients with acute dissection, paraplegia occurred in 19% of cases (20). Prevention of paraplegia remains a central focus of the perioperative management of TAAA patients. As more data accumulate about the causes of this complication, strategies evolve which have helped reduce paraplegia to low levels in experienced centers. Drainage of cerebrospinal fluid has been advocated to increase spinal cord perfusion pressure in the perioperative period (21). Crawford’s early randomized study of CSF drainage showed no benefit in preventing paraplegia; however, that study specifically limited the quantity of CSF that could be removed (22). Other reports have shown a benefit of CSF drainage in conjunction with other adjuncts (23). A recent randomized controlled trial of CSF drainage demonstrated a clear reduction in spinal cord dysfunction with the use of this technique (24). Reimplantation of intercostals vessels, especially those in the crucial T8–L1 region, has typically been advocated as a method of preventing paraplegia (25). More recently, reimplantation of intercostal vessels guided by motor-evoked potential monitoring has been used to prevent paraplegia following TAAA repair (26,27). Recent data demonstrating the adverse effect of mesenteric ischemia–reperfusion on spinal cord function in experimental and clinical studies has led some to make clear attempts to minimize mesenteric ischemia during TAAA repair (19,20). Experimental approaches to spinal cord preconditioning show some promise as potential adjunctive measures to prevent spinal cord dysfunction (28). The use of spinal cord cooling and angiographic localization of the artery radicularis magna followed by selective reimplantation of this vessel are other methods used by some to prevent spinal cord complications (11,12,29,30). Pharmacologic adjuncts such as naloxone, steroids, and mannitol have been shown to provide modest improvement in neurologic outcome following TAAA repair and are used selectively by surgeons as part of a multifactorial approach to spinal cord protection (23,31). Such a multifaceted approach has allowed rates of neuro-

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logic dysfunction to be reduced to the range of 3% to 10% in recent series. Our own approach, involving minimizing mesenteric and renal ischemia in addition to CSF drainage, passive hypothermia, and pharmacologic adjuncts, is currently being evaluated for its ability to prevent neurologic complications.

Pulmonary Complications Pneumonia and prolonged ventilatory support continue to be significant causes of postoperative morbidity in patients undergoing TAAA repair. The need for prolonged ventilatory support may occur in up to 23% of patients. Since many patients are older and have a history of COPD and tobacco abuse, their risk of pulmonary complications increases. This, in combination with the morbidity of a thoracoabdominal incision, puts these patients at increased risk of pulmonary complications. In order to minimize these complications, patients must give up smoking and undergo pulmonary function testing. Those who have a forced expiratory volume in 1 second less than 1.2 L, a forced expiratory flow, mid-expiratory phase (FEV25–75%) less than 0.5 L/s and (FEV25%) less than 2 L/s, PCO2 greater than 45 mmHg, PaO2 less than 55 mmHg, and preexisting renal failure are at increased risk of pulmonary dysfunction (32). Careful ventilatory management, chest physiotherapy, and perioperative use of bronchodilators will help in attaining satisfactory weaning from the ventilator. Patients with persistent atelectasis or infiltrates may benefit from bronchoscopy to remove mucous plugs. Those who fail to wean from the ventilator within the first postoperative week should be considered for tracheostomy. The judicious use of epidural pain management can help patients undergo chest physiotherapy more effectively and improve their pulmonary rehabilitation.

Cardiac Morbidity Since coronary artery disease remains prevalent in this patient population, perioperative cardiac events do occur. Perioperative use of beta-blockers and distal aortic perfusion to reduce cardiac strain are the techniques used to diminish cardiac complications. Adequate investigation and treatment of coronary artery disease preoperatively is the mainstay of successful prevention.

patients with a history of renal insufficiency, adequate preoperative hydration is imperative. Intraoperatively, patients should receive mannitol 25 g as well as 20 to 40 mg of furosemide. Mannitol may provide protection as a free-radical scavenger while furosemide induces a brisk diuresis. The use of dopamine or fenoldapam may improve renal blood flow in the perioperative period and reduce renal ischemia. If renal perfusion via catheters is not performed during visceral clamping, the infusion of cold Collins solution may be used to decrease renal metabolism. Our current approach, as described above, involves continuous perfusion of the kidneys with blood via catheters from a side-branch of the proximal graft. Since hypothermia may protect the kidney, it is unclear whether any benefit from perfusion of the kidneys with blood will result. Experimental evidence exists for pharmacologic agents to protect the kidneys from ischemia–reperfusion, however, these have not been widely used or studied clinically (35). It is important that postoperative fluid management involves replacing urine output with balanced salt solution. This will avoid dehydration resulting from diuresis and will maintain adequate vascular volume for renal perfusion.

Bleeding and Coagulopathy Our understanding of the coagulopathy associated with aortic aneurysms and their repair has evolved significantly. Obviously, surgical bleeding must be controlled prior to the completion of the procedure as reoperation for bleeding increases the risk of major complications. The function of the coagulation system can be profoundly affected by TAAA and its treatment. Supraceliac aortic cross-clamping results in a fibrinolytic and hypocoagulable state (36,37). It is felt that prolonged mesenteric ischemia adversely affects the coagulation system and therefore attempts to reduce this parameter are recommended (36). Cambria and colleagues have demonstrated that early reperfusion of the mesentery via the SMA can minimize the coagulation dysfunction resulting from supraceliac clamping (38,39). The judicious use of antifibrinolytic agents such as e-aminocaproic acid and aprotinin and transfusion of fresh-frozen plasma can assist in returning the patient to a normocoagulable state. Vigilant correction of coagulopathy in the postoperative period is essential.

Renal Insufficiency Patients with preexisting renal insufficiency might be expected to be at higher risk of postoperative renal failure than others. A number of patients with TAAA have renal dysfunction at the outset due to thromboembolic disease. The occurrence of instability, prolonged renal ischemia times, and cardiac pump bypass all increase the risk of postoperative renal insufficiency (9,32,33). In one series, chronic dialysis was required in 4% of patients while transient elevation of creatinine occurred in 9% (34). In

Endovascular Approach to the Thoracic Aorta The recent enthusiasm for endovascular techniques in the repair of abdominal aortic aneurysms has led to attempts at approaching TAAAs in a similar manner. If one thinks of the benefit bestowed by minimally invasive techniques, it seems intuitive that the greatest benefit would result from replacing the most invasive procedure in the sickest

Chapter 58 Thoracoabdominal Aortic Aneurysms

patients with a much less invasive alternative. While the benefit of a laparoscopic appendectomy may be minimal since most patients are young and healthy and require only a small incision for open surgery, the benefit of endovascular TAAA repair might be expected to be maximal. Indeed, patients whose comorbidities might prevent them from safely undergoing open repair might be treated with endovascular techniques. The early series of endovascular thoracic aortic devices are generally limited to use in the descending thoracic aorta. Early reports describe paraplegia rates similar to those of open repair (40–42). Stroke from wire manipulation in the aortic arch, death from device deployment, and failure due to inability to pass the delivery system occurred as well (40). Paraplegia may be related to the extent of thoracic aorta that is covered, and endoleak is predicted by shorter neck length (40). These early conclusions are drawn from relatively small series. The current trials under way in the US involve industry-made devices (Fig. 58.8). In general, repair of thoracic aneurysms with endografts is limited to lesions of the descending thoracic aorta. Adequate proximal and distal neck length makes lesions involving the aortic arch and visceral segment unacceptable for simple endovascular repair. Case reports of repair of aneurysms involving the arch or visceral segment using devices with side-branches are encouraging; however, much improvement needs to occur before endografting can be applied to complex thoracic and thoracoabdominal lesions (43,44). A creative combination of open and endovascular techniques may allow a less invasive approach to TAAA repair in some cases. Performing open abdominal aortic reconstruction and moving the visceral and renal artery orifices away from the aneurysm can permit later introduction of a thoracic endograft. Transposition of one or more arch vessels can provide sufficient length of normal proximal aorta to permit stent–graft exclusion of aneurysms involving part or all of the arch. The future of stent–graft development involves side-branch technology which will allow placement of devices across critical branch vessels while maintaining perfusion to these branches. Until that time, the use of adjunctive procedures can often facilitate endovascular repair of complex lesions. By avoiding a thoracoabdominal incision, morbidity in this debilitated population may be reduced.

Summary TAAAs occur in patients who frequently suffer from significant cardiac, pulmonary, and renal comorbidities. This fact combined with the magnitude of the physiologic insult resulting from TAAA repair results in significant perioperative complication rates. The development of neurologic, renal, and cardiac protection strategies has resulted in improved results of TAAA repair. In spite of improvements, morbidity and mortality from TAAA repair remain significant. The advent of endovascular

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techniques, alone or in combination with open techniques, represents the next phase in improving outcomes following TAAA repair. Endovascular techniques may even allow clinicians to offer TAAA repair to patients who previously would not be suitable for repair.

References 1. Etheredge SN, Yee J, et al. Successful resection of large aneurysm of the upper abdominal aorta and replacement with homograft. Surgery 1955;38:1071–1081. 2. Johnston KW, Rutherford RB, et al. Suggested standards for reporting on arterial aneurysms. J Vasc Surg 1991;13:452. 3. Bickerstaff LK, Pairolero P, Hollier LH. Thoracic aortic aneurysms: a population based study. Surgery 1982;92:1103–1108. 4. Hollier LH, Symmonds JB, et al. Thoracoabdominal aortic aneurysm repair: analysis of postoperative morbidity. Arch Surg 1988;123:871. 5. Panneton JM, Hollier LH. Nondissecting thoracoabdominal aneurysms: Part I. Ann Vasc Surg 1995;9:503–514. 6. Crawford ES, DeNatale RW. Thoracoabdominal aortic aneurysm: observations regarding the natural course of the disease. J Vasc Surg 1986;3:578–582. 7. Cambria RP, Gloviczki P, et al. Outcome and expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg 1995;170:213–217. 8. Crawford ES, Hess KR, et al. Ruptured aneurysm of the descending thoracic and thoracoabdominal aorta. Ann Surg 1991;213:417–426. 9. Crawford ES, Crawford JL, et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 1986;3:389–404. 10. Svensson LG, Crawford ES, et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17: 357–370. 11. Williams GM, Perler BA, et al. Angiographic localization of spinal cord blood supply and its relationship to postoperative paraplegia. J Vasc Surg 1991;13:23–33. 12. Kieffer E, Fukui S, et al. Spinal cord arteriography: a safe adjunct before descending thoracic or thoracoabdominal aortic aneurysmectomy. J Vasc Surg 2002;35:262–268. 13. Juvonen T, Ergin MA, et al. Risk factors for rupture of chronic type B dissections. J Thorac Cardiovasc Surg 1999;117:776–786. 14. Poldermans D, Boersma E, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch echocardiographic cardiac risk evaluation applying stress echocardiography study group. N Engl J Med 1999;341:1789–1794. 15. Morrissey NJ, Hollier LH. Anatomic exposures in thoracic aortic surgery. Sem Vasc Surg 2000;13:283–289. 16. Safi HJ, Miller CC. Spinal cord protection in descending thoracic and thoracoabdominal aortic repair. Ann Thorac Surg 1999;67:1937–1939. 17. Safi HJ, Miller CC, et al. Thoracic and thoracoabdominal aortic aneurysm repair using cardiopulmonary

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18.

19.

20.

21.

22.

23.

24.

25. 26.

27.

28.

29.

30.

Part VII Aortic and Peripheral Aneurysms bypass, profound hypothermia and circulatory arrest via left side of the chest incision. J Vasc Surg 1998;28:591–598. Vermeulen EG, Blankensteijn JD, van Urk H. Is organ ischemia a determinant of outcome of operations for suprarenal aortic aneurysms? Eur J Surg 1999;165:441–445. Morrissey NJ, Kantonen I, et al. Effect of mesenteric ischemia/reperfusion on spinal cord injury following transient aortic occlusion in a rabbit model. J Endovasc Ther 2002;9:II44:500. Coselli JS, LeMAire SA, et al. Paraplegia after thoracoabdominal aortic aneurysm repair: Is dissection a risk factor? Ann Thor Surg 1997;63:28–36. McCullough JL, Hollier LH, Nugent M. Paraplegia after thoracic aortic occlusion: influence of cerebrospinal fluid drainage. Experimental and early clinical results. J Vasc Surg 1988;7:153–160. Crawford ES, Svensson LG, et al. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg 1991;13:36–45. Acher CW, Wynn MW, et al. Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994;19:236–248. Coselli JS, LeMaire SA, et al. Cerebrospinal fluid drainage in thoracoabdominal aortic surgery. Semin Vasc Surg 2000;13:308–314. Hollier LH. Protecting the brain and spinal cord. J Vasc Surg 1987;5:524. Jacobs MJHM, Meylaerts SA, et al. Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair. J Vasc Surg 1999;29:48–59. Svensson LG, Patel V, et al. Influence of preservation of intraoperatively identified spinal cord blood supply on spinal motor-evoked potentials and paraplegia after aortic surgery. J Vasc Surg. 1991;13:355. Abraham VS, Swain JA, et al. Ischemic preconditioning protects against paraplegia after transient aortic occlusion in the rat. Ann Thorac Surg 2000;69:475–479. Cambria RP, Davison K, et al. Clinical experience with epidural cooling for spinal cord protection during thoracic and thoracoabdominal aneurysm repair. J Vasc Surg 1997;25:234–243. Sun J, Hirsch G, Svensson G. Spinal cord protection by papaverine and intrathecal cooling during aortic crossclamping. J Cardiovasc Surg 1998;39:839–842.

31. Laschinger JC, Cunningham JN, et al. Prevention of ischemic spinal cord injury following aortic crossclamping: use of corticosteroids. Ann Thorac Surg 1984;38:500. 32. Coselli JS. Perioperative management: patient selection, patient work-up, operative management and postoperative management. Semin Vasc Surg 1992;5:146. 33. Svensson LG, Coselli JS, et al. Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. J Vasc Surg 1989;10:230. 34. Hollier LH, Money SR. The risk of spinal cord dysfunction in 150 consecutive patients undergoing thoracoabdominal aortic replacement. Am J Surg 1992;164:210. 35. Joyce M, Kelly C, et al. Pravastatin, a 3-hydroxy-3methylglutaryl coenzyme A reductase inhibitor, attenuates renal injury in an experimental model of ischemia–reperfusion. J Surg Res 2001;101:79–84. 36. Gertler JP, Cambria RP, et al. Coagulation changes during thoracoabdominal aneurysm repair. J Vasc Surg 1996;24:936–945. 37. Illig KA, Green RM, et al. Primary fibrinolysis during supraceliac aortic clamping. J Vasc Surg 1997;25:244–251. 38. Cambria RP, Davison JK, et al. Mesenteric shunting decreases visceral ischemia during thoracoabdominal aneurysm repair. J Vasc Surg 1998;27:745–749. 39. Cohen JR, Schroder W, et al. Mesenteric shunting during thoracoabdominal aortic clamping to prevent disseminated intravascular coagulation in dogs. Ann Vasc Surg 1988;2:261. 40. Mitchell RS, Miller, DC, Dake MD. Stent–graft repair of thoracic aortic aneurysms. Semin Vasc Surg 1997;10:257–271. 41. Greenberg R, Resch T, et al. Endovascular repair of descending thoracic aortic aneurysms: an early experience with intermediate-term follow-up. J Vasc Surg 2000;31:147–156. 42. Temudom T, Dáyala M, et al. Endovascular grafts in the treatment of thoracic aortic aneurysms and pseudoaneurysms. Ann Vasc Surg 2000;14:230–238. 43. Chuter TA, Gordon RL, et al. An endovascular system for thoracoabdominal aneurysm repair. J Endovasc Ther 2001;8:25–33. 44. Inoue K, Hosokawa H, et al. Aortic arch reconstruction by transluminally placed endovascular branched stent graft. Circulation 1999;100(19 Suppl):11316–11321.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 59 Abdominal Aortic Aneurysm Alfio Carroccio and Larry H. Hollier

An abdominal aortic aneurysm (AAA) is a localized dilation of the subdiaphragmatic aorta to more than 1.5 times its expected diameter (1). The term ectasia is reserved for milder dilations, and arteriomegaly is commonly used to describe diffuse ectasia of the aorta and distal vessels (2). The prevalence of aortic aneurysm has been determined to be 3% to 8.9% (3–5) of adult men and 2.2% of adult woman in a population-based study (3). The rate rises to 12% among elderly males with hypertension (6,7). Screening brothers of patients with abdominal aneurysms yields an incidence of 20% to 29% (8,9). With the progressive enlargement of the aorta, there is an increased risk of vessel rupture. In the US, approximately 15,000 deaths per year are caused by ruptured abdominal aortic aneurysms, making this the 13th leading cause of death. While elective aneurysm repair has a mortality risk of 1% to 5%, emergency repair has a high risk (40–50%) of perioperative mortality. If one considers ruptured aneurysms that fail to reach medical attention, as well as operative mortality, the risk of death is 90% (10,11). Over the last 50 years, the yearly number of patients with elective aneurysm repair increased by approximately one-third. The yearly number of treated ruptures has undergone a similar increase (3). Although this increase is not substantiated by all reviews, there has been a trend for increasing volume in certain regions, which may account for the discrepancy (12). Reducing the death rate from this disease requires that the aneurysm be identified and treated before rupture can occur. The impact of early intervention may be more pronounced as our populations grow older and the inci-

dence of aortic aneurysm rises and continues to impose an increasing burden on health service resources. In this chapter, we attempt to provide a thorough review of the pathophysiology, diagnosis, and treatment of abdominal aortic aneurysm, as well as an update on the most recent advances in knowledge about this challenging disease entity.

Historical Background The first description of an abdominal aortic aneurysm is attributed to the Dutch anatomist Vesalius in the sixteenth century, but it was not until 300 years later that Astley Cooper reported treatment of a ruptured iliac aneurysm by ligation of the abdominal aorta (13). Although peripheral arterial aneurysms had been treated by ligation, aneurysms of the truncal arteries were considered sacrosanct because proximal control was not thought to be feasible. This led to the development of alternative strategies to control abdominal aneurysms, of which a technique described by Colt is particularly interesting (14). At the end of the nineteenth century, he introduced a wire via the groin into the aneurysmal lumen in an attempt to induce thrombosis by heating the wire. Although largely unsuccessful, his pioneering work can be considered a first attempt at endovascular treatment of abdominal aortic aneurysm, which currently, just over 100 years later, is a topic of discussion at every vascular meeting. Another milestone report appeared in 1940, by I.A. Bigger of Virginia (15). This surgeon ligated the neck of

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an infrarenal aortic aneurysm, using fascia, which he expected to loosen gradually. With the protection of this temporary control, the aorta was restored to its proper caliber by plication of the aneurysm. The patient apparently had a protracted survival and femoral pulses reappeared. Estes, in 1950 (16), in his classic report on the natural history of abdominal aneurysms, defined the poor prognosis of these patients, and provided the surgeon with justification for elective repair of the aneurysm, rather than reserving treatment for the nearly hopeless situation in which the aneurysm had already ruptured. The first resection and replacement with homograft of an abdominal aortic aneurysm is attributed to Charles Dubost in 1951 (17). Although the homograft at first seemed to be a quite successful substitute for the aorta, early successes were soon erased by late failures, and the search for better alternatives continued. Tuffier used rigid tubes of metal and paraffined glass in World War I, but without much success (18). Methylmethacrylate tubes, as used by Hufnagel (19,20), functioned better but tended to erode the artery at the site of anastomosis. With the introduction of various new fabrics, such as Orlon and Teflon, in the late 1950s, the era of prosthetic replacement had begun. DeBakey and co-workers (21), with the introduction of knitted Dacron in 1957, finally placed an effective graft in the hands of every surgeon. Subsequent modification, such as the addition of velour to the surface (22) and impregnation with collagen (23) or albumen (24), has further improved the results of prosthetic replacement. Creech is credited with the introduction of the inclusion technique (25), which has completely replaced total excision of the aneurysm and markedly reduced the extent of dissection and intraoperative blood loss. The latest chapter in the history of abdominal aortic aneurysm repair is that of endovascular grafting via a groin approach, as pioneered by Parodi and coworkers (26), a technique that may further decrease morbidity and mortality of aortic replacement in selected patients (4).

Screening The first requirement of successful screening is the availability of a universally applicable method of diagnosis with a high degree of patient acceptability. Scanning with ultrasonography has been shown to meet these needs. Second, for mass screening to be realistic, among those screened the prevalence of aneurysms large enough to require repair must be high. In addition, if one considers that rupture of an unsuspected abdominal aortic aneurysm is a major cause of death in men over the age of 65 years, a significant reduction in deaths is likely to result from higher rates of detection and increased numbers of elective aneurysm repairs. Also, from an economic standpoint the expense of hospital treatment for ruptured aneurysms is far greater than for elective repair.

Previous studies indicated that screening the general population may not be cost-effective (27–29); however screening of men reaching the age of 65 years has been taking place in the county of Gloucestershire, UK since 1990. The overall number of aneurysm-related deaths in men aged 65–73 years, who have been progressively influenced by the screening program, was compared with that for men of all other ages. The total number of aneurysmrelated deaths decreased progressively year by year between 1994 and 1998. Highly significant, with no such change observed in the unscreened part of the population, the authors recommend screening for asymptomatic abdominal aortic aneurysm in that age group (30). Whether or not this is cost-effective is yet to be determined. Support for an initial screen is the low rate of subsequent new aneurysm formation and thus little need for repeated scanning. In a 12-year follow-up study it was ascertained that men with an aortic diameter of less than 26 mm are considered “normal” and a clinically significant aneurysm is unlikely to develop on follow-up (31). To identify the rate at which new abdominal aortic aneurysms develop, a population of veterans without aneurysm aged 50 to 79 underwent an initial ultrasound screening and then repeated screening after an interval of 4 years. Adding the interim and rescreening diagnosis rates, a 4-year incidence rate of 2.6% was identified. As many of the aneurysms after 4 years were small, authors suggest that a second screening after longer intervals, possibly 8 years, may provide yields similar to those seen in initial screening (32). Screening of known asymptomatic aneurysms on the other hand is accepted practice and may decrease the rate of rupture by 49% (33). Likewise, screening of patients with peripheral arterial aneurysms or screening of family members of patients with abdominal aneurysms has revealed many aneurysms that require treatment (9).

Etiology and Pathogenesis Classification of abdominal aortic aneurysm according to underlying disease includes congenital lesions, inherited disorders of connective tissue metabolism, Marfan syndrome, tuberous sclerosis, trauma, infection, arteritis, and cystic medial necrosis. In most cases, since the etiology of aneurysm formation is less well understood, the Society for Vascular Surgery and the International Society for Cardiovascular Surgery Committee on Standards in Reporting have suggested the term “nonspecific” as the preferred nomenclature for these aneurysms (1). The association of atherosclerosis and aneurysm formation is not completely clear. Aneurysmal degeneration usually develops in the atherosclerosis prone infrarenal abdominal aorta. With increasing aneurysm size, one finds greater plaque area, reduced medial thickness and fewer medial elastic lamellae. These changes may be predisposing factors for the preferential development of subsequent

Chapter 59 Abdominal Aortic Aneurysm

aneurysmal dilation in the abdominal aorta (34). In contrast, most patients with atherosclerotic occlusive disease do not have aneurysms. Also, in animal studies, regression of experimental atheromatous plaques resulted in aneurysmal enlargement (35). There is some evidence in favor of genetic risk factors for abdominal aortic aneurysms. (36,37). A strong relation between a positive family history and the occurrence of abdominal aortic aneurysms has long been known (38,39). The genes involved, as well as the inheritance pattern, continue to be investigated. The possibility of an immune mediated pathogenesis for abdominal aortic aneurysms that may be modulated exists, with the result being a variable spectrum from the degenerative to inflammatory aneurysm. The preferred location for arterial aneurysm formation in the distal abdominal aorta is of interest. Factors that interfere with aortic wall structural integrity may include the following: 䊏

䊏

䊏

䊏

䊏

Mature elastin and collagen are the major structural components of the aortic wall and act in a complementary fashion. Elastin is the main load-bearing component and provides elastic recoil, while collagen constitutes a strong but inextensible “safety net” at high pressures. The elastin content falls dramatically on passing from the thoracic to abdominal aorta (40). In addition, biochemical studies have shown decreased quantities of these two proteins in both the medial and adventitial layers of the wall of aneurysmal aortas (41,42). Breakdown of aortic wall proteins by an imbalance between enzyme activity and inhibition is an area of intense research. The various enzymes including the metalloproteinases and possible inhibitors are under investigation for their potential role in the formation and expansion of aneurysms (43–45). Elevated homocysteine plasma levels have been identified in patients with aneurysms. Investigators suggest that homocysteine may induce endothelial change and stimulation of aneurysm formation in these patients (46). Apoptosis of aortic smooth muscle cells is increased and vascular smooth muscle cell density is decreased within the medial layer of aneurysmal aortic tissue (47). Increased expression of intracellular adhesion molecules (ICAM-1) in aneurysmal aorta (48) may facilitate passage of inflammatory cells with stimulation of enzymatic activity (42). The role of intramural thrombus and aneurysmal degeneration has also been investigated. While intraluminal thrombus can significantly reduce aneurysmal wall stress (49), with increasing thickness of intraluminal thrombus a localized area of hypoxia is created. This may lead to increased, localized mural neovascularization and inflammation, as well as regional wall weakening (50).

705

These structural changes, with degeneration of aortic tissue at the cellular level and the tapering abdominal aorta with increased pulsatile stress (51), may contribute to aneurysmal formation (52). Once an aneurysm is present, enlargement is governed by physical principles. The tangential stress (t) within the arterial wall becomes greater when the pressure (P) within the aneurysm increases, the radius (r) within the aneurysm increases, and/or the thickness (d) of the aortic wall decreases. t = Pr/d Often, Laplace’s law is quoted, which is more accurately used to describe thin-walled spherical structures and is not as suitable for characterizing the stresses in arterial walls. Noninvasive methods of estimating the in-vivo wall stress distribution for actual abdominal aortic aneurysms on a patient-to-patient basis have been described. Using data from spiral computed tomography scans as a means of three-dimensionally reconstructing the in-situ geometry of the intact aneurysm, the wall stress was found to be complexly distributed, with distinct regions of high and low stress. Peak wall stress among abdominal aortic aneurysms was found on the posterior surface in all cases studied. The wall stress on the nonaneurysmal aorta was relatively low and uniformly distributed. Aortic aneurysm volume, rather than diameter, was shown to be a better indicator of high wall stresses and possibly rupture (53,54). Using a combination of three-dimensional reconstruction and clinical data analysis, the annual expansion rate of maximum transverse diameter was dependent upon a combination of largest aneurysmal cross-sectional area as well as tortuosity (55). These models points to the consideration that diameter alone may be suboptimal in predicting risk of rupture and perhaps with more advanced reproduction images the risk can be more clearly defined.

Risk Factors Age The prevalence of aneurysm seems to increase with age (3).

Tobacco The prevalence of aneurysm also seems to increase with smoking history (3). Not only are smokers at an increased risk, but the risk increases with the duration of smoking (56). Current and ex-smokers have an increased risk over nonsmokers. After the cessation of smoking, there is a very slow decline in the risk of the occurrence of an abdominal aortic aneurysm. The duration of exposure rather than the level of exposure seems to determine the risk of development of an aneurysm.

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Gender

Hernia

When evaluating gender as a potential risk factor, a group of veterans aged 50 to 79 years without a previous history of abdominal aortic aneurysm underwent ultrasound screening. A total of 122,272 men and 3450 women were successfully screened. An aneurysm of 3.0 cm or greater in diameter was found in 4.3% of men and 1.0% of women (56,57).

The prevalence of abdominal aortic aneurysm in men with a history of inguinal hernia is higher than in men without such a history. This remains true when one accounts for smoking history. Men with a history of inguinal hernia are at increased risk, most notably if they are cigarette smokers (64).

Chlamydia pneumoniae Family History Family history is a risk (56) that may be even more pronounced in brothers of familial cases (58). Aging brothers of patients with known abdominal aortic aneurysm have the highest risk for developing the disease; the prevalence of the disease in siblings older than 60 years of age is 18% (59).

Diabetes There is an inverse association between diabetes mellitus (56) and the occurrence of abdominal aortic aneurysm.

Hypertension Elevated diastolic blood pressure (56) as well as a higher pulse pressure (60) have been considered risks for abdominal aneurysm.

Chronic Obstructive Pulmonary Disease (COPD) The relation between abdominal aortic aneurysms and chronic obstructive pulmonary disease has been suggested from increased elastin degradation due to a reduced level of a1-antitrypsin in COPD (61). In population screening for abdominal aortic aneurysm in 4404 men aged 65 to 73, the high prevalence of abdominal aortic aneurysm among patients with COPD is more likely to be caused by medication and coexisting diseases rather than a common pathway of pathogenesis (62). This conclusion was drawn after adjusting for coexisting diseases associated with abdominal aortic aneurysm. However, further investigation in this area is required.

Hyperlipidemia Hyperlipidemia has been suggested to be associated with aortic aneurysm but the risk is not clear (56).

Carotid Stenosis The risk of aortic aneurysm is found to be greater in patients with carotid stenosis; however, only patients without diabetes account for the increased prevalence (63).

Indicators of infection with Chlamydia pneumoniae have been reported in association with expansion of abdominal aortic aneurysm (47). The mechanism of this association remains to be defined, but progression has been correlated with evidence of chronic C. pneumoniae infection (65).

Natural History and Risk of Aneurysm Rupture Although abdominal aneurysms can occasionally cause serious consequences from fistulization, thrombosis, and subsequent distal embolization, rupture of the aneurysm remains the most frequent, and often fatal, complication. Aneurysm rupture most frequently occurs through the posterolateral aortic wall into the retroperitoneal space but may occur anteriorly, into the free peritoneal cavity. This type of rupture is under-represented in most clinical series because most patients die before reaching the hospital.

Growth Rate The growth rates of AAAs and the accompanying risk of rupture without intervention vary with initial aortic diameter, with a more rapid growth seen in aneurysms of 50 mm or more. The mean enlargement rate for smaller aneurysms (less than 5.0 cm in diameter) was found to be 0.32 cm per year, and after 5 years of observation none of these aneurysms had ruptured (66). Cronenwett et al. (61,67), however, found higher rates (0.5 cm per year) of aneurysm enlargement among small abdominal aneurysms when chronic obstructive lung disease or systolic hypertension were coexistent (61,67). Aneurysm expansion occurred at a rate of 0.4 to 0.5 cm per year in one study, in which a 5-year rupture rate of 25% was reported for aneurysms greater than 5 cm (66). It is important to recognize that, although some aneurysms show no significant increase in size (15–20%), more than 80% do show progressive enlargement, and 15% to 20% grow at a rate greater than 0.5 cm per year (68). Also evident from the literature is the fact that the expansion rate of an aneurysm is variable within the same individual; the aneurysm may remain quiescent for months or years and then show a sudden increase in rate of growth. The rate of aneurysm growth does not differ with age or sex (69). There is no evidence that rate of growth can be accurately

Chapter 59 Abdominal Aortic Aneurysm Table 59.1 Estimated yearly rupture rate based on AAA size AAA Size (cm) 3–4 4–5 5–6 6–7 ≥7

Yearly Rate of Rupture (%) £1 3–5 5–7 7–19 >20

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and highly reliant on the motivation levels and means of the individual patients. Despite the indication for surgery, often patients will fall into high-risk categories and undergo surveillance. The need for close follow-up in this population may be even greater (79). If it appears that a patient will need treatment in the future it may be worthwhile operating while the patient is in a healthier condition.

Medical Management predicted for the aneurysm in any given individual. Clearly, a method to discern more accurately which aneurysms are at greatest risk is needed.

Rupture rate As in the case of growth rate, aneurysm size has been established as the single most reliable predictor of rupture (Table 59.1). Abdominal aneurysms under 5 cm in diameter have a reported rupture rate of less than 4% to 5% per year (16,70,71). The annual risk of rupture for aortic aneurysms between 5 and 6 cm in diameter has been estimated at 7% (61,71,72). For aneurysms with a diameter of 7 cm or greater, the reported annual risk of rupture is as high as 19%, implying a 5-year rupture rate of 95% (71,73). In Great Britain, the estimated risk of rupture of an AAA with an initial diameter of 45 mm did not exceed 20% over 5 years. An aortic aneurysm with an initial diameter of 30 mm has a 4.0% or less chance of rupture over 5 years (69). The risk of rupture within 3 years was 28% for AAAs of 5.0 to 5.9 cm and 41% for AAAs of 6 cm or greater (74). The risk of rupture is independently and significantly associated with female sex, larger initial aneurysm diameter, lower FEV1 (forced expiratory volume in 1 second), higher mean blood pressure, and current smoking (75), as well as COPD (76). There is a seasonal variation in the incidence of recorded deaths from abdominal aortic aneurysm in England and Wales, with a peak of deaths in the cold winter months. The underlying cause is unknown, but hypertension and tobacco smoking are predisposing factors to aortic aneurysm rupture. Exposure to tobacco smoke is known to be greater indoors in cold weather, and there is a winter peak of blood pressure in hypertensive patients (77). In the UK, criteria for surgical planning have been suggested to be an aneurysm of 6 cm or one that has increased by more than 1 cm over a 1-year period. Using these criteria, the workload is half of what it would be with a 5-cm cutoff and one-third more than for a 4-cm cutoff. This higher cutoff would result in 1% mortality among patients with ruptures that could have been treated. This value is lower than the operative mortality (78). These parameters are not what are commonly used in the US. Also, watchful waiting programs are imperfect

Clearly, patients known to have an aneurysm should stop smoking. The next step of controlling aneurysm growth by medication is under investigation. One area studied is the benefit of controlling hypertension with beta blockade over the long term (80–82). This should be limited to patients without COPD or chronic heart failure (CHF). Preoperative short-term treatment with doxycycline can suppress matrix metalloproteinase (MMP) expression within human aortic aneurysmal tissues. Given its pleiotropic effects as an MMP inhibitor, doxycycline may be particularly effective in suppressing aortic wall connective tissue degradation. While it remains to be determined whether MMP inhibition will have a clinically significant impact on aneurysm expansion, it is expected that this question can be resolved by a properly designed prospective randomized clinical trial (83,84).

Clinical Presentation Nonruptured Aneurysm A total of 75% of patients with an intact infrarenal aortic aneurysm are asymptomatic at the time of diagnosis (85). Most aneurysms are therefore discovered on routine physical examination or during a radiographic study performed for another reason. Symptoms may be caused by pressure on adjacent structures, distal embolization, dissection, thrombosis, or rupture of the aneurysm (86,87). Chronic vague abdominal or back pain is the most common symptom, present in up to one-third of patients. The mechanism by which this occurs is not certain, but direct pressure and stretching of adjacent somatosensory nerves seems to play a role. Severe back pain in the absence of rupture has been described as a result of erosion of a large aneurysm into the spinal column. Abrupt onset of severe back pain is characteristic of aneurysmal rupture or sudden expansion. Ureteral symptoms may be a result of tethering by the aneurysm and should raise suspicion of inflammatory aneurysm, or the presence of a large iliac component (88). Many patients with an abdominal aortic aneurysm come to the physician’s attention with clinical signs of associated vascular disease. Signs of lower extremity ischemia, including “blue toe syndrome,” may be caused by an abdominal aneurysm when particles of mural

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thrombus embolize to the distal circulation. Popliteal aneurysms, for example, are markers for abdominal aneurysms: of patients with popliteal aneurysms, 64% had an aortoiliac aneurysm (87). Conversely, femoropopliteal aneurysms are found in about 15% of patients with abdominal aortic aneurysm (89), whereas associated common or internal iliac aneurysms are found in 41% (87). Evaluation of patients with carotid stenosis identified abdominal aortic aneurysms in 20% of the population (90). Interestingly, evaluation of a population of patients with tortuous internal carotid arteries revealed an abdominal aortic aneurysm rate of 40% (91), further supporting the fact that multiple factors are responsible for the development of aortic aneurysms rather than atherosclerosis alone.

Ruptured Aneurysm The classic clinical presentation of ruptured aortic aneurysm is the triad of sudden-onset mid-abdominal or flank pain, shock, and the presence of a pulsatile abdominal mass. Only one-third of patients with ruptured abdominal aneurysm, however, present with all three findings (92). The pain may radiate into the groin or thigh and is usually severe, constant, and unaffected by position. The severity of the hypotension varies from mild to profound, and the duration of symptoms may vary from a few minutes to more than 24 hours. The latter occurs when small tears in the aortic wall cause a small leak that temporarily seals with minimal blood loss. This “silent period” is usually followed within several hours by frank rupture, which produces a catastrophic medical emergency. Therefore, although such a contained rupture may occasionally become chronic, urgent repair is indicated in most instances. Not infrequently, the hypotension accompanying aneurysm rupture will lead to angina pectoris and transfer to the cardiac intensive care unit instead of the operating room. Other frequent misdiagnoses in patients with ruptured abdominal aneurysm are ureteral colic, prolapsed lumbar intervertebral disk, sciatica, perforated peptic ulcer, acute pancreatitis, acute cholecystitis, mesenteric vascular occlusion, and acute diverticulitis. If rupture occurs into the adjacent vena cava, patients may present with lower extremity edema, high-output congestive heart failure, and a continuous abdominal bruit (sometimes accompanied by a palpable thrill), or with signs of systemic arterial insufficiency including angina pectoris, oliguria, and lower extremity or intestinal ischemia. Gross hematuria from intravesicular venous hypertension is another characteristic sign of aortocaval fistula (93). Gastrointestinal bleeding may be the first sign of rupture into the gut. The initiating event is probably mechanical bowel wall erosion caused by the expanding aneurysm. The most frequent site of primary aortoenteric fistula is the fourth portion of the duodenum. Failure to diagnose a leaking or expanding aneurysm all too often delays surgical intervention and leads to frank aneurysm

rupture with massive hemorrhagic shock in the emergency room or the radiology department.

Diagnosis Physical Examination Aortic aneurysms can usually be detected during a routine physical examination as a firm, pulsatile abdominal mass. When palpating the abdomen, it should be kept in mind that the aortic bifurcation lies at the level of the umbilicus. Furthermore, if the superior border of the aneurysm can be felt (at the level of the costal margins), the aneurysm is probably confined to the infrarenal aorta. In a study to evaluate the overall accuracy of abdominal palpation for detecting aortic aneurysm, a sensitivity of 68% was found. Sensitivity increased with diameter, from 61% for aneurysms of 3.0 to 3.9 cm, to 69% for aneurysms of 4.0 to 4.9 cm, and 82% for aneurysms of 5.0 cm or larger. In subjects with an abdominal waistline of 40 inches (100 cm) or less the sensitivity was 91% vs. 53% for girth of 40 inches or greater. When girth was less than 100 cm and the aneurysm was 5.0 cm or larger, sensitivity was 100% (94). In other studies, examination was less impressive and identified a sensitivity of abdominal palpation ranging from 29% for AAAs of 3.0 to 3.9 cm to 50% for AAAs of 4.0 to 4.9 cm and 76% for AAAs of 5.0 cm or greater (95). The presence of obesity, ascites, aortic tortuosity, excessive lumbar lordosis, or other abdominal masses can affect the accuracy of physical examination findings. The presence of other clinical manifestations of atherosclerotic disease, including carotid bruits, peripheral arterial aneurysms, or absence of peripheral pulses, increases the likelihood that a vague epigastric mass is indeed caused by an aortic aneurysm. Although most large aneurysms can be detected by abdominal palpation, more objective methods are available to measure size and to detect smaller aneurysms.

Plain Radiography In approximately 70% of cases, enough calcium is present in the wall of the aorta to make the correct diagnosis of an aortic aneurysm by plain radiography. Accurate determination of size is difficult on a plain film, and a negative abdominal radiograph cannot be relied upon to exclude the diagnosis.

Ultrasound Ultrasound is a relatively simple noninvasive test that provides structural detail of the vessel wall and atherosclerotic plaques and can accurately measure the size of the aneurysm in longitudinal as well as cross-sectional directions. Studies comparing ultrasound of the in-

Chapter 59 Abdominal Aortic Aneurysm

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FIGURE 59.1 (A) CT image of the abdominal aorta showing transverse diameter with mural thrombus. (B) CT angiography identifying the longitudinal extent of the aneurysm.

A

B

frarenal aorta with intraoperative measurements demonstrated accuracy to within 3 mm (96,97). The thoracic and suprarenal aorta cannot be easily visualized by routine ultrasound examination because of the overlying aircontaining lung tissue. For the same reason, determination of the relation between the cranial extent of the aneurysm (the neck) and the renal arteries has been unsatisfactory. Imaging, especially of the iliac arteries, is also limited by bowel gas or obesity. Advantages of ultrasound are its noninvasiveness, its wide availability (some emergency departments use small, portable units for immediate diagnosis), its lack of ionizing radiation, and its relatively low cost. Thus, ultrasound is the modality of choice for the initial evaluation of patients with a suspected abdominal aortic aneurysm, for population screening, and for follow-up surveillance to determine increase in size.

Computed Tomography Computed tomography (CT) is the optimal imaging modality prior to planned abdominal aortic aneurysm

A

repair. It can identify the proximal and distal extent of aneurysm including the thoracic portion, identify occlusive or aneurysmal disease in the visceral, renal, and iliac arteries, and identify the presence of multiple and accessory renal arteries. The size of the aortic lumen, amount and location of mural thrombus, and presence of calcified plaques in the areas of intended anastomosis are represented (Fig. 59.1). Also, major venous structures, as well as their abnormalities, can be identified (Fig. 59.2). If a dissection is present, it may assist in the determination of the true and the false lumen. CT is also helpful in identifying the retroperitoneal fibrosis that is associated with inflammatory aneurysms (Fig. 59.3), and the extravasation of contrast material, which is diagnostic of aneurysm rupture. Spiral CT with multiplanar views and threedimensional reconstruction may potentially replace conventional angiography if one considers the ability to evaluate renal, visceral and iliac occlusive disease (98–100). Three-dimensional and reconstructed images must always be correlated with the thin-slice axial images, as exist an element of error exists.

B

FIGURE 59.2 (A) CT of the abdominal aorta with a left-sided vena cava (arrow). (B) Vena cava passing anterior to the aorta in a transition from left to right.

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Part VII Aortic and Peripheral Aneurysms

Magnetic Resonance Imaging

Arteriography

Magnetic resonance imaging (MRI) can obtain images in cross-sectional, longitudinal, and coronal planes, without ionizing radiation or the need for toxic contrast agents. Non-nephrotoxic contrast agents such as gadolinium can help enhance the vascular anatomy. In one study, gadolinium-enhanced three-dimensional magnetic resonance angiography (MRA) was found to be similar to conventional angiography in detecting occlusive disease of the renal and visceral vessels in terms of sensitivity specificity and accuracy (Fig. 59.4) (101). This is not the case in all of such reviews, and therefore the technique should be limited to institutions familiar with it. The presence of monitoring equipment, cardiac pacemakers, or metallic surgical clips makes MRI impossible to perform. Also, MRI is less widely available and more expensive than either ultrasound or CT.

Owing to the presence of mural thrombus, which reduces the aortic lumen to near normal in most patients with aortic aneurysm, aortography is not a reliable method to determine the diameter or extent, or even to establish the presence, of an aneurysm. It can, however, be helpful in the preoperative evaluation, by providing the surgeon with accurate information about associated arterial disease involving the renal, visceral, or distal vessels (Fig. 59.5). Risks associated with aortography include the potential of renal damage from the use of toxic contrast material, distal embolization from catheter manipulation, and bleeding or pseudoaneurysm formation at the puncture site. The use of aortography as a routine preoperative test is therefore controversial. However, selective preoperative aortography seems to be appropriate when suprarenal or thoracoabdominal aneurysm or visceral ischemia is suspected, in patients in whom there is clinical evidence of lower extremity arterial occlusive disease, in patients with uncontrolled hypertension, unexplained creatinine elevation, or suspected horseshoe kidney, or in patients with femoral or popliteal aneurysms or who have previously undergone arterial reconstruction (102,103). It should be noted that spiral CT with three-dimensional reconstruction and gadolinium-enhanced MRA are increasingly useful alternatives to contrast arteriography (66). The advantage of angiography over these modalities is its ability to detect gradients across occlusive lesions if present, and potentially to direct treatment.

Indications FIGURE 59.3 CT of the abdomen with contrast enhancing inflammatory process involving the aortic wall in an inflammatory aneurysm.

Definitive therapy for abdominal aortic aneurysm is aimed toward prevention of aneurysm rupture by replacing the dilated segment of aorta with a prosthetic graft. To

FIGURE 59.4 (A) Gadoliniumenhanced MRA of an infrarenal AAA. (B) Gadolinium-enhanced MRA with three-dimensinal reconstruction.

A

B

Chapter 59 Abdominal Aortic Aneurysm

711

FIGURE 59.5 Angiogram of an aneurysmal abdominal aorta demonstrating (A) occlusion of the right common iliac artery (arrow) and (B) stenosis of the right renal artery (arrow).

A

B

determine whether a patient is a candidate for graft replacement, many elements need to be considered, including the risk of aneurysm rupture, the risk of surgical therapy, the patient’s life expectancy, and the anticipated quality of life after aneurysm replacement. If rupture of an abdominal aneurysm has been diagnosed or is suspected, emergency repair is indicated, regardless of the size of the aneurysm or age of the patient. Also, aneurysms that have become symptomatic in the absence of signs of rupture require urgent or emergent repair. The distinction between a symptomatic aneurysm that may be just expanding and frank rupture is often difficult to make. In documenting periaortic extravasation of blood, CT or MRI may be helpful, but the absence of this finding should not lead to unnecessary postponement of operative repair; as actual rupture can occur at any time. To decide whether an asymptomatic patient is a candidate for abdominal aortic aneurysm repair several accepted guidelines to help establish the indication for surgical repair are listed. On the basis of information currently available from review of the literature (104), the following indications for aneurysm repair can be formulated: 1.

2.

3.

Ruptured abdominal aortic aneurysm. Indications: any patient with documented or suspected rupture. Relative contraindications: any underlying medical condition that would otherwise preclude significant long-term survival (e.g., terminal cancer) or underlying issues related to quality of life that make repair unreasonable (e.g., dementia, elderly nursing home patient). Symptomatic or rapidly expanding aneurysm. Indications: any patient, regardless of aneurysm size, should be considered for aneurysm repair. Relative contraindications include preterminal condition, overwhelming medical problems, or an unacceptable quality of life. Asymptomatic aneurysms. Indications: aneurysms at least 4 cm in diameter or twice the diameter of the normal infrarenal aorta. Relative contraindications: life expectancy of less than 2 years; overwhelming

4.

5.

medical problems; unacceptable quality of life. For repair of small (<5 cm) aneurysms: recent myocardial infarction (<6 months); intractable congestive heart failure; severe angina pectoris; severe renal dysfunction; decreased mental acuity; markedly advanced age. Complicated aneurysms. Indications: embolism, thrombosis, fistulization, or aneurysms associated with symptomatic intra-abdominal occlusive disease, regardless of size. Relative contraindications: life expectancy of less than 2 years; overwhelming medical problems; unacceptable quality of life. Atypical aneurysms. Indications: dissecting, false, mycotic, or saccular aneurysms, as well as penetrating ulcers, may be indications for surgical treatment, regardless of size. Relative contraindications: life expectancy of less than 2 years; overwhelming medical problems; unacceptable quality of life.

Endovascular repair of abdominal aortic aneurysms is less invasive and, therefore, some investigators have suggested that this increasingly popular technique should broaden the indications for elective AAA repair. The benefit of endovascular repair in terms of quality of life years is most noted for an older population in poor health. We feel that, for most patients, the indications for AAA repair have been changed very little by the introduction of endovascular surgery (105).

Management of “Small” Abdominal Aortic Aneurysms The ultimate goal in treatment of patients with small asymptomatic aneurysms is to minimize the risk of rupture while avoiding unnecessary operations in those who would have died from other causes before abdominal rupture could occur. In otherwise healthy patients with aneurysms >5 cm in diameter, elective repair has been shown to result in improved survival. Optimal management of patients with small, asymptomatic aneurysms (3

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Part VII Aortic and Peripheral Aneurysms

to 5 cm) is less clear. Two different clinical strategies have been widely practiced: early repair (repair of the aneurysm when diagnosed) and watchful waiting (aneurysm size is measured every 6 months and repair is performed when the diameter reaches 5 cm or when the expansion rate exceeds 0.5 cm per year). Support for early repair comes from autopsy studies in which rupture rates of 23.4% are reported for aneurysms of 4.1 to 5 cm (71). Also, current population studies report expansion to a mean of 0.7 cm per year in those aneurysms between 4.5 and 4.9 cm at entry. Authors in these studies claim that elective operation for patients with abdominal aortic aneurysms between 4.5 and 5.0 cm should be strongly considered in a fit patient (106). Support for watchful waiting comes from studies overseas. In an attempt to determine whether early prophylactic open surgery decreased long-term mortality among patients with small aneurysms, the authors randomly assigned 1090 patients aged 60–76 years, with symptomless abdominal aortic aneurysms 4.0 to 5.5 cm in diameter, to undergo elective open surgery or ultrasonographic surveillance. If the diameter of aneurysms in the surveillance group exceeded 5.5 cm, surgical repair was recommended. Patients were followed for a mean of 4.6 years. An annual rupture rate of 1% was identified. The 30-day operative mortality in the early surgery group was 5.8%, which led to a survival disadvantage for these patients early in the trial. Mortality did not differ significantly between groups at 2, 4, or 6 years. The authors suggest ultrasonographic surveillance for small abdominal aortic aneurysms. They found that early surgery does not provide a long-term survival advantage for patients with abdominal aortic aneurysms of 4.0 to 5.5 cm in diameter (75,107). Unfortunately, previous autopsy studies estimated the risk of small aneurysm rupture but were likely to have overestimated given the likelihood of autopsy in an acute death. In contrast, in population-based studies, the cumulative risk of rupture for aneurysms with a small initial diameter most likely underestimates the risk of rupture in untreated patients, as patients with more rapidly expanding aneurysms were selected for elective repair (71,75,107). If, as is seen in the UK small aneurysm trials, the risk of rupture with a 4- to 5.5-cm aneurysm is as low as 1% per year, then the operative mortality for elective repair would exceed mortality risk by surveillance the first few years. Observation may be prudent in this circumstance. Alternatively, although the annual risk of rupture of small aneurysms appears to be relatively low, a percentage of these patients with such aneurysms will eventually require elective operation. Some authors argue that early repair leads to improved survival because better surgical outcome can be expected in younger patients with fewer comorbid conditions. In that time frame the aneurysm is likely to enlarge and the patient may progress into a higher risk category than previously. The definitive

answer to the question of what to do with patients with small abdominal aortic aneurysms has yet to be confirmed. The optimal management choice will have to be based on a careful individual assessment of risks. Factors favoring early repair include young age, lack of nearby medical facilities for emergency repair, poor patient compliance, and the presence of additional risk factors for rupture (104), including diastolic hypertension or chronic obstructive pulmonary disease (61).

Risk of Repair Risk of Elective Aneurysm Repair The results of elective aneurysm repair have steadily improved since the first successful resection and graft replacement of an abdominal aortic aneurysm in the early 1950s. In several large series spanning the past few decades, operative mortality rates of between 0.9% and 7% have been reported (108–118). These include major referral centers as well as community hospitals both in the US and abroad. To better assess the operative risk, one must therefore focus on a patient’s risk stratification and whether or not the surgery will be performed in an institution of excellence. Most of the deaths resulting from aneurysm repair occur in the so-called high-risk patients. If these patients are not considered, mortality rates of elective infrarenal aneurysm repair can be expected to be as low as 1% in centers of excellence (104). Age Risk of operative mortality in a population-based study increased significantly with advancing age: less than 65 years, 2.2%; 65 to 69 years, 2.5%; 70 to 79 years, 3.5%; and more than 80 years, 7.3% (119). Not all agree that age is a risk factor. Many feel it is probably less important than once considered if one accounts for poor preoperative underlying disease such as renal or pulmonary function (120). Support for this comes from a study of abdominal aortic aneurysm repair in octogenarians. There were no perioperative deaths in patients undergoing elective repair, and even emergent repairs had a 42.8% mortality rate. The authors found that most early deaths were related to cardiac disease (121). Gender Although there is a trend for reported elective operative mortality rates to be higher among women, the values do not always reach statistical significance. When corrected for coexisting medical condition, rates may actually be similar to those for men (119,122,123). Disease There is increased operative risk for patients with renal failure (11.8%) compared with those with normal renal

Chapter 59 Abdominal Aortic Aneurysm

function 3.4% (119). To determine if COPD increases the risk of operative death, a comparison of patients with and without COPD was undertaken in a Veterans Administration Hospital from 1997 to 1998. The mortality rate in elective aneurysm patients did not differ between patients with (3.7%) or without COPD (3.7%). However, COPD patients did require ventilatory assistance for a significantly longer period as well as having increased stay in the intensive care unit (ICU) and overall length of stay (120). Severe oxygen-dependent COPD is considered by many to be a contraindication to open AAA repair. A study reviewed a small series of patients limited by home oxygen-dependent COPD who underwent elective open infrarenal aortic aneurysm repair. There were no perioperative deaths and interestingly all patients were extubated within 24 hours (124). Experience Most published studies of elective abdominal aortic aneurysm repair report operations performed in tertiary referral institutions and thus may not reflect the outcome in the surgical community at large. A population-based study in the US was undertaken to document the results obtained across a broad spectrum of clinical practice in a defined geographic area and to examine the factors that influence the outcomes. The Maryland Health Services Cost Review Commission database was used to identify all the elective abdominal aortic aneurysm repairs that were performed in all the nonfederal acute care hospitals in the state from 1990 to 1995. Elective aneurysm repair was performed on 2335 patients. The in-hospital mortality rate was 3.5% (119). Operative mortality rate was noted to be inversely correlated with hospital volume, 4.3% in low-volume hospitals and 2.5% in high-volume hospitals, with no differences noted in the mean ages or comorbidity levels of patients who underwent operations. The operative mortality rate was inversely correlated with the experience of the individual surgeon: one case, 9.9%; two to nine cases, 4.9%; 10 to 49 cases, 2.8%; 50 to 99 cases, 2.9%; and more than 100 cases, 3.8%. The increased mortality in the most experienced surgeons may be a result of higher-risk patient base in that group (119). Interestingly, cost and length of stay also decreased with increased surgeon volume. Considered at high risk for abdominal aneurysm repair are patients with coexistent cardiac disease (previous myocardial infarction, unstable angina pectoris or angina at rest, cardiac election fraction of less than 35%, or congestive heart failure), patients with renal failure (serum creatinine level greater than 3 mg/dL), and those with coexistent pulmonary disease (room air PO2 less than 50 mmHg, elevated PCO2, or a forced expiratory volume of less than 1 L/s) (125). Also, morbid obesity (>50 kg or 100% over ideal body weight) is an independent risk factor for abdominal aneurysm repair.

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When faced with a high-risk patient with a large abdominal aortic aneurysm the surgeon has three choices: 1) to defer the operation until the patient becomes symptomatic; 2) to perform a “less risky” operation; and 3) to perform conventional aneurysm repair with intensive perioperative monitoring and care. Although it has been suggested that high-risk patients invariably die of their underlying disease (74), several authors have clearly documented that aneurysm rupture remains the primary cause of death in approximately 25% of these patients and that fewer than half die of the disease for which they were denied an operation (112). Conventional repair of abdominal aortic aneurysm, performed in 106 patients who qualified as high risk according to the abovementioned criteria, has been reported to have a mortality rate of 5.7%, with all survivors returning to their normal preoperative activities (126). In addition, late survival of these patients was not statistically different from that following aneurysm repair in non-high-risk patients for the first 2.5 years following the operation. Thus, it would appear that large abdominal aortic aneurysms, even in high-risk patients, should undergo direct graft repair when resources are available for intensive perioperative support. Various extra-anatomic procedures (described in a later section of this chapter) have been promoted for their stated lower associated operative risk, but this claim has never been substantiated. Endovascular transfemoral placement of aortic grafts is a promising technique for infrarenal aortic aneurysm repair. Long-term data are only now beginning to be available to compare results of this method with those of conventional aneurysm repair.

Risk of Emergency Repair of Ruptured Aneurysm Depending on the nature of the rupture and the condition of the patient upon presentation, reported mortality rates for aneurysmal rupture range from 20% to 90%, with an average overall mortality rate of approximately 50% (127–130). The current operative results for ruptured aneurysm, although somewhat improved from nearly two decades ago, are not nearly as favorable and have not nearly approached the results of elective aneurysm repair (131–134). This is evident from the worse prognosis for patients with compromised physiologic status. Preoperative indicators of hemodynamic decompensation such as loss of consciousness, hypotension, a hemoglobin level less than 10 g/dL, and a creatinine level greater than 1.5 mg/dL have been determined to be predictive of death (135). A study model for preoperative patient risk factors associated with mortality has been suggested. The five risk factors – age (>76 years), creatinine (Cr) >190 mmol/L, hemoglobin (Hb) <9 g/dL, loss of consciousness, and electrocardiographic (ECG) evidence of ischemia – were

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recorded for each patient. Operative mortality was 43%. The cumulative effect of zero, one, and two risk factors on mortality was 18%, 28%, and 48% respectively. All patients with three or more risk factors died (136). According to reviews, the most important factors contributing to failure in the treatment of ruptured abdominal aortic aneurysm are errors in diagnosis leading to delay of the operation, technical errors during the operation (mostly venous injuries), and undue delays in the induction of anesthesia (128). A separate category is those patients who are operated upon emergently for symptomatic aneurysm, but are not found to have a rupture at the time of exploration. The operative mortality for this group is intermediate between those for elective repair and emergent repair for rupture. The reason for this increased mortality when compared with elective repair may be the lack of a thorough preoperative evaluation and preparation.

Life Expectancy Five-year survival for elective aneurysm repair, as reported in several studies using life-table analysis, ranges from 49% to 84%, with an average of 61%; 40% of patients survive for at least 10 years (111,137,138). In another study, cumulative survival rates after successful ruptured AAA repair at 1, 5, and 10 years were 86%, 64%, and 33% respectively. These were significantly lower than survival rates at the same intervals after elective repair (97%, 74%, and 43% respectively) or survival of the general population (95%, 75%, and 52% respectively) (139). In a meta-analysis of 5-year survival following abdominal aneurysm repair in unselected patients, the mean 5-year crude survival was about 70% while the expected survival of a matched population was close to 80%. Interestingly, octogenarians who survive beyond 30 days survive longer than an age-matched population (140). In a study of octogenarians undergoing aortic aneurysm repair, the 5-year survival rate was 67% in the electively managed group and 34% in the emergency group (121). The long-term survival of patients greater than 75 years of age who underwent successful repair of ruptured AAA was evaluated. The 1-, 5-, and 10-year survival rates were 88%, 59%, and 26% respectively, at a median follow-up of 54 months. The median life expectancy for this patient group was 69 months. These data are similar to those of an age- and sex-matched population and therefore suggest that survivors of ruptured AAA repair enjoy a near-normal life expectancy (141).

therefore, a thorough assessment of operative risk includes evaluation of these organ systems.

Cardiac Evaluation Cardiac risk stratification for patients who are to undergo elective repair of an abdominal aortic aneurysm has three purposes. The first is to identify patients in whom the cardiac risk is so high that it outweighs potential benefits of an operation, indicating a more conservative approach. The second purpose is to identify patients with clinical problems that may be corrected before they undergo aortic reconstruction. The third is to identify those who are most likely to benefit from risk-reducing interventions such as invasive monitoring. In addition, preoperative risk assessment should be concerned with long-term cardiac mortality to ensure that those who undergo a major operation live long enough to benefit from the procedure. Cardiac risk assessment begins with an evaluation of the history and physical examination. That a negative cardiac history does not mean the patient is “safe” was clearly demonstrated by Hertzer et al. (142,143), who obtained coronary angiograms in all patients referred for vascular operations. Of patients with no history of ischemic heart disease, 59% still had significant, angiographically documented coronary artery disease. A history of myocardial infarction within 6 months before an operation has commonly been used as a strong indicator for postoperative infarction. However, there are many single clinical variables with potential influence on postoperative outcome. Multivariate analysis of preoperative risk factors has been valuable in the general population but is a less reliable predictor of postoperative cardiac complications in patients with vascular disease. This deficiency may be explained by the limitations in exercise tolerance in these patients, which, by masking symptoms of exertional angina, can lead to falsely low scores (144). Therefore, although a high-risk index may be useful in the prediction of postoperative cardiac complications, low test scores are not sensitive enough to identify low-risk patients reliably. In fact, multivariate clinical analysis models add little to basic clinical common sense: the sicker the patient, the higher the risk. We do use clinical evaluation to identify the patients at both extremes of the cardiac risk spectrum (see below), but an additional approach for stratification seems necessary for the majority of patients who are at apparent intermediate risk. Various noninvasive cardiac function tests have been introduced for this purpose, including ambulatory electrocardiographic monitoring, exercise stress testing, gated blood pool scanning, dipyridamole–thallium scanning (DTS), and dobutamine stress echocardiography, of which the last two seem to offer the most clinically relevant information (145).

Preoperative Evaluation

Dipyridamole–Thallium Scanning

A large number of patients with AAA have associated cardiopulmonary, peripheral vascular, renal, or liver disease;

The main benefit of dipyridamole–thallium scanning (DTS) in patients with peripheral vascular disease is

Chapter 59 Abdominal Aortic Aneurysm

that this test does not require the patient to exercise. The images obtained are interpreted as normal, reversible perfusion defect, or fixed perfusion defect. Since the introduction of DTS in the mid-1980s, a multitude of reports concerning its clinical usefulness have emerged. In the preoperative cardiac evaluation of 209 patients who had aortic repair, the dipyridamole–thallium stress test (DTST) was performed in 147 (70.3%) patients. Fifty-six of these patients had a normal DTST and only one (1.8%) had a perioperative myocardial infarction (MI). Forty-six patients had a fixed defect on their DTST, and three (6.5%) had perioperative MI. Forty-five patients had reversible defects on their DTST and 2 (4.4%) had perioperative MI with one cardiac death (146). Stress Echocardiography Intravenous dobutamine is administered under twodimensional digital echocardiographic monitoring of ventricular function and segmental wall motion. Abnormalities in segmental wall motion or a reduction in ventricular ejection fraction after dobutamine-induced stress are suggestive of significant functional coronary artery disease. In one study, dobutamine stress echocardiography was performed in 98 consecutive patients scheduled to undergo aortic and peripheral vascular operations (147). Of 23 patients with an abnormal response to dobutamine, 19 underwent coronary angiography, and all were found to have greater than 50% narrowing of the arterial lumen in one or more coronary artery distributions. Thirteen of these patients underwent prophylactic coronary artery bypass grafting or angioplasty, and all had an uneventful perioperative course. Of the 10 patients with a positive study who did not undergo coronary revascularization, four experienced a perioperative event. All patients with a negative study underwent a vascular operation without cardiac complications. During long-term follow-up, cardiac events occurred in 3% of patients with normal studies and 15% with abnormal studies. Although the numbers in this study are small, the results suggest that dobutamine echocardiography can predict perioperative cardiac complications in patients undergoing vascular operations. This, in addition to its safety, low cost (approximately half that of thallium imaging), and provision of additional information such as global ventricular function, may make this test a useful alternative. However, future studies to further establish sensitivity and specificity in perioperative cardiac risk assessment are needed. If one accepts the role of noninvasive testing, two questions remain: 1.

2.

Does every patient need such a test in preparation for elective aneurysm repair and, if not, which patients do? Do all patients with a positive test result need coronary angiography and, if not, which patients do?

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Our approach (148,149) to the preoperative cardiac evaluation of a patient with an abdominal aortic aneurysm is based primarily on clinical criteria. Patients are initially screened for a history of previous myocardial infarction, previous or concurrent episodes of angina or congestive heart failure, symptoms of cardiac rhythm disturbance, and the presence of diabetes. Physical examination focuses on evidence of arrhythmia, congestive failure, or valvular heart disease. The ECG is examined for evidence of arrhythmia or previous myocardial infarction and signs of ongoing ischemia. We carefully evaluate the patient’s lifestyle and level of activity. If a patient has no history or concurrent symptoms of coronary artery disease, leads an active and vigorous lifestyle (e.g., active laborer, tennis player), and has a normal ECG and chest radiograph, we would recommend aneurysm repair without further cardiac evaluation. On the other hand, patients who have class III or class IV angina or those who have recent episodes of congestive failure would usually undergo coronary angiography and ventriculography, without an intervening noninvasive cardiac study. Between these two extremes, however, lie a large number of patients who either have mild, stable symptoms of coronary artery disease or are asymptomatic but lead a sedentary lifestyle and who might never perform activity strenuous enough to elicit any symptoms of myocardial ischemia. It is these patients, we feel, who are most likely to benefit from a preoperative noninvasive cardiac test. Unfortunately, even after the patient has been at high risk for a cardiac complication by noninvasive cardiac testing, the optimal management strategy remains controversial. No clinical trials have adequately evaluated cardiac outcome with or without preoperative coronary revascularization. Obviously, such a study should weigh the combined morbidity and mortality of the sequential cardiac and peripheral vascular procedures. Awaiting definitive data, we use preoperative coronary revascularization only when the patient’s cardiac disease warrants this procedure independently of the need for a peripheral vascular operation. When this is the case, the patient is recommended to undergo coronary angiography followed by percutaneous transluminal angioplasty, if possible, or coronary artery bypass grafting. If coronary angiography discloses noncritical lesions (<50% of lumen) or nonreconstructible lesions, or if the patient declines coronary revascularization, we will then proceed with aneurysm repair under maximum cardiac monitoring and pharmacologic support. In summary, we support the selective use of noninvasive cardiac evaluation in patients with abdominal aneurysm, based on clinical evaluation and categorization of risks. Those with severe angina and those with positive DPT scan or stress echocardiography outcome are further evaluated by coronary angiography. Prophylactic coronary angioplasty or revascularization is recommended only for those patients who appear to have truly critical lesions that might pose a threat to their life or result in the significant loss of myocardial function. Other

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patients are offered vascular reconstruction without prophylactic myocardial revascularization, but with the use of intensive perioperative monitoring and pharmacologic support.

Evaluation of Pulmonary Function Pulmonary function is initially assessed from the history, physical examination, and chest radiograph. A history of dyspnea, smoking, asthma, previous lung resection, or occupational exposure may indicate compromised pulmonary function and justify further evaluation, including arterial blood gas determination and spirometric tests. Patients who continue to smoke should be encouraged and helped to stop smoking for at least 1 month before the operation. Both obstructive and restrictive pulmonary disease can be effectively identified and quantified by spirometric testing. Parameters measured include vital capacity (VC), forced expiratory volume in 1 second (FEV1), maximal mid-expiratory flow (FEF25–75%), and maximum voluntary ventilation (MVV). Critical values for VC are 30% to 50% of predicted values (150). FEV and FEF25–75% assess the resistance of the smaller airways, with the latter being the most sensitive. Critical values are less than 50% of predicted for both tests. The MVV reflects both airway resistance and ventilatory function, with high-risk patients having values less than 50% of predicted (151). The presence of significant lung disease should not be considered a contraindication to operation but rather identify those patients that require special preoperative and postoperative pulmonary care (152).

Peripheral Vascular Disease The patient should be questioned about symptoms of extracranial carotid artery disease and examined for the presence of carotid bruits. The need to screen and repair significant carotid lesions in asymptomatic patients prior to aortic reconstruction is often mentioned. A study was undertaken to determine the true prevalence of internal carotid artery disease in asymptomatic patients. Patients with abdominal aortic aneurysms underwent duplex ultrasound screening for carotid artery disease prior to aortic reconstruction. Internal carotid artery stenosis ≥50% occurred in 26.7% of the total group. Interestingly stenosis ≥50% was more common in the aortoiliac occlusive disease group (39.6%) than in the aneurysmal group (17.3%). Severe disease (70% to 99%) was also more common in the occlusive than in the aneurysmal group (9.9% versus 3.6%) (153). If faced with a hemodynamically significant internal carotid artery stenosis in the absence of symptoms one might consider preliminary prophylactic endarterectomy in a good-risk patient. A symptomatic carotid stenosis, however, should be endarterectomized before aortic reconstruction is undertaken. Patients with complaints that suggest intestinal or lower extremity ischemia should undergo preoperative

biplanar aortography with runoff. This will allow a plan for revascularization of the involved segment, if necessary.

Evaluation of Renal and Hepatic Function Patients with unexplained renal failure manifested by elevated blood urea nitrogen and serum creatinine levels or uncontrolled hypertension should be evaluated for the possibility of renal artery stenosis. The use of intravenous radiographic contrast material should he minimized in the immediate preoperative period. Consideration in this instance should be given to MRA with gadolinium. Baseline liver function tests should be ordered for comparison to postoperative values in case of liver failure.

Perioperative Care Perioperative management of patients with abdominal aortic aneurysm involves the standard care applied to any patient undergoing a major operation. Several recent advances, however, warrant a separate discussion. There has been increased emphasis on minimizing the use of blood bank transfusions to avoid the small chance of related morbidity. Several different strategies toward this goal have been introduced. The use of intraoperative autologous blood has been a focus of attention. In a prospective randomized study it was shown to decrease homologous requirements, infectious complications, and length of stay (154); however, this finding has not been universal (155). First, the patient may “donate” his or her own blood, ideally starting 4 to 6 weeks before the anticipated aortic reconstruction (156). The starting hemoglobin level should be greater than 11 g/dL, and patients usually donate once per week, although more intensive schedules have been used. Donations are halted 1 week before the planned operation. Administration of human recombinant erythropoietin may increase the amount of blood a patient can donate over a given period (157). A second, more commonly used option is intraoperative blood salvage with the so called “cell saver” (158). Currently used systems can wash and centrifuge one unit of packed cells in 3 minutes. In one study, homologous transfusions during and after abdominal aortic aneurysm repair were avoided in 21% of patients (159). No complications or deaths could be attributed to the use of the cell saver; and frequently studied coagulation parameters were not adversely affected. The third method involves perioperative hemodilution (160). At the beginning of the operation, before the anticipated major blood loss, whole blood is removed from the patient and the lost volume is replaced with crystalloid solution. Once bleeding is controlled at the end of the operation, the removed whole blood is retransfused. Hematocrits of 20% to 24% are well tolerated by most patients but require an increase in cardiac output to com-

Chapter 59 Abdominal Aortic Aneurysm

pensate for the loss of oxygen-carrying capacity. Recent work has suggested that the incidence of paraplegia is increased after isovolemic hemodilution, reason for caution with the application of this technique during repair of suprarenal or thoracoabdominal aneurysms (161).

Perioperative Management of Patients with Severe Cardiac Disease Continuous recording of arterial blood pressure and frequent arterial blood sampling are facilitated by placement of a radial artery cannula. A flow-directed pulmonary artery catheter (Swan–Ganz) measures left ventricular filling pressure and cardiac output, thus facilitating optimal administration of intravenous fluids and inotropic or vasodilator therapy. In addition, a sudden rise in the measured end-diastolic pressure has been correlated with myocardial ischemia (162). The utility of routine pulmonary artery catheters is frequently brought into question and not agreed upon by all. Its utility in patients who undergo aortic surgery was investigated in a randomized study. It was determined that pulmonary artery catheters did not significantly aid in outcome and their use was actually associated with a greater amount of intraoperative complications. Variables such as cardiac risk factors and adenosine thallium scintigraphy may be more important predictors of cardiac events in patients who undergo aortic operations (163). An alternative, even more specific and direct, method of detecting intraoperative left ventricular filling status and myocardial ischemia is two-dimensional transesophageal echocardiography (TEE). Segmental wall motion is continuously monitored, and abnormalities are highly suggestive of myocardial ischemia, often preceding electrocardiographic changes (164). TEE may be particularly helpful during aortic clamping and unclamping. The dynamic real-time echocardiographic images provide instant information of ventricular filling status, allowing immediate adjustments with either additional volume loading or nitrate infusions (165). If, in spite of optimal fluid and blood replacement and maximal pharmacologic support, the cardiac index cannot be maintained above 2 L/min/m2, thought should be given to the institution of prophylactic intra-aortic balloon counterpulsation (126,166). After the proximal aortic anastomosis has been completed, the balloon can be introduced percutaneously through the groin and guided under direct vision or palpation through the iliac artery and passed through one limb of the graft. A tourniquet is then placed on that limb and the contralateral limb is clamped. The aortic clamp is removed and the balloon can be advanced into the proximal descending thoracic aorta. Balloon counterpulsation is started. after which completion of the iliac anastomosis can proceed in a standard fashion. Counterpulsation is generally maintained at a rate of 1:1 (balloon pulsation to cardiac contraction) for 24 to 48 hours until the patient is adequately stabilized. Balloon assist is then weaned over a 1- to 2-hour period,

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and the balloon is removed. It should be mentioned that only 6% of patients that were preoperatively considered to be at high risk required intra-aortic balloon counterpulsation, whereas the majority of patients could be managed successfully with fluid replacement and pharmacologic support.

Perioperative Management of Patients with Severe Pulmonary Disease Preoperative pulmonary preparation in these patients includes systemic antibiotics, bronchodilators, nebulizer or inhalational treatments, or postural drainage, depending upon the specific underlying pulmonary disorder. Sputum production should be quantified and minimized with cessation of smoking and removal of environmental irritants. The use of such a regimen combined with early extubation, incentive spirometry, ambulation, and aggressive pulmonary toilet has been shown to reduce postoperative pulmonary complications (151,152). Although aneurysm repair can be performed safely through a standard transabdominal approach, it has been suggested that a retroperitoneal approach may allow more rapid recovery of pulmonary function after the operation. In addition, the use of epidural catheters for pain relief without sedation may be beneficial in allowing these patients to cough more vigorously.

Epidural Anesthesia Addition of epidural anesthesia has the theoretical advantages of decreasing cardiac preload and afterload, increasing lower extremity blood flow by providing a temporary sympathectomy, and improving postoperative pulmonary function by minimizing pain (167). Potential disadvantages, however, include the increased risk of hypotension following aortic declamping, increased fluid requirements, and postoperative urinary retention. The initial fear of epidural hematoma formation in these often heparinized patients has not been substantiated (168).

Operative Techniques Nonruptured Aneurysm, Transabdominal Approach The patient is placed in a supine position on the operating table. The surgeon may stand on either side of the table, but if the number of assistants is limited the left side usually offers a better exposure and more freedom of handling. Besides personal preference, the choice between a long midline incision and a wide transverse incision depends mainly on the relative importance of the speed with which aortic control must be attained, postoperative pain, incisional strength, extent of the aneurysm, degree of obesity and coexistence of chronic pulmonary disease.

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FIGURE 59.6 Exposure of an AAA through a transabdominal midline incision with viscera mobilized to the right. Duodenum (large arrow) and sigmoid colon (small arrow) are also reflected for better exposure.

The full-length midline incision provides access to the entire abdominal cavity, including the supraceliac aorta and iliac arteries, and is easy to make and close. A wide transverse incision, just above or below the level of the umbilicus, offers similar exposure but is more time-consuming to create and to close than the midline incision. It is said to be stronger and to cause less postoperative pain (and therefore less interference with respiratory function), but objective supporting data are lacking. Both incisions permit the thorough abdominal exploration that should be a preliminary step in all elective operations. as a significant incidence of coexisting pathology has been reported, particularly in the patient with symptoms that are not clearly due to the aneurysm (169,170). The extent of the aneurysm, especially its upper and lower limits, as well as the condition of the adjacent arteries, particularly mesenteric, internal, and external iliac, is determined by palpation. Manipulation of the aneurysm itself should be avoided until proximal and distal control have been obtained, in order to minimize the chance of distal embolization. A longitudinal incision in the peritoneum overlying the distal aorta, just to the left of the base of the mesentery, is made and carried upward around the left margin of the distal duodenum to the inferior border of the pancreas, and downward over both iliac arteries. The ureters, crossing anteriorly to the common iliac arteries, are identified and protected. Especially in sexually active males, extensive dissection around the aortic bifurcation and proximal left common iliac artery needs to be avoided to minimize injury to the sympathetic nerves that course anterior to this vessel (171). After the distal duodenum has been mobilized, the small intestine may be either packed into the right side of the abdomen or eviscerated and wrapped in moistened towels or laps and retracted to the right (Fig. 59.6). The inferior mesenteric vein, which comes into view after division of the ligament of Treitz, may be ligated and divided if necessary (Fig. 59.7). The left renal

FIGURE 59.7 Intraoperative photo of an AAA requiring ligation of the left renal vein (large arrow) to improve juxtarenal aortic exposure. Also ligated is the inferior mesenteric vein exposed on the aneurysm wall (small arrow).

vein is usually found slightly more cephalad in a deeper plane. In aneurysms that extend to the renal arteries (juxtarenal) or involve them (pararenal), this vein may need to be dissected free to allow upward retraction. Prior to this maneuver, the left gonadal vein may need to be ligated and divided Occasionally, the left renal vein is found stretched tightly over the neck of the aneurysm, in which case it can usually be divided medial to its gonadal and adrenal tributaries (Fig. 59.7). Elevation of venous pressure is indicated by the degree of venous distension and does not require formal measurement. It may occasionally dictate later reanastomosis. Long-term patency in this situation is excellent due to the vein’s high flow rate (172). Fifty-eight patients who had division of the left renal vein were examined. There was no significant difference in the mortality rate when compared with the group with preserved vein. After 1 month, there was no significant difference in the number of patients who had a sustained elevation of serum creatinine level. This supports the safety and utility of renal vein division during juxtarenal aortic surgery (173). Proximal control is obtained by first dissecting down to the anterior aortic wall just proximal to the “neck” of the aneurysm, and then staying in this “inside” plane, proceeding laterally and posteriorly around the circumference of the aorta. Usually, encirclement is not recommended, as the proximal clamp can be placed while simply feeling the aorta between two fingers. Before clamping, however, the renal and superior and inferior mesenteric arteries should be palpated for pulsations and thrills. If the inferior mesenteric artery is not already occluded, it can be controlled temporarily using a small vascular clamp or a double loop of Silastic tubing. It should not be ligated at this point, especially if the hypogastric arteries are occluded or may have to be sacrificed for aneurysmal disease. A prosthetic graft of the appropriate size is selected. The choice of graft material and its mode of construction

Chapter 59 Abdominal Aortic Aneurysm

FIGURE 59.8 Bifurcated Dacron graft within aneurysm sac following aneurysmoraphy of an aortoiliac aneurysm.

are a matter of personal preference. With the advent of collagen or gelatin sealing, which averts the need for preclotting, knitted collagen-coated Dacron grafts are most popular (Fig. 59.8). At this point in the operation, adequacy of vital signs and urinary output is ensured and systemic heparin is administered, before proceeding with aortic clamping. The aneurysmal segment is excluded by placing the distal and proximal vascular clamps, and the aneurysm is opened longitudinally with the upper end of the incision “T’d” into lateral extensions in the proximal neck. The posterior wall of the aorta is not divided. All mural thrombus and atheromatous debris should be removed from the aneurysm wall. Several studies have shown a remarkably high incidence of positive bacterial cultures of this material, varying from 10% to 40% of cases. The significance of these positive cultures is not known, but most have been due to coagulase-negative Staphylococcus species, an organism commonly found in aortic graft infections. (It has been our practice to quickly irrigate the thrombectomized wall with antibiotic solution). With the inside of the aneurysm exposed, the assistant controls bleeding from the lumbar artery orifices by compression with a gauze pad. By slowly moving the pad downward, the respective orifices are oversewn with figure-of-8 suture ligatures. Once collateral flow into the opened aneurysmal sac has been controlled in this manner, the upper anastomosis is begun. From inside the lumen, a distinct ring, formed by the neck of the aneurysm, can usually be identified and used for the posterior suture line. Starting in the midline, one attempts to include a double thickness of the posterior wall for extra strength, using No. 000 polypropylene suture with double needles. The anterior half of the suture line is completed with continuous, deeply placed bites. When the aortic wall is extremely friable, pledgets of Teflon or Dacron felt may be incorporated in the suture line. These should rarely be necessary if the curve of

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the needle is carefully observed as it is pulled through the aortic wall and undue upward tension on the suture is avoided by the assistant while “following” each new suture placement. After completion of the upper anastomosis, the distal graft is clamped and the aortic clamp is slowly released to test for suture line bleeding, particularly from its posterior aspect, because this cannot be easily exposed again once the distal anastomosis has been completed. The lower anastomosis can be performed to the distal aorta if the iliac arteries are not aneurysmal. In this situation a straight tube graft can be used, which is sewn to the distal aorta at the level of the bifurcation, from the inside, encompassing both common iliac artery orifices. If iliac artery aneurysms are present, they may be incised anteriorly so that the limbs of a bifurcated graft, which are placed under the ureters, can be sewn into an oblique ellipse that includes the orifices of both the internal and external iliac arteries (Fig. 59.8). As previously described, in sexually active men, extension of the arteriotomy onto the left iliac artery should be interrupted near the “crotch” to avoid injury to the sympathetic nerves (171). Before completing each anastomosis, distal patency should be ensured by observing brisk backflow, using balloon embolectomy catheters if needed. Every effort should be made to ensure antigrade perfusion in at least one internal iliac artery in order to minimize the risk of postoperative ischemia of the left colon. Once the first iliac anastomosis has been completed, flow should be restored into that extremity. “Declamping” hypotension, caused by reperfusion of a dilated distal vascular bed with concomitant venous return of vasoactive substances and products of anaerobic metabolism, is rare when adequate intravenous fluids have been given. It can be further minimized by slowly releasing the clamp while watching the arterial pressure display on the monitor and allowing flow into the internal before the external iliac artery. This maneuver has the further advantage of diverting possible debris into the hypogastric circulation rather than into the legs. The authors have found the additional use of buffering and pressor agents rarely necessary and, if hypotension does occur, prefer to reclamp and restore blood volume rather than resorting to pressor drugs. After restoration of flow to both extremities, attention can be turned to the inferior mesenteric artery and circulation of the sigmoid colon. If the inferior mesenteric artery is already occluded, if it is small and not associated with palpable superior mesenteric artery occlusive disease, if it has brisk backflow on release of the controlling clamp, if the color of the sigmoid colon and the pulsations in its mesenteric arcades are good, and if at least one internal iliac artery is patent, reimplantation of the inferior mesenteric artery is not necessary. In questionable cases, the presence of Doppler ultrasound signals in the antimesenteric bowel wall or an adequate inferior mesenteric artery stump pressure may settle the question of

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bowel viability. In the rare instance that the circulation of the sigmoid colon seems marginal, particularly if the superior mesenteric or internal iliac arteries are occluded, a cuff of the aortic wall around the orifice of the inferior mesenteric artery may be excised and anastomosed to the left side of the graft. Finally, the remaining shell of the aneurysm is sutured back around the graft, followed by closure of the overlying peritoneum. Special care should be taken to isolate the graft and the proximal anastomosis from the overlying duodenum, to minimize the risk of aortoduodenal fistulization. If necessary, a pedicle of omenturn may be interposed for this purpose. Before closure of the abdominal wall, the small bowel is inspected and placed in its normal position.

Retroperitoneal Approach Among the advantages claimed for this approach, in which the peritoneal cavity is not entered, are less postoperative respiratory compromise, lower intravenous fluid requirements, less intraoperative hypothermia, and a shorter period of postoperative ileus with reduced need for nasogastric intubation. However, compared with a transabdominal approach in prospective studies, no significant differences were found (174,175). A study was performed comparing the transabdominal approach with the retroperitoneal approach for elective aortic reconstruction in patients who are at high risk. The retroperitoneal approach was associated with a significant reduction in cardiac and in gastrointestinal complications. Despite longer operative time and blood loss, there was a decreased need for postoperative analgesia. Hospital length of stay was significantly lower in the retroperitoneal group (176). One major disadvantage of this approach is that the contents of the peritoneal cavity are not available for inspection. In addition, access to the right iliac artery is often limited, especially if the aneurysm is large or if there is a large iliac artery aneurysm. Reports of late complications such as incisional hernias have appeared (177). Nevertheless, many surgeons prefer this approach for elective cases, and some even use it for ruptured aneurysms that are contained because of the ability to perhaps more easily control the upper aorta (178). Furthermore, the retroperitoneal approach may be particularly beneficial in patients who have undergone previous intra-abdominal operations, or in patients with inflammatory aneurysm, aneurysm with horseshoe kidney, suprarenal aneurysm, or extreme obesity (179). For the retroperitoneal approach, the patient is placed in a semilateral position with the left side up but with the hips rotated back toward the supine position, to allow access to both femoral arteries. An oblique incision extending from the left 11th intercostal space is carried down along the lateral border of the rectus sheath. The retroperitoneal space is then entered and the peritoneal sac is retracted medially, thus allowing exposure of the entire abdominal aorta. Repair of the aneurysm is then

performed in a similar fashion as was described for the transabdominal approach.

Transfemoral Endovascular Approach This technique, pioneered by Parodi and colleagues (26), is currently being applied in several centers in the US. A detailed discussion is given in Chapter 60.

Ruptured Aneurysm Every patient with a pulsatile epigastric mass or a known AAA who presents with sudden onset of abdominal or back pain is assumed to have a ruptured aortic aneurysm until proven otherwise. Emergency management prior to transportation to the operating room is controversial. It is widely believed that clot formation, retroperitoneal tamponade, and the degree of hypotension plays a critical role in the prevention of further bleeding. Thus, if the patient is in a state of hemodynamic shock, the initial urge to proceed with aggressive fluid resuscitation and restoration of blood pressure should probably be suppressed. Crawford and associates even recommend maintaining systolic blood pressure between 50 and 70 mmHg (180). Others believe that a blood pressure in the range 70 to 90 mmHg would serve the purpose of preventing further hemorrhage without severely impairing myocardial perfusion (181). The need for diagnostic tests in the setting of a suspected ruptured abdominal aneurysm is controversial. If the patient has an obvious aneurysm by physical examination and symptoms that are consistent with rupture, emergency laparotomy without further tests is justified. Computed tomography leads to unnecessary delay of therapy in this group of patients who, even if the wrong diagnosis was made, were found to benefit from emergency operation in 75% of cases (182). In hemodynamically stable patients with vague or atypical symptoms, in those with small aneurysms, and in those for whom the diagnosis is uncertain, CT may be helpful. The first priority upon arrival in the operating room is to control the hemorrhage by clamping of the proximal aorta. Emergency left thoracotomy for aortic control is almost never needed and should be considered only when cardiac arrest occurs. If the patient is hypotensive, skin preparation and draping should be performed very rapidly prior to the induction of anesthesia, since the vasodilatory effects of anesthetics, coupled with relaxation of the abdominal wall and loss of its tamponade function, may precipitate a sudden and severe drop in blood pressure. If, upon opening the abdomen through a midline incision, the rupture is found to be contained, proximal control of the aorta should be obtained before opening the retroperitoneal hematoma and is usually possible at the neck of the aneurysm, just below the left renal artery. If the hematoma is so large that proximal control cannot be easily obtained infrarenally, the supraceliac aorta can be compressed on the vertebral bodies by an assistant’s hand or a Pilling aortic compressor, without formal dissection.

Chapter 59 Abdominal Aortic Aneurysm

The hematoma can then be entered and a clamp placed proximal to the neck of the aneurysm. If it is difficult to identify the neck and the patient is rapidly deteriorating, the aneurysmal sac can be opened and clamp placement guided by palpation of the neck from within. In the authors’ experience, the problem of gaining proximal control has been greatly simplified by the use of an aortic occlusion balloon catheter. This device can be inserted into the midbrachial artery through a cutdown, while resuscitation and anesthetic induction are proceeding. Partial inflation of the balloon just as it enters the thoracic aorta will direct the catheter distally, where it is advanced to the proper level in the abdominal aorta (estimated by measuring the distance from the cutdown site to the epigastrium prior to insertion). The balloon can then immediately be inflated if the patient’s condition deteriorates. Otherwise, it is inflated only if free intraperitoneal bleeding is encountered, or immediately before entering a large retroperitoneal hematoma. Because renal flow is invariably impaired by the balloon, it should be deflated as soon as formal proximal control has been achieved by clamping. Distal control must also be achieved, and collateral bleeding into the opened aneurysmal sac is controlled systematically in the manner previously described. The remainder of the procedure is similar to that for elective aneurysm repair. After the bleeding has stopped, intravascular volume should be restored with appropriate blood products and intravenous fluids before proceeding with restoration of flow to the lower extremities. It has been our practice to administer 25 mg of mannitol and 40 mg of furosemide at this point in an attempt to reduce the incidence of postoperative renal failure.

Alternative Methods of Treatment of Aortic Aneurysm Distal ligation with extra-anatomic bypass, as a less invasive alternative for aneurysm control, has been carefully explored by Berguer and associates (183) and Karmody and colleagues (184). A preliminary axillofemoral, femorofemoral bypass is performed followed by ligation of the proximal femoral vessels. Thrombosis of the aneurysm occurred within 72 hours in more than 90% of cases. Unfortunately, however, thrombosis of the aneurysm did not prevent rupture in 10% to 20% of patients (185–187). Recently, in a small series by combining extraanatomic bypass graft and complete exclusion of the AAA by ligation of the common iliac arteries and a coil embolization, an effective, less invasive treatment option for patients with AAA and prohibitive operative risk, a 75% 1-year survival with no ruptures was achieved. The study authors emphasize the need for complete embolization documented by decreased aneurysm size (188). Although this technique initially held promise as a safer means of managing abdominal aortic aneurysm in high-risk patients, the morbidity and mortality have been shown to be at least as high as with direct repair (126).

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Exclusion of the aneurysm by means of prosthetic graft via a direct approach remains the gold standard for managing abdominal aortic aneurysm. In a suitable candidate, endovascular grafting provides a much less invasive approach, with similar short-term results as for open repair. The long-term follow-up is currently under investigation to evaluate of the impact of endovascular aneurysm repair on the rate of open surgical repair. Zarins found no significant change in the number of patients undergoing open surgical repair and no significant difference in the rate of infrarenal and complex repairs. Endovascular repair appears to have augmented treatment options rather than replaced open surgical repair for patients with AAA. Patients who previously were not candidates for repair because of medical comorbidity may now be safely treated with endovascular repair (189).

Special Considerations Associated Pathologic Conditions and Concomitant Surgical Procedures Gallstones Unexpected asymptomatic cholelithiasis is encountered in up to 20% of patients undergoing aortic aneurysm repair. Several authors have demonstrated the safety of concomitant cholecystectomy and aneurysm repair (190,191). Their argument for performing this procedure is the postulated high incidence of postoperative cholecystitis when the stone-containing gallbladder is left alone during aortic repair, coupled with a low reported incidence of graft infection. Follow-up in these studies, however, was rather short, especially when considering the often long interval between the aortic operation and the first manifestations of graft infection. Arguments against performance of incidental cholecystectomy include the finding that in most instances the cholecystitis following aortic repair has been acalculous, as well as the high reported incidence of positive bile cultures in the presence of gallstones (up to 30%). Appraising the often devastating consequences of aortic graft infection, the authors recommend performance of incidental cholecystectomy at the time of aortic reconstruction only in selected cases. Malignant Tumors Unexpected tumors, mostly colonic, are found in 4% to 5% of patients undergoing aortic aneurysm repair, particularly in those who present with abdominal pain. As outlined by Szilagyi et al. (170), colonic resection should take precedence over aneurysm repair only if an absolute indication (bleeding, perforation, or obstruction) is present. If no such compelling reason exists, aneurysm repair is performed, followed by proper evaluation and, usually 2 to 3 weeks later, resection of the colonic lesion. When the presence of a colonic malignancy is known beforehand, an

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Part VII Aortic and Peripheral Aneurysms FIGURE 59.9 (A) Aortic angiogram reveals infrarenal aneurysm with left renal artery stenosis. (B) Balloon angioplasty of the left renal artery. (C) Angiogram of left renal artery following angioplasty and stent placement.

B

A

C

estimate should be made for each individual patient as to which lesion is expected to cause a complication first. In general, aneurysm repair is performed first, as colonic resection can be performed sooner after aortic reconstruction than the opposite, especially when the latter is followed by a septic complication precluding aneurysm repair for weeks or months thereafter. Concomitant Vascular Disease Often, the question of whether to perform simultaneous prophylactic repair of asymptomatic renal artery stenosis in patients who require infrarenal aortoiliac reconstruction is discussed. A study documenting the natural history of asymptomatic renal artery stenosis in patients who require aortic reconstruction was performed. The authors found that patients with ≥70% stenosis who did not undergo simultaneous repair had, at late follow-up, an increased systolic blood pressure and a greater need for antihypertensive medications, but not decreased survival rate, dialysis dependence, or an increase in serum creatinine level. Thus, we do not recommend simultaneous repair of asymptomatic renal artery stenosis with infrarenal aortic aneurysms (192). In patients with renovascular hypertension or deteriorating renal function, concomitant repair of a renal artery stenosis may be indicated (193,194). Symptomatic visceral ischemia may necessitate concomitant repair of stenosed visceral vessels; however, morbidity and mortality of these combined procedures exceed that of aneurysm repair alone in most series, and caution is urged in the performance of so-called prophylactic revascularizations in conjunction with aneurysm repair. Preoperative renal angioplasty and stenting, if feasible, is preferable to combined AAA repair and renal artery bypass (Fig. 59.9).

FIGURE 59.10 Inflammatory AAA with duodenum adherent to the aneurysm (arrow).

Uncommon Problems Associated with Abdominal Aortic Aneurysm Inflammatory Aneurysm Inflammatory AAA is a distinct clinicopathologic entity that constitutes about 5% of abdominal aortic aneurysms. Characteristic features are fibrosis and desmoplasia of the aneurysm wall and a dense inflammatory, fibrotic reaction in the retroperitoneum that incorporates adjacent structures. (195–197). The aortic wall is thicker than normal with relative preservation of elastin, in contrast to “degenerative” aneurysms, in which the wall is thinned and attenuated and elastin content is markedly decreased (Fig. 59.10). On microscopic examination, both media and adventitia are infiltrated with a

Chapter 59 Abdominal Aortic Aneurysm

prominent acute and chronic inflammatory reaction including activated T lymphocytes, giant cells, and plasma cells. Recent evidence suggests that inflammatory AAAs arise from the same causal stimulus responsible for noninflammatory aneurysms, yet with a more progressive course (199). The inflammatory process involves the duodenum in more than 90% of cases, the inferior vena cava and left renal vein in more than 50% of cases, and the ureters in about 25% of cases. In a series of 127 patients with inflammatory abdominal aneurysms, only one patient had experienced acute rupture, but chronic, contained rupture was found in eight (197). Sixty-five percent of patients had symptoms that were attributed to the aneurysm, with abdominal or back pain present in 60%, weight loss in 20%, and anorexia in 10%; three patients with ureteral obstruction presented with colic pain. In a comparison study, inflammatory aneurysms were found to be significantly more symptomatic than noninflammatory aneurysms and larger at presentation (198). The erythrocyte sedimentation rate (ESR) was elevated in 73% of patients. The diagnosis of inflammatory aneurysm should be suspected in those patients with abdominal aortic aneurysm who present with the triad of abdominal or back pain, weight loss, and elevated ESR. Often, CT will demonstrate the typical thickening of the aneurysm wall, outside the rim of aortic calcifications (Fig. 59.3). Ultrasound may show a sonolucent halo outside the rim of calcifications. MRI also shows a characteristic appearance of inflammatory aneurysm consisting of several concentric rings surrounding the aortic lumen, while angiography is not of help in confirming this diagnosis. Excretory urography is abnormal in about one-third of cases, showing obstruction or medial deviation of the ureters (in contrast, “regular” large aneurysms tend to push the ureters laterally). It is important to make the diagnosis of inflammatory aneurysm preoperatively, as preparation and operative technique should be modified. Preoperative ureteral catheterization may facilitate identification and protection of the ureters during the dissection. Reports have suggested an advantage of the left-sided retroperitoneal approach for this condition (179). At operation, the diagnosis can be immediately confirmed by the presence of a dense, shiny, white, highly vascular reaction in the retroperitoneum, centered over the aneurysm (Fig. 59.11). No attempts should be made to dissect the duodenum from the aortic wall, because there is a high chance of duodenal injury with this maneuver. In some cases it may be helpful to expose the aorta just proximal to the renal vein or at the diaphragm to obtain proximal control safely. Concomitant ureterolysis should be performed only if there is clear evidence of obstruction, because the inflammatory process seems to be arrested, and in many cases actually regresses, following repair of the inflammatory aneurysm. On follow-up studies retroperitoneal inflammatory process resolved com-

723

FIGURE 59.11 Inflammatory AAA following aortotomy. Note the thickened aortic wall resulting from the inflammatory process.

pletely in 23% to 53% of the patients, but 35% to 47% of patients had persistent inflammation. Persistent inflammation involved the ureters in 32% and resulted in longterm solitary or bilateral renal atrophy in 47%. Formerly uninvolved organs might become included in the process despite regression. The complex nature of these aneurysms leads to considerable problems if the condition is not treated in institutions familiar with this disease (198,200). Despite technical difficulties related to the inflammatory process, the operative mortality is only slightly higher than that of ordinary aneurysm repair (4.2% vs. 2.7%). Despite higher perioperative morbidity, 5-year survival rates were similar to non-inflammatory aneurysms (198). Also, the long-term outlook for these patients is similar to that for patients who undergo regular elective aneurysm repair; and the usual criteria for recommending aneurysm repair should be applied because, in spite of the thickened aortic wall, rupture can occur (197). Suprarenal Cross-clamping As many infrarenal aortic aneurysms are managed with endovascular grafts, a larger proportion of open aneurysm repairs will have a juxta- or pararenal component. In such patients, as well as in those with concomitant renal artery occlusive disease, suprarenal cross-clamping will be required. A recent review of such a population indicated an operative mortality rate of 5.8% (201). Likewise, in a review of patients undergoing simultaneous aortic repair and renal revascularization compared with aortic repair alone, the perioperative mortality rate of 5.3% was significantly higher than for isolated aortic repair. Among survivors in the combined group, a favorable hypertension response was observed in 63%. Although contemporary perioperative mortality for combined aortic and renal repair has improved compared with earlier reports, perioperative mortality for simultaneous reconstruction remains greater than for repair of aortic disease alone. The authors suggest that aortic and

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renal artery repair should be combined only for clinical indications rather than for prophylactic repair of clinically silent disease (202).

Aortocaval Fistula Spontaneous perforation of an aortic aneurysm into the inferior vena cava has been reported in 0.2% to 1.3% of patients with AAAs (203). Its incidence is twice as high in patients presenting with a ruptured aneurysm (204). Clinically, signs of high-output cardiac failure are present in about half the patients. Manifestations of venous hypertension may be present and include lower extremity edema, priapism, rectal bleeding, and hematuria. “Steal” by the fistula may cause ischemia of the lower extremities, kidneys, and intestines. The only available therapy is surgical, with relatively high mortality rates reported (205). Repair of the caval laceration via the opened aneurysm is recommended, but in cases of significant disruption of the vein wall, inferior vena cava ligation may be necessary (205).

A

Aortoenteric Fistula Aortoenteric fistula, although uncommon, may occur primarily or following previous aortic reconstruction. The classic presentation of a low grade gastrointestinal bleed in the third and fourth portion of the duodenum followed by a massive bleed will prove fatal if untreated (Fig. 59.12A). Open exploration with repair has an associated mortality rate of 25% to 90%.

B

Horseshoe and Ectopic Kidneys The reported incidence of horseshoe kidney varies from 1:400 to 1:1000 in the general population. Its association with abdominal aortic aneurysm is rare (206). The diagnosis is usually made preoperatively by abdominal ultrasound or CT. Advanced knowledge of this condition is invaluable because it complicates aneurysm replacement (206,207). Preoperative diagnosis dictates aortography and selective renal angiography, because anomalous blood supply arising from the aneurysm or the iliac arteries is seen in 50% to 80% of cases (Fig. 59.13) (208,209). In addition, preparation for cold perfusion of the kidney during the period of interruption of blood flow can be made, and placement of ureteral stents prior to aneurysm repair may be helpful in avoiding injury to the ureters. When horseshoe kidney is encountered unexpectedly, intraoperative aortography may be performed by injecting 40 mL of contrast agent into the temporarily occluded aorta, just proximal to the aneurysm. In our experience however, this has never been necessary. The arterial orifices in the opened aneurysmal sac can be cannulated easily from within, determining the course of the vessels that supply the abnormal kidney by palpating the probe. It has been estimated that in 60% of cases the anomalous

C

FIGURE 59.12 CT scan with evidence of aortic graft infection. (A) Air within the aneurysm (arrow) from an aortoduodenal fistula. (B and C) Perigraft collection surrounding the common and external iliac arteries respectively.

renal blood supply will require some form of surgical reconstruction (210). If large anterior renal arteries are demonstrated preoperatively, a left posterolateral approach is recommended.

Chapter 59 Abdominal Aortic Aneurysm

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FIGURE 59.13 Aortic angiogram showing an aneurysmal distal aorta with a pelvic kidney (arrow) whose blood supply originates from the right common iliac artery.

The preferred surgical options for asymptomatic patients with an aortic aneurysm and a horseshoe kidney are the placement of a stent–graft or a retroperitoneal approach; both avoid many of the technical difficulties related to the presence of the horseshoe kidney. The approach of choice for a ruptured aneurysm is transperitoneal. The descending colon and the left portion of the horseshoe kidney can be retracted medially and the aneurysm opened posteriorly. In this manner, the multiple accessory renal arteries can be reimplanted into the graft as one or more Carrel patches. The isthmus or transverse portion of a horseshoe kidney almost never needs to be divided, as the aortic graft can usually be passed behind it. Separation of the renal isthmus should be avoided (211). Congenital pelvic kidneys are rare, and their occurrence in combination with abdominal aortic aneurysm is even more unusual. When encountered, the abnormal origin of the renal arteries may present the surgeon with similar problems of renal ischemia during aortic clamping, as is the case for horseshoe kidney. Although in most instances simple clamping and repair of the aneurysm can be performed, for more complex cases temporary shunting into the ischemic kidney has been recommended (212). The number of renal transplant patients who require aortic reconstruction has recently increased (86). A temporary shunt may be used to ensure adequate blood flow to the transplanted kidney during the period of aortic clamping (86).

Mycotic Aneurysms The confusing term mycotic is derived from the mushroom-shaped false aneurysm that is typical of this condi-

FIGURE 59.14 Aortic angiogram with a mycotic aneurysm shown originating below the superior mesenteric artery.

tion, and has no bearing on the causative organism. These aneurysms are believed to occur as a consequence of septic emboli that adhere to a point of the intimal surface of the aorta in high enough concentration to cause a localized transmural arteritis (Fig. 59.14).

Venous Anomalies Associated with Abdominal Aortic Aneurysm If an abnormal anatomic location of the left renal vein or the inferior vena cava is not recognized during aortic dissection and clamping, significant venous injury and subsequent exsanguinating hemorrhage may occur. A retroaortic left renal vein is encountered in 1.8% to 2.4% of patients (213,214), and is prone to injury during dissection of the aneurysm neck or placement of the proximal aortic clamp. If the surgeon cannot find the left renal vein in its usual position anterior to the aorta, the presence of this rare anomaly should be assumed, and dissection in this area limited. The presence of a retroaortic renal vein may remain unsuspected when an additional renal vein is present anteriorly, in its normal position. This configuration, named circumaortic venous collar, is found in up to 8.7% of cases (215). If injury to a retroaortic renal vein occurs, transection of the aorta may be required to offer sufficient exposure for repair.

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A double inferior vena cava, lying on each side of the aorta, is estimated to occur in up to 3% of patients, whereas an isolated left inferior vena cava is only found in 0.2% to 0.5% (215). The latter may cross from left to right, either behind or in front of the aorta, and is usually joined by a short, immobile left renal vein (Fig. 59.2). A crossing vena cava may occasionally need to be divided to provide adequate exposure of the aneurysmal neck. If the left-sided vena cava is part of a double system, it may be ligated provided that adequate drainage of the left kidney and adrenal gland is ensured.

insidious and may not manifest until 3 to 5 days postoperatively (see also Complications, below). In addition to routine outpatient follow-up of the postoperative patient, 6-monthly or annual visits with abdominal ultrasound or CT are recommended to monitor for the development of anastomotic pseudoaneurysms, aneurysmal dilation of the remaining aorta or iliac arteries, graft occlusion, or infection.

Complications Early Complications

Postoperative Care and Follow-up With major surgical procedures, the postoperative patient is cared for in a setting in which intensive monitoring is ensured, for a minimum of 24 hours. Management of the individual patient depends in part on the preoperative risk factors. Although the high-risk patient can benefit from more intensive observation in the perioperative period, the routine placement of an uncomplicated repair into an intensive care unit has been diminishing. Surgical ward admissions in one study of infrarenal aneurysms increased from 0% in 1994 to 43.6% in 1999. The average ICU length of stay declined from 4.6 to 1.2 days, whereas the hospital length of stay decreased from 12.5 to 6.8 days. This had no effect on mortality rate. With refinement in patient care, limited resources can be maximized without detrimental results (216). Fluid replacement to ensure adequate urine output is essential and may by far exceed the standard requirements due to “third-space” accumulation of fluids or highoutput renal failure or both. In patients with cardiac decompensation, the use of a balloon-directed pulmonary artery catheter is helpful to guide fluid therapy in the postoperative period. Usually, around the second or third postoperative day, third-space fluid is mobilized back into the intravascular space and intravenous fluid requirements are drastically reduced. The use of diuretics may be indicated in this period. Nasogastric decompression is usually continued until the patient show signs of restored gastrointestinal function. Prolonged ileus, often followed by a period of diarrhea, is not uncommon after aortic aneurysm repair. Careful assessment of peripheral pulses or ankle pressure monitoring by Doppler ultrasound should be done to ensure integrity of the distal circulation. Loss of a previously present palpable pulse or an abrupt decrease in ankle pressure indicate a major embolic occlusion and are indications for reexploration. Daily monitoring of basic laboratory values such as hematocrit, blood urea nitrogen, and creatinine is mandatory, especially in patients with preexisting renal insufficiency. Renal failure after aortic operations is often

Hemorrhage Abdominal aortic aneurysm repair is currently one of the major indications for the use of autotransfusion, demonstrating that intraoperative bleeding still is a considerable problem. Several causes of bleeding, however, can be easily avoided. Bleeding caused by inadvertently entering the aneurysm can be minimized by obtaining control of proximal and distal vessels before dissecting the aneurysm itself. Hemorrhage from injury to the inferior vena cava and the iliac veins is no longer the threat it used to be when the aneurysm was routinely dissected away from these venous structures. Retroaortic bleeding from injured lumbar arteries is rare if the aorta is controlled just below the renal arteries. The endoaneurysmal approach also has reduced bleeding from the posterior suture line because a double thickness of aortic wall is incorporated with this technique. Declamping Hypotension Suggested causes for the hypotension that follows restoration of distal perfusion after an extended period of aortic occlusion include inadequate intravascular volume due to sudden restoration of flow to the vasodilated distal circulation, “washout” of acidic metabolites, potassium, or vasoactive substances from the ischemic lower extremities, and “third-space loss” of protein-rich fluids into permeable distal tissues. In canine experiments in which distribution of cardiac output was measured with labeled microspheres, the senior author observed that the lower extremities share of total cardiac output was 6% before, 0.6% during, and 24% after infrarenal aortic clamping for 4 hours (104). This internal “steal”, combined with concomitant decreases in cardiac output, caused decreases in coronary, cerebral, hepatic, and renal blood flow in the range of 33% to 50%. Better monitoring and anesthetic techniques, as well as more aggressive management of intravascular volume, have importantly reduced the incidence of this problem. The surgeon can contribute by giving the anesthesiologist advanced notice of plans to restore the distal circulation, and by slowly releasing the clamps, one limb of the graft at a time. Slow clamp release has been shown to reduce the severity of reperfusion injury in animals (161).

Chapter 59 Abdominal Aortic Aneurysm

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Renal Failure

Lower Extremity Ischemia

Renal failure due to acute tubular necrosis requiring postoperative hemodialysis is another serious complication of elective infrarenal aneurysm repair that is seen less often today. Reduction of intraoperative hemorrhage and declamping shock, better intraoperative monitoring and volume replacement, and the shorter period of aortic cross-clamping associated with the endoaneurysmal technique are believed to be factors responsible for this decrease in incidence. Lesser degrees of renal failure such as a temporary high-output renal failure or transient rises in serum creatinine and blood urea nitrogen levels, however, are not infrequent, especially after suprarenal clamping (215). Renal dysfunction after repair of ruptured aneurysm is still common and was seen in 21% of survivors in one series (217). The causes of postoperative renal dysfunction, especially in the absence of hypotension or suprarenal clamping, are unclear, although reflex vasoconstriction with vascular shunting and redistribution of blood flow within the kidney have been suggested (218). Another potential cause is aortography, which may cause contrast-related nephropathy, especially if performed shortly before the operation or when combined with poor hydration. In an attempt to prevent renal failure after aortic reconstruction, administration of mannitol (12.5– 25 mg, intravenously) and furosemide (20–40 mg) shortly before aortic clamping has been widely practiced. Proof of efficacy of these maneuvers, however, is lacking and may be only at the subclinical level (219), and studies have shown that intraoperative urine volume is not predictive of postoperative renal function (218). If renal dysfunction becomes evident, volume expansion, blood pressure support, or treatment of heart failure may result in reversal of renal insufficiency. Following repletion of intravascular volume, diuretic administration may convert oliguric to nonoliguric renal failure, which facilitates management and perhaps improves the prognosis.

Following aortic aneurysm repair lower extremity ischemia may be due to embolization of dislodged mural thrombus or crushed atherosclerotic plaque, thrombosis of distal vessels during interruption of blood flow, or creation of an intimal flap at the anastomosis. Microembolization of small atheromatous particles may cause patchy areas of ischemia, usually located at the plantar aspect of the feet. With this condition, generally referred to as “trash foot,” pedal pulses are often still palpable. Measures to prevent distal ischemia include the use of heparin during the period of aortic clamping, obtaining proximal and distal control prior to manipulation of the aneurysm, and release of the internal iliac circulation before restoring flow to the extremities. Before closing the abdomen, the feet are carefully inspected. If signs of distal ischemia are present, the passage of embolectomy catheters may retrieve thrombus or debris from the extremity arteries. In cases of trash foot syndrome, lumbar sympathectomy may be beneficial in limiting or preventing full-thickness gangrene (104). If microembolization is not apparent until after the patient has left the operating room, administration of 500 mL of low-molecular-weight dextran, given over an 8- to 12-hour period may be beneficial, as may be epidural blockade to create a sympathectomy effect. If embolization has been extensive, one may need to perform direct exploration of the distal tibial vessels and extract the bulk of the embolic material with a 2- or 3-Fr. balloon catheter.

Ureteral lnjury

Ischemic Colitis

The ureters are most likely to be injured when adhesions from previous operations are present, in the hasty approach to a ruptured aneurysm, or when the ureters are displaced by the aneurysm itself or by the connective tissue reaction surrounding it. If ureteral injury occurs during the operation, immediate repair is indicated. A double J-stent can be inserted through the injury site and directed both up into the renal pelvis and down toward the bladder. The ureter can then be repaired using No. 7–0 resorbable sutures, and wrapped with a pedicle of omentum. Following copious irrigation with antibiotic-containing solution, repair of the aneurysm may be completed. If a postoperative urinoma would develop, which is unlikely with a functioning stent in place, percutaneous closed drainage can be instituted with CT or ultrasound guidance.

In a national multicenter clinical study, the incidence of bowel infarction was 1.2%. Among patients operated on for a ruptured aneurysm it was 3.1%, compared with 1.0% for patients with nonruptured aneurysm. In 67% the lesion affected the left colon (220). Other reports of ischemic colitis range from 0.2% to 10% of cases (221–224). This serious complication occurs three to four times more frequently following operations for aneurysm than following operations for occlusive disease. Although colonic ischemia may be the result of ligation of a patent inferior mesenteric artery, in most occasions this maneuver alone will not lead to significant ischemia. In many cases, the inferior mesenteric artery is already occluded preoperatively as a natural consequence of atherosclerotic disease or mural thrombus that is deposited around its orifice. Intestinal ischemia typically

Gastrointestinal Complications Some degree of paralytic ileus is the rule after aortic aneurysm repair and will usually persist for 2 to 3 days, not infrequently followed by a period of diarrhea. Occasionally, duodenal obstruction will persist longer, presumably caused by edema or hematoma in the vicinity of the proximal anastomosis. Aspiration pneumonitis may occur in these instances if nasogastric suction is discontinued and oral feedings are begun prematurely.

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Part VII Aortic and Peripheral Aneurysms

occurs when critical hypogastric arteries are not revascularized or when a patent inferior mesenteric artery is ligated in the face of superior mesenteric artery or bilateral internal iliac artery occlusion. Flow to the sigmoid colon may be apparently satisfactory at the termination of the operation, only to deteriorate later as a result of colonic distension or periods of hypotension. Another causative role may be played by the renin–angiotensin system (225,226). Intense vasoconstriction of the intestinal circulation caused by angiotensin II has been shown to lead to intestinal necrosis in animal models. The clinical features of intestinal ischemia depend on its severity. The first indication of bowel ischemia may be an inordinate intravenous fluid requirement in the first 8 to 12 hours after the operation. Diarrhea, often bloody, typically follows within the first 48 hours. Subsequent abdominal distension, unexplained fever, or elevated white blood cell count should raise the suspicion of colonic ischemia, prompting immediate sigmoidoscopy. This study typically reveals obvious mucosal changes appearing abruptly between 10 and 20 cm above the anal verge. Fortunately, necrosis is limited to the mucosa in many instances and treatment can be conservative, with bowel rest, antibiotics directed against colonic flora, and optimal fluid and electrolyte therapy. If the muscular layers are also involved, however, segmental strictures may develop that eventually require resection. The evolution of these lesions can be followed by serial barium enemas. If fullthickness necrosis is evident, or signs of peritoneal irritation are present, prompt reoperation, with resection of all ischemic bowel and creation of a terminal descending colostomy, is indicated. If the aortic prosthesis is grossly contaminated, it should be removed and replaced by extra-anatomic bypass, as described for an infected prosthesis. If the patient is hemodynamically unstable, it may be prudent to defer graft removal for several days until the condition has improved. The mortality of this dreaded complication is about 50% overall, but increases to over 90% when full-thickness gangrene and peritonitis occur. Intraoperative measures to avoid colonic ischemia are described in the discussion of operative technique in this chapter.

Spinal cord ischemia during infrarenal aortic reconstruction has been suggested to be due to interruption of a large “arteria radicularis” originating from the infrarenal aorta, a variation apparently present in almost half the population (231). However, if this were the main cause of postoperative paraplegia, one would expect a much higher incidence, indicating that other factors must play a role. At least half of the reported cases in one review followed emergency operation for ruptured aneurysm, while a third of these patients had no documented hypotension or suprarenal clamping (229). Atheroembolism or thrombosis of the spinal cord blood supply may have played a role in these cases. In reality, paraplegia after infrarenal AAA repair appears to be most closely associated with failure to adequately revascularize the hypogastric arteries. Although about 50% of the affected survivors recover some neurologic function, the mortality associated with this complication is around 50%. Graft Infection Up to 6% of patients develop graft infection, with, again, a higher incidence following emergency repair of ruptured aneurysm. Routine culture of the aneurysmal contents at the time of operation has been frequently performed with the assumption that a positive culture result would be a risk factor for secondary graft infection. In a recent study, however, in which 37% of these cultures were positive (normal skin flora in the majority of patients), no predictive value for subsequent graft infection could be demonstrated during 12 years of follow-up (232). Therefore, routine aneurysm culture does not seem to be of clinical value. Graft infection may involve the entire prosthesis or manifest itself as an indolent process at an anastomotic site (Fig. 59.15). Diffuse graft infection usually presents with a fever of unknown origin, vague back or abdominal pain, anorexia, and general malaise. Occasionally, distal manifestations of septic emboli may be the first signs of a diffuse graft infection. Indolent, more localized graft infections tend to present as anastomotic pseudoa-

Cholecystitis Acute acalculous cholecystitis is the most common postoperative biliary complication after aortic surgery. A relatively uncommon event it is often seen in conjunction with a prolonged postoperative hospital course with multisystem failure. A study of all aortic reconstructions over a 10year period identified 7 of the 996 patients who developed postoperative acute acalculous cholecystitis. Overall mortality was 71% (227). Paraplegia Encountered in up to 30% of thoracoabdominal aortic aneurysm repairs, paraplegia is an uncommon complication after infrarenal aortic reconstruction (228–231).

FIGURE 59.15 Exploration of an indolent graft infection 5 years following initial repair which identified bowel adherent to a bile stained (arrow) right iliac artery graft limb.

Chapter 59 Abdominal Aortic Aneurysm

A

729

illofemoral bypass graft) and aortic graft removal for treatment of aortic graft infection are associated with acceptable early and long-term outcomes and should remain a primary approach in selected patients with this grave problem. (236). Reports of in-situ replacement with a new prosthesis, which is subsequently wrapped in omentum, have appeared (237). Another interesting prospect demonstrated in animal studies is replacement of the infected graft by an autogenous tube graft, created from rectus abdominis muscle and underlying transversalis fascia, the feasibility of which has recently been shown (238). These techniques, however, are purely experimental and cannot be recommended at this time.

Late Complications

B

FIGURE 59.16 Leukocytoclastic vasculitis of (A) the upper extremity and (B) the lower extremity of a patient with aortic graft infection.

neurysms, graft-cutaneous sinus tracts, perigraft abscesses, or graftenteric fistula. Although rare, immune/rheumatic manifestations of graft infection may be a presenting sign (Fig. 59.16). Staphylococcus aureus has been most frequently isolated in acute, diffuse graft infections, while coagulasenegative Staphylococcus epidermidis has emerged as a major causative organism in indolent graft infections (233). Diagnosing infection can be difficult. Radionuclide imaging such as the 111In-labeled white blood cell scan and the 111In-labeled immunoglobulin G scan may be helpful (234,235). Computed tomography may show periprosthetic fluid and, more importantly, gas (Fig. 59.11). Management of diffuse graft infection has traditionally consisted of remote, extra-anatomic bypass grafting followed by complete excision of the infected graft. The long-term outcome in patients with infected prosthetic aortic grafts who were treated with extra-anatomic bypass grafting and aortic graft removal was investigated. Thirty-six patients were treated for aortic graft infection with extra-anatomic bypass grafting and aortic graft removal over a 10-year period. In the postoperative period there was an 11% mortality rate. Including the postoperative period and during follow-up the overall treatment-related mortality was 19%, whereas overall survival by means of life-table analysis was 56% at 5 years. Staged extra-anatomic bypass grafting (with ax-

Late complications occur in approximately 10% of patients after undergoing AAA repair and include graft infection (see also under Early Complications), anastomotic pseudoaneurysm, aortoenteric fistula, graft limb occlusion, secondary aneurysms, and sexual disturbances (137,226). These complications are discussed separately in this volume.

Long-term Results/Functional Outcome In an evaluation of 154 consecutive, nonemergency open repairs of infrarenal AAAs functional outcome, including ambulatory status, independent living status, current medical condition, and the patient’s perception of recovery and satisfaction were investigated. The mortality rate was 4%, the mean hospital stay was 10.7 ± 1.3 days, and 11% of the patients required transfer to a skilled nursing facility with a mean stay of 3.6 months. All patients were ambulatory preoperatively, whereas at median follow up of 25 months, 64% of the patients remained ambulatory, 22% required assistance, and 14% were nonambulatory (239). In another study regarding quality of life after the operation, virtually all patients who had undergone elective aneurysm repair stated that their quality of life had not changed, in contrast with most patients who survived emergency operations for ruptured aneurysm and seemed to have suffered a significant deterioration in life quality (240).

References 1. Johnston KW, Rutherford RB, et al. Suggested standards for reporting on arterial aneurysms. J Vasc Surg l991;13:452–458. 2. Hollier LU, Stanson AW, et al. Arteriomegaly: classifications and morbid implications of diffuse aneurysmal disease. Surgery 1983;93:700.

730

Part VII Aortic and Peripheral Aneurysms

3. Singh K, Bonaa KH, et al. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: The Tromso Study. Am J Epidemiol 2001;154(3):236–244. 4. Collin J, Aranjo L, et al. Oxford screening programme for abdominal aortic aneurysm in men aged 65–74 years. Lancet 1988;2:613–615. 5. O’Kelly TJ, Heather BP. General practice based population screening for abdominal aortic aneurysms: a pilot study Br J Surg 1989;76:479–480. 6. Bengtsson H, Bergqvist D, Ekberg O, Janzon L. A population based screening of abdominal aortic aneurysms (AAA). Eur J Vasc Surg 1991;5:53–57. 7. Scott RAP, Ashton HA, Kay DN. Abdominal aortic aneurysm in 4237 screened patients: prevalence, development and management over 6 years. Br J Surg 1991;78:1122–1125. 8. Bengtsson H, Norrgard O, et al. Ultrasonographic screening of the abdominal aorta among siblings of patients with abdominal aortic aneurysms. Br J Surg 1989;76:589–591. 9. Adamson J, Powell JT, Greenhalgh RM. Selection for screening for familial aortic aneurysms. Br J Surg 1992;79:897–898. 10. Bengtsson H, Bergqvist D. Ruptured abdominal aortic aneurysm: A population-based study J Vasc Surg 1993;18:74. 11. Katz DA, Littenberg B, Cronenwett JL. Management of small abdominal aortic aneurysms. Early surgery vs watchful waiting. JAMA 1992;268(19):2678. 12. Lawrence PF, Gazak C, et al. The epidemiology of surgically repaired aneurysms in the United States. J Vasc Surg 1999;30(4):632–639. 13. Tyrell FG. The lectures of Sir Astley Cooper, Bart, FRCS, on the principles and practice of surgery (4th American edition from the last London edition). Carey EL, Hart A, eds. Philadelphia: 1935:212–214. 14. Power PA. The palliative treatment of aneurysms by “wiring”with Colt’s apparatus. Br J Surg 1921;9:27–36. 15. Bigger IA. Surgical treatment of aneurysm of the aorta: review of literature and report of two cases, one apparently successful. Ann Surg 1940;11:879–894. 16. Estes JE Jr. Abdominal aortic aneurysm: a study of 102 cases. Circulation 1950;2:258–264. 17. Dubost C, Allary M, Oeconomos N. Resection of an aneurysm of the abdominal aorta: reestablishment of the continuity by a preserved arterial graft, with result after five months. Arch Surg 1952;64:405. 18. Tuffier M. De I’ntubation dans les plaics des grosses arteres. Bull Acad Med 1915;74:455–460. 19. Hufnagel CA. Permanent intubation of the thoracic aorta. Arch Surg 1947;54:382–389. 20. Hufnagel CA. The use of rigid and flexible plastic prosthesis for arterial replacement, Surgery 1955;37:165– 174. 21. DeBakey ME, Cooley PA, et al. Clinical application of a new flexible knitted Dacron arterial substitute. Arch Surg 1957;74:713–724. 22. Sauvage G, Berger KE, et al. An external velour surface for porous arterial prosthesis. Surgery 1971;70:940–953. 23. Quinones-Baldrick WJ, Moore WS, et al. Development of a “leak-proof’ knitted Dacron vascular prosthesis. J Vasc Surg 1986;3:895–903.

24. Guidion R, Snyder R, et al. Albumin coating of a knitted polyester arterial prosthesis: an alternative to preclorting. Ann Thorac Surg 1984;37:457–465. 25. Creech O Jr. Endo-aneurysmorhaphy and treatment of aortic aneurysm. Ann Surg 1966;164:935–946. 26. Parodi JC, Palmaz JC, Barone RD. Transfemoral inrraluminal graft implantation for abdominal aortic aneurysm. Ann Vasc Surg 1991;5:491–499. 27. Greenhalgh RM. Prognosis of abdominal aortic aneurysm. Br Med J 1990;301:136. 28. Smith T. European health challenges. Br Med J 1991;303:1395–1397. 29. Nevitt MP, Ballard DJ, Hallett JW. Prognosis of abdominal aortic aneurysms: a population based study. New Engl J Med 1989;321:1009–1114. 30. Heather BP, Poskitt KR, et al. Population screening reduces mortality rate from aortic aneurysm in men. Br J Surg 2000;87(6):750–753. 31. Crow P, Shaw E, et al. A single normal ultrasonographic scan at age 65 years rules out significant aneurysm disease for life in men. Br J Surg 2001;88(7):941–944. 32. Lederle FA, Johnson GR, et al. Yield of repeated screening for abdominal aortic aneurysm after a 4-year interval. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med 2000;160(8):1117–1121 33. Wilmink TB, Quick CR, et al. The influence of screening on the incidence of ruptured abdominal aortic aneurysms. J Vasc Surg 1999;30(2):203–208. 34. Rutledge R, Oller DW, et al. A statewide, population-based time-series Analysis of the outcome of ruptured abdominal aortic aneurysm.Ann Surg 1996;223(5):492–505. 35. Zarins CK, Xu CP, Glagov S. Aneurysmal enlargement of the aorta during regression of experimental atherosclerosis. J Vasc Surg 1992;15(1):90–98. 36. Tilson MD, Ozsvath KJ, et al. A genetic basis for autoimmune manifestations in the abdominal aortic aneurysm resides in the MHC class II locus. DR-beta-1. Ann NY Acad Sci 1996;800:208. 37. Zarins CK, Xu C, Glagov S. Atherosclerotic enlargement of the human abdominal aorta. Atherosclerosis 2001;155(1):157–164 38. Tilson MD. Generalized arteriomegaly: A possible predisposition to the formation of abdominal aortic aneurysms. Arch Surg;116:1030–1032. 39. Clifton MA. Familial abdominal aortic aneurysms. Br J Surg 1977;64:765–766. 40. Campa JS, Greenhalgh RM, Powell JT. Elastin degredation in abdominal aortic aneurysms. Atherosclerosis 1987;65:13–21, 62. 41. Busuttil RW, Abou-Zamaam AM, Machlader HI. Collagenase activity of the human aorta: comparison of patients with and without abdominal aortic aneurysms. Arch Surg 1980;115:1373–1378. 42. White JV, Haas K, Phillips S, Comerota AJ. Adventitial elastolysis is a primary event in aneurysm formation. J Vasc Surg 1993;17(2):371–381. 43. Brunelli T, Prisco D, et al. High prevalence of mild hyperhomocysteinemia in patients with abdominal aortic aneurysm. J Vasc Surg 2000;32(3):531–536. 44. McMillan WD, Pearce WH. Increased plasma levels of metalloproteinase-9 are associated with abdominal aortic aneurysms.J Vasc Surg 1999;29(1):122–129.

Chapter 59 Abdominal Aortic Aneurysm 45. Patel MI, Hardman DT, Fischer CM, et al. Current views on the pathogenisis of abdominal aortic aneurysms. J Am Coll Surg 1995;181(4):371. 46. Rasmussen TE, Hallett JW Jr, et al. Genetic similarity in inflammatory and degenerative abdominal aortic aneurysms: a study of human leukocyte antigen class II disease risk genes. J Vasc Surg 2001;34(1):84–89. 47. Davis CA, Pearce WH, et al. Increased ICAM-1 expression in aortic disease. J Vasc Surg 1993;18:875–880. 48. Mower WR, Quinones WJ, Gambhir SS. Effect of intraluminal thrombus on abdominal aortic aneurysm wall stress. J Vasc Surg 1997;26(4):602–608. 49. Knox JB, Sukhova GK, et al. Evidence for altered balance between matrix metalloproteinases and their inhibitors in human aortic diseases. Circulation 1997;95(1):205–212. 50. Moore JE, Ku DN, et al. Pulsatile flow visualization in the abdominal aorta in differing physiologic conditions: implications for increased susceptibility to atherosclerosis. J Biomech Eng 1993;115:12. 51. Vorp DA, Lee PC, et al. Association of intraluminal thrombus in abdominal aortic aneurysm with local hypoxia and wall weakening. J Vasc Surg 2001;34(2):291–299. 52. Raghavan ML, Vorp DA, et al. Wall stress distribution on three-dimensionally reconstructed models of human abdominal aortic aneurysm. J Vasc Surg 2000;31(4): 760–769. 53. Vorp DA, Raghavan ML, Webster MW. Mechanical wall stress in abdominal aortic aneurysm: influence of diameter and asymmetry J Vasc Surg 1998;27(4):632–639. 54. Hatakeyama T, Shigematsu H, Muto T. Risk factors for rupture of abdominal aortic aneurysm based on threedimensional study. J Vasc Surg 2001;33(3):453–461. 55. Blanchard JF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: results of a case-control study. Am J Epidemiol 2000;151(6):575–583. 56. Lederle FA, Johnson GR, Wilson SE. Abdominal aortic aneurysm in women. Aneurysm Detection and Management Veterans Affairs Cooperative Study. J Vasc Surg 2001;34(1):122–126. 57. Jaakkola P, Kuivaniemi H, et al. Familial abdominal aortic aneurysms: screening of 71 families. Eur J Surg 1996;162(8):611–617. 58. Salo JA, Soisalon-Soininen S, et al. Familial occurrence of abdominal aortic aneurysm. Ann Intern Med 1999;130(8):637–642. 59. Naydeck BL, Sutton-Tyrrell K, et al. Prevalence and risk factors for abdominal aortic aneurysms in older adults with and without isolated systolic hypertension. Am J Cardiol 1999;83(5):759–764. 60. CronenwettJL, Murphy TF, et al. Actuarial analysis of variables associated with rupture of small aortic aneurysms. Surgery 1985;98:472–483. 61. Lindholt JS, Heickendorff L, et al. Natural history of abdominal aortic aneurysm with and without coexisting chronic obstructive pulmonary disease. J Vasc Surg 1998;28(2):226–233. 62. Kang SS, Littooy FN, et al. Higher prevalence of abdominal aortic aneurysms in patients with carotid stenosis but without diabetes. Surgery 1999;126(4):687–692. 63. Pleumeekers HJ, De Gruijl A, et al. Prevalence of aortic

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

81.

731

aneurysm in men with a history of inguinal hernia repair. Br J Surg 2000;87(1):123–124. Rowe VL, Stevens SL, et al. Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas. J Vasc Surg 2000;31(3):567–576. Lindholt JS, Juul S, et al. Immunoglobulin A antibodies against Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm. Br J Surg 1999;86(5):634–638. Nevitt MP, Ballard DJ, Hallett JW. Prognosis of abdominal aortic aneurysms. New Engl J Med 1989;321:1009–1014. Cronenwett JL, Seargent SK, et al. Variables that effect the expansion rate and outcome of small abdominal aortic aneurysms. J Vasc Surg 1990;11:260–269. Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms J Vasc Surg 1992;15:1046–1056. Vardulaki KA, Prevost TC, et al. Growth rates and risk of rupture of abdominal aortic aneurysms. Br J Surg 1999;86(2):280. Szilagyi DE, Smith RF, et al. Contribution of abdominal aortic aneurysmectomy to prolongation of life. Ann Surg 1966;164:687–699. Darling RC, Messina CR, et al. Autopsy study of unoperated aortic aneurysms. Circulation 56(suppl 2):161–164, 177. Szilagyi DE, Elliot JP, Smith RF. Clinical fate of the patient with asymptomatic abdominal aortic aneurys m and unfit surgical treatment. Arch Surg 1972;104:600–606. Foster JH, Bolasny BL, Gobbel WG, Scott HW. Comparitive study of elective resection and expectant treatment of abdominal aortic aneurysm. Surg Gynecol Obstet 1969;129:1–9. Jones A, Cahill D, Gardham R. Outcome in patients with a large abdominal aortic aneurysm considered unfit for surgery. Br J Surg 1998;85(10):1382–1384. Brown LC, Powell JT. Risk factors for aneurysm rupture in patients kept under ultrasound surveillance. UK Small Aneurysm Trial Participants. Ann Surg 1999;230(3):289–297. Cronenwett JL. Factors increasing the rupture risk of small aortic aneurysms. In Veith FJ ed. Current Critical Problems in Vascular Surgery. Vol 3. St. Louis, Quality Medical Publishing, 1991. p. 234. Ballaro A, Cortina-Borja M, Collin J. A seasonal variation in the incidence of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 1998;15(5):429–431. Scott RA, Ashton HA, Lamparelli MJ. Vascular surgical society of great britain and ireland: fifteen years of experience using 6 cm as a criterion for abdominal aortic aneurysm surgery. Br J Surg 1999;86(5):709–710. Valentine RJ, Decaprio JD, et al. Watchful waiting in cases of small abdominal aortic aneurysms- appropriate for all patients? J Vasc Surg 2000 Sep;32(3):441–450. Englund R, Hudson P, Hanel K, et al. Expansion rates of small abdominal aortic aneurysms. Aust NZ J Surg 1998;68:21. Gadowski GR, Pilcher DB, Ricci MA. Abdominal aortic aneurysm expansion rate: Effect of size and betaadrenergic blockade. J Vasc Surg 1994;19:727.

732

Part VII Aortic and Peripheral Aneurysms

82. Leach SD, Toole AL, Stern H, et al. Effect of betaadrenergic blockade on the growth rate of abdominal aortic aneurysms. Arch Surg 1988;123:606. 83. Thompson RW, Baxter BT. MMP inhibition in abdominal aortic aneurysms. Rationale for a prospective randomized clinical trial. Ann N Y Acad Sci 1999;878:159–178. 84. Boyle JR, McDermott E, et al. Doxycycline inhibits elastin degradation and reduces metalloproteinase activity in a model of aneurysmal disease. J Vasc Surg 1998;27(2):354–361. 85. Szilagyi DE. Clinical diagnosis of intact and ruptured abdominal aortic aneurysm. In Bergan JJ, Yao JST, eds. Aneurysms: diagnosis and treatment. New York: Grune and Strtton, 1982:205–215. 86. Sterpetti AV, Fedhaus RJ, et al. Identification of abdominal aortic aneurysm patients with different clinical features and clinical outcomes. Am J Surg 1988;156:466–473. 87. Dent TL, Lindenhaur SM, et al. Multiple arteriosclerotic arterial aneurysms. Arch Surg 1972;105:338–341. 88. Hodgson KJ, Webster DJ. Abdominal aortic aneurysm causing duodenal and ureteric obstruction. J Vasc Surg 1986;3:364–368. 89. Diwan A, Sarkar R, et al. Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg 2000;31(5):863–869. 90. Karanjia PN, Madden KP, Lobner S. Coexistence of abdominal aortic aneurysm in patients with carotid stenosis Stroke 1994 Mar;25(3):627–630. 91. Mukherjee D, Mayberry JC, Inahara T, Greig JD. The relationship of the abdominal aortic aneurysm to the tortuous internal carotid artery. Is there one? Arch Surg 1989;124:955–956. 92. Kiell CS, Ernst CB. Advances in management of abdominal aortic aneurysm. Adv Surgery 1993;26:73–98. 93. Salo JA, Verkkala KA, et al. Hematuria is an indication of rupture of an abdominal aortic aneurysm into the vena cava. J Vasc Surg 1990;12:41–44. 94. Fink HA, Lederle FA, et al. The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med 2000;160(6):833–836. 95. Lederle FA, Simel DL. Does this patient have abdominal aortic aneurysm? JAMA 1999;281(1):77–82. 96. Quill DS, Colgan MP, Summer DS. Ultrasonic screening for the detection of abdominal aortic aneurysms. Surg Clin North Am 1989;69(4):713–720. 97. Gomes MN, Choyke PL. Pre-operative evaluation of abdominal aortic aneurysms: Ultrasound or computed tomography? J Cardiovasc Surg 1987;28:159–165. 98. Riecker O, Duber C, Neufang A, et al. CT angiography versus intraarterial subtraction angiography for assessmant of aortoiliac occlusive disease. AJR Am J Roentgenol 1997;169:1133–1138. 99. Cikrit DF, Harris VJ, Hemmer CG, et al. Comparison of spiral CT and arteriography for evaluation of renal and visceral arteries. Ann Vasc Surg 1996;10:109–116. 100.Pozniak MA, Bolison DJ, Lee FT, et al. CT angiography of potential renal transplant donors. Radiographics 1998;18:565–587. 101. Siegelman ES, Gilfeather M, Holland GA, et al. Pictoral essay: Breathold ultrafast three-dimentional gadolinium enhanced MRA of renovascular segment. AJR Am J Roentgenol 1997;168:1035–1040.

102. Rich NM, Clagget GP, et al. Role of arteriography in the evaluation of aortic aneurysms. In: Bergan JJ, Yao JST, eds. Aneurysms: diagnosis and treatment. New York: Grune and Strtton, 1982:233–241. 103. Friedman SG, Kerner BA, et al. Abdominal aortic aneurysmectomy without preoperative angiography: a prospective study. NY State J Med 1990;90(1):176–178. 104. Hollier LH, Rutherford RB. Infrarenal aortic aneurysms. In: Rutherford RB, ed. Vascular surgery. 3rd ed. Philadelphia: WB Saunders, 1989:909–927. 105. Finlayson SR, Birkmeyer JD, et al. Should endovascular surgery lower the threshold for repair of abdominal aortic aneurysms? J Vasc Surg 1999;29(6):973–985. 106. Brown PM, Pattenden R, et al. J Selective management of abdominal aortic aneurysms in a prospective measurement program.Vasc Surg 1996;23(2):213–221. 107. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. The UK Small Aneurysm Trial Participants Lancet 1998;352(9141):1649–1655. 108. Lloyd WE, Paty PS, et al. Results of 1000 consecutive elective abdominal aortic aneurysm repairs. Cardiovasc Surg 1996;4(6):724–726. 109. Thompson JE, Hollier LH, et al. Surgical management of abdominal aortic aneurysms. Ann Surg 1975;181: 654– 660. 110. Debakey ME, Crawford ES, et al. Aneurysms of the abdominal aorta. Analysis of results of graft replacement therapy one to eleven years after operation. Ann Surg 1964;169:622. 111. Crawford ES, Saleh SA, et al. Infrarenal abdominal aortic aneurysm. Factors influencing survival after operation performed over a 25 year period. Ann Surg 1981;193: 699–709. 112. Pairolero PC. Repair of abdominal aortic aneurysm in high risk patients. Surg Clin North Am 1989;69:755–763. 113. Robson AK, Currie IC, et al. Abdominal aortic aneurysm repair in the over eighties. Br J Surg 1989;76:1018–1020. 114. Hallin A, Bergqvist D, Holmberg L. Literature review of surgical management of abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2001 Sep;22(3):197–204. 115. Bayly PJ, Matthews JN, et al. In-hospital mortality from abdominal aortic surgery in Great Britain and Ireland: Vascular Anaesthesia Society audit. Br J Surg 2001;88(5):687–692. 116. Huber TS, Wang JG, et al. Experience in the United States with intact abdominal aortic aneurysm repair. J Vasc Surg 2001;33(2):304–310. 117. Heller JA, Weinberg A, et al. Two decades of abdominal aortic aneurysm repair: have we made any progress? J Vasc Surg 2000;32(6):1091–1100. 118. Becquemin JP, Chemla E, et al. Peroperative factors influencing the outcome of elective abdominal aorta aneurysm repair. Eur J Vasc Endovasc Surg 2000;20(1):84–89. 119. Dardik A, Lin JW, et al. Results of elective abdominal aortic aneurysm repair in the 1990s: A population-based analysis of 2335 cases. J Vasc Surg 1999;30(6):985–995. 120. Axelrod DA, Henke PK, et al. Impact of chronic obstructive pulmonary disease on elective and emergency abdominal aortic aneurysm repair. J Vasc Surg 2001;33(1):72–76.

Chapter 59 Abdominal Aortic Aneurysm 121. Falk V, Vettelschoss M, et al. Surgical treatment of abdominal aortic aneurysms of octogenarians.Cardiovasc Surg 1996;4(6):727–731. 122. Katz DJ, Stanley JC, Zelenock GB. Gender differences in abdominal aortic aneurysm prevalence, treatment, and outcome. J Vasc Surg 1997;25(3):561–568. 123. Starr JE, Hertzer NR, et al. Influence of gender on cardiac risk and survival in patients with infrarenal aortic aneurysms. J Vasc Surg 1996;23(5):870–880. 124. Eskandari MK, Rhee RY, et al. Oxygen-dependent chronic obstructive pulmonary disease does not prohibit aortic aneurysm repair. Am J Surg 1999;178(2):125–128. 125. Pilcher DB, Davis JH, et al. Treatment of abdominal aortic aneurysm in a state over 71/2 years. Am J Surg 1980;139:487–494. 126. Hollier LH, Reigel MM, et al. Conventional repair of AAA in the high risk patient: a plea for abandonment of nonresective treatment. J Vasc Surg 1986;3(5)7– 12. 127. Lawrie GM, Crawford ES, et al. Progress in the treatment of rupturesd abdominal aortic aneurysm. World J Surg 1980;4:653–660. 128. Hiatt JCG, Barker WF et al. Determinants of failure in the treatment of ruptured abdominal aortic aneurysm. Arch Surg 1984;119:1264–1268. 129. Fielding JWL, Black J et al. Ruptured aortic aneurysms: Postoperative complications and their etiologies. Br J Surg 1984;72:487–491. 130. Donaldson MC, Rosenberg JM, Buckman CA. Factors affecting survival after rupture of abdominal aortic aneurysm. J Vasc Surg 1985;2:564–570. 131. Noel AA, Gloviczki P, et al. Ruptured abdominal aortic aneurysms: the excessive mortality rate of conventional repair. J Vasc Surg 2001;34(1):41–46. 132. Kniemeyer HW, Kessler T, et al. Treatment of ruptured abdominal aortic aneurysm, a permanent challenge or a waste of resources? Prediction of outcome using a multi-organ-dysfunction score.Eur J Vasc Endovasc Surg 2000;19(2):190–196. 133. Turton EP, Scott DJ, et al. Ruptured abdominal aortic aneurysm: a novel method of outcome prediction using neural network technology. Eur J Vasc Endovasc Surg 2000;19(2):184–189. 134. Adam DJ, Mohan IV, et al. Community and hospital outcome from ruptured abdominal aortic aneurysm within the catchment area of a regional vascular surgical service. J Vasc Surg 1999;30(5):922–928. 135. Halpern VJ, Kline RG, et al. Factors that affect the survival rate of patients with ruptured abdominal aortic aneurysms.J Vasc Surg 1997 Dec;26(6):939–948. 136. Prance SE, Wilson YG, et al. Ruptured abdominal aortic aneurysms: selecting patients for surgery. Eur J Vasc Endovasc Surg 1999;17(2):129–132. 137. Reigel MM, Hollier LH, et al. Late survival in abdominal aortic aneurysm patients: The role of selective myocardial revascularization on the basis of clinical symptoms. J Vasc Surg 1987;5:222. 138. Hollier LH, Plate G, et al. Late survival after abdominal aortic aneurysm repair:influence of coronary artery disease. J Vasc Surg 1984;1:290–299. 139. Cho JS, Gloviczki P, et al. Long-term survival and late complications after repair of ruptured abdominal aortic aneurysms J Vasc Surg 1998;27(5):813–820.

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140. Norman PE, Semmens JB, Lawrence-Brown MM. Long-term relative survival following surgery for abdominal aortic aneurysm: a review. Cardiovasc Surg 2001;9(3):219–224. 141. Evans SM, Adam DJ, et al. Vascular surgical society of Great Britain and Ireland: long-term survival following repair of ruptured abdominal aortic aneurysm in patients over 75 years of age. Br J Surg 1999;86(5):696. 142. Hertzer NR, Young JR, et al. Routine coronary angiography prior to elective aortic reconstruction. Arch Surg 1979;114:1336–1344 143. Hertzer NR, Beven EG, et al. Coronary artery disease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg 1984;199:223–233. 144. Lette J, Waters D, et al. Multivariate clinical models and quantitative dipyridamole-thallium imaging to predict cardiac morbidity and death after vascular reconstruction. J Vasc Surg 1991;14:160–169. 145. Wong T, Detsky AS. Preoperative cardiac risk assessment for patients having peripheral vascular surgery. Ann Intern Med 1992;116:743–753. 146. Erickson CA, Carballo RE, et al. Using dipyridamolethallium imaging to reduce cardiac risk in aortic reconstruction. J Surg Res 1996;60(2):422–428. 147. Davila-Roman VG, Waggoner AD, et al. Dobutamine stress echocardiography predicts surgical outcome in patients with an aortic aneurysm and peripheral vascular disease. J Am Coll Cardiol 1993;21:957–963. 148. Hollier LH. Cardiac evaluation in patients with vascular disease-overview:a practical approach. J Vasc Surg 1992;15(4):726–729. 149. Wisselink W, Hollier LH, Kazmier FJ. Cardiac evaluation in patients with vascular disease:a practical approach. In: Veith FJ, ed. Current critical problems in vascular Surgery. Vol. 5 1993:340–347. 150. Williams CD, Brenowitz JB, Prohibitive lung functions and surgical procedures. Am J surg 1976;132:763. 151. Stanley JC, Wakefield TW. Cardioplumonary assessment for major vascular reconstructions. East Norwalk, Conn: Appleton and Lange, 1989:195–203. 152. Smith PK, Fuchs JCA, Sabiston DC. Surgical management of aortic abdominal aneurysms in patients with severe pulmonary insufficiency. Surg Gynecol Obstet 1980;151:407. 153. Cahan MA, Killewich LA, et al. The prevalence of carotid artery stenosis in patients undergoing aortic reconstruction. Am J Surg 1999;178(3):194–196. 154. Spark JI, Chetter IC, et al. Allogeneic versus autologous blood during abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg 1997;14(6):482–486. 155. Clagett GP, Valentine RJ, et al. A randomized trial of intraoperative autotransfusion during aortic surgery. J Vasc Surg 1999 Jan;29(1):22–30; discussion 30–31. 156. Toy PCTY, Strauss RG, et al. Predeposited autologous blood for elective surgery. N Engl J Med 1987;316:517–520. 157. Levine EA, Gould SA, et al Perioperative recombinant erythropoietin. Surgery 1989;106:432–438. 158. Hallet JW, Popovsky M, Ilstrup D. Minimizing blood transfusion during aortic surg; recent advances in autotransfusion. J Vasc Surg 1987; 5:601–660. 159. Reddy DJ, Ryan CJ, et al. Intraoperative autotransfusion in vascular surgery. Arch Surg 1990;125:1012–1016.

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160. Cutler BS. Avoidance of homologous transfusion in aortic operations: the role of autotransfusion, hemodilution, and surgical technique. Surgery 1984;95:717–723. 161. Wisselink W, Nguyen JH, et al. Ischemia-reperfusion injury of the spinal cord: the influence of normovolemic hemodilution and gradual rep[erfusion. Cardiovasc Surg 1995;3(4):399–404. 162. Whittemore AD, Clowes AW, et al. Aortic aneurysm repair reduced operative mortality associated with maintainance of optimal cardiac performance. Ann Surg 1980;120:414–421. 163. Valentine RJ, Duke ML, et al Effectiveness of pulmonary artery catheters in aortic surgery: a randomized trial. J Vasc Surg 1998;27(2):203–12. 164. Smith JS, Cahalan MK, et al. Intraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two dimensional transesophageal electrocardiography. Circulation 1985;72:1015–1021. 165.Gewertz BL, Kremser PC, et al. Transesophageal electrocardiography monitoring of myocardial ischemia during vascular surgery.. J Vasc Surg 1987;5:607–613. 166.Hollier LH, Spittell JA, Puga FJ. Intra-aortic balloon counterpulsations as adjunct to aneurysmectomyin high-risk patients. Mayo Clin Proc 1981;56(9):565. 167. Hassel EA. Intraoperative management of abdominal aortic aneurysms: the anesthesiologists viewpoint. Surg Clin North Am1989;69:775. 168. Bunt TJ, Manzuk M, Varley K. Continuous epidural anesthesia for aortic surgery: thoughts on peer review and safety. Surgery 1987;101:706–714. 169. Matsumoto K, Nakamaru M, et al. Surgical strategy for abdominal aortic aneurysm with concurrent symptomatic malignancy. World J Surg 1999;23(3):248– 251. 170. Szilagyi DE, Elliott JP, Berguer R. Coincidental malignancy and abdominal aortic aneurysm. Arch Surg 1967;95:402. 171. Weinstein MH, Machleder HI. Sexual function after aortoiliac surgery. Ann Surg 1975;181:787. 172. Szilagyi DE, Smith RF, Elliott JP, Temporary transection of the left renal vein:a technical aid in aortic surgery. Surgery 1969;65:32. 173. Elsharawy MA, Cheatle TR, et al. Effect of left renal vein division during aortic surgery on renal function. Ann R Coll Surg Engl 2000;82(6):417–420. 174. Sicard GA, Allen BJ, et al. Retroperitoneal versus transperitoneal approach for repair of abdominal aortic aneurysms. Surg Clin North Am 1989;69:795– 806. 175. Cambria RP, Brewster DC, et al..Transperitoneal versus retroperitoneal approach for aortic reconstruction. A randomized prospective study. J Vasc Surg 1990;11:314–325. 176. Kirby LB, Rosenthal D, et al. L Comparison between the transabdominal and retroperitoneal approaches for aortic reconstruction in patients at high risk. J Vasc Surg 1999;30(3):400–405 177. Honig MP, Mason RA, Giron F. Wound complications of the retroperitoneal approach to the aorta and iliac vessels. J Vasc Surg 1992;15:28–34. 178. Chang BB, Shaw DJ, et al. Can the retroperitoneal approach be used for ruptured aortic aneurysms? J Vasc Surg 1990;11:326–330.

179. Shepard AD, Tollefson DFJ, et al. Left flank retroperitoneal exposure: a technical aid to complex aortic reconstruction. J Vasc Surg 1991;14:283–291. 180. Crawford ES. Ruptured abdominal aortic aneurysm: an editorial. J Vasc Surg 1991;13(2):348–350. 181. Brimacombe J, Berry A. Controversies in the management of ruptured abdominal aortic aneurysm. Letter to the editor. J Vasc Surg 1993;17(3):625–626. 182. Valentine RJ, Barth MJ, et al. Nonvascular emergencies presenting as ruptured abdominal aortic aneurysms. Surgery 1993;113(3):286–289. 183. Berguer R, Schneider J, Wilner HI. Induced thrombosis of inoperable aneurysms. Surgery 1978;83:425. 184. Karmody Am, Leather RP, et al. The current position of nonresective treatment for abdominal aortic aneurysm. Surgery 1983;94:591. 185. Inahara T, Geary GL, et al. The contrary position to the nonresective treatment for abdominal aortic aneurysm. J Vasc Surg 1985;2:42. 186. Karmody Am, Leather RP, et al. The current position of nonresective treatment for abdominal aortic aneurysm. Surgery 1983;94:591. 187. Schwartz RA, Nichols WK, Silver D. Is thrombosis of the infrarenal abdominal aortic aneurysm an acceptable alternative? J Vasc Surg 1986;3:448. 188. Huber KL, Joseph A, Mukherjee D. Extra-anatomic arterial reconstruction with ligation of common iliac arteries and embolization of the aneurysm for the treatment of abdominal aortic aneurysms in high-risk patients. J Vasc Surg 2001;33(4):745–751. 189. Zarins CK, Wolf YG, et al. Will endovascular repair replace open surgery for abdominal aortic aneurysm repair? Ann Surg 2000;232(4):501–507. 190. String ST. Cholelithiasis and aortic reconstruction. J Vasc Surg 1984;1:664–669. 191. Ouriel K, Ricotta JJ, et al. Management of cholelithiasis in patients with abdominal aortic aneurysms. Ann Surg 1983;198:717–719. 192. Williamson WK, Abou-Zamzam AM Jr, et al. Prophylactic repair of renal artery stenosis is not justified in patients who require infrarenal aortic reconstruction. J Vasc Surg 1998;28(1):14–22. 193. Tarazi RY, Hertzer NR, et al. Simultaneous aortic reconstruction and renal revascularization: risk factors and late results in 89 patients. J Vasc Surg 1985;2:707– 714. 194. Stewart MT, Smith RB III, et al. Concomitant renal revascularization in patients undergoing aortic surgery. J Vasc Surg 1985;2:400–405. 195. Goldstone J, Malone JM, Moore WS. Inflammatory aneurysms of the abdominal aorta. Surgery 1978;83:425–430. 196. Goldstone J. Inflammatory aneurysms of the abdominal aorta. Semin Vasc Surg 1988;1:165–173. 197. Pennell RC, Hollier LH, et al. Inflammatory abdominal aortic aneurysms-a 30-year review. J Vasc Surg 1985; 198. Nitecki SS, Hallett JW Jr, et al. Inflammatory abdominal aortic aneurysms: a case-control study: J Vasc Surg 1996;23(5):860–869. 199. Rasmussen TE, Hallett JW Jr. Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis. Ann Surg 1997;225(2):155–164.

Chapter 59 Abdominal Aortic Aneurysm 200. von Fritschen U, Malzfeld E, et al. Inflammatory abdominal aortic aneurysm: A postoperative course of retroperitoneal fibrosis. J Vasc Surg 1999;30(6):1090–1098. 201. Jean-Claude JM, Reilly LM, et al. Pararenal aortic aneurysms: the future of open aortic aneurysm repair. J Vasc Surg 1999;29(5):902–912. 202. Benjamin ME, Hansen KJ, et al. Combined aortic and renal artery surgery. A contemporary experience. Ann Surg 1996;223(5):555–567. 203. Baker WH, Sharzer LA, Ehrenhalt JL. Aortocaval fistula as a complication of abdominal aortic aneurysm. Surgery 1972;72:933–938. 204. Gillig-Smith GL, Mansfield AO. Spontaneous abdominal arteriovenous fistula: report of eight cases and review of the literature. Br J Surg 1991;78:421–426. 205. Alexander JJ, Ibembo AL. Aorta-vena cava fistula. Surgery 1989;105:1–12. 206. Gutowicz MA, Smullen S. Ruptured abdominal aortic aneurysm with horseshoe kidney. J Vasc Surg 1984;1:689. 207. Connelly TL, McKinnon W, et al. Abdominal aortic surgery in horseshoe kidney. Arch Surg 1980;111: 1456. 208. Bergan JJ, Yao JST. Modern management of abdominal aortic aneurysms. Surg Clin North Am 1974;54:175. 209. Davis JT, Hardin WT, et al. Abdominal aneurysm and horseshoe kidney. South Med J 1971;64–75. 210. Hollis HW, Rutherford RB. Abdominal aortic aneurysms associated with horseshoe or ectopic kidneys. Techniques of renal preservation. Semin Vasc Surg 1988;1:148–159. 211. Stroosma OB, Kootstra G, Schurink GW. Management of aortic aneurysm in the presence of a horseshoe kidney. Br J Surg 2001;88(4):500–509. 212. Schneider JR, Cronenwett JL. Temporary perfusion of a congenital pelvic kidney during abdominal aortic aneurysm repair. J Vasc Surg 1993;17(3):613–617. 213. Brener BJ, Darling C, et al. Major venous anomalies complicating abdominal aortic surgery. Arch Surg 1974;108:160–165. 214. Kunkel JM, Weinstein ES. Preoperative detection of potential hazards in aortic surgery. Perspect Vasc Surg 1989;21:1–17. 215. Nypaver TJ, Shepard AD, et al. Supraceliac aortic crossclamping; determinants of outcome in elective abdominal aortic reconstruction. J Vasc Surg 1993;17:868–875. 216. Bertges DJ, Rhee RY, et al. Is routine use of the intensive care unit after elective infrarenal abdominal aortic aneurysm repair necessary? J Vasc Surg 2000;32(4):634–642 217. Bauer EP, Redaelli C, et al. Ruptured abdominal aortic aneurysms: predictors for early complications and death. Surgery 1993;114:31–35. 218. Alpert RA, Roizen MF, et al. Intraoperative urinary output does not predict postoperative renal function in patients undergoing abdominal aortic revascularization. Surgery 1984;95:707–711. 219. Nicholson ML, Baker DM, et al. Randomized controlled trial of the effect of mannitol on renal reperfusion injury during aortic aneurysm surgery. Br J Surg 1997;84(4):587–593. 220. arvinen O, Laurikka J, et al. Mesenteric infarction after aortoiliac surgery on the basis of 1752 operations from

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222.

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224.

225. 226.

227.

228.

229.

230. 231. 232.

233.

234.

235.

236.

237.

238.

239.

240.

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the National Vascular Registry. World J Surg 1999;23(3):243–247. Ernst CB, Hagihara PE, et al. Ischemic colitis incidence following abdominal aortic reconstruction: a prospective study. Surgery 1976;80:417. Hagihara PF, Ernst CB, Griffen WO. Incidence of ischemic colitis following abdominal aortic reconstruction. Surg Gynecol Obstet 1979;149:571–573. Smith RE, Szilagyi DE. Ischemia of the colon as a complication in the surgery of the abdominal aorta. Arch Surg 1960;80:806–821. Bailey RW, Bulkley GB, et al. The fundamental hemodynamic mechanism underlying gastric stress ulceration in cardiogenic shock. Ann Surg 1987;205:597–612. Bailey RW, Hamilton SR, et al. Pathogenesis of nonocclusive ischemic colitis. Ann Surg 1986;203:590–599. Plate G, Hollier LH, et al. Recurrent aneurysms and late vascular complications following repair of abdominal aortic aneurysms. Arch Surg 1985;120:590. Hagino RT, Valentine RJ, Clagett GP Acalculous cholecystitis after aortic reconstruction. J Am Coll Surg 1997;184(3):245–248. Picone AL, Green RM, et al. Spinal cord ischernia following operations on the abdominal aorta. J Vasc Surg 1986;3:94. Sutton J, Nesbit RR Jr. Spinal cord ischemia following surgery for aorta iliac occlusive disease. J Vasc Surg 1984;1:697. Adams HD, Van Geertruyden JJ. Neurologic complications of aortic surgery. Ann Surg 1956;144:574. Ferguson LRJ, Bergan JJ, et al. Spinal ischemia following abdominal aortic surgery. Ann Surg 1975;181:267. Farkas JC, Fichelle JM, et al. Long-term follow-up of positive cultures in 500 abdominal aortic aneurysms. Arch Surg 1993;128:284–288. Seabrook GR, Schmitt DD, et al. Anastomotic femoral pseudoaneurysm: an investigation of occult infection as an etiologic factor. J Vasc Surg 1990;11:629–634. Brunner MC, Mitchell RS, et al. Prosthetic graft infection: limitations of indium white blood cell scanning. J Vasc Surg 1986;3:42–48. LaMuraglia GM, Fischman AJ, et al. Utility of the indium 11 1-labeled human immunoglobulin G scan for the detection of focal vascular graft infection. J Vasc Surg 1989;10:20–28. Seeger JM, Pretus HA, et al.. Long-term outcome after treatment of aortic graft infection with staged extraanatomic bypass grafting and aortic graft removal. J Vasc Surg 2000;32(3):451–461. Walker WE, Cooley DA, et al. The management of aortoduodenal fistula by in situ replacement of the infected abdominal aortic graft. Ann Surg 1987;205:727–732. Core GB, Reyes E, Engels B, Vasconer LO. Complete replacement of infected vascular prosthesis with tubed myofascioperitoneal flap. Surg Forum 1993;44:360–363. Williamson WK, Nicoloff AD, et al. Functional outcome after open repair of abdominal aortic aneurysm. J Vasc Surg 2001;33(5):913–920. Magee TR, Scott DJ, et al. Quality of life following surgery for abdominal aortic aneurysm. Br J Surg 1992;79:1014–1016.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 60 Endovascular Repair of Abdominal Aortic Aneurysms Juan C. Parodi and Luis M. Ferreira

Endoluminal Treatment of Abdominal Aortic Aneurysms Currently, elective repair of abdominal aortic aneurysm (AAA) is performed with a mortality rate of less than 5% and with the expectation of a good long-term survival rate (1–4). However, there are subgroups of patients who are at increased risk during conventional repair because of their associated medical or technical problems (e.g., patients with myocardial infarction, renal or liver insufficiency, inflammatory aortic aneurysms, horseshoe kidney, hostile abdomen, among others). It is obvious that the presence of an abdominal aortic aneurysm is lifethreatening. Management of these high-risk patients could be directed toward providing them an aortic aneurysm exclusion performed endoluminally. This chapter describes three periods in the development of an endovascular treatment for AAA amenable to being treated by utilizing a combination of a stent and a vascular graft.

Early Clinical Experience In 1976, we began to develop a plan for endovascular treatment of AAA that was based on the fundamental principles of AAA replacement. Our initial experimental study had shown that stents could replace surgical anasto-

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moses by suturing a modified Palmaz stent onto a Dacron fabric graft. Stents could act as friction seals to fix the ends of the graft to the vessel wall, pressing the graft against the aortic wall to create a watertight seal. Placing of the stent–graft assembly was planned to be done by actually mounting the device on a large balloon catheter. This would be placed under fluoroscopy through a femoral arteriotomy preloaded into an introducer sheath (Fig. 60.1). This section details the endoluminal treatment of 94 patients, treated from September 1990 to March 1996 in the Cardiovascular Institute of Buenos Aires. Eight patients were considered to be in the group of acceptable risk to be treated with the standard surgical operation and were included as volunteers; 79 were clearly included in the high-risk group (ASA III or IV); and 17 were considered inoperable by at least two well-recognized vascular surgeons. A total of 51 patients underwent aortic tube graft replacement, with eight patients having only one proximal stent, and 45 received an aortoiliac stent graft (5). Of the 94 procedures for AAA exclusion, 76% were considered successful. The definition of a successful procedure includes complete exclusion of the aneurysm with restoration of the normal blood flow. On this criterion 23% in the aorto-aortic group and 24% in the aortoiliac group were considered as initial failures. Four of the failures were correctable using an additional endoluminal treatment.

Chapter 60 Endovascular Repair of Abdominal Aortic Aneurysms

FIGURE 60.1 Aorto-aortic stent graft excluding AAA.

Long-term Results All patients were followed by clinical examination, color duplex studies every 6 months, and CT scans once a year. Angiography was performed in some patients, and in everyone in whom the color duplex or CT scans indicated or suggested any sign of endoleak, or any change when compared with the study performed immediately after the procedure. Most of the patients died during the first 5 years following the endoluminal procedure. However, 30 patients were followed with an average follow-up period of 58.6 months, with a range between 22 to 119 months. Of the 15 patients who received an aorto-aortic endograft, 12 patients developed a distal aortic dilation after the initial procedure. The distal stent was placed at the aortic bifurcation. The complication was corrected in one case by adding a short segment of graft and performing a surgical anastomosis between the old graft and the aortic bifurcation. The patient recovered uneventfully. Two other patients were treated endoluminally by adding a new endograft. The aneurysm increased in size in eight patients, remained the same size in three and decreased in four patients. Three patients (20%) had a successful durable exclusion, and the size of the aneurysm decreased in all three. The aorto-aortic design was abandoned in 1994. To overcome the complications related to the aortic bifurcation dilation, the aorto-uni-iliac design was

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launched. The home-made tapered endograft led to a successful result in 10 out of 15 patients; the size of the aneurysm decreased in size in all 10 cases and no endoleak developed. Five patients developed late endoleaks: three were type I endoleaks (one proximal and two distal iliac endoleaks) and two were type II endoleaks. All five patients had their aneurysm enlarged. Careful measurement of the proximal neck indicated that neck dilation did not take place. In the 15 patients who had an aorto-aortic configuration excluding their aneurysm, the initial neck diameter was 23.9 mm and after 65 months 24.2 mm (p = 0.7). In the aorto-uni-iliac design the initial neck diameter was 25.3 mm and after 53 months was 25.7 mm (p = 0.6). Shrinkage of aneurysm was constant after 5 years when the aneurysm was effectively excluded. Presence of type I endoleaks resulted in aneurismal growth in two thirds (10 of the 15 patients). Only two out of 30 patients had persistent type II endoleaks and suffered aneurysmal growth. The fact that one-third of the patients with type I endoleaks did not result in aneurysmal growth is intriguing. The probable explanation is as follows: low-flow type I endoleaks with an appropriate outflow (several lumbar arteries) have a low pressure inside the sac, while conversely high-flow endoleaks with no outflow result in rapid aneurysmal growth and rupture. Of the patients in the initial group 70% had good results after the primary procedure until the last clinical visit or until their death from an unrelated cause. Most of the complications were correctable by additional endoluminal procedures. No neck dilation was found in the initial group of patients. Only one case (3%) of proximal endoleak resulted in the long term, in a patient in whom the proximal stent was placed distant from the renal arteries and in contact with mural thrombus. In two of our long-term cases a reduction of the diameter of the proximal neck was evident. Encapsulation of the proximal bare segment of the proximal stent was seen in the two cases in which we performed a postmortem examination (6).

Discussion After 94 procedures for treating aneurysms, some conclusions can be drawn. The procedure was simple in theory, but several details should be attended to before moving ahead with the widespread use of the method. CT scan images, intraluminal measurement, and some geometric calculations helped us to obtain reasonably reliable data. The concept of “one size fits all” was founded using a partially elastomeric balloon, an extra-large stent and an expandable fabric graft. The only variable was the length. The first lesson we learned after some initial success was that a second stent placed at the distal end was necessary in every case. The presence of reflected pressure waves from the iliac arteries was responsible of the failure of the cases in which only the proximal stent was placed. On the other hand, the distal aortic neck was often nonexistent or very short. Even the longer distal necks had a ten-

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dency to dilate and create late endoleaks. The distal neck of an abdominal aortic aneurysm has a quite different behavior when an endograft was fixed to it. Almost regularly, the distal neck of the aorta, when it exists, dilates over time. Difference in behavior of the proximal and distal neck is most probably due to the different composition of the wall. The proximal neck is richer in elastic fibers and seldom calcified. Mural thrombus in the proximal neck exists in a small proportion of patients and apparently does not have a significant impact on results. In addition, strong crisscrossing fibers in the adventitia coming from the visceral branches give strength and stability to the proximal neck adjacent to the ostia of the renal arteries. Thus, the distal landing zone for the graft should be the iliac arteries in most cases. Second, access problems were addressed and we concluded with the following recommendations: 1. 2. 3. 4.

5.

6.

Choose the straighter and wider iliac to cannulate the aorta. Avoid heavily calcified and narrow arteries. Use an extra-stiff wire to straighten the iliac arteries. If the iliac axis is too tortuous, use blunt dissection of the external iliac artery, ligating its small branches, and pull the artery down. If the iliac artery cannot be straightened or is hypoplasic, create a temporary conduit by anastomosing a 10-mm-diameter polyester graft onto the common iliac artery, bringing the other end to the groin. Place a “through and through” guidewire from the brachial artery down to the femoral artery as this often helps to advance the device inside the aorta in the presence of tortuous iliac arteries.

Although the new devices improved on the old technology, the following advantages of the basic device can be listed. One or two sizes fit all cases. The same size balloons can be used in cases with different neck diameters, just by applying different pressures. The malleability of the stent allows it to accommodate to irregular necks. The aorto-uni-iliac system developed by us made the system applicable to virtually all cases of aneurysms with suitable proximal necks. This section presents the results obtained in the initial 94 consecutive cases treated with a home-made device. During the course of this early experience, improvement in patient selection and surgical techniques have resulted in a lower incidence of surgical conversion, especially in patients with complex AAA morphology. Disadvantages of the system were mainly related to the large diameter and lower flexibility, addressed with the development of the new commercial generation. Encouraged by this promising approach, industry-made devices came to our field, opening a new and stimulating era in the endoluminal treatment of AAA. Currently, many new devices are being developed or evaluated in clinical trials around the world. In spite of its limitations this initial system is still in

use and very successful results have been reported by several investigators (7–10).

The Second Period: Vanguard Device The aim of this retrospective study was to analyze early and mid-term follow-up results and also report the anatomical changes in AAA configuration after endoluminal repair. We report our experiences with the first 100 consecutive procedures using the Vanguard® endograft (Boston Scientific Corp., Natick, MA) over a period of 4 years. From September 1996 to May 2000, the evolved Vanguard‚ endograft was used in the Instituto Cardiovascular de Buenos Aires according to a standardized protocol. Of the 204 patients with AAA who were treated in our service during this period, 100 were treated endoluminally. According to the ASA classification, 67 patients qualified as stage III and 24 as stage IV. The configuration used in all except three cases was a bifurcated version. Patients were excluded if the proximal neck was less than 10 mm in length or 29 mm in diameter, or intramural thrombus was lining all around the juxtarenal aorta (Fig. 60.2). Coil embolization, open ligation, or relocation of the hypogastric artery (11) was performed when dilation compromised the bifurcation of the common iliac arteries. An endograft extension was applied, extending the endograft to the level of the external iliac artery. In the cases of irregular or conical proximal necks, placement of an extra-large Palmaz stent covering the proximal anchoring site of the Vanguard‚ stented graft was used to seal intraoperative type I endoleak when present. To prevent damage to the endograft fabric by the metal of the Palmaz stent, an extending cuff of the Vanguard‚ was deployed beforehand. A total of 100 patients (84 men; mean aged 70.4 years, range 46–89) were treated for aneurysms with a mean maximum transverse diameter of 56 mm (range 35–92 mm). Primary technical success was achieved in 97%. Perioperative (30-day) mortality rate was 3% (three patients). Event-free survival at 54 months was 40.8%. An extra-large Palmaz stent was used to cover the proximal neck (Cordis Endovascular, Warren, NJ) in eight cases. No patient left the operating theater with a type I endoleak (Fig. 60.3). Aneurysms of the common iliac arteries were treated by hypogastric embolization using coils in 35 cases. Sixteen patients developed buttock claudication. Two patients developed colon ischemia and required colostomy and resection. Iliac relocation was performed in nine cases (Fig. 60.4). During a mean follow-up of 28 months (range 6–48 months), type I endoleaks were not found. Endoleaks caused by retrograde flow from collaterals (type II endoleak) were detected in 25 cases (25%) (Fig. 60.5). Be-

Chapter 60 Endovascular Repair of Abdominal Aortic Aneurysms

A

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A

B

FIGURE 60.2 Angiogram (A) before and (B) after AAA exclusion by a modular bifurcated stent–graft.

FIGURE 60.3 Geometric remodeling and hemostatic seal was achieved by deploying an extra-large Palmaz stent covering the proximal conical and irregular neck. (A) Plain radiograph and (B) DSA showing a complete exclusion.

cause of aneurysm enlargement, five of these patients required a secondary procedure. A limited open approach (7 cm incision) was performed in two cases, and a videoassisted clipping in the other one. In the last two cases, the endoleak was solved by inferior mesenteric artery embolization in one and hypogastric embolization and extension deployment in the other. A total of 53 patients were evaluated with plain abdominal radiographs: 13 endografts demonstrated increased distance between the struts of the stents, indicating broken sutures, and in six patients we found

broken sutures with separation of the first two rows, leading to distal migration of the segment following the proximal end of the device. Type III endoleaks were found in 10 cases. One patient suffered a rupture of the aneurysm 21 months after the endoluminal treatment. Graft wearing was the cause of the type III endoleak. In another patient, with a prosthetic limb slipped out of the main graft, a rupture was diagnosed by CT scan. He died 4 days after the exploration. Another patient died because of ruptured AAA after 14 months. Details of the cause of rupture were unavailable.

B

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Segmental separation was observed on the proximal anchorage site in six patients. Complete separation of the main body from the upper two rows of the bare stent determined distal device migration with proximal endoleak and sac re-pressurization was seen in three patients. All patients were treated by an additional proximal cuff. Component disconnection occurred in four patients. The distal component of the graft slipped into the sac, lying adjacent to the main body. In one patient the graft was

FIGURE 60.4 Relocation of the hypogastric artery in a patient with bilateral common iliac aneurysms. The contralateral hypogastric artery was coil embolized.

converted. The other patients were successfully treated endoluminally, placing an extension bridging the separate segments of the endograft. Intraluminal thrombus was seen on the contrastenhanced CT scan in six patients. This involved occlusion of one graft limb in one patient. These complications included a further seven graft limb occlusions associated with sac remodeling in patients with buckled endograft. Longitudinal shrinkage of aneurysm by >5 mm was observed in 24 cases (8.21 mm ± 6.41 mm) of which 12 had a concurrent reduction in aneurysm diameter. No significant changes were seen in aortic diameter at the level of the superior mesenteric artery (p = 0.56), renal arteries (p = 0.68) or proximal neck (p = 0.54). Transverse aneurysmals, shrinkage was seen in 73 patients (6.97 mm ± 5.94 mm). In the 13 patients in whom aneurysm enlargement (8.4 mm ± 9.3 mm) was detected, an endoleak was demonstrated (eight type II endoleaks, five type III endoleaks). In 16 patients with type II endoleaks, the aneurysm decreased in diameter (6.3 mm ± 4.5 mm), in eight patients an increase in diameter was detected (3.8 mm ± 1.9 mm), and one patient did not develop any change. Four patients with aneurysm shrinkages, presented a type III endoleak (6.6 mm ± 4.6 mm). Interestingly, pressurization of the aneurysmal sac did not preclude reduction of the aneurysm diameter in those patients. This series using the Vanguard‚ device represents the cumulative experience of our team with a modular bifurcated system over a period of almost 3 years. The good formability, flexibility, low profile, and the modular and bifurcated configuration of the device made it applicable to a large number of patients, with good early results.

FIGURE 60.5 (A, B) Endoleaks caused by retrograde flow from collaterals (type II endoleak). IMA, inferior mesenteric artery.

Chapter 60 Endovascular Repair of Abdominal Aortic Aneurysms

Endoleak Endoleak was defined as the presence of intra-aneurysm flow around an endovascular graft (12,13). This flow carries a blood pressure that potentially maintains aneurysm expansion and results in rupture. Although the causes of endoleak are many, any exposure of the residual aneurysm sac to arterial flow represents a potential persistent pressurization of the aneurysm and a potential risk for rupture. However, the natural history of endoleak remains poorly defined. If no endoleak is detectable, then the aneurysm should be maximally protected and risk of expansion or rupture minimized. Endoleaks can be detected by many forms of conventional vascular imaging, including duplex ultrasound, CT scan, magnetic resonance imaging, and angiography. Endoleak may be missed on CT scans if the images are obtained early in the cycle after infusion of the vascular contrast medium. Late CT images should be obtained. Detection of an endoleak relies on indirect evaluation of intrasac pressure, that is, observation of changes in aneurysm diameter and/or volume. The endoleaks may be due to an incomplete seal at the graft ends or between segments, thrombus interposition, incomplete deployment, or inappropriate sizing (type I endoleak). There may be flow through the graft material itself via interstices (type IV endoleak), and tears or perforations (type III endoleak). Migration or disconnection may develop over time due to arterial dilation or aneurysmal remodeling after shrinkage. Finally, non-graft-related endoleaks may be seen with retrograde flow from patent lumbar or inferior mesenteric arteries (type II endoleak). The presence of endoleaks without enlargement and enlargement without demonstrable endoleaks (endotension) allow us to justify our concept of aneurysm sac pressurization as a real cause of enlargement, ultimately leading to aneurysm rupture. Aneurysm expansion has been reported after technically successful exclusion associated with inadequate reduction of intra-aneurysmal pressure (14,15). On the other hand, not all endoleaks produce aneurysm enlargement (16,17). Some authors have reported delayed rupture in patients “waiting” for endoleak repair (18,19), while sac shrinkage with type I, II, or III endoleaks have also been described (20). Consideration of these cases, together with the experience of the nonresected treatment of AAAs (21), suggests that endoleaks can lead to aneurysm rupture. In an experimental model, we demonstrated that the presence of an endoleak causes a significant increase in aneurysm pressure (mean and diastolic pressure), the extent of which is directly proportional to the size of the endoleak. Also, a patent collateral branch depressurizes the high-pressure state made by the endoleak. Several authors studied the effect of patent lumbar arteries as the source of endoleaks (22). Lumbar endoleaks, in some cases, result in an increase of the diameter of the AAA (23). Recently, Baum et al. (24) reported two techniques to measure intrasac pressures. One involves catherization of the sac via a patent inferior mesen-

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teric artery accessed through the superior mesenteric artery. The second, which involves direct translumbar sac puncture, is particularly promising and may facilitate effective treatment and elimination of the endoleak. They demonstrated that type II endoleaks can transmit systemic pressure to the aneurysm sac.

Policy for Prevention of Endoleaks No procedure was considered finished until pressure injections of contrast media showed no type I endoleak. The infrarenal aorta was covered by an endograft from the distal edge of the lower renal artery down to the iliac artery bifurcation, or to the external iliac artery if the distal common iliac or hypogastric arteries were compromised. The device used was 20% oversized. The renal artery ostia was crossed by bare stent. Overlapping of segments extended at least 2 cm in length. Leaks from the ends were treated intraoperatively by balloon dilation, application of cuffs, or sealed by the use of a Palmaz stent and extensions. Gentle tension was applied to the device to prevent redundancy and consequent kinks, migration, or disengagement of segments. Thrombogenic materials were inserted into the aneurysm sac after the exclusion to promote sac thrombosis (Fig. 60.6). In cases of endoleak, the decision to intervene depends on the size, risks, and technical possibilities. A shrinking aneurysm may be assumed to be totally depressurized; however, aggressive intervention is mandatory for aneurysms that are enlarging. Although conservative management of type II endoleaks is an accepted approach, type I or III endoleaks should be repaired as a routine. With regard to aneurysm size, reduction is considered the criterion of successful treatment.

Endotension Sac expansion can occur even in the absence of endoleak. This condition was referred to by us as “endopressure” or “pressure leak” and is nowadays referred to as endotension. This entity has been associated not only with aneurysm expansion but also with aneurysm rupture (25–28). The transmission of pressure through a sealed or thrombosed endoleak is one of the leading explanations for endotension if it occurs (29). If endotension results from transmission from a sealed endoleak, then a highrisk group for endotension would be that group of patients who had initial endoleak, but sealed spontaneously, patient in which a migration of the endograft is seen, patients with the endograft deployed far from the renal arteries or iliac bifurcations, or on a thick layer of thrombus lining the aortic wall. This is correlated with Sanchez’s experimental demonstration that coiling with thrombosis of endoleaks fails to reduce systolic intra-aneurysmal pressures (30). Pressure transmission could also be related to porous graft fabrics. Graft material has previously been implicated in the local production of serous fluid by transudation through a polytetrafluoroethylene graft used at

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Part VII Aortic and Peripheral Aneurysms FIGURE 60.6 Insertion of thrombogenic material into the aneurysm sac and inferior mesenteric artery (IMA) coil embolization.

open AAA repair (31). In the presence of nondemonstrable endoleak, no further intervention is required if the aneurysm sac is shrinking. In the presence of expansion, however, further investigation is needed to identify the source of pressurization.

Morphologic and Structural Changes In tortuous vessels, the system can develop a kink and eventually occlude the extension, dislocate the limb graft away the iliac artery or produce disconnection between segments. It is useful to reinforce the area prone to kink with a self-expandable stent. Endograft kinking has three different causes: progressive postimplantation increase in the length of the graft, redundant stent deployment, or foreshortening of the sac. Loss of device integrity took many forms (fractures of hooks, circular and longitudinal stent wires, connections between wires loops, the polyester fabric and fabric polyester attachment mechanism) and could be demonstrated clinically by endoleaks or in the explanted specimen. None of the patients with cuff or Palmaz proximal stenting demonstrated any structural damage. Overlapping of stents avoids the complex movement of the endograft component as a whole and, among components, is probably the principal mechanism for the material fatigue. In summary, this device achieved a high initial success but our experience has documented various failure mechanisms including device component failure, migration, or disconnection. As a part of this evolution, a careful analysis of failures is particularly valuable for establishing patient selection criteria. There are some adverse results that were not anticipated when the technology was developed.

Third Period Many devices are being investigated for treatment of infrarenal abdominal aortic aneurysms. This section describes our experience with new-generation modular endografts. These were designed to overcome anticipated difficulties, like limb thrombosis, skeleton or sutures fractures, among others. This report summarizes our results using the bifurcated Excluder endoprosthesis (W.L. Gore and Associates, Flagstaff, AZ) and the Zenith device (Cook Inc., Bloomington, IN). Patients were enrolled from December 1999, through July 2001. A total of 53 subjects were enrolled (39 men; mean age 69.2 years; range 52–89 years). The mean maximum aneurysm diameter was 57.8 cm (range 4.5–9.9 cm), and the ASA classification was III for 33 patients. Two treated patients had a contained rupture aneurysm. All endoprostheses were successfully deployed, and there were no immediate conversions. No deaths have occurred. The reported type I or III endoleak rate was 0% at discharge and at 12 months follow-up. Three patients had type II endoleaks. Within this small sample size and short surveillance period, no deaths, ruptures, migrations, or occlusions have occurred. It is certain that with greater numbers of implantations and longer follow-up periods those complications might occur. At the same time, it is encouraging that these advanced device designs are not associated with limb occlusion or an inability to complete the procedure and that there has been no migration detected. What comes next? Endografts with branches to treat arch and thoracoabdominal aneurysms, the ideal systems to treat types A and B aortic dissections and thoracic aneurysms, adequate healing or incorporation of the

Chapter 60 Endovascular Repair of Abdominal Aortic Aneurysms

endograft to the aortic wall, induced thrombosis of the sac, low-profile percutaneous systems. At this stage, the procedure should be offered only to patients who present significantly impaired operative risk or have reduced life expectancy. Multiple factors must be balanced to ensure technical success. Technological advantages over the traditional procedures will soon facilitate this approach. However, longer follow-up will be needed to determine the benefits of these devices. We are finding new complications among our group of patients as late as 3 years after performing what we considered a successful procedure.

References 1. Dubost C, Chaubin F. Aortic aneurysms: technique — indications — results. Ann Chir 1997;51(5):531–536. 2. Haimovici H, Strandness DE, et al. Haimovici’s Vascular Surgery. Boston MA: Blackwell Science, 1995; 393–398. 3. Greenfield LJ, Mulholland MW, et al. Surgery: scientific principles and practice. Philadelphia PA: JB Lippincott Company, 1993; 1711–1723. 4. Rutherford RB. Vascular Surgery. Fourth Edition. Vol. 2. Philadelphia, PA: JB Lippincott Company, 1995; 1032–1060. 5. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5(6):491–499. 6. Parodi JC. Endoluminal stent grafts: overview. J Invasive Cardiol 1997;9(3):227–229. 7. Parodi JC, Ferreira LM. Historical prologue: Why endovascular abdominal aortic aneurysm repair? Sem Interv Cardiol 2000;5(1):3–6. 8. Ohki T, Veith FJ, et al. Increasing incidence of midterm and long-term complications after endovascular graft repair of abdominal aortic aneurysms: a note of caution based on a 9-year experience. Ann Surg 2001;234(3):323–334; discussion 334–335. 9. Faries PL, Burks J, et al. Current use of endovascular grafts for the treatment of abdominal aortic aneurysms. J Invasive Cardiol 2001;13(2):129–135; discussion 158–170. 10. Thompson MM, Sayers RD, et al. Aortomonoiliac endovascular grafting: difficult solutions to difficult aneurysms. J Endovasc Surg 1997;4(2):174–181. 11. Parodi JC, Ferreira M. Relocation of the iliac artery bifurcation to facilitate endoluminal treatment of abdominal aortic aneurysms. J Endovasc Surg 1999;6:342–347. 12. White, GH, May J, Waugh RC. Letter to the editors: Type I and type II endoleaks: a more useful classification for reporting results of endoluminal AAA repair. J Endovasc Surg 1998;5:189–191. 13. White, GH, May J, Waugh RC. Type III and type IV endoleak: toward a complete definition of blood flow in the sac after endoluminal AAA repair. J Endovasc Surg 1998;5:305–309. 14. Gilling-Smith, GL, Cuypers P, Buth J. The significance of endoleaks after endovascular aneurysm repair: results of a large European multicenter study (Abstr.). J Endovasc Surg 1998; 5:1–12.

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15. Chuter, TAM, Ivancev K, Malina M. Aneurysm pressure following endovascular exclusion. Eur J Vasc Endovasc Surg 1997;13:85–87. 16. May, J, White GH, Yu W. A prospective study of changes in morphology and dimensions of abdominal aortic aneurysms following endoluminal repair: a preliminary report. J Endovasc Surg 1995;2:343–347. 17. Matsumura, JS, Pearce WH, McCarthy WJ. Reduction in aortic aneurysm size: early results after endovascular graft placement. J Vasc Surg 1997;25:113–123. 18. Parodi, JC. Endovascular repair of abdominal aortic aneurysms and other arterial lesions. J Vasc Surg 1995;21:549–557. 19. Lumsden, AB, Allen RC, Chaikof EL. Delayed rupture of aortic aneurysms following endovascular stent grafting. Am J Surg 1995;170:174–178. 20. Resch, T, Ivancev K, Lindh M. Persistent collateral perfusion of abdominal aortic aneurysm after endovascular repair does not lead to progressive change in aneurysm diameter. J Vasc Surg 1998;28:242–249. 21. Resnikoff M, Clement Darling R III, et al. Fate of the excluded abdominal aortic aneurysm sac: long-term follow-up of 831 patients J Vasc Surg 1996;24(5):851–855. 22. Liewald F, Ermis C, et al. Influence of treatment of type II leaks on the aneurysm surface area. Eur J Vasc Endovasc Surg 2001;21(4):339–343. 23. Gilling-Smith GL, Martin J, et al. Freedom from endoleak after endovascular aneurysm repair does not equal treatment success. Eur J Vasc Endovasc Surg 2000;19(4):421–425. 24. Baum RA, Carpenter JP, et al. Aneurysm sac pressure measurements after endovascular repair of abdominal aortic aneurysms. J Vasc Surg 2001;33(1):32–41. 25. White GH, May J. How should endotension be defined? History of a concept and evolution of a new term. J Endovasc Ther 2000;7(6):435–438. 26. White GH, May J, et al. Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 1999;6(4):308–315. 27. Gilling-Smith G, Brennan J, Harris P. Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 1999;6(4):305–307. 28. Meier GH, Parker FM, et al. Endotension after endovascular aneurysm repair: the Ancure experience. J Vasc Surg 2001;34(3):421–427. 29. Bade MA, Ohki T, el al. Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: significance of endotension from a “virtual,” or thrombosed type II endoleak. J Vasc Surg 2001;33(6):1271–1274. 30. Marty, B, Sanchez LA, Ohki T. Endoleak after endovascular graft repair of experimental aortic aneurysms: Does coil embolization with angiographic “seal” lower intraaneurysmal pressure? J Vasc Surg 1998;27:454–462. 31. Williams GM. The management of massive ultrafiltration distending the aneurysm sac after abdominal aortic aneurysm repair with a polytetrafluoroethylene aortobiiliac graft. J Vasc Surg 1998;28:551–555.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 61 Endovascular Treatment of Ruptured Infrarenal Aortic and Iliac Aneurysms Frank J. Veith and Takao Ohki

Standard surgical treatment for ruptured abdominal aortoiliac aneurysms (AAAs) has achieved some dramatic individual results but is generally associated with substantial morbidity and an in-hospital mortality which ranges from 35% to 70% (1–8). Recent efforts to improve these poor results have not changed this bleak outlook significantly. Since 1994, we have evaluated the possibility that endovascular grafts coupled with other interventional techniques might help to improve the treatment outcomes of ruptured AAAs (9). Although we first used these grafts and techniques in a selected group of highrisk patients in whom pretreatment computed tomographic (CT) scans could be obtained, we presently believe that they should be applied more widely, to treat most patients with ruptured AAAs. The present chapter describes our experience to date with the use of endovascular grafts and other catheter-based techniques to treat ruptured AAAs.

Obstacles to Use of Endovascular Grafts in the Ruptured Aneurysm Setting The less invasive nature of endovascular treatment of ruptured AAAs offers many potential advantages. However, selection of the appropriate graft for each patient requires complex measurements of aneurysmal and adjacent arte-

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rial lengths and diameters. These measurements are usually based on high-quality contrast CT scans and arteriography that take time, which may not be available in the ruptured AAA setting. Moreover, it may not be possible to have available a stock of grafts suitable for most patients. A second obstacle to the use of endovascular grafts was that standard surgical practice mandated early proximal aortic control, and it was thought that that could be achieved most rapidly and most effectively by laparotomy with placement of a supraceliac or infrarenal aortic clamp (10).

Montefiore Endovascular Grafting System (MEGS) Since 1993, we have utilized a derivative of the original Parodi endograft (11) to treat aortic and aortoiliac aneurysms. This MEGS graft,* which is used in an aortofemoral configuration, is composed of a large proximal Palmaz balloon-expandable stent affixed to a long tulip-shaped PTFE graft (Fig. 61.1) (12). This graft is a “one size fits most” since the proximal diameter can vary between 20 and 28 mm depending on the inflation pressure applied to the deployment balloon, and the excess graft length can be cut off and tailored ap*To be commercialized as the Vascular Innovation Parodi Graft, Vascular Innovation, Inc., Perrysburg, OH 43551.

Chapter 61 Endovascular Treatment of Ruptured Infrarenal Aortic and Iliac Aneurysms

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FIGURE 61.1 MEGS graft. A large Palmaz stent is attached to the PTFE graft. The occluder device is shown on the left.

propriately before the distal graft is sutured to the graft introduction site within the common femoral artery (Fig. 61.2). Details of graft fabrication are as follows. The graft is constructed by suturing a Palmaz stent (P4010 or P5010, Cordis, Warren, NJ) to a standard ePTFE graft (6 mm ¥ 40 cm; Impra, Tempe, AZ). This stent–graft combination is then mounted onto a large percutaneous transluminal angioplasty (PTA) balloon (Maxi LD 25 mm ¥ 4 cm, Cordis) and inserted into a 16-Fr. sheath (Cook Inc., Bloomington, IN). An occluder device (for occlusion of the opposite common iliac artery) is constructed by attaching a Palmaz stent (P308 or P4014) to an ePTFE graft that is closed at one end by ligatures. This occluder device is also mounted onto a PTA balloon and inserted into either a 12-Fr. or a 16-Fr. sheath. These devices are prefabricated and are kept sterile for emergent use. Having this graft sterilized and available has the potential for eliminating the need for preoperative measurement and fabricating or procuring a suitable graft for use in the urgent ruptured aneurysm setting.

FIGURE 61.2 Schematic drawing illustrating deployment of the MEGS graft. This graft is fixed within the proximal neck with a large Palmaz stent (p). The cranial end of the graft is denoted by a metallic marker (m) attached to the graft. The bare portion of the stent is deployed across the orifice of the renal arteries so that the graft is implanted immediately below the renal arteries (r). An endoluminal anastomosis (e) is performed at the distal end of the endograft. The occluder device (o) is deployed in the contralateral common iliac artery to preserve at least one internal iliac artery (i). c, embolization coil; f, femorofemoral bypass; s, sutures to occlude the end of the occluder.

Early Experience Because of our access to the MEGS graft, on April 21, 1994, we had a patient with a ruptured abdominal aorta and all the clinical sequelae thereof, i.e., severe abdominal pain, hypotension, and a large pulsatile abdominal mass. Because the patient had had a total cystectomy and ileal bladder, and because he had severe symptomatic coronary artery disease, he was deemed unsuitable for an open repair of his ruptured aortic aneurysm. He therefore underwent a MEGS endovascular graft repair of his ruptured

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Part VII Aortic and Peripheral Aneurysms

FIGURE 61.3 Transfemoral repair of a rupture of the distal aorta. (A) A spiral CT scan demonstrates extravasation of contrast material from the aorta (arrow) into a large, partially clot-filled pseudoaneurysm (P). (B) A spiral CT scan performed after transfemoral insertion of an endovascular graft demonstrates that the pseudoaneurysm is excluded and vascular continuity within the lumen of the aorta (arrow) is preserved. (C) A postoperative transfemoral arteriogram at 1 week demonstrates vascular continuity between the aorta (open arrow) and the common femoral arteries (arrows). The inset shows flow up the external iliac artery to the right hypogastric artery. An occluder has been placed in the right common iliac artery. (Reproduced with permission from Marin ML, Veith FJ, et al. Initial experience with transluminally placed endovascular grafts for the treatment of complex vascular lesions. Ann Surg 1995;222:1–17.)

aortic aneurysm along with placement of a right common iliac artery occluder and a femorofemoral bypass (Fig. 61.3) (9). The patient did well following this procedure until he died from cardiac disease 3 years later. To our knowledge, this was the first endovascular graft repair of a ruptured aortic aneurysm, although another early case had been reported by Yusuf et al. (13). Following our experience with our first successful case, we performed similar operations on another 11 patients with ruptured aortoiliac aneurysms (12). All these patients had major contraindications to open operation,

with serious medical comorbidities (e.g., coincident major myocardial infarction, chronic obstructive pulmonary disease (COPD) requiring home oxygen therapy) or surgical problems (e.g., abdominal infection or massive recurrent incisional hernias). All 12 of these first patients had been stable enough to undergo preoperative CT scanning to confirm the aneurysmal rupture. In all cases the ruptured aneurysm was successfully excluded by the endovascular graft. Moreover, only two of the patients died within 2 months of the procedure, a 17% operative mortality.

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TABLE 61.1 Exclusion criteria for endovascular repair Proximal neck diameter larger than 28 mm Pararenal AAAs (neck length shorter than 12 mm) Bilateral, long iliac artery occlusions

Hypothesis Regarding Endovascular Treatment and Current Management Plan This low operative mortality prompted us to speculate that all ruptured AAAs could be treated endovascularly (14). Such an approach might lead to better outcomes than were currently being achieved with open repair. In 1996, we therefore adopted the following treatment plan (14). All patients with a presumed diagnosis of a ruptured AAA were taken immediately to the operating room. A diagnosis of ruptured AAA was presumed if two or more elements of the diagnostic triad were present: namely syncope, abdominal or back pain, and a known or palpable AAA (10). In the operating room, with preparation for fluoroscopy of the patient from the neck to the knees, via a brachial or femoral puncture under local anesthesia a wire was placed in the supraceliac aorta. Using this guidewire, a catheter was placed to visualize the abdominal aorta and iliac arteries angiographically. This angiogram, which was best performed with a power injector, allowed a determination of whether or not an endovascular graft repair of the ruptured AAA was possible on the basis of aortic neck and iliac artery anatomy (Table 61.1). If not, a standard repair was carried out.

Technique of Endovascular Repair If an endovascular graft repair was deemed feasible, the following technical steps were employed using local or general anesthesia to perform the bilateral open exposures of the femoral arteries. Either before or after deployment of the MEGS graft, coil embolization of the hypogastric artery ipsilateral to the side of graft insertion was performed. The MEGS graft delivery system was inserted into the aorta over a superstiff wire placed in the upper thoracic aorta. Once the graft was inserted into the proximal aneurysm neck, the delivery sheath was retracted. In order to confirm appropriate positioning in regard to the renal arteries, a repeat angiogram was performed using a catheter introduced via the brachial or contralateral femoral artery. Inflation of the deployment balloon expanded the stent and fixed the graft within the proximal neck (Fig. 61.4). By varying the inflation pressure, the MEGS graft could accommodate a wide range of proximal neck diameters ranging from 18 to 28 mm (Fig. 61.5). In each case, the length of the graft was 40 cm so that the

FIGURE 61.4 Fluoroscopic view of a proximal occlusion balloon introduced through the brachial artery.

distal end of the graft always emerged from the introduction arteriotomy site. The graft was then cut to the appropriate length and hand-sewn endoluminally within the common femoral or distal external iliac artery (Fig. 61.6). The occluder device was then placed in the opposite common iliac artery, thereby preserving at least one hypogastric artery. In addition, a femorofemoral bypass was performed (Figs. 61.7 and 61.8B).

Control of Bleeding and Blood Pressure: Restricted Resuscitation, Hypotensive Hemostasis and Proximal Balloon Control As already noted, it is widely believed that with ruptured AAAs it is necessary to perform immediate laparotomy to permit clamp control of the aorta proximal to the aneurysm. With major arterial bleeding in other circumstances, however, restricted fluid resuscitation and withholding blood transfusions have been shown to decrease blood loss and improve outcomes (15–18). Restriction of fluid resuscitation has also been advocated in the preoperative management of ruptured aneurysms (3). We also believe that restriction of fluid resuscitation and blood transfusion in the ruptured AAA setting is not only desirable but mandatory. If the blood pressure is in the 50–70 mmHg range, it should be left there. If the patient is moving and talking, no fluids should be given. This should continue when the patient is first in the operating room being prepared for treatment and having a catheter and guidewire placed in the pararenal aorta under local anesthesia via either a brachial or femoral puncture. Patients with ruptured AAAs frequently deteriorate with induction of anesthesia. If that occurs and the blood pressure falls below 50–70 mmHg or is unobtainable, administration of fluid and blood become necessary. We believe such deterioration warrants proximal balloon control and have used this technique selectively in our current management plan for ruptured aneurysms.

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Part VII Aortic and Peripheral Aneurysms FIGURE 61.5 Method for customizing the proximal stent diameter of the MEGS graft intraoperatively. (A) When the deployment balloon is inflated to 2 atm, the stent is expanded to 20 mm in diameter (small arrow). (B) Due to the compliant nature of the balloon, at 6 atm of inflation pressure the stent is expanded to 28 mm (large arrow). (Reproduced with permission

A

from Ohki T, Veith FJ, et al. Endovascular graft repair of ruptured aorto-iliac aneurysms. J Am Coll Surg 1999;189:102–123.)

B

A

B

FIGURE 61.6 Method for customizing the length of the MEGS graft intraoperatively. (A) In each case, the endograft is made long enough so that the distal end of the graft (G) emerges from the arteriotomy site. (B) The graft is cut to the appropriate length as it emerges from the femoral artery and an endoluminal anastomosis (E) is carried out. (Reproduced with permission from Ohki T, Veith FJ, et al. Endovascular graft repair of ruptured aorto-iliac aneurysms. J Am Coll Surg 1999;189:102–123.)

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A

A

B

C

FIGURE 61.7 CT scan images of a ruptured AAA. This 71year-old male was admitted to another hospital for medical treatment of his pneumonia secondary to chemotherapy for leukemia. His other comorbid diseases included severe COPD requiring home oxygen, and congestive heart failure with an ejection fraction of 25%. The patient experienced a sudden onset of severe abdominal pain with CT scan evidence of a ruptured AAA. Owing to his coexisting diseases, standard repair was deemed prohibitively risky and he was transferred to our institution. On arrival, his systolic blood pressure was 75 mmHg and his hematocrit was 18%. (A) Preoperative CT scan reveals a possible rupture site (arrow) in the AAA. (B) Preoperative CT scan showing the more distal portion of the AAA. The AAA measures 7.5 cm in diameter. In addition, a large hematoma (H) can be seen in the right retroperitoneal space with displacement of the duodenum (D). (C) Postoperative contrast CT scan. Contrast is confined within the endograft (E) with evidence of complete aneurysmal exclusion. The ureter, which is displaced by the large hematoma, is visualized. Despite his comorbid conditions, he was extubated 6 hours following the procedure and was able to eat on the second postoperative day. (Reproduced with permission from Ohki T, Veith FJ, et al. Endovascular graft repair of ruptured aorto-iliac aneurysms. J Am Coll Surg 1999;189:102–123.)

B

FIGURE 61.8 Intraoperative angiogram of the patient described in Figure 61.7. (A) Preoperative angiogram reveals a large AAA and a small right common iliac aneurysm. Because the blood pressure was low, no extravasation was noted on this arteriogram. (B) Completion angiogram. The AAA is completely excluded with no evidence of an endoleak. The bare portion of the proximal stent (S) is placed above the renal arteries, and the cranial end of the graft, which is denoted by the gold marker (arrow), is placed immediately below the renal arteries. The right internal iliac artery is opacified by retrograde flow. (Reproduced with permission from Ohki T, Veith FJ, et al. Endovascular graft repair of ruptured aorto-iliac aneurysms. J Am Coll Surg 1999;189:102–123.)

Proximal Balloon Control If and when patients deteriorate before, during or after induction of anesthesia, a larger size (14 Fr.) hemostatic sheath is inserted over the previously placed guidewire in either the brachial or femoral artery. Keeping the wire in place, a 33 or 40 mm compliant (latex) balloon is inserted

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through the sheath and inflated with dilute contrast under fluoroscopic control in either the pararenal or infrarenal aorta (depending on the length of the infrarenal neck). With the balloon inflated, the remainder of the procedure is conducted as rapidly as possible to minimize the duration of visceral and renal ischemia. If the infrarenal neck is too short for an endovascular repair, open infrarenal control is obtained and a standard AAA repair performed. If the infrarenal neck is long enough, an infrarenal balloon should replace the more proximal balloon as soon as possible, and then the endograft is placed in a deliberate fashion, although the supraceliac balloon may have to be reinflated during the graft deployment when any infrarenal balloon must be removed.

Results To date, we have treated 31 patients with ruptured aortoiliac aneurysms using endovascular techniques (14). Included are the 12 original patients already described and another 19 patients treated according to our current management plan. Of these 31 patients, six were deemed unsuitable for endovascular treatment because of their aortic neck or iliac anatomy. All six underwent open repair, only two required inflation of the proximal balloon. All six survived for more than 2 months after operation. Of the remaining 25 patients who received an endovascular graft, 17 had the graft inserted without the need for proximal balloon control and only eight required balloon control. In all 25 patients, the graft was deployed successfully and completely excluded the ruptured aneurysm. There were no significant endoleaks and all surviving patients became and remained asymptomatic. Three of the 25 patients died during the 30 days after their procedure, but all three had serious medical comorbidities (two coincident major myocardial infarctions, one oxygen-dependent COPD). Thus, in this entire series of 31 ruptured AAAs, there was a procedural mortality of only 9.7%. Two patients receiving endovascular grafts required evacuation of a large retroperitoneal hematoma for abdominal compartment syndrome. In one of these patients the decompression was required immediately after graft placement; in the other it was required 7 days later. Two groin wound infections required drainage but healed without graft involvement.

Advantages of Endovascular Treatment Among the advantages of endovascular repair of ruptured aneurysms are the ability to obtain proximal control without general anesthesia, the ability to deploy the graft from a remote access site, reduced blood loss, and minimizing hypothermia by eliminating laparotomy.

Proximal Control without General Anesthesia Patients with ruptured AAAs may be severely hypotensive. However, many patients may have their blood pressure stabilized at a nonlethal level. This is due to sympathetically mediated vasoconstriction in response to hypotension. It is not uncommon for this vasoconstriction to be released during the induction of general anesthesia, which results in a sudden drop in blood pressure. Therefore, a relatively stable patient may become severely hypotensive, mandating urgent application of a proximal aortic clamp. However, a guidewire can be inserted in the upper abdominal or lower thoracic aorta through a percutaneous puncture under local anesthesia, while maintaining the vasoconstriction. Once the guidewire is inserted in the aorta, the patient can then safely undergo induction of general anesthesia because proximal control can be rapidly and safely obtained by an occlusion balloon placed over the previously inserted guidewire.

Deployment of Graft from a Remote Access Site Endovascular grafts can be inserted and deployed through a remote access site, thereby obviating the need for laparotomy and, more importantly, eliminating the technical difficulties that are encountered when performing a standard repair in the rupture setting. With the associated bleeding, the anatomy of the retroperitoneal structures is often distorted and obscured by a large hematoma, which may lead to technical difficulties, as well as to inadvertent injury of the inferior vena cava, the left renal vein or its genital branches, the duodenum, or other surrounding structures. These iatrogenic injuries have been the cause of significant operative morbidity and mortality following standard surgery for ruptured aneurysms. In contrast, endograft repair is performed within the arterial tree, which is unaffected by extravasated blood or previous operative scarring. Thus, the technical difficulty encountered when treating a ruptured aneurysm with an endograft is similar to that for elective cases. Moreover, this approach completely eliminates the risk of inadvertent injury to surrounding structures.

Reduced Blood Loss In our experience, endovascular repair for ruptured AAA was accomplished with a relatively small amount of additional blood loss (800 mL) compared with that which occurs during open, ruptured AAA repair. This advantage is more important in patients with ruptured aneurysms because they have already lost a significant amount of blood following rupture, and coagulopathy or disseminated intravascular coagulation secondary to further blood loss can be devastating complications. There are several reasons why this limited blood loss was possible, including the maintenance of the tamponade effect within the

Chapter 61 Endovascular Treatment of Ruptured Infrarenal Aortic and Iliac Aneurysms

retroperitoneum. In addition, backbleeding from the iliac and lumbar arteries and bleeding from the anastomotic suture lines and from iatrogenic venous injuries can be completely eliminated.

Minimizing Hypothermia Hypothermia secondary to poor perfusion and laparotomy can exacerbate coagulopathy, which is one of the causes of mortality following open surgical repair. Endovascular graft repair can minimize the extent of hypothermia by avoiding laparotomy.

Conclusions The relatively low mortality rate (10%) in our group of patients was encouraging, particularly because many were high-risk patients who were not surgical candidates. Our results as well as those of others (12,14,19–21) show that endograft repair of ruptured AAAs is feasible and effective in selected cases. However, before the widespread use of this technique is adopted, further experience by other groups will be required using our graft or similar ones to treat ruptured AAAs. Nevertheless, we believe that endovascular grafts represent a potentially better way to treat this entity since previous open surgical methods have had a persistently high morbidity and mortality. Moreover, we believe that the use of fluoroscopic techniques to facilitate the placement of proximal occlusion balloons, an old idea (22–25), will make this endovascular adjunct a practical and valuable one, even if an endovascular graft procedure is not possible and an open repair is required. And finally, we believe that hypotensive hemostasis or restricted fluid resuscitation will prove valuable in the ruptured AAA setting and will become the standard of care for this entity, leading to improved treatment outcomes.

Acknowledgments This work was supported in part by grants from the William J. von Liebig Foundation, the US Public Health Service, the James Hilton Manning and Emma Austin Manning Foundation, and the Anna S. Brown Trust.

References 1. Ernst CB. Abdominal aortic aneurysms. N Engl J Med 1993;328:1167–1172. 2. Ouriel K, Geary K, et al. Factors determining survival after ruptured aortic aneurysm: the hospital, the surgeon, and the patient. J Vasc Surg 1990;11:493–496. 3. Crawford ES. Ruptured abdominal aortic aneurysm: an editorial. J Vasc Surg 1991;13:348–350.

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4. Johansen K, Kohler TR, et al. Ruptured abdominal aortic aneurysm: the Harborview experience. J Vasc Surg 1991;13:240–247. 5. Gloviczki P, Pairolero PC, Mucha P. Ruptured abdominal aortic aneurysms: repair should not be denied. J Vasc Surg 1992;15:851–859. 6. Marty-Ane CH, Alric P, et al. Ruptured abdominal aortic aneurysm: influence of intraoperative management on surgical outcome. J Vasc Surg 1995;22:780–786. 7. Darling RC, Cordero JA, Chang BB. Advances in the surgical repair of ruptured abdominal aortic aneurysms. Cardiovasc Surg 1996;4:720–723. 8. Dardik A, Burleyson GP, et al. Surgical repair of ruptured abdominal aortic aneurysms in the state of Maryland: factors influencing outcome among 527 recent cases. J Vasc Surg 1998;28:413–423. 9. Marin ML, Veith FJ, et al. Initial experience with transluminally placed endovascular grafts for the treatment of complex vascular lesions. Ann Surg 1995;222:1–17. 10. Veith FJ. Emergency abdominal aortic aneurysm surgery. Compr Ther 1992;18:25–29. 11. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5:491–499. 12. Ohki T, Veith FJ, et al. Endovascular graft repair of ruptured aorto-iliac aneurysms. J Am Coll Surg 1999;189:102–123. 13. Yusuf SW, Whitaker SC, et al. Emergency endovascular repair of leaking aortic aneurysm. Lancet 1994;344:1645. 14. Ohki T, Veith FJ. Endovascular grafts and other image guided catheter based adjuncts to improve the treatment of ruptured aortoiliac aneurysms. Ann Surg 2000;232:466–479. 15. Andresen AFR. Results of treatment of massive gastric hemorrhage. Am J Digest Dis 1939;6:641–650. 16. Andresen AFR. Management of gastric hemorrhage. NY State J Med 1948;48:603–611. 17. Shaftan GW, Chiu CJ, et al. Fundamentals of physiologic control of arterial hemorrhage. Surg 1968:58:851–856. 18. Bickell WH, Wall MJ Jr, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994;331:1105–1109. 19. Yusuf SW, Whitaker SC, et al. Early results of endovascular aortic aneurysm surgery with aortouniiliac graft, contralateral iliac occlusion, and femorofemoral bypass. J Vasc Surg 1997;25:165–172. 20. Yusuf SW, Hopkinson BR. Is it feasible to treat contained aortic aneurysm rupture by stent–graft combination? In: Greenhalgh RM, ed. Indications in vascular and endovascular surgery. London: WB Saunders, 1998:153–165. 21. Greenberg RK, Srivastava SD, et al. An endoluminal method of hemorrhage control and repair of ruptured abdominal aortic aneurysms. J Endovasc Ther 2000;7:1–7. 22. Hughes LCCW. Use of an intra-aortic balloon catheter tamponade for controlling intra-abdominal hemorrhage in man. Surgery 1954;36:65–68. 23. Hesse FG, Kletschka HD. Rupture of abdominal aortic aneurysm: control of hemorrhage by intraluminal balloon tamponade. Ann Surg 1962;155:320–322.

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24. Anastacio CN, Ochsner EC. Use of Fogarty catheter tamponade for ruptured abdominal aortic aneurysms. Am J Roentgenol 1977;128:31–33.

25. Hyde GL, Sullivan DM. Fogarty catheter tamponade of ruptured abdominal aortic aneurysms. Surg Gynecol Obstet 1982;154:197–199.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 62 Management of Infected Aortic Grafts G. Patrick Clagett

Aortic graft infections are among the most challenging and difficult problems encountered by vascular surgeons. Patients are often elderly, frail, desperately ill with multiple medical comorbidities, and unable to tolerate extensive, complex operations usually required to treat the problem. Complete resection and excision of all infected graft material and contiguous vascular wall structures are usually necessary to eradicate infection. Immediate restoration of blood flow to critical vascular beds by alternate anatomic routes or with replacement vascular conduits that minimize the risk of recurrent infection present additional challenges that tax the skill and ingenuity of vascular surgeons. Despite a great deal of progress in the treatment of vascular infections, morbidity and mortality remain among the highest of all vascular conditions (1–3).

Prevention of Aortic Graft Infections The benefit of short-term antibiotic prophylaxis in preventing wound infections after vascular surgery has been demonstrated in randomized trials (4–6). Most often, a first-generation cephalosporin is administered intravenously shortly before operation, during operation if blood loss is extensive or the operation is prolonged, and 2 hours after operation. Some evidence suggests that a more prolonged course for up to 4–5 days after operation or until all invasive lines are removed may provide additional protection (7). In circumstances where patients

have infected lower extremity ischemic lesions, culturespecific antibiotics should be administered perioperatively. Also, the use of more specific prophylactic antibiotic therapy should be considered in hospital settings where certain organisms are prevalent, especially when exposure is increased by prolonged preoperative hospitalization. Attention to intraoperative factors is also important in preventing aortic graft infections. Reoperative and emergency operations are especially prone to wound infections and present additional risks. Meticulous attention to hemostasis and avoidance of wound hematomas and seromas that can become secondarily infected are important surgical tenets that are often difficult to achieve in patients anticoagulated during the operation and who are also being treated with antiplatelet agents. If possible, these agents should be discontinued 1 week prior to operation. Ligation and control of femoral lymphatics are also important technical features in preventing vascular prosthetic infections. Electrocautery of lymphatic tissue leads to coagulation necrosis of lymphatic vessels but does not prevent extravasation of lymph fluid. Patients undergoing aortic operations are prone to intraoperative hypothermia and this condition has been shown to impair neutrophil function and increase the incidence of postoperative wound infection (8). Maintenance of normal body temperature should be the goal during major vascular operations. Additional procedures on the gastrointestinal or biliary tract that may result in intraoperative contamination of an aortic graft should be avoided unless the additional procedure is deemed necessary to

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avoid life-threatening postoperative complications. Hematogenous seeding of a vascular prosthesis is a continuing risk for as long as the prosthesis is in place. Dental work, procedures on the gastrointestinal and genitourinary tracts, and angiographic procedures should be carried out under the protection of prophylactic antibiotics.

Clinical Presentation The clinical presentation of aortic graft infections can be protean and subtle, thus making the diagnosis difficult. The tempo and severity of clinical manifestations often depend upon the microorganism. Infections from virulent organisms such as Staphylococcus aureus, Pseudomonas aeruginosa, and Escherichia coli present with systemic signs of sepsis. Methicillin-resistant Staphylococcus aureus (MRSA) can cause particularly virulent graft infections and this organism is being increasingly documented in contemporary registries of graft infections (9,10). Patients with virulent aortic graft infections may present with fever, chills, and an elevated white cell count with a left shift. Virulent microorganisms also tend to cause earlier manifestations of infections, with the interval between implantation of the graft and diagnosis of infection often being months. Very early graft infections diagnosed within weeks of implantation are most often due to wound infections that involve the aortic graft by contiguous spread. In contrast, low-virulence organisms such as Staphylococcus epidermidis present later, often years after placement. Systemic signs and symptoms are usually mild or absent. These patients most often present with local manifestations such as a chronic groin sinus that discharges small amounts of pus, exposure of the graft in a chronic wound infection, femoral anastomotic false aneurysm, or aortofemoral bypass limb thrombosis. Patients with these infections may have low-grade fever and mild constitutional symptoms, but overt systemic signs of sepsis are absent. The white count is usually normal or only mildly elevated but the erythrocyte sedimentation rate is often abnormal. A patient presenting with a femoral anastomotic false aneurysm or limb thrombosis who has an elevated erythrocyte sedimentation rate should be suspected of having a prosthetic graft infection. Patients presenting with massive gastrointestinal hemorrhage from aortoduodenal or aortoenteric fistulas will frequently have had lesser episodes of bleeding hours to days prior to the major episode. These are often referred to as “herald” or “sentinel” episodes of bleeding and offer a window of opportunity for diagnosis and management that may avert exsanguinating hemorrhage. Any patient with an aortic graft who has an episode of upper or lower gastrointestinal bleeding should be suspected of having an underlying aortoenteric fistula and expeditious workup is important. Chronic gastrointestinal bleeding can also occur in patients with aortoenteric fistulas but is more often present when enteric erosion is present. This condition is referred to as “graft-enteric erosion” and dif-

fers from aortoenteric fistula in that the body or limb of the aortic graft erodes into bowel and the aortic suture line is not involved. This produces chronic bleeding from the eroded bowel mucosa analogous to an ulcer and patients may present with chronic anemia. The diagnosis should be suspected in a patient with an aortic graft who has anemia, guaiac-positive stools, and fever. An increasingly recognized manifestation of aortofemoral and aortoiliac graft infections is hydroureteronephrosis. This may occur when the ureter becomes obstructed from periprosthetic inflammation and may be bilateral or unilateral depending on the extent of infection. It is unusual for hydroureteronephrosis to be the initial manifestation of an aortic graft infection since the urologic condition is usually asymptomatic. This complication is noted most often during the workup of a patient with an infected aortic graft, presenting with other symptoms such as a groin sinus or gastrointestinal bleeding.

Diagnosis Because the manifestations of aortic graft infections are so varied and subtle and the consequences of a missed diagnosis may be lethal, imaging tests are important (11). The types of imaging and other diagnostic tests used are based upon the clinical presentation. Computed tomographic (CT) scanning has long been the mainstay of diagnostic imaging for suspected aortic graft infection. CT findings suggestive of infection include ectopic gas, periprosthetic fluid, loss of tissue planes, periprosthetic inflammatory changes, thickening of adjacent bowel, hydroureteronephrosis, and anastomotic false aneurysm (12). These findings are most specific and useful for late infections. During the immediate period following implantation, perigraft fluid, air, and inflammatory changes may persist for 2–3 months. After 3 months, postoperative hematoma and gas should resolve and tissue planes return to normal (13). Magnetic resonance imaging (MRI) has provided an alternative to CT scanning for cross-sectional imaging. In addition to noting the same features seen on CT scanning (perigraft air, fluid, and structural abnormalities), MRI is particularly helpful in assessing perigraft inflammatory changes. These are seen as high-intensity signals on T2weighted images in the tissues surrounding the graft and accurately portray tissue edema (14). This can be particularly helpful in assessing the extent of infection that may determine the operative approach. For example, a patient with an infection localized to a single, distal limb of an aortobifemoral bypass may not need removal of the entire prosthesis to adequately treat the infection. Radionuclide scanning has also been used in the diagnosis of aortic graft infections. Scintigraphy with indium111 oxine-labeled autologous white cells is the most common technique currently used although white cells labeled with gallium-67, technetium, and other isotopes

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Chapter 62 Management of Infected Aortic Grafts TABLE 62.1 Treatment of aortic graft infections, using pooled data from major series reported since 1985

Extra-anatomic bypass In situ superficial femoral–popliteal vein replacement In situ allograft replacement In situ prosthetic replacement

Mortality (%) (Range)

Major Amputation (%) (Range) 12.1 (0–15.6) 6.1 (4.9–10.0)

Aortic Disruption (%)

Reinfection (%)

Five-Year Primary Patency (%)

8.4 0

12.0 1.5

60.3 (30–80) 84

6.5

?

15.5

?

References

Patients (n)

18–32 34,35,46

582 66

20.3 (5.0–40.6) 10.6 (6.7–20.0)

36–41

290

24.2 (8.3–36.4)

1.3 (0–3.0)

6.9

42–46

102

11.8 (4.0–21.7)

0

0

have been reported (15,16). In addition, scintigraphy based on labeling of human IgG has been used and may be more sensitive than white cell scans (17). A problem with all scintigraphic methods of diagnosing aortic graft infections is a lack of specificity due to uptake in other organs or tissues that may be contiguous. In addition, faint or no uptake may occur in the presence of limited and lowvirulence infections, giving rise to false-negative tests. Scintigraphy is most helpful in circumstances where occult aortic graft is suspected. An example would be a patient with an aortic graft who presents with a fever of unknown origin or other nonspecific symptom complex and has a positive isotope-tagged white scan that “lights up” the graft. Arteriography has limited usefulness in the diagnosis of an aortic graft infection but, on occasion, may demonstrate an aortic false aneurysm or even active leakage of contrast into bowel lumen, a pathognomonic sign of aortoenteric fistula. Aortography is helpful in planning reconstruction after removal of the infected graft and is most useful in late infections in which the vascular anatomy may have been altered by progressive occlusive disease. In patients presenting with gastrointestinal bleeding and suspected aortoenteric fistula, complete upper endoscopy with visualization of the third and fourth portions of the duodenum, the most common site of fistula, is necessary. If this study is incomplete, with inability to visualize the distal duodenum, or if gastrointestinal lesions are found that are not actively bleeding, such as chronic peptic ulcer, an aortoenteric fistula may still be present. Continued, unexplained bleeding mandates operative exploration to rule out aortoenteric fistula. At the time of operation, the duodenum, proximal jejunum, and any other bowel in contact with the aortic graft or its limbs must be dissected free in order to make or exclude this diagnosis.

Treatment The primary goals of treatment are to save life and limb, and these are best accomplished by eradicating infection

and maintaining adequate circulation to portions of the body perfused by the infected aortic graft. Secondary goals include minimizing morbidity, restoration of normal function, and maintenance of long-term function without the need for reintervention and risk of amputation. These goals are best achieved by removal of all infected graft material and vascular tissues combined with appropriate arterial reconstruction. The currently favored methods of arterial reconstruction for aortic graft infection include extra-anatomic bypass (18–32) and in situ replacement using autogenous superficial femoral popliteal veins (33–35), arterial allografts (36–41), and vascular prostheses often treated or soaked in antibiotic solutions (42–46). Pooled outcome data from contemporary series reported since 1985 are presented in Table 62.1. Direct comparisons in attempting to adjudicate the relative success of these approaches is difficult from these data because of the heterogeneity of patients with varying severity of illness and comorbidities among reported series. All of these approaches are valid and have utility depending upon patient-specific characteristics and circumstances. It is a mistake to think that a single surgical approach is applicable to all patients with this condition. These complicated patients with varying levels of illness severity require individualized attention.

Extra-anatomic Bypass Extra-anatomic bypass usually involving axillofemoral bypass is an excellent choice for infected aortoiliac reconstructions in which femoral sites are free of sepsis and the arterial runoff is good. It is also possibly less of a physiologic insult in comparison to other procedures, particularly when the operations can be staged with extraanatomic bypass preceding removal of the infected aortic prosthesis by a period of days (19). This approach has the advantage of preserving lower extremity blood flow during removal of the aortic prosthesis, thus minimizing lower extremity ischemic time. Unfortunately, extra-anatomic bypasses have limited durability in patients with multilevel occlusive disease and

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poor runoff. Most patients with infected aortic grafts have aortobifemoral bypasses and extra-anatomic bypass in such patients usually requires bilateral axillofemoral procedures with distal anastomoses to diseased and small profunda femoral or popliteal arteries. These are disadvantaged reconstructions with poor long-term patency despite antithrombotic agents. They are prone to sudden thrombotic occlusion without warning and amputation rates are high even with thrombectomy and multiple revisions. In one large series, one-third of patients required major amputation during long-term follow-up (20). In addition, reinfection of extra-anatomic bypass grafts occurs in 10% to 20% of patients and this condition is often lethal. A final problem with extra-anatomic bypass is continuing infection at the site of aortic closure or the aortic “stump.” Although an infrequent occurrence (less than 10%), aortic stump blowout is almost always fatal.

veins will also give information that may be useful if concomitant infrainguinal reconstruction or visceral/ renal reconstruction is required. Removal of an infected aortic graft in performance of a NAIS requires multiple large incisions in the abdomen and lower extremities. This extensive, lengthy exposure in a cool room results in rapid core temperature loss, potentiating coagulopathy, blood loss, metabolic acidosis, cardiac arrhythmias, and immune system depression. A concerted effort should be made to maintain the patient’s core temperature above 36 ºC. In addition to giving all fluids through blood warmers and using upper body heatedair warming blankets, the room temperature should be kept warm. In order to minimize body exposure and lower extremity ischemia, the operation is sequenced as follows:

In Situ Replacement with Superficial Femoropopliteal Veins

2. 3. 4. 5.

Dissatisfaction with the long-term patency of extraanatomic bypass led to the development of in situ autogenous vein reconstruction (33–35). Early experiences were with greater saphenous veins but rapidly evolved to the use of superficial femoropopliteal veins because of the large caliber and superior patency (33). This procedure has been referred to as creation of a “neo-aortoiliac” system or NAIS procedure. This reconstruction is most applicable in patients with extensive occlusive disease and poor runoff, a circumstance where an autogenous venous reconstruction would have better patency than a prosthetic graft bypass. The situation is analogous to the superior patency of vein grafts compared with prosthetic conduits in the performance of femoropopliteal and distal bypasses. This advantage has been realized in excellent 5-year cumulative patency rates for NAIS reconstructions of 85% for primary patency and 100% for secondary/ assisted patency (35). Long-term amputation rates have been reported to be correspondingly low. Technical Details of the NAIS Procedure Essential preoperative planning involves duplex imaging of the lower extremity deep and superficial veins. Duplex vein mapping allows preoperative determination of diameter and length of available superficial femoropopliteal veins. Findings that may mitigate against a NAIS reconstruction are deep venous thrombosis in the superficial femoropopliteal veins, recanalization changes, and congenital absence or unusually small superficial femoropopliteal veins. Fortunately, these findings are usually limited to one side. In situations where the superficial femoropopliteal vein is incomplete, absent, or unusually small (<4–5 mm in diameter), a dominant profunda femoral vein is often present. This large vein courses posteriorly through the thigh to connect with the popliteal vein and can be used as a venous autograft for the NAIS procedure. Duplex vein mapping of the greater saphenous

1.

dissect superficial femoropopliteal veins and leave in situ until needed; isolate femoral vessels; enter abdomen and obtain aortic control; remove infected graft; and perform reconstruction with superficial femoropopliteal veins.

In the initial phases of the operation, it is useful to use two surgical teams to dissect the veins and isolate the femoral vessels. Positioning of the lower limbs requires external rotation at the hips and flexion at the knees. This “frog-leg” position is facilitated by placing supports under both thighs. Bilateral superficial femoropopliteal vein harvest is required in most cases and incisions are made over the lateral border of the sartorius muscles in both thighs. In addition to allowing direct access to the contents of Hunter’s canal, the lateral orientation of the incision isolates the harvest wounds from medially located, infected femoral wounds. This approach also allows direct access to the common femoral, the profunda femoris, and the superficial femoral arteries. The sartorius muscle is reflected medially and posteriorly, allowing preservation of its medial, segmental blood supply. The subsartorial canal is initially opened in the midthigh. The superficial femoral artery is easily identified by gentle palpation and serves as a useful landmark. The superficial femoral artery is exposed along its anterior surface and the superficial femoral vein is readily identified posterior and slightly medial to the artery. The saphenous nerve is intimately involved with the artery and vein and care must be taken during the dissection to prevent injury; excessive traction or unplanned division can result in annoying postoperative medial leg neuralgia. Care must be taken when mobilizing the branches of the superficial femoral artery, especially around the adductor hiatus. These branches may represent important collaterals to distal arterial beds. Interruption of these when the superficial femoral artery is occluded may result in critical and unanticipated distal ischemia after completion of the proximal reconstruction.

Chapter 62 Management of Infected Aortic Grafts

The superficial femoropopliteal vein has multiple large and small side-branches. The larger ones are doubly ligated with 2–0 and 3–0 silk. The importance of secure branch ligature cannot be overemphasized. A “popped” tie can result in exsanguinating hemorrhage in the postoperative period. The walls of the superficial femoropopliteal vein tend to be thin and tenuous near the origin of side-branches. Torn branches can be frustrating to repair and require tedious closure with 7–0 polypropylene sutures. It is best to avoid this with careful and patient dissection of all branches. In addition, placement of branch ligatures should be close and contiguous to the vein wall. This is different from dissection of the greater saphenous vein, where emphasis is placed on securing ligatures slightly away from the vein wall so as not to constrict the vein. The superficial femoropopliteal vein is large and can easily tolerate close ligatures that are helpful in preventing tears from the thin wall near the branch origins. Dissection is carried proximally where the superficial femoral vein joins the profunda femoral vein to form the common femoral vein. The profunda femoral vein is readily identified as a large-caliber vessel penetrating deep through the fascia on the floor of Hunter’s canal. The dissection is then carried distally with division of the adductor tendons to open the adductor hiatus. This allows easy access to the popliteal vein. One must be careful during this portion of the dissection because many large branches of the popliteal vein are found in the proximal popliteal segment, often within the adductor canal. The distal dissection is carried to the level of the knee in most circumstances. If necessary, one can continue the dissection below the knee for an additional few centimeters of conduit. After complete mobilization of the superficial femoropopliteal veins, the veins are left in situ until the required length of conduit can be determined. Next, the femoral vessels and the distal limbs of the aortobifemoral bypass are isolated. In most patients, this can be accomplished by extending the vein harvest incision along the lateral border of the sartorius muscle to its attachment site at the anterior superior iliac spine. In thin patients, the entire common femoral artery can be exposed by reflecting the sartorius medially. On occasion, dissection medial to the sartorius is helpful to complete this exposure. This approach obviates the need to dissect through the old femoral incisions. In addition to controlling the distal limbs of the infected aortobifemoral bypass, complete vascular control is obtained by isolating the proximal superficial femoral, the profunda femoris, and common femoral arteries. The abdomen is then entered either through the old incision or through a left flank retroperitoneal approach. The later is particularly helpful in avoiding tedious adhesions and facilitates obtaining aortic control. The aorta is dissected above the site of the proximal anastomosis and, if this is close to the renal arteries, supraceliac or suprarenal control is appropriate.

757

The patient is then heparinized and cross-clamps are placed on the proximal aorta and the distal limbs of the aortic graft. The intra-abdominal portion of the graft is exposed and removed. It is important to carefully remove all infected graft material and sutures and perform debridement of grossly infected aorta and surrounding tissues. If the aortic anastomosis is end-to-side, balloon occlusion facilitates control of the distal aorta. The body of the graft is removed and the femoral limbs are left in place while the proximal anastomosis to the superficial femoropopliteal vein is performed. Leaving the femoral limbs in place during this period cuts down on blood loss that typically occurs when the femoral limbs are extracted from their tunnels. Prior to cross-clamping the aorta, vein grafts are removed and prepared. The lengths of superficial femoropopliteal vein required are determined by measuring the distance from the proximal anastomosis to the femoral levels on both sides. The proximal superficial femoropopliteal vein is divided flush with the profunda femoral vein and oversewn with 5–0 polypropylene continuous sutures. This allows unimpeded flow from the profunda femoral vein to the common femoral vein and minimizes the possibility of thrombus forming in a residual venous cul-de-sac of the superficial femoral vein. Vein grafts are distended with a solution consisting of Ringer’s lactate (1 l), heparin (5000 units), albumin (25 g), and papaverine (60 mg) kept at 4 ºC. Leaks are carefully sutured and adventitial bands that distort the contour of the vein graft are lysed. The three or four large valves of the superficial femoropopliteal vein are easily identified and ablated using a valvulotome or directly excised by temporarily everting the vein graft. The nonreversed configuration will allow placement of the larger end of the vein at the proximal aortic anastomosis. Vein grafts are kept in cold solution until required for reconstruction. Several configurations using superficial femoropopliteal vein grafts are possible and allow flexibility in performing the NAIS reconstruction (Fig. 62.1). The proximal end of the superficial femoral vein is frequently ≥1.5 cm in diameter and can easily be anastomosed to a normal aorta. Standard, continuous polypropylene (4–0) suture technique is used, taking care to make slightly more advancement on the aorta than the venous autograft because of the greater circumference of the aorta (Fig. 62.2A). End-to-side anastomoses are also feasible with these large vein grafts. In using endto-end anastomoses, larger aortas and greater size mismatches are sometimes encountered and require different anastomotic techniques. Plication of the distal aorta may be performed to reduce the diameter of the aorta at the anastomosis (Fig. 62.2B). If both superficial femoropopliteal vein grafts will reach to the femoral levels, a “pantaloon” vein graft configuration can be used (Fig. 62.2C). This configuration essentially doubles the circumference of the vein graft proximal anastomosis. Use of this configuration has eliminated the problem of size mismatch at the proximal anastomosis.

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Part VII Aortic and Peripheral Aneurysms

A

B

D

C

E

FIGURE 62.1 Use of the superficial femoropopliteal vein in multiple reconstructions after removal of an infected vascular prosthesis. (A) Standard aortobifemoral replacement in situ. (B) Left aortofemoral bypass in situ with leftto-right femoral crossover bypass. (C) Aortoiliac reconstruction in situ. (D) Unilateral transobturator aorta profunda bypass. (E) Femoral crossover bypass. (Reproduced with permission from Clagett GP. Vascular infections. In Greenfield, Lillemoe, et al., eds. Surgery: Scientific Principles and Practice, 3rd edn. Philadelphia, PA: Lippincott, Williams & Wilkins, 2001;1646–1658.)

FIGURE 62.2 Three anastomotic techniques to accommodate size discrepancy between the aorta and the superficial femoral–popliteal vein graft. (A) Anastomosis is performed in the majority of cases. When the size mismatch precludes comfortable end-to-end anastomosis, (B) plication of the anterior aorta can be helpful. (C) Another technique to accommodate a large aorta is to join both vein grafts together. This effectively doubles the circumference of the vein graft and is useful when there is a very large size mismatch. (Reproduced with permission

A

B

After construction of the proximal anastomosis, the superficial femoropopliteal vein graft is distended under aortic pressure. This allows careful scrutiny of the vein graft side branches prior to tunneling. Proximal suture line bleeding should be repaired and the aorta clamped to prevent tearing of the vein graft during suture placement. If iliac anastomoses are required, these are performed in a standard manner. Aortobifemoral bypass limbs are carefully removed at this point in the operation and the tunnels mechanically debrided by irrigation and passage of an open, dry gauze sponge through them. Most often, superficial femoropopliteal vein grafts are placed in the old tunnels because it is difficult to fashion new tunnels through the scarred retroperitoneum. The superficial femoropopliteal vein grafts are often larger than the tun-

C

from Clagett GP. Treatment of aortic graft infection. In Ernst C, Stanley J, eds. Current Therapy in Vascular Surgery, 4th edn. St Louis: Mosby, 2001;422–428.)

nels and, when this occurs, careful proximal and distal finger dilation can be useful to prevent vein graft luminal compromise. Care must be taken when pulling vein grafts through the tunnels as side-branch ligatures may be dislodged. To avoid this problem, vein grafts are passed nondistended. Distal femoral anastomoses are performed using standard techniques. Once again, removal of all prosthetic material and debridement of infected vascular and surrounding tissues are important. Occasionally, adjunctive profundaplasties or profunda reimplantation is required following extensive debridement of the common femoral artery and the femoral bifurcation. Care should be made to ensure some perfusion to the pelvis provided in the form of retrograde blood flow to prevent pelvic, visceral,

Chapter 62 Management of Infected Aortic Grafts

or spinal nerve root ischemia. Assessment of distal limb and foot perfusion prior to closure of wounds is important. As previously mentioned, when the superficial femoral arteries are occluded, inadvertent interruption of collaterals from the profunda femoral artery to the distal superficial femoral or popliteal arteries occurring during dissection of the superficial femoropopliteal veins can lead to leg ischemia despite excellent inflow. In addition, acute venous hypertension in the leg with prolonged limb ischemia during aortic reconstruction may cause compartment syndromes. Following operation, antibiotic coverage is continued for 5 to 7 days. Antibiotics are modified as intraoperative culture results isolate organisms sensitive to specific antibiotics. In patients who are severely immunocompromised, prolonged antibiotic therapy for 4 to 6 weeks may rarely be necessary. Intermittent pneumatic compression plus low-dose subcutaneous heparin (5000 units every 8 to 12 hours) are used for prophylaxis of venous thromboembolism. Most patients develop venous thrombosis in the residual popliteal vein segment. Aggressive prophylaxis may prevent propagation into calf veins. Full anticoagulation for this limited venous thrombosis is usually unnecessary since proximal extension and pulmonary embolism are unlikely because of the absence of the superficial femoropopliteal vein. Patients are seen every 3 months as outpatients for the first year following operation. Noninvasive vascular testing includes ankle/brachial pressure indices, and complete aortoiliac femoral graft duplex examination. Surveillance is directed at detecting vein graft and anastomotic stenoses and progression of distal disease. The principal disadvantage of the NAIS reconstruction is that it is technically demanding and a long procedure. The mean operative time is approximately 8 hours. The lower extremity ischemic time is longer than with other approaches but can be minimized using a two-team approach and carefully sequencing the procedure to shorten aortic cross-clamp time. Acute venous hypertension following harvest of the superficial femoropopliteal vein can contribute to the development of lower extremity compartment syndromes. Leg fasciotomy is required in approximately 25% of patients. Preexisting, advanced lower extremity ischemia, prolonged aortic cross-clamp times, and absence of the ipsilateral greater saphenous vein are risk factors for the development of a compartment syndrome. Prophylactic four-compartment fasciotomy should be considered when these risk factors are present. Long-term lower extremity venous morbidity is also a potential drawback to harvesting the superficial femoropopliteal veins. However, venous morbidity has been surprisingly infrequent and mild (34,35). Approximately 30% of patients will have some lower extremity swelling that requires compression stockings. This usually resolves within a period of weeks to months after operation and compression stockings are no longer necessary. The benign course following removal of the superficial

759

femoropopliteal vein is due to several compensating mechanisms (47). First, the junction of the profunda femoris and common femoral veins is carefully preserved after disconnecting the proximal superficial femoral vein, thus allowing unimpeded drainage via the profunda system. Second, there are several anatomic collateral connections between the remaining distal popliteal vein and the profunda system and many of these collaterals enlarge to accommodate the increase in volume flow following removal of the superficial femoropopliteal vein. Finally, the valves in the tibial veins and collateral circuits remain functional such that distal venous reflux does not occur. A final concern is that placing superficial femoropopliteal veins in an infected field might lead to reinfection and disruption. Experience with this approach has documented that these vein grafts resist gram-positive, gram-negative, and fungal infections and disruption of anastomoses has been rare. Long-term aneurysmal degeneration has been studied up to 10 years after placement of these vein grafts and has not occurred.

In Situ Replacement with Allograft and Antibiotic-treated Prosthetics Grafts In situ allograft replacement has been reported with varying degrees of success (36–41). Acute and delayed aortic allograft disruption has been reported and is a distinct limitation of using allografts in infected fields (38,41,48). In addition, long-term deterioration leading to thrombosis and aneurysmal degeneration have been reported. Ready availability of allograft material is another limitation of this approach in situations where emergency or urgent operations are often required. Replacement of the infected aortic graft with a new prosthesis has also been reported (40–46). Most often, the new aortic graft is soaked in an antibiotic solution prior to implantation. It is recommended that a gelatin-sealed polyester graft be soaked in a rifampin solution of 60 mg/mL for this purpose (46). This approach is most often successful with limited infections of low virulence following aggressive debridement of all infected vascular and surrounding tissues to create a clean field. Despite this, the potential for reinfection is a serious drawback (28) and patients treated in this manner require close and vigilant follow-up with frequent imaging studies such as CT scanning or MRI. They are also usually treated with lifelong oral antibiotics. In situ prosthetic and allograft reconstructions may have their greatest utility in very ill and unstable patients and also those with actively bleeding aortoenteric fistulas. Expeditious in situ replacement in these circumstances may be lifesaving. Under these circumstances, the procedure may be used as a “bridge” procedure with definitive reconstruction (extra-anatomic or NAIS) carried out at a later date when the patient has been rendered fit for such a reconstruction.

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Alternative Approaches to Removing the Entire Aortic Graft Conservative approaches that do not involve removal of the infected aortic graft have also been reported (49–52). These are based upon: aggressive drainage and debridement of infected tissues; intensive, culture-specific antibiotic therapy; meticulous wound care to achieve coverage of exposed prosthetic material; and coverage of exposed prosthetic material with muscle flaps. The most appropriate use of these conservative approaches is when infection is extracavitary and limited in extent, systemic signs of sepsis are absent, the infecting organisms are of low virulence, and anastomotic sites are uninvolved (52). As with in situ prosthetic replacement, these patients need close follow-up and indefinite oral antibiotic treatment. A conservative approach may be the only option in some frail and desperately ill patients who could not tolerate aortic graft removal. With infections that involve only one limb of an aortobifemoral bypass graft, resection of the limb is usually performed (53–57). Revascularization is often carried out via obturator bypass or other reconstructions performed in clean fields. Autogenous superficial femoropopliteal or greater saphenous vein have also been used for this purpose (57). It is important that the extent of infection is assessed with imaging studies as well as direct visual inspection. In the case of unilateral femoral infection of an aortofemoral bypass, the general approach is to begin the operation by inspection of the intra-abdominal portion of the prosthesis. If the infection grossly involves the main body of the bifurcated prosthesis, complete removal is necessary. If the suspected limb is well incorporated and free of gross infection, division of the limb, closure of the tunnel, and obturator or other extra-anatomic bypass is performed. The final portion of this operation is to remove the infected limb from below, taking care to prevent cross-contamination of other freshly placed incisions that have been closed.

Conclusion There are multiple operative management strategies that are appropriate for the treatment of infected aortic grafts. All have advantages and disadvantages that must be taken into account in dealing with individual patients. Extraanatomic bypass is a relatively straightforward procedure, can be staged, and may be physiologically less stressful than others. However, thrombectomy and revision are often required and long-term patency is only fair. The long-term amputation rates are high and anticoagulation is often used to maintain patency. In addition, reinfection of the prosthetic extra-anatomic bypass and aortic stump blowout are of concern. In situ replacement with superficial femoropopliteal vein grafts provides the best long-term patency and durability. Amputation rates are low and indefinite antithrombotic and antibiotic thera-

pies are unnecessary. However, the procedure is long, complex, and can be associated with long lower-extremity ischemia times. Leg fasciotomy is also necessary in about one-quarter of patients. In situ allograft replacement is expeditious but reinfection, allograft aneurysmal and occlusive deterioration, and limited availability make this option less attractive. In situ prosthetic replacement is also expeditious but its use is limited to low-grade, nonvirulent infections involving only part of the prosthesis. In addition, indefinite antibiotic therapy is usually required and the potential for reinfection is always present. All of these management options are appropriate in specific circumstances and judicious use of them will lead to improved outcomes.

References 1. Balas P. An overview of aortofemoral graft infection. Eur J Vasc Endovasc Surg 1997; 14 (Supplement A):3–4. 2. Kearney RA, Eisen HJ, Wolf JE. Nonvalvular infections of the cardiovascular system. Ann Intern Med 1994; 121:219–230. 3. O’Brien T, Collin J. Prosthetic vascular graft infection. Br J Surg 1992; 79:1262–1267. 4. Kaiser AB, Clayson KR, et al. Antibiotic prophylaxis in vascular surgery. Ann Surg 1978; 188:283–288. 5. Pitt HA, Postier RG, et al. Prophylactic antibiotics in vascular surgery: topical, systemic, or both? Ann Surg 1980; 192:356–364. 6. Hasselgren P, Ivarsson L, et al. Effects of prophylactic antibiotics in vascular surgery: a prospective, randomized, double-blind study. Ann Surg 1984; 200:86–92. 7. Hall JC, Christiansen KJ, et al. Duration of antimicrobial prophylaxis in vascular surgery. Am J Surg 1998; 175:87–90. 8. Kurz A, Sessler DL, Lenhardt R, Study of Wound Infection and Temperature Group. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. N Engl J Med 1996; 334:1209–1215. 9. Naylor AR, Hayes PD, Darke S on behalf of the Joint Vascular Research Group. A prospective audit of complex wound and graft infections in Great Britain and Ireland: the emergence of MRSA. Eur J Vasc Endovasc Surg 2001; 21:289–294. 10. Nasim A, Thompson MM, et al. The impact of MRSA on vascular surgery. Eur J Vasc Endovasc Surg 2001; 22:211–214. 11. Modrall JG, Clagett GP. The role of imaging techniques in evaluating possible graft infections. Sem Vasc Surg 1999; 12:339–347. 12. Low RN, Wall SD, et al. Aortoenteric fistula and perigraft infection: evaluation with CT. Radiology 1990; 175:157–162. 13. Qvafordt PG, Reilly LM, et al. Computerized tomographic assessment of graft incorporation after reconstruction. Am J Surg 1985; 150:227–231. 14. Auffermann W, Olofsson PA, et al. Incorporation versus infection of retroperitoneal aortic grafts: MR imaging features. Radiology 1989; 172:359–362.

Chapter 62 Management of Infected Aortic Grafts 15. Brunner MC, Mitchell RS, et al. Prosthetic graft infection: limitations of indium white blood cell scanning. J Vasc Surg 1986; 3:42–48. 16. Fiorani P, Speziale F, et al. Detection of aortic graft infection with leukocytes labeled with technetium 99mhexametazime. J Vasc Surg 1993; 17:87–96. 17. LaMuraglia GM, Fischman AJ, et al. Utility of the indium 111-labeled human immunoglobulin G scan for the detection of focal vascular graft infection. J Vasc Surg 1989; 10:20–28. 18. O’Hara PJ, Hertzer NR, et al. Surgical management of infected abdominal aortic grafts: review of a 25-year experience. J Vasc Surg 1986; 2:725–731. 19. Reilly LM, Stoney RJ, et al. Improved management of aortic graft infection: the influence of operation sequence and staging. J Vasc Surg 1987; 5:421–431. 20. Quinones-Baldrich WJ, Hernandez JJ, Moore WS. Longterm results following surgical management of aortic graft infection. Arch Surg 1991; 126:507–511. 21. Ricotta JJ, Faggioli GL, et al. Total excision and extraanatomic bypass for aortic graft infection. Amer J Surg 1991; 162:145–149. 22. Leather RP, Darling III RC, et al. Retroperitoneal in-line aortic bypass for treatment of infected infrarenal aortic grafts. Surg Gynecol Obstet 1992; 175:491–494. 23. Olah A, Vogt M, et al. Axillo-femoral bypass and simultaneous removal of the aorto-femoral vascular infection site: is the procedure safe? Eur J Vasc Surg 1992; 6: 252–254. 24. Bacourt F, Koskas F, and the French University Association for Research in Surgery. Axillobifemoral bypass and aortic exclusion for vascular septic lesions: a multicenter retrospective study of 98 cases. Ann Vasc Surg 1992; 6: 119–126. 25. Lehnert T, Gruber HP, et al. Management of primary aortic graft infection by extra-anatomic bypass reconstruction. Eur J Vasc Surg 1993; 7:701–707 . 26. Sharp WJ, Hoballah JJ, et al. The management of the infected aortic prosthesis: a current decade of experience. J Vasc Surg 1994; 19:844–850. 27. Kuestner LM, Reilly LM, et al. Secondary aortoenteric fistula: contemporary outcome with use of extraanatomic bypass and infected graft excision. J Vasc Surg 1995; 21:184–196. 28. Hannon RJ, Wolfe JHN, Mansfield AO. Aortic prosthetic infection: 50 patients treated by radical or local surgery. Br J Surg 1996; 83:654–658. 29. Schmitt DD, Seabrook GR, et al. Graft excision and extra-anatomic revascularization: the treatment of choice for the septic aortic prosthesis. J Cardiovasc Surg 1990; 31:327–332. 30. Bunt TJ. Vascular graft infections: a personal experience. Cardiovasc Surg 1993; 1:489–492. 31. Yeager RA, Taylor LM, et al. Improved results with conventional management of infrarenal aortic infection. J Vasc Surg 1999; 30:76–83. 32. Seeger JM, Pretus HA, et al. Long-term outcome after treatment of aortic graft infection with staged extraanatomic bypass grafting and aortic graft removal. J Vasc Surg 2000; 32:451–461. 33. Clagett GP, Bowers BL, et al. Creation of a neo-aortoiliac system from lower extremity deep and superficial veins. Ann Surg 1993; 218:239–249.

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34. Nevelsteen A, Lacroix H, Suy R. Autogenous reconstruction with the lower extremity deep veins: an alternative treatment of prosthetic infection after reconstructive surgery for aortoiliac disease. J Vasc Surg 1995; 22: 129–134. 35. Clagett GP, Valentine RJ, Hagino RT. Autogenous aortoiliac/femoral reconstruction from superficial femoral–popliteal veins: feasibility and durability. J Vasc Surg 1997; 25:255–270. 36. Kieffer E, Bahnini A, et al. In situ allograft replacement of infected infrarenal aortic prosthetic grafts: results in forty-three patients. J Vasc Surg 1993; 17:349–356. 37. Vogt PR, Pfammatter T, et al. In situ repair of aortobronchial, aortoesophageal, and aortoenteric fistulae with cryopreserved aortic homografts. J Vasc Surg 1997; 26:11–17. 38. Ruotolo C, Plissonnier D, et al. In situ arterial allografts: a new treatment for aortic prosthetic infection. Eur J Vasc Endovasc Surg 1997; 14 (Supp A):102–107. 39. Nevelsteen A, Feryn T, et al. Experience with cryopreserved arterial allografts in the treatment of prosthetic graft infections. Cardiovasc Surg 1998; 4:378–383. 40. Chiesa R, Astore S, et al. Fresh and cryopreserved arterial homografts in the treatment of prosthetic graft infections: experience of the Italian Collaborative Vascular Homograft Group. Ann Vasc Surg 1998; 12:457–462. 41. Verhelst R, Lacroix V, et al. Use of cryopreserved arterial homografts for management of infected prosthetic grafts: a multicentric study. Ann Vasc Surg 2000; 14:602–607. 42. Walker WE, Cooley DA, et al. The management of aortoduodenal fistula by in situ replacement of the infected abdominal aortic graft. Ann Surg 1987; 205: 727–732. 43. Speziale F, Rizzo L, et al. Bacterial and clinical criteria relating to the outcome of patients undergoing in situ replacement of infected abdominal aortic grafts. Eur J Vasc Endovasc Surg 1997; 13:127–133. 44. Hayes PD, Nasim A, et al. In situ replacement of infected aortic grafts with rifampicin-bonded prostheses: the Leicester experience (1992 to 1998). J Vasc Surg 1999; 30:92–98. 45. Young RM, Cherry KJ Jr., et al. The results of in situ prosthetic replacement for infected aortic grafts. Am J Surg 1999; 178:136–140. 46. Bandyk DF, Novotney ML, et al. Expanded application of in situ replacement for prosthetic graft infection. J Vasc Surg 2001; 34:411–420. 47. Wells JK, Hagino RT, et al. Venous morbidity after superficial femoral–popliteal vein harvest. J Vasc Surg 1999; 29:282–291. 48. Koskas F, Plissonnier D, et al. In situ arterial allografting for aortoiliac graft infection: a 6-year experience. Cardiovasc Surg 1996; 4:495–499. 49. Calligaro KD, Veith FJ, et al. Selective preservation of infected prosthetic arterial grafts. Analysis of a 20-year experience with 120 extracavitary-infected grafts. Ann Surg 1994; 220:461–471. 50. Morris GE, Friend PJ, et al. Antibiotic irrigation and conservative surgery for major aortic graft infection. J Vasc Surg 1994; 20:88–95. 51. Belair M, Soulez G, et al. Aortic graft infection: the value of percutaneous drainage. Amer J Radiology 1998; 171: 119–124.

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52. Calligaro KD, Veith FJ. Graft preserving methods for managing aortofemoral prosthetic graft infection. Eur J Vasc Endovasc Surg 1997; 14 (Supp A):38–42. 53. Bandyk DF, Bergamini TM, et al. In situ replacement of vascular prostheses infected by bacterial biofilms. J Vasc Surg 1991; 13:575–583. 54. Becquemin JP, Qvarfordt P, et al. Aortic graft infection: is there a place for partial graft removal? Eur J Vasc Endovasc Surg 1997; 14 (Supp A):53–58. 55. Miller JH. Partial replacement of an infected arterial

graft by a new prosthetic polytetrafluoroethylene segment: a new therapeutic option. J Vasc Surg 1993; 17: 546–558. 56. Towne JB, Seabrook GR, et al. In situ replacement of arterial prosthesis infected by bacterial biofilms: longterm follow-up. J Vasc Surg 1994; 19:226–235. 57. Sladen JG, Chen JC, Reid JDS. An aggressive local approach to vascular graft infection. Am J Surg 1998; 176:222–225.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 63 Isolated Iliac Artery Aneurysms Henry Haimovici

The majority of iliac aneurysms are associated with those of the abdominal aorta and, therefore, are not included in this chapter (see Chapter 59). Only isolated iliac aneurysms are considered here (1–5).

Incidence An isolated iliac aneurysm is a rare vascular entity. In one of the earliest comprehensive reports, published in 1961, Markowitz and Norman dealt with 30 patients from the Columbia Presbyterian Medical Center (3). They included the common, external, and internal iliac arteries as a group. The true incidence of isolated iliac aneurysm is quite small and has been considered 1.5% of that of an abdominal aortic aneurysm. In 1978, Lowry and Kraft published eight cases encountered in a 10-year period and reviewed 36 cases from the literature (2). The natural course of an isolated iliac aneurysm is toward progressive enlargement and rupture, often without much in the way of warning symptoms, with incidence of rupture ranging from 18% reported by Markowitz and Norman to 50% reported by Lowry and Kraft. Diagnosis of an isolated artery aneurysm is rendered extremely difficult because of its insidious onset and its often deep pelvic location. As these aneurysms enlarge, especially those of the hypogastric artery, they produce symptoms of compression on the intrapelvic structures, notably the lumbosacral plexus, urinary bladder, or bowel. If the significance of these symptoms is realized, the diagnosis can often be made by careful pelvic examination through

the rectum or vagina. Iliac aneurysms may rupture into the retroperitoneal space of the pelvis or, more rarely, into the rectum or sigmoid colon (Fig. 63.1). Symptoms preceding or appearing after rupture consist of abdominal and back pain in the majority of patients. Pain follows the sciatic distribution and is accompanied by straight-leg raising weakness, reflex changes, and sensory impairment. When the symptoms appear abruptly, the clinical features closely resemble the sciatica of a ruptured intervertebral disc (6). Rectal examination discloses pelvic pulsation, and x-ray films often confirm a calcific rim in the wall of the aneurysm. Most, if not all, patients are men who have associated cardiovascular and hypertensive disease. The average diameter of iliac aneurysms ranges from 7.5 to 8.5 cm. Approximately 50% of those isolated iliac aneurysms previously reported were located in the common iliac artery, with the remainder involving the internal iliac artery (2,3).

Surgical Management Surgical management of iliac aneurysms is based on general principles of adequate exposure, isolation of the artery, excision, and interposition of a graft. Any one of several surgical techniques may be applied, depending on the size of the aneurysm and its relation to the adjacent vein and the abdominal aorta: 1.

total excision of the aneurysm;

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completely from it or may be handled by opening the aneurysm, evacuating the thrombi, and controlling the bleeding from inside the sac by suture ligatures of the ostia of the collaterals (Fig. 63.2). In the first instance, a 10-mm woven or knitted Dacron graft is inserted end-to-end between the two transected ends of the common iliac and its bifurcation (Fig. 63.2A). In the second instance, the implantation of the graft is carried out by the intrasaccular method (Fig. 63.2C). If the proximal and distal ends of the aneurysm are not transected completely, the posterior row of the anastomosis is sutured through the undivided posterior wall in a fashion similar to that indicated for an abdominal aortic aneurysm (see Chapter 59). The most serious complication to avoid in mobilizing the iliac aneurysm is injury to the adjacent iliac vein or origin of the inferior vena cava and to the ureter.

Aneurysm of External Iliac Artery FIGURE 63.1 Aortogram depicting bilateral iliac aneurysms.

2. 3.

partial excision of the sac; and bypass graft combined with exclusion of the aneurysm.

For a small isolated lesion of either the common or external iliac artery, an extraperitoneal approach is desirable and may often be adequate. However, should there be any evidence of aortic or large pelvic mass, a transperitoneal approach is indicated. Mortality after elective surgery for iliac artery aneurysm is less than 10%, in contrast to the operative mortality of 52% for ruptured cases (2). Awareness of iliac aneurysms and their usual propensity to enlarge and rupture is the best approach to early diagnosis and prevention of the high mortality. B-mode ultrasonography and pelvic examination should be helpful in confirming their diagnosis. Elective repair should be carried out without delay.

Aneurysm of Common Iliac Artery Through a transperitoneal exposure using a medial xiphopubic laparotomy, the distal portion of the abdominal aorta below the inferior mesenteric artery is mobilized. The posterior wall of the aorta is freed, care being taken to avoid injuring the vena cava. Next is the exposure of the iliac arteries. On the right, this is accomplished by retracting the cecum and terminal ileum and, on the left, the sigmoid colon, after which the posterior parietal peritoneum is incised along the iliac axis. Then the origins of both the external and internal iliac arteries are mobilized. Depending on the degree of its adhesion to its satellite vein, the aneurysm may be mobilized and separated

Exposure of an external iliac aneurysm by an extraperitoneal approach is adequate, easy, and safe. (For details of exposure, see Chapter 27.) The aneurysm is mobilized after gaining control of the common, internal, and distal external iliac arteries just above Poupart’s ligament. Then, depending on the degree of adhesion between the aneurysm and adjacent structures, the lesion is excised either completely or partially, and a graft is interposed by the end-to-end procedure (Fig. 63.3).

Iliofemoral Aneurysm If the external iliac aneurysm extends beyond Poupart’s ligament, a combined iliac and femoral approach through a single incision is indicated (Fig. 63.4). The ligament is divided for the exposure, mobilization, and implantation of the graft, but it is reconstructed at the end of the procedure.

Combined Common and External Iliac Aneurysms An extraperitoneal approach to a combined common and external iliac aneurysm is often feasible if the proximal segment of the common iliac artery is uninvolved. Otherwise, a transperitoneal approach is used. Control of the proximal segment of the common iliac artery, of the distal external iliac artery, and of the internal iliac artery is achieved by observing the precautions mentioned previously for the isolated segments. In the event that the aneurysm is densely adherent to the adjacent vein, an intrasaccular procedure is carried out. In the presence of a bilateral iliac involvement, a transperitoneal approach is obviously indicated, with reconstruction of at least one of the internal iliac arteries to avoid large-bowel ischemia.

Chapter 63 Isolated Iliac Artery Aneurysms

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A

A

B

B

C

C FIGURE 63.2 Iliac aneurysms and the methods for their replacement with grafts. (Al) Isolated common iliac aneurysm. (A2) Its replacement with an end-toend prosthetic graft. (BI) Aneurysm of common and external iliac arteries. (B2) Replacement with a prosthetic end-to-end graft. Note ligation of the divided internal iliac. (C1) After partial excision of the aneurysmal sac of a common and external iliac aneurysm, prosthetic graft implantation was carried out by the intrasaccular method, using an end-to-end procedure. (C2) The residual aneurysmal sac surrounding the prosthetic graft is sutured around the latter. Note ligation of the divided internal iliac.

FIGURE 63.3 (A) Position of the patient and the line of skin incision of the abdomen for an extraperitoneal approach to the iliac arteries. (B) Isolation of the proximal and distal arterial tree to the iliac aneurysm. (C) Implantation of graft after complete excision of the aneurysm.

Aneurysm of the Internal Iliac Artery The location of an internal iliac aneurysm within the pelvis often precludes an early diagnosis. As it enlarges, it produces pressure symptoms, distorting one or both ureters, the bladder, urethra, or rectum. The aneurysm may be first noted during a rectal or vaginal examination as part of an evaluation for gastrointestinal or genitourinary symptoms. Management of the unilateral nonruptured internal iliac (hypogastric) aneurysm, and especially that of

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A

bilateral lesions, should be performed through a transperitoneal approach. Clamping of the origin of the common iliac artery and the external iliac artery close to the origin of the hypogastric artery is first carried out. Dissection of the aneurysm may be extremely laborious, and an attempt at excising the whole aneurysm or dissecting all the branches in the pelvic depth may be troublesome. After gaining control of the segment of the hypogastric beyond the aneurysm, the anterior wall is excised, and control of backbleeding is achieved by suture ligation of the ostia of the branch vessels, using the obliterative aneurysmorrhaphy technique. The distal end of the aneurysm is then oversewn. In the presence of ruptured hypogastric artery aneurysm, the reported mortality rates are high, ranging from 29% to 80%. Ligation of the hypogastric artery may suffice for small aneurysms but is inadequate for aneurysms compressing adjacent viscera. Complete resection of large hypogastric aneurysms may be difficult and dangerous because of the close proximity of the ureters, bowel, and other major vessels. The best way to deal with such an aneurysm is by ligating it, removing the laminated thrombi, excising most of the aneurysmal wall, and performing an obliterative aneurysmorrhaphy.

B

References

C FIGURE 63.4 lliofemoral aneurysm. (A) Line indicating a combined abdominal and groin skin incision for exposure of the aneurysm. (B) Note mobilization of the iliofemoral aneurysm and the ends of transected Poupart’s ligament. (C) Iliofemoral graft in place above and below Poupart’s ligament.

1. Baron HC. Isolated aneurysm of internal iliac artery. NY State J Med 1979;1884. 2. Lowry SF, Kraft RO. Isolated aneurysms of the iliac artery. Arch Surg 1978;113:1289. 3. Markowitz AM, Norman JC. Aneurysms of the iliac artery. Ann Surg 1961;154:777. 4. Silver D, Anderson EF, Porter JM. Isolated hypogastric artery aneurysm. Arch Surg 1967;95:308. 5. Wirthlin LS, Warshaw AL. Ruptured aneurysms of the hypogastric artery. Surgery 1973;73:629. 6. Chapman EM, Shaw RS, Kubik CS. Sciatic pain from arteriosclerotic aneurysm of pelvic arteries. N Engl J Med 1964;271:1410.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 64 Endovascular Grafts in the Treatment of Isolated Iliac Aneurysms Frank J. Veith, Evan C. Lipsitz, Takao Ohki, William D. Suggs, Jacob Cynamon and Alla M. Rozenblit

Although iliac aneurysms commonly occur with abdominal aortic aneurysms, isolated aneurysms of the common and hypogastric arteries can also occur and cause problems for patients. However, isolated aneurysms of the iliac arteries (IAAs) are rare, accounting for 2% to 7% of aortoiliac aneurysms (1–7). These aneurysms can rupture, embolize, thrombose, or exert pressure on surrounding viscera and they can be symptomatic. Morbidity and mortality rates of emergency surgery are much higher than for elective surgery (3). However, elective open surgical repair may also be technically challenging, especially in the setting of previous abdominal or aortic surgery. Therefore, alternative treatment modalities have been developed, including ligation proximal and distal to the aneurysm, coil embolization, and the insertion of endovascular stented grafts (6–12). Our group was the first to report on the use of transluminally placed endovascular grafts to treat iliac aneurysms (10), and has described the midterm results of these endovascular grafts and subsequent aneurysm diameter changes after the procedure (12,13). The present chapter will update our results and provide an overview of the current status of endovascular grafting in the treatment of isolated aneurysms involving the common iliac and/or hypogastric arteries.

Methods for Endovascular Graft Repair Anatomic Considerations Isolated iliac aneurysms generally involve the common iliac arteries and/or the hypogastric or internal iliac arteries. Rarely is the external iliac artery involved except with false aneurysms due to trauma or infection. As shown in Figure 64.1 isolated iliac aneurysms come in a number of varieties and combinations, and for each there is an effective method of endovascular grafting which will exclude the aneurysmal arteries from the circulation. Critical factors are the presence, location, and length of proximal and distal landing zones in which the endograft may be fixed to secure a blood-tight seal. In some circumstances, a suitable proximal landing zone may exist within the proximal common iliac artery, facilitating a unilateral endograft repair (Figs. 64.1A–D, 64.2A and B, 64.3, 64.4 and 64.5). In other circumstances no such proximal iliac artery landing zone exists and the endovascular graft proximal fixation site must be placed in the infrarenal aorta (Figs. 64.1E and F). Not shown in Figure 64.1 is the circumstance in which a standard modular or unibody bifurcated aortic graft was employed and extended distally to a normal distal landing zone

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FIGURE 64.1 Techniques used for endograft repair of isolated iliac artery aneurysms. (A) Common iliac artery (CIA) with adequate proximal and distal neck for fixation; endograft placed completely within CIA. (B) CIA with adequate proximal neck only; endograft placed in proximal CIA and extended to external iliac artery (EIA) with coil embolization of internal iliac artery (IIA). (C) CIA with adequate proximal neck only; endograft placed in proximal CIA and extended to common femoral artery for sutured anastomosis. (D) IIA with normal CIA; endograft in proximal CIA to EIA and coil embolization of branches. (E) CIA with inadequate proximal neck; endograft placed in aorta with coil embolization of IIA branches, contralateral occluding covered stent and femorofemoral bypass grafts. (F) Bilateral CIA and IIA; endograft placed in aorta and distal stent in EIA, coil embolization of IIA branches, contralateral occluding covered stent, and femorofemoral bypass graft. x, Occlusion coil; o, occluding covered stent.

within the iliac system beyond the diseased segments (Fig. 64.6). The nature and location of the distal attachment site is also an important consideration in the endograft treatment of iliac aneurysms. Rarely is a satisfactory distal landing zone present entirely within the common iliac artery (Fig. 64.1A). More commonly, the endograft will have to be extended to the external iliac or common femoral artery (Fig. 64.1B and C and Figs. 64.2–64.5). When this is required, the origin of the ipsilateral hypogastric artery must be occluded. This can be accomplished by placement of coils (Fig. 64.1B and C) or, if the distal common iliac is of normal caliber, by coverage of the

hypogastric orifice by the endograft. If the graft is unsupported, a stent may be useful in the latter circumstance. However, we generally coil embolize the proximal hypogastric artery when an endograft extension to the external iliac artery is planned. When this is done unilaterally, there have been no serious consequences except for buttock claudication which persists in about 15% of patients (14). We do not recommend bilateral hypogastric occlusion unless other options are not possible or are unsafe. However, we have not noted serious consequences when bilateral hypogastric prograde flow has been interrupted in more than 30 patients in whom preservation of flow through one hypogastric artery was not possible (14). This circumstance arises with bilateral hypogastric aneurysms or when distal common iliac aneurysms combined with calcification and tortuosity of the hypogastric artery make its reimplantation risky or impossible (14). Microembolization and hypotension may have contributed to the colon ischemia and buttock necrosis noted by others when bilateral hypogastric occlusion has been performed in association with aneurysm repairs (14–18). When large hypogastric aneurysms are present, coil embolization of all the branches of the hypogastric artery is required to prevent Type II endoleaks (Figs. 64.1D and F and 64.5). This may be a technically demanding procedure because of tortuosity. It is best performed at a separate sitting several weeks before endograft placement. Coil placement within the hypogastric aneurysm sac is inadequate, and in one of our cases led to subsequent rupture (19).

Endovascular Grafts We have used two main varieties of endografts: one is surgeon-made, the other is industry-made. Because we began endovascular graft treatment of iliac aneurysms before any commercially made grafts were available, we at first used our own surgeon-made graft largely to treat patients in whom an open operation was contraindicated because of major medical or surgical comorbidities. This Montefiore endovascular grafting system (MEGS) consisted of a polytetrafluoroethylene graft (W. L. Gore and Associates, Flagstaff, AZ, and Impra, Inc., Tempe, AZ) sutured to a Palmaz balloon-expandable stent (P308, P4014 for P4010; Cordis Corporation, Warren, NJ), with 50% to 75% of the stent covered by the overlying graft. The ends of the graft material were marked with 0.010inch radiopaque gold wire for precise proximal deployment and placement of a second distal stent across the end of the graft when necessary. Alternatively the graft extended to the common femoral artery where an endovascular anastomosis was performed (Fig. 64.1E). The endograft was coaxially mounted on an appropriately sized angioplasty balloon and packaged within a 14-Fr. to 20-Fr. introducer sheath. Informed consent was obtained from the patients before all procedures. All endografts were used under an investigator-sponsored Food and Drug Administ

Chapter 64 Endovascular Grafts in the Treatment of Isolated Iliac Aneurysms

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FIGURE 64.2 (A, B) Endovascular graft repairs of two large common iliac aneurysms. Arteriograms before and after the repairs are shown. In both cases, hypogastric coil embolization was performed before endograft placement which extended to the external iliac artery. In case A no retrograde filling of the hypogastric branches is seen, whereas it is in case B.

A

B

C B A

FIGURE 64.3 Large aneurysm involving the left distal common iliac artery. (A) Arteriogram before treatment. (B) Arteriogram after hypogastric coil embolization and endograft placement. (C) Contrast CT scan 1 year later.

ration investigational device exemption with the approval of the institutional review board. If iliac tortuosity produced kinking and narrowing of the unsupported portion of the MEGS graft, a Palmaz or Wall stent was

used to alleviate the problem and restore luminal caliber (Fig. 64.4). We have also used a variety of industry-made grafts to treat isolated iliac artery aneurysms. These grafts included

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Part VII Aortic and Peripheral Aneurysms FIGURE 64.4 Arteriograms in a patient with a 6-cm, largely clot-filled, right common iliac aneurysm. (A) Before treatment. (B) After coil embolization of the right hypogastric artery. (C) After endograft placement severe narrowing of the graft is present due to tortuosity of the iliac arteries. (D) Narrowing corrected by placement of a wall stent.

A

B

C

D

tubular self-expanding endografts (Corvita, Vanguard, AneuRx) and modular bifurcated grafts (AneuRx, Talent, Zenith). Obviously any of the commercially made tubular or bifurcated grafts could be used in patients with the appropriate anatomy.

Patient Experience Since March 1993, we have used 54 endovascular grafts to treat isolated iliac artery true aneurysms in 46 patients. Endografts have also been used during this period to treat iliac false aneurysms secondary to trauma or infection in an additional 14 patients. In most of these 60 patients, standard open surgical repair of these aneurysms would have been difficult or impossible because of the anatomic

circumstances or the patient’s medical comorbidities. The minimally invasive nature of endoluminal repair via a femoral artery approach under regional or local anesthesia allowed the procedure to be exceedingly well tolerated, and most patients required less than 3 days in hospital.

Nature of the Endovascular Graft Repair In all but four of the 60 patients, occlusion of the ipsilateral hypogastric artery was repaired. In one patient, the tubular endograft was placed only in the common iliac artery. In the three others with false aneurysms, the endograft was confined to the external iliac artery. Of the 60 patients, 48 underwent endograft repair of isolated iliac aneurysms using some variety of our MEGS graft (Fig. 64.1), while 12 patients received an industry-made

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FIGURE 64.5 Arteriograms in a patient with a 5.5-cm, largely clot-filled, right common iliac aneurysm. (A) Arteriogram before treatment shows short patulous proximal neck. (B) Arteriogram after coil embolization of the right hypogastric artery and placement of a modular bifurcated endograft (Zenith) extending from the infrarenal aorta to the right external iliac artery and the left common iliac artery. Note retrograde filling of the right hypogastric branches.

A

B

FIGURE 64.6 This patient with an implantable defibrillator had a 4-cm, largely clot-filled, right common iliac aneurysm and a 6.5-cm, largely clot-filled, right hypogastric aneurysm. (A) Arteriogram before treatment. (B) Arteriogram at the time of coil embolization of the right hypogastric branches. (C) Arteriogram after replacement of the endograft. Note coils in the hypogastric branches. (D) Contrast CT scan 4 years later showing that hypogastric aneurysm is completely excluded and has shrunk to 4.5 cm.

graft. Four received a modular bifurcated graft originating in the aorta (two AneuRx, one Talent, one Zenith); the remaining eight patients had their iliac aneurysms treated with one or more tubular grafts (three Corvita, one Vanguard and four AneuRx). In general, isolated common iliac artery aneurysms were not treated until

they exceeded 4 cm in size. Based on the work of Santilli et al., rupture of smaller iliac aneurysms appears to be unusual (7). Within the group of 60 patients, there were seven patients who had isolated hypogastric aneurysms and four others who had hypogastric and common iliac aneurysms

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FIGURE 64.7 Patient with a 4.5-cm right common iliac aneurysm containing considerable clot and involving also the proximal right hypogastric artery. (A) Arteriogram before treatment. (B) Arteriogram after coil embolization of the right hypogastric artery and placement of an endograft from the proximal common iliac artery to the external iliac artery. There is retrograde filling of hypogastric branches. Five years later the aneurysm was excluded and the right common iliac had shrunk to 3.0 cm.

(Figs. 64.5 and 64.7). All of these were true aneurysms and all ranged from 4 to 8.5 cm in maximal diameter. When such hypogastric aneurysms were present, every effort was made to occlude patent hypogastric branches. If possible, this coil embolization was performed separately several weeks before the origin of the involved hypogastric artery was to be covered by the endograft. In these eleven hypogastric artery aneurysm patients, as well as at least four others with aortoiliac and hypogastric artery aneurysms, there has been no major morbidity from such hypogastric branch occlusion.

pass in one. Two other patients developed diminished flow through their unsupported endograft in the postoperative period. This occurred without graft thrombosis due to graft kinking from iliac tortuosity. In both patients, placement of a Palmaz or Wall stent within the graft corrected the problem. Aside from one episode of colon ischemia which resolved with conservative treatment, and some minor and inconsequential groin wound problems and buttock claudication, as mentioned above, there were no important complications following these endograft repairs.

Results

Late Outcomes

Early Outcomes In the 60 patients undergoing endovascular graft treatment for isolated iliac artery aneurysm, there was only one patient who died within 30 days of the procedure. This patient, with severe intractable congestive failure, underwent endograft repair after his 8-cm iliac artery aneurysm had ruptured. His aneurysm was successfully excluded but he died 9 days later of multiorgan failure. All other 59 patients had their aneurysm successfully excluded on postoperative contrast computed tomographic (CT) scans and survived more than 1 month. Three patients had distal embolization, satisfactorily treated by thromboembolectomy in two and a distal by-

Two of the 60 patients developed late endoleaks leading to late rupture of their iliac aneurysms. In both instances, the original procedure had been flawed. In one patient the graft had been fixed proximally in a somewhat dilated clot-lined pseudoneck. After 1.5 years the graft migrated distally, leading to a type I endoleak and rupture (13). In the second patient with an 8.5-cm hypogastric aneurysm, occlusion coils had been placed in a clot-lined dilated distal hypogastric artery rather than in its branches. This resulted in a type II endoleak and rupture (19). Both patients survived open operative repair of their ruptured iliac aneurysms. In addition, one other patient had his 4.5-cm iliac aneurysm repaired in 1993 with a MEGS graft fixed proximally in a relatively normal common iliac artery. On

Chapter 64 Endovascular Grafts in the Treatment of Isolated Iliac Aneurysms

a CT scan in 2001, the aneurysm was still excluded and had shrunk to 3.3 cm in maximal diameter. A CT scan in 2002 revealed that the proximal iliac neck had enlarged and a type I endoleak had developed with enlargement of the aneurysm maximal diameter to 4.2 cm. A repair is planned. Although several patients have died from causes unrelated to their aneurysms, there have been no late deaths related to the procedure or the iliac aneurysms. Annual follow-up contrast CT scans have revealed that all the other endograft-treated iliac aneurysms have remained excluded and have decreased in size. The endografts in all these patients have remained patent, with some postprocedural follow-up observations extending to 10 years.

Indications for Endovascular Graft Repair

773

believe that endovascular graft repair is the procedure of choice for most patients with isolated iliac artery aneurysms. The exception might be a thin patient less than 65 years of age with a normal heart. Even in these circumstances, judgment and the patient’s preference must enter into the decision.

Size Considerations The observations of Santilli et al. suggest that common iliac aneurysms do not pose a great risk of rupture until they become large (>4–5 cm in maximal diameter) (7). Accordingly, we treat isolated common iliac aneurysms only when they exceed 4 cm in maximal diameter. Exceptions might be patients whose aneurysms are tender or have enlarged rapidly. Other exceptions might be small women, although there are no data to support this.

Isolated Hypogastric Aneurysms Background with Abdominal Aortic Aneurysms In the last two years, many have come to believe that endovascular grafting is the best way to repair all abdominal aortic aneurysms that are anatomically suitable for such procedures. On the other hand, because of the high early failure rates and subsequent complications, some others hold the opinion that endovascular aortic aneurysm repair (EVAR) is already “a failed experiment” (20). We have a more balanced view, based on our experience which includes many good mid- and long-term results albeit with an increasing incidence of mid- and late-term complications, many of which can be treated endovascularly (21,22). On this basis, we believe that endovascular aortic aneurysm repair is a “technique in evolution and under evaluation” and that its use should largely be restricted to patients who have limited life expectancies (age >75 years) and/or are at high risk for open repair. Younger, good-risk patients should, unless they demand an endovascular procedure, be offered an open repair (21,22). If an endograft repair is performed, close, careful CT scan surveillance at 6–12 monthly intervals is mandatory. In addition, it is only justified to perform EVAR on patients whose aortic aneurysm would be large enough (>5–5.5 cm in diameter) to warrant open repair, if endografting were not performed. At present, it is not justified to perform EVAR on smaller aortic aneurysms as some have mistakenly suggested.

Isolated Iliac Aneurysms These concepts can generally be extrapolated to isolated iliac artery aneurysms with some important exceptions. Iliac aneurysms are often more difficult to treat by open surgery than are aortic aneurysms restricted to the infrarenal aorta. Because of this and because our results have generally been favorable and durable (13), we

Similarly, there are no data to document the size at which a hypogastric aneurysm is at risk for rupture. Arbitrarily, we treat them when they exceed 4 cm in maximal diameter. Obviously, this guideline for treatment will require modification if additional data on rupture potential of hypogastric aneurysm become available.

Surveillance Considerations for Isolated Iliac Aneurysms Treated Endovascularly Since we have noted the late development of endoleaks leading to aneurysm enlargement and rupture after initially successful endograft repair of these aneurysms, we believe CT scan surveillance programmes similar to those recommended after EVAR should be employed (23). CT scans every 6–12 months are indicated, and should be performed more frequently if the aneurysm fails to decrease in size (13,23). If an endoleak is detected and the aneurysm enlarges, endovascular correction should be attempted. If the endoleak cannot be corrected, conversion to an open repair is indicated.

Conclusions Endovascular repair is an attractive method to repair isolated iliac artery aneurysms large enough to pose a risk of rupture. Because of the low morbidity of repairs carried out to date and because of their apparent durability in a limited number of cases, we believe that endovascular grafting will become the procedure of choice for these lesions. However, more experience, particularly with follow-up beyond 5 years, will be required before these beliefs can be considered proven.

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References 1. Lowry SF, Kraft RO. Isolated aneurysms of the iliac artery. Arch Surg 1978;113:1289–1293. 2. McCready RA, Pairolero PC, et al. Isolated iliac artery aneurysms. Surgery 1983;93:688–693. 3. Richardson JW, Greenfield LJ. Natural history and management of iliac artery aneurysms. J Vasc Surg 1988;8:165–171. 4. Nachbur BH, Inderbitzi RG, Bar W. Isolated iliac aneurysms. Eur J Vasc Surg 1991;5:375–381. 5. Sack NPM, Huddy SPJ, et al. Management of solitary iliac aneurysms. J Cardiovasc Surg 1992;33:679–683. 6. Krupski WC, Selzman CH, et al. Contemporary management of isolated iliac aneurysms. J Vasc Surg 1998;28:1–13. 7. Santilli S, Wernsing S, Lee E. Expansion rates and outcomes for iliac artery aneurysms. J Vasc Surg 2000;31:114–121. 8. Reuter SR, Carson SN. Thrombosis of a common iliac artery aneurysm by selective embolization and extraanatomic bypass. Am J Roentgenol 1980;134:1248–1250. 9. Vorwerk D, Gunther RW, et al. Ulcerated plaques and focal aneurysms of iliac arteries: treatment with noncovered, self-expanding stents. Am J Roentgenol 1994;162:1421–1424. 10. Marin ML, Veith FJ, et al. Transfemoral endovascular repair of iliac artery aneurysms. Am J Surg 1995;170:179–182. 11. Parsons RE, Marin ML, et al. Midterm results of endovascular stented grafts for the treatment of isolated iliac artery aneurysms. J Vasc Surg 1999;30:915–921. 12. Sanchez LA, Patel AV, et al. Midterm experience with the endovascular treatment of isolated iliac aneurysms. J Vasc Surg 1999;30:907–914. 13. Seghal A, Veith FJ, et al. Diameter changes in isolated iliac artery aneurysms 1 to 6 years after endovascular graft repair. J Vasc Surg 2001;33:289–295.

14. Mehta M, Veith FJ, et al. Unilateral and bilateral hypogastric artery interruption during aortoiliac aneurysm repair in 154 patients: a relatively innocuous procedure. J Vasc Surg 2001;33(2 Suppl):S27–32. 15. Karch LA, Hodgson KJ, et al. Adverse consequences of internal iliac artery occlusion during endovascular repair of abdominal aortic aneurysms. J Vasc Surg 2000;32:676–683. 16. Criado FJ, Wilson EP, et al. Safety of coil occlusion of the internal iliac artery during endovascular grafting of AAA. J Vasc Surg 2000;32:684–688. 17. Parodi JC. Relocation of iliac artery bifurcation to facilitate endoluminal treatment of AAA. J Endovasc Surg 1999;6:342–347. 18. Dadian N, Ohki T, et al. Overt colon ischemia after endovascular aneurysm repair: the importance of microembolization as an etiology. J Vasc Surg 2001;34:986–996. 19. Bade MA, Ohki T, et al. Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: significance of endotension from a “virtual,” or thrombosed type II endoleak. J Vasc Surg 2001;33:1271–1274. 20. Collin J, Murie JA. Endovascular treatment of abdominal aortic aneurysms: a failed experiment. Br J Surg 2001;88:1281–1282. 21. Veith FJ, Johnston KW. Endovascular treatment of abdominal aortic aneurysms: an innovation in evolution and under evaluation. J Vasc Surg 2002;35:183. 22. Ohki T, Veith FJ, et al. Increasing incidence of midterm and long-term complications after endovascular graft repair of abdominal aortic aneurysms: a note of caution based on a 9-year experience. Ann Surg 2001;234:323–335. 23. Rozenblit AM, Cynamon J, et al. Value of CT angiography for postoperative assessment of patients with iliac artery aneurysms who have received endovascular grafts. Am J Roentgenol 1998;170:913–917.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 65 Para-anastomotic Aortic Aneurysms: General Considerations and Techniques Daniel J. Char and John J. Ricotta

Surgical repair of abdominal aortic aneurysms can be accomplished with excellent results and good long-term outcomes. Modern series of open elective surgical repair have achieved mortality rates less than 5% (1,2). Although long-term survival of patients following abdominal aortic aneurysm repair is less than age- and sex-matched normal population, good long-term survival has been reported (3). However, during the long-term follow-up of patients after open surgical repair, recurrent aortic pathology can arise. Progression of the original aortic pathology can result in a true aneurysm of the arterial wall, either proximal or distal to the initial aortic graft. Alternatively, disruption of the original suture line can result in a false anastomotic aneurysm. These two processes may be indistinguishable prior to operation. Taken together, they represent para-anastomotic aortic aneurysms (PAAAs). PAAAs resulting from infection or aorto-enteric erosion present a special circumstance that is dealt with in Chapter 00.

Incidence of Para-anastomotic Aortic Aneurysms The reported incidence of PAAAs varies widely in the literature (Table 65.1). The true incidence of PAAAs is

unknown. In several reports, PAAAs were incidental findings detected in asymptomatic patients (4–6). In the Northwestern series (6), one-third of PAAAs were nonpalpable. While several authors have recommended routine imaging of patients at intervals after aortic reconstruction, there is scant prospective data on this topic in the literature (5,7). DeMonti et al. reported six new aneurysms in 95 patients subjected to routine ultrasound follow-up surveillance 3 to 13 years postoperatively (5). Berman et al. followed 178 patients with aortic prostheses implanted for a mean of slightly less than 4 years. During that time, complications occurred in 24 patients (13.5%), including 15 (8%) PAAAs (8). In clinical series of PAAAs, most aneurysms are discovered more than 5 years after the original graft implantation (4,6,9). Mii et al. estimate an incidence of PAAAs of 0.5% at 5 years, 6.2% at 10 years, and 35.8% at 15 years, although routine surveillance was not performed (10). Edwards et al., using yearly ultrasound surveillance, found PAAAs in 10% of patients after aortic grafting. They estimated a 27% incidence of PAAAs 15 years after implantation (7), a number similar to that reported by Mii (10). In a late follow-up after ruptured AAAs, Cho et al. reported PAAAs in 15% of these patients (11). From these reported experiences, one may conclude that PAAAs are not an uncommon late complication after

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TABLE 65.1 Incidence of proximal aortic anastomotic aneurysms Author

Reference

Year

Initial Surgery

13 1 21 7

1985 1999 1989 1992

AAA AAA AOD AAA + AOD

Plate Kalman Van Den Akker Edwards

Patients (n)

True Aneurysm

False Aneurysm

Overall Incidence (%)

1087 94 438 111

7 3 0 4

4 9 21 7

1 13 4.8 10

AAA, abdominal aortic aneurysm; AOD, aortoiliac occlusive disease.

aortic surgery. The incidence of PAAAs is under-reported in the current literature since most studies identify PAAAs only when they become clinically obvious. Surveillance studies have not been carried out for long intervals, but those reported suggest as many as one-third of patients with aortic surgery may develop PAAA if followed long enough. Since the emergent or urgent repair of PAAA is associated with poor results, surveillance imaging studies should be considered with the aim of early detection and repair. The ideal surveillance protocol is not clear, but recommendations include annual physical examination and periodic ultrasound every 1 to 2 years. Since secondary aneurysms may arise in the popliteal or thoracic aorta, these areas should also be evaluated. Our policy is annual physical examination (including the femoral and popliteal arteries) with chest radiographs and abdominal ultrasound at 2 to 3 years and CT imaging of the chest and abdomen at 5 years. Thereafter, CT scans are repeated every 24 to 30 months.

True PAAAs Several investigators have noted that true juxtaanastomotic aneurysms tend to occur only in patients who originally had aortic grafting for aneurysmal rather than occlusive disease (4,7,12). This is not surprising since the underlying degenerative process in the aorta remains unaltered. True PAAAs may result from either inadequate resection of the abdominal aortic aneurysm at the time of the original surgery or from continued dilatation of the aortic neck and adjacent aorta over time. The importance of placing the proximal anstomosis immediately below the renal arteries during aneurysmectomy was emphasized by Plate et al. in 1985. Their initial failure to do this resulted in infrarenal dilatation of the remaining native aorta during follow-up (18). With attention to this technical detail, leaving an aneurysmal aorta at the initial operation has become a less common cause of PAAA. Edwards and colleagues were able to document the development of true PAAAs in patients with normal proximal juxtaanastomotic aortas, suggesting that these PAAAs were due to subsequent proximal aneurysmal dilation of the initially normal aorta and not a result of residual unresected aneurysmal aortic necks untreated at the original operation (7). Continued dilation of the aorta has been recognized as increasingly important. Data obtained from

serial CT studies after aortic aneurysm repair support the hypothesis of progressive dilation and elongation of the remaining aorta. Illig et al. (14) studied 33 patients for an average of 89 months after aneurysmectomy. While the mean increase in aortic diameter was only 4 mm, onethird of their patients experienced significant neck dilation to greater than 30 mm. Hallet et al. noted 13% of patients followed after aortic surgery exhibited a proximal aortic neck greater than 30 mm (9). While these data are of greatest interest for patients who undergo endografting, they shed important light on the development of PAAA after open surgery. The fact that most PAAAs are found 8 to 10 years after open repair is important in this regard, reemphasizing the need for late follow-up in all patients with AAA repair.

False PAAAs False PAAAs occur with equal frequency after operations for aneurysmal and occlusive disease (4,6). Etiologies include fatigue of the arterial wall, suture material, or aortic prosthesis. Older reports on false aneurysms (15,16) implicated both suture material and graft fabric, although these problems are less common with modern materials. Several detailed pathologic studies (17–19) implicate arterial degeneration and failure as the primary etiology of pseudoaneurysm formation. Recent reports by Shah et al. (20) on over 1000 polytetrafluoroethylene (PTFE) grafts with 94% complete follow-up demonstrate no false aneurysms, implying a benefit of this material. The importance of fabric was also noted in the follow-up study by Berman et al., who noted significantly more mean percentage dilation of aortic grafts made from knitted Dacron (49%) than either woven Dacron (28.5%) or PTFE (20%) (8). In patients operated on for occlusive disease, performance of both an endarterectomy (10) and an end-to-side anastomosis (21) was associated with the development of a false PAAA. These data have implications for both material selection and operative technique in the prevention of false aneurysms. Of most importance to the surgeon is selection of a relatively normal arterial segment for anastomosis. In this regard, the increasing attention to disease of the perirenal aorta and comfort with suprarenal or even supraceliac clamping to allow access to normal aorta for the initial anastomosis have been great advances in the

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prevention of para-anastomotic aneurysms in the perirenal area. When a less-than-optimal proximal aortic segment must be used for anastomosis, or when proximal endarterectomy is required, the development of late pseudoaneurysm must be an increased concern.

Presentation Characteristically, aortic anastomotic aneurysms present several years after the original aortic grafting. Allen and colleagues reported a mean interval to diagnosis of 9.4 years for proximal aortic anastomotic aneurysms. However, over one-third of these patients were noted to present within 5 years of their original aortic surgery (12). Similarly, Curl and colleagues reported a mean interval of 9.9 years from initial surgery to presentation (4). The presentation of patients with PAAAs varies. Patients may be asymptomatic and their PAAA is discovered incidentally on physical examination or during radiological evaluation for unrelated conditions. By using routine yearly abdominal ultrasonography to follow patients after aortic grafting, Edwards and colleagues were able to detect 11 PAAAs in 111 patients, all of whom were asymptomatic (7). However, when surveillance is not performed, 42% to 79% of patients from different series have presented with symptoms related to their PAAA (12,22). Common symptoms include abdominal pain, back pain, and gastrointestinal bleeding. The number of patients presenting with a ruptured PAAA varies between series. Coselli and colleagues reported that 4.9% of their patients with PAAAs presented with rupture (23). Plate and colleagues reported that 6 of 11 PAAAs presented with rupture, all of which resulted in death (13). Matsumura et al. noted an 88% mortality rate in eight PAAAs operated on emergently for rupture (6). The high mortality of rupture forms the basis for recommendation of routine surveillance by most authors reporting on this topic. Curl and colleagues observed that patients who presented with ruptured PAAAs (three of their 21 patients) had undergone their original aortic surgery for aneurysmal disease. Those patients who had aortoiliac occlusive disease as their original surgical indication were asymptomatic and no PAAA ruptures were reported in this group (4). This last group consisted entirely of pseudoaneurysms, many of which were identified by a palpable groin mass. This stresses the importance of complete graft evaluation when a femoral anastomotic aneurysm is discovered.

Management Diagnostic Evaluation When a PAAA is suspected on physical examination or after surveillance imaging, complete diagnostic evaluation should be done whenever possible. This includes contrast-enhanced CT scanning and detailed aortography

FIGURE 65.1 Angiogram of patient with recurrent aneurysms above and below an aortofemoral graft placed 12 years earlier.

(Fig. 65.1). The purpose of these studies is to define the extent of the PAAA, determine its relationship to the visceral vessels, and to identify any occlusive lesions of the visceral vessels which may need to be addressed at the time of surgical repair.

Indications for Repair Repair of PAAAs should be individualized according to the patient’s presentation (symptomatic vs. asymptomatic), pathology (true vs. false aneurysm), aortic anatomy, and medical comorbidities. Symptomatic PAAAs should be repaired as expeditiously as possible. Patients who present with symptomatic PAAAs suggestive of impending rupture should be approached urgently because of the poor outcome associated with rupture. As noted above, preoperative computed tomography and angiography are helpful to identify the extent of the PAAA and its relationship to the visceral aorta and should be obtained whenever possible. However, the ability to obtain preoperative imaging will be dictated by the patient’s hemodynamic status.

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The management of asymptomatic PAAAs should be predicated on the natural history of true versus false PAAAs. Asymptomatic true PAAAs should be repaired according the generally accepted criteria for primary infrarenal abdominal aortic aneurysms. One should consider repair of asymptomatic true PAAAs as they approach 5 cm in diameter. However, these aneurysms can extend proximally from the juxta-anastomotic aorta to involve the visceral aorta. Therefore, the anatomy of a true PAAA in relationship to the suprarenal aorta can weigh heavily in both the decision to proceed with repair and the selection of operative approach. Studies to define the anatomy in as much detail as possible are imperative. The management of asymptomatic false PAAAs remains unsettled and revolves around aneurysm size, aortic anatomy, and the patient’s medical comorbidities. Since false PAAAs represent a contained suture line disruption, one should consider repair of all false aneurysms. In addition, the poor outcome associated with rupture of these aneurysms suggests that all false PAAAs should be repaired (22,24). However, medical comorbidities or the patient’s refusal of further intervention may preclude repair. Edwards and colleagues report observation of four false PAAAs ranging in size from 4.1 to 6.2 cm for a mean period of 18 months. No symptoms developed or ruptures occurred during this period (7). Others have suggested repair of all false PAAAs that measure more than 50% of the diameter of the aortic graft (25).

Interventions and Results PAAA is usually treated by open surgical repair, although there have recently been reports of endovascular repair in selected patients. Preoperative evaluation of medical comorbidities will be dictated by the urgency of the repair. For elective procedures, a standard preoperative evaluation should be performed, as these patients are elderly and suffer from the expected comorbidities associated with aneurysmal or occlusive aortoiliac disease. When planning the open surgical approach, one must consider the method of exposure (transperitoneal vs. retroperitoneal) and the site for placement of the proximal aortic clamp. The relative advantages and disadvantages of the surgical exposures will be discussed subsequently. The position of the aortic cross-clamp will be dictated by the proximal extent of the PAAA and can be placed infrarenal, suprarenal or supraceliac. Infrarenal clamping is preferable when possible in patients with either false PAAAs or those with true aneurysms that do not require concomitant renal or visceral artery reconstruction. In the series by Curl and associates, 60% of patients with false PAAAs had infrarenal clamping while this maneuver was impossible in patients with true aneurysms. Patients requiring emergency surgery are best managed by supraceliac clamping, as this limits perianastomotic dissection (4). Endoluminal balloon catheter con-

trol may be considered. When this is utilized, the transbrachial approach is preferred, as the risk of distal balloon migration is reduced (36). Suprarenal or supraceliac aortic cross-clamping are required for patients who need renal or visceral artery reconstruction or when dissection of the juxtarenal aorta is hazardous as a result of prior surgery or perianastomotic hemorrhage. In the series by Allen and associates, 37% of patients who underwent open surgical repair of a PAAA required supraceliac aortic cross-clamping. After completion of the proximal anastomosis the clamp can be moved to the graft, restoring visceral flow. Suprarenal aortic cross-clamping was not associated with an increase in postoperative complications or mortality in this series (12). The reported results of open surgical repair of PAAAs vary. Overall, mortality rates have ranged from 21% to 37.5% (4,12,22,24). Table 65.2 summarizes the surgical results for repair of false and true PAAAs. In the series by Locati and colleagues, the mortality rate for repair of false PAAAs was 42% versus 20% for true PAAAs. However, almost half of the patients with false PAAAs presented with rupture (22). For patients who present with symptomatic PAAAs, there is a trend towards increased mortality, especially in those patients who present with rupture (4,6,13). Table 65.3 summarizes the surgical results for repair of symptomatic and asymptomatic PAAAs. In addition to open surgical repair, endovascular treatment of PAAAs is evolving. Morrissey and colleagues reported on 12 patients with PAAAs who underwent endovascular repair with no perioperative deaths (26). Although these results are encouraging, other smaller series of endovascular repair have reported up to a 50% perioperative mortality rate (27). Proposed benefits of this approach include avoidance of operative dissection through a scarred field, reduced blood loss, and the ability to perform the procedure under regional anesthesia (26). However, the anatomy of the PAAA and its relationship to the renal arteries may preclude safe repair with an endovascular device. For instance, the length of the infrarenal aortic neck above the PAAA available for securing an endovascular device may not be adequate. As newer devices become available for suprarenal fixation, the required length of the normal infrarenal aortic neck will diminish, allowing more PAAAs to be treated by endovascular means. Currently, endovascular repair has its greatest utility in the management of distal PAAAs, where consideration of visceral anatomy is less important. In these circumstances, an endovascular approach can greatly simplify management.

Open Technique Proximal PAAAs can be approached via a transperitoneal or retroperitoneal approach. Each approach has advantages and disadvantages to be considered when planning the surgical repair of a PAAA.

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TABLE 65.2 Open surgical results for PAAA repair: true vs. false aneurysms Mortality Author

Reference

Year

Patients (n)

False Aneurysm

True Aneurysm

Overall

22 4 24 35

2000 1992 1988 1993

24 21 18 25

8/12 (42%) 3/12 (25%) 5/18 (28%) 6/25 (25%)

1/5 (20%) 2/9 (22%) NA NA

9/24 (37.5%) 5/21 (24%) 5/18 (28%) 6/25 (25%)

Locati Curl Treiman McCann

TABLE 65.3 Open surgical results for PAAA repair: symptomatic vs. asymptomatic aneurysms Mortality Author

Reference

Year

Patients (n)

Symptomatic Aneurysm

Asymptomatic Aneurysm

Overall

Locati Curl Allen

22 4 12

2000 1992 1993

24 21 29

7/10 (70%) 2/7 (29%) 5/23 (22%)

2/14 (14%) 3/14 (21%) 1/6 (17%)

9/24 (37.5%) 5/21 (24%) 6/29 (21%)

The anterior transperitoneal approach is familiar to most surgeons and provides easy access for supraceliac, suprarenal, and infrarenal aortic cross-clamping. In addition, the aortic bifurcation and both iliac arteries are easily accessible if distal aortic or iliac artery aneurysms are present. Left medial visceral rotation involving mobilization of the left colon, spleen, pancreas, stomach, and left kidney can be accomplished via a transperitoneal approach. This allows exposure of the proximal abdominal aorta and the visceral aortic segment for reconstruction when needed although significant mobilization is required and visceral (especially splenic) damage may occur (Fig. 65.2). The transperitoneal approach is most useful when an infrarenal repair can be anticipated, when distal reconstruction is required, or when infection is suspected. Its major advantages lie in its familiarity and the ability to expose the infrarenal aortoiliac segments. Its major disadvantage is in exposing the visceral aorta and the problem of adhesions associated with prior surgery. The extended left retroperitoneal approach allows for the wide exposure of the abdominal aorta, particularly the visceral portion (28) (Fig. 65.3). Intraperitoneal adhesions from prior abdominal procedures are avoided and the left renal vein does not obstruct the aortic exposure if the left kidney is mobilized medially during the dissection. The major advantage of this approach is the easy exposure of the supraceliac aorta through nondissected tissue planes. However, this approach is limited in its exposure of the right iliac artery and the right renal artery beyond its origin. In addition, the left ureter needs to be identified and mobilized with caution, as it may be adherent to the aorta as a result of prior dissection. This approach is preferred when surgery is limited to the proximal anastomosis, when visceral reconstruction is anticipated, and in cases of the “hostile abdomen.” Whether the transperi-

FIGURE 65.2 Transabdominal exposure of suprarenal aorta via medial visceral rotation. This approach is best when the proximal extent of the aneurysm is perirenal rather than suprarenal.

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FIGURE 65.3 Extended left retroperitoneal approach. This gives the best exposure to the visceral aorta and allows the surgeon to reach the lower thoracic aorta by incising the diaphragmatic crus. However, access to the visceral vessels (except the left renal) is more limited than with the anterior approach. An incision is made superior to the 11th (or, occasionally, the 10th) rib (A). The dissection occurs behind the kidney (B).

toneal or retroperitoneal approach is used, the key to success is flexibility on the surgeon’s part, and the ability to make intraoperative adjustments. After achieving exposure of the aorta, proximal aortic control needs to be established. Supraceliac, suprarenal, or infrarenal aortic cross-clamping will be dictated by the level of involvement of the PAAA and the exposure of the aorta. Suprarenal aortic clamping will be necessary for renal or visceral reconstruction. Suprarenal aortic cross-clamping need not be associated with an increase in perioperative morbidity or mortality (12). With proximal aortic control achieved, interposition grafting to repair the PAAA can be accomplished by two general approaches. An interposition graft can be placed between the normal proximal aorta and the proximal end of the old aortic graft (Fig. 65.4). This is the preferred approach when distal vascular reconstruction is not required. The old aortic graft can usually be clamped easily to obtain distal vascular control. Once the proximal aorta is clamped, the aneurysm sac can be opened and the old

graft easily dissected out. This approach obviates the need for further distal dissection, saves time and blood loss, and minimizes the chance for venous or ureteral injury. Alternatively, when aneurysmal degeneration occurs at both the proximal and distal ends of the graft, then the entire graft must be replaced. Unless there is evidence of graft infection, this is performed in situ. Antibioticsoaked grafts may be used as an additional precaution (29). When total graft replacement is required, the operation begins in the manner described above, i.e., with proximal aortic control. Following proximal control, dissection of a segment of noninvolved iliac artery is achieved. After noninvolved aorta and iliac vessels are clamped, the sac of the PAAA is entered, and the graft replaced. If a proximal suture line disruption and false PAAA are present, a different approach to vascular control can be employed. Appropriate proximal aortic control is established as described above. If distal vascular control is difficult secondary to anatomy, reoperation, or obscured exposure due to an overlying large false aneurysm, distal vascular control is easily obtained by clamping the old graft after incising the false aneurysm sac (Fig. 65.5). With proximal aortic control, the false aneurysm sac surrounding the aorta can be entered with relative impunity. With the aorta controlled proximally and the graft clamped within the false aneurysm sac (providing distal vascular control), dissection is continued within the aneurysm sac to minimize damage to adjacent organs. Dissection proceeds first towards the proximal suture line. Debridement of the aorta is performed as required and a new graft sewn proximally. An end-to-end anastomosis of the distal end of the new graft to the proximal end of the old graft completes the reconstruction. By working within the aneurysm sac, the sites for the new anastomoses are exposed with minimal external dissection. When replacement of the visceral aortic segment is needed, the techniques used for type IV thoracoabdominal aneurysm repair are applied. The visceral vessels may be replaced into a tube graft using Carrel patches, or a posterior “tongue” of aortic graft may be used, preserving the anterior half of the visceral aorta in a long suture line (Fig. 65.6).

Endovascular Technique The principles of endovascular repair for infrarenal abdominal aortic aneurysms apply. The major concern with endovascular repair is secure proximal fixation. Accurate measurement of the proximal aortic neck is crucial, requiring techniques of computed tomography and angiography. Since reported experience suggests that two-thirds of PAAA repairs can be performed infrarenally, an endovascular approach should be considered in appropriate patients. Patients with false PAAA are the most likely candidates for endovascular repair with current endografts. Currently a 1-cm proximal aortic neck is required for en-

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B

A

C

dovascular repair, although improvements in proximal fixation may change this. For isolated proximal PAAAs, a simple extension cuff may be placed transfemorally (Fig. 65.7). The cuff must be of sufficient diameter to create a secure proximal and distal seal.

FIGURE 65.4 Repair of recurrent true proximal aneurysm. (A) Suprarenal (or suprailiac) control is obtained in proximal normal aorta. Distal control is obtained after opening the aneurysm sac and clamping the graft. (B) Proximal aorta is opened and a new proximal anastomosis is constructed with a new graft. In this case, this is at the level of the renal arteries which is often possible. Suprarenal control allows good visualization of the sewing ring. (C) Distal anastomosis completed to old graft. The majority of dissection occurs either proximal to the first operation or within the aneurysm sac, reducing risk of injury to surrounding structures.

When the PAAA is distal, endovascular intervention may be particularly useful, provided that the proximal graft is not too dilated to allow a proximal seal. In general, a bifurcated graft, seated just below the renal arteries and extending into each iliac artery beyond the PAAA, is the preferred approach. Again, presence of adequate

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Part VII Aortic and Peripheral Aneurysms FIGURE 65.5 Repair of a false aneurysm. Expeditious distal control is obtained after suprarenal clamping and incising false aneurysm sac (A). Distal control is obtained by clamping the old graft (B). Repair of the proximal suture line (C) or graft replacement can be performed as in Figure 65.4.

FIGURE 65.6 Repair of recurrent aneurysm involving visceral vessels. Use of an oblique incision (A) allows incorporation of the visceral vessels with a single suture line (B). After the proximal suture line is completed, the graft is clamped below the visceral vessels and the distal reconstruction is performed. (Note: Head is to right of figure.)

proximal and distal landing zones is of paramount importance. Distal PAAAs may involve the common iliac vessels. In this case, embolization of one or both internal iliac arteries may be required to allow sealing of the endograft in the external iliac artery. While bilateral hypogastric artery embolization should be avoided (30), it is not absolutely contraindicated (31,32). Endovascular repair of iliac artery aneurysms are discussed in detail elsewhere (see Chapter 63). However, there is an unusual condition, aneurysmal dilation of the blind iliac stump, which is amenable to combined endovascular and open repair. This situation occurs when the common iliac artery or the aortic bifurcation has been oversewn and a distal end-to-side anastomosis is per-

formed to the external iliac or common femoral artery to permit retrograde perfusion of the hypogastric artery. When the retrograde perfused segment dilates, there is the risk of rupture. A combined approach including transfemoral coil embolization of the iliac artery aneurysm and feeding hypogastric artery, followed by open ligation of the external iliac artery through a groin incision, provides effective treatment of this difficult problem with minimal morbidity (Fig. 65.8). There have been reports of endovascular approaches for aneurysms involving the visceral vessels. In some cases, endovascular branch grafting has been suggested (33,34). In other cases, a combination of open extraanatomic visceral revascularization has been combined with visceral aortic endografting. These novel approaches might also be applied to treatment of PAAAs involving the visceral aorta. At present, the use of endovascular techniques in such cases remains anecdotal.

Surveillance Although aortic grafting for aneurysmal and occlusive disease is a durable procedure, late complications do occur. As noted by Edwards and colleagues, the incidence of para-anastomotic aneurysms was 27% at 15 years by life-table analysis (7). Cho and colleagues observed a statistically significant greater number of para-anastomotic aneurysms after repair of ruptured AAAs compared with elective cases (11). In addition, a trend is seen toward increased mortality in patients with symptomatic or ruptured PAAAs. Given the moderate but progressive incidence of late complications after aortic grafting, many of which are asymptomatic, and the noted poor outcome for symptomatic or ruptured PAAAs, life-long surveillance of all patients following aortic grafting should be pursued (13,22,35). However, most complications are discovered after an extended period. Therefore, followup CT scanning performed 5 years after aortic grafting in asymptomatic patients has been recommended (1). How-

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FIGURE 65.7 Repair of proximal false aneurysm (A) by placement of a proximal extension cuff (B). A secure proximal landing zone may require using a graft with suprarenal fixation using bare stent technology. The cuff must be large enough to provide a distal seal with the old graft. An entire bifurcated endograft with extension to both iliac arteries may be used.

FIGURE 65.8 Endovascular exclusion of recurrent iliac aneurysm after aortofemoral bypass and oversewing of common iliac artery. This patient presented 8 years after AAA repair. Angiogram shows large left common iliac artery aneurysm (A). Via cutdown, the native common femoral artery was accessed and catheters were placed into the common iliac aneurysm. Coil embolization of both the internal iliac artery and common iliac aneurysm was performed (B). Finally, the distal external iliac artery was ligated, preventing retrograde flow.

ever, the ideal surveillance protocol is not clear. As stated earlier, our policy is annual physical examination (including the femoral and popliteal arteries) with chest radiographs and abdominal ultrasound at 2 to 3 years and CT imaging of the chest and abdomen at 5 years. Thereafter, CT scans are repeated every 24 to 30 months.

References 1. Kalman PG, Rappaport DC, et al. The value of late computed tomographic scanning in identification of vascular abnormalities after abdominal aortic aneurysm repair. J Vasc Surg 1999;29:442–450.

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2. Huber TS, Wang JG, et al. Experience in the United States with intact abdominal aortic aneurysm repair. J Vasc Surg 2001;33;304–311. 3. Johnston KW. Nonruptured abdominal aortic aneurysms: six-year follow-up results from the multicenter prospective Canadian aneurysm study. J Vasc Surg 1994;20:163–170. 4. Curl GR, Faggioli GL, et al. Aneurysmal change at or above the proximal anastomosis after infrarenal aortic grafting. J Vasc Surg 1992;16:855–860. 5. DeMonti M, Ghilardi G, et al. Recurrent aneurysms: late complications for patients previously submitted to graft replacement for abdominal aortic aneurysm. Minerva Cadioangiol 1999;47:329–338. 6. Matsumura JS, Pearce WH, et al. Reoperative aortic surgery. Cardiovasc Surg 1999;7:614–621. 7. Edwards JM, Teefey SA, et al. Intraabdominal paraanastomotic aneurysms after aortic bypass grafting. J Vasc Surg 1992;15;344–353. 8. Berman SS, Hunter GC, et al. Application of computed tomography for surveillance of aortic grafts. Surgery 1985;118:8–15. 9. Hallett JW, Marshall DM, et al. Graft-related complications after abdominal aneurysm repair: reassurance from a 36-year population-based experience. J Vasc Surg 1997;25:277–284. 10. Mii S, Mori A, et al. Para-anastomotic aneurysms: incidence, risk factors, treatment and prognosis. J Cardiovasc Surg 1998;39:259–266. 11. Cho JS, Gloviczki P, et al. Long-term survival and late complications after repair of ruptured abdominal aortic aneurysms. J Vasc Surg 1998;27:813–820. 12. Allen RC, Schneider J, et al. J Vasc Surg 1993;18:424–432. 13. Plate G, Hollier LA, et al. Recurrent aneurysms and late vascular complications following repair of abdominal aortic aneurysms. Arch Surg 1985;120:590–594. 14. Illig KA, Green RM, et al. Fate of the proximal aortic cuff: implications for endovascular aneurysm repair. J Vasc Surg 1997;26:492–502. 15. Starr DS, Weatherford SC, et al. Suture material as a factor in the occurrence of anastomotic false aneurysms. Arch Surg 1979;114:412–415. 16. Clagett GP, Salander JM, et al. Dilation of knitted Dacron aortic protheses and anastomotic false aneurysms: etiologic considerations. Surgery 1983;93:9–16. 17. Gaylis H. Pathogenesis of anastomotic aneurysms. Surgery 1981;90,509–515. 18. Dennis JW, Littoy FN, et al. Anastomotic pseudoaneurysms. Arch Surg 1986;121:314–317. 19. Drury JK, Leiberman DP, et al. Operation for late complications of aortic grafts. Surg Gynecol Obstet 1986;163:251–255. 20. Shah DM, Darling C, Kreienberg PB, et al. A critical approach for longitudinal clinical trial of stretch PTFE aortic grafts. Cardiovasc Surg 1997;5:414–418.

21. Van Den Akker PJ, Brand R, et al. False aneurysms after prosthetic reconstructions for aortoiliac obstructive disease. Ann Surg 1989;210:658–666. 22. Locati P, Socrate AM, Costantini E. Paraanastomotic aneurysms of the abdominal aorta: a 15-year experience review. Cardiovasc Surg 2000;8:274–279. 23. Coselli JS, LeMaire SA, et al. Subsequent proximal aortic operations in 123 patients with previous infrarenal abdominal aortic aneurysm surgery. J Vasc Surg 1995;22:59–67. 24. Treiman GS, Weaver FA, et al. Anastomotic false aneurysms of the abdominal aorta and iliac arteries. J Vasc Surg 1988;8:268–273. 25. Schwartz LB, Clark ET, Gewertz BL. Anastomotic and other pseudoaneurysms. In: Rutherford (ed). Vascular Surgery, 5th edn. Philadelphia: WB Saunders, 2000: 755. 26. Morrissey NJ, Yano OJ, et al. Endovascular repair of para-anastomotic aneurysms of the aorta and the iliac arteries: preferred treatment for a complex problem. J Vasc Surg 2001;33:503–512. 27. Liewald F, Kapfer X, et al. Endograft treatment of anastomotic aneurysms following conventional open surgery for infrarenal aortic aneurysms. Eur J Vasc Endovasc Surg 2001;21:46–50. 28. Ricotta JJ, Williams GM. Endarterectomy of the upper abdominal aorta and visceral arteries through an extraperitoneal approach. Ann Surg 1980;192: 633–638. 29. Bandyk DF, Novotney ML, et al. Expanded application of in situ replacement for prosthetic graft infection. J Vasc Surg 2001;34:411–420. 30. Karch LA, Hodgdon KJ, et al. Adverse consequences of internal iliac artery occlusion during endovascular repair of abdominal aortic aneurysms. J Vasc Surg 2000;32:676–683. 31. Criado FJ, Wilson EP, et al. Safety of coil embolization of the internal iliac artery in endovascular grafting of abdominal aortic aneurysms. J Vasc Surg 2000;32:684–688. 32. Mehta M, Veith FJ, et al. Unilateral and bilateral hypogastric artery interruption during aortoiliac aneurysm repair in 154 patients: a relatively innocuous procedure. J Vasc Surg 2001;33:S27–32. 33. Anderson JL, Berce M, Hartley DE. Endoluminal aortic grafting with renal and superior mesenteric artery incorporation by graft fenestration. J Endovasc Ther 2001;8:3–15. 34. Chuter TA, Gordon RL, et al. An endovascular system for thoracoabdominal aortic aneurysm repair. J Endovasc Ther 2001;8:25–33. 35. McCann RL, Schwartz LB, Georgiade GS. Management of abdominal aortic graft complications. Ann Surg 1993;217:729–734. 36. Ohki T, Veith FJ. Endovascular grafts and other imageguided catheter-based adjuncts to improve the treatment of ruptured aortoiliac aneurysms. Ann Surg 2000;232:466–479.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART VIII Cerebrovascular Insufficiency

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery Anthony M. Imparato

Indications The ideal candidate for carotid endarterectomy, gleaned from the accumulated experience of the past four decades since Eastcott, Pickering, and Rob reported the first successful carotid operation for prevention of stroke (1), would be a normotensive individual without cardiac symptoms, younger than 70 years, preferably male, who had suffered one or more focal cerebral hemispheric transient ischemic neurologic episodes within the preceding 120 days and was found to have 70% to 99% stenosis of the appropriate ipsilateral internal carotid artery at its origin, in the absence of other intracranial or extracranial arterial lesions on cerebral angiography. The cerebral angiogram ideally should show that the involved cerebral hemisphere received its blood supply via the circle of Willis from the contralateral unaffected internal carotid artery and that the posterior communicating arteries were patent. Scans of the brain obtained by computed tomography (CT) or magnetic resonance imaging (MRI) should not show any sign of cerebral infarction. The patient should have tolerated daily aspirin ingestion of as much as 1300 mg, and would be expected to continue to tolerate it for the rest of his life, which should be at least 5 years. This patient would then have the procedure performed by a surgeon who performs at least 50 such operations per year with an operative mortality or neurologic complication rate of 1% to 3%. Unfortunately, few patients about to suffer ischemic strokes conform to the criteria described. Equally unfortunately, many strokes occur without warning symptoms, and once they have occurred it is usually impossible to reverse the ischemia completely and bring about full functional and anatomic recovery (2). One is faced, therefore,

with the need to detect which patients are at risk for stroke so that it can be prevented. That stroke can be prevented in symptomatic patients with severe carotid stenoses has been clearly demonstrated by three prospective multicenter randomized clinical trials of carotid endarterectomy (3–5). Though differing considerably in the manner of estimating carotid stenosis for randomization to medical or surgical treatment, they illustrated the essential facts that 70% to 99% diameter reduction of an ipsilateral internal carotid artery measured on a conventional biplane angiogram, ipsilateral to either focal hemispheric symptoms [transient ischemic attack (TIA), small stroke] or amaurosis fugax, surgically treated by endarterectomy as practiced by one of a number of participating surgeons, with 5.3% to 7.5% operative mortality and morbidity, resulted in marked reduction in follow-up stroke rates when compared with those of patients randomized to medical treatment that included aspirin. Improved results were strikingly apparent within 18 months of follow-up. The variations in presentation, which may markedly influence surgical risk and long-term outcome, are almost innumerable; therefore it is essential to determine what factors must be considered in evaluating individual patients for operations, as alternative nonsurgical and less invasive surgical therapies have been proposed (6–8) and may be especially useful in the treatment of patients not suitable for conventional operations (9,10). The factors that influence immediate surgical outcome can be classified as 1) the nature and extent of arterial pathology including the carotid plaque and the extent of carotid pathology; 2) the clinical condition of the patient, including both neurologic condition comprising functional state and nonneurologic factors such as age,

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sex, cardiac condition, and other vascular factors; 3) cerebral pathology; and 4) the experience of the surgeon. The factors that influence late outcome and disease modification can be classified as 1) specific therapy such as antiplatelet administration and cessation of smoking; and 2) modification of risk factors including hypertension, cardiac risk factors, and others. This chapter discusses factors influencing immediate surgical outcome. Late outcome and disease modification are beyond the scope of this chapter and so will be mentioned only in passing.

Nature and Extent of Carotid Pathology The Carotid Plaque The carotid bifurcation plaque, responsible for approximately 70% of all ischemic strokes, is found in various stages of evolution in both symptomatic and asymptomatic patients (11–13). In its least complex form it is composed almost entirely of fibromuscular intimal thickening, grossly pearly white with a smooth lumenal surface made up of flattened cells, probably transformed smooth muscle cells, forming a nonthrombogenic surface. Its characteristic location, best observed in early and intermediate stages of development, is at the lateral surface of the carotid bulb and origin of the internal carotid artery, where it may produce degrees of stenosis varying from barely perceptible to almost total occlusion. At this fibrous stage of development, symptoms occur probably entirely as the result of flow restriction, which, by causing marked stasis of blood, may finally end in thrombosis of the vessel. Referred to as “hard” plaque, it is sonaropaque and appears to pose lesser risks for symptoms to occur than do “soft,” sonar-lucent plaques, until occlusion occurs (14). Ulceration of the lumenal surface does not seem to occur at this fibrous stage. The “soft” sonalucent plaque contains either clotted blood or toothpaste-like atheromatous debris encysted within the walls of the original myointimal fibrous plaque (15–17). Histologic study of many such plaques suggests that intrafibrous plaque hemorrhage, which may occur repeatedly (18–20), degenerates gradually to form encysted atheromatous debris (11,12) and is quite different in appearance and location from the sometimes seen fat-laden macrophages that form seemingly innocuous neighboring fatty streaks. This soft plaque is associated more often with symptoms. It can enlarge rapidly and obstruct flow, ulcerate, and discharge its contents as embolic material to the brain, or accumulate thrombus and result in total occlusion of the vessel, thus threatening ischemia either through flow impedance or through embolization (21–24). Almost unobtrusively, many plaques are encountered that, though nonstenotic, have deep smooth craters devoid of thrombus, suggesting that they are the healed remains of soft plaques after encysted hemorrhage or atheromatous debris erupted into the vessel lumen. Although plaque regression has been de-

scribed based on decrease of plaque stenosis (25) as measured by ultrasound, at the carotid bifurcation this may well mean pathologic progression exemplified by embolization. From both pathologic and noninvasive sonographic studies of plaques, neurologic symptoms and stroke correlate not only with the degree of stenosis, which may impede flow, but also with the nature of the plaque, whether it be “simply” fibrotic or a “complex” compound plaque containing hemorrhage, atheromatous debris, or thrombus on an ulcerated, thrombogenic surface, characteristics predictable from the apparent severe degree of stenosis as well as from the echolucency on sonographic survey. To date, criteria for operability derived from the randomized clinical trials (3–5) are based on degrees of stenosis derived from biplane angiograms, a technique whose validity has been challenged on several counts. Carotid bifurcation plaques are of excentric configuration (11,12), so that minor variations in either the angle of the angiographic x-ray beam or the degree of rotation of the head and neck may produce significant variations in the measured degree of diameter reduction. In addition, the concept of determining diameter restriction has been questioned in favor of determining cross-sectional area by ultrasonography (26). Of equal consequence is the question of what constitutes “significant” stenosis, with estimates ranging from 30% diameter reduction to 85% (27–30). As the carotid plaque is the result of a sometimes rapidly evolving process and strokes frequently occur without warning, one must conclude that a minimum of 50% to 70% diameter reduction (75% cross-sectional area) by an echolucent plaque in the presence of symptoms characteristic of transient cerebral ischemic attacks, with no other detectable source of microemboli, constitutes an indication for operative intervention if no contraindications exist. Indeed, even in the absence of symptoms, operative intervention for that degree of arterial involvement is supported by two randomized clinical trials (31,32) and by several nonrandomized trials to be described (33–35), supporting the concept that precise determination of the nature of the pathologic process at the carotid bifurcation is the primary determinant of risk requiring correction to prevent strokes (36–38).

Extent of Carotid Pathology Carotid bifurcation plaques, conveniently for the surgeon, most often involve the area of the common carotid bifurcation extending only 1 to 3 cm into the origin of the internal carotid artery, beyond which the intima is uninvolved, to its intracranial segment, where it exits from the petrous bone, the siphon, where a second, usually smooth, plaque may be found. On occasion the internal carotid origin plaque extends above a line drawn from the angle of the mandible to the mastoid process, a configuration predictable from the appearance of the bifurcation, which then is quite low in the neck, resulting in a very acute angle at the common carotid bifurcation, between the internal and external carotid arteries. This creates a difficult prob-

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

lem of surgical exposure, increasing the risk of perioperative stroke. The plaque in the common carotid artery may be extensive and friable, well below the crossing of the omohyoid muscle, increasing the risk of embolization to the brain on application of occluding vascular clamps. Unilateral Carotid Involvement Unilateral and isolated carotid involvement presents the ideal pathologic lesion for surgical intervention because, unless there are major gaps in the circle of Willis, compensatory flow can occur during carotid clamping needed to perform endarterectomy. On occasion, however, even unilateral involvement may be associated with carotid clamping intolerance. Bilateral Carotid Involvement As with atherosclerosis elsewhere, paired vessels are usually simultaneously involved, although the extent of involvement may be bilaterally unequal. Most patients require only unilateral operations either for relief of symptoms or to deal with hemodynamically significant lesions. Bilateral operations, in some series, are done 10% to 25% of the time, for a variety of reasons including for relief of symptoms, or to correct hemodynamically significant contralateral lesions. One series reported the performance of staged bilateral operations based upon the stage of the pathologic process on th symptomatic side (39). If the symptomatic plaque was complex, containing hemorrhage, atheromatous debris, thrombus, or ulceration at operation, then endarterectomy was performed as well on the contralateral carotid artery if it appeared to cause 50% or more lumen diameter constriction on a biplane angiogram. This resulted in a threefold lesser incidence of late strokes in follow-up when compared with those who had had unilateral operations. The performance of bilateral operations is considered by some to be unnecessarily risky (40,41) although not found to be so in the series cited above. Indeed, simultaneous bilateral carotid endarterectomies have been reported with no apparent increase in operative complications (42). It would seem, however, that the risk and catastrophic consequences of producing bilateral cranial nerve injuries to the laryngeals, to the glossopharyngeals, and to the hypoglossals would far outweigh any potential benefits of simultaneous bilateral operations. Although the incidence of later stroke referable to the unoperated contralateral artery varies considerably in different surveys (43,44), it is essential to note that the decision to perform the contralateral operation in this author’s series (39) was based on the premise that not all carotid plaques become converted from simple fibrous to compound, complex ones, and that if such conversion occurs it is in response to particular factors inherent in particular patients, which may continue, unpredictably, to exert an influence upon plaque conversion from simple fibrous to compound complex. When bilateral markedly stenotic plaques are encountered, an order of precedence must be decided based on cerebral angiography. Unless one plaque is outstanding because of symptoms threatening early stroke,

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the concept of carotid predominance has been a useful guide (45). The carotid artery that supplies the contralateral hemisphere (the “predominant” or “major” artery) is susceptible to clamping intolerance. Therefore the nonpredominant or “minor” artery is operated on first, followed by operation one or more weeks later on the predominant artery, by which time the newly reopened artery may have assumed predominance, increasing the likelihood that clamping will be tolerated. When a balanced circulation is encountered with bilaterally severe stenosis, either or both may fail to tolerate clamping, precipitating the need for intraluminal shunting. Stenosis and Occlusion Stenosis opposite an occlusion requiring operation offers the greatest risks of clamp intolerance and creates the greatest risk of perioperative stroke (46,47). This may be due in part to intolerance to carotid clamping and in part to failure of the collateral circulation to compensate for operative complications that result in decreased cerebral perfusion, such as thrombosis at the site of endarterectomy, intracerebral embolization, systemic deficits in arterial perfusion pressure as from carotid sinus hypersensitivity, cardiac arrhythmias, myocardial infarctions, or drug administration. Operations in this cohort of patients may incur 10% to 15% operative risk requiring extraordinary measures beyond merely employing shunts routinely. It is essential, as well, to avoid hemodynamic instability, which, even in the presence of a patent intraluminal shunt, may predispose to stroke. Nevertheless, a number of strategies have been used to ensure safety of operations on stenotic carotid arteries opposite occlusions, ranging from operating on conscious patients with selective shunting (48) to the routine use of shunts under general anesthesia (49). Carotid Occlusion Internal carotid occlusion may occur as an isolated lesion in association with bifurcation plaques (50) or may be part of extensive thrombosis of the common and internal carotid arteries (51). The usual bifurcation plaque that progresses to total occlusion accumulates “flow thrombus” at the origin of the internal carotid, which may be limited to the proximal 1 or 2 cm of that vessel for as long as 1 month, or may develop “stasis” clot in the vessel beyond, extending a variable distance distally, and may eventually occlude the entire vessel to the first major branch, the ophthalmic artery. Though red in color, and initially gelatinous in consistency, and of fair tensile strength, easily separated from normal intima, it becomes friable, granular, and maroon in color after a few days, finally becoming organized to form a fibrous cord, attached to intima only by thin strands that can be easily broken, permitting its extraction. If thrombus and clot do not extend to the intracranial internal carotid artery, total occlusion can be relieved by routine endarterectomy and clot extraction. If, after the first 24 to 48 hours after formation of stasis clot, there is extension to the intracranial portion, restoration of unim-

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peded flow is possible in perhaps only 10% of patients. Reports of very high success rates with disobliteration of totally occluded internal carotid arteries usually refer to angiographic occlusions and fail to specify in detail the pathologic findings. In my experience, such cases reveal that anatomical occlusion has not occurred but that rather there is preocclusive stenosis, which masquerades as total occlusion both on various types of angiography as well as on ultrasound studies. Sufficient flow may be maintained to the internal carotid artery to prevent thrombosis with extension of clot to the intracranial segment. Total occlusion of the internal carotid artery creates a grave risk of later stroke if it has not occurred at the time of occlusion, and results in areas of brain that are marginally nourished and subject to serious functional and metabolic disturbances from even minor changes in arterial perfusion pressure (52). How then select patients for operation for complete occlusion? Duplex scans, MRI, and CT scans with or without rapid sequential imaging are techniques that will help to identify totally occluded internal carotid arteries that have patent segments beyond the bifurcation which permit restoration of flow. When the common carotid artery is occluded, the techniques enumerated will identify whether internal or external carotid branches or both are patent, thereby permitting reopening of totally occluded common carotid arteries (53). Intracranial Involvement: Siphon Lesions A doctrine was proposed as a result of the experience gained through the Joint Study of Extracranial Arterial Occlusion (JSEAO). Carotid bifurcation stenosis in association with a tandem siphon lesion of even greater stenosis did not merit operation and, if performed, might precipitate total internal carotid occlusion. Since then the dictum has been repeatedly challenged (54). In evaluating the reported experience with such tandem lesions, it is important to realize that nonflow-impeding lesions at the carotid siphon are frequently reported to be present by the neuroradiologist and appear as irregularities in the column of contrast medium. Pinhole preocclusive lesions, however, are much less frequently encountered, and these are the lesions that may create grave risks of carotid endarterectomy precipitating total internal carotid occlusion, and are therefore still considered by many to be contraindications to carotid endarterectomy. Noninvasive evaluation of carotid siphon lesions for their hemodynamic effects has been reported (55) and may help in more clearly defining a prudent strategy for management in the presence of such lesions. Extracranial Involvement Brachiocephalic Trunk Arteries The possible combinations of occlusive lesions of aortocranial arteries that occur in association with carotid bifurcation lesions number in the hundreds, yet relatively few studies contribute to an understanding of their role in the causation of is-

chemic strokes. Ulcerating lesions that could result in embolization to intracranial vessels are relatively infrequently recognized, though they do occur (56). Seemingly greater emphasis has been on hemodynamically significant lesions (57–59), on mechanisms that lead to symptoms, and on means of correction (60). When symptomatic carotid lesions occur in association with nonembolizing lesions of other brachiocephalic arterial lesions, the carotid lesions are dealt with first, and only if symptoms persist are other hemodynamically significant lesions corrected (61). Vertebral Artery Lesions Symptomatic lesions of the vertebral arteries are in most instances bilaterally flow obstructing, but only occasionally the source of emboli. A relatively small clinical experience compared with the experience with carotid arteries has justified the policy of correcting carotid lesions first when found in combination with vertebral lesions (62,63). Only if symptoms then persist is a unilateral repair of bilaterally involved vertebral arteries performed (64). External Carotid Artery Indications for primary endarterectomy of the external carotid artery for stroke prevention are not usually encountered. Its preservation as a part of carotid bifurcation endarterectomy and its role in serving as outflow for revascularized occluded common carotid arteries (65,66) emphasize its role as a valuable collateral pathway in the presence of internal carotid occlusion (67). Whether these maneuverscanprevent strokes from occurring is not clear. They may, however, serve to relieve eye symptoms, amaurosis fugax, occurring either from hypoperfusion or from microembolization and possibly transient cerebral ischemic attacks, although this is difficult to document except with narrative data (68).

Clinical Condition of the Patient Neurologic Condition Occlusive arterial disease of the cerebral circulation, which lends itself to carotid endarterectomy, manifests in a variety of ways. Some are typical and easily recognized, others are more subtle, frequently masquerading as nonischemic conditions. In part, symptoms are determined by whether ischemia results from either macroembolization or microembolization, usually from the carotid bifurcation, and in part through the occurrence of territorial or global ischemia secondary to major vessel obstructions for which compensation does not occur through collateral vessels, either because of gaps in the circle of Willis or because of multiple vessel occlusions. Symptoms may occur unexpectedly and suddenly from massive cerebral infarction causing catastrophic nonremediable stroke, or may be evanescent and sometimes difficult to recognize as of cerebral origin because of their focal and limited extent and duration. They may be rapidly recurring as from repeated embolization from even small carotid bifurca-

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

tion plaques. Transient symptoms may also occur with complete carotid occlusion and rapid alterations of arterial perfusion pressure related to cardiac events such as arrhythmias, myocardial infarctions, or valvular disorders. Symptoms may originate from the brain in the vertebrobasilar watershed, usually in association with a combination of carotid and vertebral arterial lesions. They may be difficult to characterize as to site of origin because of their diffuse nature, involving cognitive, ideational, and emotional functions. The severity of the pathologic process in the arteries is not necessarily reflected in the severity of symptoms or in the degree and extent of existing cerebral damage. Frank infarcts may present with minimal or no symptoms as may multiple occlusive or embolizing arterial lesions. The neurologic status therefore becomes a vital issue in selection of patients for operation, not only to attempt to recognize those who, with minimal or no symptoms, are at risk of suffering catastrophic stroke, but also to estimate operative risks as they relate to clinical status. Of equal importance is whether clinical improvement can be expected to occur in the presence of neurologic impairment. Of note in evaluating clinical status is the role of silent cerebral infarcts (69,70) detected on CT or MRI scans of the brains in patients who are asymptomatic, have suffered transient symptoms, or are minimally neurologically impaired. Patients to be considered for carotid endarterectomy therefore may present with acute strokes of varying severity at one end of a spectrum whose other end includes those who have no neurologic symptoms. Between these two extremes are a variety of symptom complexes that include transient symptoms with complete recovery between attacks (TIA), transient symptoms with increase in frequency, duration or severity (crescendo TIAs), stuttering progressive or waxing and waning symptoms with incomplete recovery (stroke in evolution), and an ill-defined syndrome of transient attacks with persistence of mild, temporary impairment beyond the 24 hours characteristic of the TIA (RIND). Of possibly equal consequence is whether evidence of cerebral infarction is detected by CT or MRI scans regardless of the neurologic condition of the patient. Functional Stroke Acute Stroke The first prospective randomized clinical trial of carotid endarterectomy, the Joint Study of Extracranial Arterial Occlusion (1962–1972) (2,62), established that carotid endarterectomy performed on patients who had suffered acute hemispheric strokes resulted in 40% mortality if conciousness was impaired, twice that observed in similar patients randomized to medical therapy. On the other hand, there were observed instances, since confirmed by other isolated reports (71), of dramatic reversal of major impairment following carotid endarterectomy in such severely afflicted patients. The conclusion of that initial study was that, for operative intervention to be effective, it had to be prophylactic,

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before major impairment had occurred. These observations, perhaps, spurred a number of surgeons to continue to investigate the feasibility of restoring neurologic function in patients with acute strokes (72) by revascularization of a large “penumbra” of ischemic, but not infarcted and therefore recoverable, brain surrounding the “umbra” of irrecoverable infarction. There are now reports, exemplified by that of Whittemore and Mannick (73), of series of patients with acute strokes subjected successfully to carotid endarterectomy if over a period of hours or days they achieve neurologic stability and are found to have appropriate preocclusive carotid lesions, even in the presence of small (1-cm) cerebral nonhemorrhagic infarcts on CT brain scans. Operations are done under general anesthesia with routine shunting during the phase of carotid clamping and careful blood pressure control, and immediate results are comparable to those of operations performed electively in intact patients. This strategy is in contrast to that used for some patients with profound neurologic deficits in whom emergency operations are performed in the face of severe neurologic dysfunction, but CT scans are persistently negative for infarction or hemorrhage, finding that are considered contraindications to operation (71). Strokes in Evolution, Crescendo TIAS Neurologic instability has appeared to worsen the risk of carotid endarterectomy. Strokes in evolution, in which neurologic deficit worsens during the ensuing hours or days after initial onset, indicate a poor prognosis both for survival and for neurologic recovery. Millikan (74) reported 14% mortality within 2 weeks of onset of strokes in evolution and only 12% complete recovery, while two-thirds remained hemiparetic. A number of reports referring to early operations in neurologically unstable patients collated by Rosenberg from five series indicated that 55% of operated patients improved while 10% died and another 10% worsened (75). Clearly, operative risk is greater than that in neurologically stable patients, but the prospect of complete recovery may be improved over that in nonoperated patients. A less severe type of neurologic instability, crescendo TIAs, in which symptoms abate between attacks of increasing frequency and severity of duration, has lent itself to successful early surgical intervention. In the Veterans Administration Symptomatic Carotid Endarterectomy trial, 12 patients with crescendo TIAs and severe carotid stenoses of 70% or greater reduction treated initially with intravenous heparin had urgent carotid endarterectomies, with no deaths and no neurologic deficits. Mean followup of 12 months indicated complete freedom from neurologic symptoms, leading to the characterization of crescendo TIAs as a “surgical imperative” (76). Although there are no recent randomized clinical trials to evaluate either operative results in neurologically unstable patients or criteria for selection of patients, for timing of operations, or for operative management, there is a trend toward operating more frequently in neurologically unsta-

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ble patients whose clinical courses indicate an otherwise poor prognosis. It would seem advisable, however, to avoid operations in semiconscious or unconscious patients in whom airway and nutritional problems compromise operative recovery. Equally to be avoided are operations during the acute phases of strokes on patients who have CT or MRI evidence of cerebral hemorrhage or who have massive infarcts. The risk of precipitating massive and fatal cerebral hemorrhage in patients with massive acute infarcts was reported by Blaisdell et al., antedating the era of CT and MRI cerebral studies. Unless a surgeon or an operating team has established a credible record of low complication rates (77–79) in operations on neurologically stable patients (1% to 5%) and is prepared to function according to a strict protocol to accurately define the population operated upon and to record accurately the mechanisms of possible failures, neurologically acutely afflicted patients should not be operated upon. The need for carefully controlled trials in the category of neurologically unstable patients is apparent (80). TIA or Amaurosis Fugax Three prospective multicenter randomized clinical trials (3–5) have conclusively established carotid endarterectomy as superior to medical therapy in patients who have suffered TIA or amaurosis fugax or minor stroke during the preceding 3 months in the presence of 70% to 99% stenosis of an ipsilateral carotid artery measured as lumen restriction on conventional angiography when performed with a combined mortality or neurologic complication rate of 5.2% and 7.2% for the two largest trials, the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) (2,3). The superiority of surgical treatment became apparent within 18 months of follow-up and was of increasing benefit as the degree of stenosis progressed from 70% to 99% (3). Stenoses of 0% to 30% were considered unsuitable for further randomization in view of the low event rate in the study groups, precluding the likelihood that meaningful statistical differences between medically and surgically treated groups would become apparent within the foreseeable future. The end points in the two largest studies were stroke, and the results are therefore considered “hard data,” literally applicable to the problem of stroke prevention. The long awaited results of the NASCET trial of carotid endarterectomy for symptomatic patients with intermediate, 30% to 69% stenosis, seem to point to a long suspected 50% stenosis threshold for advantageous carotid endarterectomy. When patients who had experienced ischemic symptoms on the same side as the operated stenosis within 180 days before entry into the study were stratified into two groups, one with less than 50% stenosis and the other with 50% to 69% stenosis, the stroke rates for both disabling and non disabling strokes in the 50% to 69% group were favorably influenced by carotid endarterectomy over medical therapy alone; 15.7% versus 22.2% for non disabling strokes and 2.8% versus 7.2% for disabling strokes. The investigators found surgical in-

tervention to be most beneficial in men who had suffered recent strokes with recent hemispheric symptoms and those taking 650 mgm. of aspirin daily. Only minimal and not significantly decreased risk of stroke was conferred by operation for less than 50% carotid stenosis (81). In a more recent review of randomized clinical trials, Barnett and Meldrom (82) conclude that with intermediate 50% to 69% stenosis by angiography and low operative risk, males with hemispheric non disabling strokes and appropriate lesions will benefit from carotid artery endarterectomy. On the other hand, patients with TIA or retinal symptoms alone, especially if female, will not benefit from operation with these intermediate lesser degrees of stenosis. Of particular interest is that some groups previously considered unlikely to benefit from operation are considered to be particularly at risk from medical treatment alone. These include symptomatic patients with associated intracranial stenoses, with extensive white matter lesions, with lacunar syndromes, with intralumenal carotid artery thrombus and those with poor collateral circulation. Good long term results occurred with carotid endarterectomy irrespective of age if those with advanced cardiac disorders are excluded. These studies validated the observations by a number of other investigators, among them Hertzer and colleagues (33), who reported similar beneficial results of surgically versus medically treated symptomatic patients with a considerably lower operative complication rate, more representative of what has been achieved by a large number of experienced surgical groups (47,83–85). In the selection of patients for operation according to the criteria established by the aforementioned studies, questions have been raised regarding the validity of adhering to the fine dividing line between 69% and 70% diameter restriction on biplane angiography without critically establishing the ranges of errors of measurements among different observers and among different views of the same arteries. The issue of establishing the significance of diameter reduction as opposed to crosssectional area reduction, as proposed by Alexandrov et al. (26) and discussed by Barnett (86), is another, at present unresolved, problem. The validity of considering the degree of stenosis as a criterion of operability is apparent not only from the flow restriction produced, but also from the correlation between degree of stenosis and the severity of the pathologic process apparent even on gross inspection of carotid plaques in situ at operations (18). Another observation that may indicate the severity of the pathologic process in instances of questionable indication for operation based on stenosis as defined above is the nature of the plaque on ultrasonography (15,16,87), which differentiates hard fibrotic plaque from soft blood clot or fat-laden plaque. Asymptomatic Patients Many series of reported results of carotid endarterectomy include as many as 50% of the patients as “asymptomatic,” a group selected for operations usually because of the findings of “significant”

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

carotid stenosis, a criterion poorly defined as it derived using a variety of techniques that include conventional biplane angiography, sonography (duplex scanning), and variations of contrast radiography, including intravenous and intra-arterial contrast ministration. The protocol of the Veterans Affairs Cooperative Study Group on the Efficacy of Carotid Endarterectomy for Asymptomatic Carotid Stenosis (31) indicated that patients be screened for carotid stenosis by duplex scans of the neck. If these were indicative of 50% or greater stenosis and were followed by confirmatory conventional biplane angiography, they led to randomization for operation or for medical therapy. End points were TIA, stroke, or death. Five-year follow-up after operations performed with a 5.5% serious complication rate revealed definite improvement in combined TIA and stroke rate, but only a trend for improvement for stroke alone as an end point, ascribable to the too-small population sample. No mention is made of the character of plaques on sonography. This study, though criticized adversely for its “soft” end points, needs to be evaluated on the basis of the significance of TIA in predicting future stroke occurrence, and in how well other carefully controlled nonrandomized studies conform to its reported results. The ominous implication of TIAs, argued and estimated differently by different observers (88–90), has most recently been emphasized by both the NASCET and the ECST trials (3,4) to be worse than frequently calculated. This can probably be attributed to the fact that these later studies estimated stroke risk only in patients with advanced carotid lesions and TIA and not in groups suffering TIAs from one of a variety of causes as had often been reported. These findings further emphasize the primacy of carotid plaque in determining stroke risk and the need for operation. The reports of Thompson et al. (33) and Hertzer et al. (34,35) attesting to the beneficial effects of carotid endarterectomy for marked carotid stenosis in asymptomatic patients appear now to have been validated by the recently reported results of the Asymptomatic Carotid Endarrterectomy Study (ACAS), which found that the aggregate risk reduction for stroke and death when carotid endarterectomy was performed as part of a prospective randomized clinical trial in patients with “hemodynamically significant” asymptomatic carotid stenosis was 53% after a median followup of 2.7 years. Hemodynamic significance was defined as 60% or greater diameter reduction, calculated as the ratio of the minimal residue lumen over the distral lumen (1 - [MRL/DL] ¥ 100) from an angiogram, or as estimated from specific findings on ultrasonography. These results confirm the previously mentioned findings of other nonrandomized clinical studies, emphasize the danger of advanced carotid bifurcation atherosclerosis even in asymptomatic patients and raise the challenge of how best to detect these lesions before they cause devastating strokes (32). On the other hand, in the previously cited reference to Barnett and Meldrum (82), appears an opposing view that serious doubt exists regarding the advisability of operating upon asymptomatic patients since even with the upper

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limit of 3% operative risk from carotid endarterectomy, cited as a desirable upper limit of acceptable risk, 111 patients would have to be subjected to CAE to prevent one large artery stroke in 5 years. Although the terms “scientific” and “unscientific” are used by some to characterize some studies as opposed to others, all existing studies suffer from the fact that certain determinations such as duplex scans are markedly technician dependent and not reproducible, and that there is not a full understanding of what particular measurements of arterial stenoses signify in terms of arterial and brain pathology. Rigid classifications as symptomatic versus asymptomatic, for example, are based upon the reports of untrained observers (patients) who monitor their neurologic wellbeing for only a portion of each day (while awake) in disregard of the facts of arterial and brain pathology determinable by methods more apt to yield reproducible results (91). Though much is made of the randomization process as a means of securing accurate, reproducible, and convincing data, the Carotid Surgery versus Medical Therapy in Asymptomatic Carotid Stenosis (The Casanova Study Group) trial of carotid endarterectomy, which reported no beneficial effects of carotid endarterectomy in asymptomatic patients (92) has been severely criticized for a number of protocol defects that render its results uninterpretable. Patients with 90% or greater stenosis of carotid arteries were excluded for randomization. Those with bilateral carotid lesions of unequal degrees of stenosis, operated electively for their markedly stenotic lesions, were then included in randomization to medical treatment to serve as controls. As early as 1998, Kusey, Bowyer et al. (93), following their evaluation of the determinants of outcome after carotid endarterectomy and how to generalize the results of various clinical trials to average surgical practice concluded that although adoption of the recommendations of the symptomatic endarterectomy trials was appropriate, endarterectomy for asymptomatic patients was of uncertain benefit on a regional basis and should be individualized to the experience of individual surgeons. Indeed some reported series indicate that operation rates for asymptomatic patients can be as low as 1% (94). Established Strokes “Established stroke” may refer to a wide spectrum of clinical conditions ranging from dense, unremitting hemiplegia without appreciable recovery to less severe impairment with lesser degrees of persistent deficits weeks to years after an acute event. An almost bewildering variety of combinations of arterial lesions may be found in such instances, ranging from inoperable occlusions that cause marked impairment of cerebral blood flow to minor stenoses that may have been the site of origin of cerebral emboli. Available data are narrative. Revascularization weeks to months after a major neurologic deficit has been incurred cannot be expected to restore function; therefore the justification for surgical intervention, other than feasibility, should be that mortality and further morbidity can be postponed or prevented in stricken patients who are “functional.”

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The accumulated experience with carotid endarterectomy in patients with residual neurologic deficits pertains to those with mild to moderate disturbances, those with hemiplegia and aphasia having been excluded from consideration for operations. Carotid endarterectomy in such patients is reported to definitely decrease long-term neurologic deterioration from recurring strokes when compared with similar not operated patients, and to have a perhaps negligible effect on survival. Operative complication rates can be expected to be somewhat higher than in neurologically intact patients, but are otherwise acceptable (95–97). The timing of operations in patients was established when Whittemore and Mannick (73) successfully operated on patients as soon as neurologic stability had been achieved (within hours to days), but Giordano et al. report that operation during a critical 5-week period after stroke is associated with a nearly one in five incidence (18.5%) of marked worsening or death (98). Nonfocal Symptoms in Neurologically Intact Patients Although much attention has been devoted to the study and treatment of ischemic syndromes clearly due to cerebral hemispheric origin, relatively little has been directed at those that are either nonlocalizing or are related to the basivertebral circulation. As with cerebral hemispheric disorders, the extracranial lesions may be single or multiple and are often amenable to surgical correction, which if successful may result in marked improvement in cerebral circulation through the remarkable circle of Willis. Basivertebral Symptoms Nonlocalizing symptoms such as dizziness, syncope, and vague sensory disorders, which occur frequently in the aged without specific arterial lesions, may on the other hand occur in association with occlusive lesions of the vertebrobasilar arterial system, just as the “classic” symptoms of posterior fossa circulatory insufficiency, symmetrical motorsensory disorders, diplopia, and dysarthria can. Often these symptoms occur in combinations of arterial lesions that include carotid lesions amenable to endarterectomy. Patients referred for correction of lesions for these classes of symptoms appear to be suffering from regional flow disturbances, rather than from microembolization, so it is not surprising that correction of usually severely stenotic carotid arteries, if present, has often resulted in relief of these symptoms (63,99). There remains, however, a group of patients with nonhemispheric symptoms, sometimes clearly of posterior circulatory origin, whose symptoms persist after correction of carotid lesions, who then experience relief after correction of usually paired unilateral, surgically accessible vertebral arterial lesions (64,100). Other Nonlocalizing and Localizing Symptoms Although gradual deterioration of intellectual function is often ascribed to aging, and conditions such as Alzheimer’s disease are not ordinarily thought to be associated with specific vascular lesions, any surgeon who has performed large

numbers of carotid endarterectomies has of necessity been impressed with a small but definite cohort of patients whose intellectual functions have improved during follow-up after carotid endarterectomy for severely stenotic carotid lesions. Deteriorated personalities have largely recovered, and job performances have improved as well, as reported by coworkers. Multi-infarct dementia is now recognized as such and is ascribable to lesions in the cervical arteries. There is growing interest in developing criteria for the diagnosis of vascular dementia in the hopes of forestalling what has appeared to be the inevitable consequences of aging by correcting accessible occlusive arterial lesions (101). Similarly, there is growing interest in more clearly defining the entity of “lacunar ischemia” to ascertain whether there is a cohort of patients whose symptoms derive from microembolization from the carotids or whose symptoms, often presenting as TIAs, might influence the outcome of clinical trials of carotid endarterectomy (102,103). The issue is perhaps partially resolved by the conclusions of Barnett and Meldrum (85) that lacunar syndromes at presentation respond to carotid endarterectomy but with less benefit than can be expected from operation in some other groups.

Non-neurologic Factors Age Although age is heavily weighted in evaluating patients for operative procedures, it has become apparent that age itself need not be considered a contraindication to carotid endarterectomy. Conditions that are found with greater frequency in patients of advanced years, in the eighth decade of life and older, such as coronary artery disease, chronic obstructive pulmonary disease, cancers, and diabetes mellitus, are the determinants of operative risk in general. Therefore, estimation of surgical risks in octagenarians and older individuals should be with reference to specific risk factors other than age. Long-term results of operations achieved with a somewhat higher perioperative complication rate justify surgical intervention for threatened stroke. When one considers the devastating effects that even relatively minor neurologic impairment imposes on the quality of life of the aged, it is evident that the concept of long-term outcome must be viewed from a different perspective from that for younger individuals (104,105). Coronary Artery Disease The concurrence of coronary and carotid artery disease has been frequently convincingly documented as has the impact of one upon the other in the operating room. Riles et al. found an 8% myocardial infarction rate in patients undergoing carotid endarterectomy under local anesthesia if artificial elevation of blood pressure with vasopressors was used (106). Ennis et al. reported that 13% of 77 patients with severe heart disease undergoing carotid

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

endarterectomy suffered acute myocardial infarctions (107). Even in the absence of clinical symptoms, 14% of patients without cardiac symptoms considered for carotid endarterectomy had angiographic evidence of severe operable coronary artery disease. Conversely, patients undergoing coronary artery bypass surgery have variable stroke rates that range between 2% and 15.6%, depending upon the patient population. Brener et al. reported that patients without carotid disease had less than 2% stroke rate related to coronary surgery while the risk increased to 4% to 5% for unilateral or bilateral stenoses and 15.6% for unilateral carotid occlusion (108). In the absence of coronary artery disease, for which patients must be screened in one of a number of ways, carotid endarterectomy can safely be performed with minimal cardiac risk. Patients with severe coronary artery disease manifested by unstable angina, recent acute myocardial infarction, low left ventricular ejection fractions, markedly positive stress tests, left main coronary stenosis, or “triple vessel disease” require particular consideration for how to manage symptomatic or severely stenotic carotid disease. Strategies range from performing both operations at the same operative session, with neurologic complication rates that range from low to as high as 9.5%, to attempting to “uncouple” the procedures by operating on the more threatening procedure first, except in cases of the most severe coronary artery disease, as defined, when combined procedures are done. As examples, Ivey (109) screens patients with ischemic heart disease and neck bruits with carotid duplex scans. He recommends coronary artery bypass first in patients who have 80% or greater carotid stenosis and, at a later date, carotid endarterectomy, since the incidence of stroke in this group without carotid operation is 35% within 6 months. Patients with stable angina pectoris and symptomatic carotid artery disease are subjected to angiography and carotid endarterectomy with delayed coronary artery bypass surgery. Simultaneous coronary artery endarterectomy and bypass graft were performed when both cerebral and cardiac symptoms were severe, when symptomatic carotid artery disease was associated with left main coronary artery stenosis, or when triple coronary artery disease was associated with left ventricular dysfunciton. Brener follows a similar protocol, based on his study of 4047 patients undergoing cardiac surgery over a 7-year period during which a number of carotid studies were performed prior to performing heart surgery (108). He reported that 9.2% of patients with greater than 50% stenosis diameter reduction suffered a combined neurologic complication rate (TIA and stroke) after heart operations as opposed to a 1.9% incidence in those with less than 50% carotid stenoses, 15.6% in those with inoperabele occluded carotids, and 7.4% in those with operable stenotic lesions. Combined operations resulted in an 8.8% neurologic complication rate, leading to the decision to perform combined operations very selectively only

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in those with symptomatic carotid disease and severe coronary artery disease. As combined operations may result in a higher than acceptable neurologic complication rate, and carotid operations under general anesthesia result often in a high cardiac complication rate, an alternative approach has been suggested: namely, to perform carotid endarterectomy when indicated by the severity of the carotid stenoses or the threatening nature of carotid symptoms under local or regional block anesthesia, avoiding the use of vasopressors, except to maintain arterial blood pressure, rather than to artificially elevate it. This approach appears to minimize cardiac risks of carotid endarterectomy, permitting “unbundling” of the two procedures except in instances of severe left main coronary artery stenoses, in which the risk of sudden death is ever present, or when crescendo angina is so alarming that even a few hours’ delay in performing cardiac surgery could prove fatal, in which cases combined operations might be indicated despite increased neurologic risk (110–112,113b). Realizing the need for further clarification of the indications for combined versus staged operations in the presence of clinically significant carotid and coronary arterial occlusive disease, Ricotta et al. review past operative results and conclude that randomized clinical trials of combined versus staged surgical procedures are warranted, in which patient cohorts are defined on the basis of recognized risk factors for both cerebral and myocardial ischemic events, for example, smoking, hypertension, diabetes mellitus, left ventricular, hypertrophy, prios cerebrovascular events, etc. (113a). The need for such studies seems justified on the basis of the lack of unanimity regarding outcomes in series reporting results of combined operations. Carotid Artery Disease and Other Operations Although the incidence of stroke associated with operations other than for coronary artery disease is quite low, their prevention is desirable if accomplished with minimal mortality and morbidity. Patients who have symptomatic carotid artery disease can be evaluated on the basis of neurologic status and degree of stenosis of the carotid arteries as described. Problems arise in attempting to discover, evaluate, and treat patients who are asymptomatic but who nevertheless have “significant” carotid artery disease. No randomized clinical trial of carotid endarterectomy in patients proposed for unrelated major operative procedures has been completed, although such a cohort was included in the protocol of the Veterans Affairs Cooperative Study Group (31). That phase of the study could not be completed because of insufficient patient accrual. For patients in the atherosclerotic age groups, however, just as screening is done for coronary artery disease, renal function, and a number of other risk factors, screening for severe carotid artery disease seems logically to be indicated and can be done noninvasively by duplex carotid scans. Preocclusive lesions (>75% stenosis) can then be evaluated by angiography, or MRA and comparative

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risks of the operative procedures contemplated can be estimated. When major hemodynamic aberrations such as might occur during abdominal aortic aneurysm operations are anticipated, preliminary carotid endarterectomy should be considered. On the other hand, when hemodynamic instability is unlikely to occur (laparoscopic cholecystectomy), the more pressing or symptomatic procedure might be performed first. In emergency situations such as impending rupture of abdominal aortic aneurysms, preoperative screening for asymptomatic carotid artery disease is unlikely to be fruitful (114–116).

Cerebral Pathology It has become apparent that selection of patients for operation on the basis of clinical criteria by which to estimate surgical risks and predict long-term outcome and functional recovery has marked limitations. Regional hemodynamics and the state of health of ischemic neurones, whether suffering from completely reversible metabolic deficits or having already undergone irreversible structural changes even in the presence or absence of symptoms (117), are vital issues that require investigation and understanding to further refine and improve management. As an example, in a series of intracerebral hemorrhages after carotid endarterectomy, 10 of 11 patients so afflicted had merely had TIAs as their presenting symptoms, a cohort representative of more than one-half of the patients operated upon, and had no distinguishing characteristics other than that severe carotid stenoses had been surgically corrected 11 days earlier (118). Scans obtained by CT, MRI, and positron emission tomography (PET), and perhaps other parameters of brain physiopathology, would be needed to identify patients at risk of suffering this most serious of consequences from an otherwise seemingly successfully performed operative procedure. The selection of patients with severe acute neurologic deficits for surgical correction of severe carotid stenoses with the prospect of inducing complete or almost complete recovery of function remains a major challenge three decades after the participants in this JSEAO attempted and occasionally succeeded in achieving this result, but at a cost of a high operative mortality. For the present, the suggestion that a persistently negative CT scan in the presence of severe and extensive symptoms identified the patient suitable for attempting to reverse the course of catastrophic stroke rests on sparse data. The CT scan characteristically may not register severe cerebral damage for many hours after the onset of symptoms and therefore either may mislead the surgeon to operate or may cause a reversible situation to become irreversible while awaiting an appropriate time lapse to establish the validity of the test. Whether or not MRI or PET scans will add clarity remains to be determined.

Techniques Carotid endarterectomy, the single most commonly performed operation in many busy vascular surgical services,

is unique. It is predominantly prophylactic, performed on patients with often severe coronary artery disease, in an anatomic area crowded with vital structures of great functional significance, requiring interruption of blood supply to the organ in the body most sensitive to ischemia, to remove often friable atherosclerotic plaque whose location and distribution are predictable and stereotyped, leaving behind a large area of thrombogenic collagen exposed to flowing blood, to then act as a long-lasting vascular conduit to an organ whose incomparable complexity defies full recovery once damaged. A successfully performed operation requires strict adherence to a set of principles aimed at avoiding a number of well-defined operative complications, any one of which can destroy the effectiveness of the procedure. The complications to be avoided are 1) cerebral clamping ischemia, 2) cerebral embolization, 3) operative site thrombosis, 4) hyperperfusion including cerebral edema and hemorrhage, 5) myocardial infarction, 6) cranial nerve palsies, and 7) delayed restenosis or occlusion. The first four mechanisms listed above can be incriminated in 80% of the neurologic complications encountered in a large series of patients operated upon under local or cervical block anesthesia, and occurred in equal frequency, each accounting for an 0.5% incidence of neurologic events, nearly two-thirds of which were transient, the remainder permanent. The remaining 0.5% of events could not be accurately diagnosed as to mechanism (47). The particular maneuvers used by different vascular surgeons to avoid the complications listed differ sometimes so markedly as to seem contradictory. For this reason, the description of techniques will emphasize avoiding complications, and finally detail the technique used, with only slight modifications, by the author and his associates for the past three decades, with a neurologic complication rate (major and minor) and mortality in a mixed population of high- and low-risk patients consistently below 3.0%.

Cerebral Clamping Ischemia The design of the intracerebral circulation, with its circle of Willis, was seemingly to ensure adequate total cerebral blood flow from any one of the extracranial cervical arteries. Its execution, however, has resulted in various gaps in the circle through defects or absences of various communicating arteries that complete the circle, as occurs in 30% of humans even without arterial occlusive disease (119). Nevertheless, although Boysen recorded a reduction of regional hemispheric blood flow per 100 g/min from 51 to 30 mL using intra-arterial 133Xe following carotid clamping under general anesthesia (120), Imparato et al. reported that only 7% of conscious patients developed neurologic symptoms on carotid clamping (47). Sundt et al. detected a 26.7% incidence on electroencephalograms (EEG) of severe abnormalities requiring shunting on carotid clamping under general anesthesia (121). When cerebral ischemia occurs, signs may appear within seconds of application of clamps (8 to 30 seconds under local anesthesia and on EEG), and recovery is equal-

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

ly prompt on their removal or on restoration of flow through temporary inlying shunts. The longest duration of total ischemia compatible with complete recovery in humans is not known (122) but may be as short as 2 to 5 minutes, in any event much too short to permit the completion of a well-performed carotid endarterectomy. The problem is complicated by the fact that unilateral carotid endarterectomy rarely results in total ischemia because some circulation is usually maintained through collaterals, and only when regional flow is decreased 64% to 18 mL/min/100 g do EEG signs of cerebral ischemia appear (120). Recognition of this problem led to a variety of monitoring techniques aimed either at detecting signs of cerebral ischemia or at critical lowering of cerebral blood flow, as well as techniques to either correct or prevent this ischemia. No generally agreed upon strategy to deal with it exists, with proponents of different approaches citing low neurologic morbidity and mortality results of carotid endarterectomy to support their preferred techniques. Comparably excellent results have been reported using a variety of approaches. No strategy, however, except operating upon conscious patients to permit differentiation of clamping ischemia from intraoperative microembolization ischemia, plus exhaustive diagnostic measures aimed at elucidating the probable mechanism of a neurologic deficit, avoids the need to make presumptive rather than definitive diagnoses of the mechanisms of perioperative strokes under general anesthesia, regardless of what monitoring or protective measures are used (123) (Table 66.1). Conscious patients who do not tolerate carotid clamping do not appear to tolerate any additional ischemia, as evidenced by the fact that increasing the interval of clamping intolerance ischemia even seconds beyond when either consciousness is lost or neurologic deficit occurs, markedly and disproportionately increases recovery time. In this group of clamp-intolerant patients identified under local anesthesia, but not identifiable under general anesthesia except possibly with EEG (124–126), shunting techniques require that ischemia times for shunt insertion and removal be minimized. Most conscious patients who TABLE 66.1 Summary of monitoring and protective measures to deal with clamping ischemia Monitoring Direct Conscious patient EEG Evoked potential response Indirect Carotid stump pressure Transcranial Doppler ultrasound Cerebral arteriovenous oxygen Jugular venous oxygen Protective measures Metabolic General anesthesia Hypothermia Hemodynamic Artificial hypertension Carbon dioxide inhalation or carbonic anhydrase Mechanical Intralumenal shunts

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have not tolerated internal carotid clamping have tolerated isolated common carotid clamping, the internal and external carotids left open to each other. Based on this fact, a technique for reversal of the usually recommended sequence of shunt insertion (i.e., internal insertion followed by common insertion) has been used and will be described. An added advantage of the technique is that free flow from the common carotid through the shunt can be verified before the internal carotid is clamped, only then commencing ischemia time. In 10 patients highly intolerant to internal carotid clamping while awake, common carotid clamping alone was tolerated. When the shunts were inserted into the common carotid artery by the technique described, they became filled with debris, requiring extension of the arteriotomy proximally in the common carotid artery, adding another 20 to 35 minutes to operating time. During this extended interval, they remained neurologically intact, apparently because of retrograde flow from the external to internal carotid artery. Had all vessels been clamped for shunt insertion, as usually recommended, clamping ischemia times of 20 to 35 minutes would have occurred in patients ischemic on initial application of internal carotid clamps for only 8 to 30 seconds. Monitoring of the neurologic status of conscious patients undergoing carotid endarterectomy was adapted by the author over four decades ago, originally as a means of evaluating monitoring and protective techniques as they were described through the years. No monitoring technique correlated well with the neurologic status of conscious patients. Electroencephalography, though a direct evaluation of the status of the status of the brain, reflects brain surface abnormalities and has been found wanting for a number of reasons, including failure to reflect ischemic changes and difficulty in interpretation in the presence of preexisting neurologic deficits. Depending upon the variable criteria empolyed to determine the need for intraluminal shunts under general anesthesia, it may lead to as high as a 20% to 25% incidence of intraluminal shunting. The incidence of shunting in a similar population of conscious patients is only 7%. Yet EEG has been quite successfully used to monitor CAE, most recently reported by Pinkerton et al. (128), who relied on EEG to limit shunting in their patients. Evoked potential response as a means of monitoring the activity of the brain during carotid endarterectomy is a refinement that has been relatively recently introduced. It is reported upon by a few surgeons who describe some of its drawbacks, including the fact that responses are affected by change in head positions, by temperature variations, and probably by a number of other conditions that have not yet been completely elucidated. Considerably more experience with the technique is required before its usefulness and drawbacks will be completely known (127,130), as is true of transcranial ultrasonography (129,131,132). Carotid stump pressure, used for nearly three decades by some, has been found to poorly reflect regional ischemia in conscious patients, so that pressures of 70 mmHg have been recorded in severely compromised patients rendered so by carotid clamping, and pressures as

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low as 20 mmHg have been observed in clamp-tolerant patients. In addition, the measurements are made at the outset of carotid clamping and so do not reflect the hemodynamic or airway changes that can occur during operation, which could result in cerebral ischemia, otherwise undetected under general anesthesia. Correlations between stump pressures and EEG findings are relatively poor (133–135). Protective measures resulting from decreasing cerebral metabolism by administration of general anesthesia (136,137) or induction of hypothermia (138) are difficult to document for the patients undergoing carotid endarterectomy who are intolerant of carotid clamping, and so are rarely relied upon. Induction of hemodynamic changes in cerebral circulation by induction of hypercarbia, either with carbon dioxide inhalations or by administration of carbonic anhydrase inhibitors (Diamox), to produce cerebral vasodilatation have not been shown to be effective, and this failure is explained by the fact that nonischemic brain rendered hyperemic by gengeralized hypercarbia competes with the already hypercarbic, vasodilated ischemic brain, further enhancing ischemia (139,140). Hypertension artificially induced with drugs during carotid clamping is the only pharmacologically dependent technique that has converted patients from intolerance to carotid clamping to tolerance. Elevations to well over 200 mmHg may be required to do so. Hypertensive agents increase the intraoperative incidence of acute myocardial infarction eightfold and so are not used (106). Well-functioning intralumenal shunts (141,142) are the most reliable devices that correct clamping cerebral ischemia. They can interfere with performance of carotid endarterectomy through long arteriotomies under direct vision to obtain unobstructed visualization of the entire operative site. Shunts may act as conduits for emboli originating in the common carotid artery. Placing shunts in the manner usually described—internal limb first, common limb second—may not only predispose to embolization but also unduly prolong ischemia time in the 7% or so of patients who tolerate less than 1 minute of ischemic time before developing signs of severe cerebral ischemia. The alternative technique to be described is preferred, when used selectively.

Cerebral Embolization Cerebral embolization from the operative site is often presumptively and probably erroneously cited as the most common cause of neurologic deficits encountered upon awakening from general anesthesia after carotid endarterectomy, since most surgeons either monitor for or protect against clamping ischemia, and a number of “control series” (46,142) attest to the safety of carotid clamping except in certain defined instances, notably when stenosis opposite occlusion is the operative indication. Embolization may occur at any phase of the operation. During dissection of the carotid bifurcation, small or large

aggregates may be dislodged from the frequently ulcerated carotid plaque unless precautions are taken to occlude the outflow by application of vascular clamps to the internal carotid artery beyond the distal end of the plaque before completing the exposure of the carotid bulb. Occluding clamps applied to the common carotid artery similarly may dislodge debris, prevented by clamping well below the friable portion of the plaque using the omohyoid muscle as a landmark, clamping at or below the lower border of that muscle, or clamping at an even lower site if indicated by the preoperative angiograms. Loose shreds of tissue, usually bands of smooth muscle of the media, may be dislodged as emboli unless the endarterectomy site is made smooth by removing the grossly visible circular bands of smooth muscle, leaving behind a smooth, glistening surface devoid of circular striations. This maneuver also helps prevent the trapping of platelet clumps that may embolize, a complication further protected against by the preoperative administration of aspirin and by liberal irrigation of the operative site to remove the red stasis clot, which may deposit at the endarterectomy site during arteriotomy closure in spite of systemic heparinization. A third critical phase when embolization may occur is at removal of vascular clamps, when emboli may be dislodged from any of the aforementioned sites. A routine of flushing all vessels into the operative site before final closure of the arteriotomy and of restoring flow to the internal carotid last helps to protect the brain from embolization. During the early postoperative period, thrombi may form at any of the previously clamped carotid sites and embolize, a complication difficult to guard against except by applying clamps to relatively normal segments of carotid arteries, by liberal flushing prior to final closure of the arteriotomy, by intraoperative heparinization without heparin neutralization at the conclusion of the operation, by aspirin administration preoperatively, and by constructing a free-flowing carotid system. Detection of potential sites for embolization intraoperatively requires visualization of the entire endarterectomy site, performing intraoperative completion angiography or inspecting sonographic images. Microembolization may be impossible to detect may but be suspected when a neurologic deficit is noted after the postendarterectomy patient wakens. By performing intraoperative transcranial Doppler monitoring, it is possible to detect cerebral embolization of even minute particles whose clinical significance is not always apparent (144–146). EEG may not reflect the ischemic brain produced by small emboli under general anesthesia. Embolic ischemia can be differentiated from clamping ischemia in the conscious patient. Removal of clamps or restoration of flow upon the appearance of a neurologic deficit from clamping ischemia results in prompt recovery, while embolic ischemia persists either for some time after restoration of flow or permanently. “Silent” embolization may be detected on ophthalmoscopic examination, said to reveal this phenomenon relatively frequently following carotid endarterectomy.

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

A pathway for cerebral embolization exists through temporary inlying shunts used either routinely or selectively in patients who exhibit ischemic symptoms on carotid clamping. The technique usually recommended for shunt insertion involves placing the shunt in the internal carotid artery first, flushing retrograde to remove air, then inserting it into the common carotid, a sequence that does not permit flushing debris from the sometimes abnormal common carotid artery, thus permitting cerebral embolization to occur. The technique for shunt placement to be described reverses the order of shunt placement, accomplishing two aims: it minimizes the possibility of embolization while markedly decreasing the ischemia time required for shunt insertions.

Operative Site Thrombosis Operative site thrombosis may occur in the absence of symptoms, may cause only transient ischemic neurologic deficits, or may precipitate catastrophic stroke and death. Neither the mode of onset of symptoms and signs, which may be present on awakening from anesthesia, nor duration indicates that operative site thrombosis has occurred. Mechanisms leading to thrombosis usually result from technical errors such as incomplete removal of plaque, from ledges or intimal flaps in the internal carotid artery at the distal termination of the endarterectomy, from uncorrected kinks of the internal carotid artery that become accentuated following endarterectomy, from stenosis produced by primary arteriotomy closure, from posterior wall buckling caused by too short a roof patch for the length of the arteriotomy, from stasis clot forming in the isolated endarterectomized segment during arteriotomy closure, due to inadequate heparinization, insufficient flushing, or from insufficient irrigation of the endarterectomy site just prior to final closure of the arteriotomy. A so-called white clot is composed mainly of platelet aggregates possibly induced paradoxically by heparin (143), perhaps preventable by preoperative aspirin administration. Its formation is favored by leaving multiple partially raised circular bands and strands of smooth muscle media at the endarterectomy site. As the thrombosed vessel can be reopened and the mechanism precipitating thrombosis corrected, reexploration of the operative site is usually indicated upon detection of an early neurologic deficit. Delay beyond 1 or 2 hours may result in permanent neurologic damage. Undetected chronic asymptomatic occlusion may predispose to late stroke. Prevention of operative site thrombosis requires attention to details of technique that lead to a smooth endarterectomy site and to correction of kinks (147). When long arteriotomy incisions to permit inspection of the entire endarterectomized segment and adjacent areas of intima in the common and internal carotid artery are not used or an inlying temporary shunt prevents such inspection, completion angiography or ultrasound scan of

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the operated segment should be performed and technical errors immediately corrected.

Hyperperfusion: Cerebral Edema or Hemorrhage When a relatively ischemic area of brain distal to marked carotid stenosis is revascularized by carotid endarterectomy, transient hyperemia results, apparently owing to loss of intrinsic vascular reflexes. It may last 24 to 72 hours and cause a spectrum of symptoms ranging from mild to severe headache, or periodic lateralizing epileptiform seizures due to cerebral edema, or coma, and in the most severe cases, death from intracerebral hemorrhages (118,148,149). Hemorrhages may occur anytime between the first and tenth postoperative days (mean 3.3 days), the common denominator in all cases being that a successful operation was performed to relieve either total occlusion or severe stenosis of the internal carotid. Hypertension, systolic pressure over 200 mg Hg, is recorded in only about half the cases. Evidence of frank cerebral infarction, long thought to be a prerequisite for this most severe manifestation of hyperperfusion, is only occasionally recorded. Mortality ranges from 36% to 60%. One report indicates that craniotomy and evacuation of intracerebral hematoma may increase survival but not necessarily improve neurologic recovery (118). For less severe forms of hyperperfusion, anticonvulsants and antihypertensive agents are used to control symptoms. Although the incidence of cerebral hemorrhage varies considerably in different series and at different times for unknown reasons, it is universally recommended that postoperative hypertensive crises be avoided by preserving the carotid baroreceptors, by the judicious use of vasoactive substances to prevent blood pressure elevations beyond 160 to 175 mmHg postoperatively, and by avoiding operations on patients with large (>1 cm) cerebral infarcts for 4 to 5 weeks after the appearance of symptoms. A recent report by Dalman et al. (146) suggests that transcranial Doppler monitoring helped identify patients at risk of developing post-operative hyperperfusion by revealing a marked increase in middle cerebral artery velocity. When this finding was encountered patients had close blood pressure monitoring and control. Although minor hyperperfusion syndromes might have been prevented from progression, it is not clear that these maneuvers prevented intracerebral hemorrhages.

Myocardial Infarction The coincidence of coronary artery and carotid artery atherosclerosis predispose the carotid endarterectomy patient to suffer perioperative acute myocardial infarction (150,151). Varying in incidence depending upon the severity of the coronary artery disease as manifested by cardiac symptoms, the various strategies adopted by different clinicians have already been discussed and include the critical elements of avoiding the use of vasopressors to artificially raise the arterial blood pressure above levels

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ordinarily recorded in each patient and, conversely, avoiding lowering the blood pressure with vasolytic substances to attempt to correct the 10 to 20 mmHg compensatory pressure elevation that often occurs on carotid clamping, to maintain cerebral perfusion. Local anesthesia, which has a lesser effect on cardiohemodynamics, is favored by some and said to be associated with fewer cardiac complications than general anesthesia (111).

Cranial Nerve Damage Cranial nerve injuries (152) may escape detection unless specifically sought out or may be distressingly evident, as when a markedly deviated chewed-up tongue (cranial nerve XII) is detected or there is marked hoarseness from vocal cord paralysis (cranial nerve X) or difficulty swallowing from paralysis of the middle pharyngeal constrictor (cranial nerve IX) or drooling of saliva (cranial nerve VII). Very few injuries occur from cutting any of these nerves except in the presence of undetected anomalies. Most are the result of traction, compression, or heating from the use of electrocautery. Incidence varies dramatically depending on the manner used to detect deficits, and the particular nerve involved, from 1.8% for the superior laryngeal nerve to 15% for the recurrent laryngeal nerve, for an overall incidence for all cranial nerves of from 7.9% to 15%. In most instances, dysfunction is transient but may be particularly distressing when the tongue becomes chewed upon, the voice fails, or swallowing becomes virtually impossible. The marginal mandibular nerve must be protected from retractors placed to elevate the mandible to secure exposure of high internal carotid lesions and from incisions which should pass posterior to the angle of the mandible and a line extending posterior to the earlobe to avoid its transection. The hypoglossal nerve, which limits exposure of the distal portion of the internal carotid artery, is directly in the operative field but can be removed from danger by transecting the sternocleidomastoid artery and vein which keep it tethered in a lateral position (153). Often the descending branch of the hypoglossal nerve prevents upward dislocation of the main trunk and so must be transected. Performance of these two maneuvers not only displaces the nerve out of harm’s way without retraction but also yields the added dividend that if reoperation is required at a later date, cranial nerve XII will be found to be permanently retracted out of the operative field by scar. On occasion, small facial vein tributaries that cross the carotid bifurcation anteriorly are adherent on their posterior aspects to a low lying hypoglossal nerve. These veins, therefore, must be completely cleared of areolar tissue before being divided (as they must be to gain exposure) to avoid transecting the nerve. Recurrent laryngeal nerve palsy probably usually results from main vagal trunk injuries (154), except when it has an unusually high origin from the parent trunk, when hoarseness may result from direct injury including transection. The main vagal trunk is situated posterior to the

carotid arteries and jugular veins, and although it is rarely seen during the operation, awareness of its location is essential to prevent its being injured during high dissection of the internal carotid artery while applying clamps to the common carotid artery, which must be skeletonized before clamping, during retraction, and during the use of electrocautery. Not infrequently with either local anesthetic infiltration or incident to cervical block anesthesia, hoarseness will occur and persist for the duration of effective anesthesia, after which function returns. The superior laryngeal nerve, however, passing obliquely downward from its origin from the main vagus trunk at the level of the jugular foramen behind the internal and external carotid arteries, to reach the cricothyroid muscle and inferior pharyngeal constrictor is subject to injury from the internal carotid clamp and from dissections around the external carotid and superior thyroid arteries. Its injury results in easy fatigability of the voice, which patients say they cannot project well. Shouting becomes difficult. The glossopharyngeal nerve becomes susceptible to injury when high exposure of the internal carotid artery is required by transection of the digastric muscle. The proximity of the nerve to the muscle must be appreciated so that the muscle will be well delineated before it is transected, preferably avoiding the use of cautery, and watchful for the presence of the nerve, which can often be visualized during high dissection (155). Injury to the great auricular nerve from retraction in the upper angle of a vertical incision may cause painful paresthesia of the earlobe and may be avoided by avoiding forceful stretching of the upper angle of the wound.

Late Restenosis and Occlusion Late restenosis at the carotid endarterectomy site, reported with an incidence that varies from 3% to 25%, is arbitrarily divided into myointimal hyperplasia, usually discovered within 6 months to 2 to 3 years of operation, and recurrent atherosclerosis, occurring beyond this early postoperative period (156,157). A third category, emphasized by Barnes et al. (158), is classified as residual plaque, and is incomplete removal of the plaque at the original operation, detectable if looked for in the immediate postoperative period. Comparisons of plaques removed at the initial operation with those that recur and are removed months to years later suggest that the spectrum of pathologic change observed at the initial operations, at which plaques range from purely and simply fibrous to frankly atherosclerotic with fibrosis, intraplaque hemorrhages, encysted atheromatous debris, ulceration, and thrombosis, is reproduced by the recurrent plaques— those discovered early being simple and fibrous, those found later, compound and characteristic of full-blown atherosclerosis. Residual plaque need never be left behind if proper exposure of the involved vessels is obtained from proximal to common carotid plaque to distal to internal carotid plaque, which permits a long arteriotomy to be made and

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

an appropriately deep endarterectomy to be performed. If there is a question regarding complete removal because of an inlying shunt or for whatever other reason, completion of visualization of the operative site, angiographically, with ultrasound. Routine completion surveillance is advocated by several authors as a method to reduce both early and late complications. When restenosis occurs early (6 months to 2 years) in spite of complete initial removal of plaque, discovered either by routine postoperative duplex scan or because of return of symptoms, simple fibrous myointimal hyperplasia should be suspected. The locations of these early lesions vary in distribution and configuration. They may be sharply defined at the terminal ends of primarily closed arteriotomies where minimal stenosis may have been produced at the uppermost angle, perhaps predisposing to acceleration of flow or, perhaps, analogous what has been observed experimentally in vein grafts, to low shear which predisposes to myointimal hyperplasia (160). If roof patch closure of arteriotomies is done, similar lesions may occur at the end of the patched segment if too abrupt a taper results from the closure. The site of transection of intima in the common carotid artery may result in a ledge where abnormal flow may also occur, preventable by suturing down the proximal intima with simple sutures across the edge of the intima in the longitudinal orientation of the artery. On the other hand, diffuse thickening of the entire endarterectomized segment may occur, possibly because of incomplete removal of media with the original plaque, possibly for as yet unknown metabolic or hemodynamic factors. It is possible, from the diverse appearances that these lesions present, that there are multiple etiologies, further evident from the fact that they occur more often in women and smokers (159,161). The early myointimal plaque can be produced in the experimental laboratory in a variety of animal models that range from alteration of arterial configuration to produce specific modifications of flow (accelerated flow, marked slowing of flow, absence of flow) (162,163), to myointimal injuries produced with balloon catheters (164), to endothelial injuries produced by air-drying of the intima (165). The experimental lesions can be prevented by avoiding making geometric configurations that result in specific flow abnormalities. A host of pharmacologic agents, seemingly unrelated, which range from heparin (166,167), to eicosopentoic acid (168), to antiplatelets (169), corticosteroids (170), and immunosuppressive agents such as cyclosporine (171), although not preventing the formation of experimental lesions, have been reported to at least partially suppress their development, a finding not apparent in human operations. In the human model, claims have been made for the preventive effects of patch closure of arteriotomies to change the configuration of the carotid bifurcation and thereby change the flow conditions that existed during development of the initial atherosclerotic plaque (172,173). Autologous vein substitution of the stenotic segment if found in women, rather than repeat endarterectomy and roof patching, if not initially performed, has also

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been suggested as preventing the all too frequent rerecurrences. Cessation of smoking and administration of antiplatelets is advisable, although not firmly established as preventive. Vitamin E administration, long-term heparinization, or administration of the non-anticoagulant fraction of heparin are as yet unproved. Although early lesions, presumably those that are simply fibrous have been reported to regress when followed by repeated duplex scans, symptomatic lesions and those that result in severe stenosis, of whatever age, merit serious consideration for reintervention. When patch closure of arteriotomies is initially performed, if the patching results in too voluminous a lumen, gelatinous platelet fibrin flow thrombus similar to that found in spontaneously occurring aneurysms may be deposited and may be the source of recurrent cerebral emboli or the nidus for continuing thrombus deposition leading to stenosis. When this is encountered, reoperation is almost always mandatory, but prevention is possible by suturing roof patches of dimensions suitable for changing the shape of the vessels without attempting to enlarge the lumen.

Carotid Endarterectomy in the Conscious Patient The following technique is used for carotid endarterectomy in the conscious patient (174,176,178,179). With minimal premedication only, insufficient to cause drowsiness and inability to respond promptly to verbal commands, the patient is positioned on the operating table supine, the head turned away from the operative side with a small pillow under the shoulders. A compressible squeaker toy is strapped in the palm of the hand opposite the side of operation. Cervical block anesthesia is administered using a three-needle technique, injecting a total of 10 mL of 0.5% marcaine. Surgical preparation of the skin of the neck and groin is performed and skin drapes are placed. The groin ipsilateral to the carotid to be operated is infiltrated to permit removal of the greater saphenous vein for vein patching (Figs. 66.1–66.4). Ankle veins are avoided because of their tendency to rupture. Skin incision is made in the neck along the anterior border of the sternocleidomastoid muscle extending from the level of the lower border of the thyroid cartilage to the level of the angle of the mandible, curving along the upper border of the incision posteriorly to avoid the great auricular nerve. The platysma and investing layer of deep cervical fascia are cut in the direction of the skin incision, exposing the anterior facial vein, which is divided between ligatures after ensuring that it has been dissected from a sometimes adherent cervical nerve XII. The carotid sheath is exposed along the common and internal carotid arteries. The hypoglossal nerve is identified. The sternocleidomastoid artery and vein are divided between ligature. The descending branch of the nerve is also divided to permit cervical nerve XII to retract away from the internal carotid artery, which is now dissected free above the estimated termination of plaque and encircled with an elastic vessel loop.

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FIGURE 66.1 The anatomy. Anatomic landmarks upon which the operation of carotid endarterectomy is based. The dotted line indicates the location and extent of the vertical incision that is favored to obtain maximal exposure.

FIGURE 66.2 The endarterectomy. (A) The internal carotid artery is clamped prior to completion of the dissection of the bulb to prevent embolization to the brain. (B) The relation of the arterial clamps to the carotid bifurcation plaque are placed so as to avoid crushing, thereby protecting against another source of intraoperative embolization. (C) After the plaque has been completely removed, tacking sutures are placed proximally and distally unless no ledge is evident at either end of termination of the endarterectomy. (D) A 12-Fr. catheter is used as a stent to guide the suturing of the vein roof patch used for closure of the long arteriotomy. A similar stent is used if primary closure is elected. (E) Vein roof patch closure is completed.

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

A

B

C

D

FIGURE 66.3 The plication. (A) When there is redundancy or kink of the internal carotid artery, plication is performed. The proximal thick intima of the common carotid artery, if present, is tacked down. (B) Plication sutures are tied outside the artery as shown. (C) Detail for suture closure of “dog ears” resulting from plication. (D) Plication completed showing externalized “dog ears” and completed vein roof patch.

Three thousand units of heparin is administered by the anesthesiologist intravenously. The anterior belly of the omohyoid muscle is identified in the lower angle of the wound and used as a landmark to identify the common carotid artery well below the plaque at the carotid bulb. Test clamping of the internal carotid is done, the clamps applied to the segment of vessel that has come into view when the hypoglossal nerve has retracted, a level usually well above the distal end of the plaque. The patient is asked to count and squeeze the compressible squeaker for a test period of at least 3 minutes. During this maneuver, attention is directed to the groin for harvest of the saphenous vein. The line between the anterior superior iliac spine and the public tubercle, indicating the location of the inguinal ligament, is followed until the femoral pulse is encountered. From this intersection an incision is made directed obliquely medially and downward for a distance of 10 cm. Sweeping the groin fat downward with the back of the knife handle usually

803

promptly exposes the greater saphenous vein, which is resected from the saphenofemoral junction downward for a distance of 7.5 cm. It is irrigated with heparinized saline solution without distending it and is placed in dilute heparin solution. Test clamping having been tolerated, dissection of the common and external carotid and superior thyroid arteries is completed, leaving the clamp on the internal. The external and superior thyroid arteries are clamped, and finally a clamp is placed on the common carotid artery well below plaque, using the lower border of the anterior belly of the omohyoid muscle as a landmark. A long arteriotomy is made on the anterior wall of the vessel, extending from below the plaque in the common carotid to normal intima above the plaque in the internal. If marked tortuosity or redundancy is encountered or was seen on the preoperative angiogram, the arteriotomy extends to beyond it. A cleavage plane through media is developed with a Freer elevator. The plaque is liberated under direct vision from the common and internal carotids by performing an eversion endarterectomy of the external carotid and superior thyroid arteries. Its removal in one piece is accomplished by sharp transection of usually only slightly thickened intima in the common carotid and by “feathering” the plaque in the internal carotid, which usually results in its breaking away at normal, firmly attached intima. Circular bands of media are removed from the endarterectomized segment until a smooth surface is exposed. Saline irrigation will reveal loose shreds requiring removal and unattached distal intima, which, if not removable to firmly attached intima, may require tacking sutures. The transected intima in the common carotid artery is often thick though pearly white. Its edge requires tacking sutures to eliminate the ledge that may be present. If there is redundancy of the internal carotid artery, this is corrected by performing plication of that vessel using longitudinally placed sutures. A 10-Fr. catheter is placed in the lumen of the internal carotid to act as a stent for roof patching performed with the now longitudinally opened saphenous vein (175–177). When there remains only a quarter-inch opening in the closing suture line, the catheter is removed and a flushing routine is instituted, flushing the internal and external carotid arteries retrograde, reapplying clamps, and liberally irrigating the endarterectomized segment through the remaining opening with dilute heparinized saline solution until clear. The suture line is completed with a blunt needle through which dilute heparinized saline is injected into the endarterectomized segment. The flushing routine is now carried out. The internal carotid is backbled into the bulb and reclamped, and the common and external carotid clamps are removed. After 1 minute, the internal clamp is removed. The wounds are closed in layers. If test clamping of the internal carotid is not tolerated, the clamp is removed. Blood pressure is checked to be certain that hypotension has not occurred. If it has, blood pressure is restored but is not permitted to rise above

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A

D

E

B

F

C

G

FIGURE 66.4 The shunt. (A) Common carotid artery at the level of the omohyoid muscle is isolated between vascular clamps and an arteriotomy is made for insertion of the proximal end of the shunt. Temporary clamping of the internal carotid artery is performed while the common carotid clamps are being applied to prevent cerebral embolization. (B) Proximal end of shunt inserted into the common carotid artery and flushed, the internal and external carotid arteries remaining in continuity with each other during these maneuvers. (C) Distal end of shunt inserted into the internal carotid and flow restored to the brain. (D) Vein roof patch closure while shunt is in place allowing both limbs of the shunt to protrude through the same opening. (E) Internal and external carotids open to each other after removal of shunt and flushing. Patch closure can then be done without haste if the patient is one of the majority who tolerate common carotid clamping through internal or external clamping. (F) Basting stitch closure to minimize clamping ischemia in those who fail to tolerate even common carotid clamping. (G) Side-biting clamp technique. Basting stitch clusure of the roof patch to permit removal of the shunt while minimizing clamping ischemia time.

basal levels, with nitroprusside solution, and test clamping is repeated. If still not tolerated, the clamp is removed, recovery is permitted to occur, and test clamping of the common carotid is done. The common carotid clamp is applied only after the internal carotid is temporarily clamped to prevent embolization to the brain. If common carotid clamping is tolerated, the clamp is removed, an additional 2000 units of heparin is administered, and the neck incision is enlarged downward to well below the anterior belly of the omohyoid muscle to permit additional exposure of the common carotid artery so that a 3-cm segment well below the upper border of the omohyoid muscle can be isolated between clamps. Double clamping of the common carotid at this low level is done while temporarily occluding the internal carotid. (see Fig. 66.4) An arteriotomy is made between the common carotid artery clamps, and the lower end of a clamped Javid shunt is inserted into the common carotid artery and affixed in place with a Javid clamp. The shunt is flushed with blood from the common carotid, and if it flows freely without visible yellow flakes, it is clamped distally. The internal and external carotid and superior thyroid arteries are clamped, the upper common carotid clamp is removed, and the arteriotomy is extended distally to normal internal carotid artery. The flushed, blood-filled, air-free distal end of the

shunt is inserted into the internal carotid artery and flow is restored. Upon completion of the endarterectomy and closure of arteriotomy, one of three techniques is used to remove the shunt while not exceeding a period of 1 to 2 minutes of clamping ischemia. The preferred technique is to suture the vein patch to completion except where the two limbs of the shunt are permitted to extrude as a loop. A basting stitch is placed at the remaining opening, and occluding clamps are placed on the shunt and on each of the three major arteries as the shunt is extracted. Flushing is performed as described. The endarterectomized segment is irrigated and filled with saline. The basting stitch is snugged to close the suture line, and flow is restored in the usual way. The second technique is a reversal of the technique of shunt insertion in that the vein patch closure is done to well below the carotid bifurcation, whereupon the internal portion is removed after it is clamped and the internal and external carotid are opened to each other by clamping with a vascular clamp well below the bifurcation. The remainder of the closure is accomplished, and common carotid flow to the distal vessels is restored. The third technique relies upon closure of the vein patch around the shunt as before. When it is removed, a

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery

curved side-biting clamp is applied to the edges of the unclosed arteriotomy, which is sutured after flow has been restored to the distal vessels.

4.

Experience of the Surgeon A critical factor in the outcome of carotid endarterectomy is the experience of the surgeon. The first randomized clinical trial of carotid endarterectomy (27) failed to provide answers to some of the critical questions regarding selection of patients for operations because of the high operative complication rates, which ranged from 2% to over 20% among various participating groups, averaging 11.0%. In more recent times, although many experienced teams of surgeons reported complication rates of 1% to 3% (33,34,47,73,85,98) operating on groups of patients that included both high- and low-risk situations, there were repeated expressions of concern about the appropriateness of carotid endarterectomy because of the much higher incidence of complication discovered on sampling of institutions where these procedures were being done. Indeed, there was skepticism about the recording methods of highly successful teams. The randomized clinical trials of recent vintage have been performed by groups of surgeons who have satisfied both experience requirements (3,31,32) based on numbers of operations performed and expertise analyses based on calculations of complication rates, which though higher than achieved by many experienced surgeons, nevertheless indicate the need for constant monitoring of performance. Operations on asymptomatic, neurologically intact patients with unilateral lesions can be done with 1% to 3% mortality/morbidity, while symptomatic, neurologically intact patients with bilateral operations should bear no more than 1% to 5% operative mortality/morbidity. Indeed, with proper monitoring and selective shunting, selected patients with contralateral occlusions, a high-risk group, can be operated upon within the 1% to 3% complication rate (47,72,73). Operations on higher-risk patients that are severely impaired, neurologically unstable, or have acute stroke should probably be performed only by those who have established records of excellence in lesser-risk patients, who are prepared to function with guidance of established protocols aimed at achieving accurate classifications of patients with studies of brain pathology and arterial pathology, with adherence to standardized surgical techniques, and prepared to investigate all operative and postoperative complications to satisfactory diagnosis as to mechanisms of monitoring failure, possible in at least 80% of perioperative complications.

References 1. Eastcott HHG, Pickering GW, Rob CG. Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 1954;13:994–996. 2. Blaisdell FW, Clauss RH, et al. Joint study of extracranial arterial occlusions: a review of surgical considerations. JAMA 1969;209:1889. 3. North American Symptomatic Carotid Endarterectomy

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

805

Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445–453. European Carotid Surgery Trialists’ Collaborative Group. MCR European Carotid Surgery Trial: interim results for patients with severe (70% to 99%) or with mild (0% to 29%) carotid stenosis. Lancet 1991;337:1235–1243. Mayberg MR, Wilson SE, et al. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA 1985;266:3289–3294. American-Canadian Co-Operative Study Group. Persantine aspirin trial in cerebral ischemia: Part II. Endpoint results. Stroke 1985;16:406–415. The SALT Collaborative Group. Swedish Aspirin LowDose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischaemic events. Lancet 1991;338:1345–1349. The Dutch TIA Trial Study Group. A comparison of two doses of aspirin (30 mg vs 283 mg) a day in patients after a transient ischemic attack or minor ischemic stroke. N Engl J Med 1991;325:1261–1266. Brandier JF, Licht PB, Roder O, et al. Endovascular treatment of severe symptomatic stenosis of the internal carotid artery: early and late outcome. Eur J Vasc Endovasc Surg 2001;22:205–210. Al-Murak N, Colombo A, Gaines PA, et al. Multicenter evaluation of carotid artery stenting with filter protection. J Amer Coll Cardiol 2002;39:841–846. Imparato AM. The carotid bifurcation plaque. A model for the study of atherosclerosis. J Vasc Surg 1986;3:249–255. Imparato AM, Riles TS, Gorstein F. The carotid bifurcation plaque: pathologic findings associated with cerebral ischemia. Stroke 1979;10:238. Yuan C, Zhang S-x, Polissar NL, et al. Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attacks or stroke. Circulation 2002;105:181–185. Fisher CM, Ojemann RG. A clinico-pathologic study of carotid endarterectomy plaques. Rev Neurol (Paris) 1986;142:573–589. O’Donnell TF Jr, Erdoes L, et al. Correlation of B-mode ultrasound imaging and arteriography with pathologic findings at carotid endarterectomy. Arch Surg 1985;120:443–449. Sterpetti AV, Schulz RD, et al. Ultra-sonographic features of carotid plaque and the risk of subsequent neurologic deficits. Surgery 1988;104:652–660. Gomez CR. Carotid plaque morphology and risk for stroke. Curr Concepts Cardiovasc Dis Stroke 1989;24:25–29. Imparato AM, Riles TS, et al. The importance of hemorrhage in the relationship between gross morphologic characteristics and cerebral symptoms in 376 carotid artery plaques. Ann Surg 1983;197:195–203. Lusby RJ, Ferrell LD, et al. Carotid plaque hemorrhage. Its role in the production of cerebral ischemia. Arch Surg 1982;117:1479–1488. Ammar AD, Ernst RL, et al. The influence of repeated carotid plaque hemorrhages on the production of cerebrovascular symptoms. J Vasc Surg 1986;3:857–859. Pessin MS, Hinton RC, et al. Mechanisms of acute strokes. Ann Neurol 1979;6:245–252.

806

Part VIII Cerebrovascular Insufficiency

22. Avril G, Batt M, et al. Carotid endarterectomy plaques: correlation of clinical and anatomic findings. Ann Vasc Surg 1991;5:50–54. 23. Torvik A, Svindland A, Lindboe CF. Pathogenesis of carotid thrombosis. Stroke 1989;20:1477–1483. 24. Ogata J, Masuda J, et al. Rupture of thrombotic occlusion of stenotic internal carotid artery. Stroke 1990;21:1740–1745. 25. Norris JW, Bornstein NM. Progression and regression of carotid stenosis. Stroke 1986;17:755–757. 26. Alexandrov AV, Bladin CF, et al. Measuring carotid stenosis. Time for reappraisal. Stroke 1993;24:1292–1296. 27. Fields WS, Maslenikov V, et al. Joint study of extracranial arterial occlusion: V. Progress report of prognosis following surgery or nonsurgical treatment for transient cerebral ischemic attacks and cervical carotid artery lesions. JAMA 1970;211:1993–2003. 28. Breslau PJ, ed. Hemodynamics of arterial stenosis. In: Ultrasonic duplex scanning in the evaluation of carotid artery disease. Voerendal, Holland: Herleen, 1981. 29. May AG, Van den Berg L, et al. Critical arterial stenosis. Surgery 1963;54:250–259. 30. Roederer GO, Langlois YE, et al. The natural history of carotid arterial disease in symptomatic patients with cervical bruits. Stroke 1984;15:605–613. 31. Hobson RW II, Weiss DG, et al. The Veterans Affair Cooperative Study Group. Efficacy of carotid endarterectomy for symptomatic carotid stenosis. N Engl J Med 1993;328:221–227. 32. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273: 1421–1428. 33. Thompson JE, Patman RD, Talkington CM. Asymptomatic carotid bruit: long-term outcome of patients having endarterectomy compared with nonoperative controls. Ann Surg 1978;188:308–316. 34. Hertzer NR, Flanagan RA Jr, et al. Surgical versus nonoperative treatment of symptomatic carotid stenosis, 211 patients documented by intravenous angiography. Ann Surg 1986;204:154–162. 35. Hertzer NR, Flanagan RA Jr, et al. Surgical versus nonoperative treatment of asymptomatic carotid stenosis, 290 patients documented by intravenous angiography. Ann Surg 1986;204:163–171. 36. Moore WS, Boren C, et al. Natural history of nonstenotic asymptomatic ulcerative lesions of the carotid artery. Arch Surg 1978;113:1352. 37. Svindland A, Torvik A. Atherosclerotic carotid disease in asymptomatic individuals. A histologic study of 53 cases. Acta Neurol Scand 1988;78:506–517. 38. Imparato AM. Carotid endarterectomy to prevent stroke III based on pathologic findings at the carotid bifurcation. In: Veith FJ, ed. Current critical problems in vascular surgery. St Louis: Quality Medical Publishing, 1989:548–552. 39. Riles TS, Imparato AM, et al. Comparison of results of bilateral and unilateral carotid endarterectomy five years after surgery. Surgery 1982;91:258–262. 40. Bernstein EF, Humber PB, et al. Life expectancy and late stroke following carotid endarterectomy. Ann Surg 1983;198:80–84.

41. Schroeder T, Sillesen H, Engell HC. Staged bilateral carotid endarterectomy. J Vasc Surg 3:355. 42. Dimikakos PB, Kotsis TF, Tsiligiris B, et al. Comparative results of staged and simultaneous bilateral carotid endarterectomy: a clinical study and treatment. Cardiovasc Surg 2000;8:10–17. 43. Sobel M, Imparato AM, et al. Contralateral neurologic symptoms after carotid surgery: a nine year follow-up. J Vasc Surg 3:623. 44. Levin SM, Soldheimer FK. Stenosis of the contralateral carotid artery—to operate or not? Vasc Surg 1973;7:3. 45. Imparato AM. The “major” and “minor” carotid artery in arterial reconstruction. Stroke 1974;9:15–21. 46. Baker WH, Littooy FN, et al. Carotid endarterectomy without a shunt: the control series. J Vasc Surg 1984;1:50–56. 47. Imparato AM, Ramirez AA, et al. Cerebral protection in carotid surgery. Arch Surg 1982;117:1073–1078. 48. Riles TS, Imparato AM, Kopelman I. Carotid artery stenosis with contralateral occlusion with long-term results in fifty-four patients. Surgery 1980;87:363–368. 49. Patterson RH. Risk of carotid surgery with occlusion of the contralateral carotid artery. Arch Neurol 1974;30:188–189. 50. Riles TS, Imparato AM, et al. The totally occluded internal carotid artery: preliminary observations using rapid sequential computerized tomographic scanning. Arch Surg 1982;117:1185–1188. 51. Riles TS, Imparato AM, et al. Common carotid occlusion: preoperative assessment of the distal vessels. Ann Surg 1984;199:363–366. 52. Yamauchi H, Fukuyama H, et al. Hemodynamics in internal carotid artery occlusion examined by positron emission tomography. Stroke 1990;2:1400–1406. 53. Martin RS, Edwards WH, et al. Common carotid occlusion: surgical treatment and imaging of distal vessels. J Vasc Surg 1992;15:244. 54. Matos MA, van Bemmelen PS, et al. The influence of carotid siphon stenosis on short- and long-term outcome after carotid endarterectomy: fact or fiction? J Vasc Surg 1992;16:475–476. 55. Ley-Pozo J, Ringelstein EB. Non-invasive detection of occlusive disease of the carotid siphon and middle cerebral artery. Ann Neurol 1990;28:640–647. 56. Laro RSA, Berry NA. Atherosclerotic ulceration of the brachiocephalic artery. Aust NZ J Surg 1974;44:370–374. 57. Nichols SC, Koutlas TC, Strandness DE Jr. Clinical significance of retrograde flow in the vertebral artery. Ann Vasc Surg 1991;5:331–336. 58. Fronek A. Comments on the diagnosis of subclavian (or innonimate) artery steal syndromes. J Vasc Surg 1992;15:938–940. 59. Grosvell WJHM, Lawson JA, et al. Clinical significance of innominate artery lesions evaluated by ultrasonography and digital angiography. Stroke 1988;19:958–961. 60. Brewster DC, Moncure AC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985;2:99–112. 61. Imparato AM, Riles TS. Surgery of vertebral and subclavian artery occlusions. In: Bergan JJ, Yao JST, eds. Cerebrovascular insufficiency. New York: Grune and Stratton, 1983.

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery 62. Blaisdell FW, Clauss RH, et al. Joint Study of Extracranial Arterial Occlusion: a review of surgical considerations. JAMA 1969;209:1889. 63. Ouriel K, Ricotta JJ, et al. Carotid endarterectomy for non-hemispheric cerebral symptoms: patient selection with ocular pneumoplethysmography. J Vasc Surg 1986;4:116–118. 64. Imparato AM. Vertebral arterial reconstruction: a ninteen year experience. J Vasc Surg 1985;2:626. 65. O’Hara PJ, Hertzer NR, Beven EG. External carotid revascularization: review of a ten year experience. J Vasc Surg 1985;2:709–714. 66. Friedman SG, Lamparello PJ, et al. Revascularization of the external carotid artery. Arch Surg 1988;123:497. 67. Zarins CK, DelBeccaro EJ, et al. Increased cerebral blood flow after external carotid revascularization Surgery 1981;89:730–734. 68. Countee RW, Viyayanathan T. Intracranial embolization via external carotid artery: report of a case with angiographic documentation. Stroke 1980;11:465–468. 69. Berguer R, Sieggren MY, et al. The silent brain infarct in carotid surgery. J Vasc Surg 1986;3:442. 70. Gregg MJ, Papadakis C, et al. The significance of CT scan infarcts and atrophy in patients with amaurosis fugax. J Vasc Surg 1988;7:215. 71. McKenzie RL, Awad IA. Reversal of a dense persistent, holohemispheric neurological deficit after an endarterectomy of the carotid artery: case report. Neurosurgery 1991;29:261–264. 72. Goldstone J, Moore WS. A new look at emergency carotid operations for the treatment of cerebrovascular insufficiency. Current concepts of cerebrovascular disease. Stroke 1978;9:599. 73. Whittemore AD, Mannick JA. Surgical treatment of carotid disease in patients with neurologic deficits. J Vasc Surg 1987;5:190. 74. Millikan CH. Discussion in cerebral diseases. In: McDowell FH, Brennan RW, eds. Transactions of the 8th Princeton Conference on Cerebral Vascular Disease. New York: Greene and Stratton, 1973:209. 75. Rosenberg H. Handbook of carotid artery surgery. Boca Raton, Fla: CRC Press, 1989:93. 76. Wilson SE, Mayberg MR, et al. Crescendo transient cerebral attacks: a surgical imperative. J Vasc Surg 1993;17:249. 77. Hertzer MR. Carotid endarterectomy and common sense [editorial]. Surg Gynecol Obster 1978;147:235. 78. Kempczinski RF, Brott TG, Labretta RJ. The influence of surgical specialty and caseload on the results of carotid endarterectomy. J Vasc Surg 1986;3:911. 79. Ernst CB. Update on manpower issues in vascular surgery. Who is performing vascular operations and who should be performing them. In: Veith F, ed. Current critical problems in vascular surgery. St Louis: Quality Medical Publishing, 1989:3. 80. Imparato AM. Is there a need for prospective randomized clinical trials of carotid endarterectomy. In: Veith FJ, ed. Current critical problems in vascular surgery. St Louis: Quality Medical Publishing, 1989:553. 81. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998; 339:1415–1425.

807

82. Ingall TJ, Dodick DW, Zimmerman RS. Carotid endarterectomy. Which patients can benefit? Postgrad Med 2000;107:97–109. 83. Thompson JE. Complications of carotid endarterectomy and their prevention. World J Surg 1979;3:155–165. 84. Hertzer NR, Avellone JC, et al. The risk of vascular surgery in a metropolitan community. J Vasc Surg 1984;1:13–21. 85. Sundt TM Jr, Sharbrough FW, et al. The risk benefit ratio of intraoperative shunting during carotid endarterectomy. Relevancy to operative and postoperative results and complications. Ann Surg 1986;203:196–204. 86. Barnett HJM, Warlow CP. Carotid endarterectomy and the measurement of stenosis. Stroke 1993;24:1281–1284. 87. Langsfeld M, Lusby RJ. The spectrum of carotid artery disease in asymptomatic patients. J Cardiovasc Surg 1988;29:687–691. 88. Toole JF, Janeway R, et al. Transient ischemic attacks due to atherosclerosis. Arch Neurol 1975;32:5. 89. Goldner JC, Whisnant JP, Taylor WJ. Long-term prognosis of transient ischemic attacks. Stroke 1971;2:160. 90. Ziegler DK, Hassanein RS. Prognosis in patients with transient ischemic attacks. Stroke 1973;4:666. 91. Gorelick PB. Carotid endarterectomy. Where do we draw the line? Stroke 1999;30:1745–1750. 92. The Casanova Study Group. Carotid surgery versus medical therapy for asymptomatic atherosclerosis. Stroke 1991;22:1229–1235. 93. Kusey DS, Bowyer B, Iron K, et al. Determinants of outcome in carotid endarterectomy. J Vasc Surg 1998;28:1051–1058. 94. Norman PE, Semmens JB, Laurvick CL, et al. Long term relative survival of elderly patients after carotid endarterectomy. Stroke 2003;34:95–98. 95. Bardin J, Bernstein EF, et al. Is carotid endarterectomy beneficial in preventing recurrent stroke? Arch Surg 1982;117:1401. 96. McCullough JL, Mentzer RM, et al. Carotid endarterectomy after completed stroke: reduction in long-term neurologic deterioration. J Vasc Surg 1985;2:7. 97. Rubin JR, Goldstone J, McIntyre KE Jr, et al. The value of carotid endarterectomy in reducing the morbidity and mortality of recurrent stroke. J Vasc Surg 1986;4: 443–449. 98. Giordano JM, Trout HH, et al. Timing of carotid endarterectomy after stroke. J Vasc Surg 1985;2:250. 99. Ouriel K, May AG, et al. Carotid endarterectomy for nonhemispheric symptoms: predictors of success. J Vasc Surg 1984;1:339. 100. Habozit B. Vertebral artery reconstruction: results in 106 patients. Ann Vasc Surg 1991;5:61–66. 101. O’Brien MD. Vascular dementia is underdiagnosed. Arch Neurol 1988;45:797–798. 102. Bamford JM, Warlow CP. Evolution and testing of the lacunar hypothesis. Stroke 1988;19:1074–1082. 103. Bamford JM. Carotid endarterectomy for lacunar ischemia. In: Cao P, Ricci S, eds. Update in carotid disease. Italy: Esam Futura, 1991:23–28. 104. Fisher SS, Malenka DJ, et al. Risk of carotid endarterectomy in the elderly. Am J Publ Health 1989;79:1617–1620.

808

Part VIII Cerebrovascular Insufficiency

105. Pinkerton JA, Gholkar VR. Should patient age be a consideration in carotid endarterectomy? J Vasc Surg 1990;11:650–658. 106. Riles TS, Kopelman I, Imparato AM. Myocardial infarction following carotid endarterectomy: a review of 683 operations. Surgery 1979;85:249–252. 107. Ennis CL, Lawrie GM, et al. Improved results in patients with symptomatic coronary disease: an analysis of 1, 546 consecutive carotid operations. Stroke 1979;10:122. 108. Brener BJ, Brief DL, et al. The risk of stroke in patients with asymptomatic carotid disease undergoing cardiac surgery: a follow-up study. J Vasc Surg 1987;5:269. 109. Ivey TD. Combined carotid and coronary disease—conservative strategy. J Vasc Surg 1986;3:687–689. 110. Connolly JE. Carotid endarterectomy in the awake patient. Am J Surg 1985;150:159–165. 111. Gableman CG, Gann DS, et al. One hundred consecutive carotid reconstructions—local versus general. Am J Surg 1983;145:477–482. 112. Corson JD, Chang BB, et al. Influence of anesthetic choice on carotid endarterectomy outcome. Arch Surg 1987;122:807–812. 113a. Ricotta JJ, Char DJ, Cuadra SA, et al. Modeling stroke risk after coronary artery bypass and combined coronary artery bypass and carotid endarterectomy. Stroke 2003;34:1212–1217. 113b. Rockman CB, Su W, Lamparello P, et al. A reassessment of carotid endarterectomy in the face of contralateral carotid occlusion. J Vasc Surg 2002;6:668–673. 114. Gutierrez IZ, Barone DL, et al. The risk of perioperative stroke in patients with asymptomatic carotid bruits undergoing peripheral vascular surgery. Am Surg 1987;5:487. 115. Wong EHW. Perioperative stroke: Part I. General surgery, carotid artery disease, and carotid endarterectomy. Can J Anaesth 1991;38:347. 116. Barnes RW, Marsalek PB, Rittgers SE. Asymptomatic carotid disease in preoperative patients. Stroke 1980; II,VII:8,136. 117. PET scanning: can it help resolve management issues in cerebral ischemic disease? Stroke 1986;17:803–807. 118. Pomposelli EB, Lamparello P, et al. Intracranial hemorrhage after carotid endarterectomy. J Vasc Surg 1988;7:248–255. 119. Alpers B, Berry RG. Circle of Willis in cerebrovascular disorders. The anatomical structure. Arch Neurol 1963;8:398–402. 120. Boysen G. Cerebral hemodynamics in carotid surgery. Acta Neurol Scand Suppl 1973;52:1–6. 121. Sundt TM, Sharbrough FW, Piepgras DG. The significance of cerebral blood flow measurements during carotid endarterectomy. In: Bergan JJ and Yao JST, eds. Cerebrovascular Insufficiency. New York: Grune and Stratton, 1983. Chapt. 19. 122. Carter PL, Yamagata S, Erspamer R. Time limits of reversible cortical ischemia. Neurosurgery 1983;12:620–623. 123. Imparato AM, Riles TS, et al. The management of TIA and acute strokes after carotid endarterectomy. In: complications in vascular surgery. New York: Grune and Stratton, 1985:735–738. 124. Siegert BS, Koumoudouros E, et al. Comparison of the processed electroencephalogram and awake neurologic

125.

126.

127.

128. 129.

130.

131.

132.

133.

134.

135.

136.

137.

138.

139.

140.

141.

assessment during carotid endarterectomy. Anaesth Intens Care 1989;17:298–304. Marowetz RB, Zeiger HE, et al. Correlation of cerebral blood flow and EEG during carotid occlusion for endarterectomy (without shunting) and neurologic outcome. Surgery 1984;96:184–189. Kresowik TJ, Worsey JM, et al. Limitations of electroencephalographic monitoring in the detection of cerebral ischemia accompanying carotid endarterectomy. J Vasc Surg 1991;13:439–443. Andrews RJ. Retraction brain ischemia: cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model. Neurol Res 1992;14:12–18. Pinkerton, Jr. JA. EEG as a criterion for shunt need in carotid endarterectomy. Ann Vasc Surg 2002;6:756–761. Halsey JH, McDowell HA, Gelman S. Transcranial Doppler and CBF compared in carotid endarterectomy. Stroke 1986;17:1206–1208. Lam AM, Manninem PH, Ferguson GG, et al. Monitoring electrophysiologic function during carotod endarterectomy. A comparison of somatosensory evoked potentials and conventional electrograms. Anesthesiology 1991;75:15–21. Arnolds BJ, von Reutern GM. Transcranial Dopplersonography. Examination technique and normal reference values. Ultrasound Med Biol 1986;12:115–123. Naylor AR, Wildsmith JAW, et al. Transcranial Doppler monitoring of middle cerebral artery blood flow velocity during carotid endarterectomy. Br J Surg 1991;78:1264–1268. Archie JP, Technique and clinical results of carotid stump back pressure to determine selective shunting during carotid endarterectomy. J Vasc Surg 1991;13: 319–327. Kwaan JM, Peterson GJ, Connolly JE. Stump pressure an unreliable guide for shunting during carotid endarterectomy. Arch Surg 1980;115:1083–1085. Beebe HG, Starr C, Slack D. Carotid artery stump pressure: its variability when measured serially. J Cardiovasc Surg 1989;30;419–423. Young WL, Prohovnik I, et al. Cerebral blood flow and metabolism in patients undergoing anesthesia for carotid endarterectomy. A comparison of isoflurane, halothane, and fentanyl. Anesth Analg 1989;68:712–717. Neter FB. Cerebral protection during aneurysm surgery with isoflurane anesthesia. J Neurosurg 1992;756:541–543. Saccani S, Beghi C, et al. Carotid endarterectomy under hypothermic extracorporeal circulation: a method of brain protection for special patients. J Cardiovasc Surg 1992;33:311–314. Bloodwell RD, Halman GL, et al. Carotid endarterectomy without a shunt: results using hypercarbia general anesthesia to prevent cerebral ischemia. Arch Surg 1968;96:644–652. Lassen NA. The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localized within the brain. Lancet 1966;2:1113–1115. Strawn DJ, Hunter GC, et al. The relationship of intraluminal shunting to technical results after carotid endarterectomy. J Cardiovasc Surg 1990;31:424–429.

Chapter 66 Carotid Endarterectomy: Indications and Techniques for Carotid Surgery 142. Whitney DG, Kahn EM, et al. Carotid artery surgery without a temporary indwelling shunt: 1917 consecutive cases. Arch Surg 1980;115:1363. 143. AbuRhama AF, Boland JP, Witsberger T. Diagnostic and therapeutic strategies of white clot syndrome. Am J Surg 1991;162:175–179. 144. Ackeroff RGA, Jansen C, Moll FL. Carotid endarterectomy and intraoperative embolization detection: correlation of clinical, transcranial Doppler and magnetic resonance findings. Echocardiography 1996;13:543–550. 145. Gaunt ME. Clinical relevance of intraoperative embolization detected by transcranial Doppler ultrasonography during carotid endarterectomy: a prospective study of 100 patients. Br J Surg 1994;81:1435–1439. 146. Furst H, Hartl WH, Habrl R, et al. Silent cerebral infarction: risk factors complicating carotid endarterectomy. World J Surg 2001;25:969–974. 147. Imparato AM. Surgery for extracranial cerebrovascular insufficiency. In: Ransohoff J, ed. Modern techniques in surgery. Volume Neurosurg. Mt. Kisco, NY: Futura Publishing Co., 1980:14–38. 148. Macfarlane R, Moskowitz MA, et al. The role of neuroeffector mechanisms in cerebral hyperperfusion syndromes. J Neurosurg 1991;75:845–855. 149. Piepgras DG, Morgan MK, et al. Intracranial hemorrhage after carotid endarterectomy. J Neurosurg 1988;68:532–536. 150. Bernhard VM, Johnson WS, Peterson JJ. Carotid artery stenosis: association with surgery for coronary artery disease. Arch Surg 1972;105:837–840. 151. Rubio PA, Grunir GA. Myocardial infarction following carotid endarterectomy. Cardiovasc Dis 1975;2: 402–406. 152. Hertzer NR, Feldman BJ, et al. A prospective study of the incidence of injury to the cranial nerves during carotid endarterectomy. Surg Gynecol Obstet 1980;151: 781–784. 153. Imparato AM, Bracco A, et al. The hypoglossal nerve in carotid artery reconstructions. Stroke 1972;3:576–578. 154. Welch EL, Geary WE. Vocal cord paralysis following carotid endarterectomy. J Cardiovasc Surg 1979;29:393–397. 155. Rosenbloom JM, Friedman SG, et al. Glossopharyngeal nerve injury complicating injury endarterectomy. J Vasc Surg 1987;5:469–471. 156. Stoney RJ, String ST. Recurrent carotid stenosis. Surg 1976;80:705–710. 157. Imparato AM, Weinstein GS. Clinic-pathologic correlation in post carotid endarterectomy recurrent stenosis. J Vasc Surg 1986;3:657–662. 158. Barnes RW, Nix ML, et al. Recurrent versus residual carotid stenosis. Ann Surg 1986;203:652–660. 159. Ouriel K, Green RM. Clinical and technical factors influencing recurrent carotid stenosis and occlusion after endarterectomy. J Vasc Surg 1987;5:702–706. 160. Meyerson SL, Skelly CL, Curi MA, et al. The effects of extremely low shear stress on cellular proliferation and neointimal thickening in the failing bypass graft. J Vasc Surg 2001;34:90–97. 161. Washburn WK, Mackey WC, et al. Late stroke after carotid endarterectomy: the role of recurrent stenosis. J Vasc Surg 1992;15:1032–1037.

809

162. Imparato AM, Baumann FG. Consequences of hemodynamic alterations of the arterial wall after revascularization. In: Towne JB, Bernhard VM, eds. Complications in vascular surgery. New York: Grune and Stratton, 1980:107–121. 163. Nathan IM, Imparato AM. Vibration analysis in experimental models of atherosclerosis. Brill. NY Acad Med 1977;58:849–868. 164. Spaet TH, Stemmerman MB, Lejneikis I. The role of smooth muscle cells in repopulation of rabbit aortic endothelium follwong balloon injury. Fed Proc 1973;32: 219. 165. Fishman JA, Ryan GB, Karnowsky MJ. Endothelial regeneration in the rat carotid artery and the significance of endothelial denudation in the pathogenesis of myointomal thickening. Lab Invest 1975;32:339–351. 166. Clowes AW, Clowes MM. Inhibition by heparin of smooth muscle hyperplasia. J Vasc Surg 1989;5:589–590. 167. Gryton JR, Rosenberg RD, et al. Inhibition of rat arterial smooth cell proliferation by heparin. In vivo studies with anticoagulant and nonanticoagulant heparin. Circ Res 1980;46:625–634. 168. De Campli WM, Kosek JC, et al. Effects of aspirin, dipyridamole, and cod liver oil on accelerated myointimal proliferation in canine veno-arterial allografts. Ann Surg 1988;208:746–754. 169. Bush HL, Jakubowski JA, Sentissi JM. Early healing after carotid endarterectomy: effect of high and low dose aspirin on thrombosis and early neointimal hyperplasia. J Vasc Surg 1988;7:275–283. 170. Chervu A, Moore WS, et al. Efficacy of corticosteroids in suppression of intimal hyperplasia. J Vasc Surg 1989;10:129–134. 171. Uretsky BF, Murali S, et al. Development of coronary artery disease in cardiac transplant patients receiving immunosuppressive therapy with cyclosporin and prednisone. Circulation 1987;76:827–834. 172. Imparato AM. The role of patch angioplasty in carotid endarterectomy [editorial]. J Vasc Surg 1988;7:715–716. 173. Archie JPJ. Prevention of early restenosis and thrombosis occlusion after carotid endarterectomy by saphenous vein patch angioplasty. Stroke 1986;17:901–905. 174. Imparato AM. Extracranial vascular disease: advances in operative indications and techniques. World J Surg 1988;12:756. 175. Abu Rhama AF, Kahn, JH, Robinson PA, et al. Prospective randomized trial of carotid endarterectomy with primary closure and patch angioplasty with saphenous vein, jugular vein and polytetraflourethylene: perioperative (30 day) results. J Vasc Surg 1996;6:998–1006. 176. Moore WS. Technique of carotid endarterectomy. In: Moore WS, ed. Surgery for cerebrovascular disease. New York: Churchill Livingstone, 1987:491–502. 177. Imparato AM, Riles TS, Ramirez A, et al. Early complications of carotid surgery. Int Surg 1984;69:223–230. 178. Smith LL. Standard and extensive exposure of the carotid artery. In: Moore WS, ed. Surgery for cerebrovascular disease. New York: Churchill Livingstone, 1987:449–456. 179. Fisher DF, Clagett PG, et al. Mandibular subluxation for high carotid exposure. J Vasc Surg 1984:1:727–733.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 67 Eversion Carotid Endarterectomy R. Clement Darling, III, Manish Mehta, Philip S.K. Paty, Kathleen J. Ozsvath, Sean P. Roddy, Paul B. Kreienberg, Benjamin B. Chang, and Dhiraj M. Shah

Several randomized trials have validated the use of carotid endarterectomy (CEA) for management of hemodynamically significant symptomatic and asymptomatic carotid artery stenosis (1–3). Classically, CEA has been accomplished through a longitudinal arteriotomy either primarily closed or with a patch comprised of autogenous or prosthetic material (4–6). The incidence of recurrent stenosis following CEA ranges from 2% to 30% (7,8). Although patch angioplasty closure decreases carotid restenosis, this involves either vein harvest or the use of a prosthetic, which may increase the incidence of bleeding and infection (9–13). Furthermore, even patch closure of the longitudinal carotid arteriotomy may not reduce restenosis of the distal internal carotid artery (ICA) where it is most narrow. In order to successfully negotiate these technical hurdles and minimize restenosis, occlusion, and stroke, some surgeons have turned to the alternative technique of eversion CEA (14–23). Eversion CEA has a history almost as old as CEA itself. An early report by DeBakey et al. illustrated the use of one everting technique in which the distal common carotid was transected and the atheroma removed by everting the bifurcation with both the attached internal and external carotid arteries (14). Unfortunately, leaving both branches connected limited cephalad plaque exposure and, therefore, visualization of the distal end point.

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Hence, this technique was considered unreliable in patients whose disease extended beyond the bifurcation, and the eversion technique never gained acceptance. For many years, the most effective application of the eversion endarterectomy technique involved its use in the external iliac and common femoral arteries, where surgeons were able to visualize the end points and perform autogenous arterial reconstructions with excellent results (24). Kasparzak and Raithel in 1989 revised the DeBakey eversion CEA technique by transecting the ICA at the carotid bulb, and reported their results of decreased recurrent stenosis and occlusion (15). In contrast to the earlier procedure, transection of the ICA at the carotid bulb allows better visualization and, therefore, complete removal of plaque in almost all cases of carotid artery stenosis. The primary advantage of eversion CEA is that the ICA is divided at the largest part of the two vessels, and the subsequent anastomosis onto the common carotid artery (CCA) is easier, with less potential for a closure-related restenosis (18–23). This avoids a distal ICA suture line where the artery is narrow and its closure is prone to restenosis. Furthermore, the improved visualization facilitates plaque extraction and management of the end points. These two seemingly small advantages can result in reduced carotid cross-clamp time, total procedure operative time, incidence of carotid restenosis, and stroke mortality.

Chapter 67 Eversion Carotid Endarterectomy

The technique of standard CEA has been performed with excellent results over the past three decades. Most surgeons are reluctant to change but there is always room for improvement. The eversion CEA technique offers just that by displacing the anastomosis from a narrow distal ICA to a larger carotid bulb and proximal internal carotid arteries. In this chapter, we report the details of eversion endarterectomy—the technique, its variations, and limitations—as well as our experience and results to date.

Methods Selection of Cases Surgeons adopting eversion CEA need not change the majority of their technique. The anesthetic choice as well as methods of cerebral monitoring and protection can be the same for both eversion and standard CEA. We prefer eversion CEA under cervical block anesthesia, with selective shunting only in patients that develop neurologic deterioration during cross-clamping (25). As currently conceived, eversion CEA can be used to treat almost all cases of primary carotid bifurcation disease and selective cases of recurrent stenosis. This technique is ideal for treatment of carotid arteries with kinks or loops, as shortening of the artery can be incorporated within the process of eversion. The use of shunts is fairly straightforward and can be safely accomplished (18–20,23–25). Actually, in some cases, the use of a shunt can facilitate the procedure. Once the shunt is inserted, it can be used as a mandrel to evert the ICA and adequately remove the atherosclerotic plaque. However, certain types of shunts are probably more amenable to eversion than others, and the specifics of shunt use will be detailed later in this chapter. The extent of disease at the carotid bifurcation may affect one’s ease in performing CEA by any method. Disease limited to or near the bifurcation is easier to treat than disease that extends distally in the ICA. External visualization of the ICA should be used to adequately evaluate the distal extension of the atherosclerotic plaque prior to division of the ICA. Treatment of extensive disease in the ICA up to or beyond the level of the anterior digastric muscle can be challenging at times. Such cases should be kept in reserve until ample experience of eversion CEA is gained on simpler cases with low bifurcation and limited disease. Although the eversion technique can also be used in selective cases for treatment of recurrent carotid stenosis, it is contraindicated in patients that had the original CEA with the standard technique and prosthetic patch angioplasty. Carotids patched with autogenous vein material may sometimes be suitable for the eversion technique, but these operations may not be universally successful. Early and late recurrent stenoses may be removed by eversion technique, although the long-term results remain to be defined.

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Perioperative Management The preoperative workup of the patient presenting with carotid artery stenosis is similar for both the eversion and the standard CEA. All patients are evaluated clinically and with a duplex scan. If indicated, magnetic resonance or standard arteriography is selectively used for further delineation of the lesions. Postoperatively, patients remain in the postanesthesia care unit for 2 hours and, once their neurologic and hemodynamic status are assessed to be stable, they are transferred to the vascular surgical floor. Usually, patients are discharged within 24 hours of surgery and are routinely seen in office at 2 weeks. Subsequent follow-up by carotid duplex and clinical examination is at 3 months, 6 months, and once a year thereafter.

Technique In the operating room, superficial and deep cervical plexus block anesthesia is performed in an awake patient. A small IV bag attached to a pressure transducer is placed in the patient’s contralateral hand, which is squeezed intermittently by the patient to monitor motor function. In addition, the ability to follow commands, and other aspects of neurologic function during and after clamping, are monitored. No other methods of neurologic assessment (EEG/SEPS) are used. Exposure of the carotid artery is identical with either method of endarterectomy. Although circumferential dissection of the ICA along its length is a necessary part of eversion endarterectomy, this is probably best completed after clamping and division of the artery. Thus, only sufficient dissection to accommodate clamps need be performed initially. Following carotid artery exposure, the patient is systemically anticoagulated (30 u/kg body weight of intravenous heparin) and the carotid arteries are clamped. The ICA should be externally examined. The end of the plaque may be seen as the transition from the yellowish diseased artery to the normal bluish artery. Ideally, the clamp should be placed across the normal artery well above the transition zone as this makes eversion of the ICA and examination of the end point easier. If a more cephalad exposure is required, the usual measures include division of the ansa cervicalis, mobilization of the hypoglossal nerve and division of the digastric muscle may be performed. If the atherosclerotic disease extends superior to this point, an endarterectomy will be difficult by any technique and the operator should use whatever method is more familiar. The ICA is obliquely divided at the carotid bulb (Fig. 67.1). The line of transection should be in the range of 30 to 60º from the horizontal. It is relatively important for the line of transection to end in the crotch of the carotid bulb and not higher up into the internal or external carotid arteries; failure to do so is not necessarily catastrophic but can result in an increased complexity of the anastomosis. After the ICA is divided, cephalad and lateral traction on the artery helps in circumferential mobilization of the artery. This consists of the carotid

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Part VIII Cerebrovascular Insufficiency Superior thyroid artery

Segment excised

External carotid artery Hypoglossal nerve

Arteriotomy extended Kinked internal carotid artery

Common carotid artery Internal carotid artery

FIGURE 67.3 Management of extremely redundant ICA by segmental excision. (Copyright 1997 William B. Westwood.)

FIGURE 67.1 Oblique transection of internal carotid artery (ICA) at the carotid bulb. (Copyright 1997 William B. Westwood.) Atheromatous core

Common carotid artery

Adventitia, outer layer of media everted

External carotid artery

Intimal edge

15-30 mm CCA caudal extension

ICA cephalad extension

Internal carotid artery Redundant internal carotid artery

FIGURE 67.2 Cephalad and caudal extension of common and internal carotid arteriotomies, respectively, to accommodate the redundant ICA. (Copyright 1997 William B. Westwood.)

sinus tissue medially and the looser areolar tissue adherent posteriorly, in which the vagus nerve usually resides. Dissection close to and along the divided ICA mobilizes the remaining length of artery while avoiding injury to the adjacent structures. Once freed from the surrounding tissue, some ICA redundancy is generally recognized in relation to the common carotid artery (CCA). This may range from a very few millimeters to several centimeters, depending on carotid kink or loop. The heel of the ICA (side formerly adherent to the carotid body) is then divided longitudinally so it lines up with the upper end of the common carotid arteriotomy (Fig. 67.2). The anterolateral border of the CCA is extended proximally to match the length of internal carotid arteriotomy. The resultant arteriotomies, of 15 to 30 mm length, allow a wider anastomosis that is easily performed with a lower chance of restenosis. In patients with an extensively redundant ICA, the proximal

A

B

FIGURE 67.4 Eversion of atherosclerotic plaque from the ICA with visualization of internal end point. (Copyright 1997 William B. Westwood.)

artery can be obliquely excised and tailored to match the common carotid arteriotomy (Fig. 67.3). Removal of the bulk of the internal carotid plaque is a simple maneuver that usually proceeds expeditiously. The standard CEA plane is established and the plaque is elevated from the adventitia circumferentially. For optimum exposure, the adventitia is everted along the entire length of the atherosclerotic plaque until a distal intimal end point is observed, similar to rolling up a sleeve (Fig. 67.4). One forceps holds the plaque in place while the other provides cephalad traction of the adventitia. If the plaque is merely pulled out of the ICA without eversion, the end point will often be poorly visualized. If the adventitia is merely pushed cephalad without complete eversion, its redundancy will obstruct the view of the end point. As the end point is reached, the bulk of the plaque usually separates from the distal intima relatively cleanly. Alternatively, the plaque may be sharply divided with either fine scissors or a scalpel blade. Loose atherosclerotic debris can be shaved off from the wall and a carotid shunt can be inserted either before or following the endarterectomy as needed.

Chapter 67 Eversion Carotid Endarterectomy

The superior visualization of the end point prior to closure of the artery is one of the advantages of this technique compared with conventional endarterectomy. This is the most critical step of the procedure and the operator should take the time to make the end point as perfect as possible. Sometimes, gentle irrigation of the end point with heparin saline solution will cause loose strands of tissue to float away from the adventitia such that they can be easily visualized and removed. If the end point is not well visualized, the operator should make sure the artery is maximally everted. If necessary, the distal ICA clamp should be moved further cephalad. Bulky clamps can sometimes obscure and hinder eversion; therefore, we prefer smaller Yasargil clamps. If the end point is not satisfactory and loose intimal flaps are detected, tacking sutures can be placed. Although there are several ways to secure the intima, the most reliable method requires the assistant to hold the bulk of the everted adventitia at two points. Tacking can be done from inside when the artery is still everted by using fine 8–0 Prolene interrupted suture in approximately three or four areas or with inside/outside sutures by everting and inverting the internal carotid artery and tying the knot outside. Either way, it can be done as effectively as in standard endarterectomy. We do not use indirect visualization, such as angioscopy, to inspect the distal intima as this may pose an extra risk of dissection or injury to the end point. The technique of common and external CEA is similar to that of standard CEA. The plaque is circumferentially elevated from the adventitia of the CCA. The external carotid artery (ECA) plaque is circumferentially mobilized and extracted by a combination of everting the external carotid adventitia, and applying counter-traction on the plaque. As long as the plaque extends proximal to the end of the CCA by no more than 2 to 3 cm, it may be grasped and the CCA everted to expose its proximal end, where it is transected. Often this maneuver may be facilitated by further circumferential mobilization of the CCA externally and, if necessary, by moving the clamp more caudad. If the plaque runs so proximally that it cannot adequately be extracted by everting the CCA, the arteriotomy should simply be extended proximally to facilitate complete endarterectomy. Closure of the additional common carotid arteriotomy may usually be performed primarily, as this artery is relatively large. This will result in a Y-shaped suture line where the linear common carotid closure meets the circumferential proximal suture line connecting the distal CCA to the ICA. Although some operators have voiced reluctance to reconstruct the artery in this fashion, we have done this in more than 100 cases without any short- or long-term complications. A fine monofilament nonabsorbable suture (e.g., 6–0 polypropylene) is used to reattach the internal to the distal common carotid artery. The suture is usually started at the most cephalad ends of both arteriotomies and completed using a parachuted technique (Fig. 67.5). The major advantage of eversion endarterectomy is that both the com-

813

Internal carotid artery

FIGURE 67.5 End-to-side internal carotid anastomosis at the carotid bulb. (Copyright 1997 William B. Westwood.)

mon and internal carotid arteriotomies (15 to 30 mm) are used to “patch” each other. It is fairly straightforward to sew the arteries together without producing a stenosis. The anastomosis is done in the more accessible center of the wound, not in the upper reach. Clamps are released in a similar fashion to that in standard CEA; flow is first established into the ECA and subsequently into the ICA. Flow is assessed by Doppler ultrasound and the patients monitored for neurologic changes (cervical block cases). Wounds are closed and drains are used as needed, upon the discretion of the surgeon. When patients present with extensive ECA disease that is inaccessible through the CCA, it is sometimes necessary to extend the external carotid arteriotomy cephalad, and match the ICA arteriotomy in a similar fashion. The resulting reanastomosis is then performed as a cephalad advancement bifurcation-plasty. If there was unusual extension of the atheroma beyond the reach in the neck, we sharply divided the atheroma and tacked the distal intima.

Use of a Shunt Probably the most frequent objection or perceived contraindication to eversion CEA raised by surgeons (some of whom use eversion endarterectomy) is that the use of a shunt is difficult or impossible. We usually perform eversion CEAs under cervical block in awake patients and assess their neurologic function throughout the case. Shunts are used on the basis of neurologic deterioration during the procedure. However, shunts can be used routinely during all eversion CEAs, as needed (18–21,23–25). Several simple points illustrated below detail a practical manner to incorporate shunt placement with eversion CEA. Certain shunts work better than others with eversion. Those shunts that are fixed at either end via an internal balloon (Pruitt–Inahara type) or external clamping (Javid type) are both eminently suitable for eversion techniques.

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Part VIII Cerebrovascular Insufficiency

Furthermore, they may actually facilitate eversion of the distal ICA. Unfortunately, straight shunts (Edwards type) may not be easy to use as traction on the arteries during eversion can cause these shunts to slip out. Shunt insertion may be accomplished in the following fashion. After the ICA is divided from the CCA and mobilized, the arteriotomy is extended cephalad a variable distance. In some cases, this extension goes through the end point, and normal lumen is visible. A shunt can be inserted at this time (Fig. 67.6). If the plaque end point is not encompassed by the arteriotomy, the bulk of the plaque is quickly everted and removed to expose the normal lumen. Shunt insertion then may be performed. Although the second method may seem time-consuming, usually shunt insertion can be accomplished within one minute of initial clamping. Proximal insertion of a shunt is facilitated by the usual caudad extension of the common carotid arteriotomy. This allows the surgeon to visualize a relatively clean artery for shunt placement. After flow is reinstituted, the ICA is everted over the shunt. If the clamp is placed cephalad enough, the shunt acts as a mandrel over which the artery is everted. This allows for excellent visualization of the end point. Endarterectomy of the CCA is completed in standard fashion. Reanastomosis is accomplished by completing as much of the suture line as possible while leaving the shunt protruding from the anterior surface. The shunt is then removed, the arteries are reclamped, and the suture line is completed in the standard fashion.

Limitations There are few limitations of the use of eversion endarterectomy for carotid bifurcation stenosis. One such contraindication is early recurrent stenosis as a result of neointimal hyperplasia. However, eversion endarterectomy can be used for proximal and distal atheromatous recurrence. This technique may also be inappropriate for radiation-related carotid stenosis since the separation of

Atheromatous core

Eversion of outer vessel wall

Shunt

Internal carotid artery

FIGURE 67.6 The atheromatous plaque is everted over the ICA shunt in order to adequately visualize the end point. (Copyright 1997 William B. Westwood.)

the intima and outer layer may not be possible. Under those circumstances either patch angioplasty or bypass is a better option. If the plaque unexpectedly extends higher beyond reach, and the ICA has been divided from the CCA, one may choose to do an interposition bypass graft to the distal ICA and transect the diseased segment. The eversion technique should not be used for reexploration of early occlusion following standard CEA due to the presence of a longitudinal suture line. However, eversion CEA has been used for recurrent stenosis after the standard technique once the longitudinal suture line has healed.

Troubleshooting The adoption of any significant modification in technique is often unsettling, especially when the conventional technique seems to provide adequate results. Although eversion CEA can be used effectively in the vast majority of patients with primary carotid bifurcation disease, there is a gradual curve which will lead to comfort and confidence with the technique. The most significant issue with any endarterectomy is proper management of the end point. Even though we find end-point management to be easier in most cases with eversion CEA, during the learning period the surgeon may feel unsure about this. The first requires the operator to finish the rest of the endarterectomy as previously described and to reanastomose the ICA to the CCA. However, the arteries are left clamped and a short longitudinal arteriotomy is made over the end point. The end point may be examined, flaps removed, and tacking sutures inserted by conventional techniques. The arteriotomy can then be closed with a small patch of autogenous vein or prosthetic. Alternatively, a transverse arteriotomy may be made on the distal ICA and the end point examined. This may be closed primarily. The second method involves amputating the proximal ICA distal to the end point and performing a CCA–ICA bypass. This solves the problem of a difficult end point by anchoring the entire circumference of the distal intima within a suture line. The choice of conduit material could be either polytetrafluoroethylene (PTFE) or autogenous vein. Both produce similar results when used in this position with a restenosis rate of 5% to 10% (26–28). The diameter of the ICA may often dictate the type of graft used: smaller carotids are easier to size-match with vein whereas it is more convenient to use PTFE for the larger carotids. We have had to apply these techniques in less than 0.5% of cases; most were performed in the first year of adopting the eversion technique and are rarely necessary with experience.

Results Eversion endarterectomy was introduced at our institution in 1993. All surgeons adopted this technique as their

Chapter 67 Eversion Carotid Endarterectomy

primary method of CEA over a 2-year period. Since 1993, more than 5000 CEAs have been performed using this method. The indications for operation included symptomatic disease in 32% of patients. The demographic data show that 57% were men, 25% were diabetic, 32% were active smokers, 60% had hypertension, and 50% had coronary artery disease. The mean age was 70 years, with a range of 30 to 92 years. Regional anesthesia was preferred and used in 85% of patients. Shunts were placed in 4% of patients for neurological deterioration in patients undergoing cervical block anesthesia. Of the remaining 15%, the majority (>95%) needed general anesthesia because of simultaneous coronary artery bypass (CABG). During this period, the stroke/mortality was 1.2% for all eversion CEAs: 0.8% for CEA alone, and 3.4% for combined CABG/CEA procedures. In addition, nonfatal cardiac events occurred in 0.9% of patients, 0.8% developed a transient neurologic deficit that resolved by the time of discharge, and 0.2% developed cranial nerve injuries. Additionally, incidence of wound infection was 0.1%, intracerebral bleed 0.2%, and asymptomatic early occlusion 0.2%. Return to the operating room for evacuation of hematoma occurred in 1.4% of patients. Overall, the complication rate in patients undergoing eversion CEA was 1.6%, and for combined CABG/eversion CEA was 4.9%. Routine follow-up at our institution included serial duplex scans at 1 month, 6 months, and yearly thereafter. With this surveillance, the carotid restenosis rate was 0.7%, the patency of eversion endarterectomy was 98%, and the cumulative stroke-free survival was 84.5%.

Conclusion Carotid endarterectomy by the eversion technique has proven to be a durable method that encompasses the entire scope of normal carotid surgeries. Although it is uniquely useful for the treatment of redundant ICAs, it can be used for treatment of almost all symptomatic and asymptomatic carotid stenosis. The major advantage of this technique is that the closure of the artery is no longer a technical challenge. Instead, by using the arteries to patch each other, there is little chance of producing a substantial recurrent stenosis. Furthermore, vein or prosthetic materials are not needed. Eversion technique can also be used on smaller-caliber carotid arteries. This is further evidenced by the fact that female patients undergoing CEA are more likely to require patch closure or have a higher rate of restenosis in long-term follow-up (29). As elaborated in this chapter, the eversion technique may be routinely used with or without shunts. Our results with this technique demonstrate a recurrence rate in women that is less than 1%, identical to that in men. Management of the end point requires the surgeon to learn how to evert the ICA. This is not technically challenging and requires a minimum of effort to learn. In many cases, visualization of the end point is superior to

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standard techniques, thereby simplifying the other major technical issues facing the operative surgeon. However, ICAs with long-running plaques will be difficult to manage regardless of the technique. We discourage indirect visualization of the end point via angioscopy in favor of direct visualization and complete removal of the plaque. Although it is always difficult to improve on a wellaccepted technique, we believe that eversion endarterectomy is truly an advance in carotid surgery and one that we have adopted enthusiastically with improved results. Whether this becomes the principal technique or merely an occasional technique of the operator, it is an important and useful tool for the surgeon who performs carotid procedures.

References 1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445–453. 2. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. J Am Med Assoc 1995;273:1421–1428. 3. Moore WS, Mohr JP, et al. Carotid endarterectomy: practice guidelines. Report of the ad hoc committee to the joint council of the Society of Vascular Surgery and the North American Chapter of the International Society of Cardiovascular Surgery. J Vasc Surg 1992;15: 469–479. 4. Entz L, Jaranyi Z, Nemes A. Comparison of perioperative results obtained with carotid eversion endarterectomy and with conventional patch plasty. Cardiovasc Surg 1997;5:16–20. 5. Hertzer NR, Beven EG, et al. A prospective study of vein patch angioplasty during carotid endarterectomy: three year results for 801 patients and 917 operations. Ann Surg 1987;206:628–635. 6. Vanmaele R, VanSchil P, et al. Closure of the internal carotid artery after endarterectomy: the advantages of patch angioplasty without its disadvantages. Ann Vasc Surg 1990;4:81–84. 7. Healy DA, Zierler RE, et al. Long-term follow-up and clinical outcome of carotid restenosis. J Vasc Surg 1989;10:662–669. 8. Healy D, Clowes AW, et al. Immediate and long-term results of carotid endarterectomy. Stroke 1989;20: 1138–1142. 9. Archie JP. Prevention of early restenosis and thrombosisocclusion after carotid endarterectomy by saphenous vein patch angioplasty. Stroke 1986;17:901–905. 10. Schultz GA, Zammit M, et al. Carotid artery Dacron patch angioplasty: a ten-year experience. J Vasc Surg 1987;5:475–478. 11. Hertzer NR, Beven EG, et al. A prospective study of vein patch angioplasty during carotid endarterectomy: three year results for 801 patients and 917 operations. Ann Surg 1987;206:628–635. 12. Lord RSA, Raj B, et al. Comparison of saphenous vein patch, polytetrafluoroethylene patch and direct arteri-

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13.

14.

15.

16.

17.

18.

19.

20.

21.

Part VIII Cerebrovascular Insufficiency otomy closure after carotid endarterectomy. Part I. Perioperative results. J Vasc Surg 1989;9:521–529. Riles TS, Lamparello PJ, et al. Rupture of the vein patch: a rare complication of carotid endarterectomy. Surgery 1990;107:10–12. DeBakey ME, Crawford ES, et al. Surgical considerations of occlusive disease of innominate, carotid, subclavian and vertebral arteries. Ann Surg 1959;149: 690–710. Kasparzak PM, Raithel D. Eversion carotid endarterectomy: technique and early results. J Cardiovasc Surg 1989;30:495. Darling RC III, Paty PSK, et al. Eversion endarterectomy of the internal carotid artery: technique and results in 449 procedures. Surgery 1996;120:635–640. Shah DM, Darling RC III, et al. Carotid endarterectomy by eversion technique: its safety and durability. Ann Surg 1998;228:471–478. Shah DM, Darling RC III, et al. Carotid endarterectomy by eversion technique. In: Whittemore A, ed. Advances in Vascular Surgery, Volume 7. St Louis: Mosby, 1999:55–76. Shah DM, Darling RC III, et al. Carotid endarterectomy by eversion technique. In: Cameron JL ed. Advances in Surgery, Volume 33. St Louis: Mosby, 1999:459–476. Shah DM, Leather RP, et al. Technique of eversion carotid endarterectomy and contemporary results. In: Perry MO ed. Perspectives in Vascular Surgery. New York: Thieme, 1997:49–62. Darling RC III, Shah DM, et al. Carotid endarterectomy using the eversion technique. Semin Vasc Surg 2000;13 (1):4–9.

22. Shah DM, Darling RC III, et al. Technical aspects of eversion carotid endarterectomy for atherosclerotic disease. In: Ernst C, Stanley J, eds. Current Therapy in Vascular Surgery, 4th edn. St. Louis: Mosby 2000: 42–44. 23. Shah DM, Darling RC III, et al. Carotid endarterectomy by eversion technique. Loftus CM, Kresowik TF, eds. Textbook of Carotid Artery Surgery. New York: Thieme 2000:271–280. 24. Darling RC III, Leather RP, Chang BB, et al. Is the iliac artery a suitable inflow conduit for iliofemoral occlusive disease? An analysis of 514 aortoiliac reconstructions. J Vasc Surg 1993;17:15–19. 25. Chang BB, Darling RC III, et al. Use of shunts with eversion carotid endarterectomy. J Vasc Surg 2000;32: 655–662. 26. Umemura A, Yamada K, et al. Common carotid-internal carotid interposition vein graft bypass for carotid restenosis after repeated percutaneous transluminal angioplasty. Acta Neurochir (Wien) 2000;142(8): 947–949. 27. Brennan JW, Morgan MK, et al. Recurrent stenosis of common carotid-intracranial internal carotid interposition saphenous vein bypass graft caused by intimal hyperplasia and treated with endovascular stent placement: case report and review of the literature. J Neurosurg 1999;90(3):571–574. 28. Paty PSK, Darling RC III, et al. Carotid artery bypass in acute postendarterectomy thrombosis. Am J Surg 1996;172(2):181–183. 29. Hurlbert SN, Krupski WC. Carotid artery disease in women. Semin Vasc Surg 1995;8(4):268–276.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 68 Complications and Results in Carotid Surgery Michael S. Conners, III, and Samuel R. Money

The death rate secondary to cerebral infarction has been declining over the last half-century; however, this does not necessarily translate into a declining incidence of stroke (1). Currently stroke is the third leading cause of death in the United States and the second leading cause of cardiovascular death (1). In addition to being a cause of mortality, stroke can leave victims severely debilitated. This in turn is a tremendous burden on family members as well as a financial strain on the healthcare system. The ability to make a real impact on the incidence of stroke makes the surgical approach to cerebrovascular disease attractive. Carotid endarterectomy is the procedure of choice for atherosclerotic disease involving the carotid bifurcation. From an occurrence standpoint, it is by far the most common surgical procedure concerning the carotid artery. For this reason, discussion in this chapter will revolve around complications and results of carotid endarterectomy. Atherosclerotic disease of the carotid artery is felt to be the result of intimal injury followed by smooth muscle proliferation and finally calcium deposition. This leads to stenotic lesions that encroach on the area of the vessel lumen. Further injury leads to plaque rupture and hemorrhage into the lesion (2). This predisposes these areas to fragmentation and subsequent embolization of particles into the cerebral circulation. It is unknown what determines the exact timing of these events, so predicting which patients are at high risk is virtually impossible. What we do know, as will become evident in the follow paragraphs, is that once individuals show they are prone to embolization (transient ischemic attack, transient monocular blindness or hemispheric stroke) their risk of ensuing stroke is greatly increased. Much attention has been

directed at trying to identify these patients in hopes that intervention prior to plaque rupture and subsequent embolization will prevent a potentially fatal disaster. It is appropriate that we begin our discussion with these asymptomatic patients.

Results of Carotid Endarterectomy Asymptomatic Carotid Stenosis Endarterectomy for asymptomatic stenosis of the internal carotid artery (ICA) has been the subject of much debate in the past. Unlike the symptomatic counterpart, there is still some controversy regarding the actual benefit (or lack thereof) offered to the asymptomatic patient. Table 68.1 lists four randomized trials that have attempted to answer this difficult question. Over the following paragraphs, it will become obvious that the major determinant in achieving a benefit from carotid endarterectomy in the asymptomatic patient is avoiding perioperative complications. The 2% to 5% rate of stroke in the absence of a preceding transient ischemic event mandates that operative intervention be accomplished with minimal morbidity to justify use in an asymptomatic individual (3). An early report from Europe, the CASANOVA study group, evaluated the benefit of carotid endarterectomy in patients with asymptomatic ICA stenosis between 50% and 90% (4). Patients were randomized to either receive surgery plus medical treatment (330 mg acetylsalicylic acid and 75 mg dipyridamole orally three times daily) or

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TABLE 68.1 Comparison of asymptomatic carotid endarterectomy trials

Trial CASANOVA Study Group Mayo Asymptomatic Carotid Endarterectomy Study Group Veterans Affairs Cooperative Study Group Asymptomatic Carotid Atherosclerosis Study

Degree of Stenosis (%)

410

Perioperative Stroke/Death Rate

Mean Followup (months)

Angiography Complication Rate (%)

Surgical (%)

Medical (%)

50–90

42.9

0.7

4.2

NA

71

≥50*

23.6

NA

4.0

NA

444

u50*

47.9

0.4

4.3

0.9

1662

>60*

32.4

1.2

2.3

0.4

n

Comments Many crossovers and exclusion of >90% stenosis No ASA in the surgical group; terminated early 2o to MI rate in surgical group Benefit in prevention of TIA Early termination secondary to benefit of surgery

*Total occlusion excluded. ASA, acetylsalicylic acid; MI, myocardial infarction; NA, not available; TIA, transient ischemic attack.

medical treatment alone. This study has been criticized for its design flaws. First, asymptomatic patients with greater than 90% ICA stenosis were excluded from participation and operation recommended. Although the asymptomatic carotid atherosclerosis study (ACAS), which will be covered later, showed no additional benefit provided to patients with severe (>90%) stenosis, it is generally felt there is a higher risk of stroke associated with tighter lesions. Excluding this high-risk population prevents a true comparison of this group’s results with those of other large trials. Second, patients who were originally randomized to nonoperative therapy then subsequently developed stenosis greater than 90%, bilateral stenosis greater than 50%, or experienced a transient ischemic attack in the region supplied by the ICA of interest proceeded to operative intervention. All together 118 carotid endarterectomies were performed on patients initially randomized to medical therapy alone. Understanding the shortcomings of this study, investigators found no significance difference between the 10.7% of surgical patients and 11.3% of medical patients who experienced at least one end point using the intent-to-treat analysis. End points were defined as stroke or death due to surgery or stroke. Based on their analysis, they did not recommend offering a carotid endarterectomy to individuals with ICA stenosis <90%. A second study that found no demonstrable benefit to carotid endarterectomy in the asymptomatic population was the Mayo asymptomatic carotid endarterectomy study group (5). Likewise, this study evaluated individuals with ICA stenosis of ≥50% but included the “high-risk” (>90%) group. Patients in this study were randomized to either medical treatment (80 mg of acetylsalicylic acid orally four times daily) or surgery alone. A

couple of concerns with this trial are 1) a small number of randomized patients and 2) aspirin use in the surgical arm was discouraged in hopes of avoiding complications associated with bleeding. The trial was terminated early secondary to a significant difference (p = 0.036) in the rate of myocardial infarction, favoring the use of aspirin. Altogether 22% (8 of 36) of patients in the surgical group experienced a myocardial infarction, none of whom were taking aspirin. Of these eight infarctions, five were not temporally related to the surgical procedure (four occurred before surgery and the other 5 months after endarterectomy). Neurologic events occurred with equal frequency in the two groups. Despite no real evidence for or against carotid endarterectomy, the importance of aspirin use throughout the perioperative period was recognized. Of note, each of the other trials listed in Table 68.1 utilized aspirin in their surgical groups without experiencing a significant rate of bleeding. Contrary to the CASANOVA and Mayo trials, the Veterans Affairs (VA) cooperative study group found a significant reduction in neurologic events after carotid endarterectomy in asymptomatic patients with ≥50% ICA stenosis (6). This was an all-male study with a mean follow-up of 48 months and a primary objective of determining the efficacy of carotid endarterectomy in reducing the incidence of neurologic outcome events. Neurologic events were defined either as a transient ischemic attack (TIA), transient monocular blindness or stroke. Patients were randomized to carotid endarterectomy plus medical therapy (325–1300 mg acetylsalicylic acid orally four times daily) or medical therapy alone. All patients meeting criteria for inclusion were required to undergo a carotid arteriogram prior to randomization. Three (0.4%) patients suffered a stroke secondary to the arteriogram. This

Chapter 68 Complications and Results in Carotid Surgery

was similar to the angiography associated cerebral infarction rate experienced in the CASANOVA trial (0.7%). Analysis of all (ipsilateral and contralateral) neurologic events demonstrated an absolute reduction in risk of 11.6% (p <0.002) in favor of the surgical group. If confined to the ipsilateral carotid distribution, the absolute reduction climbed to 12.6% (p < 0.001) or the risk of an ipsilateral neurologic event in the surgical group was 62% less than that of the medical group (8.0% vs. 20.6%). This is encouraging; however, exclusion of transient neurologic events exposes an ipsilateral permanent stroke rate of 4.7%. Although investigators were successful in showing a significant reduction in neurologic outcome events, when the rate of ipsilateral stroke suffered by the surgical cohort was compared to the 9.4% rate endured by the medical treatment group, preference towards surgical intervention was suggested but no significant benefit was demonstrated (p < 0.06). Despite no advantage seen in protection from cerebral infarction, it seems logical that reducing the number of transient events would reduce the number of subsequent strokes. It is well recognized that an individual who experiences a transient ischemic event is at a 10% risk of suffering a cerebral infarction over the next year (3). One could argue that the sample size was too small to detect a significant difference. This brings to question the risk–benefit ratio. As alluded to earlier, a low perioperative complication rate plays a major role in determining the benefit achieved by asymptomatic patients. In this particular trial, the combined 30-day operative mortality and stroke rate was 4.7%. This not only compares unfavorably to the 0.9% rate experienced by the medical arm but also is noticeably higher than other trials of comparable size. So one must conclude from this study that surgery in addition to medical therapy is preferable to medical therapy alone in the prevention of ipsilateral neurologic events; however, in the absence of low perioperative complications, patients may be subjected to a substantial risk for prevention of a transient event. The largest and most compelling trial to date is the asymptomatic carotid atherosclerosis study (ACAS) (7). Its goal was to determine if the addition of carotid endarterectomy to the best medical management (325 mg acetylsalicylic acid orally four times daily plus risk factor modification) could reduce the incidence of fatal and nonfatal ipsilateral cerebral events in the asymptomatic population with > 60% ICA stenosis. As Table 68.1 shows, this trial was much larger than the trials previously discussed. A total of 828 patients were randomized to the surgical arm and 834 were managed with risk factor modification and aspirin only (medical arm). Altogether 101 patients assigned to the surgical group never proceeded to surgery but following the intent-to-treat rule all were included in the final analysis. Perioperatively 19 (2.3%) surgical patients had a stroke or died. Three of these complications occurred before operative intervention. Evaluating at the actual numbers, 16 (2.2%) of 724 patients who had an endarterectomy died or suffered a stroke. Five were a direct result of angiography and the remaining 11 (1.5%) were

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associated with the surgical procedure. A criticism of this study, offered by advocates of carotid endarterectomy, is the unacceptably high stroke rate (1.2%) experienced as a result of the arteriogram. A total of 414 patients underwent an arteriogram after randomization. This is approximately half the number of patients who had an arteriogram in the VA study but three times the complication rate. The medical arm had two patients experience a cerebral infarction and one died, yielding a “perioperative” stroke and mortality rate of 0.4%. Comparing these statistics, it is easy to see that the greatest risk to the surgical patient is early on or perioperatively. Realizing this, organizers of ACAS were prudent in establishing strict guidelines for surgeon and center participation. The importance of a low perioperative complication rate was emphasized in selecting highly competent surgeons. Surgeon requirements included a minimum of twelve carotid endarterectomies per year with a combined death and stroke rate of £ 3% for asymptomatic patients and £ 5% for symptomatic individuals. Altogether 117 surgeons were selected, with an overall combined mortality and stroke rate of 1.5%. In the ACAS trial they were able to accomplish similar results. The study was terminated after a mean of 2.7 years of follow-up. A significant difference in favor of surgery had been achieved. Applying a Kaplan–Meier estimate demonstrates a projected 5-year ipsilateral stroke and death rate of 11% for the medical cohort and 5.1% for the surgical cohort (p = 0.004). This translates to over 50% reduction in the risk of stroke or death with endarterectomy. Similar to the VA study, ACAS investigators found a significant advantage with endarterectomy when ipsilateral transient events were included in the analysis (8.2% vs. 19.2%; p < 0.001). Assuming all surgical patients (724) had been subjected to the high complication rate associated with angiography, 19 carotid endarterectomies would need to be performed to prevent one stroke over 5 years. Additional subgroup analysis suggested that men benefit more than women (66% vs. 17%) but significance was not achieved. A small number of women patients and a higher percentage experiencing a perioperative complication may be responsible for preventing a significant difference. Similarly, evaluating benefit related to grade of stenosis revealed no difference in 5-year stroke risk; however, like the number of women patients, sample sizes were too small (70% of patients had <80% stenosis). Despite the low perioperative complication rate, the risk associated with surgery remains higher than the risk experienced by the medical cohort for the first 10 months. After this point, surgical patients enjoy an advantage and become “significantly protected” at 3 years. Reducing the complications associated with angiography could provide further benefit. Many centers today are substituting duplex ultrasonography for angiography in a substantial number of patients. Elimination of all angiographyrelated complications would reduce the number of endarterectomies required to prevent a stroke within 5 years from 19 to 15.

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Carotid endarterectomy in asymptomatic patients for protection from cerebral infarction has received extensive evaluation with many questionable results. The most convincing data to date provide evidence that surgical intervention in addition to medical therapy and risk factor modification offers superior protection over medical therapy alone in patients with ICA stenosis > 60%. This stands true only if endarterectomy can be performed with a less than 3% rate of perioperative complications. Hopefully advancements in noninvasive imaging techniques will reduce the number of patients prone to angiographyrelated complications and further increase the benefit provided by carotid endarterectomy. Further studies are needed to identify certain subgroups of patients who stand to gain more than the routine asymptomatic individual.

Symptomatic Carotid Stenosis Unlike the continuing debate surrounding carotid endarterectomy in asymptomatic patients, strong evidence has been set out for patients with symptomatic disease. Those patients with greater degrees of stenosis stand to benefit a substantial amount while those with lesser degrees show only moderate benefit. The necessity of a low perioperative complication rate mandated for patients with asymptomatic ICA stenosis is likewise paramount for individuals with symptomatic atherosclerotic ICA disease. The North American symptomatic carotid endarterectomy trial (NASCET) was a landmark study establishing overwhelming support in favor of carotid endarterectomy in patients with symptomatic ICA stenosis (8). The study divided symptomatic patients into either high-grade (70% to 99%) or moderate to severe (<50%, 50% to 69% respectively) ICA stenosis. Beneficial effects of carotid endarterectomy in patients with symptomatic high-grade stenosis became evident early in the study. The average duration of follow-up was only 18 months when randomization to this arm was halted secondary to a significant treatment benefit achieved in the surgical patients. This was a randomized trial that involved patients under 80 years of age, who had experienced either a hemispheric transient ischemic attack (TIA), monocular blindness persisting less than 24 hours, or a nondisabling stroke within 120 days of randomization. A total of 331 patients placed in the medical group received 1300 mg of aspirin daily (less if side effects developed) and 328 patients in the surgical group underwent carotid endarterectomy in addition to medical therapy. At 2 years, surgical patients were found to have a 17% absolute reduction in risk of ipsilateral cerebral infarction. This translated to a 65% relative risk reduction or prevention of one stroke for every six patients treated with endarterectomy. Investigators also found a correlation between absolute risk reduction and severity of stenosis. Individuals with 90% to 99% ICA stenosis had an absolute risk reduction in ipsilateral strokes within 2 years of 26% while those with 80% to

89% and 70% to 79% ICA stenosis had reductions of 18% and 12% respectively. Like the ACAS trial, surgeons were required to have low perioperative complication rates. Prerequisites included 50 consecutive carotid endarterectomies within the previous 24 months with perioperative complication rates of <6%. In the perioperative period (within 30 days of surgery for surgical patients and within 32 days of randomization for the medical group), 18 surgical patients suffered cerebral infarctions, one of which was fatal. One other patient died shortly after surgery, yielding a perioperative stroke and death rate of 5.8% (Table 68.2). The medical group had 11 strokes, one of which was fatal, generating a 3.3% peri-randomization stroke and death rate. Although the surgical cohort was at a higher risk for stroke and/or death in the perioperative period, this disadvantage was overcome at 3 months and persisted throughout the study. Similar to the ACAS trial, credit for success is attributed to the high competency demonstrated by the surgeons. Patients with moderate (<50%) to severe (50–69%) degrees of ICA stenosis were followed out to 5 years (9). The benefit achieved by individuals with 50% to 69% ICA stenosis was found to be similar to that seen in asymptomatic patients. Absolute reduction in risk of ipsilateral stroke in this group was 6.5% or, for every 15 patients treated, one ipsilateral cerebral infarction was prevented over the next 5 years. Advantages over medical therapy were experienced in the first 2 to 3 years. After this period the risk of ipsilateral stroke in the medically treated patients was similar to that among surgically treated patients. Another interesting point observed, which was also suggested in the ACAS study, was that women benefit less than men. Secondary subgroup analysis reveals that 12 men need to be treated to prevent one ipsilateral stroke of any severity. The corresponding number of women needed to achieve the same result is 67. Investigators found no benefit offered by endarterectomy to individuals with <50% ICA stenosis. A second trial, which supported NASCET’s findings, was the European carotid surgery trial (ECST) (10). This particular trial enrolled all symptomatic patients regardless of stenosis severity. Altogether, 3018 patients were randomly divided to either the surgical (1807) or medical (1211) groups. Analysis based on degree of ICA stenosis found that patients with > 80% stenosis had a substantial benefit with endarterectomy over medical treatment alone. These findings correlate with those of the NASCET trial, in the high-grade stenosis portion. The difference in the degree of stenosis between the two trials is a result of angiographic measuring differences and not actual differences in the degree of stenosis. Another similarity to the NASCET trial was that researchers experienced the same phenomenon of increasing benefit with increasing stenosis. Absolute risk reduction was 5.7% and 14.2% for patients in the 80% to 89% and 90% to 99% range respectively. Combining these two subgroups results in one major stroke and/or death eliminated for each nine

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Chapter 68 Complications and Results in Carotid Surgery TABLE 68.2 Perioperative stroke and death rates Perioperative Mortality Rate (%) Trial

Perioperative n

CASANOVA Mayo

334* 36

VA Coop

211

ACAS

724

NASCET (high-grade)

328

NASCET (moderate–severe)

1087

ECST

1807

Total

4527

Stroke

Nonstroke

1.2 NA 0.0 0.0 1.9 0.5 0.2 0.0 0.6 0.3 1.2 0.6 1.2 0.8 0.9 0.4

3.0 NA 4.0 0.0 2.8 1.4 2.1 0.2 5.5 0.3 6.2 0.6 6.6 0.4 4.1 0.5

Perioperative Stroke Rate (%)†

Stroke and Death Rate (%)

4.2

3.7‡

4.0 4.3 2.3 5.8

6.5†

6.7 7.0 4.8

*Includes endarterectomies preformed in the crossover patients.

†Does not always equal the sum of the perioperative mortality rate and the perioperative stroke rate. Individuals who died as a result of stroke are counted twice. ‡Average perioperative stroke and death rate. NA, not available

carotid endarterectomies performed safely. This benefit appeared to be the greatest over the first 2–3 years, then the risk of stroke and/or death was similar to that experienced by the medical patients. However, the perioperative complication rate was higher than that of either NASCET trial. In conclusion, these three trials have demonstrated that a carotid endarterectomy performed by an experienced surgeon can significantly reduce the risk of stroke in patients with high-grade (70–99%) symptomatic ICA stenosis. One stroke is prevented for every six to nine endarterectomies in this patient population. Evaluating subgroups suggests that men benefit more than women and beneficial effects correlate with degree of ICA stenosis. Individuals with lesser degrees of stenosis (50–69%) are similar to asymptomatic patients, such that the benefits are not always clearly greater than the risks and patients with minimal disease (<50%) are not offered any advantage over medical treatment alone. As would be expected, perioperative complications were consistently higher in the symptomatic trails. Despite this, surgeons were still able to demonstrate a clear reduction in the risk of stroke in patients with > 70% ICA stenosis.

Complications An uncomplicated carotid endarterectomy is ordinarily well tolerated, frequently with the patient discharged on the first postoperative day. However, if complications occur, they can be devastating, and the benefits of this pro-

cedure might be eliminated by a high complication rate. As addressed earlier in this chapter, the morbidity and mortality must be kept quite low to justify use in routine clinical practice. Benefits enjoyed by this prophylactic procedure are highly dependent on low perioperative complication rates. Complications associated with carotid endarterectomy include neurologic, cardiac and, as with any surgical procedure, a multitude of generic complications (respiratory, infection, hematoma, etc.). Hematoma formation deserves special attention because limitations to tissue expansion make this a serious problem in the neck. Compression of the trachea can occur when postoperative bleeding is not recognized. Meticulous hemostasis is obligatory if hematoma formation is to be avoided. Further discussion in this text will be limited to the major complications of neurologic and cardiac origin. These are the precise perioperative problems that determine whether a carotid endarterectomy is beneficial or hazardous to the individual.

Mortality Death secondary to a carotid endarterectomy can and does occur but fortunately the rate is quite low. Most deaths occur as a result of either a neurologic insult or a myocardial infarction. Rothwell et al. reviewed 21 studies that included 2521 operations for asymptomatic stenosis and 9529 procedures for symptomatic lesions (11). The overall death rate was 1.31% for asymptomatic patients

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and 1.81% for patients with symptomatic disease. Reviewing the causes of death, Rothwell found similarities between the asymptomatic (0.81%) and symptomatic (0.80%) patients with respect to nonstroke deaths. The most common cause of a nonstroke death was cardiac in nature, with the vast majority being the result of a myocardial infarction. Not surprisingly, death secondary to a fatal stroke was 40% higher in the symptomatic population (0.91% vs. 0.47%). Table 68.2 reviews the 30-day mortality rates from the various trials discussed in this chapter. By comparing the perioperative death rate among asymptomatic and symptomatic patients one can see differences similar to those found by Rothwell. Although the perioperative stroke death rate and the nonstroke death rate are slightly less than Rothwell’s findings, the same trends are identified. Cardiac disease among this patient population is common. It was the leading cause of death in the ACAS, VA, and both NASCET trials and was responsible for 75% of the surgical perioperative deaths in the VA study. Riles and associates found 41% of patients undergoing a carotid endarterectomy to have preexisting significant heart disease as manifested by angina, congestive heart failure, previous myocardial infarction, or the use of significant cardiac medication (12). Bardin and coworkers demonstrated that approximately one-third of patients undergoing carotid endarterectomy have a history of myocardial infarction and approximately one-third have occasional bouts of clinical angina (13). Goldman et al. devised a scoring system, which used independent preoperative variables, in hopes of identifying patients at high risk for adverse cardiac events (14). In this system, patients receive points for each variable, then are grouped (I–IV) by sum of points. Musser and colleagues found in carotid endarterectomy patients that individuals in Goldman classes III and IV were at a significantly higher risk of experiencing an adverse cardiac event or death (15). In summary, perioperative mortality rates are very important in determining the beneficial effect of carotid endarterectomy and these rates are quite low. Death rate secondary to stroke is higher in symptomatic individuals, whereas nonstroke death rates are essentially the same for asymptomatic and symptomatic patients with the leading cause of death being myocardial infarction. Efforts should be directed at preoperative identification and intraoperative monitoring of patients at high risk for cardiac events.

Morbidity Mechanisms of Perioperative Neurologic Deficits Carotid endarterectomy is an unusual procedure in the fact that the exact end point it is trying to avoid is also one of its most common complications. Examination of Table 68.2 allows one to appreciate how frequent these major complications occur. These rather disturbing rates and the

uncertainty behind the cause prompted Riles and coworkers at New York University to study perioperative strokes with an emphasis on the cause of such events (16). Upon review of their database, they identified 66 (2.2%) patients who had suffered a perioperative stroke related to a carotid endarterectomy. The most probable cause was obvious in 63 of these patients. Causes of stroke were classified into one of six categories: 1. 2. 3. 4. 5. 6.

ischemia during carotid artery clamping; postoperative thrombosis and embolization; intracerebral hemorrhage; stroke from other mechanisms related to surgery; stroke unrelated to the reconstructed artery; and unknown.

The most common cause, thrombosis and embolization, accounted for 40% of the strokes and was felt to be the result of a technical imperfection. This category was further subdivided into immediate postoperative ICA thrombosis with embolization and postoperative embolization without evidence of arterial occlusion. The classification difference between these subcategories is based solely on the amount of thrombus formed at the endarterectomy site. Postoperative thrombosis with embolization accounted for 15 (60%) strokes, 13 of which occurred within 12 hours of the procedure. An interesting side point was that these patients had their procedure performed under a local anesthetic and tolerated clamping of the carotid artery without evidence of ischemia. This incriminates embolization as the culprit for the infarction and not the actual thrombosis. On reexploration of these patients, problems identified included clamp injuries, kinks in redundant vessels, distal intimal flap elevations, stenosis at the closure of the arteriotomy, and rough endarterectomy surfaces. Platelet aggregates were usually found at the defect site. Similar findings were noted by Bandyk and colleagues when they evaluated 250 endarterectomies using intraoperative ultrasonography and found 4% of patients to have severe flow disturbances related to either vessel stricture, intimal flap formation, or fibrin-platelet aggregates (17). Patients who suffered embolization in the absence of arterial thrombosis accounted for 10 strokes in Riles’ series and generally presented later than patients with occluded vessels (70% presented on or after postoperative day 1). These strokes were usually milder than those seen with vessel thrombosis. The second most prevalent cause was that of intracerebral hemorrhage (19%) and was almost always associated with reopening of a severely stenotic lesion. Reflex contraction then relaxation of intracranial vessels in the normal brain serves as a protective mechanism against variations in systemic blood pressure. In the ischemic brain, this autoregulation is lost and the vessels remain maximally dilated. Sundt and coworkers have demonstrated that patients with critical high-grade carotid stenosis have abnormally low blood flow to the ipsilateral cerebral hemisphere (18). Removal of the stenosis increas-

Chapter 68 Complications and Results in Carotid Surgery

es flow to as much as three to four times preoperative levels. This exposes capillary beds to profound increases in pressure that can subsequently lead to edema and hemorrhage (hyperperfusion syndrome). Pomposelli et al. demonstrated that patients who, either intraoperatively or postoperatively, are hypertensive and whose blood pressure is difficult to control perioperatively are at increased risk of developing an intracranial hemorrhage (19). The patients with near-total occlusive lesions (>95%) may also manifest postoperative neurologic dysfunction characterized by severe temporal headaches, nausea, vomiting, and even seizures. Reigel et al. demonstrated that these patients have lateralizing epileptiform discharges on electroencephalograms (20). The third most common cause, ischemia during carotid artery clamping, is a consequence of hypoperfusion. This was felt to be the cause of 10 (16%) strokes, five of which were clearly related to difficulties with shunt placement and the other five were consequences of hypoperfusion related to hypotension, bradycardia, or contralateral ICA occlusion with a delay in shunt placement. The major problem in this grouping is the lack of adequate cerebral perfusion. In an effort to overcome problems such as these, surgeons began using an intra-arterial shunt. There are basically three trains of thought: those who always shunt, those who selectively shunt and those who never shunt. Advocates of always shunting feel that experience is gained with repetition and complications are minimized (technical difficulties with shunt placement or delay in shunt placement accounted for 60% on the complications in the category) (21). Surgeons who selectively shunt prefer not dealing with the technical issues associated with working around the shunt so they attempt to identify individuals who would benefit from the use of a shunt. Over the years, techniques have evolved in an attempt to identify patients who cannot tolerate clamping of their internal carotid artery. Early criteria used focused on backbleeding of the internal carotid artery. Pulsatile backbleeding was an indication that no shunt was needed. In an effort to quantify backbleeding, surgeons started monitoring stump or distal arterial pressures (22,23). Hayes and colleagues recognized a stump pressure of 50 mmHg as being protective and today this is generally felt to be safe (22). Another method in use today utilizes intraoperative electroencephalography. By measuring changes in brain wave activity, surgeons are able to identify patients who experience cerebral hypoxia with carotid clamping. A third method is to perform the endarterectomy under local anesthesia. This allows the surgeon to do a test clamping of the ICA while monitoring the awake patient. The fourth category, strokes from other mechanisms related to surgery, accounted for 13% of the perioperative strokes. This category encompassed a potpourri of problems ranging from vessel dissection to global anoxia related to premature extubation. Strokes unrelated to the operated artery, category 5, accounted for 13% of the neurologic deficits. This class included entities such as car-

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diac thrombus embolization, cerebral infarctions in other vascular territories, and infarctions associated with angiography. Riles et al. divided the causes of stroke into either technically related (categories 1, 2, and 4) or technically unrelated (categories 3, 5, and 6) and discovered that at least 65% of perioperative cerebral infarctions were related to technical aspects of the procedure (16). This reiterates the concern of many trial collaborators regarding the importance of a highly competent surgeon performing the endarterectomy. In an effort to suggest minimum standards for carotid endarterectomy, the American Heart Association consensus panel was created (3). Table 68.3 shows the 30-day combined mortality and neurologic deficit rates considered to be the maximum acceptable levels, based on indications for operation (24). It is also recommended that actual data be kept with the results of each given surgeon and suggests that surgeons with unacceptably high complication or death rates be limited in their privileges to carry out carotid endarterectomy. Looking back at Rothwell’s work, the overall risk of stroke and/or death was 3.35% for asymptomatic lesions and 5.18% for the symptomatic counterparts (11). This is in accord with the recommendations set out by the American Heart Association. Of note, although the trends suggest asymptomatic lesions result in a lower combined perioperative stroke and death rate, Rothwell failed to identify a single study in which the perioperative stroke and death rate was significantly lower in asymptomatic patients (11). However,on viewing some of the larger multicenter studies, the lower perioperative stroke and death rate in asymptomatic individuals seems intuitive. In conclusion, a perioperative stroke is not only a physically devastating event but a psychologic insult as well. In lieu of the fact that most perioperative strokes occur as a result of technical imperfections, extreme care and meticulous detail must be directed toward each step of the procedure. If a patient awakens with a neurologic deficit and intraoperative imaging (ultrasonography or angiography) was not used, we suggested immediate reexploration. If no obvious source of the neurologic deficit is present, or if the source of the deficit is not reparable (such as one originating from the siphon or A-1 segment of the carotid artery), then the patient should be treated with anticoagulation and antiplatelet agents. Some authors suggest that immediate thrombolysis delivered directly into the carotid artery may prove beneficial (25, 26). We have utilized this technique on few occasions, with normalization of neurologic function. Due to timing we are not cer-

TABLE 68.3 Maximum acceptable 30-day combined mortality and stroke rate for carotid endarterectomy Asymptomatic stenosis Transient ischemic attacks Ischemic stroke Recurrent disease after previous endarterectomy

<3% <5% <7% <10%

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Part VIII Cerebrovascular Insufficiency

tain whether the patients were suffering a TIA or a true stroke. Presently, no untoward events have occurred using this protocol.

Postoperative Blood Pressure Problems Alterations in blood pressure are common after carotid endarterectomy. The actual incidence varies depending on the defining criteria but can be as high as 50% for both hypo- and hypertension. In the VA cooperative study, 30% of patients experienced postoperative blood pressure instability (5% hypotension and 25% hypertension). The leading theory regarding the etiology centers on changes in baroreceptor activity. Baroreceptors located in the carotid sinus detect changes in blood pressure by monitoring wall stretch. Stretching of the carotid sinus secondary to increases in blood pressure ordinarily cause a reflexive bradycardia and reduction in blood pressure. Removal of calcified plaque from the arterial wall changes the compliance of the wall from a fixed rigid condition to a more elastic state. Subsequent exposure of the endarterectomized vessel to systemic blood pressure leads to an overreactive response; thus bradycardic hypotension. A similar response can be encountered during the surgical dissection if the carotid sinus is manipulated too aggressively. During dissection this is best treated by injection of the area with a local anesthetic such as lidocaine. Postoperative hypertension is particularly worrisome. As described above, loss of autoregulation predisposes this patient population to a potential fatal cerebral hemorrhage. The most important risk factor for developing hypertension postoperatively is a preoperative history of hypertension. Towne and Bernhard noted that most of these patients returned to normal levels within 12 hours, but some (20%) remained hypertensive for more than 24 hours (27). Also, those with uncontrolled hypertension preoperatively had a significantly greater chance of developing postoperative hypertension than nonhypertensive control subjects. Ahn and associates proposed an intracranial cause for hypertension following carotid endarterectomy after they found postoperative jugular venous blood levels of norepinephrine and renin to be elevated (28). Regardless of the cause, prompt treatment is mandatory. Currently we favor sodium nitroprusside because of its rapid onset of action and its ability to be “dialed to effect.” We attempt to keep the systolic blood pressure not more than 10% to 15% above baseline preoperative values, with the maximum accepted systolic pressure being less than 170 mmHg. We also use clonidine, as its effect is via a central pathway and it has a rather rapid effect (<1 hour).

but have been reported as high as 16% (5,6). Injury rates also vary depending on the specialty of the evaluating individual. Evans and coworkers found a 16% incidence of local nerve dysfunction; however, when speech pathologists evaluated the same patients a 38% deficit rate was discovered (29). Despite the fact that most of these deficits resolved over a 6-week period, local nerve injury is a real problem considering it is an avoidable phenomenon. A review of the local anatomy will accompany the following discussion (Fig. 68.1). Branches of the Cervical Plexus Injuries to branches of the cervical plexus are frequently unavoidable and occur with the skin incision. The transverse cervical nerve (C2 and C3) exits near the anterior border of the sternocleidomastoid (SCM) muscle and supplies cutaneous sensation to the anteriolateral neck. Damage to this branch results in an insensate area medial to the incision (30). Men should be warned preoperatively that shaving in this area might be difficult because of the numbness. The greater auricular (C2 and C3) nerve exits the SCM muscle, then ascends the upper neck to supply sensation to the skin overlying the inferior parotid gland and the lower earlobe. This nerve is likewise injured with the skin incision but near the superiormost aspect of the wound. Lost of sensation secondary to injury to these two nerves is usually temporary, with return of sensation over a maximum period of 6 to 12 months. Cranial Nerve VII The main trunk of the facial nerve is not typically in jeopardy. However, two of its branches are subject to injury. As the facial nerve exits the parotid gland the most inferior branch, the cervical, descends into the neck to supply

Local Nerve Injury During Carotid Endarterectomy The most common complication after carotid endarterectomy is local nerve injury. Rates of local nerve injury, from trials discussed in this chapter, vary from 3.8% to 11%

FIGURE 68.1 Anatomy of cervical carotid artery with nerves in situ. N, nerve; V, vein; A, artery; SCM, sternocleidomastoid muscle.

Chapter 68 Complications and Results in Carotid Surgery

motor innervation to the platysma muscle. This nerve is routinely sacrificed without postoperative disability (30). A second branch, the marginal mandibular nerve, courses inferior and parallel to the edge of the mandible to supply facial muscles responsible for maintaining proper function of the lateral mouth. Injury to this branch occurs secondary to aggressive retraction and results in a lower lip droop on the ipsilateral side. Recovery is generally the rule with this type of injury. Injury to other branches (posterior auricular nerve and the nerve to the posterior belly of the digastic muscle) can occur with exposure to high carotid lesions. Cranial Nerve IX The glossopharyngeal nerve is found high in the neck, running between the internal and external carotid arteries. This nerve carries taste and sensation to the posterior onethird of the tongue as well as sensory fibers to the pharynx and middle ear. It is injured during high dissection of the internal carotid artery. The nerves of Herring (or DeCastro), which supply the carotid sinus, are branches of the ninth cranial nerve. Postoperative blood pressure instability can result with transection. Cranial Nerve X The vagus nerve usually descends the neck posteriolateral to the carotid artery and posteriomedial to the internal jugular vein. In the proximal neck its relation with these large vessels remains fairly constant. Injury to the vagus nerve and its branches are the most commonly injured clinically important nerves. Most injuries to the main vagus trunk are clamp related and are sustained when vascular clamps are applied to the carotid artery. A branch of the vagus nerve, the superior laryngeal nerve, travels with the superior thyroid artery. Injury to this nerve ordinarily occurs while gaining control of the superior thyroid artery (a branch of the external carotid artery) (31). Care must be taken to dissect the artery and not simply place a vascular clamp in the area around it, because the nerve is frequently adherent to the posterior portion of this artery. This nerve divides into an internal branch, which supplies sensation to the glottic area, and an external branch, which supplies motor innervation to the cricothyroid muscle. Denervation of the cricothyroid muscle results in difficulty singing and talking, with limitations on high notes. A second branch of the vagus nerve, the recurrent laryngeal nerve, is rarely injured during a carotid endarterectomy. However, the possibility of a “nonrecurrent” recurrent laryngeal nerve must be kept in mind. The nonrecurrent nerve will run posteriorly to the common carotid artery and is more commonly seen on the right side (32). Injury to this nerve results in vocal cord paralysis. This becomes of vital interest when bilateral carotid procedures are planned. Prior to proceeding with the second endarterectomy, vocal cord function must be assessed with direct laryngoscopy (33). If vocal cord paralysis is present, the contralateral endarterectomy should be postponed until cord function is regained.

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Cranial Nerve XI The spinal accessory nerve exits the base of the skull through the jugular foramen and courses beneath the posterior belly of the digastric and SCM muscles to supply innervation to the SCM and the trapezius. Injury results in complete paralysis of the SCM muscle and partial paralysis of the trapezius muscle. Deficits are noted by the presence of a winged scapula and difficulty in raising the shoulder. Cranial Nerve XII The hypoglossal nerve is found frequently during a carotid endarterectomy dissection. Its course is usually above the bifurcation and anterior to the internal and external carotid arteries. Frequently it is tethered down by an artery and vein to the SCM muscle. These vessels are routinely divided in order to allow medial retraction of the hypoglossal nerve, exposing the more cephalad portion of the internal carotid artery. Division of the hypoglossal nerve produces ipsilateral deviation of the tongue and can be quite debilitating causing trouble with speech, eating, and drinking. Fibers of the hypoglossal nerve descend joining fibers of C1 to form the anasa cervicalis. Division of this nerve is done with impunity leaving no obvious loss of function. Local nerve injury is an avoidable complication. Despite most injuries resulting in only a temporary deficit, some can be permanent and utterly debilitating. Knowledge of regional anatomy is vital in preventing these serious complications.

Conclusion This chapter has concentrated on results and complications of carotid surgery with an emphasis on carotid endarterectomy. Current literature supports the use of endarterectomy in both asymptomatic and symptomatic patients with the appropriate indications. Because of the fact that most perioperative strokes occur as a result of technical imperfections, meticulous care must be given to all aspects of the procedure in order to avoid potentially fatal complications. Thorough knowledge of anatomy is required to prevent inadvertent local nerve injury and subsequent disability.

References 1. Moore WS. In Rutherford RB, et al. (eds). Vascular Surgery, 5th edn. Vol 2. Philadelphia: W.B. Saunders Company 2000: 1713–1730. 2. Clowes AW. In Greenfield LJ, Mulholland M, et al. (eds). Surgery: Scientific Principles and Practice, 2nd edn. Philadelphia: Lippincott-Raven Publishers, 1997: 1585–1596. 3. Guidelines for Carotid Endarterectomy. A Multidisciplinary Consensus Statement From the Ad Hoc Committee,

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4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

Part VIII Cerebrovascular Insufficiency American Heart Association. Circulation 1995; 91:566–579. The CASANOVA Study Group. Carotid surgery versus medical therapy in asymptomatic carotid stenosis. Stroke 1991; 22:1229–1235. Mayo Asymptomatic Carotid Endarterectomy Study Group. Results of a randomized controlled trial of carotid endarterectomy for asymptomatic carotid stenosis. Mayo Clin Proc. 1992; 67:513–518. Hobson RW 2nd, Weiss DG, Fields WS, et al. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Eng J Med 1993; 328:221–227. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. J Am Med Assoc 1995; 273:1421–1428. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial Effect of Carotid Endarterectomy in Symptomatic Patients with High-Grade Carotid Stenosis. N Eng J Med 1991; 325:445–453. Barnett H, Taylor D, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Eng J Med 1998; 339:1415–1425. European Carotid Surgery Trialists’ Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 1998; 351:1379–1387. Rothwell PM, Slattery J, Warlow CP. A systematic comparison of the risks of stroke and death due to carotid endarterectomy for symptomatic and asymptomatic stenosis. Stroke 1996; 27:266–269. Riles TS, Kopelman I, Imparato AM. Myocardial infarction following carotid endarterectomy: a review of 683 operations. Surgery 1979; 85:249–252. Bardin JA, Berstein EL, et al. Is carotid endarterectomy beneficial in prevention of recurrent stroke? Arch Surg 1982; 117:1401–1407. Goldman L, Caldera DL, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977; 297:845–850. Musser DJ, Nicholas GG, Reed JF 3rd. Death and adverse cardiac events after carotid endarterectomy. J Vasc Surg 1994; 19:615–622. Riles TS, Imparato AM, et al. The cause of perioperative stroke after carotid endarterectomy. J Vasc Surg 1994; 19:206–216. Bandyk DF, Kaebnick HW, et al. Turbulence occurring after carotid bifurcation: a harbinger of residual and recurrent carotid stenosis. J Vasc Surg 1988; 7:261–274. Sundt TM, Sharbrough FW, et al. Correlation of cerebral

19.

20.

21.

22.

23.

24. 25.

26.

27.

28.

29.

30. 31.

32.

33.

blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clinic Proc 1981; 56:533–543. Pomposelli FB, Lamparello PJ, et al. Intracranial hemorrhage after carotid endarterectomy. J Vasc Surg 1988; 7:248–255. Reigel MM, Hollier LR, et al. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. J Vasc Surg 1987; 5:628–634. Baker WH. In Bernhard VM, Towne JB. Complications in Vascular Surgery. St. Louis: Quality Medical Publishing, Inc., 1991: 466–470. Hayes RJ, Levinson SA, Wylie EJ. Intraoperative measurement of carotid back pressure as a guide to operative management for carotid endarterectomy. Surgery 1972; 72:953–960. Moore WS, Hall AD. Carotid artery back pressure: a test of cerebral tolerance to temporary carotid occlusion. Arch Surg 1969; 99:702–710. Beebe HG, Clagett GP, et al. Assessing risk associated with carotid endarterectomy. Stroke 1988; 20: 314–315. Eckstein H, Hupp T, et al. Carotid endarterectomy and local intraarterial thrombolysis: simultaneous procedure in acute occlusion of the internal carotid artery and middle cerebral artery embolism. J Vasc Surg 1995; 2:196–198. Perler BA, Murphy K, et al. Immediate postoperative thrombolytic therapy: an aggressive strategy for neurologic salvage when cerebral thromboembolism complicates carotid endarterectomy. J Vasc Surg 2000; 5:1033–1037. Towne JB, Bernhard VM. The relationship of postoperative hypertension to complications following carotid endarterectomy. Surgery 1980; 88:575–580. Ahn SS, Marcus DR, Moore WS. Post-carotid endarterectomy hypertension: association with elevated cranial norepinephrine. J Vasc Surg 1989; 9:351–360. Evans WE, Mendelowitz DS, et al. Motor speech deficit following carotid endarterectomy. Ann Surg 1982; 196:461–464. Bryant MF. Complications associated with carotid endarterectomy. Am Surg 1976; 42:665–669. Verta MJ, Applebaum EL, et al. Cranial nerve injury during carotid endarterectomy. Ann Surg 1977; 185:192–195. Wells SA. In Nyhus LM, Baker RJ, Fischer JE. Mastery of Surgery, 3rd edn. Vol 1. Boston: Little, Brown & Company, 1997: 496–507. Matsumoto GH, Crossman D, Callow AD. Hazards and safeguards during carotid endarterectomy. Am J Surg 1977; 133:458–462.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 69 Carotid Stenting: Current Status and Clinical Update Robert W. Hobson, II

Carotid endarterectomy (CEA) is the currently preferred method for cerebral revascularization in patients with symptomatic (1–3) and asymptomatic (4,5) high-grade carotid stenoses, displacing optimal medical management alone as a reasonable alternative. However, during the last decade, carotid angioplasty and stenting (CAS) has been recommended by some clinicians (6–15) due to its lesser invasiveness as well as an emerging position of clinical equipoise (16) as different specialists use CEA or CAS to manage comparable patients with cerebrovascular insufficiency. Stroke is the third most common cause of death in North America, and approximately 600,000 new strokes are reported annually in the United States (17,18). However, stroke is the second leading cause of death in a recent review of the worldwide experience due in part to aging populations (19,20). Sacco (21) has reported that up to 20% of cases of stroke are due to extracranial carotid occlusive disease; 30-day and 5-year mortality rates for strokes that occur in the carotid distribution are 17% and 40% respectively, (17), while as many as 160,000 strokerelated fatalities are documented annually. It has also been estimated that 4–5 million Americans are alive with stroke disability, making it the most common form of disability among the elderly. The American Heart Association has estimated its annual cost as $18–20 billion during the last decade (22). CEA reduces the reported incidence of stroke alone as well as stroke and death in symptomatic patients with high-grade (≥70%) stenoses (1). In addition, recent data presented by the North American symptomatic carotid endarterectomy trial (NASCET) investigators (23) has

confirmed the efficacy of CEA for carotid stenosis in the moderate range (50–69%). The procedure also reduces the incidence of combined neurologic events in male patients with asymptomatic stenoses > 50% (4), and ipsilateral stroke or any peri-procedural stroke or death in patients with asymptomatic stenoses > 60% (5). Although CAS has been proposed as an alternative to CEA, the safety and clinical effectiveness of CAS has not been established and no prospective comparisons of CAS and CEA have been completed successfully in the US. Furthermore, a Science Advisory from the American Heart Association (24) concluded that “. . . with few exceptions, use of carotid stenting should be limited to well-designed, wellcontrolled randomized studies with careful dispassionate oversight.” CEA, performed with a low peri-procedural complication rate, is the only form of mechanical cerebral revascularization for which definitive evidence of clinical effectiveness has been reported. In the NASCET data )(1), life-table estimates of the cumulative risk of stroke at 2 years were 26% in the medical group vs. 9% in the surgical group (absolute risk reduction (±SE): 17 ± 3.5%, p < 0.001). The corresponding estimates for major or fatal ipsilateral stroke were 13.1% vs. 2.5% (absolute risk reduction (±SE): 10.6 ± 2.6%, p < 0.001) and for any stroke or death were 32% vs. 16% (absolute risk reduction: 16.5 ± 4.2%, p < 0.001). Complementary findings were reported in the European carotid surgery trial (ECST) (2) and the VA symptomatic endarterectomy trial (3). Although recent presentation of data by the NASCET investigators on patients with symptomatic disease (23) also has confirmed efficacy of CEA in male patients with 50%

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to 69% stenosis, the benefit was not confirmed in women with the same degree of stenosis. In ACAS (5), after a median follow-up of 2.7 years, the aggregate risk over 5 years for ipsilateral stroke and any peri-procedural stroke or death was estimated to be 5.1% for surgical patients and 11% for patients treated medically (relative risk reduction: 53%, p < 0.001). Results from these trials have dictated current indications for carotid endarterectomy throughout the US and abroad.

Carotid Angioplasty and Angioplasty–Stenting Numerous case reports and clinical series have been published (6–15). The first report of a multicenter prospective protocol-based study of CAS, the North American percutaneous transluminal angioplasty Registry (NACPTAR) (8,9), was published in 1993. Interim results were reported on 165 angioplasties in 147 symptomatic nonsurgical patients. The average stenosis pre-angioplasty was 84% (range: 70–99%). The average stenosis immediately postangioplasty was 37% (p < 0.01). This corresponded to an immediate success rate of 83% (95% CI, 76–88%). Death from all causes occurred in 3% of procedures, and stroke in an additional 6%. The 30-day combined rate of death and stroke from all causes was 9% (95% CI, 5–15%). Data concerning the rate of restenosis in 44 lesions with angiographic follow-up at a mean of 260 days has also been reported (9). The definition of restenosis was angiographic documentation of stenosis exceeding 70%. Of the 37 lesions that were less than the original 70% stenosis after the initial dilatation, restenosis occurred in eight (22%; 95% CI, 10–38%). Of the patients who had restenosis, five of eight (63%) were symptomatic at the time of follow-up. Cox proportional hazards modeling demonstrated that symptoms and the degree of stenosis pre-angioplasty were independent predictors of angiographic restenosis in follow-up. These data suggested that restenosis after angioplasty alone would be a significant problem and stimulated clinicians to perform stenting after angioplasty as a routine practice. In 1996, Diethrich and coworkers (10) reported results of carotid angioplasty-stenting in 110 symptomatic patients with ≥70% stenoses from a single institution. One procedure failed (0.9%) for technical reasons and was converted to CEA. Two deaths (1.8%) were observed (one from stroke and one due to a cardiac event). Seven strokes [two major (1.8%) and five minor (4.5%)] and five transient neurological events (4.5%) occurred. Based on this early experience, the authors concluded that the incidence of peri-procedural neurological complications was excessive. In an accompanying editorial by Diethrich (25), he suggested that CAS be restricted to cases of carotid restenosis after prior CEA, instances in which the internal carotid stenosis was anatomically higher than readily treated by CEA, and radiationinduced stenosis.

A larger prospective protocol-based study of CAS in 204 patients was reported by Roubin and colleagues (11). Patients ranged in age from 36 to 86 years, 75% had significant coronary artery disease, and 70% of the patients had medical comorbidities that would have made them ineligible for the NASCET study. Of the 238 arteries treated (204 patients), 145 arteries (61%) presented in patients with ipsilateral symptoms (60 strokes, 85 TIAs), while 93 arteries were treated in asymptomatic patients. Altogether 9% of the patients had an occluded contralateral carotid artery and 15% had restenosis following prior CEA; 18% of the patients had complex lesions with ulcerated plaques. Technical success was achieved in 99% of patients. In two patients, the carotid artery could not be accessed via the transfemoral approach. In one patient, the procedure was aborted after initial angiography was complicated by an air embolism. Of the 204 patients, one death (0.5%) and two major (0.98%) (NIH stroke scale > 4 with residual disability > 30 days) strokes were reported. One was due to the single episode of stent thrombosis and the second due to a cardiogenic embolus causing a contralateral stroke on the second post-procedural day. Minor strokes (NIH stroke scale < 3 and resolution within 30 days) were observed in 15 patients (7.4%). During follow-up, one minor ischemic stroke has occurred in these 204 patients. Three patients have suffered TIAs with no evidence of stent restenosis. Four patients died during follow-up [one from congestive heart failure, one from pneumonia, one from intracranial hemorrhage (patient not on anticoagulation), and one from renal failure]. Repeat carotid imaging (angiography or ultrasound) has been performed in 75% of patients reaching 6 months of follow-up. Restenosis (>70% diameter reduction) has been documented in 5 of 104 (5%) patients re-studied. Stent deformation occurred in 14% of balloon expandable stents deployed. On the basis of these results, self-expanding stents have been recommended by the authors and other skilled interventionalists. Recently, Roubin, et al. (26) updated their previous reports. These data included 528 consecutive patients in whom carotid stenting was performed on 604 arteries. The stroke and death rate was 2.6% and the overall 30day stroke and death rate was 7.4% (including the minor stroke rate of 4.8%). A total of 48% of the patients treated were asymptomatic. Of the symptomatic patients, 83% would have been ineligible for inclusion in the NASCET protocol (1). Of greatest concern was the elevated 30-day stroke and death rate among patients over 80 years of age. Among this elderly group, the 30-day stroke and death rate was 16% as compared with 6% of patients under 80 years of age (p < 0.01). In comparison, Gomez and colleagues (15) reported comparability of complications between CEA and CAS in patients eligible for the NASCET protocol. These investigators reported one transient (2.5%) neurologic event and no deaths, major stroke, or myocardial infarctions among 40 NASCET-eligible patients.

Chapter 69 Carotid Stenting: Current Status and Clinical Update

Recently, one randomized clinical trial from Europe designed to compare the efficacy of CAS and CEA has reported its results. The CAVATAS investigators (27,28) randomized 504 symptomatic patients primarily to angioplasty alone (25% also had stenting) and reported comparable complication rates for CEA and CAS (disabling stroke and death for CEA 6.3% and for CAS 6.4%). Phase II of the CAVATAS investigation comparing CEA and CAS was initiated this year. The National Institute of Neurological Disorders and Stroke (NINDS) NIH is currently sponsoring CREST (carotid revascularization endarterectomy vs. stent trial) in North America (29), while a group of investigators in Germany has initiated the SPACE (30) trial. Two other aborted attempts at clinical trials to compare the efficacy of these two procedures were discontinued by their clinicians (31) or the manufacturer (32) because of high complication rates in the CAS group (10–12%). However, both groups have acknowledged that the trials were underpowered and lacked significant credentialing for interventionalists. Conclusions regarding the results of these retrospective analyses and clinical trials await further review. However, it now appears that in selected patients, CAS can be used to treat extracranial carotid stenosis in NASCETeligible patients with peri-procedural complications which may approach those reported for CEA.

Technical Considerations: Initial Results Based on the conclusions of a multi-disciplinary panel at a recent Montefiore Vascular Symposium (33), subgroups of patients were recommended for CAS. These included high-risk patients with significant medical comorbidities, patients with carotid restenosis after prior CEA, anatomically inaccessible lesions above C2, and radiationinduced stenoses. As an example, our group (34) recently documented the comparability of results between CAS and surgical intervention for restenosis after primary CEA. However, in the absence of randomized clinical trial methodology, we are currently unwilling to expand use of CAS beyond these defined subgroups of patients. We have restricted our use of CAS to patients with carotid restenosis after CEA (34) and those with high-risk medical comorbidities (35). Symptomatic or asymptomatic carotid restenosis after CEA is relatively uncommon and is generally attributed to myointimal hyperplasia during the early postoperative period (within 36 months) or recurrent atherosclerosis thereafter (36–40). Surgical management of carotid restenosis is controversial for two major reasons:

2.

Indications for operative management in the asymptomatic patient with high-grade (≥80%) restenosis remain controversial due to the low risk of stroke or progression to total occlusion (36).

Reoperation is associated with an increased risk of perioperative neurological events and cranial nerve palsies (41,42).

Because of these issues, some authors (34,43–45) recommend CAS as an alternative to operative management. However, lack of efficacy data comparing endovascular management and carotid endarterectomy has created additional controversy in the choice of treatment among specialists seeing patients with carotid restenosis as well as those with primary atherosclerotic occlusive disease. We prospectively collected data and intervened using endovascular techniques on patients with symptomatic and asymptomatic (≥80%) carotid restenosis due to myointimal hyperplasia for the purpose of defining technical feasibility and periprocedural outcomes (35). Technical considerations in the performance of CAS are outlined in Table 69.1. A more recent example of pre- and postprocedural arteriograms (Figs. 69.1) demonstrate use of an antiembolic device (ACCUNET, Guidant, Santa Clara, CA) and a nitinol stent (ACCULINK, Guidant, Santa Clara, CA). Balloon angioplasty for placement of the antiembolic device and stent was not required. Currently, predilatation is generally necessary in lesions > 90% stenoses or when associated with angiographic evidence of a string sign. In these cases and all but one other case, stents were placed across the carotid bifurcation. Serial duplex ultrasonography has demonstrated persistent patency of all external and internal carotid arteries. In our series of 46 patients undergoing 50 CAS procedures (34,35), all procedures were completed technically. One 72-year-old woman with severe coexisting coronary

TABLE 69.I Updated protocol for carotid stent (CAS) procedure (modified/updated from reference 34) 䊏

䊏 䊏 䊏 䊏

䊏

䊏 䊏

1.

829

䊏 䊏

Transfemoral approach; open carotid cannulation considered in presence of severe aortoiliac disease; pre-procedural aspirin and Clopidogrel. Heparinization to ACT >300 (with introduction of antiembolic device) 5-Fr. Vitek catheter for cannulation of aortic arch branches. 0.035-in. coated Terumo long exchange guidewire to external carotid artery. 6-Fr. guide sheath (100 cm length) to common carotid artery proximal to lesion; occasional use of the 0.035-in. Amplatz stiff guidewire is recommended to advance the Vitek catheter or 6 F guide sheath into the common carotid artery. 0.014-in. guidewire to cross common–internal carotid stenosis, and place an antiembolic device (ACCUNET, Guidant, Santa Clara, CA); 3-mm or 4-mm low-profile balloon for predeployment dilatation as required. Deployment of a nitinol self-expanding stent (ACCULINK, Guidant, Santa Clara, CA). Post-stent dilatation using 5-mm or 6-mm balloons. Intermittent hand-injection angiography during procedure; utilize bony landmarks for balloon and stent placements. Remove sheath once ACT <180; continue aspirin, while Clopidogrel is continued for a minimum of 1 month after CAS.

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A

B

FIGURE 69.1 (A) Selective lateral carotid angiogram demonstrating a high-grade restenotic lesion in the proximal internal carotid artery near the apex of a Dacron patch angioplasty used in this patient. (Modified from Hobson RW II, Lal BK, et al. Carotid artery closure for endarterectomy does not influence results of angioplastystenting for restenosis. J Vasc Surg 2002; In Press, with permission.) (B) Selective angiogram demonstrating

passage of the guidewire for placement of a selfexpandable nitinol stent. Please note the center location of the wire which was confirmed during CAS; an antiembolic device was used (ACCUNET, Guidant, Menlo Park, CA) during this procedure. (Modified from

C

artery disease had undergone coronary angioplastystenting during the week before a right carotid angioplasty-stent procedure for symptomatic high-grade carotid stenosis. Discharged on the morning after CAS, the patient was alone at home and died suddenly 10 days later, presumably due to an acute myocardial infarction or cardiac arrhythmia. She represented the only mortality (2.2%) in our initial series of 50 CAS procedures. All patients were discharged on the morning following the

Hobson RW II, Lal BK, et al. Carotid artery closure for endarterectomy does not influence results of angioplastystenting for restenosis. J Vasc Surg 2002; In Press, with permission.) (C) Final selective angiogram demonstrated a satisfactory post-stent result. (Modified from Hobson RW II, Lal BK, et al. Carotid artery closure for endarterectomy does not influence results of angioplastystenting for restenosis. J Vasc Surg 2002; In Press, with permission.)

procedure and no subsequent peri-procedural strokes or deaths have been observed. Based on our experience with CAS as well as a review of results from retrospective analyses and one prospective clinical trial, these data suggest that an efficacy trial comparing the results of CEA and CAS should proceed in the US. Furthermore, it would appear that the safety of the procedure is now approaching that of carotid endarterectomy, particularly with the addition of an

Chapter 69 Carotid Stenting: Current Status and Clinical Update

antiembolic device (46,47). These protective devices can be categorized in one of three general areas: distal balloon occlusion, distal filter devices, and proximal occlusion devices accompanied by balloon occlusion of the external carotid artery occlusion (47). Currently, the distal devices appear to be most practical; however, both require crossing the lesion before the antiembolic device is in place, while the third device allows performance of CAS without crossing the lesion. In our current practice, we have moved from balloon and self-expanding stainless steel stents to self-expanding nitinol stents and currently use a distal filter device for its antiembolic protection. That CAS can be performed safely after primary closure of the carotid arteriotomy or patch angioplasty also has been documented recently (48). We reviewed our experience with 54 cases of carotid restenosis after prior CEA. Eight cases (15%) had primary closure, five (9%) had patch closure with autologous vein and 41 (76%) operations utilized Dacron patch closures. All patients were successfully managed by CAS using predeployment angioplasty with low-profile balloons, self-expanding stents and post-stent angioplasty. No instance of contrast extravasation, arterial disruption, or subintimal dissection was observed. In this particular series, one stroke (1.8%) was observed, and a retinal infarction with partial permanent field of vision loss occurred in a patient with prior CEA and Dacron patch closure, while no deaths were observed in the series. The incidence of in-stent restenosis after CAS also appears to be reassuringly low. While several authors have documented restenosis rates of <5% (10,48–50), followup has been brief in these series. Appearance of high-grade (>80%) in-stent restenosis (35) has now been documented in four of our 50 CAS procedures (8%) after a mean follow-up of 18 ± 10 months. One example (Fig. 69.2) was documented which was treated by repeat angioplasty without the necessity for operative intervention. Cases have been managed by angioplasty (n = 3) or angioplasty and re-stenting (n = 1) and all continue to be asymptomatic. As this series has been followed for an additional year, the incidence of in-stent restenosis has been observed in about 5% of cases, which appears to be substantially lower than the 16% to 59% incidence with coronary stenting and 13% to 39% with iliac stenting.

Organizational Plan Stimulated by our clinical experience and the referenced reports, the CREST investigators received approval for funding from the NINDS, NIH for a trial to compare efficacy of CEA and CAS in symptomatic patients with diameter reducing stenoses >50%. The executive committee for CREST (Table 69.2) designed a protocol to compare the efficacy of these two procedures. However, recognizing that CAS is a relatively new procedure, each participating center will be required to complete a credentialing phase so as to reassure clinicians that the safety of these

831

procedures has been reviewed and established before proceeding with the randomized phase of the trial. Assuming that a credentialing phase, which requires performance of up to 20 interventional procedures at each of 50 or more participating centers, is completed to the satisfaction of the study’s interventional management committee, randomization of patients between the two treatments will then proceed. The primary outcome events for this clinical trial will include: 1. 2.

any stroke, myocardial infarction or death during the 30-day perioperative or peri-procedural period; or ipsilateral stroke after 30 days.

End points will be reviewed by an adjudication committee blinded to the assigned treatment. Stroke will be determined by a positive TIA/stroke questionnaire confirmed by an evaluation of a neurologist. Myocardial infarction will be determined by ECG and enzyme abnormalities. Secondary goals include: 1. 2.

3. 4. 5.

describe differential efficacy of the two treatments in men and women; contrast perioperative procedural (30-day) morbidity and post-procedural (after 30 days) mortality for CEA and CAS; estimate and contrast the restenosis rates for the two procedures; identify subgroups of participants at differential risk for the two procedures; and evaluate differences in health-related quality-of-life issues and cost effectiveness.

Differential efficacy assessment of CEA and CAS based on gender is a secondary goal for CREST. In patients with high-grade asymptomatic stenosis reported by ACAS, CEA offered a 66% reduction in events over a 5year period for men, but only a 17% reduction for women (5). In NASCET, while no differential gender effects were reported among symptomatic patients with stenosis greater than 70%, male patients demonstrated greater benefit after CEA than women for stenoses of 50–69% (23). While the causes for these examples of differential efficacy between genders are not well understood, the effect may be attributed to a higher complication rate for CEA in women, possibly caused by their reported smaller arterial sizes and a greater surgical morbidity. Unfortunately, neither ACAS or NASCET suspected the possibility of a differential gender effect. However, given the results of these two randomized clinical trials, a requirement for a priori plans to evaluate the possibility of a differential gender effect has become an important component of CREST. Centers are being selected with a goal as high as 50% women in the randomized sample of patients and a minimum of 40%. Patients will be evaluated at baseline, 24 hours postprocedure, 30 days, 6 months and thereafter at 6-month intervals. Baseline procedures will include a brief medical

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A

B

C

D

FIGURE 69.2 (A) Selective angiography in a symptomatic patient presenting with a single episode of amaurosis fugax 11 months after prior right carotid endarterectomy demonstrating a focal high-grade restenosis. (B) Poststent deployment angioplasty resulted in a technically satisfactory angiographic results. (C) In-stent restenosis was defined angiographically in two areas in this patient 6 months after CAS. (D) Angioplasties of both areas reduced the lesions to less than 30% residual stenoses, which have not recurred during clinical follow-up. (Modified from Chakhtoura EY, Hobson RW, et al. In-stent restenosis after carotid angioplasty-stenting: incidence and management. J Vasc Surg 2001; 33:220–226. J Vasc Surg 2001; 33:220–226, with permission.)

Table 69.2 Executive committee, CREST Robert W. Hobson II, MD, principal investigator Thomas Brott, MD, J.P. Mohr, Co-PIs neurology Robert Ferguson, MD, Co-PI, intervention (radiology) Gary S. Roubin, MD, PhD, Co-PI, intervention (cardiology) Wesley Moore, MD, Co-PI, vascular surgery L.N. Hopkins, MD, Co-PI, neurosurgery George Howard, Dr PH, Co-PI, statistical analysis Richard Kuntz, MD, Co-PI, data management D.E. Strandness, MD, Co-PI, ultrasound Jeff Popma, MD, Co-PI, angiography Beverly Huss, intervention device guidant John Marler, MD, project officer, NINDS

history and physical examination, a risk factor evaluation, performance of neurologic status questionnaires, a neurologic examination, ECG, and a baseline carotid duplex scan. The 30-day follow-up will include evaluation of the neurologic status through questionnaires, ECG, and a follow-up carotid duplex scan. All 6-month followup visits will include a brief physical, completion of the neurologic questionnaire, risk factor evaluation and carotid duplex scan. All patients with a positive neurologic status questionnaire will be evaluated by a neurologist. The sample size for the study is approximately 2,500 symptomatic patients, which will be sufficient to detect a

Chapter 69 Carotid Stenting: Current Status and Clinical Update

relative difference of 25–30% between treatment groups. Lesser differences would be considered sufficiently small to declare the treatments equivalent. Opinions have varied about the participation of vascular surgeons in randomized clinical trials on carotid endarterectomy. While the value of our participation has been recommended, the emergence of clinical equipoise (16) between treatment groups as supported by a rigorous credentialing phase of CREST should reassure our colleagues about their participation as well as the ethical conduct of this trial.

Conclusions Current clinical practice dictates that CAS be considered in limited subsets of patients. The results of clinical trials (CREST and others) will provide level I, II evidence upon which to establish a firm clinical recommendation. Clinicians are urged to support these clinical trial efforts in participating institutions, while those in other institutions should refer their patients for randomization or rely on the gold standard, CEA for the majority of symptomatic patients.

References 1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325:445–453. 2. European Carotid Surgery Trialists’ Collaborative Group. MCR European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70–99%) or with mild (0–29%) carotid stenosis. Lancet 1991; 337:1235–1243. 3. Mayberg MR, Wilson SE, Yatsu F, and the VA Symptomatic Carotid Stenosis Group. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. J Am Med Assoc 1991; 266: 3289–3294. 4. Hobson RW, Weiss DG, et al., and the Veterans Affairs Cooperative Study Group. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Engl J Med 1993; 328:221–227. 5. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study: Endarterectomy for asymptomatic carotid stenosis. J Am Med Assoc 1995; 273: 1421–1428. 6. Namaguchi Y, Puyau FA, et al. Percutaneous transluminal angioplasty of the carotid artery: its application to post surgical stenosis. Neuroradiology 1984; 26: 527–530. 7. Theron J, Raymond J, et al. Percutaneous angioplasty of atherosclerotic and postsurgical stenosis of carotid arteries. AJNR 1987; 8:495–500. 8. The NACPTAR investigators. Update of the immediate angiographic results and in-hospital central nervous system complications of cerebral percutaneous transluminal angioplasty. Circulation 1995; 92(8):1–383.

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9. NACPTAR Investigators: Ferguson R, Schwarten D, Purdp, et al. Restenosis following cerebral percutaneous transluminal angioplasty. Stroke 1995; 26:186. 10. Diethrich EB, Ndiye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996; 3:42–62. 11. Mathur A, Roubin GS, et al. Predictors of stroke following carotid stenting: univariate and multivariate analysis. Circulation 1997; 96:A1710. 12. Roubin GS, Yadav S, et al: Carotid stent-supported angioplasty: a neurovascular intervention to prevent stroke. Am J Cardiol 1996; 78:8–12. 13. Bergeron P, Chambran P, et al. Cervical carotid artery stenosis. J Cardiovasc Surg 1996; 37(suppl 1–5):73–75. 14. Shawl FA, Efstratiou A, et al. Combined percutaneous carotid stenting and coronary angioplasty during acute ischemic neurologic and coronary syndromes. Am J Card 1996; 77:1109–1112. 15. Gomez CR, Roubin GS, et al. Safety of carotid artery stenting in NASCET-comparable patients. Neurology 1998; 50:76A. 16. Freedman B. Equipoise and the ethics of clinical research. N Engl J Med 1987; 317:141–145. 17. Chambers BR, Norris JW, et al. Prognosis of acute stroke. Neurology 1987; 37:221–225. 18. Wolf PA, Kannel WB, McGee DL. Epidemiology of strokes in North America. In: Barnett HJM, Stein BM, Mohr JP, Yatsu FM, eds. Stroke: Pathophysiology, Diagnosis and Management. New York: Churchill Livingstone, 1986: 19–29. 19. World Health Organization. The World Health Report 1999. Geneva, Switzerland: WHO, 1999. 20. Bonita R. Stroke prevention: a global perspective. In: Norris JW, Hachinski V, eds. Stroke Prevention. New York: Oxford University Press, 2001: 259–274. 21. Sacco RL. Extracranial carotid stenosis. N Engl J Med 2001; 345(15):1113–1118. 22. 1993 Heart and Stroke Facts Statistics. American Heart Association, Dallas, 1992: 18. 23. Barnett HJM, Taylor DW, et al. for the North American Symptomatic Carotid Endarterectomy Trial Collaborators. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998; 339:1415–1425. 24. Bettmann, MA, Katzen BT, et al. Carotid stenting and angioplasty: a statement from the Councils on Cardiovascular Radiology, Stroke, Cardio-thoracic and Vascular Surgery, Epidemiology and Prevention, and Clinical Cardiology, American Heart Association. Stroke 1998; 29:336–346. 25. Diethrich EB. Indications for carotid artery stenting: a preview of the potential derived from early clinical experience. J Endovasc Surg 1996; 3:132–139. 26. Roubin GS, New G, et al. Immediate and late clinical outcomes of carotid artery stenting patients with symptomatic and asymptomatic carotid artery stenosis. Circulation 2001; 103:532–537. 27. Major ongoing stroke trials: carotid and vertebral artery transluminal angioplasty study (CAVATAS). Stroke 1996; 27:358. 28. CAVATAS. Endovascular versus surgical treatment in patients with carotid stenosis in the carotid and vertebral artery transluminal angioplasty study (CAVATAS): a randomized trial. Lancet 2001; 357:1729–1737.

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29. Hobson RW II, Brott T, et al. CREST: Carotid Revascularization Endarterectomy versus Stent Trial. Cardiovasc Surg 1997; 5(5):457–458. 30. SPACE trial, personal communication, Professor Stefan von Sommoggy. 2001. 31. Naylor AR, Bolia A, et al. Randomized study of carotid angioplasty and stenting versus carotid endarterectomy: a stopped trial. J Vasc Surg 1998; 28:326–334. 32. Alberts MJ, McCann R, et al. A randomized trial: carotid stenting versus endarterectomy in patients with symptomatic carotid stenosis, study designs. J Neurovas Dis 1997; Nov–Dec:228–234. 33. Veith FT, Amor M, et al. Consensus Panel on Carotid Angioplasty-Stent. Marcel-Dekker Publications, In Press, 2000. 34. Hobson RW II, Goldstein JE, et al. Carotid restenosis: operative and endovascular management. J Vasc Surg 1999; 29:228–238. 35. Chakhtoura EY, Hobson RW II, et al. In-stent restenosis after carotid angioplasty-stenting: incidence and management. J Vasc Surg 2001; 33:220–226. 36. Lattimer CR, Burnand KG. Recurrent carotid stenosis after carotid endarterectomy. Br J Surg 1997; 84: 1206–1219. 37. Stoney RJ, String ST. Recurrent carotid stenosis. Surg 1976; 80(6):705–710. 38. Bartlett FF, Rapp JH, et al. Recurrent carotid stenosis: operative strategy and late results. J Vasc Surg 1987; 5:452–456. 39. Atnip RG, Wengrovitz M, et al. A rational approach to recurrent carotid stenosis. J Vasc Surg 1990; 11: 511–516.

40. Sterpetti AV, Schultz RD, et al. Natural history of recurrent carotid artery disease. Surg Gynecol Obstet 1989; 168:217–223. 41. Treiman GS, Jenkins JM, et al. The evolving surgical management of recurrent carotid stenosis. J Vasc Surg 1992; 16:354–363. 42. Das MD, Hertzer NR, et al. Recurrent carotid stenosis: a five-year series of 65 operations. Ann Surg 1985; 202(1):28–35. 43. Bergeron P, Chambran P, et al. Recurrent carotid disease: Will stents be an alternative to surgery? J Endovasc Surg 1996; 3:76–79. 44. Yadav JS, Roubin GS, et al. Angioplasty and stenting for restenosis after carotid endarterectomy. Initial experience. Stroke 1996; 27:2075–2079. 45. Yadav JS, Roubin GS, et al. Elective stenting of the extracranial carotid arteries. Circ 1997; 95:376–381. 46. Reimers B, Corvaja N, et al. Cerebral protection with filter devices during carotid artery stenting. Circulation 2001; 104:12. 47. Parodi JC, La Mura R, et al. Initial evaluation of carotid endarterectomy and stenting with three different cerebral protection devices. J Vasc Surg 2000; 32:1127–1136. 48. Hobson RW II, Lal BK, et al. Carotid artery closure for endarterectomy does not influence results of angioplastystenting for restenosis. J Vasc Surg 2002; In Press. 49. Theron JG. Carotid artery stenosis: treatment with protected balloon angioplasty and stent placement. Radiology 1996; 201:627–636. 50. Wholey MH, Wholey M, et al. Current global status of carotid artery of carotid artery stent placement. Cathet Cardiovasc Diagn 1998; 44:1–6.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 70 Vertebrobasilar Disease: Surgical Management Ronald A. Kline and Ramon Berguer

This chapter deals specifically with ischemic manifestations derived from arterial disease of the vertebrobasilar trunk or of its arteries of supply. Excluded are the ischemic manifestations and neurologic diseases that are presumed to be secondary to diffuse obliteration of small arteries, such as the perforating branches of the basilar artery. In patients with the latter conditions, the arteriogram usually fails to identify the site of occlusion (the branches are small beyond the resolution power of the arteriogram) or the potential source of microembolization. It is important to introduce at the beginning of this discussion the concept of the two most common mechanisms of vertebrobasilar ischemia: hemodynamic and embolic (1). The indications for treatment and the specific surgical techniques used depend on the identification of the underlying mechanism. As in the carotid territory, ischemia in the vertebrobasilar territory may be due to a hemodynamic or to an embolic mechanism. There is, however, a group of patients, discussed below, in whom it is difficult to determine which of the two mechanisms is operative or whether, in some cases, both may be responsible for the patient’s symptoms.

Hemodynamic Mechanism This mechanism implies that there is a condition of low blood flow or pressure affecting the vertebrobasilar territory. Some of these patients have stenosis or occlusion of one or both vertebral arteries that is not fully compensated for by existing anastomoses with the carotid system.

This situation creates a drop in the perfusion pressure in the vertebrobasilar territory that is not critical. However, when there is an additional central pressure drop, because of arrhythmia, orthostatic hypotension, or as the peak effect of an antihypertensive drug, superimposed on an already hypotensive system, symptoms result. A second mechanism for hemodynamic symptoms is the intermittent external compression of the vertebral arteries, which may occur with neck rotation and is particularly common in patients with osteoarthritis of the cervical spine. This can occur anywhere along the V2 or V3 segments of the vertebral artery.

Embolic Mechanism The embolic mechanism, as in the carotid territory, usually represents microembolization from proximal lesions impacting in the branches of the vertebral or basilar arteries. The sources of embolization are the heart, the proximal subclavian arteries, and the vertebral and basilar arteries. Plaques found in the subclavian and vertebral arteries show the same degenerative features that have been demonstrated in carotid plaques: intraplaque hemorrhage, ulceration, and surface thrombus (2). The latter two may cause embolization. Embolization may also occur as a result of mural thrombosis, which can develop at the site of compression and repeated trauma of the vertebral arteries by an osteophyte or other extrinsic compressive element. Repeated trauma may result in injury to the vertebral artery wall and formation of a mural throm-

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bus or an aneurysm laden with potentially embologenic thrombus. The latter may be dislodged, causing central embolization (Fig. 70.1).

Mixed Etiology In some patients, it is difficult to know if the mechanism is thromboembolic or hemodynamic. This is the case in patients with intramural dissection in whom the possibility of microembolization is obvious but there is also severe compromise of the lumen of the artery by the intramural hematoma. In patients with intermittent occlusion of the vertebral arteries, it is difficult to determine if the cause of the symptom is the intermittent occlusion of the artery (hemodynamic mechanism) or if thrombus at the site of local extrinsic compression and repeated trauma has given source to an embolus (embolic mechanism). In published series in which an effort has been made to differentiate the mechanisms of vertebrobasilar ischemia, the group denominated “mixed” oscillates between 9% and 23% (1,3) of the total number of patients. The rest of the patients are classified either as hemodynamic (52% to 79%) or thromboembolic (12% to 24%). The importance of the embolic mechanism in the production of vertebrobasilar ischemia has only recently become a concern on the part of clinical neurologists. Although the mechanism of embolic ischemia was anticipated by the classic pathologic study of Hutchinson and Yates (2), the tendency in neurologic services has been to ascribe the symptoms to disease of the small (and hence invisible to the eye) branches of the basilar artery. In 1973

the postmortem studies of Castaigne et al. (4), Amarenco and Hauw (5), and others indicated that perhaps in 30% of the cases of vertebrobasilar ischemia the etiology is embolic. It will probably take some years before this notion is applied to differential diagnosis in clinical practice as it took nearly two decades to routinely incorporate the notion of microembolization in the management of carotid bifurcation disease. The relevance of embolization as a cause of ischemia in the vertebrobasilar territory has been superbly summarized by Caplan and Tettenborn (6).

Pathology of the Vertebral Artery Although the majority of vertebral artery lesions are atherosclerotic, the entire array of arterial pathology is observed. Atherosclerotic stenoses are particularly common at the origin of the vertebral arteries. Occasionally, atheromatous plaques are also seen at the point where the artery penetrates the atlanto-occipital membrane or in its fourth portion. External compression (Fig. 70.1) is an important mechanism for temporary occlusion, and occasionally thrombosis, of the vertebral arteries. It is most commonly seen in its V2 segment. The most common elements of compression are osteophytes, the edge of the transverse foramina, and the intervertebral joints (3). This type of compression is usually prompted or aggravated by rotation or extension of the neck. In its V3 segment, the artery is somewhat redundant and must accommodate to the greatest rotational displacement of any vertebral segment in the neck (C1–2). At this level the artery is vulnerable to direct trauma and

FIGURE 70.1 Intraluminal mural thrombus is evident on the right vertebral artery at the site of compression by an osteophyte. Embolization from this site has occluded the right posterior. lnferior cerebellar artery (middle) and caused a right cerebellar infarction (right), as seen in the MRI scan.

Chapter 70 Vertebrobasilar Disease: Surgical Management

stretch injury. The latter is most likely a frequent cause of vertebral artery dissection although in some cases no specific traumatic injury can be recalled by the patient. It is also in this C1–2 segment that the artery is particularly prone to arteriovenous fistulas and aneurysm. Some of them appear spontaneously; others are the result of trauma. It is suspected that a number of these spontaneous aneurysms have their origin in birth or childhood trauma that has gone unnoticed, and are not congenital. This is supported by the absence of arteriovenous malformation in the surrounding bone or in the overlying skin. At the C1–2 level the artery is surrounded by a plexus of vertebral veins: trauma causing a tear in the artery is likely to produce a tear of the concomitant vein. This will result in the establishment of an artenovenous fistula, which will eventually form an “arteriovenous aneurysm.”

Syndrome of Vertebrobasilar Ischemia The manifestations of vertebrobasilar ischemia may appear spontaneously or follow specific postural changes such as standing up, or rotating the neck, and may result in transient or permanent neurologic deficits. The classic symptoms of vertebrobasilar ischemia are dizziness, vertigo, diplopia, perioral numbness, alternating paresthesiae, tinnitus, dysphasia, dysarthria, and imbalance. Rancurel and associates analyzed the clinical and anatomic findings in a series of 402 patients presenting with vertebrobasilar ischemia (1). Those with “hemodynamic” vertebrobasilar ischemia had repetitive, stereotyped symptoms, nearly always prompted by positional changes, and tended to have a good prognosis. Most of the disability seen in patients with hemodynamic vertebrobasilar ischemia is not due to strokes in the vertebrobasilar territory but rather to the limitations that these symptoms pose in daily life (inability to drive, climb stairs, etc.). Occasionally patients suffer traumatic injuries due to sudden visual disturbances or imbalance. On the contrary, patients with “embolic” ischemic attacks in the vertebrobasilar territory had longer-lasting transient deficits, which were varied and nonrepetitive, occurring less frequently but lasting longer, were usually independent of body and neck position, and were not relieved by lying down. This group of patients with thromboembolic vertebrobasilar ischemia had bad prognosis with progressive deterioration of neurologic function and even death. The workup of patients with vertebrobasilar ischemia must establish whether there is any relation between activity, posture, and the appearance of symptoms. In addition, one should inquire about any association of palpitations of the chest or arrhythmia with a bout of vertebrobasilar ischemia. In patients who have positionally induced symptoms, one must inquire what antihypertensive drugs they are taking and consider whether the peak levels of this medication may be influencing their central aortic pressure, causing relative hypotension and symptoms.

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The examination should always include the recording of pressure in both brachial arteries and of the pulses in both upper extremities and the neck. Whenever there is a difference in pressure between the brachial arteries greater than 20 mmHg, the possibility of a subclavian– vertebral steal being the cause of symptoms must be considered. The workup of patients with vertebrobasilar ischemia should include a magnetic resonance imaging (MRI) scan of the brain. Brain computed tomography (CT) scans, even the newer generations, are not reliable in identifying small infarctions of the brain stem because of the bone density surrounding the hindbrain. The advent of MRI scanning of the brain into clinical practice has shown that some patients thought to have had transient ischemic attacks of the vertebrobasilar territory, in fact had had small infarctions of this territory. Patients with an infarction in the vertebrobasilar territory must be thoroughly evaluated for an embolic source from either the heart or the arteries leading to the basilar artery. Duplex ultrasound has limited usefulness in the management of the vertebrobasilar ischemic syndromes. While the vertebral arteries can be identified in the neck, it is seldom possible to make any statements other than documenting the presence and direction of flow. Reversal of flow in the vertebral arteries can be easily identified by duplex scanning. We have been dissatisfied with the information provided by transcranial Doppler instrumentation and have not been able to use this equipment reliably as a screening tool in the diagnosis of postural intermittent compression of the vertebral arteries in the neck. The final diagnostic test for both diagnosis and selection of therapy in vertebral artery disease is a full arteriographic study. We routinely use a four-vessel arteriogram that includes an arch injection in two projections (RPO and LPO) and selective anteroposterior and lateral views of each common carotid artery and each subclavian artery, with attention to the origin of the vertebral arteries. This permits outlining the entire vertebrobasilar system from origin to the top of the basilar artery. In patients who have symptoms triggered by a particular neck position, the arteriogram is obtained with the neck in the specific trigger position, ideally while the patient is having symptoms. In patients who only have symptoms when standing, we place them in approximately 15° Trendelenburg position with the head supported by a block and then turn the neck into the trigger position. Owing to the weight of the head, the head-down position simulates the compression of the cervical spine that takes place when standing. This combination of maneuvers, called dynamic arteriography, is necessary if one is to identify points of compression or occlusion of the vertebral artery triggered by neck positions. The relevance of the arteriographic findings in determining the indication for surgery is different for patients with hemodynamic versus thromboembolic vertebrobasilar ischemia. In hemodynamic vertebrobasilar ischemia, we require that both vertebral arteries (or the single one if

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only one is present) have a cross-sectional area stenosis of 75% or more or be occluded. In patients with bilateral occlusion of the vertebral artery who present with hemodynamic vertebrobasilar ischemia, one may see retrograde filling of the basilar artery from the posterior communicating arteries after a common carotid injection. In thromboembolic vertebrobasilar ischemia, effort is directed toward identifying the source of the thromboembolus. This source may be fixed (ulceration, thrombus) or intermittent, as may be the case when an osteophyte is seen to impinge and occlude a vertebral artery during neck rotation. A cardiac source of embolization should be ruled out in all these patients. This usually implies both Holter monitoring to exclude an arrhythmia and transesophageal echocardigraphy to exclude an intracardiac thrombus. Aneurysms of the vertebral artery may also be a source of embolization. Other sources of emboli include intramural dissection, with or without associated fibromuscular dysplasia, or nonexcluded subclavian atheromata. As an example, an atheroma of the subclavian artery may manifest primarily by embolization into the hand. If this is improperly treated by a carotid–subclavian bypass without ligation of the proximal subclavian artery

(Fig. 70.2), the latter may embolize the vertebrobasilar territory.

Surgical Management Ligation of the vertebral artery is rarely indicated in management of lesions producing vertebrobasilar ischemia. The dangers of ligating a vertebral artery, whether single or not, are well documented in the surgical literature. We have used ligation rarely in patients who have a traumatic aneurysm causing embolization and who have an intact contralateral vertebral artery. Ligation of the vertebral artery in these patients may be done by endovascular procedures, keeping in mind that the artery must be occluded above and below the aneurysm. Proximal ligation alone results in continuing expansion of the aneurysm by the pulsatile pressure transmitted from the opposite vertebral artery. In the rare patient that requires endovascular or direct ligation of a vertebral artery and has a proven intact opposite vertebral artery, we use systemic heparinization for 3 days following the occlusion to prevent the ascending thrombus from reaching the vertebrobasilar junction. For most embolic disease, the best alternative is to divide the vertebral artery above the embolus-bearing lesion and

FIGURE 70.2 This patient had a carotid–subclavian bypass to treat embolization of the hand from a left subclavian lesion. The patient continued to have ischemic episodes in the hand and eventually developed infarctions in the vertebrobasilar territory. An endovascular balloon occlusion of the proximal subclavian artery cured her symptoms.

Chapter 70 Vertebrobasilar Disease: Surgical Management

to reconstruct it distal to the excluded lesion by means of a transposition or an exclusion bypass.

Reconstruction of the Proximal Vertebral Artery The proximal vertebral artery (V1 segment) is usually reconstructed to exclude the plaque at the origin of the vertebral artery and revascularize the latter. The most common and best technique to do this is a transposition of the vertebral artery to the posterior wall of the common carotid artery. In cases in which the opposite carotid system is occluded, one may not want to clamp the ipsilateral common carotid artery. In this case a subclavian–vertebral artery bypass using saphenous vein is the preferred alternative. Rarely, a patient has a redundant vertebral artery that allows its division above the plaque and its transposition to another subclavian site. Even more rarely, one may have to go to the ascending aorta or to the opposite side of the neck to tap into an arterial source for a bypass in order to revascularize a single vertebral artery. This is usually required in patients who have bilateral occlusion of the internal carotid arteries. For a vertebral artery–carotid transposition, the vertebral artery is exposed using the medial approach. As soon as an adequate length of vertebral artery has been exposed, the patient is systemically heparinized. With the available length of vertebral artery the anticipated site for its anastomosis to the posterior wall of the common carotid artery is estimated and marked with a surgical pen. The vertebral artery is then clamped below the longus colli muscle. A suture ligature of 6–0 polypropylene is placed at its origin. The artery is divided above this ligature, passed between the sympathetic loop that surrounds it (Fig. 70.3), and, once freed, brought into

FIGURE 70.3 (Left) Relation between the vertebral artery and the middle and lower cervical sympathetic ganglia. (Right) Severance of the origin of the vertebral artery. The latter has been pulled through the intact sympathetic loop and can now be prepared for the anastomosis.

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proximity to the common carotid artery. With the end of the artery spatulated, the common carotid artery is crossclamped, an arteriostomy is made in which an aortic punch and an end-to-side anastomosis is constructed (Fig. 70.4) between the vertebral and common carotid arteries using an open continuous suture. Before completing the suture, the vessels are backbled into the wound, the suture is tied, and flow is re-established first in sequence to the distal common carotid and then the vertebral artery. If the proximal vertebral artery is reconstructed by means of a subclavian–vertebral saphenous vein bypass, the distal segment of V1 is used for the anastomosis under systemic heparinization. The anastomosis is an oblique end-to-side type. Once constructed, flow is restored in the native vertebral artery and the proximal end of the vein graft is brought to the subclavian artery at the site selected for anastomosis. The arteriostomy in the subclavian artery is performed with a 5.2-mm aortic punch. The proximal end of the vein graft is anastomosed to the upper wall of the subclavian artery avoiding any redundancy. Occasionally this proximal anastomosis is made to the thyrocervical trunk after amputation of its branches (7). Once the proximal anastomosis is constructed, flow is resumed and the vertebral artery is tied immediately below the anastomosis of the graft, excluding its proximal portion.

FIGURE 70.4 The vertebral artery is being transposed to the posterior wall of the common carotid artery by a continuous “open” suture technique. The vertebral vein and the thoracic duct have been divided.

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FIGURE 70.5 Common carotid to distal vertebral artery bypass. A clip below the anastomosis occludes the proximal vertebral artery.

Reconstruction of the Distal Vertebral Artery Patients undergoing reconstruction of the distal vertebral artery (V3 segment) have disease or occlusion involving the V2 segment of the vertebral artery. Two different techniques are commonly used. The most common operation is a saphenous vein bypass from the common carotid artery to the vertebral artery at the level of C1–2 (Fig. 70.5). This implies the availability of a good segment of saphenous vein, a matter that should be determined preoperatively by duplex ultrasound. If the bypass is done as an end-to-side anastomosis (which we prefer), the proximal vertebral artery is ligated immediately below the anastomosis, transforming the latter into a functional end-to-end junction. An alternative technique to repair the distal vertebral artery is to skeletonize the external carotid artery, dividing its branches and transposing it to the vertebral artery at the C1–2 level (Fig. 70.6). This latter technique is not used in patients who have atherosclerotic occlusive disease involving the external carotid artery or in those in whom the anatomy of the external carotid artery in the arteriogram suggests that there will not be sufficient length of the trunk to reach the vertebral artery. On the contrary, patients who have osteophytic compression of the V2 segment and who are in the younger age group are less likely to have atheroma of the carotid bifurcation and usually undergo an external carotid transposition as described above, provided the anatomy of the

FIGURE 70.6 Transposition of the external carotid artery to the distal vertebral artery.

external carotid in the preoperative arteriogram indicates that there is a good-sized trunk that matches well the diameter of the vertebral artery. This transposition technique is also the choice in any patient who requires a distal vertebral artery reconstruction and does not have a saphenous vein of appropriate caliber. We recommend a minimum vein caliber of 3.0 mm and prefer at least 3.5 mm. A third technique that may be used for reconstruction of the distal vertebral artery is the division of the artery above the transverse process of C2 and its anterior transposition, to the wall of the upper cervical internal carotid artery by means of an end-to-side anastomosis (Fig. 70.7). Needless to say, this technique should not be used when the opposite internal carotid artery is occluded.

Suboccipital Approach Some patients present with occlusion of a single and dominant vertebral artery by bone or ligamentous structures between the atlas and the occipital bone. These patients may need decompression of the artery and often removal of the offending bone, usually the posterior arch of the atlas. Access to the artery at the supra-atlantal portion may also be needed in patients who have aneurysms that extend higher than C1. The access to the vertebral artery at this level has been described in Chapter 23.

Chapter 70 Vertebrobasilar Disease: Surgical Management

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FIGURE 70.9 Cumulative (secondary) patency rate of proximal vertebral artery reconstruction. Numbers indicate patients at risk. (Reproduced by permission from Berguer R. Long-term results of reconstructions of the vertebral artery In. Yao J, Pierce W. Long-Term Results in Vascular Surgery. Norwalk, CT: Appleton & Lange, 1993.)

FIGURE 70.7 Transposition of the distal vertebral artery to the high cervical internal carotid artery.

FIGURE 70.10 Life-table analysis of patients after distal vertebral artery reconstruction. Numbers indicate patients at risk. (Reproduced by permission from Berguer R. Long-term results of reconstructions of the vertebral artery. In: Yao J, Pierce W. Long-Term Results in Vascular Surgery. Norwalk, CT: Appleton & Lange, 1993.)

FIGURE 70.8 Life-table analysis of patients after proximal vertebral artery reconstruction. Numbers indicate patients at risk. (Reproduced by permission from Berguer R. Long-term results of reconstructions of the vertebral artery. In: Yao J, Pierce W. Long-Term Results in Vascular Surgery. Norwalk, CT: Appleton & Lange, 1993.)

Outcome There are now data from three series with follow-up extending for at least 10 years (3,8,9). Patency rates and life expectancy tables for our proximal and distal vertebral artery operations are shown in Figures 70.8 through 70.11. Analysis of the experience accumulated in vertebral artery reconstruction leads to some noteworthy

FIGURE 70.11 Cumulative (secondary) patency rate of distal vertebral artery reconstruction. Numbers indicate patients at risk. (Reproduced by permission from Berguer R. Long-term results of reconstructions of the vertebral artery. In: Yao J, Pierce W. Long-Term Results in Vascular Surgery. Norwalk, CT: Appleton & Lange, 1993.)

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conclusions. When one studies the incidence of postoperative complications, a learning curve is detectable. This is evidenced, for instance, by the high incidence of lymphoceles in the early part of series on proximal vertebral artery reconstructions and in the high rate of immediate failure in the first 5 years of experience in performing distal vertebral artery revascularization. The two most common reasons for failure of a distal reconstruction were: 1. 2.

a poor anastomosis that thrombosed immediately after operation and was usually revised; or a design flaw, such as double reconstructions (external carotid and vertebral artery), creating a situation of competitive flow.

The introduction of routine intraoperative digital arteriography has drastically reduced the incidence of postoperative occlusion. The patency rates of vertebral reconstruction are superior to those obtained with carotid operations. Operations restricted to the proximal vertebral artery have remarkably low mortality and morbidity (less than 1%). However, when the vertebral artery operation is combined with a carotid endarterectomy, the mortality and morbidity increase more than the sum of the mortality and morbidity for each individual component operation. These patients in whom combined carotid–vertebral reconstructions were done probably form a special subgroup with extensive arterial disease, which may be the explanation for their increased morbidity. It appears that the life expectancy of patients undergoing vertebral artery reconstruction is considerably better than that found in patients undergoing carotid reconstruction. This may very well be due to the fact that we include in the vertebral artery series a number of pa-

tients who have external compression who are generally younger and are without the cardiac comorbidity characteristic of patients with carotid artery disease.

References 1. Rancurel C, Kieffer E, et al. Hemodynamic vertebrobasilar ischemia: differentiation of hemodynamic and thromboembolic mechanisms. In: Berguer R, Caplan L, eds. Vertebrobasilar Arterial Disease. St Louis: Quality Medical Publishing, 1992:40–51. 2. Hutchinson EL, Yates PO. The cervical portion of the vertebral artery: a clinico-pathological study. Brain 1956;79:319. 3. Kieffer E, Koskas F, et al. Reconstruction of the distal cervical vertebral artery. In: Berguer R, Caplan L. eds. Vertebrobasilar Arterial Disease. St Louis: Quality Medical Publishing, 1992:279–289. 4. Castaigne P, Lhermitte F, et al. Arterial occlusions in the vertebral-basilar system. Brain 1973; 96:133–154. 5. Amarenco P, Hauw J-J. Cerebellar infarction in the territory of the superior cerebellar artery. Neurology 1990; 40:1383–1390. 6. Caplan I-R, Tettenborn B. Embolism in the posterior circulation. In: Berguer R, Caplan L, eds. Vertebrobasilar arterial disease. St Louis: Quality Medical Publishing, 1992:52–65. 7. Berguer R, Kieffer E. Surgery of the arteries to the head. New York: Springer-Verlag, 1992. 8. Berguer R. Long-term results of reconstructions of the vertebral artery. In: Yao J, Pierce W, eds. Long-term results in vascular surgery. Norwalk, CT: Appleton & Lange, 1993:69–80. 9. Branchereau A, Rosset E, et al. Proximal reconstructions. In: Berguer R, Caplan L, eds. Vertebrobasilar arterial disease. St Louis: Quality Medical Publishing, 1992:265–278.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 71 Nonatherosclerotic Cerebrovascular Disease Gary R. Seabrook

Atherosclerosis is the predominant disease process affecting the extracranial arterial circulation, with much clinical attention focused on the relation between internal carotid artery stenosis and stroke. A variety of other disease processes, however, also can afflict the extracranial cerebral circulation, and an understanding of these clinical syndromes is important for accurate diagnosis and treatment of the vascular patient. Although these non occlusive entities may not require operative intervention, effective and successful therapy does require the vascular surgeon to be skilled and expert in their diagnosis, assessment, and treatment, be it surgical or medical. Nonatherosclerotic processes involve changes to the arterial wall including various forms of inflammation, architectural abnormalities involving elongation and coiling of the carotid artery, structural defects in the arterial wall encompassing aneurysmal degeneration and spontaneous dissection, fibromuscular dysplasia, the effects of adjacent pathology such as a carotid body tumor, and responses to manipulation of the carotid vessels including irradiation-induced carotid artery disease and restenosis from myointimal hyperplasia after carotid endarterectomy.

Inflammatory Processes Diverse inflammatory processes of the cerebral vascular circulation may be described as arteritis, defined as transmural injury or invasion of the arterial wall by bacteria, chemical toxins, mechanical trauma, immunologic complexes, or ionizing radiation. Histologic examination of

the infiltrate will reveal granulomatous lesions with giant cells congregating along the internal elastic membrane, neutrophils dispersed through all layers of the arterial wall, and fibrosis of the intimal layer with the internal elastic lamina remaining intact. As the lumen becomes more obliterated with these changes in the vessel wall, thrombosis may occur, particularly in the microcirculation. After the acute inflammatory process has resolved, there may be recanalization of a thrombosed vessel, but often the arterial structure is left as fibrous scar tissue. Arterial inflammation may also be termed vasculitis, which is nomenclature usually associated with a noninfectious process. Both arteries and veins are affected, and the inflammation is more likely to be associated with vascular occlusion resulting in destruction of the vascular tree and the tissue that it supplies. Most researchers now believe that the vasculitides involve immune complex-mediated injury at the luminal surface of blood vessels. Whether the cellular elements of the vessel wall serve as an antigen, or the endothelial surface provides a bed for the deposition of antigen–antibody complex, the pathology results in an immune-mediated process. Given the wide variety of vasculitides (polyarteritis nodosa, giant cell arteritis, Takayasu’s arteritis, Behçet’s disease, thromboarteritis obliterans), a specific antigen has yet to be identified. The inflamed endothelial cell, regardless of etiology, becomes a site for platelet adhesion, activation, and aggregation, which incites thrombosis. In the vessels supplying the cerebral circulation, this occlusive process will produce symptoms and findings similar to arteries affected by atherosclerotic disease. The more significant physiologic consequence, however, may be due to the

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aftermath of the inflammatory process with the release of cytokines, procoagulant factors, and metabolic byproducts from the fibrinolytic system or the endothelial cell.

Temporal Arteritis Temporal arteritis and Takayasu’s arteritis are giant cell arteritides that present as a systemic granulomatous panarteritis affecting large and medium-sized arteries, but not the arterioles and capillary beds, most often in the head and neck (1). In both conditions, the arterial wall is infiltrated with mononuclear leukocytes and giant cells involving the circumference of the vessel. The giant cells usually lodge adjacent to the internal elastic lamina, and its structural integrity may be disrupted or focally absent (2). The intimal proliferation, in response to the inflammation, can result in thrombosis of the constricted lumen. However, the inflammation does not affect the artery in a uniform longitudinal pattern, so that the process presents with “skip lesions,” which can frustrate the clinician seeking a diagnosis by arterial biopsy (3). Systemically, granulomatous regions may be found in the vasculature supplying the skeletal musculature throughout the body. Women are affected at least twice as frequently as men, and the average age of onset is usually in the eighth decade (1,4). The disease process presents with a variety of symptoms including headache, pyrexia, myalgia, scalp tenderness, jaw claudication, and generalized malaise and/or depression. Specific visual symptoms (diplopia, blurred vision, or amaurosis fugax) occur in less than a quarter of the patients. Laboratory findings indicative of the process include an elevated erythrocyte sedimentation rate. It is extraordinarily rare for a patient to have the diagnosis of temporal arteritis with a normal sedimentation rate (5). Although angiography is not routinely indicated in the diagnostic workup of temporal arteritis, imaging of the vessels with intra-arterial contrast material will frequently reveal multiple segments of smooth stenoses. Because treatment involves the administration of systemic steroids with the attendant complications involved in this therapy, histologic confirmation of the inflammatory process may be beneficial before undertaking therapy. Because the temporal artery is involved in a majority of the patients afflicted with this systemic condition, and because this is one of the few peripheral arteries in the human circulation that is both easily accessible and sacrificed without harm for biopsy, attention given the disease is frequently focused at the temporal artery. However, patients with giant cell arteritis may not always have symptoms specifically referable to the temporal artery (headache, superficial tenderness, or adverse visual symptoms). Conversely, the lack of symptoms referable to the temporal artery, or even histologic involvement of the artery following biopsy, does not negate the need for treatment or eliminate the risk of visual damage if the inflammatory process involves the blood supply to the retina.

Biopsy of the superficial temporal artery can easily be performed under local anesthesia. The artery crosses over the zygomatic process of the temporal bone, where it is readily palpated. The frontal branch, which courses near the patient’s hairline, is the common site for biopsy. The auriculotemporal nerve, which usually accompanies the artery but in a posterior relation, may result in some confusion for the surgeon securing the biopsy specimen. A more proximal biopsy, taken where the artery courses in the preauricular region, poses a greater risk for injury to the auriculotemporal branch of the facial nerve, which controls motor function to the periorbital musculature. Attempts should be made to harvest up to 2 cm of artery to ensure an adequate specimen for diagnosis, given the variable distribution of the inflammatory infiltrates. Biopsy of bilateral temporal arteries will increase the yield of positive findings by approximately 15% (6,7). Treatment of the inflammatory process involves administration of corticosteroids. If symptoms suggest impending visual loss, administration of steroids should be commenced even before a histologic diagnosis is secured (8). Untreated temporal arteritis can result in ischemia to the optic nerve by involvement of the ophthalmic or posterior ciliary branches of the internal carotid artery. Blindness may occur (9).

Takayasu’s Arteritis Although Takayasu’s arteritis is rare, it is included for discussion because of its fascinating presentation. The eponym dates back to a description made at the Japan Ophthalmology Society in 1908 by Mikito Takayasu, which involved a symptom complex including ocular disturbance and diminished pulses in the upper extremities (10). The classic disease presents with the discovery of weakened pulses in the upper extremities, and a concomitant reduction in blood pressure when compared with that of the lower extremities, hence the nomenclature pulseless disease or reversed coarctation. Global neurologic symptoms may include dizziness or syncope. Focal neurologic deficits can vary from limb weakness and paresthesias to complete hemiparesis, representing end stages of the disease. An anatomic study of the patient’s great vessels reveals marked thickening of the arterial wall as branches originate from the aortic arch. This process can result in critical stenosis or occlusion of the extracranial cerebral vasculature, resulting in one of the more serious complications of the disease. Symptoms referable to the carotid circulation include visual field defects, retinal hemorrhages, and atrophy of the irides, leading to partial or total blindness. Takayasu’s arteritis has been divided into four presentations. Type I, involving the aortic arch and arch vessels, and type III, involving the arch vessels as well as the abdominal aorta and its branches, play a role in the analysis of patients with cerebral vascular symptoms. Type II involves the descending thoracic and abdominal aorta,

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

while type IV involves obliterative changes of the pulmonary artery and its branches (11–13). Takayasu’s arteritis occurs predominantly in females, the typical onset occurring between 10 and 25 years of age. Although the constitutional findings associated with the prodrome may be better appreciated retrospectively as a constellation of symptoms, they include fever, weight loss, arthralgias, anorexia, and an elevated erythrocyte sedimentation rate. A specific clinical phase associated with the initial development of arterial inflammation may be present in only half of the cases diagnosed. Even when the patient is undergoing a diagnostic evaluation, many of these generalized symptoms are often attributed to another disease process or discounted as a viral syndrome, fatigue, or depression (14). The diagnosis should be entertained when occlusive disease is discovered unexpectedly in a young, otherwise healthy, patient. Focused cardiovascular examination of a patient with arterial obliteration secondary to Takayasu’s arteritis will usually reveal a diminished pulse pressure. Patients may have an elevated systemic blood pressure to compensate for reduced flow from the stenotic proximal aorta. Systolic vascular bruits are frequently audible and originate from the segmental arterial stenoses or from high-frequency flow jets occurring in collateral beds that may have developed in the circulation to circumvent a stenosis of one of the major conduits from the aorta. Because Takayasu’s arteritis is an inflammatory process, early therapy involves intensive and often lengthy courses of corticosteroid therapy. Steroid treatment failures may be treated with cyclophosphamide. The progress of various therapeutic regimens is usually monitored by the patient’s erythrocyte sedimentation rate. Serial arteriography may demonstrate a measurable improvement in the occlusive segments in response to medical therapy. Failure of medical therapy and the progression of symptoms leading to potential complications of arterial ischemia may indicate the need for a surgical intervention. Arterial bypass construction between uninvolved arterial segments is the appropriate operation (15–17). Surgery should be timed during a quiescent period of the disease to avoid operating on arteries that are acutely inflamed. Because the process is a panarteritis and endarterectomy planes cannot be established, direct operation on the involved segments will often lead to the destruction of the arterial wall (14). Patients should be maintained on corticosteroid therapy in the perioperative period to protect against the inflammatory process developing at the anastomotic site of the bypass graft. In some patients, transluminal balloon angioplasty may be considered, if for no more than a temporizing measure, when involved arterial segments may not be amenable to surgical bypass (e.g., involvement of the entire aortic arch and great vessel orifices) (18,19). The role of intravascular stenting provides an attractive therapeutic approach; however, the effect of a foreign body lodged within an already inflamed arterial segment has the potential to further provoke the constrictive process. Because of the infrequent occurrence

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of this inflammatory process, large series evaluating or comparing various treatment modalities do not exist.

Behçet’s Disease Behçet’s disease is another rare inflammatory process that may affect the walls of both arteries and veins in contrast to other arteritides. Its presentation may lead the clinician to suspect a diagnosis of Takayasu’s arteritis or Buerger’s disease; however, the systemic manifestations of Behçet’s disease present a different clinical scenario. In 1937, Hulusi Behçet, a Turkish dermatologist, reported a disease associated with iritis and ulcerations of the mucous membranes of the oral cavity and genitalia (20). These findings were only a few of the systemic manifestations of the disease including peripheral vascular changes involving aneurysmal degeneration that often leads to occlusion of the affected artery. Behçet’s disease, most frequently affecting Mediterranean and Asian populations in the third and fourth decades of life, is associated with other systemic findings including cutaneous erythematous nodules and pustules, arthralgias, and inflammatory processes of the gastrointestinal and respiratory tracts (21). Aneurysmal formation is likely to occur at the branch points of the tributaries of the aortic arch. This degeneration of the artery wall architecture may be prompted by obliteration of the vasa vasorum, resulting in disruption of the nutrient flow to the arterial walls. The ischemic insult can lead to perforation and pseudoaneurysm formation (22,23). Histologic examination of involved specimens reveals a panvasculitis with edematous changes of the endothelial cells. The underlying medial layer is disrupted owing to disorganization of the elastic components of the vessel wall. Inflammatory cells invade the outer layers of the artery and infiltrate the perivascular tissue. Laboratory studies will often reveal a markedly increased erythrocyte sedimentation rate, an increased C-reactive protein, and positive HLA typing for the (BS) antigen. Surgical procedures to bypass aneurysmal or occlusive arterial segments are frequently fraught with complications, including early anastomotic disruption and recurrent stenosis (24). Similarly, invasive percutaneous arterial procedures, including diagnostic angiography, should be approached with caution, as the vessel wall is likely to rupture. The physical characteristics of the involved artery are reminiscent of surgeons’ experience with patients afflicted with Ehlers–Danlos syndrome, in whom an aneurysmal artery does not have the structural integrity to sustain vascular reconstruction. In this setting, vascular occlusion may have a better prognosis than aneurysm formation, as exsanguination following aneurysm rupture is avoided when the vessel thromboses (25). The etiology of the apparent associated hypercoagulable state has not been clearly defined. Fibrinolytic therapy may be considered in the peripheral circulation, but it may be hazardous to open occluded

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segments of vessels with aneurysmal changes owing to the frequent occurrence of subsequent arterial rupture. Use of fibrinolytic therapy in the carotid circulation is not recommended because of the risk of embolization from an aneurysmal site. Systemic therapy is directed at defusing the inflammatory process by administering corticosteroids, nonsteroidal anti-inflammatory agents, colchicine, and immunosuppression. Because the process is obscure, there are no widely tested or accepted treatment protocols.

Elongation and Coiling of the Carotid Artery Elongation and coiling of the carotid artery is usually due to an embryologic event, but may result from changes in the arterial wall caused by fibromuscular dysplasia or atherosclerosis. In fetal development, the fused dorsal aortae combine with the truncus arteriosus to form the aortic arch, from which arise major branches associated with the embryonic pharyngeal arches. The common carotid and proximal internal carotid artery form from the third arch, while the distal internal carotid artery has as its anlage the cranial segment of the dorsal aorta. The external carotid artery also has its origin in the third aortic arch. In early fetal stages, the third and fourth arches are significantly angulated at the point where they are fused by the carotid duct. As the embryonic pharynx matures, the fetal neck lengthens, with the migration of the great vessels and heart caudally into the chest cavity. Failure of complete migration may leave a redundant loop of the internal carotid artery, and this is thought to account for approximately half of the coils and angulations detected in the pediatric population (26,27). Patients with a carotid coil many have symptomatic atherosclerotic disease of the carotid bifurcation and internal carotid artery, but seldom is the tortuosity of the vessel considered the etiology of neurologic events. In contrast, kinks and coils may be found in a symptomatic patient when no disease of the vascular wall is present (28). Flow disturbances result from constriction of the lumen due to acute angulation of an artery that is not compliant enough to maintain an adequate cross-sectional area throughout the change in direction that the artery may take (Fig. 71.1). In addition to the diameter-reducing character of the lesion, the disruption of laminar flow can result in the propagation of intraluminal thrombus that may further restrict the arterial diameter or serve as a source for distal embolization. Extensive compression by the angle of the mandible, or processes of the cervical spine and their associated tendinous attachments, may also contribute to arterial angulation and further diameter reduction. In patients presenting with symptoms of transient ischemic attack (TIA) or amaurosis fugax in association with lateral movement of the neck or exaggerated flexion or extension, flow changes may be documented angio-

FIGURE 71.1 Carotid arteriogram of a coiled right internal carotid artery with a focal stenosis (arrow), from a patient with symptoms of right eye amaurosis fugax. The stenosis was caused by a nonatherosclerotic fibrous band, which was resected with the adjacent coiled arterial segment.

graphically by executing those maneuvers (29,30). Because of the embryologic factors contributing to the maturation of the carotid artery, any focal neurologic events occurring in children that could be attributed to altered cerebral blood flow must prompt investigation of the carotid artery for coiling. Tortuosity of the internal carotid artery may also be acquired in adulthood after normal fetal development. In addition to atherosclerotic degeneration, weakening of the elastic components of the medial layers of the artery, which are exposed to shear forces from hypertension or flow disturbances, may lead to an elongation of portions of the arterial wall architecture resulting in coils or kinks. The development of kinking in the abnormal carotid segment is further explained, given that the vessel is relatively fixed at where it originates at the aortic arch, and the distal internal carotid vessel is fixed at the petrous bone as the internal carotid crosses the foramen lacerum. Branches of the external carotid artery further stabilize the carotid bifurcation so that the unfettered internal carotid artery is prone to becoming tortuous as the result of shear stresses and hemodynamic forces running counter to the axial stream. Systemic hypertension, producing increased pressure on the longitudinal elastic fibers comprising the wall

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

structure of the vessel, could be postulated as an etiology for elongating the carotid artery, but no direct correlation between hypertension and carotid artery kinking has been established (31). Before modern imaging techniques were available, the abnormal tracking of the carotid artery was most likely to be diagnosed when dental abscesses eroded into the tortuous vessels, or when a segment of the errant artery was inadvertently excised while a patient was undergoing a tonsillectomy or adenoidectomy. Carotid kinks and coils are now most frequently found incidentally by angiography being performed to evaluate neurologic symptoms, or by screening procedures employing a color flow duplex scanner. The true incidence of carotid kinking and coiling is difficult to establish. To properly identify a carotid coil that is not associated with hemodynamic changes requires an experienced technologist. As blood moves through a coiled arterial segment, the changes in the direction of the flow in relation to the duplex transducer can easily be interpreted as a stenosis if only flow velocities from spectral analysis are being used as the criterion for assessing diameter reduction. However, if recognized, duplex scanning can provide excellent imaging of carotid coils and kinks that are not caused by atherosclerotic occlusive disease. Most symptomatic patients will require angiography, and asymptomatic patients may also be referred for radiographic contrast studies to provide the most precise definition of the arterial anatomy. Surgery is recommended when it is determined that the tortuosity of the vessel is serving to restrict blood flow to the brain or that the irregular vessel wall is providing an embolic source. A variety of surgical procedures have been described to return an elongated, coiled carotid artery to a more axial orientation (27). At one time, operations employed pexis of the arterial wall to the adjacent sternocleidomastoid muscle without interrupting blood flow. Such maneuvers are mentioned now only for historical interest, as surgeons have learned that the tortuous vessel has significant potential recoil owing to the “memory” of the elastic fibers within the arterial wall. Attempts to straighten a coiled carotid artery may result in the vessel becoming kinked. To eliminate flow abnormalities, the vessel must be straightened in the longitudinal plane; due to the rotational forces that have influenced the development of the vessel, there is a significant axial twist that must also be corrected. For this reason, attempts to correct arterial coils require transection of the vessel and frequently resection of a segment of the redundant structure. At times, improved flow can be restored by simply resecting a kink, but it may be necessary to resect a normal segment of the common carotid artery or adjacent internal carotid artery to provide the appropriate foreshortening to correct the aberrant artery’s course. Vein patch angioplasty may open the vessel across a kinked segment. Use of a prosthetic patch of polytetrafluoroethylene or Dacron may provide more structural support to a floppy arterial segment than would be obtained with a vein. Be-

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cause the disease process is frequently associated with atherosclerosis, when approaching patients with these anatomic variants the carotid surgeon must be prepared to undertake a complex reconstruction of the entire bifurcation. This may involve a segmental resection of the carotid artery including the bifurcation with interposition vein grafting, or resection of redundant artery with primary repair. Sometimes an end-to-end anastomosis cannot be performed and the artery is re-approximated by suturing the back walls together and completing the anastomosis with a patch angioplasty of the anterior component of the vessel.

Aneurysms of the Extracranial Carotid Artery Aneurysms of the extracranial carotid artery are rare in comparison with aneurysms in other major arterial segments of the body (32). Most observers attributed an apparent recent increased incidence to more vigorous screening programs, often using noninvasive modalities while searching for carotid lesions than can be repaired to reduce the incidence of stroke. Historically, syphilitic aneurysms contributed the greatest incidence to this malady, but primary infections of the carotid circulation have become rare with the availability of modern antimicrobial therapy (33). As might be expected, altered flow characteristics and accelerated shear stress, thought to be responsible for atherosclerotic plaque formation at the carotid bifurcation, may also contribute to aneurysm formation (34,35). Nonatherosclerotic carotid aneurysms caused by blunt trauma typically affect the internal carotid artery (36). The relative mobility of this segment, with no tethering side-branches, places it at greater risk of injury from blunt forces than the remainder of the extracranial carotid circulation. Penetrating trauma is another acquired type of aneurysmal formation in the carotid artery. Patients with penetrating neck trauma and a focal neurologic deficit should prompt suspicion that an injury leading to an aneurysm may have occurred. Because of the proximity of major venous tributaries to the carotid artery, aneurysms that form as the result of penetrating injury may be associated with arteriovenous fistulas (Fig. 71.2). Pseudoaneurysms of the carotid artery may occur following endarterectomy and reconstruction. These aneurysmal changes are frequently associated with recurrent occlusive disease from atherosclerosis or from a complication of the surgical procedure (37). Carotid aneurysms result in pain and swelling in the neck. Symptoms may also result from direct compression of the aneurysm on the adjacent cranial nerves or from an inflammatory reaction secondary to the expansion of the aneurysm. Irritation of the vagus or recurrent laryngeal nerve can result in hoarseness, while noxious stimulation of the 12th nerve will be manifested by difficulty in swal-

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FIGURE 71.2 Selective right carotid artery injection following a low-velocity gunshot wound to the neck. The intimal arterial defect (arrow) was associated with a pseudoaneurysm encroaching on the adjacent jugular vein, and an arteriovenous fistula communicating between the vessels. For illustrative purposes the arterial phase (white) is imposed on a mask of the opacified vein (black).

lowing and mastication. It is not uncommon that these associated symptoms are noted by the patient before appreciating a palpable, pulsating neck mass. Duplex scanning provides an excellent modality for evaluating carotid aneurysms. B-mode gray-scale imaging allows excellent definition of the size and extent of the arterial dilation, and the use of color flow imaging can determine which portions of the aneurysmal vessel are filled with thrombus and which are carrying an active flow stream. A coiled internal artery may initially be interpreted as an aneurysm, but detailed interrogation of the direction of blood flow should enable the operator to discriminate abnormal flow caused by a coil from that of turbulence in an aneurysmal sac. Aneurysms of significant size should be repaired (38). Because the incidence of carotid aneurysms is low, it is difficult to predict the natural history and risk of rupture of these abnormalities. Using criteria applied to other peripheral aneurysms would dictate that an aneurysmal dilation twice the diameter of the adjacent normal vessel would be an appropriate indication for repair. Replacement of the aneurysmal segment with an interposition vein graft has the best chance of restoring the circulation to a normal state and achieving long-term patency. The external carotid artery may have to be sacrificed during these procedures. A more complex arterial reconstruction can include reanastomosis of the external carotid artery or, if available, use of a bifurcated segment of saphenous vein to replace the resected bifurcation. Autogenous material is a more attractive conduit if the patient is faced with any risk of infection. If a vein of adequate diameter is not available, however, prosthetic material should be used. In general, the surgical tech-

niques for routinely treating carotid artery occlusive disease are used when correcting aneurysmal changes. When an interposition graft is utilized, proximal and distal arterial control is obtained, and a straight intraluminal shunt may be placed for preservation of cerebral blood flow during the repair. The aneurysm is opened to provide access points for the shunt. The conduit to be used is telescoped over the shunt before its insertion. The shunt is secured proximally and distally within the artery using a Rummel tourniquet. End-to-end anastomoses can then be constructed while internal carotid artery blood flow is maintained. The shunt is removed just before completion of the proximal anastomosis. Saphenous vein, harvested from the thigh, usually provides a good size match for replacement of the internal carotid artery (39). Simple ligation of a carotid aneurysm was first successfully accomplished and reported nearly two centuries ago by Sir Astley Cooper in London (40). Surgeons developed instruments such as the Selverstone clamp that was ratcheted closed over several days, allowing for collateral circulation to develop while the patient’s neurologic status was observed (41). With the advent of endovascular covered stents, a large or symptomatic distal internal carotid aneurysm may be excluded with catheter-guided techniques. Although internal carotid occlusion should not be considered if reconstruction is possible, aneurysms involving the very distal artery may preclude construction of an anastomosis before the vessel becomes intracranial. Occlusion is appropriate to consider in the face of embolic symptoms or impending aneurysm rupture. Aneurysmal changes of branch vessels of the external carotid artery may be amenable to simple ligation without neurologic sequelae or to treatment with percutaneously directed intra-arterial catheters and balloon embolization. This technique is attractive for use in those patients with external carotid aneurysms that would require disfiguring dissections by direct surgical techniques, particularly those lying adjacent to branches of the facial nerve, the base of the skull, oropharynx, or maxillary sinus structures.

Carotid Dissection Dissection of the carotid artery is a rare event, and although sometimes described as “spontaneous,” the process is usually associated with some mechanical insult to the vessel. Trivial trauma, often remote from the onset of symptoms, such as exaggerated extension, flexion, or rotation of the neck, or even vigorous coughing or noseblowing, may result in an intimal disruption that forms the entry point into the wall of the artery. True spontaneous dissections may be associated with ruptured atherosclerotic plaques, fibromuscular dysplasia, or cystic medial necrosis. Carotid dissection is usually associated with a focal neurologic deficit, which may include hemispheric motor and sensory losses, Homer’s syndrome, dysgeusia, loss of vagal and hypoglossal nerve function, neck pain, scalp

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

tenderness, or headache (42,43). An inflammatory response surrounding the arterial dissection is attributed as the etiology of the various neural defects. Arteriography demonstrates a tapered narrowing in the cervical portion of the carotid artery (Fig. 71.3). A tapered pattern created by the bulging subadventitial hematoma may create a long “string sign,” as the false channel compromises flow in the normal lumen (44). Computed tomography or magnetic resonance imaging provides excellent crosssectional demonstration of an arterial dissection and the extent of the false channel (45,46). The origin of the dissection occurs with a rent in the intima that extends into the outer layers of the tunica media but is confined by the adventitial tissue. In addition to the presence of organized thrombus penetrating the smooth muscle layers of the arterial wall, histologic study of dissection specimens reveals disruption of the internal elastic laminae and decreased amounts of elastic tissue (42). Although a long “string sign” should lead the clinician to entertain the diagnosis of spontaneous dissection, this arteriographic finding is present in other conditions with luminal narrowing including atherosclerosis, fibromuscular dysplasia, arteritis, moyamoya disease, and vasospasm. Initial experience with dissections of the internal carotid artery prompted surgeons to pursue operative repair, with fenestration and obliteration of the false lumen

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to return blood flow to normal anatomic channels; however, this approach was associated with disappointing results including a high incidence of perioperative stroke and occlusion of the reconstructed segment (42). Better outcomes are recorded with a nonoperative technique of systemic anticoagulation with heparin for 10 to 14 days. During this treatment interval, there is evidence that the subadventitial clot impinging on the carotid lumen retracts and that the intimal defect heals. An anticoagulated state reduces the risk of internal carotid artery thrombosis as well as distal cerebral embolization from the site of injury (47). Heparin should be avoided if the dissection has resulted in stroke associated with intracerebral hemorrhage, or if the dissection extends past the base of the skull, in which case anticoagulation may be associated with a prohibitive risk of subarachnoid hemorrhage. Heparin therapy may be replaced with warfarin, which can be administered in an outpatient setting, until the lesion has resolved. The progress of the healing dissection can easily be monitored by duplex ultrasonography without risk to the patient. Operative intervention, including replacement of the dissected segment with a vein interposition graft, is recommended if the dissection hematoma does not resolve and the patient has deterioration of neurologic status or recurrent neurologic deficits. Persistent symptoms not amenable to reconstruction of the cervical carotid circulation have been treated with internal carotid

B

FIGURE 71.3 (A) Spontaneous dissection of the carotid artery imaged via selective injection of the true lumen. The borders of the false lumen (arrows) form a tapered “beak” at the distal point of the dissection. The origin of the external carotid artery is not perfused, as the dissection extends through the bulb. (B) Selective injection proximal to the origin of the dissection obliterates the false channel and completely opacifies the bifurcation and its branches.

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artery ligation and extracranial–intracranial bypass grafting (48).

Fibromuscular Disease of the Carotid Artery Fibromuscular dysplasia is an entity that is well characterized but whose etiology is not well understood. Patients are afflicted with sequential stenoses of the internal carotid artery and experience symptoms related to cerebrovascular insufficiency. Long, mobile, medium-sized arteries (e.g., the internal carotid artery) are afflicted more often than those that are more arborized (e.g., the external carotid artery) (49). Most theories implicate some form of chronic trauma to the artery resulting in a compromised blood supply from the vasa vasorum, primarily affecting the medial layer of the artery (50). This leads to disorganization of the internal elastic lamina and marked thickening of the medial layer owing to hypertrophy of the smooth muscle cells and infiltration and proliferation of fibroblasts. The process often affects the artery in a segmental fashion, with hypertrophic segments being associated with the disruption of the elastic membranes. Because of the uneven changes in the vessel wall, angiographic studies reveal a beading characteristic. The artery also may become tortuous or kinked as the hypertrophied artery is affected by sequential areas of stenosis. Patients with fibromuscular hyperplasia of the internal carotid artery are more likely to have other arterial segments involved, including the vertebral, tibial, renal, and visceral arteries. Pathologic study of intracranial berry aneurysms suggests that a similar etiology may contribute to this arterial anomaly. Fibromuscular abnormalities may be diagnosed following focal, hemispheric neurologic symptoms including limb paresis or amaurosis fugax. As might be expected in an arterial segment plagued with sequential stenosis, carotid bruit is the most significant finding on physical examination. The symptom complex is indistinguishable from atherosclerotic occlusive disease, and the clinical diagnosis of fibromuscular dysplasia is usually made at the time of arteriography. The disease process most frequently affects the internal carotid artery distal to the bifurcation. It commonly extends past the angle of the mandible and may advance close to the intracranial portion of the vessel. Findings are usually bilateral. Fibromuscular changes are associated with concomitant atherosclerotic changes in less than one-fourth of the patients affected. Angiographically the “string of beads” appearance is noted in more than 75% of patients studied. This angiographic finding is considered pathognomonic for fibromuscular dysplasia. A less common arteriographic finding is a tubular stenosis, which may occur singly or in multiple segments of the affected artery (51). Because the disease process occurs nearly 10 times more frequently in women, investigators have focused on a link between fibromuscular changes and estrogens, con-

traceptive hormones, and sex-linked genetic factors. Changes in the media of medium- and large-sized arteries during pregnancy have been well described (52). Others have implicated the administration of female reproductive steroids either for contraception or postmenopausal therapy, but these associations have not been proved (53). A modified hormonal environment and the concomitant shear stresses that occur in the relatively unfixed middle segment of the internal carotid artery probably both contribute to the changes in the wall structure of the artery that result in the typical segmental changes. Patients with neurologic symptoms in the absence of dissection are considered surgical candidates because there is a strong relation between the abnormal arterial architecture and stroke (54,55). The multiple stenotic sites identified by arteriography can easily be implicated as an embolic source for blood clots and platelet aggregates that may form on the irregular wall surfaces and their associated webs and luminal stenoses. Symptoms may also be attributed to decreased flow given that multiple stenoses of significant diameter reduction frequently occur in series. Unlike atherosclerotic disease affecting the extracranial carotid circulation, endarterectomy is not effective or appropriate for patients with fibromuscular dysplasia, and transluminal dilation has become the accepted treatment (54). At surgery, the common carotid artery, its bifurcation, and the external and internal branches should be thoroughly mobilized, with the dissection of the internal carotid being carried to its most distal point. Vascular control of the internal carotid artery should be achieved using a nontraumatic technique. A pliable arterial loop effectively controls backbleeding and provides a method of supporting and manipulating the diseased arterial segment. Access to the internal carotid artery should be gained by a longitudinal incision in the carotid bulb. Following arteriotomy, graded intravascular dilators are sequentially advanced into the vessel, initially sounding the vessel with a probe 1.5 or 2 mm in diameter. The diameter of the dilator is increased in 0.5-mm increments, passing it through the stenotic area by applying gentle pressure when resistance is encountered. The maximal dilator size to avoid damage to the intimal surface that might occur with graded dilation of the segment has been accepted as 4 mm. After maximal dilation, vigorous backbleeding is permitted to evacuate any clots or fragments of disrupted debris that may have accumulated during the procedure. An alternative technique uses an intraluminal balloon for dilation (56). A balloon size should be selected with a length that can be easily manipulated into the involved segment and with a diameter to achieve results similar to those described with the graded dilators. Because of the risk of thromboembolization, some surgeons advocate an open technique and, following maneuvers with the balloon, backbleeding is allowed to clear the vessel of any debris or clot. As carotid stenting procedures become more sophisticated, dilating these lesions from a remote site with a percutaneously directed catheter with the use of

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

a protection device may reduce the risk of distal embolic complications. The use of stents may augment balloon interventions, but their efficacy remains anecdotal in the early experiences reported.

Carotid Body Tumors Carotid body tumors, which are more precisely characterized in the nomenclature of human pathology as carotid body paraganglionomas, are the most common extraadrenal paraganglionoma (57). Although not directly originating from the extracranial carotid circulation, these lesions are reviewed because of their intimate relation with the carotid vessels and because vascular surgeons often diagnose and treat these lesions when therapeutic intervention is required. The normal carotid body is a small mass of neurovascular tissue located bilaterally in the medial valley of the carotid artery bifurcation. The fetal carotid body develops within the arterial wall between the medial and adventitial layers. The blood supply originates predominantly from the branches of the external carotid artery, and the structure is innervated by a tiny branch of the nerve of Hering, whose fibers traverse to the inspiratory center of the medulla along with the glossopharyngeal nerve. It has a rich vascular supply and, when compared with equivalent masses of tissue, the carotid body receives a blood volume that is 10 times that delivered to the heart and 25 times that to the brain (58). Chemoreceptors in the carotid bodies are sensitive to hypoxia, hypercapnia, and acidosis, and the substantial blood flow allows these cells to participate in the control of respiration, although their exact mechanism of action has not been well defined. The carotid body should not be confused with the carotid sinus, located within the wall of the proximal internal carotid artery, which regulates blood pressure. Carotid body paragangliomas also arise from neuroectodermal tissue that migrates embryologically with the autonomic ganglion cells that form the carotid body. Histologically, carotid body tumors actually represent an exuberant growth of paraganglionic cells. In addition to occurring at the site of the carotid body, these lesions may occur adjacent to the vagus nerve as it traverses from the aortic arch into the base of the skull. Intracranially, paragangliomas can affect the nervous innervation of the middle ear. Although the lesions are usually discrete, at times the abnormal paraganglion cells can proliferate from the carotid body to invade the cranium. Although the term “tumor” has historically been assigned to these masses, they are not carcinomas, and the neoplastic process is actually hypertrophy of the carotid body tissue. Carotid body hypertrophy has been associated with chronic hypoxia; however, most patients with these tumors have experienced neither environmental nor physiologic oxygen deprivation (59). The lesions are considered to be malignant if there is infiltration of the paraganglionic tissue into adjacent lymph nodes or distant

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metastasis, and approximately 10% of reported cases meet this definition of malignancy. In approximately 10% of patients the lesions will be bilateral. There is a familial predisposition for the development of carotid body tumors and, when a patient is diagnosed, siblings should be screened for early detection (60). Other paragangliomas in the cervical region include jugular body tumors and glomus tumors, which can involve the middle ear structures after penetrating the skull base (61). In patients with carotid body tumors, symptoms usually result from their mass and compression on adjacent structures in the relatively confined space of the carotid sheath. In addition to noting a fullness or pressure at the angle of the mandible, the patient may experience dysphagia, hoarseness, tinnitus, or headache. The tumor frequently will have a pulsatile character due to its intimacy with the carotid bifurcation; however, the vascularized mass itself is not actually pulsatile and usually is mobile enough to be rotated radially about the axis of the carotid vessels. Because the mass has a propensity to stimulate the adjacent carotid sinus, patients may experience bradycardia or syncope. Ultrasonography provides a useful diagnostic modality to delineate carotid body tumors from simple neck cysts or thyroid pathology. Because of the significant vascularity of these lesions, the addition of color flow waveform analysis to B-mode imaging can define the limits of a carotid body tumor and determine its association with the carotid bifurcation. Computed tomography or magnetic resonance imaging of the neck confirms the extent of the lesion and its anatomic relation to adjacent structures (Fig. 71.4). Preoperative planning requires a selective carotid arteriogram to provide a record of the arterial anatomy and the relation of the carotid body tumor to the carotid bifurcation. A classic splaying of the internal and external carotid arteries around the highly vascularized tumor mass is pathognomonic for the lesion (Fig. 71.5). Significant blood supply to the carotid body tumor usually originates from branch vessels of the external carotid artery, and knowledge of the specific arterial anatomy is important in establishing intraoperative vascular control. Embolization of the tumor may also be achieved through these branch vessels, particularly in cases in which the lesion extends over a considerable distance and may approach the base of the skull. There is no role for biopsy of carotid body tumors using either an open or a percutaneous needle technique. Any plans to approach the tumor surgically must include complete resection and reconstruction of the arterial tree as may be indicated. Surgical resection is the treatment for carotid body tumors, and the procedure should be undertaken unless the patient has a prohibitive operative risk or is asymptomatic at an advanced age. In all other patients, even small lesions should be resected as they will continue to enlarge over time. More extensive tumors are associated with increased surgical morbidity as they become adherent to and invade adjacent structures. Surgical excision is techni-

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FIGURE 71.4 Computed axial tomography of a patient with bilateral carotid body tumors. The patient was evaluated for complaints of dysphagia having previously undergone a thyroidectomy for a suspected malignancy. Note the relation of the internal and external carotid arteries opacified by contrast material (arrows) to the substance of the lesions.

cally challenging owing to the hypervascularity of the lesions, which can result in significant intraoperative blood loss, and the intimacy that the mass will have with adjacent structures in the neck, particularly the vagus and hypoglossal cranial nerves. When the tumor has actually invaded the wall of the carotid artery, a segment of the vessel may be excised to eradicate all of the tissue. Carotid body tumors are approached through a standard cervical incision used for carotid bifurcation reconstruction. Plans for intraoperative blood cell salvage are appropriate, as significant blood loss is routine in the dissection of these lesions. For some lesions, a subadventitial plane can be created, and the tumor is resected by removing the most superficial cellular layer of the artery’s adventitial investment. Handling the tumor, which has the consistency of wet tissue paper, requires slow, meticulous dissection with careful control of hemorrhage using suture ligature, electrocautery, and topical hemostatic agents. It can be expected that the major blood supply to the tumor will come from the external carotid artery, and division of the many small feeding vessels to the paraganglioma may be facilitated by controlling the external carotid artery at the level of the bifurcation and at a point distal to the carotid body tumor. This segment of the external carotid artery may even be excised en bloc with the carotid body tumor. Lesions that have invaded and are inseparable from the internal carotid artery may also require excision of that segment of artery. In these cases, for preservation of cerebral blood flow, an arterial recon-

FIGURE 71.5 Arteriogram of a carotid bifurcation involved with a carotid body tumor. Note the splaying of the internal and external branches and the dense vascularity of the tumor mass.

struction should be performed using autogenous vein graft, with the proximal saphenous vein providing the best size match. Maximal tumor dissection and hemostatic control should be accomplished before internal carotid artery replacement, which requires systemic heparinization of the patient. To maintain distal internal carotid artery blood flow during the resection, the shunt is first passed through the vein graft, and end-to-end anastomoses can then be constructed to fashion an interposition graft, with the shunt being removed just before restoration of blood flow. In extensive tumors, particularly those involving the distal internal carotid artery, the surgeon should elect to leave residual tumor rather than face ligation of the artery, which has been associated with significant risks of stroke and hemiplegia (62). As dissections progress closer to the skull base and exposure of the anatomy becomes more constrained, there is increased risk of cranial nerve damage. Both the hypoglossal and vagus nerves may be covered or entwined in the abnormal carotid body. Embolization of the lesions by a percutaneously directed catheter may be effective in reducing blood supply to the paraganglioma; however, this method should be utilized only as an adjunct to operative resection (63).

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

Embolization alone will not occlude enough of the blood supply to eradicate the tumor. Surgery should promptly follow an embolization procedure, as the vast collateral network supplying these tumors will quickly restore blood supply to the areas that have been embolized. When planning percutaneous intervention, the risks of significant catheter manipulation in the region of the carotid bifurcation must also be considered, and injury or the introduction of debris into the internal carotid artery must be avoided. Currently, excision of the carotid body tumor should be undertaken with a stroke and mortality rate of less than 1% (64). Surgical resection is usually definitive therapy for these lesions. However, microscopic residual disease may be missed with recurrence of the tumor. Surgical patients should be followed in a long-term surveillance program, because one or two decades may elapse before metastatic disease is clinically evident (60).

Injuries to the Carotid Artery from Radiation High-dose radiation therapy is commonly prescribed for treating squamous cell carcinoma of the head and neck structures, both as adjunctive therapy to extensive surgical resection of the disease and in lieu of surgery, in which case it is employed as the primary treatment modality. Radiation therapy may also be used to treat other small malignant neoplasms in the cervical region, including Hodgkin’s disease, non-Hodgkin’s lymphoma, adenocarcinoma of the parotid gland, and metastatic breast or thyroid cancer. With the successful treatment of these malignancies and long-term patient survival, radiationinduced carotid artery disease has become a more common clinical problem (65). Radiation-induced changes to otherwise normal arteries are very similar to the atherosclerotic degeneration that occurs in patients with hypercholesterolemia, chronic smoking, and advanced age. The clinical presentation is similar to that of carotid artery occlusive processes occurring because of atherosclerosis, but changes are most likely to be present in the irradiated arteries of patients who are otherwise free of atherosclerotic disease (65). Because patients surviving significant malignancies of the head and neck are usually under vigilant surveillance, most of the lesions are discovered before the patient becomes symptomatic; however, focal neurologic deficits referable to irradiation-induced carotid stenosis have been reported (66). These changes may manifest years after the patient received the radiation therapy. There is no evidence that the physiology of the artery is adversely affected by any direct influence of the malignant process in these patients. The effects of external beam radiation on normal arteries result in both acute and chronic histologic changes. Within 48 hours of radiation exposure there is significant sloughing of endothelial cells with disruption of their

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nuclei (67). The medial and adventitial layers are spared from this acute response. As would be expected with intimal injury, a reparative process soon begins with associated platelet aggregation and fibrin deposition at the involved site. Although the intimal surface is soon covered with a new layer of endothelial cells, they may lack normal morphology and physiology. Chronic changes include disruption of the medial layer with the infiltration of fibrocytes. Focal areas of medial necrosis develop as well as focal disruption of parts of the adventitial layer, as would be seen in a chronic inflammatory process. With altered smooth muscle function, the vessel has increased wall permeability allowing the infiltration of circulating lipids. The healed artery may be devoid of its normal elastic characteristics, leading to chronic fibrosis, fatty infiltration, and disruption of the adventitia. Injury to the vasa vasorum may further compromise the integrity of the vessel. The changes to the periadventitial tissue that occur from the radiation exposure may further impede the compliance and adaptation that a normal artery should be able to endure. Radiation injuries will result in a narrowed arterial lumen, often indistinguishable from that of a patient with advanced atherosclerotic disease. However, in addition to stenosis and occlusion, these arteries are at significant risk of rupture because of the damaged adventitial layers. Arterial blowout is more common in patients who have undergone extensive surgery combined with radiation therapy for their malignancy. These patients may have only a layer of skin covering the carotid artery, and in the presence of infection this protective barrier is violated. Frequently, vascular catastrophes are associated with infection as a complication of a malignancy involving the oral cavity or as the result of skin flap breakdown from chronic ischemia after extensive cervical dissections. Any bleeding from such a wound should be treated as a surgical emergency, with preparations being made to immediately replace the involved carotid artery segment (68). The potential of identifying an impending arterial catastrophe warrants an ongoing surveillance program. As McReady and associates reported, for 11 carotid artery ruptures, ligation was required to treat nine of the patients, with stroke or death resulting in five of these nine (69). Two patients in this series who had undergone only cervical irradiation for neck carcinomas developed subcutaneous bleeding of the carotid artery. The incidence of carotid artery stenosis is significantly higher in irradiated than in nonirradiated necks (70). Duplex scanning surveillance of patients undergoing carotid irradiation is appropriate, as the test is sensitive enough to detect injuries to the vessel before symptoms occur. In a report by Moritz et al. concerning a group of patients with advanced neck carcinomas, 30% of the patients having undergone radiation therapy exhibited stenotic carotid artery lesions compared with 5.6% in a nonirradiated control group (66). This imaging modality is able to detect the presence of evolving plaque, often

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composed of infiltrated lipids and fresh thrombus, as well as grade the degree of associated arterial stenosis. In addition to averting vascular catastrophes, surgical intervention to correct these lesions is indicated to prevent stroke, which can be even more devastating in a patient who is already disabled from a radical neck dissection or laryngectomy. Because of the extensive changes that occur to the entire arterial wall after exposure to irradiation, standard endarterectomy is usually not an appropriate surgical therapy. Even if a medial dissection plane can be established within the artery, the integrity of the damaged adventitia will usually preclude it from safely remaining in the arterial circulation. Replacement of the involved segment with an autologous interposition graft is recommended, utilizing saphenous vein harvested from the thigh. Frequently this will require resection of a portion of the common carotid artery, the bifurcation, and the involved internal carotid artery in the cervical region. The external branches can usually be ligated with impunity, although care must be taken in developing skin flaps that may rely on their collateral circulation. If intraluminal shunting is required to maintain adequate cerebral profusion, a shunt may be placed through the saphenous vein graft before constructing an end-to-end anastomosis at the common and internal carotid segments. The advancement of muscle flaps are often required to ensure adequate coverage of the carotid repair. If adequate skin coverage is unavailable following arterial reconstruction in the irradiated field, a myocutaneous flap may be utilized to close the defect.

Recurrent Carotid Stenosis after Endarterectomy As large series of patients undergoing carotid endarterectomy are followed, it has become apparent that the procedure is not 100% durable. Although the subset of patients is small, recurrent stenosis of the carotid artery will occur following a technically error-free endarterectomy closed either primarily or with patch angioplasty. In some patients, atherosclerotic disease will be the cause of the recurrent stenosis. These patients usually have evidence of restenosis later than 2 years after the initial endarterectomy (Fig. 71.6). This recurrent disease is treated with techniques similar to the primary operation performed for atherosclerosis, with removal of the plaque at the interface of the reformed medial and adventitial layers. In another group of patients, during an interval within 2 years of endarterectomy, restenosis will occur that is not due to atherosclerosis (71). In these patients, intimal fibrosis at the site of the previous endarterectomy is usually identified as the etiology of the recurrent occlusive process. As surgeons have begun to follow their patients undergoing carotid endarterectomy with a postoperative surveillance protocol, these recurrent lesions are more clearly understood (72). When a patient is followed longitudinally after carotid reconstruction, beginning with a perioperative evaluation of the repair, it is possible to determine that a restenosis is not a postoperative residual, and it is possible to identify patients at risk of an adverse neurologic event before they become symptomatic from the process.

FIGURE 71.6 (A) Carotid arteriogram of a patient with hemispheric motor transient ischemic attacks. The patient was treated with carotid endarterectomy and primary closure of the bifurcation. (B) Seven years later a repeat carotid arteriogram demonstrates recurrent stenosis. An atheromatous plaque containing cholesterol clefts was excised.

A

B

Chapter 71 Nonatherosclerotic Cerebrovascular Disease

A

B

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C

FIGURE 71.7 (A) Carotid arteriogram with a high-grade focal stenosis of the proximal internal carotid artery in a patient with amaurosis fugax. (B) Following carotid endarterectomy, arteriography demonstrates normal flow in the reconstructed internal carotid artery segment. (C) Eight months later a postoperative surveillance program detected a recurrent stenosis, which was imaged by repeat arteriography. The lesion, which proved to be fibrointimal hyperplasia, was treated with vein patch angioplasty.

Myointimal cell proliferation occurs as a normal response to arterial injury with a slow, orderly recruitment and proliferation of a multicellular layer at the site of the intimal damage. Myointimal cell hyperplasia, which occurs in a subset of patients having had carotid artery reconstruction, is an exaggeration of the normal endothelial repair process in which there is an uncontrolled proliferation of smooth muscle cells in the medial layer of the arterial wall. In these patients it is believed that the smooth muscle layer, exposed in the carotid artery during the creation of an endarterectomy plane, reacts with circulating blood elements and induces this exuberant proliferative response (73). Investigators theorize that smooth muscle cells from the media replicate and migrate across the internal elastic lamina to the intimal layer; where they multiply and secrete an extracellular matrix which, along with connective tissue, contributes to the intimal thickening resulting in recurrent stenosis of the vessel (74). On gross appearance, this is a pale, firm, homogeneous layer with a shiny, smooth surface lining the lumen of the artery (71). Histologically, there is a diffuse fibrous layer underneath the intimal layer of endothelial cells and above the reformed medial layer. This thickening is composed of mucopolysaccharide ground substance infiltrated with an array of loosely connected fibrocytes. The infiltrations of cholesterol and lipid elements seen in atherosclerotic lesions are absent. Angiographically, these lesions are seen as smooth stenoses occurring in the region of the endarterectomy (Fig. 71.7). When studied with duplex scanning, the lesions will demonstrate some degree of diameter reduction by velocity criteria, but seldom progress to critical, preocclusive lesions. Noting these wall characteristics of the arterial lumina, recurrent stenosis from myointimal

hyperplasia is less likely to be symptomatic than a primary atherosclerotic stenosis of similar degree. The smooth myointimal proliferation is less prone to the thrombotic process and distal embolization that will occur in the more irregular atherosclerotic lesions. Because of the hope that the proliferative process occurring from an interaction with blood elements could be blocked, surgeons have routinely prescribed chronic antiplatelet therapy for their patients after carotid endarterectomy. However, research has been unable to substantiate that proliferative myointimal disease can be blocked by decreased platelet adhesion and aggregation. Antiplatelet agents may be more effective in protecting the patient with recurrent atherosclerotic disease from neurologic sequelae. In addition to an interaction between blood elements and the endarterectomized arterial wall, technical factors from the surgical procedure including clamp trauma, residual intimal flaps, or atherosclerotic plaque or stenosis of the arteriotomy repair may result in flow disturbances that contribute to myointimal cell proliferation. Because stroke may be the first clinical symptom for patients with early recurrent carotid stenosis, the value of a vigorous postoperative surveillance program cannot be underestimated (74). Regular sequential monitoring of patients must occur during the first 2 years after arterial reconstruction, when stenosis from myointimal hyperplasia is most likely to occur. An early postoperative study must be performed to document any residual stenosis lest it be confused with recurrent disease (75). When a significant lesion is identified in the surveillance program, aggressive surgical treatment should be considered (76). A recurrent stenosis from myointimal hyperplasia has traditionally been treated by patch angiography without endarterectomy, as it is frequently impossible to re-establish

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the medial dissection plane from the initial operation. Disruption of a myointimal lesion can result in destruction of the adventitial layers of the artery wall, which provides its structural integrity. Interposition grafting, therefore, must remain an option to replace a damaged site of restenosis in secondary reconstructions of the carotid artery. Balloon angioplasty and stenting are rapidly becoming attractive therapeutic alternatives in the management of recurrent carotid artery stenosis. Catheter directed therapy avoids reoperation in the neck and the attendant potential injury to the cranial nerves. As cerebral protection devices become available, the risk of distal embolization and stroke will decrease. Long-term results do not exist to substantiate the durability of catheter-directed therapy for recurrent carotid stenosis in this setting. Recurrent lesions believed to be caused by myointimal hyperplasia that are not symptomatic may be followed. A significant proportion of these lesions may actually regress as they are studied over time in a surveillance program. Just as the etiology of primary carotid occlusive lesions is not completely understood, the factors controlling this remodeling process need more study.

References 1. Huston KA, Hunder CC, et al. Temporal arteritis: a 25-year epidemiologic, clinical and pathologic study. Ann Intern Med 1978;88:162–167. 2. Mambo NC. Temporal (granulomatous) arteritis: a histopathological study of 32 cases. Histopathology 1979;3:209. 3. Klein RG, Campbell RJ, et al. Skip lesions in temporal arteritis. Mayo Clin Proc 1976;51:504. 4. Huston KA, Hunder GG. Giant cell (cranial) arteritis: a clinical review. Am Heart J 1980;100:99. 5. Wong RL, Korn JH. Temporal arteritis,without an elevated erythrocyte sedimentation rate. Am J Med 1986; 80:959. 6. Allsop CJ, Gallagher PJ. Temporary artery biopsy in giant-cell arteritis. Am J Surg Pathol 1981;5:317–323. 7. Hall S, Persellin S, et al. The therapeutic impact of temporal artery biopsy. Lancet 1983;2:1217–1220. 8. Rosenfeld SI, Dosmorsky GS, et al. Treatment of temporal arteritis with ocular involvement. Am J Med 1986; 80:143. 9. Bengtsson BA, Malmvall BE. Giant cell arteritis. Acta Med Scand 1982;658:1. 10. Takayasu M. Case with unusual changes of the central vessels in the retina. Acta Soc Ophthalmol Jpn 1908;12:554. 11. Veno A, Awane Y, et al. Successfully operated obliterative brachiocephalic arteritis (Takayasu) associated with elongated coarctation. Jpn Heart J 1967;8:538. 12. Lupi HE, Sanchez TG, et al. Pulmonary artery involvement in Takayasu’s arteritis. Chest 1975;67:69. 13. Lupi-Herrera E, Sanchez, et al. Takayasu’s arteritis: clinical study of 107 cases Am Heart J 1977;93:94–103. 14. Wolfe SM. Takayasu’s arteritis. J Am Med Assoc 1989;89:90–94.

15. Lagneau P, Michel JB, Vuong PN. Surgical treatment of Takayasu’s disease. Ann Surg 1987;205:157–168. 16. Robbs JV, Human RR. Rajaruthnam P. Operative treatment of nonspecific aortoarteritis (Takayasu’s arteritis). J Vasc Surg 1986;3:605–616. 17. Bloss RS, Duncan JM, et al. Takayasu’s arteritis: surgical considerations. Ann Thorac Surg 1979;27:574. 18. Hodgins GW, Dutton JH. Transluminal dilation for Takayasu’s arteritis. Can J Surg 1984;27:355. 19. Hodgins GW, Dutton JH. Subclavian and carotid angioplasties for Takayasu’s arteritis. Can Assoc Radiol J 1982;33:205. 20. Behçet H. Ucher rezidivierende, aphthoese, durch em Virus verursachte Geschwuere am Mund, am Auge und an den Genitalien. Dermatol Monatsschr 1937;105:1152–1157. 21. James DG. Behçet’s syndrome. N Engl J Med 1979;301:431–432. 22. Enoch BA, Castillo-Olivares JL, et al. Major vascular complications in Behçet’s syndrome. Post Grad Med J 1968;44:453–459. 23. Little AG, Zarins CK. Abdominal aortic aneurysm and Behçet’s disease. Surgery 1982;91:359–362. 24. Schwartz P, Weisbrot M, et al. Peripheral false aneurysms in Behçet’s disease. Br J Surg 1987;74:67–68. 25. Hamia M. Large artery involvement in Behçet’s disease. J Rheumatol 1987;14:554–559. 26. Sarkari NBS, MacDonald Holmes J, Bickerstaff ER. Neurological manifestations associated with internal carotid loops and kinks in children. J Neurol Neurosurg Psychiatr 1970,33:194–200. 27. Vannix RS, Joergenson FJ, Carter R. Kinking of the internal carotid artery: clinical significance and surgical management. Am J Surg 1977;134:82. 28. Quartlebaum JK Jr, Wade JS, Whiddon CM. Stroke associated with elongation and kinking of the carotid artery: long-term follow-up. Arch Surg 1973;177:572. 29. Freeman RT, Lippitt WH. Carotid artery syndrome due to kinking: surgical treatment in forty-four cases. Am Surg 1962;28:745. 30. Stanton PE Jr, McClusky DA Jr, Lamis PA. Hemodynamic assessment and surgical correction of kinking of the internal carotid artery. Surgery 1973;84:793. 31. Metz H, Murray-Leslie RM, et al. Kinking of the internal carotid artery in relation to cerebrovascular disease. Lancet 1961;1:424. 32. McCollum CH, Wheeler WG, et al. Aneurysms of the extracranial carotid artery. Am J Surg 1979;137:196. 33. Kirby CK, Johnson J, Donald JG. Aneurysms of the common carotid artery. Ann Surg 1949;130:913–920. 34. Mokri B, Piepgras DC, et al. Extracranial internal carotid artery aneurysms. Mayo Clin Proc 1982;57:310. 35. Perdue CD, Barreca JP, et al. The significancc of elongation and angulation of the carotid artery: a negative view. Surgery 1975;77:45. 36. Welling RE, Kakkasseril JS, Pechiera J. Pseudoaneurysm of the cervical internal carotid artery secondary to blunt trauma. J Trauma 1985;25:1108. 37. Bergamini TM, Seabrook CR, et al. Symptomatic recurrent carotid stenosis and aneurysmal degeneration after endarterectomy. Surgery 1993;113:580–586. 38. El-Sabrout, R, Cooley, DA. Extracranial carotid artery aneurysms: Texas Heart Institute experience. J Vasc Surg 2000;31:702–712.

Chapter 71 Nonatherosclerotic Cerebrovascular Disease 39. Busuttil RW, Davidson RK, et al. Selective management of extracranial carotid arterial aneurysms. Am J Surg 1980;140:85–91. 40. Cooper A. Account of the first successful operation performed on the common carotid artery for aneurysm in the year of 1808 with post mortem examination in the year 1821. Guy’s Hosp Rep 1836:1:53. 41. Webb RC, Barker WF. Aneurysms of the extracranial internal carotid artery. Arch Surg 1969;99:501. 42. Ehrenfeld WK, Wylie EJ. Spontaneous dissection of the internal carotid artery. Arch Surg 1976;111: 1294–1301. 43. Bogousslavshy J, Despland P, Regli F. Spontaneous carotid dissection with acute stroke. Arch Neurol 1987;44:137. 44. Bradac GB, Kaerobach A, et al. Spontaneous dissecting aneurysm of cervical cerebral arteries. Neuroradiology 1981:21:149–154. 45. Petro CR, Witwer CA, et al. Spontaneous dissection of the cervical internal carotid artery: correlation of arteriography, CT and pathology. Am J Radiol 1987;148:393. 46. Goldberg HI, Grossman RI, et al. Cervical internal carotid artery dissecting hemorrhage: diagnosis using MR. Radiology 1986:158:157. 47. McNeill DH, Dreisbach J, Marsden RI. Spontaneous dissection of the internal carotid artery: its conservative management with heparin sodium. Arch Neurol 1980; 37:54. 48. Miyamoto S, Kikuchi H, et al. Surgical treatment for spontaneous carotid dissection with impending stroke. J Neurol 1984;61:382. 49. Ehrenfeld WK, Wylie EJ. Fibromuscular dysplasia of the internal carotid artery: surgical management. Arch Surg 1974;109:676. 50. Stanley JC, Gewertz BL, et al. Arterial fibrodysplasia: histopathologic character and current etiologic concepts. Arch Surg 1975;110:561. 51. Osborn AG, Anderson RE. Angiographic spectrum of cervical and intracranial fibromuscular dysplasia. Stroke 1977;8:617. 52. Manalo-Estrella P, Barker AE. Histopathologic findings in human aortic media associated with pregnancy: a study of 16 cases. Arch Pathol 1967;83:336. 53. Irey NS, Norris HJ. Intimal vascular lesions associated with femal reproductive steroids. Arch Pathol 1973;96:227. 54. Effeney DH, Ehrenfeld WK, et al. Fibromuscular dysplasia of the internal carotid artery. World J Surg 1979;3:179–186. 55. Effeney DJ, Ehrenfeld WK, et al. Why operate on carotid fibromuscular dysplasia? Arch Surg 1980;115: l261. 56. Smith LL, Smith DC, et al. Operative balloon angioplasty in the treatment of internal carotid artery fibromuscular dysplasia. J Vasc Surg 1987;6:482. 57. Glenner GG, Grimely PM. Tumors of the extraadrenal paraganglion system (including chemoreceptors). In:

58.

59.

60. 61.

62. 63.

64.

65. 66.

67.

68.

69. 70.

71. 72.

73. 74.

75.

76.

857

Atlas of Tumor Pathology, second series, fasc 9. Washington, DC: Armed Forces Institute of Pathology, 1973. Daly MD, Lambertsen CJ, Schwietzer A. Observations on the volume of blood flow and oxygen utilization of the carotid body in the cat. J Physiol 1954;125:67–89. Pacheco-Oieda L, Durango E, et al. Carotid body tumors at high altitudes: Quito, Ecuador, 1987. World J Surg 1988;12:856–860. Dent TL, Thompson NW, Fry WJ. Carotid body tumors. Surgery 1976;80:365–372. Lack FE, Cubilla AL, et al. Paragangliomas of the neck and head region: a clinical study of 69 patients. Cancer 1977;39:397–409. Lahey FH, Warren KW. Tumors of the carotid body. Surg Gynecol Obstet 1947;85:281–288. Schick PM, Hieshima GB, et al. Arterial catheter embolization followed by surgery for large chemodectoma. Surgery 1980;87:459–464. Hallett JW, Nora JD, et al. Trends in neurovascular complications of surgical management for carotid body and cervical paragangliomas: a fifty-year experience with 153 tumors. J Vasc Surg 1988;7:284–291. Silverberg GD, Britt BH, Goffinet RD. Radiation induced carotid artery disease. Cancer 1978;41:130–137. Moritz MW, Higgins RF, Jacobs JR. Duplex imaging and incidence of carotid radiation injury after high-dose radiotherapy for tumors of the head and neck. Arch Surg 1990;125:1181–1183. Fonkalsrud EW, Sanchez R, et al. Serial changes in arterial structure following radiation therapy. Surg Gynecol Obstet 1977;145:395. Marcial-Rojas RA, Castro JR. Irradiation injury to elastic arteries in the course of treatment for neoplastic disease. Ann Otol 1962;71:945–958. McCready RA, Hyde GL, et al. Radiation-induced arterial injuries. Surgery 1983;93:306–312. Elerding SC, Fernandez RN, et al. Carotid artery disease following external cervical irradiation. Ann Surg 1981;194:609–615. Stoney RJ, String ST. Recurrent carotid stenosis. Surgery 1976;80:705–710. Zierler RE, Bandyk DF, et al. Carotid artery stenosis following endarterectomy. Arch Surg 1982;l17:1408– 1415. Chervu A, Moore WS. An overview of intimal hyperplasia. Surg Gynecol Obstet 1990;171:433–447. Clowes AW, Clowes MM, et al. Regulation of smooth muscle cell growth in injured artery. J Cardiovasc Pharmacol 1989;14 (Suppl 6):512–515. Kinney EV, Seabrook GR, et al. The importance of intraoperative detection of residual flow abnormalities after carotid artery endarterectomy. J Vasc Surg 1993;17:912–923. O’Hara, PJ, Hertzer NR, et al. Reoperation for recurrent carotid stenosis: early results and late outcome in 1999 patients. J Vasc Surg 2001; 34:5–12.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART IX Visceral Vessels

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 72 Surgery of Celiac and Mesenteric Arteries Stephen P. Murray, Tammy K. Ramos, and Ronald J. Stoney

Visceral ischemic syndromes represent a diverse spectrum of disease that presents a challenge in both diagnosis and treatment. Acute visceral ischemia is a medical and surgical emergency in which timely diagnosis and treatment are critical in obtaining bowel salvage and survival of the patient. Chronic visceral ischemia is frequently overlooked in assessing patients with abdominal pain, and a delayed diagnosis subjects the patient to undue suffering, weight loss, and the threat of fatal intestinal gangrene. This chapter reviews the historical background of visceral ischemic syndromes and discusses the overall management of patients with both acute and chronic ischemia. The etiology, clinical presentation, diagnostic evaluation, perioperative management, options for therapy, operative techniques, and results of therapy are presented.

Historical Background Gradual occlusion of one or all of the aortic visceral branches may occur without producing any abdominal symptoms, provided that adequate intestinal blood supply is maintained through the abundant collateral pathways. Chiene, in 1869, noted occlusion of all three major visceral arteries in a patient who had no abdominal symptoms and who died from other causes (1). The fact that all three visceral vessels could occlude without universally producing intestinal ischemia or infarction was probably responsible for a great deal of the delay in recognizing chronic visceral ischemia as a distinct disease. In 1894, Councilman proposed that abdominal

pain could result from obstruction of the visceral arteries (2); unfortunately, this report was generally overlooked. Indeed, Osler believed that the abdominal complaints of patients with atherosclerotic disease of the visceral arteries was in fact atypical angina pectoris. Proponents of this theory persisted, and Bacelli in 1918 was the first to use the term “angina abdominis” to describe these patients (3). Then in 1921, Davis likened mesenteric ischemia to intermittent claudication (4). In 1936, Dunphy reported 7 of 12 patients dying of mesenteric infarction who had premorbid complaints consisting of abdominal pain, weight loss, and altered intestinal motility (5). He correctly established the relation between chronic visceral ischemia and subsequent fatal intestinal gangrene. Mikkelsen proposed surgical revascularization to relieve intestinal ischemia and coined the term intestinal angina in 1957 (6). Within a year, Shaw and Maynard reported two patients with intestinal gangrene successfully treated with thromboendarterectomy and bowel resection (7). Before this, surgical treatment of acute intestinal ischemia consisted only of intestinal resection, as reported by Elliott in 1985 (8). In 1959, surgical relief of chronic intestinal ischemia by superior mesenteric transarterial endarterectomy was accomplished, and thus began the modern management of this disease (9). During the same year, alternative techniques for surgical reconstruction were introduced when Derrick et al. reported use of autogenous iliac artery with bifurcation intact as an antegrade bypass from the supraceliac aorta to the celiac and superior mesenteric arteries (10). The first retrograde Dacron bypass was described by Morris and Crawford (11). The following year, Fry and

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Kraft reported use of an autogenous vein bypass originating from the supraceliac aorta that was exposed by a thoracoabdominal medial visceral rotation approach (12). They pointed out that the absence of disease in this location made the proximal anastomosis easier. In 1966 the technique of transaortic thromboendarterectomy was introduced, as well as antegrade prosthetic bypass from the supraceliac aorta to one or both major visceral arteries (13). More recently, percutaneous methods of revascularization have emerged (14–19) and are seeing increasing utilization with little yet in the way of documented longterm efficacy. It seems intuitive that short-term morbidity and mortality should be improved; however, data has arisen to the contrary (14,19).

Acute Visceral lschemia Etiology Acute visceral ischemia results from acute thrombotic occlusion of the major visceral branches of the aorta—the ultimate complication of chronic visceral ischemia due to atherosclerosis—or from embolic occlusion of the superior mesenteric artery. Nonocclusive mesenteric ischemia (NOMI) is usually a manifestation of cardiac dysfunction and is not within the scope of this chapter. Patients with acute ischemia are immediately endangered by the development of irreversible intestinal infarction and gangrene, thus necessitating its early recognition and treatment.

Embolic Occlusion Clinical Presentation and Diagnosis Embolic occlusion most commonly involves the superior mesenteric artery and the presentation of these patients is sufficiently distinct to allow its early differentiation from thrombotic occlusion, thus enabling early intervention (20–23). Because of the acute obstruction of mesenteric blood flow, there is insufficient time for the development of protective visceral collaterals. The initial response of the ischemic small bowel is vigorous contraction and spasm. This is perceived by the patient as severe periumbilical abdominal pain frequently associated with gut emptying. At this early stage, peritoneal inflammation is not yet present, and physical examination may demonstrate active bowel sounds and only minimal tenderness. Surgical exploration at this stage has occasionally resulted in a missed diagnosis because the intestines are pale in color and vigorously contracting (24). Almost all patients have an obvious cardiac source as origin for the embolus, and embolic occlusion of other vascular beds (cerebral, renal, or extremity) is present in approximately one-third of the patients with emboli to the superior mesenteric artery. A plain x-ray film and/or CT scan is obtained to rule out other intra-abdominal catastrophes. In acute intesti-

nal ischemia this film might show a gasless abdomen or, later, bowel dilation and/or thickening. The definitive diagnosis is obtained by preoperative arteriogram or by laparotomy. Biplanar arteriograms demonstrate minimal or no blood flow to the superior mesenteric artery. However, on the lateral views, the superior mesenteric artery orifice and proximal 5 to 7 cm are patent. This is because the embolus most often lodges near the takeoff of the middle colic artery. Surgical Treatment Although nonoperative management with dextran has been described (25), salvaging both the threatened bowel and the patient requires a timely operation after aggressive resuscitation. Preoperative management with cardiac and hemodynamic monitoring to control arrhythmias and to maximize cardiac output by instituting appropriate volume replacement and, if necessary, myotropic support are essential for a successful outcome. The abdominal exploration is usually performed through a midline incision. Characteristically, the duodenum and the first several centimeters of the jejunum are normally perfused and viable, whereas the remainder of the small bowel and right colon show evidence of ischemia. With prolonged ischemia, the bowel begins to manifest evidence of hemorrhagic infarction, with edema, dilation, and hemorrhage into the mesentery. However, revascularization at this point will allow normal bowel color and motor activity to return. Palpating the superior mesenteric artery can identify the point of obstruction. The superior mesenteric artery is exposed by elevating the transverse colon and incising the base of the overlying transverse mesocolon. A transverse arteriotomy is made in the superior mesenteric artery distal to the middle colic artery. Bidirectional catheter thromboembolectomy is then completed, and the vessel is flushed with a heparinized saline solution. After closure of the arteriotomy with fine interrupted sutures, the bowel is returned to its normal anatomic position for observation. Viability is reassessed after an observation period of 30 to 45 minutes. Areas of obvious gangrene must be resected. The assessment of bowel viability may be aided by the use of a Doppler probe or by fluorescin injection and inspection under ultraviolet light (26,27). In the absence of extensive intra-abdominal contamination, primary intestinal anastomosis is performed. Before completion of the procedure, a decision has to be made regarding the advisability of a second-look operation within 24 to 48 hours. Once a second-look procedure is planned, the subsequent postoperative course should not alter this decision.

Thrombotic Occlusion of Visceral Arteries Clinical Presentation and Diagnosis Acute mesenteric ischemia due to thrombotic occlusion of the superior mesenteric or celiac arteries is the consequence of gradual atherosclerotic occlusion of these ves-

Chapter 72 Surgery of Celiac and Mesenteric Arteries

sels with superimposed thrombosis. The progressive stenosis of the visceral vessels allows collateral pathways to develop. The collaterals provide a marginal blood supply to the intestines and are responsible for blunting the initial severity of the thrombosis. The symptomatology is similar to that of intestinal ischemia caused by emboli, but its onset is more insidious, and it may initially be intermittent and reminiscent of abdominal angina as first reported by Dunphy (5). The liberal use of arteriography early in the evaluation of patients with suspected bowel ischemia is critical (28). If the etiology of the bowel ischemia is due to visceral artery thrombosis, the aortogram will frequently show extensive occlusive disease involving the visceral arteries. Lateral aortography will reveal occlusions near the origin of the celiac or superior mesenteric arteries or both. As in embolic visceral artery occlusion, aggressive preoperative resuscitation is essential. Surgical Treatment An assessment of the extent of visceral ischemia and viability is mandatory; therefore the exploration is best accomplished through a midline laparotomy. Attention is first directed toward determining the extent and pattern of visceral ischemia. This will help differentiate the etiology of the ischemia. Visceral artery occlusion secondary to thrombosis is frequently associated with ischemia of the upper abdominal viscera including the proximal jejunum. This finding is in contrast to the pattern of ischemia associated with acute embolic occlusion of the superior mesenteric artery. In addition, the pattern of ischemia associated with mesenteric artery thrombosis is continuous as compared with the segmental pattern of ischemia that is seen with embolic disease. Next, intestinal viability is assessed to determine whether acute visceral artery reconstruction is indicated. The risk of contamination from necrotic bowel is considered a contraindication to the use of prosthetic grafts. Autogenous reconstruction by transaortic thromboendarterectomy or by antegrade aortovisceral saphenous vein bypass is safe in this situation. However, when intra-abdominal contamination can be excluded, antegrade prosthetic aortovisceral bypass may be performed. Exposure of the mesenteric arteries and the technique for reconstruction are described below under Chronic Visceral Ischemia. After revascularization the bowel is observed for viability and is resected as indicated.

Chronic Visceral Ischemia Etiology Atherosclerosis Chronic visceral ischemia is overwhelmingly (95%) caused by atherosclerosis. One-third of the patients have coexisting atherosclerotic disease in the aorta and other aortic branches (29). In the abdominal aorta, the disease occupies a predominantly ventral position and encroaches upon the lumen of the major visceral arteries

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(30,31). Derrick et al., in 1958, first noted that the extension of aortic plaque into the lumen of the visceral arteries was limited to the first 1.5 to 2 cm, with sparing of the arteries beyond this point (10). This finding has been repeatedly demonstrated in our own experience, with few exceptions. Rarely, an eccentric calcified polypoid lesion originating from the posterior surface of the upper abdominal aorta encroaches upon the lumen of the major visceral arteries. This “coral reef” atherosclerosis should be considered if symptoms of visceral ischemia are associated with symptoms of chronic aortic obstruction (32). Involvement of multiple visceral branches is common. In our series of 77 patients, only one had singlevessel involvement. There is, however, no constant correlation between the number of branches involved and the severity of symptoms. Isolated celiac artery lesions might be symptomatic; on the other hand, lesions of the superior or inferior mesenteric arteries alone rarely cause symptoms. In some cases occlusion of all three branches might be asymptomatic because of a well-developed collateral system. The pathophysiology of postprandial pain is not known. It is felt to be the result of ischemia, leading to acidification of bowel wall interstitium (33). This results in a decrease of resistance of the mesenteric vascular bed. This decreased resistance ordinarily results in an increase in blood flow but, in the presence of proximal stenosis, blood flow to the mesenteric bed is actually decreased. As the characteristic postprandial pain usually occurs within 20 minutes of eating and the food bolus has not reached the small intestine within that period, the mechanisms leading to symptoms may be, in part, mediated by unknown humoral factors. Celiac Axis Compression Atherosclerosis is the most frequently encountered lesion in chronic visceral ischemic syndromes, but other rare causes also exist. The most common of these is the socalled celiac axis compression syndrome, or median arcuate ligament syndrome, originally described by Dunbar et al. (34). The clinical relevance and the pathophysiologic background of this syndrome are still a matter of discussion (35–38). It is generally presumed to be caused by an anatomic abnormality in the relation between the celiac axis and the median arcuate ligament, resulting in external compression of the celiac axis, which occasionally involves the superior mesenteric artery as well. This presumption is opposed by the fact that celiac artery compression has been demonstrated in asymptomatic patients (38). In this disease, the aorta and its other branches are free from lesions, and the collateral circulation is less evident than in patients with chronic visceral ischemia caused by atherosclerosis (39).

Other Rare Cases External compression of the celiac axis by neural and fibrous tissue has been reported to cause symptomatic

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chronic visceral ischemia in patients with pathologic processes involving these tissues (e.g., neurofibromatosis) (40,41). Spontaneous intimal dissection in the superior mesenteric artery has also been reported to cause symptomatic chronic visceral ischemia (42). Fibromuscular hyperplasia can involve the celiac and superior mesenteric arteries, but its relation to symptoms of chronic visceral ischemia is unclear (43). Finally, chronic visceral ischemia has been described as a consequence of radiation and in association with systemic vasculitides (44).

Collateral Pathways Proximal branches of the major and minor visceral arteries are of great importance in preventing bowel ischemia and symptoms in patients with occlusive visceral artery disease. The fact that gradual occlusion of all major visceral branches can occur without causing bowel infarction or ischemic symptoms demonstrates the great capacity of the visceral collaterals. These collateral branches are located beyond the flow-limiting lesions and are capable of enlarging and reversing their flow into the ischemic splanchnic bed. In celiac axis occlusion, the major collateral flow connects the hepatic artery with the superior mesenteric artery through the gastroduodenal artery and the inferior

A

and superior pancreaticoduodenal arteries. This collateral pathway is known as the pancreaticoduodenal arcade. A less common collateral pathway develops between the middle colic and the dorsal pancreaticosplenic arteries. When the superior mesenteric artery is occluded, the most important collateral pathway is the pancreaticoduodenal arcade. However, the inferior mesenteric artery also provides collateral blood flow to the superior mesenteric artery through branches of the left and middle colic arteries (arc of Riolan). In combined celiac axis and superior mesenteric artery occlusion, the inferior mesenteric artery provides major collaterals through the marginal anastomotic arteries, the arc of Riolan, and the pancreaticoduodenal arcade. In obstruction of all three aortic visceral branches, one or both internal iliac arteries may provide afferent splanchnic blood flow through the inferior and superior mesenteric artery collateral pathways described above (Fig. 72.1).

Clinical Presentation Atherosclerosis Chronic visceral ischemia caused by atherosclerosis usually develops in the fifth through seventh decades (mean

B

FIGURE 72.1 (A) The visceral arteries and collateral pathways. (B) Arteriogram (anteroposterior projection) showing the main collateral pathways—the pancreaticoduodenal arcade, the meandering mesenteric artery (arc of Riolan), and branches of the inferior mesenteric artery extending down to the hypogastric artery. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols I and 2. New York: Springer Verlag, 1980.)

Chapter 72 Surgery of Celiac and Mesenteric Arteries

age, 59 years), with a female to male ratio of 3 : 1. A typical postprandial abdominal pain, termed intestinal angina (6), is the most common symptom in chronic visceral ischemia due to atherosclerosis (90% to 95%). This pain is mostly located in the epigastrium and is of a colickycramping or dull-aching character. It typically starts 15 to 30 minutes after food ingestion and lasts for 1 to 3 hours. Significant weight loss is the second most common symptom (79%) and, without weight loss, the diagnosis should be suspect. The weight loss is secondary to the postprandial pain that causes the patient to ingest smaller meals or only fluid. Ultimately, food intake is avoided altogether (“food fear”) (29). Accordingly, starvation is the likely cause of weight loss rather than malabsorption as originally suggested (7). About 25% of the patients are initially seen with protean motility disturbances such as nausea and vomiting, diarrhea, or constipation. Physical examination commonly reveals signs of substantial weight loss and advanced systemic atherosclerosis. An epigastric bruit is present in 85% of the patients (29,45–49). Frequently, the symptoms of chronic visceral ischemia are misinterpreted as being due to gastrointestinal malignancy. These patients have often undergone an extensive gastrointestinal workup before being referred to a vascular surgeon (29,46,48). However, knowing that chronic visceral ischemia is a possibility, in most cases, a thorough history and physical examination is all that is necessary to lead one to suspect the correct diagnosis. Use of aortography, with both anteroposterior and lateral

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views, is necessary to confirm the diagnosis and to plan subsequent surgical intervention. The anteroposterior aortogram will disclose the collateral vessels and allow assessment of the renal arteries and the infrarenal aorta, which frequently have coexisting atherosclerotic disease (see Fig. 72.1B). A lateral aortogram provides visualization of the origins of both the superior mesenteric and celiac arteries (Fig. 72.2). Celiac Axis Compression As with atherosclerosis, chronic viscera ischemia due to celiac axis compression primarily affects women (76%). However, unlike atherosclerosis, these patients develop symptoms at a younger age (mean age 47) (33), and the symptoms are not always characteristic of “intestinal angina.” Only 37% of patients have postprandial symptoms, and in one-quarter of these patients, the symptoms are related to body position. Nausea, vomiting, and diarrhea occur in 65% of patients. Weight loss is less pronounced when compared with that of patients with atherosclerotic chronic visceral ischemia, and occurs in only 61% of patients. Around 23% of patients have a history of psychiatric disorder or alcohol abuse before the onset of symptoms. A history of previous abdominal operations is common. Compared with atherosclerotic chronic visceral ischemia, physical findings of malnutrition are uncommon. An epigastric bruit is common (85%) and typically varies with respiration, being more pronounced during expiration.

B

FIGURE 72.2 (A) Aortograms (lateral projection) showing occluded superior mesenteric artery (a) and severely stenosed celiac artery (b). (B) Digital subtraction angiography after transaortic visceral thromboendarterectomy. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

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Part IX Visceral Vessels FIGURE 72.3 Aortograms (lateral view) during expiration (A) and inspiration (B) in a patient with celiac axis compression syndrome. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

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B

Lateral aortographic projections during both inspiration and expiration will unmask the typical lesion in celiac axis compression (Fig. 72.3). In 78% of angiographies performed in patients with celiac axis compression, a diameter reduction of more than 50% was found in the celiac axis (39).

Treatment Options Surgical Treatment: Transabdominal Exposure Atherosclerosis All patients with a history suggestive of chronic visceral ischemia and a negative gastrointestinal workup should undergo biplanar aortography if the patient is a candidate for visceral artery reconstruction. The goal of operative treatment is relief of pain, reversal of inanition, and prevention of disease progression, which ultimately results in visceral infarction. Because multiple arteries are commonly involved, many authors suggest revascularization of as many arteries as possible (45–48). In our experience, the first priority is the celiac axis, and then the superior mesenteric artery. This is based on the observation that only postoperative celiac reocclusion was associated with recurrent ischemic symptoms. This was true even when the superior mesenteric artery was patent. Furthermore, reocclusion of the superior mesenteric artery does not always cause ischemic symptoms provided that the celiac artery is patent. The only indications for revascularization of the inferior mesenteric artery, which is rarely performed, are distal superior mesenteric artery lesions, failure of previous aortovisceral bypass, or a common celiac and superior mesenteric artery trunk (50). Concomitant

aortic repair including both renal arteries is frequently required because of the extension of advanced atherosclerotic disease to the infrarenal aorta (29). Exposure and reconstruction of the visceral arteries are very challenging (11,51,52), and a variety of techniques have been used. The early operative experience in treatment of chronic visceral ischemia included transmesenteric arterial thromboendarterectomy, saphenous vein bypass, arterial autograft, and vessel reimplantation (7,53–55). In our experience, these procedures had a high rate of early and late failures, which prompted the development of transaortic visceral thromboendarterectomy and antegrade aortovisceral bypass. These are the methods with which we have achieved significantly improved outcome for our patients. The choice of procedure has to be individualized according to the pattern of disease. In general, we perform thromboendarterectomy in patients with relatively low operative risks and when reconstruction of both the celiac axis and the superior mesenteric artery is feasible. This is also the preferred procedure when there is concomitant renal artery or infrarenal aortic disease. Anregrade aortovisceral grafting is reserved for elderly, high-risk patients without significant concomitant renal or infrarenal aortic disease (13,29–31). Celiac Axis Compression Because of the atypical presentation of chronic visceral ischemia in patients with celiac axis compression, a thorough examination to rule out other causes for their symptoms should be carried out, and the patient should be carefully selected for surgery. In our experience, relief of symptoms was most likely when the patient was female with a typical postprandial pain pattern and a weight loss greater than 20 pounds (9 kg) (39).

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FIGURE 72.4 This operative photograph demonstrates the unlimited exposure of the distal thoracic aorta and the entire abdominal aorta and its major visceral branches provided by the medial visceral rotation approach. (Reproduced by permission from Stoney RJ, Effeney DJ. Wylie’s atlas of vascular surgery: thoracoabdominal aorta and its branches. Philadelphia: JB Lippincott, 1992.)

Perioperative Management Considering the high incidence of other problems in patients with visceral atherosclerosis (80% smokers, 32% coronary artery disease, 66% hypertension, 36% renal insufficiency), preoperative cardiopulmonary optimization is frequently needed. Because of significant weight loss, nutritional repletion should be considered. Antibiotics are regularly started 12 hours before surgery and are continued for 48 hours. Supraceliac cross-clamping is associated with a high incidence of myocardial ischemia and an increased risk for myocardial infarction. The use of intraoperative cardiac monitoring with two-dimensional transesophageaI echocardiography has increased our ability to discover and treat cardiac complications at a very early stage (56). Also, the use of table-fixed self-retaining retractors has significantly improved the exposure facilitating the reconstruction of the aorta and its branches (Fig. 72.4) (57). Following reconstruction, intraoperative duplex ultrasound has proved invaluable for assessment of vessel patency and for disclosing technical errors before closure (58). Before discharge from the hospital, the patients have a digital subtraction arteriogram to determine patency of the reconstruction (see Fig. 72.2B). These technical advances have led to improved patient outcomes.

Transabdominal Exposure of Mesenteric Arteries Medial Visceral Rotation Approach The medial visceral rotation approach provides unlimited exposure of the distal thoracic and entire abdominal aorta including the major visceral and renal branches (51,57,59). The patient is positioned supine on the operating table and the abdomen is entered through a fulllength midline abdominal incision. After exploratory

laparotomy, the small bowel is placed in an intestinal bag and displaced to the right. Incising the lateral peritoneal reflection begins mobilization of the sigmoid and descending colon. This peritoneal incision is carried cephalad through the phrenocolic and lienorenal ligaments. Using gentle blunt and occasional sharp dissection, a plane is developed between the pancreas and Gerota’s fascia. The descending colon, pancreas, spleen, and stomach are then rotated anteriorly and medially, leaving the gonadal vein, ureter, left kidney, and adrenal gland in situ. The spleen and pancreas are protected with moistened pads, and a self-retaining retractor system is positioned to hold all of the anteriorly mobilized viscera to the right. The peritoneum is reflected from the left crus of the diaphragm, and the triangular ligament and left lobe of the liver are freed. The aorta is now clearly in view, crossed only by the left renal vein, the autonomic ganglia tissue, and the left crus of the diaphragm. Exposure of the upper abdominal aorta requires circumferential dissection of the left renal vein to its junction with the inferior vena cava, so that it can be widely displaced as needed. The superior mesenteric artery and celiac axis are exposed by excising the dense autonomic ganglia on the left lateral surface of the aorta, and by incising the left crus of the diaphragm. These vessels can then be circumferentially dissected. Resection of the median arcuate ligament and separation of the muscle fibers of the diaphragm exposes the supraceliac abdominal aorta and distal thoracic aorta. The major advantages of this approach are the unlimited exposure and the lack of constraint on the choice of technique used for visceral artery reconstruction. This approach is used preferentially when complex aortic and multiple-branch reconstructions are required (59). The thoracoretroperitoneal approach to the upper abdominal aorta and visceral arteries has been abandoned because substantially more pulmonary morbidity is associated

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with its use in patients undergoing visceral reconstruction for chronic mesenteric ischemia (60).

Techniques for Visceral Artery Reconstruction in Atherosclerosis

Transcrural Approach

Thromboendarterectomy

Transcrural exposure of the celiac and superior mesenteric arteries is performed through an upper two-thirds midline incision (57,61). The lesser peritoneal sac is entered through a vertical incision in the gastrohepatic ligament placed just to the right of the midline. The stomach and the esophagus are retracted to the left. The triangular ligament is divided to allow retraction of the liver to the right. The midline posterior peritoneum is incised. The muscle fibers of the diaphragm are separated and the median arcuate ligament is divided, exposing the distal thoracic aorta and supraceliac abdominal aorta. Excision of the dense autonomic ganglion tissue along the left anterolateral surface of the aorta allows the celiac axis to be mobilized and the common hepatic and splenic arteries to be freed from their position along the upper border of the pancreas. Then caudal retraction of the pancreas exposes the proximal superior mesenteric artery, allowing for its circumferential dissection.

As visceral artery thromboendarterectomy aims at removal of both the aortic atheroma and the orifice lesions that cause the visceral artery obstruction, a transaortic endarterectomy is preferred. This procedure requires unrestricted access to the distal thoracic aorta and upper abdominal aorta, which is achieved with the medial visceral rotation approach (see Fig. 72.4). The aorta is crossclamped above and below the major visceral branches, which are temporarily controlled. A U-shaped “trapdoor” aortotomy is performed, partially surrounding the orifices of the celiac axis and the superior mesenteric artery. The aortic orifice atheroma is removed, using extraction endarterectomy (Fig. 72.5A and B) (61). If the renal arteries are included in the thromboendarterectomy, the distal portion of the aortotomy is extended to an infrarenal level, with care not to encroach too closely upon the lumen of the left renal artery. This allows en bloc removal of the diseased intima from the aorta and the orifice

FIGURE 72.5 “Trapdoor” aortotomy (A) used for transaortic visceral artery extraction thromboendarterectomy (B). (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

Chapter 72 Surgery of Celiac and Mesenteric Arteries

lesions from all involved branches (Fig. 72.6). After checking the backbleeding from the visceral branches, the aortotomy is closed with a running suture. When the superior mesenteric artery (SMA) is totally occluded, a separate longitudinal arteriotomy may be created in the SMA after the aortotomy is closed, to allow direct visual control of the distal end point of the thrombotic occlusion. This allows removal of the “tail-thrombus,” which extends distally to the level of the reentry collateral 5 to 7 cm from the orifice. The arteriotomy is then closed with an autogenous vein patch to avoid narrowing (Fig. 72.7). Aortovisceral Bypass Grafting Aortovisceral bypass grafting can be performed with a variety of arterial substitutes and can be constructed to provide antegrade or retrograde flow. Autogenous vein or artery grafts used in a retrograde orientation with proximal infrarenal anastomosis have been abandoned because of unacceptably high early and late failure rates (43–49,53–54). The following basic principles for aortovisceral bypass grafting have been associated with a significantly improved patency and are therefore recommended:

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An undiseased aortic segment, with little risk for future disease developing at the origin of the graft. An antegrade alignment of the graft to minimize turbulence and kinking. A prosthetic Dacron graft, which, in our experience, has not developed degenerative changes. A flanged knitted Dacron prosthesis, created from a bifurcated graft, is preferred for a single-vessel bypass, and bifurcated graft (10 ¥ 5 mm or 12 ¥ 6 mm) is used when both vessels are reconstructed.

2. 3.

The transcrural approach is used. A length of supraceliac aorta 3.5 to 5 cm is controlled between vascular clamps. For celiac axis reconstruction, an elliptical aortotomy is created on the anterior aspect of the aorta for anastomosis of the beveled end of the prosthetic graft. Aortic flow can then be restored and the graft clamped separately. The celiac artery is transected beyond the lesion, and the proximal stump is oversewn; then the distal end is sutured end-to-end to the graft limb (Fig. 72.8). For combined celiac axis and superior mesenteric artery reconstruction, the aortotomy is placed on the right anterolateral aspect of the aorta, allowing placement of one limb of the graft in a retropancreatic position for end-

B

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FIGURE 72.6 “Trapdoor” aortotomy extended to include the renal arteries (A) for a combined transaortic extraction thromboendarterectomy of the visceral and renal arteries (B). (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

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B

FIGURE 72.7 (A) Separate arteriotomy for thromboendarterectomy of the totally occluded superior mesenteric artery. (B) Closure of the arteriotomy with a venous patch to avoid narrowing. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

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to-end anastomosis to the divided superior mesenteric artery. The visceral arteries are grafted sequentially to minimize ischemia (Fig. 72.9).

Results and Complications The most recent update of patients treated at University of California, San Francisco, encompasses 109 patients who underwent primary visceral revascularization between 1959 and 1997 (14). Of these, 90 (83%) achieved symptom relief and 19 (17%) had recurrent symptoms— 12 chronic and seven acute. Of the 12 with chronic recurrent symptoms, 10 underwent reoperation. There were 94 patients who underwent the preferred method of revascularization (transaortic endarterectomy or antegrade prosthetic bypass grafting). Transaortic endarterectomy was performed in 60 patients (126 arteries) with seven deaths and long-term symptom relief in 51 (85%). Antegrade bypass was perfomed in 34 (57 arteries) with three deaths and long-term symptom relief in 29 (85%) (62). Average follow-up for 66 months was 80%. Transaortic endarterectomy and antegrade visceral bypass provide long-term relief from visceral ischemic symptoms and prevent visceral gangrene. The durability of these procedures is attributed to the elimination of turbulent blood flow by using endarterectomy and antegrade graft placement and by the avoidance of conduit complications inherent in retrograde graft alignment.

Celiac Artery Compression Syndrome With the exception of patients having multiple previous abdominal operations, a standard transabdominal approach is used. Principally, celiac axis compression is treated in three different ways: decompression alone, decompression and dilation, or decompression and celiac artery reconstruction. Decompression means resection of the median arcuate ligament and the celiac ganglion fibers. If a flowlimiting fibrotic stenosis has resulted from the compression, it can be dilated by use of retrograde intraluminal grade dilators (Fig. 72.10). This procedure is performed through a transverse arteriotomy in the splenic artery. If dilation fails to restore good celiac inflow, as demonstrated by duplex scanning or a residual pressure gradient, aortoceliac bypass is performed. The celiac artery can be reconstructed by a short interposition Dacron graft proximally anastomosed to the celiac axis stump and distally to the divided end of the celiac artery (63).

FIGURE 72.8 (A) Excision of celiac ganglion fibers for exposure of the celiac axis. (B) Segmental aortic clamping and aortotomy for proximal anastomosis of aortovisceral graft. (C) Flanged Dacron graft, cut from a bifurcated graft (inset), used for aortoceliac reconstruction with antegrade alignment. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

Results and Complications In a series of 51 patients treated between 1964 and 1981, each of the three different principal treatments was used with roughly the same frequency (33). No mortality occurred. A total of 44 patients (86%) were available for late

Chapter 72 Surgery of Celiac and Mesenteric Arteries

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follow-up after a mean period of 9 years. Of these patients 30 were cured and 14 were still symptomatic. The cure rate was higher when decompression was combined with dilation or reconstruction than when it was used alone (79% and 73% vs. 53% asymptomatic patients). Combined with the fact that decompression alone had a high rate of pressure gradients, these results might suggest that decreased celiac flow really is a significant factor in this syndrome.

Endoluminal Therapy The advent of minimally invasive percutaneous therapy for these conditions deserves mention, although longterm results and head-to-head comparison with the surgical treatments presented does not yet exist. The first successful visceral angioplasty was reported by Furrer et al. in 1980 when they angioplastied a superior mesenteric artery (64). Since then numerous case reports have appeared (65–67). A comparison between treatment rendered percutaneously and with open surgery with short-term follow-up was reported by the Cleveland Clinic recently (14). They compared a prospectively gathered group of 28 patients undergoing percutaneous therapy (82% with stenting) over a 3.5-year period with a historic surgical control group of 85 treated between 1977 and 1997. Significantly more vessels were revascularized with open surgery and only one completely occluded vessel was addressed percutaneously versus treatment of 62 of 122 occluded vessels in the open surgery group. Of interest, there was no statistically significant difference in length of hospital stay, perioperative complications, or mortality. In addition, the 3-year survival between these two groups was not statistically different. Of particular interest was the fact that in the 11 of 28 patients treated percutaneously who had recurrent symptoms; only one of seven who received duplex interrogation of the treated vessel had a restenosis of that vessel— begging the question as to what was the cause of the recurrent symptoms. Overall, percutaneously treated patients had a 34% incidence of recurrent symptoms at 3 years compared with only 13% of those treated with open surgery. Similar results were obtained in the course of a smaller review done in Seattle (68). Clearly, the retrospective nature of these reviews limits the ability to prognosticate for individual patients. Sicker patients are more likely to undergo percutaneous treatments on the whole and 䉳 FIGURE 72.9 (A) Exposure of celiac axis and superior mesenteric artery and placement of the aortotomy for combined aortovisceral reconstruction. (B) Separate clamping of the bifurcated graft restores aortic flow. End-to-end anastomosis between prosthetic graft limb and the transected celiac artery is performed. (C) Restored flow to the celiac artery and completion of anastomosis between graft and the superior mesenteric artery. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

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FIGURE 72.10 Technique for exposure in the surgical treatment of celiac axis compression. Right-angle clamp is used to separate the median arcuate ligament and the underlying artery (A) before triangular excision of the ligament (B). (C) Midline division of the muscular fibers of the diaphragmatic crus exposes the celiac origin and the thoracic aorta. (D) Dilation of the celiac axis through a transverse arteriotomy in the splenic artery. (Reproduced by permission from Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vols 1 and 2. New York: Springer Verlag, 1980.)

surgical patients, while relatively healthier presumably, also were more likely to have multiple vessel bypass. Unfortunately, given the rare occurrence of this disease in all but the busiest centers, prospective data comparisons are not likely to be made. It is important to always keep a surgical option open when planning and performing endovascular therapies.

Acknowledgments This work was supported in part by the Pacific Vascular Research Foundation, San Francisco, CA. Special thanks to Darren Schneider, MD, for his contribution to the results section.

Chapter 72 Surgery of Celiac and Mesenteric Arteries

References 1. Chiene J. Complete obliteration of the celiac and mesenteric arteries. J Anat Physiol 1869;3:65. 2. Councilman WT. Three cases of occlusion of the superior mesenteric artery. Boston Med Surg J 1894:130:4. 3. Goodman EH. Angina abdominis. Am J Med Sci 1918;155:524. 4. Davis BB. Thrombosis and embolism of the mesenteric vessels. Nebraska Med J 1921;6:101. 5. Dunphy JE. Abdominal pain of vascular origin. Am J Med Sci 1936;192:102. 6. Mikkelsen WP. Intestinal angina: its surgical significance. Am J Surg 1957;99:262. 7. Shaw RS, Maynard EP III. Acute and chronic thrombosis of mesenteric arteries associated with malabsorption: report of two cases successfully treated with thromboendarterectomy. N Engl J Med 1958;258:874. 8. Elliott JW. Operative relief of gangrene of the intestine due to occlusion of the mesenteric vessels. Ann Surg 1985;21:9. 9. Mikkelsen WP, Zaro IA. Intestinal angina: report of a case with preoperative diagnosis and surgical relief. N Engl J Med 1959;260:912. 10. Derrick J, Pollard H, et al. The pattern of arteriosclerotic narrowing of the celiac and superior mesenteric arteries. Ann Surg 1959;149:684. 11. Morris GC, Crawford ES, et al. Revascularization of the celiac and superior mesenteric arteries. Arch Surg 1962;84:95. 12. Fry WD, Kraft RO. Visceral angina. Surg Gynecol Obstet 1963;117:417. 13. Stoney RJ, Wylie EJ. Recognition and surgical management of visceral ischemic syndromes. Ann Surg 1966;164:714. 14. Kasirajin K, O’Hara P, et al. Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 2001;33(1):63–71. 15. Allen RC, Martin GH, et al. Mesenteric angioplasty in the treatment of chronic intestinal ischemia. J Vasc Surg 1996;24(3):415–423. 16. Schneider DB, Schneider PA, et al. Reoperation for recurrent chronic visceral ischemia. J Vasc Surg 1998; 27(2):276–286. 17. Maspes F, Mazzetti di Pietralata G, et al. Percutaneous transluminal angioplasty in the treatment of chronic mesenteric ischemia: results and 3 years follow-up in 23 patients. Abdom Imag 1998;23:358–363. 18. Nyman U, Ivanciv K, et al. Endovascular treatment of chronic mesenteric ischemia: report of five cases. Cardiovasc Interv Radiol 1998;21:305–313. 19. Rose SC, Quigley TM, Raker EJ. Revascularization for chronic mesenteric ischemia: comparison of operative arterial bypass grafting and percutaneous transluminal angioplasty. J Vasc Interv Radiol 1995;6(3):339–349. 20. Bergan JJ. Recognition and treatment of superior meseneric artery embolization. Geriatrics 1969;24:118. 21. Bergan JJ. Recognition and treatment of superior mesenteric artery embolization. Surg Clin North Am 1967;47:109. 22. Bergan JJ, Dean RH, et al. Revascularization in the treatment of mesenteric infarction. Ann Surg 1975;182: 430.

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23. Bergan JJ, Dry L, et al. Intestinal ischemia syndromes. Ann Surg 1969;169:120. 24. Wilson GSM, Block J. Mesenteric vascular occlusion. Arch Surg 1956;73:330. 25. Serjeant JCE. Mesenteric embolus treated with low molecular weight dextran. Lancet 1965;1:139. 26. Marfuggi RA, Greenspan M. Reliable intraoperative prediction of intestinal viability using fluorescent indicator. Surg Gynecol Obstet 1980;152:33. 27. Wright CB, Hobson RW. Prediction of intestinal viability using Doppler ultrasound technique. Am J Surg 1975; 129:642. 28. Wittenberg J, Asthanasoulis CA, et al. A radiological approach to the patient with acute, extensive bowel ischemia. Radiology 1973;106:13. 29. Rapp JH, Reilly LM, et al. Durability of endarterectomy and antegrade grafts in the treatment of chronic visceral ischemia. J Vasc Surg 1986;3:799. 30. Stoney RJ, Ehrenfeld WK, Wylie EJ. Revascularization methods in chronic visceral ischemia caused by atherosclerosis. Ann Surg 1977;186:468. 31. Stoney RJ, Olcott C IV. Visceral artery syndrome and reconstructions. Surg Clin North Am 1979;59: 637. 32. Qvatfordt PG, Reilly LM, et al. “Coral reef” atherosclerosis of the suprarenal aorta: a unique clinical entity. J Vasc Surg 1984;1:903. 33. Poole JW, Sam Martano BS, Boley SJ. Hemodynamic basis of the pain of chronic mesenteric ischemia. Am J Surg 1987;153:171. 34. Dunbar JD, Molner RL, et al. Compression of the celiac trunk and abdominal angina: preliminary report of 15 cases. Am J Roentgenol 1965;95:731. 35. Evans WE. Long-term evaluation of the celiac band syndrome. Surgery 1974;76:867. 36. Brandt IJ, Boley SJ. Celiac axis compression: a critical review. Am J Dig Dis 1978;23:633. 37. Rogers DM, Thompson JE, et al. Mesenteric vascular problems: a 26-year experience. Ann Surg 1982;195:554. 38. Szilagyi DE, Rian RL, et al. The celiac axis compression syndrome. Does it exist? Surgery 1972;72:849. 39. Reilly LM, Ammar AD, et al. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg 1985;2:79. 40. Snyder MA, Mahoney EB, et al. Symptomatic celiac artery stenosis due to constriction by the neurofibrous tissue of the celiac ganglion. Surgery 1967;61:372. 41. Harlola PT, Lahtiharjn A. Celiac axis syndrome: abdominal angina caused by external compression of the celiac artery. Am J Surg 1968;115:864. 42. Krupski WC, Effeney DJ, Ehrenfeld WK. Spontaneous dissection of the superior mesenteric artery. J Vasc Surg 1985;2:731. 43. Pallubinskas AJ, Ripley HR. Fibromuscular hyperplasia in extrarenal arteries. Radiology 1964;82:451. 44. Williams LF Jr. Vascular insufficiency of the intestines. Gastroenterology 1971:61:757. 45. Connolly JE, Kwaan JHM. Management of chronic visceral ischemia. Surg Clin North Am 1982;62:345. 46. Baur GM, Millay DJ, et al. Treatment of chronic visceral ischemia. Am J Surg 1984;148:138. 47. Hollier LH, Bernatz PE, et al. Surgical management of

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48. 49.

50.

51.

52.

53.

54.

55. 56.

57.

Part IX Visceral Vessels chronic intestinal ischemia: a reappraisal. Surgery 1981;90:940. Connelly TJ, Perude GD, et al. Elective mesenteric revascularization. Am J Surg 1980;115:497. Zelenock GB, Graham LM, et al. Splanchnic arteriosclerotic disease and intestinal angina. Arch Surg 1980;115:497. Schneider DB, Nelken NA, Messina LM, et al. Isolated inferior mesenteric artery revascularization for chronic visceral ischemia. J Vasc Surg 1999;30(1): 51–58. Murray SP, Keustner L, Stoney RJ. Transperitoneal medial visceral rotation. Ann Vasc Surg 1995;9(2): 209–216. Keustner L, Murray SP, Stoney RJ. Transaortic renal and visceral endarterectomy. Ann Vasc Surg 1995;9(3): 302–310. Dean RH, Wilson JP, Burko H. Saphenous vein aortorenal bypass grafts: serial arteriographic study. Ann Surg 1974;180:469. Stanley JC, Ernst CB, Fry WJ. Fate of 100 aortorenal vein grafts: characteristics of late graft expansion, aneurysmal dilation, and stenosis. Surgery 1973;74:931. Stoney RJ, DeLuccia N, et al. Aortorenal arterial autografts: long term assessment. Arch Surg 1981;116:1416. Sohn YJ, Cronnelly R, et al. Monitoring with twodimensional transesophageal echocardiography: comparison of myocardial function in patients undergoing supraceliac, suprarenal, infraceliac or infrarenal aortic occlusion. J Vasc Surg 1984;1:300. Ramos TK, Stoney RJ. Exposure of the abdominal aorta and its branches using the Omni-Tract. In: Tawes RL, ed. International surgical technology II. London: Century Press of London Corp., 1993.

58. Okuhn SP, Reilly LM. Intraoperative assessment of renal and visceral artery reconstruction: the role of duplex scanning and special analysis. J Vasc Surg 1987;5: 137. 59. Reilly LM, Ramos TK, et al. Optimal exposure of the proximal abdominal aorta: a critical appraisal of transabdominal medial visceral rotation. J Vasc Surg 1993; 60. Cunningham CG, Rapp J, et al. Chronic intestinal ischemia: three decades of surgical progress. Ann Surg 1991;14:76–88. 61. Wylie EJ, Stoney RI, Ehrenfeld WK. Manual of vascular surgery Vol. 1. New York: Springer-Verlag 1980;207. 62. Darren Schneider, personal communication. March 2002. 63. Wylie EJ, Stoney RJ, et al. Manual of vascular surgery, vol.2. New York: Springer-Verlag 1980;210. 64. Furrer J, Gruntzig A, Kugelmeier J, Goebel N. Treatment of abdominal angina with percutaneous dilation of an arteria mesenterica superior stenosis. Cardiovasc Intervent Radiol 1980;3:43–44. 65. Nyman U, Ivancev K, et al. Endovascular treatment of chronic mesenteric ischemia: report of five cases. Cardiovasc Intervent Radiol 1998;21:305–331. 66. Allen R, Martin G, et al. Mesenteric angioplasty in the treatment of chronic intestinal ischemia. J Vasc Surg 1996;24(3):415–421. 67. Maspes F, Mazzetti G, et al. Percutaneous transluminal angioplasty in the treatment of chronic mesenteric ischemia: results and 3 years of follow-up in 23 patients. Abdominal Imaging 1998;23:358–363. 68. Rose S, Quigley T, Raker E. Revascularization for chronic mesenteric ischemia: comparison of operative arterial bypass grafting and percutaneous transluminal angioplasty. J Interv Radiol 1995;3:339–349.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 73 Mesenteric Ischemia Julie A. Freischlag, Michael M. Farooq, and Jonathan B. Towne

Mesenteric ischemia encompasses a wide variety of clinical syndromes with symptoms that range from subtle complaints in patients with chronic ischemia to septic shock in patients with acute mesenteric ischemia that has progressed to bowel gangrene (1–6). Mesenteric ischemia is difficult to diagnose. Intervention, whether it is surgical or nonsurgical, carries a high morbidity and mortality rate. This chapter will review the historical background of mesenteric ischemia and discuss the pathophysiology, clinical presentation and treatment of acute and chronic mesenteric ischemia as well as mesenteric venous thrombosis (Table 73.1). Diagnosis with duplex ultrasonography, computed tomography (CT) and angiography are reviewed. Indications for percutaneous balloon angioplasty and stenting for high-risk cases and recurrent disease are addressed.

Historical Background Initially, observations were made that the mesenteric arteries could become occluded without causing symptoms; it was not until 1936 that Dunphy first reported upon a small series of patients who died from chronic mesenteric ischemia (7). He was the first to correlate the complaints of abdominal pain and weight loss with the absence of adequate arterial blood supply to the intestine. The term “intestinal angina” was initially used by Mikkelsen in 1957 (8) and is the most frequently used term for such complaints of postprandial pain by patients with symptomatic chronic mesenteric ischemia. Shaw and Maynard described two patients with mesenteric ischemia that had resulted in bowel infarction who were treated by bowel

resection and endarterectomy of the visceral vessels (9). Further studies of endarterectomy were reported (10–13). Eventual operative treatment involving the use of synthetic and autologous bypass grafts from the supraceliac aorta and the infrarenal aorta was utilized to remedy the low-flow state responsible for chronic mesenteric ischemia in these patients (14–18).

Acute Mesenteric Artery Ischemia Diagnosis Acute mesenteric ischemia has been diagnosed with increasing frequency over the past few decades (19–23). The reasons for this appear to be heightened physician awareness of the problem and the aging of our population. Elderly patients with serious medical illnesses survive in intensive care units and develop acute mesenteric ischemia late in the course of recovery from other disease processes. Acute mesenteric ischemia is manifested by the sudden loss of blood supply in the distribution of the superior mesenteric artery. Acute mesenteric ischemia can occur secondary to embolization or thrombosis of a previously stenotic lesion. The metabolic alterations seen as a consequence of the occlusion include dehydration, metabolic acidosis, and hyperkalemia. A third cause of acute mesenteric ischemia that must be differentiated from embolus or thrombosis is nonocclusive mesenteric ischemia resulting from low cardiac output in patients who tend to be hospitalized for other serious medical conditions (24). Acute mesenteric ischemia carries a 60% to 70% morbidity and mortality rate that has not changed for

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TABLE 73.1 Mesenteric ischemia Acute Arterial Superior mesenteric artery embolism

Superior mesenteric artery thrombosis

Nonocclusive mesenteric ischemia

many decades despite early aggressive treatment (25). Boley and colleagues noted a decreased mortality rate of 54% in patients with acute mesenteric ischemia who were treated aggressively with early angiography and intraarterial papaverine (26). The high morbidity and mortality rates, most notably in patients with nonocclusive mesenteric ischemia, indicate that these patients have other medical conditions which require intensive perioperative management and care (27). The physician should not be reluctant when investigating these patients if the question of possible mesenteric ischemia arises. Delay in diagnosis adds to the high morbidity and mortality rates, while early aggressive intervention combined with the liberal use of second-look laparotomy has resulted in increased early survival (27). Despite improvements in diagnostic, operative, and anesthetic techniques, these patients continue to be a challenge for the physicians who care for them. However, beyond the perioperative period, patients successfully treated for acute mesenteric ischemia demonstrate similar long-term survival compared with patients revascularized for chronic disease (28).

Embolic Occlusion Acute mesenteric occlusion occurring secondary to embolization is the most common cause of mesenteric infarction (18). The patient with acute embolic occlusion of the superior mesenteric artery experiences severe periumbilical pain most often accompanied by gut emptying, which can be accompanied by nausea and vomiting (23). On physical examination, in the early phases of this ischemic process, minimal tenderness is found on palpation of the abdomen. At this time as well, before the development of peritonitis secondary to bowel infarction, normal to hyperactive bowel sounds will be heard on auscultation (19). The most frequent site of origin of the embolus is the heart, as almost all of these patients have a history of cardiac disease (20). Classically, the triad of acute abdominal pain, bowel evacuation, and cardiac disease that could be responsible for the source of embolization was described by Boley (29). Echocardiography should be performed postoperatively to reveal any residual thrombus. In almost one-third of these patients who have a superior mesenteric artery embolus, additional emboli can be identified in other arterial beds such as the renal, cerebral, or peripheral extremities (30). Laboratory evaluation may initially reveal no abnormalities. As the illness progresses, tests can reveal leuko-

Venous

Chronic Arterial

Mesenteric venous thrombosis

Chronic mesenteric ischemia

cytosis and coagulopathy as the ischemia leads to infarction, resulting in bowel death and sepsis (31). Other metabolic changes can then be seen, as described above, leading to the patient’s demise due to septic shock. A plain film of the abdomen should be ordered to rule out other causes of abdominal pain such as a perforated ulcer, which can be diagnosed by the presence of free air. If the abdominal film is normal, then the existence of mesenteric ischemia is even more plausible in this setting. A plain radiograph is rarely diagnostic of acute mesenteric ischemia. Bowel dilation or a paucity of gas is usually seen but is nondiagnostic. Computed tomography can document bowel infarction by the presence of bowelwall thickening that can be seen with ascites, but it cannot accurately document mesenteric artery occlusion (32,33). If the patient does not have documented signs and symptoms of peritonitis, diagnostic evaluation of the abdominal vasculature is best obtained by use of an angiogram that selectively images the superior mesenteric artery. Angiography classically will demonstrate no flow into the superior mesenteric artery at a short distance from its origin from the aorta, just at the branching point of the middle colic artery. This is referred to as the “mercury meniscus” sign (34). Lateral angiographic views of the superior mesenteric artery can be helpful to delineate the embolus. Sometimes a nonoccluding thrombus will allow a small amount of contrast material into the more distal superior mesenteric artery. In approximately one-third of these patients, even more distal propagation of thrombus beyond the embolus can be seen.

Thrombotic Occlusion Acute mesenteric thrombosis occurs with a thrombosis at the site of a previously stenotic site in the artery, which arises most commonly secondary to atherosclerosis (35). Because collateral vessels will enlarge over time when a stenosis forms, the symptoms experienced by the patient with acute mesenteric thrombosis are less severe and are slowly progressive (17). The whole picture of abdominal pain, bowel emptying, and distention may develop over 12 to 24 hours, rather than abruptly as it does in acute mesenteric occlusion secondary to embolus (19,21).

Nonocclusive Mesenteric Artery Ischemia Nonocclusive mesenteric ischemia has no structural lesion causing occlusion of the mesenteric arteries. The

Chapter 73 Mesenteric Ischemia

most common cause is poor cardiac output, which then leads to mesenteric ischemia due to a relatively low output to the intestines (24). The physiologic mechanism of preserving blood flow to vital organs, such as the kidneys and the brain, allows a state of low flow to the intestine. Associated disease states that lead to nonocclusive mesenteric ischemia are congestive heart failure, cardiac arrhythmias, myocardial infarction with left ventricular failure, septic shock, trauma associated with hypotension, extensive body burns, hypovolemia from any cause, the use of inotropic cardiac drugs, especially digitalis, and aortic insufficiency (26). Vasoconstrictors also contribute to the development and worsening of mesenteric ischemia. Digitalis and its derivatives are splanchnic vasoconstrictors that can contribute to mesenteric insufficiency secondary to low-output failure (37–39). Symptoms are similar to those with the development of acute mesenteric ischemia from either embolus or thrombosis of the superior mesenteric artery. Abdominal pain may be absent in up to one-quarter of these patients; however, unexplained abdominal distention or upper gastrointestinal bleeding may be the initial symptom (40). The diagnosis is sometimes obscured by the complexity of the patient’s other medical problems. Diagnosis is again made by the use of angiography. Angiography should not be performed until the patient has been adequately resuscitated. Patients with hypotension or hypovolemia will demonstrate similar findings on the angiogram; therefore hydration and treatment of the underlying cardiac problem should be attempted before angiography. Unlike the angiogram obtained with either embolus or thrombosis of the superior mesenteric artery, in this case the superior mesenteric artery appears in spasm and many of its branches can be narrowed either focally or diffusely (41). The lesions themselves are smooth in contour without total occlusion. Other classic angiographic findings are impaired filling of the intramural mesenteric artery, vasculature arcades, or alternating dilation and narrowing of the mesenteric vessels, which is referred to as the “string-of-sausage sign.”

Treatment Surgical intervention is the treatment of choice for both embolic and thrombotic mesenteric occlusion. Systemic heparinization should be started before the operation to prevent propagation of thrombus beyond either the embolic or thrombotic occlusion. Through a midline incision, the small bowel and its mesentery are inspected for viability. The superior mesenteric artery can be found easily by mobilization of the fourth portion of the duodenum and transverse colon so that the aorta can be visualized just at the origin of the superior mesenteric artery. The superior mesenteric artery can be isolated for the length needed by careful dissection through the mesentery. By palpating the artery itself, the area of lodgment of the embolus can be readily identified. An arteriotomy can then be

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planned to be placed at that point. A transverse arteriotomy is most frequently made, which allows use of a No. 3 Fogarty balloon catheter to extract the embolus. The artery is then irrigated with heparinized saline and closed with interrupted 6–0 polypropylene suture. Intraoperative thrombolytic therapy can be used if the embolus has caused distal thrombosis in smaller vessels that cannot be reached by the Fogarty catheter (42,43). Owing to the slow progression of their symptoms, patients with thrombotic occlusion will not come to medical attention until the disease process has gone on to cause bowel infarction. These patients often have other signs and symptoms of atherosclerosis and may be elderly (21). If questioned specifically, these patients will also relate a history of mesenteric angina, which includes pain after eating, weight loss, and often fear of eating due to the pain incurred. Again, angiography is the best method to make the diagnosis if the patient does not already have signs and symptoms of infarcted bowel that would warrant immediate laparotomy and bowel resection. The angiogram will reveal mesenteric artery stenoses and occlusions near the origin of the mesenteric vessels from the aorta (36). Often all three mesenteric vessels—the celiac, superior mesenteric, and inferior mesenteric arteries—will be involved, which makes reconstruction a surgical challenge. The bowel is again inspected (44). Any areas of bowel that are obviously necrotic and nonviable should be resected at this first operation. Any segments of bowel that are questionable in appearance should be left to be checked in 24 hours (45,46). The use of fluorescein can be helpful (47,48). Using a Wood’s ultraviolet light, areas of viable bowel will reveal a fine reticular vascular pattern, whereas those segments that are gangrenous will have no fluorescein appear in their walls. The Doppler probe can identify a return of signal in certain areas of the bowel but cannot differentiate viable from nonviable bowel (49–51). This “second-look” operation then is performed to reinspect those areas. After 24 hours, the bowel will either become more necrotic, necessitating resection, or it will appear viable and therefore can be left in place. The decision to perform a “second-look” operation should be made at the primary operation, and it should always be carried out despite the patient’s condition. The clinical course over those 24 hours often does not reflect the nature of the bowel’s viability. Postoperatively, patients who have embolized to their superior mesenteric artery need to remain on anticoagulation therapy. Systemic heparinization should be followed by the administration of warfarin for life, as the recurrence rate for embolization to other vascular beds approaches 50% in some series (29). There have been a few isolated reports of lytic therapy being used for patients with acute mesenteric ischemia secondary to an embolus (52–55). These patients were thought not to be surgical candidates and therefore underwent attempted lysis of the embolic occlusion. This treatment is to be used with caution because most patients

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require more immediate attention due to progressive bowel ischemia that cannot await the utilization of lytic therapy. If the underlying cause of the mesenteric ischemia is thrombosis of a preexisting arterial stenosis, the angiogram will help the surgeon to plan the reconstruction needed. The superior mesenteric artery is exposed and dissected distally until a segment beyond the occlusion is found suitable for a bypass graft to be placed (56,57). If the celiac artery is not stenotic or occluded, a bypass graft taken from either the suprarenal or infrarenal aorta can be performed to the superior mesenteric artery alone. Saphenous vein is the conduit of choice; however, polytetrafluoroethylene can be used when the saphenous vein is not available. If the aorta is severely atherosclerotic, placement of the proximal anastomosis may not be feasible at that location. Replacement grafting of the aorta can be performed in the good-risk patient, or placement of the origin of the graft to the iliac artery can be performed in the poor-risk patient (58). When multiple mesenteric arteries are involved, thromboendarterectomy can be utilized to open the orifices of the celiac, superior mesenteric, and inferior mesenteric arteries through either a thoracoabdominal approach or an intra-abdominal approach using a medial visceral rotation to gain access to the aorta (59). Other methods may include replacement of the infrarenal aorta with a synthetic graft with limbs sewn in place, made from either saphenous vein or polytetrafluoroethylene, which can be brought to all or one of the mesenteric branches. The bowel needs to be similarly inspected following revascularization, and a “second-look” procedure may be necessary (60). Anticoagulation is not indicated in these patients who have suffered a thrombotic occlusion. Nonocclusive mesenteric ischemia does not warrant surgical intervention unless the patient has signs and symptoms of bowel infarction, which would require emergent bowel resection. The treatment of choice for nonocclusive mesenteric ischemia is perfusion of the superior mesenteric artery with papaverine via a selectively placed catheter at the time of angiography (20). An initial bolus of 30 mg can be instilled, followed by an infusion of 30 to 60 mg/h for a 24-hour period. A repeat angiogram is then obtained to determine if the spasm has improved and vascular perfusion has returned to a normal-appearing state. During this 24-hour period, all other medical means should be used to improve cardiac output. Some series have reported the use of papaverine for up to 5 days without complication (17).

Mesenteric Venous Thrombosis Mesenteric venous thrombosis is a rare entity that can cause acute mesenteric ischemia. Its signs and symptoms are similar to those seen in acute arterial mesenteric ischemia; however, the presentation initially tends to be less acute and severe (61–64). It is not unusual for patients to

have a slow progressive course that lasts from hours to days to weeks, whereas other patients can have acute abdominal symptoms (54,65). Mesenteric venous thrombosis occurs most commonly in the superior mesenteric vein but can arise in smaller veins of the mesentery or the portal vein (66,67). In up to one-third of cases of mesenteric venous ischemia, no underlying cause can be identified. Many hematologic abnormalities can be associated with mesenteric venous thrombosis, including antithrombin III deficiency (68), protein C and S deficiency (69–72), sickle-cell anemia, and polycythemia vera. Intra-abdominal infections can lead to the development of mesenteric venous thrombosis (73). Low-flow states, regional venous congestion, and abdominal trauma all can be associated with mesenteric venous thrombosis as well (74). Some patients who have developed mesenteric venous thrombosis used oral contraceptives (75–77) (Table 73.2). Abdominal pain is frequently present and can vary greatly in location and severity. Abdominal distension is more frequently seen in mesenteric venous thrombosis than in mesenteric arterial thrombosis (64). Fever, nausea, vomiting, diarrhea, and hematemesis can be part of the presenting picture, depending on the extent of bowel infarction (65). Fluid sequestration is evident in severe cases along with intestinal hemorrhage. Because of the varying locations of the site of the mesenteric venous thrombosis, the symptoms can mimic many other disease states, and the diagnosis can be very difficult to make. No laboratory tests are diagnostic of mesenteric venous thrombosis. A plain abdominal radiograph usually reveals a nonspecific ileus pattern or no abnormality. A test for occult blood in the stool can be positive in up to 50% of patients with acute mesenteric venous thrombosis (62). Angiography can be diagnostic if thrombus is identified in the superior mesenteric vein (78,79). Computed tomography has emerged as a diagnostic tool in mesenteric TABLE 73.2 EtioIogy of mesenteric venous thrombosis Primary (unknown) Secondary Abdominal trauma Oral contraceptives Low-flow states Pregnancy Liver cirrhosis Abdominal infection/inflammation Cholecystitis/cholangitis Appendicitis Diverticulitis Ulcerative colitis Crohn’s disease Hematological abnormalities Antithrombin III deficiency Protein C or S deficiency Polycythemia vera Sickle-cell disease Thrombocytosis Carcinomatosis/compression of mesenteric veins by tumor

Chapter 73 Mesenteric Ischemia

venous thrombosis. A CT scan can reveal a superior mesenteric vein thrombus if present along with ascites, thickened bowel walls, and abnormal venous collateralization, which characterize the findings of mesenteric venous thrombosis (80–83). Computed tomography can also identify the mesenteric venous thrombosis early, which often allows the diagnosis to be made before bowel infarction and peritonitis. In those cases, the patient can undergo systemic anticoagulation and may not require a laparotomy or bowel resection. Duplex scanning can be utilized as well to visualize thrombus of the superior mesenteric vein and the portal vein (63,84). Because the quality of duplex scanning is more operator dependent, the diagnosis is more difficult to make. Some authors have advocated use of laparoscopy to identify mesenteric venous thrombosis in the early stages, which would avoid a laparotomy as the patient could initially be treated with anticoagulation (85). Despite attempts at diagnosis prior to laparotomy in those patients with peritonitis, most cases of mesenteric venous thrombosis are diagnosed at the time of laparotomy (86,87). The bowel is inspected for viability, and any segments of bowel that appear grossly necrotic should be resected. If portions of the small intestine are marginal in appearance, a “second-look” operation should be planned for 24 hours later. Postoperatively, the patient should be systemically heparinized followed by lifelong administration of warfarin to prevent further episodes of venous thrombosis. The mortality rates reported for mesenteric venous thrombosis are lower than those for arterial mesenteric ischemia, ranging from 10% to 30% (64,66). This is because these patients tend to be younger and do not have the same medical illnesses that are prevalent in patients with arterial mesenteric ischemia. Lytic therapy has been used in a few isolated reports to attempt to open up areas of thrombosed mesenteric veins, but no benefit has been shown in overall outcome (88).

Chronic Mesenteric Artery Ischemia Diagnosis The classic clinical picture of chronic mesenteric ischemia includes a history of abdominal pain after eating, which some authors have described as intestinal angina (89). Patients are usually in their fifth to seventh decade; women are affected three times as often as men, with a predominance of tobacco use (90). Initially, pain may only occur after large meals, hut then it begins to happen following smaller meals. The pain is located in the epigastrium, but it may radiate to the back. Diarrhea, secondary to malabsorption, may also be part of the clinical history. Other ischemia-induced motility problems may be seen such as constipation, nausea, and vomiting (1). As the syndrome progresses over time, the pain becomes more severe in nature and duration. The patient becomes fearful of eating

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and loses weight due to the decreased intake of food. These patients have other stigmata of peripheral vascular disease such as a history of cardiac disease, stroke, claudication, or previous vascular operative procedures (5). On physical examination, an abdominal bruit may be heard by auscultation. No other findings on physical examination are particular to those patients with chronic mesenteric ischemia (16). The diagnosis of chronic mesenteric ischemia is a difficult one to make as the findings of abdominal pain, weight loss, and diarrhea can be associated with a multitude of other medical problems (91). Often, patients have undergone both upper and lower endoscopy, ultrasound, and computed tomography before seeing the vascular surgeon. Peptic ulcer disease, cholecystitis, diverticulitis, and carcinoma of the pancreas, stomach, or intestine can have similar presentations. Therefore, preliminary investigations are often appropriate; however, the time until the diagnosis is made and an angiogram is obtained can be very long in some cases, with a mean interval till diagnosis of over a year in one review (90,92,93). Duplex scanning can be used to document noninvasively the presence of stenoses or occlusions of the visceral vessels (94–99). Ideally, the patient should fast for 8 hours before the examination to decrease the amount of gas present, which allows better visualization of the mesenteric arteries. B-mode probes with a low frequency of 2 to 3 MHz are used. The mesenteric arteries are identified as they branch off the aorta (100). The inferior mesenteric artery is the most difficult to identify. The vessels are inspected for size and patency as well as for their flow characteristics. The celiac artery normally has a low resistance pattern with forward flow throughout diastole (101,102). The superior mesenteric artery has a high-resistance appearance with a triphasic signal (103,104). With progressive stenosis of these arteries, a monophasic signal can be identified along with spectral broadening and increased systolic velocities that can be quite impressive. With occlusion, no flow can be seen in the identified artery. Some authors advocate comparing the mesenteric vessels’ flows at rest with their flows following a meal (105). In those with mesenteric ischemia, no increase in systolic velocity is seen, which is the normal response. Angiography is the best diagnostic test to identify mesenteric arteries involved in the atherosclerotic process. As atherosclerotic disease most frequently begins at the origin of the vessels off the aorta, a lateral angiogram is best to visualize the nature of the stenoses or occlusions. Unusual meandering collateral vessels are seen that have enlarged over time as the main mesenteric arteries have been narrowed. Celiac axis compression (or arcuate ligament) syndrome can also cause signs and symptoms of chronic mesenteric ischemia in patients usually somewhat younger than patients with atherosclerotic mesenteric ischemia. The majority of patients afflicted are women (106). The complaints are often even less specific, with abdominal pain that may or may not be associated with eat-

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ing (107). Weight loss is less often seen along with other characteristic complaints of diarrhea, nausea, and vomiting (108). An epigastric bruit can be heard in the epigastrium in well over half the patients (109). Duplex scanning can reveal stenoses and occlusions of the celiac artery that may be caused by the classic fibrous bands which cause obliteration of the lumen, resulting in mesenteric ischemia (110). Over time, the celiac artery can develop a stenosis or occlusion as a result of the fibrous bands (Figs. 73.1 and 73.2). Lateral angiography is the best diagnostic test to identify celiac compression syndrome. During expiration, the fibrous bands can be

shown to impinge on the origin of the celiac artery, which then, during inspiration, releases the celiac artery and allows revisualization.

Treatment Those patients identified as having symptomatic mesenteric ischemia should undergo revascularization to relieve the pain, allowing them to eat and regain their weight. Without intervention, the intermittent nature of the mesenteric ischemia can become worse, resulting in bowel infarction, peritonitis, and death (16). Patients with

FIGURE 73.1 Selective superior mesenteric artery angiogram demonstrates brisk opacification of the celiac trunk and its branches with hypertrophied gastroduodenal arcade arteries. The celiac artery was occluded in this 17year-old female with celiac artery compression.

FIGURE 73.2 Lateral view of the celiac artery after injection of dye in the superior mesenteric artery demonstrated occlusion of the celiac trunk at its origin.

Chapter 73 Mesenteric Ischemia

asymptomatic visceral artery stenoses or occlusions should not have revascularization unless aortic reconstruction is planned for other reasons. With atherosclerosis, multiple visceral arteries are commonly affected, and therefore most authors recommend that multiple arteries be revascularized (15,18). The celiac and superior mesenteric artery are both considered vital in order to maintain adequate intestinal perfusion. If one of them were to subsequently become occluded, intestinal perfusion would be adequate through the patency of the other one. The inferior mesenteric artery is rarely revascularized owing to its relatively small size and the fact that adequate collaterals do appear over time from the superior mesenteric artery. Indications for inferior mesenteric artery revascularization include failure of previous bypasses to the celiac or superior mesenteric arteries, or extensive disease in the distal branches in these same arterial distributions. Alternatively, Porter and colleagues have argued that isolated bypass to the superior mesenteric artery provides comparable long-term graft patency and patient survival when used in the treatment of chronic disease (111). Their findings did not hold true for patients treated similarly for acute mesenteric ischemia, although their anecdotal findings in three such patients all involved cases of prior revascularization and resulted in death. Transluminal angioplasty has been advocated by some as the initial treatment of choice for patients with nonorificial stenoses of the celiac and superior mesenteric arteries (112–118). Patients with signs and symptoms of chronic mesenteric ischemia who undergo angiography are candidates for percutaneous transluminal angioplasty if the appropriate lesions are seen (Figs. 73.3, 73.4, and 73.5). If the atherosclerotic lesion involves the aorta or the orifice of the celiac or superior mesenteric arteries, percutaneous transluminal angioplasty is often not successful due to the calcific nature of these aortic “spill-over” plaques. If there is inadequate filling of distal collaterals, angioplasty can be dangerous as the inflated balloon could thrombose or dissect the artery, and therefore it should not be attempted (119,120). Angioplasty of the inferior mesenteric artery is rarely indicated unless abnormalities exist in the celiac and superior mesenteric arteries that are not amenable to intervention (121). Patients with radiographic evidence of celiac artery compression are not candidates for percutaneous transluminal angioplasty, which is routinely unsuccessful because the lesion is secondary to external compression and not intraluminal obstruction. Reports have been favorable for initial success with percutaneous angioplasty in the appropriately selected patient (ie. < 30% residual stenosis), and limited longer-term success has been cited by absence of recurrent symptoms, not documented patency of the treated vessel (122). Conversely, patients receiving percutaneous interventions demonstrated a higher rate of symptom recurrence in one series (123). Many of these patients received treatment of only one vessel. The paucity of data thus far provides only speculation as to whether this could be related to progression of disease in the untreated

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FIGURE 73.3 Lateral view aortogram of a 64-year-old woman with chronic mesenteric ischemia. The celiac artery is occluded, as is the inferior mesenteric artery. A tight stenosis is seen distal to the orifice of the superior mesenteric artery.

FIGURE 73.4 This patient was considered a poor surgical candidate; therefore superior mesenteric artery angioplasty was performed. The balloon is shown inflated.

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FIGURE 73.6 Single celiac–superior mesenteric artery bypass. The proximal anastomosis acts to both patch open the stenotic celiac segment as well as serve as inflow to the bypass graft.

FIGURE 73.5 Postangioplasty film demonstrates an excellent result with minimal residual stenosis. The patient has remained symptom-free for 6 months.

vessels compared with the treated segment. Percutaneous treatment of recurrent disease after bypass grafting has been performed successfully in some patients with prohibitive comorbidities and hostile abdomens (90). A myriad of operations can be performed to provide better blood supply to the mesenteric circulation. No one operation has proved clearly superior to another, mainly because each case is approached individually depending on the vascular anatomy seen. Aortomesenteric bypasses are performed most frequently, using both antegrade and retrograde approaches (126). The antegrade approach involves isolation and dissection of the supraceliac aorta. This portion of the aorta is rarely diseased, so this bypass is preferred for the good-risk patient (59). To expose this portion of the aorta, a midline incision is made and the left lobe of the liver is mobilized medially after the triangular ligament is incised. The esophagus is identified, which is facilitated by placement of a nasogastric tube. The crura of the diaphragm are divided so that the aorta is visualized. The celiac artery is found as one progresses inferiorly upon the anterior surface of the aorta. The superior mesenteric artery is easily dissected free just inferiorly to the pancreas. The bypass the authors prefer is to utilize a 10- or 12-mm polyester or polytetrafluoroethylene graft

whose proximal anastomosis is performed at the orifice of the celiac artery, resulting in a patch angioplasty of that area. The tunnel from the celiac to the superior mesenteric artery can be made either anteriorly or behind the pancreas, depending on the patient’s anatomy. The distal anastomosis is then fashioned to the superior mesenteric artery in an end-to-side manner (127) (Fig. 73.6). Gewertz and colleagues have proposed a modification of this bypass configuration for those patients with smaller arteries (123). A bifurcated 16 ¥ 8 mm polyester graft is modified to a spatulated proximal anastomosis by incorporating an oblique bevel of the graft barrel down into the contralateral graft limb. This provides a natural heel to the aortic anastomosis, allowing a more contoured graft orientation relative to the aorta, which avoids kinking. Meanwhile, the celiac artery is divided beyond its proximal lesion, and sewn end-to-side to the dorsal surface of the graft hood. The distal bypass limb is tunneled and sewn to the superior mesenteric artery in the usual fashion. The preferred retrograde approach involves the use of the infrarenal aorta for bypass grafting to the superior mesenteric artery, celiac artery, or both. If the infrarenal aorta is too diseased, the aorta can be replaced with a graft in a good-risk patient. If the patient is not a candidate for aortic replacement and an antegrade approach is not appropriate, then the iliac artery can be used as the origin of the graft (128). A single or bifurcated polyester or polytetrafluoroethylene graft can be tunneled in the retroperitoneum to the celiac artery, superior mesenteric artery, or both. If there is evidence of ischemic bowel or peritonitis, autologous tissue should be employed using saphenous vein as the conduit. The bypass from the iliac artery needs to be made rather redundant so that the small-bowel mesentery does nor compress it and occlude the graft once the bowel is placed back in the abdominal cavity (129). Thromboendarterectomy has been utilized by some groups to treat chronic mesenteric ischemia, with excel-

Chapter 73 Mesenteric Ischemia

lent results (130). Because the lesions are most commonly orificial, an intraluminal approach to the aorta will allow direct removal of the occluding plaques without the placement of bypass grafts and synthetic substances. Only if the plaques extend into the main celiac or superior mesenteric arteries themselves must an arteriotomy be made more distally in the artery to completely remove the lesion or to place a graft more distally. A retroperitoneal thoracoabdominal approach is required to expose the aorta in its entire length at this level. Poor-risk patients, especially those with severe pulmonary and cardiac disease, are not candidates for this approach. A “trapdoor” arteriotomy is made around the celiac and superior mesenteric arteries as they emerge off the aorta, and the orifices then can be seen easily. The arteriotomy is then closed with running polypropylene sutures. Duplex scanning can be utilized in the operating room to document patency of mesenteric bypass grafts and completeness of endarterectomized vessels. Angiography has been used routinely by some in the postoperative period to document graft patency before the patient is discharged. Duplex scanning has been used as an alternative to follow patency after bypass grafting and endarterectomy. Series of patients who have been treated surgically for chronic mesenteric ischemia secondary to atherosclerosis do not show any major differences in outcome regardless of the procedure that has been chosen for revascularization (90). Because of the risk of acute bowel ischemia occurring if a bypass were to thrombose, most authors agree that reconstruction should be aimed at bypassing to as many vessels as possible, which usually include the celiac and the superior mesenteric arteries (124,125). Mortality rates of between 4% and 100% are reported, with myocardial disease the primary cause of death in the majority of patients (126,127). Technical problems identified with surveillance also warrant early correction, as mortality rates due to early graft failure can exceed 40% (90). Prophylactic revascularization of mesenteric artery stenoses and occlusions has been performed by some authors, but it has not been shown to have an impact on patients who have not yet developed symptoms (131). Those patients with celiac artery compression or arcuate ligament syndrome should undergo surgical intervention to relieve their symptoms. Angioplasty is most often unsuccessful because the ligament compressing the celiac artery does not allow the artery to expand and dilate with the balloon. The artery can be seen angiographically to recoil back into the stenotic position after angioplasty attempts. The surgical procedure is to expose the celiac artery, and in doing so the median arcuate ligament and the ganglionic fibers that are responsible for the compression are excised, which releases the artery (132). The celiac artery can then be inspected using the duplex scanner intraoperatively to assess the flow. Celiac artery stenosis and occlusion can result from the chronic compression and may require repair. Some authors have advocated intraoperative dilation through a transverse arteriotomy in

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the splenic artery. For more severe lesions, interposition grafting using an autologous or synthetic graft can be performed. The celiac artery can be directly reimplanted into the aorta in some cases if the lesion is limited in length (133). Outcomes from celiac artery decompression procedures are good, with low morbidity and mortality rates and good overall resolution of symptoms.

Conclusion Mesenteric ischemic syndromes are variable in presentation and complexity and may present acutely or in a chronic fashion. Early, aggressive intervention is necessary in cases of acute mesenteric ischemia as the morbidity and mortality rates are high. Chronic mesenteric ischemia syndromes are more of a diagnostic dilemma for the clinician. Once diagnosed, intervention should be aimed at relieving symptoms and preventing progression to bowel infarction. The procedures available are diverse and should be tailored to the individual patient for excellent results.

References 1. Bergan JJ. Recognition and treatment of intestinal ischemia. Surg Clin North Am 1967;47:109. 2. Morris GC Jr, DeBakey ME, Bernhard V. Abdominal angina. Surg Clin North Am 1966;46:919. 3. Bergan JJ Dry L, et al. Intestinal ischemic syndromes. Ann Surg 1969;169:120. 4. Fry WJ, Kraft RO. Visceral angina. Surg Gynecol Obstet 1963;117:417. 5. Boley SJ, Brandt U, Veith FJ. Ischemic disorders of the intestines. Curr Probl Surg 1978;15:6. 6. Sachs SM, Morton JH, Schwartz SI. Acute mesenteric ischemia. Surgery 1982;92:646. 7. Dunphy JE. Abdominal pain of vascular origin. Am J Med Sci 1936;192:109. 8. Mikkelsen WP. Intestinal angina. Am J Surg 1957;94:262. 9. Shaw RS, Maynard F.P III. Acute and chronic thrombosis of mesenteric arteries associated with malabsorption: report of two cases successfully treated with thromboendarterectomy. N Engl J Med 1958;258:874. 10. Stoney RJ, Wylie EJ. Recognition of surgical management of visceral ischemic syndromes. Ann Surg 1966;164:714. 11. Mikkelsen WP, Zaro JA. Intestinal angina: report of a case with preoperative diagnosis and surgical relief. N Engl J Med 1959;260:912. 12. Bergan JJ, Dean RH, et al. Revascularization in treatment of mesenteric infarction. Ann Surg 1975;182:430. 13. Ortinger LW, Austen WG. A study of 136 patients with mesenteric infarction. Surg Gynecol Obstet 1967;124:251. 14. Morris GC, Crawford ES, et al. Revascularization of the celiac and superior mesenteric arteries. Arch Surg 1962;84:95.

884

Part IX Visceral Vessels

15. Stoney RJ, Ehrenfeld WK, Wylie EJ. Revascularization methods in chronic visceral ischemia caused by atherosclerosis. Ann Surg 1977;186:468. 16. Stoney RJ, Olcott C IV. Visceral artery syndrome and reconstructions. Surg Clin North Am 1979;59:637. 17. Ottinger LW. Mesenteric ischemia. N Engl J Med 1982;307:535. 18. Levy PJ, Krausz MM, Manny J. Acute mesenteric ischemia: improved results: a retrospective analysis of ninety-two patients. Surgery 1990;107:372. 19. Wilson C, Gupta R, et al. Acute superior mesenteric ischemia. Br J Surg 1987;74:279. 20. Kaleya RN, Sammartano RJ, Boley SJ. Aggressive approach to acute mesenteric ischemia. Surg Clin North Am 1992;72:157. 21. Finucane PM, Tilakaprakash A, et al. Acute mesenteric infarction in elderly patients. J Am Geriatr Soc 1989;37:355. 22. Samuels LE, Gensler Tw, Kerstein MD. Acute mesenteric ischemia: a simple and practical approach. Vasc Surg 1992;26:272. 23. Clavien PA. Diagnosis and management of mesenteric infarction. Br J Surg 1990:77:601. 24. Rivers SP. Acute non-occlusive intestinal ischemia. Semin Vasc Surg 1990:3:172. 25. Endean ED, Barnes SL, et al. Surgical management of thrombotic acute intestinal ischemia. Ann Surg 2001;233:801. 26. Boley SJ, Sprayregen S, et al. Initial results from an aggressive roentgenological and surgical approach to acute mesenteric ischemia. Surgery 1977;82:848. 27. Park WM, Gloviczki P, et al. Contemporary management of acute mesenteric ischemia: factors associated with survival. J Vasc Surg 2002;35:445. 28. Cho JS, Carr JA, et al. Long-term outcome after mesenteric artery reconstruction: a 37-year experience. J Vasc Surg 2002;35:453. 29. Boley SJ, Feinstein FR, et al. New concepts in the management of emboli of the superior mesenteric artery. Surg Gynecol Obstet 1981:153:561. 30. Batellier J, Kieny R. Superior mesenteric artery embolism: eighty-two cases. Ann Vasc Surg 1990;4:112. 31. Clavien PA, Muller C, Harder F. Treatment of mesenteric infarction. Br J Surg 1987;74:500. 32. Clark RA. Computed tomography of bowel infarction. J Comput Assist Tomogr 1987;11:757. 33. Alpern MB, Glazer GM, Francis IR. Ischemic or infarcted bowel: CT findings. Radiology 1988;166:149. 34. Bergan JJ, McCarthy W, et al. Non-traumatic mesenteric vascular emergencies. J Vasc Surg 1987;5:903. 35. Kaleya RN, Boley SJ. Acute mesenteric ischemia: an aggressive diagnostic and therapeutic approach. 1991 Roussel Lecture. Canad J Surg 1992;35(6):613. 36. Moskowitz M, Zimmerman H, Felson B. The meandering mesenteric artery of the colon. Am J Radiol 1964; 92:1088. 37. Ferrer MI, Bradley SE, et al. The effect of digoxin in the splanchnic circulation in ventricular failure. Circulation 1965;32:524. 38. Mikkelsen F, Andersson KE, Pedersen OL. Effects of digoxin on isolated human mesenteric vessels. Acta Pharmacol Toxicol 1979;45:25. 39. Kim EH, Gewertz BL. Chronic digitalis administration

40.

41.

42.

43.

44. 45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56. 57. 58.

59.

alters mesenteric vascular reactivity. J Vasc Surg 1987;5:382. Gazes PC, Holmes CR, et al. Acute hemorrhage and necrosis of the intestines associated with digitalization. Circulation 1961;23:358. Siegelman SS, Sprayregen S, Boley SJ. Angiographic diagnosis of mesenteric arterial vasoconstriction. Radiology 1974;112:533. Flickinger EG, Johnsrude IS, et al. Local streptokinase infusion for superior mesenteric artery thromboembolism. Am J Radiol 1983;140:771. Sande E, Johnsen G, et al. Intraoperative streptokinase in the treatment of superior mesenteric artery embolization case report. Eur J Surg 1991;157:615. Horgan PG, Gorey TF. Operative assessment of intestinal viability. Surg Clin North Am 1992;72:143. Lindblad B, Hakansson H. Rationale for second-look operation in mesenteric vessel occlusion. Acta Chir Scand 1987;153:531. Levy PJ, Krausz MM, Manny J. The role of second-look procedure in improving survival time for patients with mesenteric venous thrombosis. Surg Gynecol Obstet 1990;170:287. Carter M, Fantini G, et al. Qualitative and quantitative fluorescein fluorescence for determining intestinal viability. Am J Surg 1984;147:117. Bulkley GB, Zuidema GD, et al. Intraoperative determination of viability following ischemic injury: a prospective, controlled trial of adjuvant methods (Doppler and fluorescein) compared to standard clinical judgment. Ann Surg 1981;193:628. Wright CB, Hobson RW. Prediction of intestinal viability using Doppler ultrasound technique. Am J Surg 1975;129:642. Cooperman M, Martin EW Jr, Carey LC. Evaluation of ischemic intestine by Doppler ultrasound. Am J Surg 1980;139:73. Whitehill TA, Pearce WR, et al. Detection thresholds of nonocclusive intestinal hypoperfusion by Doppler ultrasound, photoplethysmography, and fluorescein. J Vasc Surg 1988;8:28. Pillari G, Doscher W, et al. Low dose streptokinase in the treatment of celiac and superior mesenteric artery occlusion. Arch Surg 1983;118:1340. Vujic I, Stanley J, Gobien RP. Treatment of acute embolus of the superior mesenteric artery by topical infusion of streptokinase. Cardiovasc Intervent Radiol 1984;7:94. Schoenbaum SW, Pena C, et al. Superior mesenteric artery embolism: treatment with intraarterial urokinase. J Vasc Interv Radiol 1992;3:485. Hillers TK, Ginsberg JS, et al. Intraarterial low-dose streptokinase infusion for superior mesenteric artery embolus. Can Med Assoc J 1990;142:1087. Williams LF Jr. Vascular insufficiency of the intestines. Gastroenterology 1971;61:757. Bergan JJ. Unexpected vascular problems at laparotomy. Prob Gen Surg 1984;1:190. Hermreck AS, Thomas JH, et al. Role of supraceliac aortic bypass in visceral artery reconstruction. Am J Surg 1991;162:611. Beebe HG, MacFarlane S, Raker EJ. Supraceliac aortomesenteric bypass for intestinal ischemia. J Vasc Surg 1987;5:749.

Chapter 73 Mesenteric Ischemia 60. Clavian PA, Muller C, Harder F. Treatment of mesenteric infarction. Br J Surg 1987;74:500. 61. Naitove A, Weismann RE. Primary mesenteric venous thrombosis. Ann Surg 1965;161:516. 62. Grendell JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology 1982;82:358. 63. Harward TRS, Green D, et al. Mesenteric venous thrombosis. J Vasc Surg 1989 ;9:328. 64. Font VE, Hermann RE, Longworth DL. Chronic mesenteric venous thrombosis: difficult diagnosis and therapy. Cleve Clin J Med 1989;56:823. 65. Grieshop RJ, Dalsing MC, et al. Acute mesenteric venous thrombosis: revisited in a time of diagnostic clarity. Am Surg 1991;57:573. 66. Abdu RA, Zakhour BJ, Dalis DJ. Mesenteric venous thrombosis: 1911–1984. Surgery 1987;101:383. 67. Kitchens CS. Evolution of our understanding of the pathophysiology of primary mesenteric venous thrombosis. Am J Surg 1992;163:346. 68. Maung R, Kelly JK, et al. Mesenteric venous thrombosis due to antithrombin III deficiency. Arch Pathol Lab Med 1988;112:37. 69. Green D, Ganger DR, Blei AT. Protein-C deficiency in splanchnic venous thrombosis. Am J Med 1987;82:171. 70. Olson JF, Steuber CP, et al. Functional deficiency of protein C associated with mesenteric venous thrombosis and splenic infarction. Am J Pediatr Hematol Oncol 1991;139(2):168. 71. De Stefano V, Leone G, et al. Mesenteric vein thrombosis in protein S congenital deficiency. Thromb Res 1990;57:935. 72. Broekmans AW, Van Rooyen W, et al. Mesenteric vein thrombosis as presenting manifestation of hereditary protein S deficiency. Gastroenterology 1987;92:240. 73. Fogartie JA, Adams DB, et al. Splanchnic venous obstruction: a complication of chronic pancreatitis. Am Surg 1989;55:191. 74. Engelhardt C, Kerstein MD. Pregnancy and mesenteric venous thrombosis. South Med J 1989:82:1441. 75. Collier TM, Coopwood TB, Treadaway JP. Mesenteric thrombosis associated with oral contraceptives. Angiology 1975;26:518. 76. Nesbit RR, Deweese JA. Mesenteric venous thrombosis and oral contraceptives. South Med J 1977;70:360. 77. Schneiderman DJ, Cello IP. Intestinal ischemia and infarction associated with oral contraceptives. West J Med 1986:77:350. 78. Gertsch P, Matthews J, et al. Acute thrombosis of the splanchnic veins. Arch Surg 1993;128:341. 79. Tey PH, Sprayregen S, et al. Mesenteric vein thrombosis: angiography in two cases. Am J Radiol 1981:136:809. 80. Rosen A, Kirobkin M, et al. Mesenteric vein thrombosis: CT identification. Am J Radiol 1984;143:83. 81. Clavien A, Huber O, et al. Contrast enhanced CT scan as a diagnostic procedure in mesenteric ischaemia due to mesenteric venous thrombosis. Br J Surg 1989;76:93. 82. Karawi MA, Quaiz M, et al. Mesenteric vein thrombosis, non-invasive diagnosis and follow-up (US + MRI), and non-invasive therapy by streptokinase and anticoagulants. Hepatogastroenterology 1990;37:507. 83. Kim JY, Ha HK, et al. Intestinal infarction secondary to mesenteric venous thrombosis: CT-pathologic correlation. J Comput Assist Tomogr 1993;17(3):382.

885

84. Flinn WR, Rizzo RJ, et al. Duplex scanning for assessment of mesenteric ischemia. Surg Clin North Am 1990;70:99. 85. Serreyn RF, Schoofs PR, et al. Laparoscopic diagnosis of mesenteric venous thrombosis. Endoscopy 1986;18:249. 86. Matthews JE, White RR. Primary mesenteric venous occlusive disease. Am J Surg 1971;122:579. 87. Grendall JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology 1982;82:358. 88. Robin P, Gruel Y, Lang M. Complete thrombolysis of mesenteric vein occlusion with recombinant tissue-type plasminogen activator. Lancet 1988;1:1391. 89. Reinus JF, Brandt U, Boley SJ. Ischemic diseases of the bowel. Gastroenterology Clin North Am 1990;19:319. 90. Mateo RB, O’Hara PJ, Hertzer NR, et al. Elective surgical treatment of symptomatic chronic mesenteric occlusive disease: early results and late outcomes. J Vasc Surg 1999;29:821. 91. MacFarlane SD, Beebe HG. Progress in chronic mesenteric arterial ischemia. J Cardiovasc Surg 1989;30:178. 92. Connolly JE, Kwaan JRM. Management of chronic visceral ischemia. Surg Clin North Am 1982;62:345. 93. Baur GM, May DJ, et al. Treatment of chronic visceral ischemia. Am J Surg 1984;148:138. 94. Buchardt-Hansen HJ, Engell HC, et al. Splanchnic blood flow in patients with abdominal angina before and after arterial reconstruction: a proposal for a diagnostic test. Ann Surg 1977;186:216. 95. Jager KA, Fortner GS, et al. Noninvasive diagnosis of intestinal angina. J Clin Ultrasound 1984;12:588. 96. Nicholls SC, Kohler TR, et al. Use of hemodynamic parameters in the diagnosis of mesenteric insufficiency. J Vasc Surg 1986;3:507. 97. Bowersox JC, Zwolak RM, et al. Duplex ultrasonography in the diagnosis of celiac and mesenteric artery occlusive disease. J Vasc Surg 1991;14:780. 98. Moneta GL, Yeager RA, et al. Duplex ultrasound criteria for diagnosis of splanchnic artery stenosis or occlusion. J Vasc Surg 1991;14:511. 99. Harward TRS, Smith S, Seeger J. Detection of celiac axis and superior mesenteric artery occlusive disease with use of abdominal duplex scanning. J Vasc Surg 1993;17:738. 100. Muller AF. Role of duplex Doppler ultrasound in the assessment of patients with postprandial abdominal pain. Gut 1992;33:460. 101. Quamar MI, Read AE, et al. Transcutaneous Doppler ultrasound measurement of celiac axis blood flow in man. Br J Surg 1985,72:391. 102. Healy DA, Neumayer MM, et al. Evaluation of celiac and mesenteric vascular disease with duplex ultrasonography. J Ultrasound Med 1992;11:481. 103. Quamar MI, Read AE, et al. Transcutaneous Doppler ultrasound measurement of superior mesenteric artery blood flow in man. Gut 1986;27:100. 104. Lilly MP, Harvard TRS, et al. Duplex ultrasound measurement of changes in mesenteric flow velocity with pharmacological and physiologic alteration of intestinal blood flow in man. J Vasc Surg 1989;9:18. 105. Moneta GL, Taylor DC, et al. Duplex ultrasound measurement of postprandial intestinal blood flow: effect of meal composition. Gastroenterology 1988;95:1294. 106. Snyder MA, Mahoney EB, et al. Symptomatic celiac artery stenosis due to constriction by the neurofi-

886

107.

108. 109. 110.

111.

112.

113.

114.

115.

116.

117.

118.

119.

120.

Part IX Visceral Vessels brous tissue of the celiac ganglion. Surgery 1967;61(3): 372. Hariola PT, Lahtiharin A. Celiac axis syndrome: abdominal angina caused by external compression of the celiac artery. Am J Surg 1968;115:864. Szilagyi DE, Rober MD, et al. The celiac axis compression syndrome. Does it exist? Surgery 1972;72:849. Gupta S. Surgical and hemodynamic considerations in middle aortic syndrome. Thorax 1979;34:470. Taylor DC, Moneta GL, et al. Extrinsic compression of the celiac artery by the median arcuate ligament of the diaphragm: diagnosis by duplex ultrasound. J Vasc Technol 1987:11:236. Gentile AT, Moneta GL, et al. Isolated bypass to the superior mesenteric artery for intestinal ischemia. Arch Surg 1994;129:926. Furrer J, Gruntzig A, et al. Treatment of abdominal angina with percutaneous dilation of an arteria mesenterica superior stenosis: preliminary communication. Cardiovasc Intervent Radiol 1980;3:43. Golden DA, Ring EJ, et al. Percutaneous angioplasty in the treatment of abdominal angina. Am J Radiol 1982;139:247. Castaneda-Zuniga WR, Gomes A, et al. Transluminal angioplasty in the treatment of abdominal angina. ROFO 1982;137:330. Roberts L, Wertman DA, et al. Transluminal angioplasty of the superior mesenteric artery: an alternative to surgical revascularization. Am J Radiol 1983;141:1039. Mani J, Courtheoux P, et al. Endoluminal angioplasty of atheromatous stenoses of gastrointestinal arteries. Ann Radiol 1986,29:589. Levy PJ, Haskell L, Gordon RL. Percutaneous transluminal angioplasty of splanchnic arteries. Eur J Radiol 1987;7:239. Odurney A, Sniderman KW, Colapinto RF. Intestinal angina: percutaneous transluminal angioplasty of the celiac and superior mesenteric arteries. Radiology 1988;167:59. McShane MD, Proctor A, et al. Mesenteric angioplasty for chronic intestinal ischaemia. Eur J Vasc Surg 1992;6:333. Warnock NG, Gaines PA, et al. Treatment of intestinal angina by percutaneous transluminal angioplasty of a

121.

122.

123.

124.

125.

126.

127.

128.

129. 130.

131.

132.

133.

superior mesenteric artery occlusion. Clin Radiol 1992;45:18. Crotch-Harvey MA, Gould DA, Green AT. Case report: percutaneous transluminal angioplasty of the inferior mesenteric artery in the treatment of chronic mesenteric ischaemia. Clin Radiol 1992;40:408. Maspes F, Mazzeti di Pietralata G, et al. Percutaneous transluminal angioplasty in the treatment of chronic mesenteric ischemia: results and 3 years of follow-up in 23 patients. Abdom Imaging 1998;23:358. Wolf YG, Berlatzky Y, Gewertz BL. Sequential configuration for aorto-celiac-mesenteric bypass. Ann Vasc Surg 1997;11:640. Johnston KW, Lindsay TF, et al. Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia. Surgery 1995;118:1. Moawad J, McKinsey JF, et al. Current results of surgical therapy for chronic mesenteric ischemia. Arch Surg 1997;132:613. Hollier LH, Bernatz PE, et al. Surgical management of chronic intestinal ischemia: a reappraisal. Surgery 1981;90:940. Geelkerken RH, van Bockel H, et al. Chronic mesenteric vascular syndrome: results of reconstructive surgery; Arch Surg 1991;126:1101. Cormier JM, Fichelle JM, et al. Atherosclerotic occlusive disease of the superior mesenteric artery: late results of reconstructive surgery. Ann Vase Surg 1991;5: 510. Connelly TJ, Perdue GD, et al. Elective mesenteric revascularization. Am Surg 1981;47(1):19–25. Rapp JH, Reilly LM, et al. Durability of endarterectomy and antegrade grafts in the treatment of chronic visceral ischemia. J Vasc Surg 1986:3:799. Valentine RJ, Martin JD, et al. Asymptomatic celiac and superior mesenteric artery stenoses are more prevalent among patients with unsuspected renal artery stenoses. J Vasc Surg 1991;14:195. Reilly LM, Ammar AD, et al. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg 1985;2:79. Skillman JJ, Orron D, et al. Piggy-back mesenteric arterial reconstruction. J Cardiovasc Surg 1992;33:189.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 74 Renal Artery Revascularization Keith D. Calligaro and Matthew J. Dougherty

Renal artery stenosis has become increasingly recognized as a cause of intractable hypertension. In addition, thousands of patients in the United States develop renal failure, many because of renal artery disease. Many controversies exist concerning evaluation and treatment of renal artery occlusive disease and its relationship to hypertension and renal failure. Indications for renal artery revascularization remain somewhat ill defined despite the fact that renal artery operations have been performed for decades. Choosing the optimal technique for renal artery revascularization, whether by minimally invasive interventions such as balloon angioplasty and stent placement or by traditional open surgery, may not be straightforward. In some centers of excellence, morbidity and mortality of surgical renal revascularization are low, even when combined with aortic surgery. On the other hand, some series cite high complications of these operations. In this chapter we will review the scientific basis, evaluation, and indications for revascularization for renovascular disease, along with the results of endovascular and surgical procedures.

Background Systemic hypertension may be due to a multitude of causes. Renal artery occlusive disease is the etiology in less than 5% of hypertension among all patients (1). Hemodynamically significant renal artery stenosis or occlusion results in renovascular hypertension in less than half of patients with this anatomic abnormality (2). Chronic renal failure is usually due to causes other than renovascu-

lar disease. However, the chance of hypertension being due to renal artery disease increases significantly as the severity of hypertension increases. Since there are approximately 25 million hypertensive patients in the US, there are potentially hundreds of thousands of patients with curable, or at least more easily controlled, hypertension. Renovascular hypertension may very well be the most common surgically correctable cause of hypertension, even when considering other etiologies such as hyperparathyroidism, Cushing’s disease, renal parenchymal disease, pheochromocytoma, and primary aldosteronism (Conn’s syndrome). Many patients with hypertension or renal failure could potentially benefit from more aggressive evaluation of renal artery stenosis to prevent or minimize complications of renal artery disease.

Pathology of Renovascular Hypertension Stenosis or occlusion of the renal artery may be due to atherosclerosis, fibromuscular dysplasia, renal artery aneurysm, and renal artery dissection (Figs. 74.1 and 74.2). Atherosclerosis is the most common cause of renovascular hypertension. An atherosclerotic lesion typically involves the proximal renal artery and usually involves the ostium as an extension of aortic atherosclerosis. Renovascular hypertension secondary to renal atherosclerosis occurs most commonly in the sixth and seventh decades of life and accounts for approximately two-thirds of new-onset renovascular hypertensive cases in this age group (2).

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Part IX Visceral Vessels FIGURE 74.1 Aortograms depicting two types of arteriosclerotic renal artery lesions. (Left) Focal right renal artery stenosis of proximal main renal artery. (Right) Diffuse arteriosclerosis involving aorta and its branches. The right renal artery is occluded at ostium. Left renal artery ostial stenosis is an extension of aortic disease.

and fifth decades of life. Intimal fibroplasia (5%) occurs equally in males and females and is more likely to be found in children and young adults than in older persons. Other causes of renovascular hypertension include renal artery aneurysms, arteriovenous malformations of the renal parenchyma, coarctation of the abdominal aorta, Takayasu’s aortitis, embolic lesions, renal artery dissections, and traumatic lesions (4). Renal artery aneurysms probably cause hypertension only if a coexisting stenosis is present in the adjacent artery or if emboli to the terminal arterial branches in the kidney result in increased renin release (4). Similarly, arteriovenous malformations of the kidney rarely cause hypertension (4). Other etiologies such as Takayasu’s aortitis, coarctation, dissection, and trauma result in occlusive disease of the renal artery and stimulate the renin–angiotensin–aldosterone mechanism.

Physiology of Renovascular Hypertension FIGURE 74.2 Selective right renal arteriogram of a typical medial fibrodysplastic lesion. Tandem stenoses involve the distal renal artery. The proximal main renal artery appears normal.

Fibromuscular dysplasia is the second most common cause of renovascular hypertension and accounts for about one-quarter of cases. This disorder usually involves the mid- and distal portions of the renal artery and may extend into the primary branches. Fibromuscular dysplasia comprises a heterogeneous group of diseases including intimal fibroplasia, medial fibrodysplasia, and perimedial dysplasia (3). Medial fibroplasia is the most common subtype (85%) and almost exclusively affects women in their fourth and fifth decades. The typical angiographic appearance is a “string-of-beads” or multiple tandem stenoses with alternating aneurysmal outpouchings (Fig. 74.2). Perimedial dysplasia (10%) often coexists with medial fibrodysplasia and usually affects women in their fourth

Renin is the cause of renovascular hypertension due to a complicated but well-defined pathway in which vasoconstrictive and volume-dependent mechanisms interact (5). The renin–angiotensin–aldosterone axis acts to maintain normal blood pressure and blood volume and is closely related to sodium balance. The juxtaglomerular complex is comprised of cells in the afferent arterioles feeding the glomerulus. The afferent arterioles of the glomerulus contain cells of smooth muscle cell origin that synthesize and store renin. These cells respond to changes in renal artery perfusion pressure. The macula densa is a specialized tubular area marking the transition from the ascending loop of Henle to the distal convoluted tubule. The macula densa is responsible for detecting changes in sodium chloride concentration and affects renin release (5). The renal sympathetic nerves innervate the juxtaglomerular apparatus and also modulate renin release. Renin is a proteolytic enzyme and converts angiotensinogen, which is produced in the liver, to

Chapter 74 Renal Artery Revascularization

angiotensin I. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II in the lung. Angiotensin II is the most powerful naturally occurring vasoconstrictor in the body and also stimulates release of aldosterone from the adrenal cortex. Aldosterone stimulates sodium retention in the kidney, promoting fluid retention and potentiating the vasoconstrictor effects of circulating catecholamines.

Clinical Diagnosis of Renovascular Hypertension One of the biggest challenges for a clinician treating renovascular hypertension is identifying patients who might benefit from renal artery revascularization. Clinical evaluation can raise suspicions but is insufficient to prove the diagnosis. The Cooperative Study of Renovascular Hypertension compared 339 patients with essential hypertension with 175 patients with renovascular hypertension secondary to atherosclerosis (91 patients) or fibromusclar dysplasia (84 patients) and reported that no characteristic had sufficient negative predictive value to exclude anyone from further investigation for renovascular disease (6). However, certain findings should arouse suspicion that renovascular disease may be the cause of hypertension. The typical patient evaluated by a vascular surgeon is someone in the sixth or seventh decade of life with new onset of severe hypertension. These patients usually have other manifestations of atherosclerosis but do not demonstrate features consistent with endocrine causes of hypertension (pheochromocytoma, Cushing’s disease, Conn’s syndrome, hyperparathyroidism). Patients with renovascular hypertension frequenty have a history of coronary artery disease manifested by myocardial infarction or angina, cerebrovascular disease manifested by stroke or transient ischemic attacks, or lower extremity arterial occlusive disease manifested by claudication, rest pain, or lower extremity ischemic lesions. In addition, these patients usually have other risk factors for atherosclerosis such as diabetes mellitus, hypertension, hyperlipidemia/ cholesterolemia, and history of tobacco use. Severe elevation of diastolic blood pressure should arouse suspicion, specifically, pressure greater than 105 mmHg. The higher the untreated diastolic blood pressure, the greater the likelihood of a renovascular origin of hypertension. A sudden worsening of previously well-controlled hypertension may also indicate a renovascular cause. Dramatic improvement in blood pressure in response to an ACE inhibitor is one of the strongest clues that hypertension is secondary to renovascular disease (1,5,7–9). In general, patients are generally not considered for endovascular or surgical treatment of renovascular hypertension unless the hypertension is considered refractory to medical management. This definition usually implies that the patient requires more than three medications to satisfactorily control the blood pressure. Many patients can be well controlled with a lesser number of medications for the

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remainder of their lives and do not need to be subjected to endovascular treatment or surgery. Despite the fact that clinical evaluation alone cannot prove renovascular hypertension, some authorities recommend that history and physical examination of the patient is more important than any screening test and that renal arteriography and revascularization should be performed regardless of the findings of most of the following tests (10). As previously mentioned, women in their third to fifth decades of life with new-onset hypertension should be suspected of having renal artery stenosis secondary to fibromuscular dysplasia. Since this disorder commonly affects the carotid arteries also, findings in women in this age range of a carotid bruit or history of stroke, transient ischemic attack, or amaurosis fugax should heighten suspicion of fibromuscular dysplasia as a cause of renovascular hypertension. In pediatric patients, hypertension is unusual and most likely due to renovascular disease or coarctation of the aorta. Other etiologies such as tumors can usually be easily ruled out.

Laboratory and Radiologic Diagnosis of Renovascular Hypertension Laboratory Tests Clinical suspicion remains the most critical element of considering renovascular disease as a cause of hypertension but also for suspecting other etiologies. These other causes can usually be evaluated with relatively simple blood tests or radiologic studies. A thorough clinical evaluation along with normal serum sodium, potassium, and calcium levels and normal urinary catecholamine and cortisol levels can effectively rule out pheochromocytoma, Conn’s syndrome, hyperparathyroidism, and Cushing’s disease. No current diagnostic study is both easy to perform and accurate at diagnosing or excluding renovascular hypertension. Azotemia secondary to renal artery occlusive disease may be more straightforward to diagnose but other causes of chronic renal insufficiency are far more common. These patients must have bilateral significant renal artery stenosis or occlusion if poor perfusion of the kidneys is the cause of kidney failure.

Plasma Renin Levels With and Without Captopril Determination of random plasma renin activity alone is not considered to be an effective method of screening for renovascular hypertension (11). Patients with renovascular hypertension increase plasma renin activity after administration of an ACE inhibitor such as captopril. A screening test has been proposed to diagnose renovascular

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hypertension in which plasma renin activity is determined before and 60 minutes after an oral dose of this drug. Patients with renovascular hypertension usually demonstrate higher plasma renin activity than patients with essential hypertension (12–14). However, others have reported much lower sensitivities and specificities with this test (8,9). Patients with renal insufficiency or those taking diuretics or alpha-adrenergic blocking agents have been shown to demonstrate less accurate results. Since patients with renovascular disease frequently have elevated creatinine or are taking these medications, this diagnostic method has not gained widespread approval.

Renal Vein Renin Assays A previously widely used method to confirm a renovascular cause of hypertension was to measure renal vein renin activities of each kidney and simply compare these levels with each other. By calculating a ratio comparing the hypertensive kidney with the normal kidney, lateralizing results were strongly associated with renal artery stenosis resulting in elevated renin levels and renovascular hypertension (15). Elevation of the renal vein renin ratio has been reported to discriminate between those patients who benefited by operation and those in whom surgical treatment did not cure or improve their hypertension (15,16). However, renin ratios were shown to have an overall accuracy of only 80% among patients with proven renovascular hypertension, i.e., those who have benefited from renal revascularization. This lack of sensitivity may be due to many factors, including suppression of renin release by antihypertensive drugs (most notably alphaadrenergic blocking agents), poor sampling techniques, and significant collateral blood flow that may prevent lateralization of renin (17). A potentially more accurate method using renal vein renin levels is the renal systemic renin index (RSRI) (16). The RSRI is calculated by subtracting systemic renin from the individual kidney vein renin divided by the systemic renin activity. The systemic renin level is obtained by measuring renin activity in the inferior vena cava. The individual renal vein renin is obtained by selectively catheterizing each renal vein by passing a catheter from the femoral vein through the inferior vena cava into each renal vein. An RSRI greater than 0.48 from one kidney or from both kidneys reflects renin production that exceeds hepatic clearance and suggests hyperreninemia. Beneficial responses to unilateral renal revascularization are most likely with an RSRI greater than 0.48 in the ischemic kidney and an RSRI approaching zero in the opposite kidney (16). Although this test was previously considered one of the most accurate and necessary tests in the evaluation of renovascular hypertension, it has fallen into disfavor for several reasons. Results vary greatly with the experience of the laboratory performing the test. The laboratory results often take two or more weeks to be completed. The patient must stop taking certain antihypertensive medications (for example, alpha-adrenergic blocking agents) to

improve accuracy. By stopping these medications, marked elevation of blood pressure may result unless a suitable alternative medication is administered. The accuracy of the test is diminished when bilateral renal artery stenosis exists, a common scenario in the atherosclerotic populaton. For of all these reasons, a false-negative rate of 35% persists in some studies, meaning a significant percentage of patients would be denied potentially useful renal revascularization if decisions were based on this screening test (18). Lastly, the test is invasive and requires catheterizing the inferior vena cava and both renal veins. Complications such as bleeding from the puncture site and allergies to contrast material (necessary to administer to identify the renal vein origins) may occur. We and others rarely perform renal vein renin samplings at the present time.

Captopril Renal Scintigraphy Radionuclide renography provides functional evaluation of renal glomerular filtration and tubular secretion. These studies are accomplished by administration of radiolabeled agents with subsequent scintigraphy to analyze renal function. The agent commonly used to evaluate glomerular function has been diethylenetriamine pentaacetic acid (DTPA). Both mertiatide (MAG3) and O-Ihippurate (HIP) have been used to evaluate tubular secretion. The effects of angiotensin II on glomerular filtration have been used to improve radionuclide renography accuracy. Angiotensin II causes vasoconstriction of both afferent and efferent arterioles in the kidney. In renovascular hypertension, angiotensin II-mediated vasoconstriction of efferent arterioles maintains glomerular filtration pressure in spite of the decreased renal blood flow caused by renal artery occlusive disease. When an ACE inhibitor such as captopril is administered to a patient with renal artery stenosis, efferent arteriolar vasoconstriction is diminished and glomerular filtration decreases. This effect also explains why renal function frequently worsens in patients with renovascular hypertension who are given ACE inhibitors (19). Patients suspected of having renovascular hypertension undergo baseline and post-captopril radionuclide renography. In patients with renovascular hypertension, radionuclide renography performed with DTPA after captopril administration should show a decrease in radiolabeled tracer accumulation in the involved kidney due to decrease in glomerular filtration induced by administration of the ACE inhibitor. Captropril renal scintigraphy has been reported to have high accuracy in diagnosing renovascular hypertension, over 90% in several studies (20,21). There has been widespread acceptance of this screening method in many centers. However, several problems exist with this diagnostic tool also. There is significant variability in the accuracy of this test from institution to institution. Patients with either bilateral renal artery occlusive disease or chronic renal failure have lower sensitivity and specificity with this test. As with several of the previously mentioned

Chapter 74 Renal Artery Revascularization

tests, negative results should not prevent further evaluation of patients if renovascular hypertension is suspected. Nonetheless, some authorities believe that a normal captopril renogram helps to exclude renovascular hypertension with a high degree of accuracy, and a positive finding suggests a high likelihood of renovascular hypertension in subjects with preserved renal function (5). Until recently we routinely performed this test to evaluate patients with renovascular hypertension prior to revascularization, but because of false-positive and -negative results, we no longer routinely use this technique.

Duplex Ultrasonography Duplex ultrasonography (DU) has evolved as a very useful technique to noninvasively evaluate patients for renal artery stenosis. DU is a safe, relatively inexpensive diagnostic test compared with other radiologic imaging studies and is easily repeatable. The test involves a combination of B-mode ultrasound to visualize the arteries and determination of blood flow velocity. Severity of renal artery stenosis is determined by measuring peak systolic velocity (PSV) in the renal artery and adjacent aorta. A 60% to 99% renal artery stenosis is suspected when the PSV in the stenotic renal artery is greater than 3.5 times the PSV in the adjacent aorta (22,23). DU has been reported to have a 95% sensitivity, 98% specificity, 98% positive predictive value, 94% negative predictive value, and overall accuracy of 96% if single renal arteries are present (23). DU requires experienced and highly trained technologists and expensive equipment. In addition, accuracy of the examination may be limited by obesity, excessive bowel gas, previous abdominal operations, or anatomic variants such as multiple renal arteries. Adequate studies can be expected to be performed in 75% to 92% of patients, although more recent reports from centers of excellence routinely obtain technically adequate studies in more than 90% of patients (22,24). In our practice, DU is uniformly part of the initial evaluation of patients with suspected renovascular hypertension. If an adequate study can be performed and is not limited by the previously mentioned factors, the study is very useful to rule in or rule out renal artery stenosis. When equivocal results are obtained or the study is limited for technical reasons, magnetic resonance angiography or contrast arteriography is performed. However, if an excellent technical study reveals normal renal arteries from the ostium to the branch arteries, generally no further studies are performed. If a 60% to 99% stenosis is found using DU, contrast arteriography is then performed to determine if endovascular or surgical intervention is warranted.

Magnetic Resonance Angiography Magnetic resonance angiography (MRA) is another noninvasive method of evaluating renal artery stenosis. Radiation and intravascular contrast media exposure are not required. MRA has proven useful to diagnose proxi-

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mal renal artery stenosis (25). Overall, MRA has significant limitations as a screening examination for renovascular hypertension. MRA is highly dependent on the software available at each institution. At some centers, this diagnostic tool has proven very useful to help quantify the degree of renal artery stenosis, whereas at others the tendency to overestimate stenoses severely limits its usefulness. Some patients cannot tolerate the study because of claustrophobia. At our hospital, we perform MRA to investigate renal artery stenosis when DU cannot be performed for technical reasons. Of note, if results are borderline for significant renal artery stenosis, MRA is generally not performed because of the likelihood of overestimation of the degree of stenosis, and instead contrast arteriography is performed.

Helical (Spiral) Computed Tomography This technique has emerged as a promising diagnostic method to evaluate renal artery stenosis. The primary advantage of this technique compared with standard arteriography is the avoidance of an arterial puncture and passage of a catheter through a possibly diseased aorta. However, administration of iodinated contrast into a peripheral vein is required. In addition, arterial calcification obscures the renal artery lumen and prevents accurate measurement of the degree of stenosis (26).

Contrast Arteriography Renal arteriography remains the gold standard to diagnose renal artery stenosis. In infancy and childhood, flush aortography alone is usually performed. Selective arterial catheterization with oblique filming techniques is reserved for older children and adults. Contrast arteriography remains essential in the ultimate diagnosis of renal artery stenosis warranting intervention. Patients with an elevated serum creatinine can have the contrast load minimized by performing aortography with carbon dioxide and then injecting only 10 to 20 mL of contrast for renal artery imaging and endovascular intervention. Most surgeons prefer preoperative renal artery imaging with contrast material to confirm that hemodynamically significant renal artery stenosis truly exists but also to best plan surgical intervention. If a spleno- or hepatorenal bypass is considered, lateral views of the aorta are necessary to insure a widely patent celiac artery. Disadvantages of contrast arteriography include access-related complications such as hematoma, contrast allergy, peripheral or renal emboli, and worsening renal failure. However, the irreversible risk of contrast toxicity may be overestimated. As long as patients are well hydrated, nondiabetic individuals with moderate elevations in serum creatinine can safely undergo contrast arteriography. In a review of 244 aortograms performed at our hospital, the incidence of permanent renal failure following contrast arteriography was only 0.8% (2).

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Of note, many elderly patients with other manifestations of atherosclerosis have renal artery stenosis or occlusion that does not cause hypertension. In a report of 350 patients who underwent aortography for peripheral vascular disease, 25% of patients had greater than 50% stenosis of at least one renal artery but had mild or no hypertension (28). Endovascular or surgical intervention for renal artery disease is indicated only for medically intractable hypertension or for renal salvage in a small proportion of patients. Indications for intervention are more clear-cut for renal salvage because these patients always have rising serum creatinine and must have bilateral renal occlusive disease or unilateral stenosis in a solitary functioning kidney. Unilateral disease does not cause azotemia in the setting of a normal contralateral kidney. Revascularization for unilateral renal artery stenosis is thus rarely indicated in the absence of sever hypertension.

Summary of Diagnostic Protocol to Evaluate Renal Artery Disease Although exceptions exist, our strategy regarding evaluation of patients with suspected renovascular hypertension includes a thorough history and physical examination as the first step. If previously mentioned clinical findings suggest the possibility of renovascular disease as the etiology, as the next step we would perform DU of the renal arteries in an accredited noninvasive vascular laboratory experienced in renal evaluation. Other authorities agree that this direct screening method should be the preliminary study of choice for both renovascular hypertension and ischemic nephropathy (1). If DU suggests a 60% to 99% stenosis, the next step would be contrast arteriography. Appropriate intervention with balloon angioplasty and stent placement, or surgery, would be pursued. If a high-quality DU was performed, and clearly less than 60% stenosis is identified bilaterally, then no further studies are performed and the patient is managed medically. However, if the hypertension is extremely severe and uncontrollable, an argument can be made to proceed to contrast arteriography to identify distal and accessory renal artery lesions (1). If DU is equivocal, suggesting borderline hemodynamically significant renal artery stenosis, contrast arteriography is performed. If DU is poor quality due to previously mentioned factors such as obesity or excessive bowel gas, an MRA is obtained. If the MRA suggests a 60% to 99% stenosis, then contrast arteriography is performed. If the MRA clearly shows normal bilateral renal arteries, no further studies are performed and the patient is managed medically. If a patient has rising serum creatinine and indications for renal revascularization are renal salvage and not necessarily renovascular hypertension, the same protocol generally applies. The only need for intervention for renal salvage is when these imaging studies confirm the presence of bilateral renal artery occlusive disease or significant renal artery stenosis in the setting of a solitary functioning kidney. Although renal vein renin sampling

and captopril renal scintigraphy may play a role in the evaluation of patients with suspected renovascular hypertension, our nephrologists and we do not believe they need to be performed on a routine basis. These tests have a significant rate of false-negatives and therefore a large number of patients may be denied potentially curable intervention. Others also favor a strategy of renal arteriography when a thorough clinical evaluation supports the diagnosis of renovascular hypertension without obtaining many of the available screening tests previously mentioned such as captopril renal scans or renal vein renins (10).

Endovascular Treatment of Renovascular Disease Since the early 1990s, endovascular treatment of renovascular disease has dramatically changed the indications for traditional open surgery of diseased renal arteries. Balloon angioplasty and stenting of renal artery stenosis is clearly associated with lower morbidity and mortality than surgery. The question remains whether long-term patency rates of endovascular intervention for renal artery disease approximates surgical treatment and whether relatively good-risk patients with few comorbid conditions are better treated with surgery than temporizing treatment with balloon angioplasty. On the other hand, many patients who require renal revascularization have significant coronary artery, pulmonary, or cerebrovascular disease that may preclude major surgery and endovascular treatment remains a reasonable alternative. Balloon angioplasty alone for renovascular disease is indicated to treat a focal, atherosclerotic, nonostial lesion when appropriate indications exist (1). Complication rates of these interventions are less than 5% and longterm results are reasonable. A compilation of recent series has shown an 83% 1-year patency rate, although a significant percentage of patients had fibromuscular dysplasia (26). Cure of hypertension or a beneficial response was found in 84% of patients with atherosclerotic stenosis (26). More recently, even ostial lesions have been increasingly treated by endovascular means with stent placement across the renal ostium following balloon dilation of the stenosis (29). These lesions represent higher-risk cases and long-term results are not as favorable as nonostial lesions. A compilation of single-center series showed immediate technical success in 99%, cure or improvement in blood pressure in 68%, worsening of renal function in 14%, and restenosis in 13% to 39% of patients during follow-up of approximately 6 to 16 months (1,30). On the other hand, some surgical authorities continue to recommend operative intervention for ostial lesions because of better patency rates and improved blood pressure management (31). Some interventionalists argue that, even when recurrent stenosis develops, repeat balloon angioplasty with stenting may be performed to maintain patency. Of note, a

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prospective randomized trial that compared balloon angioplasty with medical therapy on blood pressure and renal function did not find any significant differences between blood pressure response and renal function parameters unless bilateral renal artery stenosis was present (32). Fibromuscular dysplasia resulting in severe hypertension is best treated by balloon angioplasty as long as the lesions are confined to the main renal artery. Arteriographic findings typically include a “string-of-beads” appearance due to consecutive stenoses and aneurysmal dilation. Five-year patency rates of 80% to 90% have been reported following endovascular treatment of these lesions (26,30). However, if the fibromuscular dysplasia extends into branch arteries, then surgical treatment is best performed to avoid complications of balloon angioplasty such as rupture, dissection, and occlusion of adjacent branches. Renal artery aneurysms larger than 2 to 3 cm in diameter should generally be treated to avoid rupture (4). Occasionally a renal artery aneurysm smaller than this can cause intractable hypertension and require treatment for this reason. Although in the past surgery was considered the only reasonable treatment, there have been more reports suggesting that endovascular intervention may be appropriate, especially in high-risk patients. A segment of autologous vein or prosthetic graft can be sutured to a stent and positioned across the aneurysm. Placement of a stent-graft across the aneurysm may achieve satisfactory results (4). Potential complications of endovascular treatment of renal artery disease include puncture site hematoma, emboli to the renal parenchyma, contrast dye allergy, nephrotoxicity, renal artery occlusion, perforation with hemorrhage, dissection, and early restenosis.

disease, assuming the patient has acceptable low-risk factors for surgery.

Operative Management

7.

Indications for Surgery for Renovascular Disease Most patients with focal renal artery stenosis are best treated by balloon angioplasty, and possibly stenting, if these procedures are performed by experienced interventionalists with documented low complication rates. In a prospective, randomized study comparing surgery with endovascular treatment of renal artery disease, balloon angioplasty of renal artery stenosis resulted in a 75% primary 2-year patency (33). Based on favorable morbidity and mortality rates for endovascular intervention, the authors recommended that balloon angioplasty be performed first for focal renal artery stenosis instead of surgery (33). On the other hand, excellent contemporary results of operative management argue for an aggressive surgical approach to renovascular disease that is causing hypertension or renal insufficiency (31). We believe there are seven indications for surgery for renal artery occlusive

1.

2.

3.

4.

5.

6.

Surgery may be considered the first-line treatment for patients with focal renal artery stenosis if they are relatively young (less than 70 years old) with few medical comorbidities and expected long-term survival and have intractable renovascular hypertension or impending renal failure (1). Operation may be especially recommended in these patients with long ostial lesions where endovascular treatment has thus far yielded suboptimal long-term patency rates. The risks and benefits of endovascular intervention compared with surgery should be carefully weighed and presented to the patient before any elective intervention is performed. Surgery is best for patients with nonfocal, long, or multiple atherosclerotic lesions in the main renal artery. Surgery is indicated for recurrent stenosis following endovascular treatment of renal artery stenosis when repeat balloon angioplasty is not reasonable or has failed. Operative management is indicated if endovascular intervention is not possible or is unsuccessful because a guidewire cannot be passed across a tight stenosis or occlusion. Surgery is indicted for complications of endovascular intervention such as renal artery or aortic rupture and renal artery dissection or occlusion following balloon angioplasty. Clearly these operations have high morbidity and mortality rates compared with elective renal artery revascularizations. Surgery is indicted for patients with renal artery branch lesions. Balloon angioplasty is generally contraindicated for these patients due to risk of rupture or occlusion of adjacent branches. Lastly, surgery may be preferred if the patient requires open surgery for other reasons, namely repair of aortic aneurysm or aortoiliac occlusive disease. Although some older series reported higher morbidity and mortality rates of elective aortic surgery when concomitant renal artery revascularization is performed, more recent reports have demonstrated acceptable results with a perioperative mortality of approximately 5% (31,34,35). If the patient has intractable renovascular hypertension or worsening renal function with bilateral renal artery occlusive disease, we believe concomitant aortic and renal artery surgery is indicated. An argument has been made to treat renal artery stenosis with endovascular intervention first and then perform open aortic surgery, and occasionally this may be preferable. We are generally conservative regarding renal artery surgery at the time of aortic surgery for patients with well-controlled blood pressure or normal serum creatinine. However, in relatively young, good-risk patients we will perform renal artery revascularization

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at the time of aortic surgery. We are more aggressive in patients with bilateral disease and in nondiabetic patients with diminished renal function.

Preoperative and Intraoperative Assessment Because most patients who require surgery for renovascular disease are elderly and atherosclerosis is the underlying cause of the disease, coronary artery evaluation is essential before an elective operation. Most operative deaths are due to cardiac complications. Death is rare after renal artery reconstruction for fibromuscular dysplasia because these patients tend to be younger and healthier. Antihypertensive medications should be continued throughout the preoperative, operative, and postoperative periods to maintain blood pressure in a normal range. All patients should have pulmonary artery and radial artery catheters placed for blood pressure and fluid status monitoring.

Surgical Techniques for Renal Artery Reconstruction Renal artery revascularization is performed by: 1. 2. 3.

FIGURE 74.3 Approach to the right renal artery through a transverse supraumbilical incision. The duodenum and ascending colon are mobilized by an extended Kocher maneuver providing exposure of the right renal artery, vena cava, and aorta. (Reproduced by permission from Stanley JC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

bypassing the stenotic or occluded segment with a graft; performing endarterectomy; or anastomosing the patent distal renal artery segment to an inflow artery.

Bypasses are performed with autogenous saphenous vein, hypogastric artery or prosthetic grafts depending on the patient and underlying etiology. Inflow sources for bypasses or renal artery implantation include the aorta and iliac, splenic, or hepatic arteries. Endarterectomy is generally applicable only for atherosclerotic orificial lesions.

Aortorenal Bypass For an aortorenal bypass procedure, we generally prefer a midline abdominal incision with the patient in the supine position, although others have favored an upper transverse abdominal incision (Figs. 74.3 and 74.4). If only a left renal artery bypass is required, a left retroperitoneal approach is acceptable. The infrarenal aorta in these patients frequently is densely calcified and cannot be used as an inflow source. In these cases, the aorta can either be replaced with a prosthetic graft or an alternative inflow artery, such as the iliac, splenic, or hepatic arteries, may be utilized. In addition, the supraceliac aorta is usually disease-free and may be another option. Access to the right renal artery is obtained by incising the peritoneum lateral to the ascending colon and mobilizing and reflecting the colon and duodenum to the left as an extended Kocher maneuver. Dissection is continued in an extraperitoneal plane posterior to the colon and ante-

FIGURE 74.4 Approach to the left renal artery through a midline incision. The descending colon and abdominal contents are mobilized to the right in an extraperitoneal plane anterior to the kidney, providing exposure to the renal vessels and aorta. The hypogastric arteries are readily accessible. (Reproduced by permission from Stanley JC, Ernst CR, Fry WJ, eds. Renovascular hypertension. Philadelphia. WB Saunders, 1984.)

Chapter 74 Renal Artery Revascularization

rior to the kidney. The distal right renal artery is identified posterior and superior to the right renal vein and inferior vena cava. The origin of the right renal artery is approached close to the aorta after reflecting the small bowel to the right and retracting the vena cava laterally. Exposure of the left renal artery is obtained via a midline incision by reflecting the small bowel to the patient’s right and taking down the ligament of Treitz, similar to obtaining control of the juxtarenal aorta. On the left, the adrenal and gonadal veins frequently need to be divided while the left renal vein is mobilized. This facilitates dissection of the left renal artery toward the hilum. After a suitable segment of appropriate renal artery is mobilized distal to the diseased segment, the infrarenal aorta is dissected about its circumference between the renal and the inferior mesenteric arteries. Grafts to the right kidney are usually placed in a retrocaval position, taking origin from a lateral aortotomy. Although autogenous saphenous vein has been reported to be the preferred graft for aortorenal bypass in adults, most recent series show that prosthetic grafts function as well in terms of long-term patency (1). For children, the hypogastric artery is preferred because of the propensity of autogenous vein to dilate and become aneurysmal. Low-dose dopamine is started at the beginning of the operation and 12.5 g of mannitol is administered intravenously to enhance diuresis. For aortorenal bypass, the aortic anastomosis is performed first, after the patient has been systemically heparinized (Fig. 74.5). Although it is tempting to place a side-biting vascular clamp midway between the renal vessels and the inferior mesenteric artery to partially occlude the aorta, we prefer to place totally occluding proximal and distal aortic clamps to allow deep aortic bites while performing the aortic anastomosis. Infrarenal total aortic occlusion is well tolerated for far longer than the time required for this anastomosis. The length of the aortotomy should be approximately two to three times the graft diameter. After the aortic anastomosis is complete, a clamp is applied to the renal graft and flow is restored to the lower extremities. This technique also allows for determining the appropriate length of the renal graft since the graft is distended with arterial blood. The proximal renal artery is clamped, transected and oversewn with a 4–0 silk suture. Microvascular clamps or double-looped vessel loops are applied to the distal renal artery or branches. The renal ischemic time is therefore only about 20 min while the renal artery anastomosis is performed and is usually well tolerated, especially in patients with chronic stenosis or occlusion because collaterals have developed. Irrigating the distal renal artery with cooled solution is not necessary in these cases. We prefer an end-to-end anastomosis in these cases because of the greater technical ease of this type of reconstruction and better flow characteristics. Renal anastomoses are facilitated by spatulation of the graft and renal artery (Fig. 74.6). We generally do not administer protamine to reverse the heparin unless the activated

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FIGURE 74.5 Anastomosis of end-to-side vein graft to aorta. The aorta is side-clamped. The aortotomy length is two to three times the diameter of the vein. The graft may be positioned either anterior or posterior to the vena cava depending on local anatomy. (Reproduced by permission from Stanley IC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

FIGURE 74.6 Adjunctive arterial dilation of the primary renal artery branch using olive-tipped stainless steel dilators. (Reproduced by permission from Stanley JC, Ernst CB, Fry WI, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

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clotting time (ACT) remains elevated and diffuse oozing occurs. Management of stenotic disease affecting multiple renal arteries or segmental branches represents a particularly challenging problem. For these cases, autologous tissue grafts using saphenous vein or hypogastric artery is recommended so that branch points of these conduits can be anastomosed to the branched renal arteries. Also, renal arterial branches are much smaller diameter than the main renal artery, and autologous tissue will likely result in less intimal hyperplasia and better patency rates. Creativity may be required in certain cases where some branches are sewn end-to-side to the graft and some endto-end (Figs. 74.7 and 74.8). In some instances, it is best if the involved kidney is freed away from surrounding tissue and placed on the patient’s abdomen for construction of the renal artery anastomosis. In other cases, a “bench” approach is used where the renal artery and vein and ureter are temporarily divided and the renal anastomosis performed at a separate table where the kidney is continually perfused with chilled solution.

Renal Endarterectomy

FIGURE 74.7 Anastomosis of end-to-end vein graft to renal artery. The graft is spatulated anteriorly and the renal artery is spatulated posteriorly. (Reproduced by permission from Stanley IC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

Exposure for endarterectomy differs somewhat from that for aortorenal bypass because the aorta immediately proximal to the renal arteries must be dissected to enhance exposure and apply a proximal aortic clamp. This clamp may also be placed proximal to the celiac artery by approaching the aorta through the gastrohepatic ligament. Dense neural tissue and the crura of the diaphragm should be divided just above the renal arteries to facilitate proximal exposure. For exposure of the left renal artery, the left renal vein anterior to the aorta should be completely mobilized. Division of the adrenal and gonadal veins enhances exposure and allows the left renal vein to be retracted cephalad or caudad. However, we would caution FIGURE 74.8 Technique of in situ reconstruction of multiple renal arteries. The lower branch is anastomosed to a sideof-vein graft. The upper branch is anastomosed in an end-to-end manner to the vein graft. Microvascular lowtension clamps facilitate repair. (Reproduced by permission from Ernst CB, Stanley JC, Fry WJ. Multiple primary and segmental renal artery revascularization utilizing autogenous saphenous vein. Surg Gynecol Obstet 1973;137:1023.)

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A FIGURE 74.9 Technique of anastomosing renal artery branches in a side-to-side manner followed by endto-end vein graft to a common renal artery orifice anastomosis. (Reproduced by permission from Stanley JC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

that these veins should only be divided once the surgeon is certain that the left renal vein itself need not be divided to obtain adequate exposure. We have previously shown that a left renal vein stump pressure less than 35 mmHg is well tolerated because adequate venous collaterals exist to allow left renal vein sacrifice (36). Low stump pressures suggest that the left kidney will not swell significantly or lose significant function because of venous hypertension. However, if the collaterals are already divided, the left renal vein may not be safely divided in some cases when adequate collaterals do not exist. We liberally divide the left renal vein since this maneuver greatly enhances juxtarenal aortic exposure, especially in obese patients or those with juxtarenal aortic aneurysms. When bilateral renal endarterectomy is performed, a transverse aortotomy allows excellent visualization of the end points of the renal endarterectomy since the arteriotomy can be extended far onto each renal artery (Fig. 74.9). A longitudinal aortotomy beginning just distal and to the left of the superior mesenteric artery and carried distally to below the renal arteries is used when infrarenal aortic reconstruction is to be performed (Figs. 74.10 and 74.11). The suprarenal aortic clamp is then repositioned immediately below the renal arteries after the juxtarenal aortotomy is closed with a running Prolene suture. Completion studies using intraoperative DU should be routinely performed to insure technical perfection of the revascularization (37,38). Any significant residual renal plaque that is identified may be removed through a separate transverse renal arteriotomy (Fig. 74.12).

Spleno- and Hepatorenal Artery Bypasses In some patients the infrarenal aorta is not a suitable or ideal inflow source for a renal artery bypass. The presence of a severely calcified aorta renders that vessel unsuitable for clamping unless it is replaced with a prosthetic graft.

B FIGURE 74.10 Transrenal endarterectomy which is reserved for focal proximal renal artery arteriosclerosis. (A) Aorta side-clamped and endarterectomy performed. (B) Patch angioplasty closure.

FIGURE 74.11 Technique of transaortic renal endarterectomy. The aortotomy extends from a point lateral to the superior mesenteric artery to below the renal arteries. (Reproduced by permission from Stanley JC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

Previous aortic surgery may result in dense periaortic scar tissue and may be associated with higher risk of hemorrhage or other surgical complications. Also, some patients have comorbid conditions such as severe cardiac disease that renders aortic clamping unattractive. In these cases, the use of the hepatic or gastroduodenal artery for an in-

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the proximal greater saphenous vein. We therefore prefer performing a hepatorenal vein bypass in most cases.

Renal Artery Aneurysm Repair

FIGURE 74.12 Technique of removing aortorenal arteriosclerotic plaque. Traction on the transected aortic intima facilitates renal ostium endarterectomy. (Reproduced by permission from Stanley JC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984.)

flow source for a right renal artery bypass or the splenic artery for a left renal artery bypass may be more appealing (39,40). Other alternatives include the iliac artery or the supraceliac aorta as inflow arterial sources. Prior to performing a hepato- or splenorenal bypass, a lateral aortogram should be performed to insure wide patency of the celiac artery. A right or left subcostal incision is recommended for these operations. For splenorenal reconstruction, the splenic artery is exposed along the superior-posterior aspect of the pancreas. The splenic artery is extremely tortuous and has many small, friable side-branches. Therefore, dissection of the artery must be performed most carefully. The splenic artery is ligated distally and then brought posterior to the pancreas and caudally to the left renal artery. After the proximal renal artery is divided, the two arteries are spatulated and anastomosed in a tension-free manner using an end-to-end anastomosis. For hepatorenal reconstruction, the common hepatic artery and its branches are identified in their course through the hepatoduodenal ligament. A segment of greater saphenous vein can be sutured in an end-to-side fashion to the hepatic artery and then sutured end-to-end to the right renal artery. Another option is to dissect the hepatic artery onto the gastroduodenal artery and free away this artery for several centimeters. The gastroduodenal artery can then be anastomosed end-to-end to the right renal artery and only one anastomosis is required. However, we have found that the gastroduodenal artery is prone to spasm and usually has a smaller diameter than

Renal artery aneurysms are extremely rare. At Pennsylvania Hospital in Philadelphia, we have documented renal artery aneurysms in only 0.1% (1/845) of consecutive abdominal aortograms, although others have reported somewhat higher prevalence (4). Renal artery aneurysms may result from atherosclerosis, congenital medial degenerative process, fibromuscular dysplasia, or dissection. The clinical significance of renal artery aneurysms relates to renovascular hypertension and potential for rupture. Although rupture from renal artery aneurysms is probably less common than previously thought and fewer than 3% of renal artery aneurysms rupture, pregnant women are particularly vulnerable to rupture and have high associated mortality rates (4). Hypertensive patients who have a renal artery aneurysm should be fully evaluated for a renovascular origin of their hypertension. Although the association of hypertension with renal artery aneurysms may approach 80%, many patients who undergo repair of these aneurysms continue to have unimproved hypertension. Hypertension may be associated with renal artery aneurysms due to renal artery thrombosis, renal parenchymal emboli originating from aneurysm thrombus, and underlying stenosis in the renal artery. Currenty accepted criteria for surgery for renal artery aneurysms include symptoms which imply impending or actual rupture, aneurysms causing renovascular hypertension, aneurysms in pregnant or childbearing-age women, and aneurysms greater than 3 cm in diameter (4).

Operative Techniques The objective of renal artery aneurysm repair is excision of the aneurysm with preservation of the kidney. Because most renal artery aneurysms involve the bifurcation of the main renal artery, the surgeon must be prepared to repair the involved branches by in situ or ex vivo reconstructive techniques. Autogenous saphenous vein is preferred for these complex in situ reconstructions because of the small diameter of these renal artery branches. The three most commonly used techniques are aneurysm excision plus: 1. 2. 3.

primary arteriorrhaphy or end-to-end anastomosis (Fig. 74.13); aortorenal grafting; patch graft angioplasty (Fig. 74.14).

Exposure of the renal arteries is obtained as described in the discussion of aortorenal bypass reconstruction. Some repairs can be accomplished without removing the kidney from its retroperitoneal position. However, occasionally ex vivo reconstruction may be required, particu-

Chapter 74 Renal Artery Revascularization

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FIGURE 74.13 Technique of excision of distal main renal artery aneurysm followed by primary arteriorrhaphy. (Reproduced by permission from Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

FIGURE 74.14 Technique of excising aneurysm arising from renal artery bifurcation. Vein patch angioplasty ensures patulous reconstruction of primary renal arterial branches. (Reproduced by permission from Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

larly when multiple primary branches are involved in the aneurysmal process.

Results of Renal Artery Reconstruction Operative mortality rates for renal artery revascularization performed for atherosclerotic renovascular disease range from 0.9% to 12% with most recent series reporting a 3% mortality rate (31). Recent series have shown that renal artery revascularization performed concomitantly with aortic surgery have an acceptable perioperative mortality rate of 5% (31). Patients undergoing surgery for fibromuscular dysplasia generally have lower morbidity and mortality rates than those with renal atherosclerosis because the former tend to be younger and have fewer comorbid conditions (31). Beneficial blood pressure responses mainly relate to proper patient selection and technical precision in performing the reconstruction. Overall cure and improvement rates range are generally more than 90% (31). Patients undergoing renal artery revascularization for fibromuscular dysplasia generally have better long-term results in terms of blood pressure control than those with atherosclerosis (31). At centers of excellence, 30-day patency rates of renal artery bypasses have been reported to be more than 98%

(31). Late stenoses requiring reoperation for recurrent renovascular hypertension are rare and may occur in only 5% of grafts on late follow-up (41). About 20% to 40% of aortorenal vein grafts undergo expansion. Aneurysmal changes in aortorenal vein grafts affect 5% of such conduits (42). These alterations occur most frequently among children (43). Because of the yet unknown but worrisome potential problems associated with aortorenal vein grafts in children, autogenous arterial segments, most commonly hypogastric artery, have been used.

References 1. Hansen KJ. Renovascular disease: an overview. In: Rutherford, ed. Vascular Surgery, 5th edn. Philadelphia: WB Saunders, 2000:1593–1600. 2. Gifford R.V Jr. Epidemiology and clinical manifestations of renovascular hypertension. In: Stanley JC, Ernst CB, Fry WJ, eds. Renovascular hypertension. Philadelphia: WB Saunders, 1984:77–99. 3. Stanley JC, Gewertz BC, et al. Arterial fibrodysplasia: histopathologic character and current etiologic concepts. Arch Surg 1975;110:561–565. 4. Calligaro KD, Dougherty MJ. Renal artery aneurysms and areriovenous fistulae. In: Rutherford, ed. Vascular Surgery, 5th edn. Philadelphia: WB Saunders, 2000:1697–1705.

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5. Ferrario CM, Levy PJ. Pathophysiology, functional studies, and medical therapy of renovascular hypertension. In: Rutherford, ed. Vascular Surgery, 5th edn. Philadelphia: WB Saunders, 2000:1600–1611. 6. Simon N, Franklin SS, et al. Clinical characteristics of renovascular hypertension. J Am Med Assoc 1972;220:1209. 7. Mann SJ, Pickering TG. Detection of renovascular hypertension. State of the art: 1992. Ann Intern Med 1992;117:845. 8. Postma CT, Van der Steen PH, et al. The captopril test in the detection of renovascular disease in hypertensive patients. Arch Intern Med 1990;150:625. 9. Elliott WJ, Martin WB, Murphy MB. Comparison of two noninvasive screening tests for renovascular hypertension. Arch Intern Med 1993;153:755–764. 10. Krijnen P, van Jaarsveld BC, et al. A clinical prediction rule for renal artery stenosis. Ann Int Med 1998;129:705–711. 11. Dean RH. Renovascular hypertension. In: Moore WS, ed. Vascular surgery: a comprehensive review, 3rd edn. Philadelphia: WB Saunders, 1991:403–424. 12. Muller FB, Sealey JE, et al. The captopril test for identifying renovascular disease in hypertensive patients. Am J Med 1986;80:633. 13. Hansen PB, Garsdal P, Fruergaard P. The captopril test for identification of renovascular hypertension: value and immediate adverse effects. Ann Intern Med 1990;228:159. 14. Frederickson ED, Wilcox CS, et al. A prospective evaluation of a simplified captopril test for the detection of renovascular hypertension. Arch Intern Med 1990;150:569. 15. Ernst CB, Rutkow IM, et al. Vascular surgery in the United States: report of the Joint Society for Vascular Surgery–International Society for Cardiovascular Surgery Committee on Vascular Surgical Manpower. J Vasc Surg 1987;6:611. 16. Stanley JC, Fry WJ. Surgical treatment of renovascular hypertension. Arch Surg 1977;112:1291. 17. Ernst CB, Daugherty ME, Kotchen TA. Relationship between collateral development and renin in experimental renal arterial stenosis. Surgery 1976;80:252. 18. Roubidoux MA, Dunnick NR, Cotman PE. Renal vein renins: inability to predict response to revascularization in patients with hypertension. Radiology 1991:178:819–822. 19. Textor SC, Tarazi RC, et al. Regulation of renal hemodynamics and glomerular filtration in patients with renovascular hypertension during converting enzyme inhibition by captopril. Am J Med 1984;76 (Suppl 5B):29. 20. Setaro JF, Saddler MC, et al. Simplified captopril renography in diagnosis and treatment of renal artery stenosis. Hypertension 1991;18:289–298. 21. Meier GH. Diagnosis of renovascular hypertension: an overview. In: Calligaro KD, Dougherty MJ, Dean RH, eds. Modern management of renovascular hypertension and renal salvage. Media, PA: Williams & Wilkins, 1996:47–74. 22. Taylor DC, Kettler MD, et al. Duplex ultrasound in the diagnosis of renal artery stenosis: a prospective evaluation. J Vase Surg 1988;7:363–367.

23. Hansen KJ, Tribble RW, et al. Renal duplex sonography: evaluation of clinical utility. J Vasc Surg 1990;12:227–231. 24. Hansen KJ, Reavis SW, Dean RH. Duplex scanning in renovascular disease. Geriatr Nephrol Urol 1996;6:89. 25. Kent KC, Edelman RR, et al. Magnetic resonance imaging: a reliable test for the evaluation of proximal atherosclerotic renal artery stenosis. J Vasc Surg 1991;13:311–317. 26. Slonim SM, Dake MD. Radiographic evaluation and treatment of renovascular disease. In: Rutherford, ed. Vascular Surgery, 5th edn. Philadelphia: WB Saunders, 2000:1611–1639. 27. Schindler N, Calligaro KD, et al. Has arteriography gotten a bad name? Current accuracy and morbidity of contrast arteriography for aortoiliac and lower extremity arterial disease. Ann Vasc Surg 2001;4:417–421. 28. Valentine RJ, Clagett GP, et al. The coronary risk of unsuspected renal artery stenosis. J Vasc Surg 1993;18:433–440. 29. Rees CR, Palma JC, et al. Palmaz stent in atherosclerotic stenoses involving the ostia of the renal arteries: preliminary report of a multicenter study. Radiology 1991;181:507–511. 30. Martin L. Renal revascularization using percutaneous balloon angioplasty for fibromuscular dysplasia and atherosclerotic disease. In: Calligaro KD, Dougherty MJ, eds. Modern management of renovascular hypertension and renal salvage. Media, PA: Williams & Wilkins, 1996:47–74. 31. Hansen KJ, Starr SM, et al. Contemporary surgical management of renovascular disease. J Vasc Surg 1992;16:319. 32. Webster J, Marshall F, et al. Randomized comparison of percutaneous angioplasty vs. continued medical therapy for hypertensive patients with atheromatous renal artery stenosis. J Hum Hypertens 1998;12:329–334. 33. Weibull H, Bergqvist D, et al. Percutaneous transluminal renal angioplasty versus surgical reconstruction of atherosclerotic renal artery stenosis: a prospective randomized study. J Vasc Surg 1993;18:841–852. 34. Atnip RG, Neumyer MM, et al. Combined aortic and visceral arterial reconstruction: risks and results. J Vasc Surg 1990;12:705. 35. Tollefson DF, Ernst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg 1991;14:327. 36. Calligaro KD, McCoombs P, et al. Division of the left renal vein during aortic surgery. Am J Surg 1990;160:192–196. 37. Dougherty MJ, Hallett JW Jr, et al. Optimizing technical success of renal revascularization: the impact of intraoperative color-flow duplex ultrasonography. J Vasc Surg 1993;17:849–856. 38. Hansen KJ, O’Neil EA, et al. Intraoperative duplex sonography during renal artery reconstruction. J Vasc Surg 1991;14:364–374. 39. Moncure AC, Brewster DC, et al. Use of the splenic and hepatic arteries for renal vascularization. J Vasc Surg 1986:3:196. 40. Novick AC. Alternative renal artery reconstructive techniques: hepatorenal, splenorenal, and other bypass

Chapter 74 Renal Artery Revascularization procedures. In: Ernst CB, Stanley JC, eds. Current therapy in vascular surgery, 3rd edn. Philadelphia: BC Decker, 1994. 41. Dean RH, Krueger TC, et al. Operative treatment of renovascular hypertension: etiology, diagnosis, and operative treatment. Arch Surg 1981;116:669.

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42. Ernst CB, Stanley JC, et al. Autogenous saphenous vein aortorenal grafts: a ten-year experience. Arch Surg 1972;105:855. 43. Stanley P, Gyepes MT, et al. Renovascular hypertension in children and adolescents. Radiology 1978;129: 123.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 75 Visceral Artery Aneurysms Matthew J. Dougherty and Keith D. Calligaro

Although rare, aneurysms of the visceral arteries (VAA) have been extensively described in the surgical literature. Most reports consist of only a few patients, with varying aneurysm etiology, location, clinical presentation, and treatments employed. In this context is difficult to get a clear view of the natural history of untreated VAA, or a consensus on the optimal approach for managing splenic artery aneurysms that should be treated. However with increasing recognition of these lesions and more reports on new treatment approaches, principles of management are being formulated. Of VAAs on the whole, splenic artery aneurysms are most common (approximately 60% of all), followed by hepatic artery aneurysms (20%). Far fewer celiac and superior mesenteric artery aneurysms present, and fewer still branch vessel aneurysms (gastroduodenal, pancreaticoduodenal, jejunal, ileal, colic.) Inferior mesenteric artery aneurysm is least common (Fig. 75.1). As the etiology and clinical implications of VAA vary by site, we will consider aneurysms of these vessels separately by group.

Splenic Artery Aneurysm Since Beaussier’s first report in 1770 (1), nearly 2000 cases of splenic artery aneurysm (SAA) have been reported (2–6) and these account for about 60% of all visceral aneurysms. The prevalence of SAA has been reported to be as low as less than 0.1% on a large autopsy series (7) to over 10% in another postmortem report on patients over 60 (8). The true incidence remains unknown and depends upon defining criteria for what constitutes an aneurysm of the splenic artery. The increasingly common use of sophis-

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ticated abdominal imaging has led to increasing recognition of SAA in asymptomatic patients.

Etiology In early reports infectious etiologies were prevalent but in the last few decades the most common cause of SAA has been medial fibrodysplasia (9). Although atherosclerosis has been frequently observed in SAA, in most cases these histologic changes are thought to be secondary related to turbulent flow. However primary atherosclerotic degeneration may be a more common cause of other true visceral artery aneurysms. Unlike most other aneurysms, where male gender and older age are predominant features, splenic artery aneurysms exhibit a 4 to 1 female to male ratio with a mean age at presentation of 51 years (3,5,10,11).

Pregnancy The influence of pregnancy on both the development and behavior of SAA has long been recognized. The female predominance for SAA (2,10–12) may be a reflection of this. Multiparity has been noted by some to be associated with SAA, reinforcing the notion that gestational influences play a role in the pathophysiology of SAA development (12). The association of female gender and pregnancy is of course also well recognized with fibromuscular dysplasia. Stanley and Fry theorized that elevated visceral flow rates associated with pregnancy combined with the effect of circulating relaxins and other gestational hormones on the internal elastic lamina of the splenic artery, leading to intramural medial disruption and aneurysmal degeneration (5,13). Patients with preex-

Chapter 75 Visceral Artery Aneurysms

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celiac artery hepatic 20-40 % left gastric & gastroepiploic 3-5 % splenic ~60%

aneurysm

gastroduodenal & pancreaticoduodenal 3-5 %

splenic artery superior mesenteric 3-5 %

jejunal / ileal / colic 1-3 %

inferior mesenteric < 1 %

FIGURE 75.1 Distribution of VAA. Percentages reflect ranges in published reports.

isting systemic fibromuscular dysplasia seem to be at particular risk, exhibiting a six-fold increase in incidence of SAA (12).

Portal Hypertension The prevalence of SAA in patients with cirrhosis and portal hypertension has been noted more frequently in the last decade (6,13–18). The incidence of SAA may be as high as 7 to 9% in patients undergoing orthotopic liver transplant (15,19), although in their review of the University of Pittsburgh’s last decade of liver transplantation, Lee et al. noted a much lower (0.46%) incidence of SAA treated after transplant. Post-transplant patients appear to be at higher risk than patients with untreated portal hypertension. Hyperdynamic splenic artery flow is noted after transplant due to normalization of portal venous pressures in the dilated mesenteric venous bed (16,20). It is notable that six of seven SAA ruptures were observed less than 16 days after liver transplant in the Pittsburgh series (6). Screening transplant candidates for SAA and concomitant SAA repair with transplant has been recommended (15).

Other Factors The influence of systemic blood pressure on SAA is less clear than for other nonvisceral arterial aneurysms, but essential hypertension may be a risk factor for SAA rupture (6). Hypertension has been associated with SAA in approximately 40% of patients (21). Pseudoaneurysms of the splenic artery are associated with trauma and inflammation. This entity is distinct from true SAA and behaves differently. The most common scenario is in association with pancreatitis (both acute and chronic). Inflammatory degeneration and enzymatic digestion of the arterial wall is the likely mechanism for pseudoaneurysm development.

FIGURE 75.2 Depiction of mid-splenic artery aneurysm. Note multiple contributing vessels which allow for splenic preservation with ligation or embolization. When rupture occurs, hemorrhage may initially be contained in the lesser sac, with secondary free peritoneal hemorrhage representing the “double rupture” phenomenon. (By permission of Lumsden AB, Riley JD, Skandalakis JE. Splenic artery aneurysms. Probl General Surg 1990;7(1):113–121.)

As with other locations, infection with mycotic aneurysm development is an occasional mechanism for SAA formation. These also represent pseudoaneurysms rather than true aneurysms.

Clinical Presentation Most splenic artery aneurysms are asymptomatic. When presenting with symptoms, left upper quadrant pain is most common. As unexplained abdominal pain is a frequent indication for radiographic evaluation, the causal relationship between chronic or subacute pain and an SAA may be difficult to establish. While nonruptured SAA rarely cause symptoms, rupture of SAA typically presents with severe upper abdominal pain and tenderness associated with hypovolemic shock. The classic picture, described by Brockman, is of a “double rupture,” with initial tamponade of bleeding within the lesser sac, and subsequent free intraperitoneal rupture through the foramen of Winslow with hemodynamic collapse (13,22,23). This delay between initial symptoms and free rupture can be minutes or days (4) and is observed in approximately one-quarter of patients who present with rupture (24) (Fig. 75.2). Approximately 13% of SAA ruptures occur into the gastrointestinal tract (10). These present with upper gastrointestinal bleeding from fistulization with the duodenum, the stomach, or pancreatic duct. This presentation is more common with pancreatitis-related splenic pseudoaneurysm. Rupture appears to be more common during pregnancy. Most ruptures occur during the third trimester and

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are probably influenced by the same factors that lead to aneurysm formation, namely, circulating hormones such as relaxin and the hyperdynamic state of pregnancy.

Diagnosis The diagnosis of SAA was classically made by plain abdominal radiograph, the appearance of a “signet ring” opacity in the left upper quadrant representing the calcified shell of the aneurysm. Approximately 70% of SAA are calcified and the diagnosis of asymptomatic SAA is most commonly made based on this finding (3). While color duplex imaging has become the mainstay for diagnosis and surveillance for most other aneurysms, its sensitivity for SAA has been less (25). Although arteriography has been the gold standard for defining SAA, in recent years computed tomography has supplanted this role. Particularly with the newer generation of highresolution machines with angiographic capabilities, the need for diagnostic arteriography is less clear unless catheter-based treatments are elected (Fig. 75.3). Likewise magnetic resonance angiography has been reported to be an effective imaging modality.

Treatment While there is consensus on the treatment of symptomatic SAA, the approach to small and asymptomatic SAA remains controversial. Rupture of SAA has been said to occur in as few as 0.5% (5) to up to 10% of cases not initially treated. The actual annual incidence of rupture for a given size SAA remains unknown due to lack of uniform reporting, small

FIGURE 75.3 CT demonstrating splenic artery aneurysm. Note eccentric calcification, frequently visible on plain abdominal radiograph as a “signet ring” on the left upper quadrant.

numbers, and few longitudinal natural history reports. This is especially true for larger SAA. Trastek noted few ruptures for SAA followed up to 9 years at the Mayo Clinic, however the cohort followed was only 19 patients and mean aneurysm size was small at 1.4 cm (3). Using a 2-cm threshold and an assumed 25% ultimate rupture mortality risk, Stanley recommended elective repair of SAA if a less than 0.5% mortality could be anticipated. There is a consensus that larger SAA should be treated. Whether the threshold value should be as high as 3 cm or as low as 2 cm cannot be stated with certainty based on currently available data. Calcification, previously thought to be of prognostic significance and protective from rupture, is no longer felt to be relevant (2,10). The mortality of rupture of SAA is 25% to 50%, and as high as 75% (with 95% fetal mortality) in the gravid female. Given the high risk of rupture and its high mortality in pregnant patients, repair of SAA has been recommended for all patients presenting while pregnant or planning future pregnancies. Patients with portal hypertension present a special challenge. SAA in these patients tends to be at the hilum, and splenomegaly is frequently associated (13). Although the risk of rupture in patients with portal hypertension may be higher than for other SAA, the morbidity of surgery is likewise higher. Repair is not recommended for SAA of 1.5 cm or less (16). Patients undergoing liver transplant with SAA should have concomitant repair of the SAA given the high risk of postoperative rupture. The traditional treatment for SAA has been surgical. The aneurysm is exposed through the lesser sac and proximal and distal arterial control is obtained (Fig. 75.2). For smaller or mobile aneurysms, complete excision is employed. For larger lesions and those associated with pancreatic inflammation, proximal and distal ligation with oversewing communicating vessels from within the aneurysm is a better option. The spleen usually derives adequate arterial flow from the short gastric vessels; however, for SAA involving the hilum of the spleen, splenectomy is warranted. SAA secondary to pancreatitis may best be treated by distal panceatectomy. Laparoscopic SAA ligation has been reported and advocated for pregnant women (26). In recent years, angiographic embolization has been more frequently employed for definitive treatment of SAA (27) (Fig. 75.4). The splenic artery is selectively catheterized and occluded proximal and distal to the aneurysm. Although Gelfoam has been utilized as an embolizing agent in the past, the tendency toward recanalization makes it less attractive. Gianturco coils are the most utilized technique in recent reports. This approach has been successful in over 80% of patients in many reports, although most of these are from specialized centers. In a recent pooled community hospital report, technical success with SAA embolization was only 20% (11). Delayed recanalization has been observed in a few patients, and has been successfully treated by repeat embolization. Radiographic embolization is certainly a more appealing ap-

Chapter 75 Visceral Artery Aneurysms

A

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B

FIGURE 75.4 (A) Arteriogram showing large, multilobulated SAA. (B) After transcatheter embolization. (By permission of Messina LM, Shanley CJ. Visceral artery aneurysms. Surg Clin North Am 1997;77:425–442.)

proach for high-risk surgical patients, such as those with portal hypertension (13). Some authors believe this should be the preferred approach for all patients (28,29). In general, the efficacy of embolization therapy for VAA will depend upon the maintenance of alternate perfusion pathways to sustain end-organ function, and the ability to effectively and permanently occlude the aneurysmal vessel. Figure 75.5 depicts anatomic features most amenable to embolization. With improving technologies, open repair will likely be replaced by endovascular occlusion for most SAA.

Hepatic Artery Aneurysm Hepatic artery aneurysm (HAA) was first described by Wilson in 1809 (30). Over 400 cases of HAA have been reported (31), and HAA has previously been thought to constitute about 20% of all visceral aneurysms (2,10). However, in recent years HAA has supplanted SAA as the most frequently reported visceral artery aneurysm (10,32). This may reflect literature bias toward case reports of less common entities; however, HAA also appears to be increasing in frequency in combined reports of visceral aneurysm (28,33,34).

Etiology While in early reports infectious and luetic causes for HAA were most common, mycotic aneurysm now represents a small proportion of reported HAA, perhaps 3%. Mycotic HAA may occur from metastatic infection in intravenous drug abusers (31) or extension of biliary sepsis (10,31,35). However, false aneurysm and pseudoaneurysm of the hepatic artery are increasingly being ob-

FIGURE 75.5 Arterial and aneurysmal anatomy favorable for percutaneous ablation procedures. Type I depicts small-necked pseudoaneurysm where ablation can be successful while maintaining patency of artery. Types II and III demonstrate collateral pathways that can be recruited with aneurysm occlusion. (By permission of Kasirajan K, Greenberg R, et al. Endovascular management of visceral artery aneurysm. J Endovasc Ther 2001;8:150–155.)

served and account for approximately 50% of all HAA (10). Many of these are iatrogenic, related to percutaneous biliary procedures, penetrating or blunt trauma, and biliary surgery. In contradistinction to SAA, true HAA are more frequently atherosclerotic aneurysms than secondary to medial dysplasia (31,34,35), although again atherosclerotic changes may in some cases be secondary rather than primary (2,10). Medial degeneration is observed in about a quarter of lesions, although these too appear to be acquired rather than congenital abnormalities (2). The association of atherosclerotic aneurysms of nonvisceral vessels with HAA also points toward atherosclerosis as a primary cause (35,36).

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Rare causes of HAA include arteritis (particularly polyarteritis nodosa), cholecystitis, and perihepatic inflammation. HAA has also been observed in patients with long-term amphetamine abuse (37) and cirrhosis (38,39).

Location Owing to the increasing incidence of iatrogenic and traumatic HAA, intrahepatic HAA have increased in prevalence. However extrahepatic lesions still represent approximately two-thirds of all HAA (10). About 40% involve the common or proper hepatic artery, half involve the right hepatic artery, and the left hepatic and more peripheral branches are infrequently involved (32,34). Multiple aneurysms occur in about 4% (40). In contrast to SAA, there is a preponderance of male patients for HAA, and average age at presentation is 52, with true aneurysm patients older than false aneurysm patients (32).

FIGURE 75.6 Contrast-enhanced computed tomography demonstrates large intrahepatic HAA with thrombus. (By permission of Dougherty MJ, Gloviczki P, et al. Hepatic artery aneurysms. Int Angiol 1993;12:178–184.)

Clinical Presentation As with SAA, the majority of HAA are asymptomatic. When symptoms occur, abdominal pain is the most common complaint. Up to 46% present with hematobilia or gastrointestinal bleeding (10). Jaundice may occur from extrinsic bile duct compression or thrombus in the duct. Quincke’s classic triad of jaundice, biliary colic, and gastrointestinal bleeding is observed in only one-third of patients (41). In contrast to SAA, rupture is frequent for HAA and approximately two-thirds of current reports describe ruptured HAA (10,32). Rupture into the bile duct, duodenum, or stomach is more common than free intraperitoneal rupture.

Diagnosis Patients may occasionally have a pulsatile mass in the right upper quadrant on abdominal examination; however, most HAA are discovered by ultrasound or computed tomography (Fig. 75.6). Precise localization of HAA for definitive planning of therapy requires angiography with selective celiac artery injection (Fig. 75.7).

Treatment Treatment of HAA has evolved significantly in the last decade. For extrahepatic aneurysms in good-risk patients, surgery is still probably the most common approach. For aneurysm of the common hepatic artery, surgery may involve simple ligation proximal and distal to the aneurysm. The gastroduodenal artery will usually provide adequate collateral flow to the more distal hepatic artery, so this approach is reasonable. However we prefer vascular reconstruction if feasible in most cases (Fig. 75.8). Aneurysms extending to the proper hepatic artery should be treated with vascular reconstruction as the risk of liver necrosis is substantial with ligation alone (31,35). Miani and co-

FIGURE 75.7 Flush aortogram demonstrates fusiform aneurysm of common hepatic artery. (By permission of Dougherty MJ, Gloviczki P, et al. Hepatic artery aneurysms. Int Angiol 1993;12:178–184.)

authors noted two patients with failed grafts to the proper hepatic artery who suffered fatal liver necrosis (33). Liver necrosis with ligation alone may be more likely to occur in patients explored for rupture with hemorrhagic shock, and in this setting vascular reconstruction should be attempted even for common hepatic aneurysm. For lesions involving the intrahepatic vessels, liver resection has sometimes been required, with significant attendant morbidity. It is for these lesions, as well as the increasingly common traumatic or iatrogenic false aneurysm, that catheter-based treatments have been embraced. Indeed this is currently the most commonly employed treatment for HAA (32), and some authors prefer endovascular treatment for all cases where technically feasible, including extrahepatic lesions, particularly in higher-risk patients (28,40,42,43).

Chapter 75 Visceral Artery Aneurysms

A

907

B

FIGURE 75 8 (A) Surgical exposure of HAA visualized on arteriography in Figure 75.7. (B) Interposition saphenous vein graft reconstruction (LHA, left hepatic artery; GDA, gastroduodenal artery; SA, splenic artery; CA, celiac artery). (By permission of Dougherty MJ, Gloviczki P, et al. Hepatic artery aneurysms. Int Angiol 1993;12:178–184.)

For endovascular treatment, transarterial access to the hepatic vessels is preferred, although direct percutaneous embolization has been successfully employed in patients whose anatomy was unfavorable for the conventional approach (45) (Fig. 75.9). Delivery of the embolizing agent both proximal and distal to the aneurysm, as well as to any other feeding vessels, appears to be critical to sustained success (42). Microcoils are preferred to Gelfoam given the danger of the higher delivery pressure required with the latter, especially in thin-walled pseudoaneurysms, and because recanalization has been observed with the Gelfoam (28,46,42,43). However, late recurrence of HAA has been observed even with microcoil treatment (28) so careful postoperative surveillance with color duplex imaging is critical to ensure ongoing success. The newly available covered stent technology will undoubtedly be employed for the treatment of HAA, and certainly this is an attractive concept with advantages over embolization. Burger and co-authors recently reported successful stent–graft repair of a perforated hepatic artery secondary to sepsis (47). The ability to preserve prograde flow to the affected organ is a major advantage of stent–graft technology compared with more commonly employed embolization techniques (Fig. 75.10). As with embolization therapy, duplex or other surveillance will be critical to ensuring durable exclusion of HAA.

Superior Mesenteric Artery Aneurysm Accounting for about 5% of visceral artery aneurysms, superior mesenteric artery aneurysm (SMAA) is the third most common VAA (2,10). These aneurysms may be fusiform or saccular and tend to involve the proximal 5 cm of the SMA (10). In contrast to splenic and hepatic aneurysms, the most common cause of SMAA is still infection, frequently secondary to bacterial endocarditis

from nonhemolytic Streptococcus and Staphylococcus species. Indeed, the SMA is the most common site for infection of a muscular artery (10,48). Atherosclerotic true aneurysms are increasing in incidence with the aging population, and false aneurysms from pancreatitis are also growing in prevalence (10). Although dissecting aneurysm involving the SMA is rare, the SMA is the visceral vessel most commonly affected by dissection (49). SMAA has been associated with a1-antitrypsin deficiency (50). In recent years SMAA has been observed in males in two-thirds of cases. Abdominal pain is associated with SMAA in twothirds of cases, with less frequent findings of abdominal mass, fever, gastrointestinal bleeding, jaundice, and shock (51). Occasionally patients present with symptoms of intestinal angina due to associated SMA stenosis. Rupture has been noted in 70% of symptomatic patients (48). The location of SMAA may allow for diagnosis with ultrasound, although CT scanning provides a better study (Fig. 75.11). Arteriography is necessary to define the exact location of the aneurysm and its relationship to other SMA branches. The first successful surgical treatment for SMAA was reported by DeBakey and Cooley in 1953 (52). Transabdominal, transperitoneal exposure is most frequently utilized, but for proximal SMAA a retroperitoneal approach may be preferable. Probably because of the prominent role of infection in these aneurysms, the majority of reports describe ligation or ablation without revascularization. The presence of extensive collateral flow via pancreaticoduodenal and middle colic branches, as well as the proximal location of most SMAA, enables this approach, although adjunctive bowel resection may be necessary. Temporary occlusion of the SMA, with intraoperative observation with fluoroscein dye and a Woods lamp prior to SMA ligation has been advocated to reduce the risk of bowel necrosis (48). When not contraindicated by extensive sepsis, revascularization with autogenous conduit is probably a preferable approach.

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A

B

FIGURE 75.9 (A) CT demonstrating large intrahepatic HAA. (B) Selective celiac arteriography demonstrates saccular common hepatic artery pseudoaneurysm. (C) After successful Gianturco coil embolization. (By

C

Transcatheter embolization has been successfully employed for ruptured SMAA (53), however recurrent hemorrhage requiring laparotomy and endoaneurysmorrhaphy was noted in another patient after initially successful coil embolization (54). The obvious concern with transcatheter therapy for SMAA is the inability to directly assess bowel viability. Nonetheless, percutaneous approaches may occasionally be warranted for SMAA.

Celiac Artery Aneurysm Although the fourth most common visceral artery aneurysm, accounting for about 4% of all VAA (2,10), in the decade from 1985 through 1995 there were only 29 case reports of celiac artery aneurysm (CAA) (32). Of these small numbers, two-thirds of patients were male, and average age was 56 years. While in the historic era the common causes of celiac artery aneurysm were syphilis and other infections, the etiology of true aneurysm of the

permission of Reber PU, Baer HU, et al. Superselective microcoil embolization: Treatment of choice in high-risk patients with extrahepatic pseudoaneurysms of the hepatic arteries. J Am Coll Surg 1998;186(3):325–330.)

celiac artery in the modern era is most commonly atherosclerotic, with medial dysplasia associated with most others (55,56). Rupture was the common presentation for CAA in earlier years, but more recently most have been diagnosed and treated prior to rupture. Mortality with rupture approaches 100%. Vague abdominal pain was the symptom leading to diagnosis in over two-thirds of patients, with occasional patients exhibiting gastrointestinal bleeding, jaundice, hemoptysis, or a palpable mass (32). Although treatment of CAA with revascularization has only been reported in about a quarter of published cases (57), this would appear to be the preferred approach. When infection or other factors preclude revascularization, ligation may be safe if patency of the superior mesenteric artery and portal vein can be ensured. Endovascular treatment of celiac artery aneurysm is feasible but will likely be more difficult than for other VAA given the early branching to major vessels. As with endovascular treatment for VAA in general, while the presence of

Chapter 75 Visceral Artery Aneurysms

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B

C

D

FIGURE 75.10 (A) and (B) demonstrate contrast extravasation with leaking proper hepatic artery pseudoaneurysm secondary to sepsis. (C) Percutaneous transluminal dacron covered stent deployed (Wallgraft) Boston Scientific, Watertown, MA. (D) Successful exclusion of HAA. (E) Follow-up CT Scan at 10 months. (By permission of Burger T, Halloul Z, et al. EmerE

gency stent–graft repair of a ruptured hepatic artery secondary to local postoperative peritonitis. J Endovasc Ther 2000;7(4):324–327.)

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Common hepatic a.

Inferior pancreaticoduodenal a.

Posterior inferior pancreaticoduodenal a.

Superior mesenteric a.

Anterior inferior pancreaticoduodenal a.

FIGURE 75.11 Computed tomography scan depicting large superior mesenteric artery aneurysm. (By per-

FIGURE 75.12 Arterial anatomy of pancreaticoduodenal aneurysm. Superior mesenteric artery compression by the aneurysm may be responsible for symptoms of chronic mesenteric ischemia. (By

mission of Kopatsis A, D’Anna JA, et al. Superior mesenteric artery aneurysm: 45 years later. Am Surg 1998;64:263–266.)

permission of Chiou AC, Josephs LG, Menzoian JO. Inferior pancreaticoduodenal artery aneurysms: Report of a case and review of the literature. J Vasc Surg 1993;17:784–789.)

multiple collaterals may allow for sacrifice of the artery, these pathways may also lead to recanalization of the aneurysm (Fig. 75.5).

Diagnosis may occasionally be made with contrastenhanced CT scanning, but arteriography is a more sensitive and specific test, and is essential to planning therapy. Because of the rich collateral circulation around the pancreas, ablative treatment is the preferred approach for most GDAA and PDAA. Surgical ligation or aneurysmectomy has been most commonly employed. Revascularization has been employed in only a handful of cases, accounting for no more than 5% of case reports (51). Although surgical ablation is effective, the morbidity is significant, particularly when aneurysms are associated with pancreatic inflammation. Hence, catheter-based techniques have been preferred in most recent reports. Embolization of the feeeding vessels of the aneurysm using microcoils is the preferred option. Deployment of coils both proximal and distal to the aneurysm, as well as into any other feeding vessels, is critical to sustained success. Gelfoam has been successfully used here, particularly for pseudoaneurysms. Direct deposition of Gelfoam (and thrombin in some cases) into the aneurysmal sac may be sufficient for pseudoaneurysms. Success with endovascular treatment of peripancreatic VAA is in the range of 80% (46,60).

Gastroduodenal and Pancreaticoduodenal Aneurysms Gastroduodenal and pancreaticoduodenal aneurysms (GDAA and PDAA) are very rare, accounting for approximately 3.5% of all VAA (10). Fewer than 100 cases were reported between 1970 and 1995. In more recent reports, pseudoaneurysms outnumber true aneurysms and are associated with acute or chronic pancreatitis or biliary disease in more than half of cases. However, for true aneurysms, atherosclerosis appears to be the most common etiology and is observed in 58% of cases (51,58). Males outnumber females by more than 2 to 1, and most patients present in their fifth decade (10). Although abdominal pain is the most frequently associated symptom, the most common presentation of GDAA and PDAA is rupture. This is usually manifest by gastrointestinal bleeding, occurring in over half of cases (59). Gastrointestinal bleeding occurs secondary to erosion into the duodenum or stomach, or with involvement of the pancreatic duct (hemosuccus pancreaticum) or bile duct (hemobilia). Retroperitoneal bleeding occurs in about half as many cases as gastrointestinal bleeding, and free peritoneal rupture about half as often as this (59). Jaundice may accompany these aneurysms, either from related hepatobiliary disease or from common bile duct obstruction. Occasionally, patients present with symptoms of chronic mesenteric ischemia such as weight loss and postprandial pain (58). This may be secondary to compression of the SMA by the aneurysm (Fig. 75.12).

Gastric and Gastroepiploic Artery Aneurysm Although these rare aneurysms have been said to account for up to 4% of VAA in prior reviews (2,34), they appear to be less commonly reported more recently. Etiologies include medial degeneration, inflammatory degeneration of the media, and observed histologic changes of atherosclerosis are probably secondary in most cases (2). Most present in elderly patients, with a preponderance of men. In earlier reports, gastric artery aneurysms

Chapter 75 Visceral Artery Aneurysms

were much more common than gastroepiploic aneurysms. The majority of reported cases present with rupture, most frequently causing gastrointestinal bleeding. Associated mortality is as high as 70% (12). Treatment has generally been surgical, with aneurysmectomy, often with excision of involved gastric tissue, as the standard. As with gastroduodenal and pancreaticoduodenal aneurysms, endovascular therapy will likely assume a larger role in the future.

Rare Visceral Artery Aneurysms Although all VAA are rare, least common of all are aneurysms of the jejunal, colic, and other SMA branches, and aneurysms of the inferior mesenteric artery, with only 23 cases reported between 1970 and 1995 (51). The majority of these cases were false aneurysms, with a roughly even sex distribution. The large majority (21 of 23) involve the middle colonic distribution. Congenital and acquired medial defects, septic or immunogenic endarteritis (e.g., polyarteritis nodosa) and atherosclerosis have all been described as causes (2,10). Most reported patients present with rupture, and treatment has been with ligation, excision, or embolization. Aneurysms of the inferior mesenteric artery are extraordinarily rare, with only a handful reported. True aneursyms outnumber false aneurysms. Most were treated with ligation, although bypass is occasionally necessary to preserve colonic perfusion (51).

References 1. Beaussier M. Sur un aneurisme de l’artere splinique don’t les parroie se sont ossifiees. Journal Medical Toulose 1770;32:157. 2. Zelenock GB, Stanley JC. Splanchnic Artery Aneurysms. In: Rutherford RB, ed. Vascular Surgery. 5th edn. Philadelphia: WB Saunders, 2000:1369–1382. 3. Trastek VF, Pairolero PC, et al. Splenic artery aneurysms. Surgery 1982;91:694. 4. Lumsden AB, Riley JD, Skandalakis JE. Splenic artery aneurysms. Probl Gen Surg 1990;7(1): 113–121. 5. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 1974;76:898. 6. Lee PC, Rhee RY, et al. Management of splenic artery aneurysms: the significance of portal and essential hypertension. J Am Coll Surg 1999;189(5): 483–490. 7. Moore SW, Guida PM, Schumacher HW. Splenic artery aneurysm. Bull Soc Int Chir 1970;29:210. 8. Bedford PD, Lodge B. Aneurysm of the splenic artery. Gut 1960;1:312–320. 9. Stanley JC, Gewertz BL, et al. Arterial fibrodysplasia: histopathologic character and current etiologic concepts. Arch Surg 1975;110:561. 10. Messina LM, Shanley CJ. Visceral artery aneurysms. Surg Clin North Am 1997;77:425–442.

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11. Carmeci C, McClenathan J. Visceral artery aneurysms as seen in a community hospital. Am J Surg 2000;179: 486–489. 12. Stanley JC, Thompson NW, Fry WJ. Splanchnic artery aneurysms. Arch Surg 1970;101:689. 13. Mattar SG, Lumsden AB. The management of splenic artery aneurysms: experience with 23 cases. Am J Surg 1995;169:580–584. 14. Brems JJ, Hiatt JR, Klein AS. Splenic artery aneurysm rupture following orthotopic liver transplantation. Transplantation 1988;45:1136–1137. 15. Ayalon A, Wiesner RH, et al. Splenic artery aneurysms in liver transplant patients. Transplantation 1988;45:386. 16. Puttini M, Aseni P, et al. Splenic artery aneurysms in portal hypertension. J Cardiovasc Surg 1982;23:490–493. 17. Hossain A, Reis ED, et al. Visceral artery aneurysms: experience in a tertiary-care center. American Surgeon 2001;67:432–437. 18. Bronsther O, Merhhav H, et al. Splenic artery aneurysms occurring in liver transplant patients. Transplantation 1991;52:723–724. 19. Pomerantz RA, Eckhauser FE, et al. Splenic aneurysm rupture in cirrhotic patients[letter]. Arch Surg 1986;121:2095. 20. Ohta M, Hashizume M, et al. Hemodynamic study of splenic artery aneurysm in portal hypertension. Hepatogastroenterology 1994;41:181 21. Boisjen E, Efsing HO. Aneurysm of the splenic artery. Acta Radiol(Stockh) 1969;8:29. 22. Spittel JA, Fairbairn JF, et al. Aneurysm of the splenic artery. J Am Med Assoc 1961;175:452. 23. Holdsworth RJ, Gunn A. Ruptured splenic artery aneurysm in pregnancy: a review. Br J Obstet Gynaecol 1992;99:595–597. 24. O’Grady JP, Day EJ, et al. Splenic artery aneurysm rupture in pregnancy: a review and case report. Obstet Gynecol 1977;50:627. 25. Kolmannskog F, Jakobsen JA, et al. Duplex doppler sonography and angiography in the evaluation of liver transplants. Acta Radiol 1994;35:1–5. 26. Hashizume M, Ohta M, et al. Laparoscopic ligation of splenic artery aneurysm. Surgery 1993;113:352–354. 27. McDermott VG, Shlansky-Goldberg R, Cope C. Endovascular management of splenic artery aneurysms and pseudoaneurysms. Cardiovasc Intervent Radiol 1994;17:179–184. 28. Salam TA, Lumsden AB, et al. Nonoperative management of visceral aneurysms and pseudoaneurysms. Am J Surg 1992;164:215–219. 29. Reidy JF, Rowe PH, Ellis FG. Splenic artery embolisation: the preferred technique to surgery. Clin Radiol 1990;41:281–282. 30. Guida PM, Moore SW. Aneurysms of the hepatic artery: report of five cases with a brief review of the previously reported cases. Surgery 1966;60:299–310. 31. Lumsden AB, Mattar SG, et al. Hepatic artery aneurysms: the management of 22 patients. J Surg Res 1996;60:345–350. 32. Shanley CJ, Shah NL, Messina LM. Common splanchnic artery aneurysms: splenic, hepatic and celiac. Ann Vasc Surg 1996;10(3):315–322. 33. Miani S, Arpesani A, et al. Splanchnic artery aneurysms. J Cardiovasc Surg 1993;34:221–228.

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34. Rokke O, Sondenaa K, , et al. Review: the diagnosis and management of splanchnic artery aneurysms. Scan J Gastroenterol 1996;31:737–743. 35. Dougherty MJ, Gloviczki P, et al. Hepatic artery aneurysms Int Angiol 1993;12:178–184. 36. Busuttil RW, Brin BJ. The diagnosis and management of visceral artery aneurysms. Surgery 1980;88:619–624. 37. Welling TH, Williams DM, Stanley JC. Excessive oral amphetamine use as a possible cause of renal and splanchnic arterial aneurysms: a report of two cases. J Vasc Surg 1998;28:727–731. 38. Tarazov PG, Polysalov VN, Ryzhkov VK. Transcatheter treatment of splenic artery aneurysms. J Cardiovasc Surg 1991;32:128–131. 39. Tarazov PG, Ryzhkov VK, et al. Extraorganic hepatic artery aneurysm: failure of transcatheter embolization. HPB Surgery 1998;11:55–60. 40. Noah EM, Psathakis D, et al. Perforated aneurysm of the left hepatic artery. Zentralbl Chir 1992;117:556–560. 41. Stouffer JT, Weinman MD, Bynum TE. Hemobilia in a patient with multiple artery aneurysms: a case report and review of the literature. Am J Gastroenter 1989;84:59. 42. Reber PU, Baer HU, et al. Superselective microcoil embolization: treatment of choice in high-risk patients with extrahepatic pseudoaneurysms of the hepatic arteries. J Am Coll Surg 1998;186(3):325–330. 43. Kasirajan K, Greenberg R, et al. Endovascular management of visceral artery aneurysm. J Endovasc Ther 2001;8:150–155. 44. Carr SC, Pearce WH, et al. Current management of visceral artery aneurysms. Surgery 1996;120:627–634. 45. Araoz PA, Andrews JC. Direct percutaneous embolization of visceral artery aneurysms: techniques and pitfalls. J Vasc Intervention Radiol 2000;11:1195–1200. 46. Mandel SR, Jaques PF, et al. Nonoperative management of peripancreatic arterial aneurysms: a 10-year experience. Ann Surg 1987;205:126–128. 47. Burger T, Halloul Z, et al. Emergency stent–graft repair of a ruptured hepatic artery secondary to local postoperative peritonitis. J Endovasc Ther 2000;7(4):324–327. 48. Kopatsis A, D’Anna JA, et al. Superior mesenteric artery aneurysm: 45 years later. Am Surg 1998;64:263–266.

49. Cormier F, Ferry J, et al. Dissecting aneurysms of the main trunk of the superior mesenteric artery. J Vasc Surg 1992;15:424–430. 50. Mitchell MB, McAnena OJ, Rutherford RB. Ruptured mesenteric artery aneurysm in a patient with alpha 1antititrypsin deficiency: etiologic implications. J Vasc Surg 1993;17:420–424. 51. Shanley CJ, Shah NL, Messina LM. Uncommon splanchnic artery aneurysms: pancreaticoduodenal, gastroduodenal, superior mesenteric, inferior mesenteric and colic. Ann Vasc Surg 1996;10(5):506–515. 52. DeBakey ME, Cooley DA. Successful resection of mycotic aneurysm of superior mesenteric artery. Am Surg 1953;19:202–212. 53. Tan BS, Reidy JF. Case report: transcatheter embolization of a superior mesenteric artery pseudoaneurysm with interlocking detachable coils. Clin Radiol 1998;53(6):455–457. 54. Bindman DJ, Rogoff PA, et al. Transcatheter embolization of a ruptured superior mesenteric aneurysm with Gianturco coils: a case report. Cardiovasc Intervent Radiol 1990;13:289–290. 55. Graham LM, Stanley JC, et al. Celiac artery aneurysms: historic (1745–1949) vs contemporary (1950–84) differences in etiology and clinical importance. J Vasc Surg 1985;2:757–764. 56. Baily RW, Riles TS, et al. Celiacomesenteric anomaly and aneurysm: clinical and etiologic features. J Vasc Surg 1991;14:229–234. 57. Risher WH, Hollier LH, et al. Celiac artery aneurysm. Ann Vasc Surg 1991;5:392–395. 58. Chiou AC, Josephs LG, Menzoian JO. Inferior pancreaticoduodenal artery aneurysms: report of a case and review of the literature. J Vasc Surg 1993;17: 784–789. 59. Iyomasa S, Matsuzaki Y, et al. Pancreaticoduodenal artery aneurysm: a case report and review of the literature. J Vasc Surg 1995;22:161–166. 60. Waltman AC, Luers PR, et al. Massive arterial hemorrhage in patients with pancreatitis: complementary roles of surgery and transcatheter occlusive techniques. Arch Surg 1986;121:439–443.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART X Upper Extremity Conditions

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 76 Vasospastic Diseases of the Upper Extremity Scott E. Musicant, Gregory L. Moneta, James M. Edwards, and Gregory J. Landry

Vasospastic diseases of the upper extremity encompass many distinct disease processes. Clinical manifestations of these conditions are varied and range from episodic digital vasospasm to severe hand and finger ischemia, occasionally progressing to gangrene. Symptoms of digital artery vasospasm occur in response to cold exposure or emotional stress. In the absence of fixed arterial obstruction, patients are generally asymptomatic between episodes. A small minority of patients with episodic digital vasospasm, when followed long term, eventually will develop diffuse palmar and digital arterial occlusions due to their underlying disease process. Only a tiny percentage of patients with Raynaud’s will have a surgically correctable disease. Palliative medical therapies are therefore the mainstay of treatment of upper extremity vasospastic disorders. In the Division of Vascular Surgery at Oregon Health & Science University we have been conducting a 30-year prospective evaluation of over 1300 patients with vasospastic and/or occlusive diseases of the upper extremity (1–3). The content of this chapter is based on analyses and observations made from this clinical database and will focus on the clinical presentation, pathophysiology, diagnosis, and management of vasospastic diseases of the upper extremity.

Raynaud’s Syndrome Raynaud’s syndrome (RS) is a common clinical condition which is characterized by episodic digital ischemia

secondary to cold exposure or emotional stimuli. The ischemia is due to vasospasm of the palmar and digital arteries. Raynaud’s syndrome is classified as either vasospastic or obstructive. Patients with vasospastic RS have vasospasm only and have normal arterial perfusion between episodes of vasospasm. Patients with obstructive RS have fixed arterial obstruction of small arteries in the hands and sometimes the feet as well. It is very uncommon to see patients with vasospastic RS present with ischemic ulceration of the digits. Virtually all patients with digital ulceration will have fixed palmar and digital arterial obstruction (4). Maurice Raynaud was the first to describe a group of 25 patients with digital ischemia which he attributed to digital artery vasospasm (5). Raynaud proposed that the pathophysiology was secondary to sympathetic overactivity. However, many of the patients he described had digital gangrene and therefore likely suffered from distal arterial occlusion and not simply vasospasm. Allen and Brown were the first to recognize that many patients with symptoms of episodic digital vasospasm have associated diseases. They recommended distinguishing patients with idiopathic Raynaud’s disease from those with Raynaud’s phenomenon in whom associated systemic disorders are present (6). Subsequently, many have examined the natural history of RS and have observed some patients who, at first, appear to have only isolated idiopathic Raynaud’s attacks but, over time, begin to show signs and symptoms of a systemic disease (7–9). It is our preference to classify patients according to whether their Raynaud’s symptoms are vasospastic only

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or also associated with an obstructive component. In this chapter we will refer to the disorder as Raynaud’s syndrome and specify whether the patient has primarily a vasospastic or obstructive component.

Epidemiology Epidemiologic data regarding the prevalence of Raynaud’s syndrome in the general population is probably inaccurate. The syndrome is probably underreported. Many patients with mild to moderate cold-induced symptoms likely do not seek medical treatment. Available data suggests a higher incidence in regions with lower mean annual temperatures. The prevalence of patients with symptoms of Raynaud’s syndrome in Spain was found to be 2.8% in men and 3.4% in women (10). Similarly, in Charleston, South Carolina, the prevalence of Raynaud’s symptoms in men was found to be 4.7% and in women 5.7% (11). In comparison, in Tarentaise, France, the prevalence was 20.1% in women and 13.5% in men. In Portland, Oregon, the prevalence in a randomly selected group of 150 individuals was 30% (4,11). Approximately 70% to 90% of patients presenting with symptoms of RS are women (12). Younger women are more likely to have vasospastic RS, however, RS has been linked to unopposed estrogen replacement therapy in postmenopausal women (13). Older men with symptoms of RS usually have digital arterial occlusive disease, often secondary to atherosclerosis or embolization from an atherosclerotic source. Occupational exposure to vibrating equipment has been shown to predispose workers to developing RS (14,15). Vibrating tools such as chain saws, jack hammers, pneumatic air knives, and mining tools when used frequently and for a prolonged period of time can cause symptoms of RS in over 50% of workers (14–16). The development of symptoms and the degree of arterial damage appear directly related to the frequency at which the tools operate (above a threshold frequency of 125 Hz) and to the total number of hours of use.

Pathophysiology The classic triphasic Raynaud’s attack initially manifests itself as an abrupt onset of digital pallor or blanching after cold exposure or emotional stress. This is followed by cyanosis and then rubor with rewarming. The typical length of a Raynaud’s attack is between 15 and 45 minutes. The initial blanching is likely due to spasm and closure of the digital arteries and arterioles, resulting in cessation of capillary blood flow. The patient may experience parasthesias or pain in conjunction with the pallor. After a variable period of time the capillaries, and likely the venules, will dilate in response to the relative hypoxia and resulting byproducts of anaerobic metabolism. After relaxation of the arterial spasm, a small amount of blood reenters the capillary bed and rapidly desaturates, causing the digits to be cyanotic. Increasing amounts of blood flow

into the dilated capillaries results in hyperemia and digital rubor. Finally, the capillaries constrict down to near normal diameter, the digital arterial perfusion returns to baseline, and the digits return to normal. Not all patients exhibit classic tricolor changes during a Raynaud’s attack. Some may have only pallor and cyanosis along with cold sensation. Some may not experience color change at all and have a heightened cold sensation or digital numbness as their only complaint. Because patients with the classic tricolor presentation have similar angiographic and hemodynamic abnormalities as those patients who experience no color change, the diagnosis of RS does not require classic findings of pallor followed by cyanosis and then rubor. Maurice Raynaud hypothesized in 1888 that the symptoms his patients experienced were caused simply by arterial vasospasm (5). It is, however, now clear that there is more involved in the pathophysiology of RS than just digital artery vasospasm. Normal individuals experience, to some degree or another, a vasospastic response to cold. Such individuals, however, do not experience the classic symptoms of RS. Patients with RS actually have a period of complete cessation of arterial flow into the digits. This is more pronounced if there is an element of preexisting arterial obstruction. Normal subjects, although experiencing vasospasm, will not have complete cessation of blood flow. It is imperative to understand the distinction between obstructive and vasospastic RS. In patients with obstructive RS, fixed obstruction of the digital and palmar arteries causes a decrease in the intraluminal distending pressure which, when coupled with a normal vasoconstrictive response to cold, results in complete arterial closure. The fixed obstructions can be due to many causes. The most common are atherosclerosis and arteritis associated with autoimmune connective tissue disorders (18). Patients who have vasospastic RS do not have arterial obstruction and have normal digital artery pressures and essentially normal digital perfusion at room temperature. Cold exposure produces a markedly exaggerated vasospastic force resulting in arterial closure. Krahenbuhl and associates measured digital artery pressures in patients with vasospastic RS after external finger cooling (19). They were able to show that, once a critical temperature of 28 ºC was reached, complete digital artery closure occurred and digital artery blood pressure was no longer measurable (Fig. 76.1). At one time, simple sympathetic nerve overactivity was thought to be responsible for the vasospastic responses seen in RS. Sir Thomas Lewis in the 1920s attempted to disprove this hypothesis (7). He demonstrated that blocking the digital nerves with a conduction anesthetic did not prevent digital artery vasospasm. He postulated a “local vascular fault” was responsible for the hyperreactivity to cold seen in patients with vasospastic RS. Newer evidence suggests alterations in adrenergic receptor activity are responsible for the vasospastic responses seen in patients suffering Raynaud’s attacks. Coffman

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TABLE 76.1 Diseases associated with Raynaud’s syndrome Autoimmune connective tissue diseases Scleroderma Rheumatoid arthritis Dermatomyositis Systemic lupus erythematosus Polymyositis Mixed connective tissue disease Sjogren’s syndrome Vasculitis induced by hepatitis B antigen Drug-induced vasculitis Undifferentiated connective tissue disease

FIGURE 76.1 Alterations in digital blood pressure with decreasing temperature. The top black curve depicts the normal decrease in finger pressure seen with decreasing finger temperature. The middle grey curve depicts the finger pressure in a patient with vasospastic Raynaud’s syndrome in response to decreasing temperature. The curve parallels normal until a critical temperature is reached, at which time there is an abrupt decrease in finger pressure, often to zero. The bottom dotted curve represent patients with obstructive Raynaud’s syndrome. The finger pressure starts off below normal, and the decrease parallels the normal curve unless there is a vasospastic component also (not shown).

and Cohen showed a decrease in nutrient blood flow in patients with RS as compared to controls and this was reversed after sympathetic blockade with reserpine (20). Rosch and associates also showed a decrease in digital artery spasm after intra-arterial infusion of reserpine in patients with vasospastic RS (21). The distinction between a1- and a2-adrenergic receptors has furthered understanding of the pathophysiology of vasospasm. a2-Adrenergic receptors are the predominant adrenergic receptors in the extremities and are responsible for peripheral resistance and peripheral vasospasm. Keenan and Porter showed circulating platelets of patients with vasospastic RS have significantly higher levels of a2-adrenergic receptors compared to both controls and patients with obstructive RS (22). Edwards et al. demonstrated that a2 receptor levels can be reduced in normal platelets if incubated with serum from patients with vasospastic RS (23). They hypothesized that the decrease in the levels of adrenoreceptors could be explained by circulating antireceptor antibodies which may constitute the primary pathophysiologic abnormality in Raynaud’s patients. Such antibodies, however, have yet to be identified directly. Endothelial cell contracting factors have also been implicated in the pathogenesis of RS. Endothelin, a 21amino-acid peptide, has a contractile effect on vascular tissue that in some (24,25), but not other (26) studies, is enhanced with cooling. Calcitonin gene-related peptide (CGRP) levels in cutaneous neurons are decreased in patients with RS, particularly those with scleroderma (27–29).

Obstructive arterial diseases Atherosclerosis Thromboangiitis obliterans Thoracic outlet syndrome Environmental conditions Vibration injury Frostbite injury Direct arterial trauma Drug-induced Raynaud’s syndrome without vasculitis Ergot Cytotoxic drugs Birth control pills Miscellaneous Vinyl chloride disease Chronic renal failure Cold agglutinins Cryoglobulinemia Neoplasm Neurologic disorders Central Peripheral Endocrinology disorders

Associated Diseases Many conditions are associated with RS (Table 76.1). Many of these disorders are associated with distal arterial obstruction. The presence of digital artery obstruction underlies digital ischemic ulceration. The evaluation of a patient with hand ischemia begins with interrogation for proximal arterial obstruction or a proximal embolic source. Emboli from a cardiac chamber source are too large to cause isolated digital artery obstruction. Emboli restricted to digital arteries tend to be smaller and composed of platelet aggregates. Once proximal lesions are excluded, a more focused investigation of potential autoimmune or connective tissue diseases should be undertaken. In our early experience as many as 70% of patients referred with RS had one of these associated diseases. More recently, patients are being referred with milder symptoms and presently only about 30% of patients with RS in our tertiary referral center are now found to have an associated disorder. The most frequent disorders associated with digital ischemic ulceration are the autoimmune connective tissue

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TABLE 76.2 Diagnostic evaluation of upper extremity ischemia Routine

In Selected Patients

Laboratory

Complete blood count Chemistry panel Sedimentation rate Urinalysis Immunology screen (Table 76.3)

Hypercoagulable screen Thyroid panel

Radiographic

Hand films

Chest films Arm/hand arteriography Barium swallow

Vascular laboratory

Finger plethysmography Digital hypothermic challenge test

Toe plethysmography Segmental arm pressures

Other

disorders. They typically manifest as progressive obstruction of small and medium-sized arteries of the hands. The most common association is with scleroderma or its CREST variant. Almost all patients with scleroderma will develop RS, and the symptoms may precede the diagnosis of scleroderma by many years (30). Buerger’s disease, or thromboangiitis obliterans, is another cause of distal arterial obstruction and ischemic gangrene. This condition typically occurs in young male cigarette smokers and involves segmental thrombotic occlusions of the distal arteries of the hands and feet. The term “hypersensitivity angiitis” has been applied to a group of patients who present with acute onset digital ischemia severe enough to cause ulceration or gangrene, but do not have a history of similar episodes or a history of vasospastic symptoms (31). These patients often have no serologic abnormalities on immunologic evaluation. Arteriography reveals digital arterial obstruction, which remains persistent over time despite the resolution of symptoms with conservative treatment. Long-term follow-up of these patients fails to elicit an immunologic or connective tissue disease etiology (31). Patients with digital arterial obstruction, with or without ulceration, who have a negative serologic workup should be evaluated for the presence of a malignancy. In such cases digital artery obstruction is thought to be due to either primary arterial thrombosis from a hypercoagulable state or an inflammatory arteritis (32,33).

Diagnosis Evaluation of a patient with suspected RS should begin with a history and physical examination that focuses on signs and symptoms of connective tissue diseases (arthritis, sclerodactyly, telangectasia, myalgia, skin rash, xerostomia, xeropthalmia, dysphagia, oropharyngeal ul-

Schirmer’s test Skin/mucosal biopsy Nerve conduction Electromyography

TABLE 76.3 Immunologic tests Essential

Antinuclear antibody Rheumatoid factor assay

Complete

Cryoglobulins Serum protein electrophoresis Cold agglutinins Anti double-stranded DNA antibody SSA SSB VDRL Hep-2 antinuclear antibody Extractable nuclear antigen Hepatitis panel

ceration, hand swelling, and cutaneous cutis). A history of coronary artery disease, cerebral vascular disease, vasculogenic claudication, or diminished peripheral pulses should initiate a workup for a possible atherosclerotic source. A distinction between digital vasospasm, carpal tunnel syndrome, or thoracic outlet syndrome must be made. A history of frostbite, use of vibratory tools, ingestion of ergot, or exposure to vinyl chloride or heavy metals should be elicited. Physical examination includes palpation of all pulses, bilateral brachial and wrist blood pressure determinations, as well as palpation for cervical ribs or evidence of clavicular abnormalities.

Laboratory Evaluation Tables 76.2 and 76.3 outline the routine and selective diagnostic, serologic and immunologic tests which should be employed when evaluating a patient with symptoms consistent with RS. Once a diagnosis of RS is made by the presence of cold-induced or emotionally induced digital ischemia, effort should be made to quantify the

Chapter 76 Vasospastic Diseases of the Upper Extremity

A

B

degree of ischemia and identify the presence of associated diseases. The baseline laboratory evaluation consists of a complete blood count to evaluate for anemia, which can exacerbate cold-induced vasospasm and is present in up to one-third of patients with scleroderma; a chemistry panel to screen for viral hepatitis; and a erythrocyte sedimentation rate which, if elevated, is a nonspecific indicator of inflammation and may indicate presence of arteritis. A positive serum rheumatoid factor assay or elevated antinuclear antibody (ANA) titer can screen for patients with rheumatoid arthritis, systemic lupus erythematosus, scleroderma, and mixed or undifferentiated connective tissue disease. Evaluation by a rheumatologist is indicated if a patient has either an elevated ANA titer or a positive serum rheumatoid factor assay. The rheumatologist can then determine which of the specialized tests listed in Table 76.3 to obtain.

Noninvasive Vascular Laboratory Evaluation Noninvasive vascular laboratory evaluation is useful in distinguishing between obstructive and vasospastic RS. Patients with symptomatic vasospasm who do not experience the classic tricolor changes and patients with obstructive RS who do not present with digital ulceration or gangrene may still have noninvasive vascular laboratory findings which confirm the diagnosis of RS. Patients with medicolegal or worker’s compensation claims need objective evidence of pathology and the establishment of a prognosis which can be accomplished by noninvasive methods. Patients with vasospastic RS may demonstrate a digital photoplethysmographic waveform characterized by a “peaked pulse.” This “peak” in the digital artery waveform occurs at the apex of the waveform or on the proximal portion of the systolic downstroke. A peaked pulse is present in up to 78% of patients with cold-induced vasospasm compared with only 3% of asymptomatic controls (34) (Fig. 76.2). Digital artery blood pressures are determined with finger pneumatic cuffs. Digital blood pressures and photoplethysmographic waveforms can be used to quantitate the degree of digital artery obstruction

C

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FIGURE 76.2 Photoplethysmographic digital artery waveforms objectively document arterial occlusive disease and diminish the need for angiography. (A) A normal tracing. (B) A tracing from a patient with vasospastic Raynaud’s syndrome demonstrating a peaked pulse. (C) A tracing from a patient with obstructive Raynaud’s syndrome.

(35). A digital blood pressure 20 to 30 mmHg lower than the brachial blood pressure is evidence for digital arterial obstruction. It must be kept in mind that digital artery pressures may be normal even in the presence of digital artery obstruction. This occurs when the cuff is placed proximally on the digit but the occlusion is located on the distal aspect of the phalanx or when only a single digital artery is occluded while the other artery is uninvolved. The ice water immersion test determines fingertip temperatures with a thermistor probe after the hand is immersed in ice water for 30 seconds. After drying the hand, fingertip pulp temperatures are measured every 5 min for 45 min or until the temperatures return to preimmersion level. The preimmersion temperature must be at least 30 ºC. The digital temperature of normal persons will return to baseline within 10 min (Fig. 76.3). This test has high specificity, but low sensitivity (36). This test is often difficult for patients to tolerate and is not widely utilized. The digital hypothermic challenge test described by Nielsen and Lassen quantifies decreases in finger blood pressure evoked by digital cooling (37). Patients are examined at a room temperature of 21 ºC. Local cooling is achieved by placing a double-inlet cuff over the proximal phalanx of the test finger (most often the right second digit). Baseline blood pressures are determined in the reference and a test finger distal to the occlusive cuff (Fig. 76.4). The test finger is then subjected to 5 min of ischemic hypothermic perfusion. After cooling, the tourniquet is released and digital blood pressure recovery is recorded. The results are expressed as the percentage of decrease in the systolic pressure of the cooled finger on reperfusion, as compared with pressure in the reference finger. A decrease in digital blood pressure of more than 20% in the cooled finger compared to the reference finger is diagnostic for RS. The “Nielsen” test has been shown to have a specificity of 80% and a sensitivity of 100%; it is 97% accurate in identifying patients with vasospastic RS (38). Other tests have been developed to detect RS such as thermal entrainment, venous occlusion plethysmography, and digital thermography (39,40). These tests may be useful, but do not appear to equal the accuracy of the Nielsen test.

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Part X Upper Extremity Conditions FIGURE 76.3 Digital temperature after ice water immersion. The normal curve is shown as a solid line, with recovery within 5 to 8 minutes. The dotted line represents temperature recovery in patients with Raynaud’s syndrome.

FIGURE 76.4 Setup for the Nielsen digital hypothermic challenge test. The double inlet cuff is around the test finger (right second digit), while the fourth digit serves as the reference finger.

Angiography In general, angiography in the evaluation of a patient with RS is most useful in identifying a surgically correctable condition that is flow limiting or serving as an embolic source. This is further discussed in Chapter 80 on arterial surgery of the upper extremity. Angiography is also useful in establishing whether the disease is bilateral in early cases of connective tissue disease. However, due to the accuracy and cost-effectiveness of vascular laboratory tests such as the Nielsen test, angiography is rarely required in patients with vasospastic RS. It is usually reserved for patients with either an abnormal pulse examination or unilateral symptoms of RS.

Treatment and Outcomes Vasospasm There is no known cure for Raynaud’s syndrome and therefore the goal of treatment is palliation of symptoms.

The natural history of the disease is usually benign. Most patients experience symptomatic periods alternating with periods of improvement. Often symptoms diminish or disappear with aging. Progression of the disorder to severe ischemia and gangrene is rare and, if present, virtually always signifies underlying digital artery occlusions. The avoidance of excessively cold temperatures and tobacco are important initial steps in controlling vasospastic symptoms. Drug therapy is of little value in treating patients with obstructive RS. There has been a paucity of level I, double-blind, placebo-controlled studies of pharmacotherapy for the treatment of vasospastic RS. Vasodilator therapy, particularly a-adrenergic blocking drugs, historically were the mainstay of attempted palliative treatment for RS. More recently calcium channel blockers have become the first-line therapy due to improved efficacy (41). Nifedipine extended release, 30 mg once daily during periods of increased symptoms, can be useful for some patients. Several controlled double-blind trial have shown significant improvement in both the frequency and severity of attacks in up to two-thirds of patients treated with nifedipine compared with placebo (41–43). Many patients, however, discontinue use of calcium channel blockers due to side effects such as lightheadedness, weakness, lethargy, and headaches. If patients are intolerant of calcium channel blocking agents, the next category of drug therapy is either angiotensin-converting enzyme inhibitors or angiotensin II receptor-blocking agents such as captopril or losartan (44–46). Pancera and colleagues showed significant improvement in the number and severity of vasospastic attacks with losartan compared with thromboxane A2 inhibition or placebo (45). A recent randomized, controlled trial showed a clinical benefit with losartan over nifedipine in the treatment of vasospastic RS (46). The addition of a-adrenergic blockers such as prazocin can sometimes further improve symptoms which are incompletely controlled by calcium channel blockers, but these reports are anecdotal (2). Other anecdotal evidence suggests that selective serotonin reuptake inhibitors may reduce the frequency and severity of vasospastic attacks (47).

Chapter 76 Vasospastic Diseases of the Upper Extremity

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FIGURE 76.5 Ischemic digital ulcer in a patient with scleroderma. Total healing was achieved using the conservative treatment regimen outlined.

The oral prostaglandin analogs prostaglandin E (PGE1) and prostaglandin I2 (prostacyclin) are platelet aggregation inhibitors and potent arterial vasodilators. Anecdotal studies suggest moderate symptomatic improvement in patients with digital ulceration, but a randomized double-blind trial showed no benefit (48,49). Sympathetic blockers such as reserpine, given as an intra-arterial infusion, had shown promise in relieving vasospasm as evidenced by both symptomatic and angiographic improvement; however, there were significant side effects from the drug and it has since been withdrawn from the market (50). Oral reserpine is not effective in the treatment of RS.

Digital Ulceration and Gangrene Most patients with digital gangrene and RS do not have surgically correctable lesions. As noted above, the digital lesions arise from occlusive disease distal to the wrist in patients with scleroderma, Buerger’s disease, and CREST syndrome, for example. The management of ischemic ulceration and gangrene in patients with occlusive RS therefore primarily centers on local ulcer care and selected digital amputation. Simple soap and water scrubs, conservative local debridement, and/or amputation of nonviable tissue and culture-specific antibiotics for obvious cellulitis comprise the basis for management of digital gangrene (Fig. 76.5). It is important to adhere to the principle of length conservation in digital amputation to allow for optimal hand function after healing. Pentoxifylline, a hemorrheologic agent, which decreases blood viscosity and may also provide a relaxing effect on vascular smooth muscle, may be effective in promoting healing, although controlled trials have yet to be done. Appropriate therapy for the associated diseases leading to finger gangrene or ulceration must also be ad-

ministered under the supervision of specialists in rheumatology or immunology (51,52).

Surgical Treatment There are limited surgical options for treating digital artery vasospasm. Surgical management of vasospastic RS has historically focused on surgical sympathectomy for the control of symptoms. Lumbar sympathectomy for lower extremity vasospastic disease has been shown to produce long-term benefit (53). In contrast, cervicothoracic sympathectomy has frequently been performed in an attempt to control upper extremity vasospasm. Symptomatic improvement can be achieved; however, the benefits are short-lived (54,55). The rate of symptomatic recurrence is high and it is not clear whether this is due to incomplete sympathectomy, receptor hypersensitivity, or possibly sympathetic nerve regeneration. Cervical sympathectomy is not currently recommended for treatment of upper extremity RS whether it be primarily obstructive or vasospastic. More recently investigators have attempted local or periarterial sympathectomy as an alternative to cervical sympathectomy. The adventitial tissue from distal digital arteries is stripped and the terminal sympathetic nerve branches are divided with microscopic assistance (56). This has been reported to lower recurrence of Raynaud’s symptoms; however, these reports are anecdotal and still lack support by prospective controlled trials (57).

Summary RS manifests as episodic digital vasospasm produced by cold exposure or emotional stimulation. The classic tricolor changes are seen in many, but not all, patients with

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vasospastic RS. The disorder affects a significant proportion of the population, with the majority of patients being women. Vasospastic RS is likely caused by excessive vascular smooth muscle contractions, whereas obstructive RS is often associated with an autoimmune or connective tissue disease which produces palmar or digital artery occlusion. The natural history of vasospastic RS is intermittent symptomatic episodes interspersed with periods of remission. For the majority of patients vasospastic RS is a nuisance condition. Progression to digital ulceration or gangrene requiring amputation in patients with vasospastic RS is rare. Positive serologic tests can help predict which patients have an associated autoimmune or connective tissue disease, and are more likely to have progression of symptoms. There is no cure for RS. Management consists of attempts at symptomatic control as well as smoking cessation. Vasodilating agents such as calcium channel blocking agents, a-adrenergic blockers, or ACE inhibitors provide relief of symptoms in about 50% of patients. There is no long-term benefit of surgical sympathectomy for upper extremity vasospastic disease.

References 1. Landry GJ, Edwards JM, et al. Long-term outcome of Raynaud’s syndrome in a prospectively analyzed patient cohort. J Vasc Surg 1996;23:76–85; discussion 85–86. 2. Landry GJ, Edwards JM, Porter JM. Current management of Raynaud’s syndrome. Adv Surg 1996;30:333–347. 3. McLafferty RB, Edwards JM, et al. Diagnosis and longterm clinical outcome in patients diagnosed with hand ischemia. J Vasc Surg 1995;22:361–367; discussion 367–369. 4. Porter JM, Bardana EJ, Jr., et al. The clinical significance of Raynaud’s syndrome. Surgery 1976;80:756–764. 5. Raynaud M. On local asphyxia and symmetrical gangrene of the extremities. Selected Monographs. London: New Sydenham Society, 1888. 6. Allen E. Raynaud’s disease: a review of minimal requisites for diagnosis. Am J Med Sci 1932;83:187–200. 7. Lewis TP. Observations upon maladies in which the blood supply to the digits ceases intermittently or permanently and upon bilateral gangrene of the digits: observations relevant to so-called Raynaud’s disease. Clin Sci 1934;1:327–366. 8. de Takats G, Fowler, EF. Raynaud’s phenomenon. J Am Med Assoc 1962;179:99. 9. Gifford RJ, Hines EJ. Raynaud’s disease among women and girls. Circulation 1957;16:1012–1021. 10. Roman Ivorra JA, Gonzalvez Perales JL, et al. Prevalence of Raynaud’s phenomenon in general practice in the east of Spain. Clin Rheumatol 2001;20:88–90. 11. Maricq HR, Carpentier PH, et al. Geographic variation in the prevalence of Raynaud’s phenomenon: Charleston, SC, USA, vs Tarentaise, Savoie, France. J Rheumatol 1993;20:70–76.

12. Porter JM, Edwards JM. Occlusive and Vasospastic Diseases Involving the Distal Upper Extremity Arteries — Raynaud’s Syndrome. In: Rutherford RB, ed. Vascular Surgery. Philadelphia: WB Saunders, 2000:1170–1183. 13. Wigley FM. Raynaud’s phenomenon is linked to unopposed estrogen replacement therapy in postmenopausal women. Clin Exp Rheumatol 2001; 19:10–11. 14. Taylor W, Pelmear PL. Raynaud’s phenomenon of occupational origin: an epidemiological survey. Acta Chir Scand Suppl 1976;465:27–32. 15. McLafferty RB, Edwards JM, et al. Raynaud’s syndrome in workers who use vibrating pneumatic air knives. J Vasc Surg 1999;30:1–7. 16. Taylor W. The hand–arm vibration syndrome — diagnosis, assessment and objective tests: a review. J R Soc Med 1993;86:101–103. 17. Mackiewicz Z, Piskorz A. Raynaud’s phenomenon following long-term repeated action of great differences of temperature. J Cardiovasc Surg (Torino) 1977;18:151–154. 18. Cupps T, Fauci A. The Vasculitides. Philadelphia: WB Saunders, 1981:116–118. 19. Krahenbuhl B, Nielsen SL, Lassen NA. Closure of digital arteries in high vascular tone states as demonstrated by measurement of systolic blood pressure in the fingers. Scand J Clin Lab Invest 1977;37:71–76. 20. Coffman JD, Cohen AS. Total and capillary fingertip blood flow in Raynaud’s phenomenon. N Engl J Med 1971;285:259–263. 21. Rosch J, Porter JM, Gralino BJ. Cryodynamic hand angiography in the diagnosis and management of Raynaud’s syndrome. Circulation 1977;55:807–814. 22. Keenan EJ, Porter JM. Alpha-adrenergic receptors in platelets from patients with Raynaud’s syndrome. Surgery 1983;94:204–209. 23. Edwards JM, Phinney ES, et al. Alpha 2-adrenergic receptor levels in obstructive and spastic Raynaud’s syndrome. J Vasc Surg 1987;5:38–45. 24. Zamora MR, O’Brien RF, et al. Serum endothelin-1 concentrations and cold provocation in primary Raynaud’s phenomenon. Lancet 1990;336:1144–1147. 25. Fyhrquist F, Saijonmaa O, et al. Raised plasma endothelin-I concentration following cold pressor test. Biochem Biophys Res Commun 1990;169:217–221. 26. Harker C, Edwards J, et al. Plasma endothelin-1 concentration during cold exposure. Lancet 1991;337:1104–1105. 27. Shawket S, Dickerson C, et al. Prolonged effect of CGRP in Raynaud’s patients: a double-blind randomised comparison with prostacyclin. Br J Clin Pharmacol 1991;32:209–213. 28. Bunker CB, Terenghi G, et al. Deficiency of calcitonin gene-related peptide in Raynaud’s phenomenon. Lancet 1990;336:1530–1533. 29. Turton EP, Kent PJ, Kester RC. The aetiology of Raynaud’s phenomenon. Cardiovascular Surgery 1998;6:431–440. 30. Dabich L, Bookstein JJ, et al. Digital arteries in patients with scleroderma: arteriographic and plethysmographic study. Arch Intern Med 1972;130:708–714. 31. Baur GM, Porter JM, et al. Rapid onset of hand ischemia of unknown etiology: clinical evaluation and follow-up of ten patients. Ann Surg 1977;186:184–189.

Chapter 76 Vasospastic Diseases of the Upper Extremity 32. Taylor LM, Jr., Hauty MG, et al. Digital ischemia as a manifestation of malignancy. Ann Surg 1987;206:62–68. 33. Paw P, Dharan SM, Sackier JM. Digital ischemia and occult malignancy. Int J Colorectal Dis 1996;11:196–197. 34. Sumner DS, Strandness DE, Jr. An abnormal finger pulse associated with cold sensitivity. Ann Surg 1972;175:294–298. 35. Holmgren K, Baur G, Porter J. Vascular laboratory evaluation of Raynaud’s syndrome. Bruit 1981;5:19–22. 36. Porter JM, Snider RL, et al. The diagnosis and treatment of Raynaud’s phenomenon. Surgery 1975;77:11–23. 37. Nielsen SL, Lassen NA. Measurement of digital blood pressure after local cooling. J Appl Physiol 1977;43:907–910. 38. Gates K, Tyburczy J, et al. The non-invasive quantification of digital vasospasm. Bruit 1984;8:34. 39. Lafferty K, de Trafford J, et al. Raynaud’s phenomenon and thermal entrainment: an objective test. Br Med J 1983;286:90–92. 40. Chucker F, Fowler RC, et al. Induced temperature gradients in Raynaud’s disease measured by thermography. Angiology 1971;22:580–593. 41. Corbin DO, Wood DA, et al. A randomized double-blind cross-over trial of nifedipine in the treatment of primary Raynaud’s phenomenon. Eur Heart J 1986;7:165–170. 42. Gjorup T, Kelbaek H, et al. Controlled double-blind trial of the clinical effect of nifedipine in the treatment of idiopathic Raynaud’s phenomenon. Am Heart J 1986;111:742–745. 43. Smith C, McKendry R. Controlled trial of nifedipine in the treatment of Raynaud’s phenomenon. Lancet 1982;2:1299. 44. Madsen JL, Hvidt S. Raynaud’s disease treated with captopril (Capoten): a randomized double-blind cross-over study. Ugeskr Laeger 1984;146:2695–2697. 45. Pancera P, Sansone S, et al. The effects of thromboxane A2 inhibition (picotamide) and angiotensin II receptor blockade (losartan) in primary Raynaud’s phenomenon. J Intern Med 1997;242:373–376.

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46. Dziadzio M, Denton CP, et al. Losartan therapy for Raynaud’s phenomenon and scleroderma: clinical and biochemical findings in a fifteen-week, randomized, parallel-group, controlled trial. Arthritis & Rheumatism 1999;42:2646–2655. 47. Coleiro B, Marshall SE, et al. Treatment of Raynaud’s phenomenon with the selective serotonin reuptake inhibitor fluoxetine. Rheumatology (Oxford) 2001;40:1038–1043. 48. Belch JJ, Capell HA, et al. Oral iloprost as a treatment for Raynaud’s syndrome: a double blind multicentre placebo controlled study. Ann Rheum Dis 1995;54:197– 200. 49. Mohrland JS, Porter JM, et al. A multiclinic, placebocontrolled, double-blind study of prostaglandin E1 in Raynaud’s syndrome. Ann Rheum Dis 1985;44:754–760. 50. Nobin BA, Nielsen SL, et al. Reserpine treatment of Raynaud’s disease. Ann Surg 1978;187:12–16. 51. Block JA, Sequeira W. Raynaud’s phenomenon. Lancet 2001;357:2042–2048. 52. Isenberg DA, Black C. ABC of rheumatology: Raynaud’s phenomenon, scleroderma, and overlap syndromes. Br Med J 1995;310:795–798. 53. Janoff KA, Phinney ES, Porter JM. Lumbar sympathectomy for lower extremity vasospasm. Am J Surg 1985;150:147–152. 54. Gifford RJ, Hines EJ, Craig W. Sympathectomy for Raynaud’s phenomenon: follow-up study of 70 women with Raynaud’s disease and 54 women with secondary Raynaud’s phenomenon. Circulation 1958;17:5. 55. Hall K, Hillestad L. Raynaud’s phenomenon treated with sympathectomy: a follow-up study of 28 patients. Angiology 1960;11:186. 56. Flatt AE. Digital artery sympathectomy. J Hand Surg [Am] 1980;5:550–556. 57. el-Gammal T, Blair W. Digital periarterial sympathectomy for ischaemic digital pain and ulcers. Hand Surgery 1991;16:382.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 77 Neurogenic Thoracic Outlet Syndrome Richard J. Sanders and Michael A. Cooper

Thoracic outlet syndrome (TOS) is defined as upper extremity symptoms due to compression of the neurovascular bundle in the supraclavicular area. First used in 1956, TOS is a general term that encompasses a large number of syndromes which can involve the brachial plexus, subclavian artery, or subclavian vein. The term TOS has replaced names that describe specific causes for neurovascular compression, such as scalenus anticus, scalenus medius, cervical rib, or first rib syndrome, to name just a few (1,2).

The last period began in 1956 with the introduction of the term TOS. This era begins with emphasis on the normal first rib as the common denominator in treating TOS. This modern era includes several approaches to removing the first rib, total anterior and middle scalenectomy, angiography, neuroelectric physiologic testing, and recognition of microscopic abnormalities in the scalene muscles of patients with TOS (see Table 77.1).

Anatomy Historical Background Historically, TOS was originally thought to be caused by subclavian artery occlusion brought on by a congenital cervical rib. Over the past 100 years, this view has changed. Currently, most cases of TOS are neurogenic rather than vascular and are caused by brachial plexus compression from injured scalene muscles. Among our patients fewer than 5% have cervical ribs. Development of current theories regarding TOS follows three arbitrary time periods. The cervical rib period, from 1740 to 1920, saw the introduction of knowledge regarding cervical ribs, subclavian artery aneurysms, and the description of loss of the radial pulse with the arm held in certain positions (3) (Table 77.1). The second period, 1920 to 1956, recognized the cervical rib syndrome in a variety of instances in which there was no cervical rib. The new etiologic factors included rudimentary first ribs, congenital ligaments and bands, middle scalene muscle variations, and scalene minimus muscles.

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The nerves, artery, and vein to the upper extremity pass from the chest and neck to the arm by traveling through a long tunnel whose walls are muscles, bones, and ligaments. Any number of abnormalities can occur in the walls of the tunnel and will cause narrowing of the neurovascular space, resulting in symptoms. There are three distinct anatomic spaces within the thoracic outlet area: the scalene triangle, the costoclavicular space, and the pectoralis minor space. Compression in the scalene triangle is the commonest form of TOS; costoclavicular compression is seldom seen, and pectoralis minor compression is also rare (Fig. 77.1).

Comparison of Neurogenic, Arterial, and Venous Thoracic Outlet Syndromes The three types of TOS have major differences that usually make them easy to differentiate. The only symptom

Chapter 77 Neurogenic Thoracic Outlet Syndrome

common to the three is arm pain. Neurogenic TOS is distinguished by paresthesia, neck pain, and headaches; venous TOS by swelling and cyanosis; and arterial TOS by ischemic hand symptoms. The etiology, treatment, and TABLE 77.1 Three historical periods in the development of thoracic outlet syndrome Period 1: cervical rib, 1740–1927 Anatomy: Galen, Vesalius, Hunauld, 1749; Gruber, 1842 Embryology: Todd, 1912; Jones, 1913 Clinical description: Cooper, 1821 Surgical resection: Coote, 1861 Physiology of subclavian artery stenosis and aneurysms: Halsted, 1916 Period 2: cervical rib syndrome without cervical rib, 1920–1956 Congenital bands and ligaments: Law, 1920 Scalenus anticus syndrome: Adson, 1927 Costoclavicular syndrome: Eden, 1939; Falconer, 1943 Normal first rib: Bramwell, 1903; Murphy, 1910 Abnormal first rib: Keen, 1907 Middle scalene muscle variations: Stiles, 1929 Pectoralis minor syndrome: Wright, 1945 Period 3: Modern era of thoracic outlet syndrome, first-rib resection, 1956–present The name, TOS: Peet, 1956; Rob, 1958 Approaches to first rib: posterior, Clagett, 1962; transaxillary, Roos, 1966; infraclavicular, Gol, 1968 Histochemical microscopy: fiber change, Machleder, 1986; increased connective tissue, Sanders, 1990 Anterior and middle scalenectomy: Sanders, 1979

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incidence also differ for each and are summarized in Table 77.2. These will be more fully discussed in this and the next two chapters. The term TOS indicates compression in the supraclavicular area. Used alone, the term TOS implies neurogenic TOS. When dealing with a vascular form of TOS, it should be labeled arterial TOS or venous TOS.

Etiology Neurogenic TOS is usually caused by a combination of two factors: 1. 2.

anatomic narrowing of the space around the brachial plexus; and some type of trauma that precipitates symptoms.

This theory is based on a history of neck trauma in more than 80% of several hundred patients with a diagnosis of neurogenic TOS (Table 77.3), as well as observations in the operating room of a variety of anatomic variations and anomalies of the scalene muscles (4–9).

Anatomic Predisposition Several anatomic structures can narrow the scalene triangle or costoclavicular space, predisposing the patient to develop neurogenic TOS. Cervical ribs, rudimentary first ribs, and fractures of the clavicle or first rib are the easiest

FIGURE 77.1 Anatomy of the thoracic outlet area showing all spaces. (Reproduced by permission from Sanders RJ, Haug CE. Thoracic outlet syndrome: a common sequella of neck Injuries. Philadelphia: JB Lippincott, 1991.)

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TABLE 77.2 Differences between three types of thoracic outlet syndromes Type Neurogenic TOS

Incidence 97%

Commonest Etiology

Symptoms

Diagnosis

Treatment

Neck trauma plus anatomic predisposition

Hand paresthesia, headache, neck pain, arm pain

History, often trauma; phys. exam, scalene tender and symptoms at 90° AER

Excise scalene muscles and/or first-rib resection

Venous TOS

2%

Narrow costoclavicular space plus arm trauma

Swelling, cyanosis, arm pain

Dynamic venogram

Dissolve/remove clot; divide costoclavicular ligament, resect first rib; enlarge or bypass vein

Arterial TOS

1%

Cervical or rudimentary first rib

Ischemic fingers, arm claudication, arm pain

Plain x-ray; arteriogram

Excise abnormal rib, repair or replace artery; thromboembolectomy; dorsal sympathectomy

TABLE 77.3 Etiology of neurogenic thoracic outlet syndrome in 492 patients operated on between 1982 and 1992 Trauma Rear-end auto accident Side or front auto accident Specific neck injuries at work Repetitive activity at work, no specific injury Other neck trauma Cervical or rudimentary first rib (without trauma) Axillary/subclavian vein occlusion Subclavian artery insufficiency No obvious etiology, no trauma history

90% 26% 24% 5% 21% 14% 2% 1% 1% 6% 100%

to recognize because they are visualized radiographically. The ratio of females to males for abnormal first ribs is 50 : 50, whereas for cervical ribs the ratio is 70 : 30 (10). It is unknown why cervical ribs occur twice as frequently in women as in men. The large majority of people with extra or abnormal ribs go through life without symptoms from their osseous abnormalities. It has been estimated that only 12% ever become symptomatic (11). Although the incidence of cervical and rudimentary first ribs is only 0.3% of the population (10), in the authors’ experience, 4.5% of patients undergoing surgery for neurogenic TOS have bony abnormalities. Thus, the presence of extra or anomalous ribs appears to be a predisposition to develop TOS. Why do patients with cervical ribs develop symptoms at all? One explanation is neck trauma. In reviewing the onset of symptoms in patients with cervical ribs, most in our series had a history of neck trauma immediately before the onset of symptoms (12). Thus, the presence of a bony abnormality narrowing the scalene triangle may predispose a person to develop TOS; but symptoms usually do not develop unless there is a precipitating event, specifically neck trauma.

Several investigators have recorded muscle and ligament variations and anomalies in the scalene triangle. These include anterior scalene muscles splitting around the C5 and C6 nerve roots; interdigitating muscle fibers between anterior and middle scalene muscles; scalenus minimus muscles covering C8 and T1 nerve roots; and a variety of thickened bands of fascia and dense ligaments lying against one or more of the nerves (4–9,13). Although it has been assumed that these anatomic variations are responsible for TOS symptoms, this has yet to be fully proved. These anatomic variations have also been seen in many cadaver dissections. Further studies are needed to prove cause and effect. Perhaps the most significant anatomic variation is the width of the interscalene space as measured at the first rib. The distance between anterior and middle scalene muscles varies from 0.3 to over 2.3 cm (4). Clinical observations in the operating room have shown that more than 80% of TOS patients have narrow scalene triangles (7) (Fig. 77.2).

Trauma Hyperextension neck injuries (whiplash) are the most frequent type of neck trauma reported (see Table 77.3). Rear-end collisions are the most common cause, but many head-on and lateral accidents are reported as well. Although many patients do not recall what occurred in their motor vehicle accident, those that do can usually report that their necks were forced forward and backward. Other types of accidents that cause hyperextension neck injuries include slipping on ice, falling off ladders, or being hit in the head or arm while at work. The second most common group of injuries are work related. They occur in workers whose hands are engaged on a keyboard or assembly line. The etiology of TOS in these patients is obscure but it is presumed that quick twists of the neck frequently occur because of an inability to release the hands in order to turn the body. Holding a

Chapter 77 Neurogenic Thoracic Outlet Syndrome

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B A FIGURE 77.2 Variations in the relations within the scalene triangle. (A) The usual relation found in most cadavers. The triangle is wider and the nerves emerge a little lower in the triangle than in most patients with TOS. (B) The nerve emerge high in the triangle, touching the scalene muscles as they emerge. (Reproduced by permission from Sanders RJ, Roos DB. The surgical anatomy of the scalene triangle. Contemp Surg 1989;35:11–16.)

telephone by squeezing it between head and shoulder while continuing to use one’s hands is another way to stretch neck muscles. These activities may result in repeated small trauma to the scalene muscles that eventually leads to scarring and spasm of the muscles.

later. It is the responsibility of the examiner to probe deeply on interview to elicit this history. In a minority of patients, there is no history of trauma and no obvious osseous abnormality. A diagnosis of TOS may still be made in these patients if the symptoms and physical findings are appropriate.

Histopathology of Scalene Muscles Microscopic examination of the scalene muscles of patients with TOS reveals significant histochemical changes that are not observed in control patients. Type 1 fiber predominance and type 2 fiber atrophy and pleomorphism are common findings, but these are nonspecific changes that are seen in a variety of myopathies (14). However, a unique finding in patients with TOS has been the consistent observation of increased connective tissue (scar tissue) in all studied patients. In 45 TOS patients the scalene muscles had an average connective tissue content of 36% compared with only 14% in control patients, a difference that was highly significant (15).

Clinical Manifestations History Many patients give a history of trauma prior to the onset of symptoms. Some patients have sustained injuries but have forgotten them or do not relate them to their symptoms. It is not unusual for a patient to recall a neck injury during the middle of the examination, or even several days

Symptoms The typical symptoms of TOS are paresthesia or numbness and tingling in the hand, weakness of the hand and arm, and pain involving the upper extremity, head, and neck. Headaches are specifically in the occiput. Headaches in the parietal and frontal regions are probably not due to TOS although the occipital headaches of TOS can radiate forward. Pain in the neck, shoulder, axilla, arm, forearm, hand, and anterior chest wall are characteristic of TOS. Pain in the dorsal spine and over the trapezius muscles is commonly seen in TOS patients, but these complaints may be due to other diagnoses. Pain in the jaw or side of face is not typical of TOS, but more likely to be temporomandibular joint (TM) dysfunction. Numbness and tingling most frequently involve the fingers, but in some cases can involve the hand, forearm, and even the upper arm. Although most texts typically describe TOS as involving the fourth and fifth fingers (ulnar nerve distribution), the most common involvement in our patients has been all five fingers (median and ulnar nerves). Many patients with involvement of all five fingers state that the symptoms are worse in the fourth and fifth fingers. During history-taking they often do not mention

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involvement of the first three fingers unless specifically asked. This may explain the differences reported by different investigators. Arm and hand weakness is common in most patients. Dropping things, such as coffee cups, is frequent. Coldness in the hand is a common complaint, while color changes are less common. These symptoms are usually from irritation of sympathetic nerve fibers that run with the lower nerves of the brachial plexus. They represent neurogenic, not vascular, symptoms. True Raynaud’s disease (pain, color changes, coldness, hyperhidrosis, and hyperesthesia) is seldom seen. The anatomic explanation for “Raynaud’s type symptoms” in patients with neurogenic TOS is the accompaniment of sympathetic nerve fibers to the hand with the C7 and C8 nerve roots. Compression of these roots also stimulates these sympathetic nerves and increases sympathetic activity. Symptoms are often intermittent but in severe cases may be constant. They tend to occur or be aggravated by elevating the arms to comb one’s hair or drive a car. In many patients, using the arms for household chores, particularly heavy work like vacuuming and window washing, results in symptoms later that day or evening. Differentiating upper plexus from lower plexus symptoms is sometimes possible, but in most patients, the symptoms are a combination of upper and lower plexus compression. We have not relied on differentiating upper and lower plexus symptoms to help decide the type of operation to be performed when surgery is indicated.

FIGURE 77.3 Point of tenderness over scalene muscles.

Physical Examination Supraclavicular tenderness over the scalene muscles (2.5 cm above the clavicle and 2.5 cm lateral to the midline) is present in more than 90% of TOS patients. Absence of this finding should make one question the diagnosis. Pressure for 20 to 30 seconds in the same area, which is directly over the brachial plexus, usually elicits pain or paresthesia in the arm or hand. Tinel’s sign in the same spot is often positive as well. In patients with unilateral symptoms, the presence of these findings on the symptomatic side and their absence on the contralateral side is a helpful diagnostic sign (Fig. 77.3). Duplication of symptoms with the arms in the 90° abduction external rotation (AER) or “stick-em-up” position is the other physical finding that is present in more than 90% of patients (Fig. 77.4). The arms are held in this position for 3 minutes. Although some examiners have patients open and close their fingers, this activity is not necessary. Position alone will elicit symptoms in those with neurogenic TOS. Radial pulses may or may not disappear with the arms in the 90° AER position. This has been called the modified Adson’s test. At one time, positional loss of radial pulses was regarded as the definitive diagnostic sign of TOS. However, more than one study has revealed that many normal subjects cut off their pulses with their arms in elevated positions (4,16,17). Further, most

FIGURE 77.4 The 90° abduction external rotation (AER) position.

patients with neurogenic TOS do not cut off their pulses. Therefore positional pulse loss is no longer regarded as a significant sign in establishing or ruling out this diagnosis. Pain in the contralateral neck when tilting or rotating the head to the side is commonly seen in patients with TOS. This is also seen in patients with cervical spine strain and cervical disc disease, but in those conditions, the pain is usually on the ipsilateral side. Tenderness over the rotator cuff and biceps tendons of the shoulders are commonly seen in TOS patients. The ability to abduct both arms to 180° is important. Failure to reach 180° is abnormal and usually indicates shoulder tendinitis, impingement syndromes, tendon tears, or frozen shoulder. However, in some instances, shoulder tenderness is due to brachial

Chapter 77 Neurogenic Thoracic Outlet Syndrome

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FIGURE 77.5 (A) MRI of neck indicating mild disc degeneration with minimal compression of cervical spine at C2–3, C4–5, C5–6, and C7–8. (B) MRI in normal patient.

A

B

plexus compression. This may be detected by the scalene muscle block described below. The hands should be examined in TOS patients for signs of carpal tunnel syndrome. If Tinel’s or Phelan’s sign is positive, carpal tunnel syndrome should be considered in the differential diagnosis or as an associated diagnosis. Neurologic examination of the upper extremities is often normal. Reduced sensation to light touch on the involved side is the most frequent neurologic finding. In rare cases (under 1%), muscle wasting of the thenar muscles is present and is usually associated with weakness of other intrinsic hand muscles (18). The upper limb tension test, similar to straight leg raising in the lower extremity, is usually positive in TOS patients (19).

Diagnostic Tests Neurophysiologic Tests Electromyography, nerve conduction velocities, somatosensory evoked potentials, F-waves, cervical root stimulation, and other neuroelectric tests are useful for the diagnoses of other compression syndromes such as carpal and cubital tunnel syndromes. Most patients with neurogenic TOS have normal results on electrophysiologic studies; when they are abnormal, the changes are usually nonspecific. However, if there is muscle wasting and significant weakness, ulnar sensory action potentials show a characteristic reduction in amplitude without a comparable change in velocity. While studies of nerve

conduction velocity and somatosensory-evoked potential have been reported to be of value in TOS by some investigators (20–22), their findings have not gained popularity (23).

Imaging Cervical spine and chest x-rays detect cervical ribs, abnormal first ribs, and the callous of healed clavicular and firstrib fractures. Cervical arthritis and degenerative cervical spine disease will also show changes on radiographic films. The availability of magnetic resonance imaging (MRI) has made detection of cervical disc disease with spinal cord and nerve root compression much easier (Fig. 77.5).

Scalene Muscle Block The scalene muscle block has proved to be the most helpful diagnostic test for neurogenic TOS. With the patient sitting or recumbent and the neck hyperextended, 4 ml of 1% procaine is infiltrated throughout the belly of the anterior scalene muscle, which is located by palpation (10,24). A good block is recognized by loss of tenderness over the scalene muscle. Following the block, physical examination is repeated to determine if there is improvement in neck motion, head tilt, abduction of the arm to 180°, 90° AER, and reduced tenderness over the trapezius muscle and shoulder tendons. In addition, if patients had headaches or hand paresthesia at rest before the block, they are asked if the headache and hand symptoms have disappeared. A positive test is improvement in most

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physical findings and symptoms at rest. There is good correlation between response to the block and response to operation (10,25).

with both shoulder tendinitis and TOS, once the shoulder has been treated the TOS component may improve with conservative, nonoperative therapy.

Cervical Spine Disease

Differential and Associated Diagnoses Symptoms of pain and paresthesia in the upper extremity are common to a variety of musculoskeletal disorders. These conditions may mimic TOS and must be differentiated from it, or they may coexist with TOS and be regarded as associated diagnoses. The term “double crush syndrome” refers to two entrapment syndromes, usually TOS and carpal tunnel syndrome, which exist together (26,27). When two conditions coexist, each is treated separately.

Carpal and Cubital Tunnel Syndromes Carpal tunnel syndrome presents with pain and paresthesia in the fingers and hand. The pathology is entrapment of the median nerve at the wrist with symptoms in the first three fingers. However, many patients have ulnar nerve compression too so that all five fingers experience pain and paresthesia. Carpal tunnel syndrome tends to be job related, occurring in persons who use their hands a lot for repetitive activities such as typing, data entry, or assembly-line work. It can cause pain and paresthesia in the forearm, but seldom higher than this. Pain in the shoulder and neck is seldom from carpal tunnel syndrome. Not uncommonly, carpal tunnel and thoracic outlet syndromes coexist as “double crush syndrome” and both must be treated. Cubital tunnel syndrome is ulnar nerve compression or irritation at the elbow. It causes pain in the elbow with radiation into the ulnar forearm and last two fingers of the hand. Like carpal tunnel syndrome, it can occur alone or in association with TOS or carpal tunnel syndrome. The existence of the three conditions together has sometimes been referred to as “triple crush syndrome.”

Cervical disk strains, sprains, arthritis, and even spinal cord tumors can each present with symptoms similar to TOS: pain in the neck, shoulder, and arm as well as paresthesia in the fingers. Cervical spine pathology should be ruled out or treated before TOS surgical treatment. Disc abnormalities and tumors are usually diagnosed by MRI or computed tomography (CT) scans and occasionally by myelography. Arthritis is recognized on plain cervical spine x-rays and its compression of the spinal cord is demonstrable by CT scan and MRI. Cervical strains and sprains are difficult to diagnose because they are soft-tissue injuries and are not visualized radiographically. They present with neck pain, tightness, and stiffness. The range of neck motion may be restricted, and the neck may be tender on palpation over the cervical spine. Strains and sprains are treated with medication and physical therapy, similar to conservative measures for TOS. They frequently coexist with TOS, and their symptoms may persist after TOS symptoms have been relieved.

Brachial Plexus Injury Stretch injuries of the brachial plexus can be difficult to recognize. They must be suspected by the nature of the injury. One diagnostic feature is that the paresthesia is constant, not intermittent. In addition, the paresthesia from nerve injury is usually seen immediately after an injury while the paresthesia from TOS is usually delayed a few days to weeks following an injury. Symptoms can still be aggravated by working with the arm. Diagnosis can sometimes be made by electromyography, but in minor plexus injuries electrophysiologic studies may be normal. There is no treatment for minor plexus injuries, but their recognition is important to avoid misdiagnoses and incorrect treatment.

Fibromyalgia Rotator Cuff and Biceps Tendinitis Inflammation or tears of the tendons around the shoulder are commonly seen in association with TOS. This condition presents with shoulder pain, particularly on abducting or extending the arm. There is tenderness over the shoulder at the biceps and rotator cuff tendons. Some patients are unable to abduct their arm to 180°. When these findings are present, the shoulder must be evaluated by more detailed examination and possibly MRI or arthrography. Treatment of shoulder pathology can be carried out during conservative therapy for TOS. Operations for TOS should not be done until the shoulder problem has been treated as extensively as possible. In some patients

Fibromyalgia is inflammation in stretched, pulled, or injured muscles. It occurs in the trapezeii and in other muscles of the shoulder girdle following injuries. It is diagnosed clinically by symptoms of pain over these muscle areas, tenderness on examination, and sometimes the presence of trigger points. These are localized points over the muscles that are particularly tender. Fibromyalgia is treated by muscle-stretching exercises, heat, massage, ultrasound, and trigger point injections. In some patients, fibromyalgia is resistant to treatment and leads to chronic pain. Fibromyalgia should be considered in the differential diagnosis and frequently is an associated diagnosis with TOS.

Chapter 77 Neurogenic Thoracic Outlet Syndrome

Pectoralis Minor Syndrome (Hyperabduction Syndrome) Pectoralis minor syndrome is compression of the neurovascular bundle by the pectoralis minor tendon when the arm is abducted over the head. It usually causes numbness and tingling in the hand but seldom pain. The symptoms occur primarily at night. It may or may not be accompanied by loss of the radial pulse with the arm hyperabducted to 180°. It is treated by instructing the patient to sleep with the arm at the side at night. Surgery is seldom necessary, but in severe cases the pectoralis minor tendon can be divided, a relatively minor operation. Pectoralis minor syndrome is seldom seen. Although the senior author (RS) has performed more than 1500 operations for TOS, only three were pectoralis minor tenotomy.

Temporomandibular Joint Dysfunction TMJ dysfunction has been recognized more often since 1980. The symptoms are pain in the jaw and sometimes the ear, a popping sensation when opening and closing the mouth, facial numbness, and headaches. It frequently accompanies TOS in patients who have had whiplash injuries. The only common symptom with TOS is headaches. Patients with the other symptoms should be evaluated by a dentist or oral surgeon with experience diagnosing and treating TMJ disorders. A number of TOS patients have enjoyed significant improvement in their headaches when the TMJ dysfunction was treated.

Angina Pectoris Anterior chest wall pain occurs in 10% to 20% of patients with TOS. In a few patients, this is the predominant symptom and can resemble angina pectoris when present on the left side. Cardiac evaluation, electrocardiography, and stress tests should rule out coronary artery disease. Occasionally, angiograms have been obtained before the diagnosis of TOS was considered.

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Neck-stretching exercises stretch the appropriate injured muscles in most cases of TOS. In addition, posture correction and abdominal breathing instructions are added to the program because the neck muscles are used as accessory muscles of breathing. By using abdominal muscles to breathe instead of neck muscles, spasm and tightness in the scalenes may be reduced. Patients are instructed to perform stretching at home, with supervision by a physical therapist. Once the therapist is convinced the patient is performing the exercises correctly, the patient can continue the program alone. Duration of the program varies. It should be tried for at least 3 months. If symptoms improve, it should be continued as long as any symptoms are present and resumed if symptoms recur. If symptoms do not improve at all after 3 months, stretching will probably not be successful. In recent years, the Feldenkrais method has been added to the armamentarium of therapy modalities. This technique of gentle, slow movements and exercises is designed to help improve the patient’s ability to perform activities of daily living. We have found it helpful to the majority of our patients. Physical Therapy Other forms of physical therapy, besides neck stretching, are indicated for the associated injuries, such as tendinitis and fibromyalgia. Passive stretching exercise programs for the shoulders and arms are frequently selected. However, active exercises against resistance, therabands, strengthening exercises, and work hardening programs often aggravate TOS symptoms and are not recommended. Medication In the acute stages of TOS, a variety of medications are tried. These include anti-inflammatory drugs, muscle relaxers, tranquilizers, and analgesics. Narcotics should be avoided. In their place, combinations of the above medications should be tried. Treatment of All Associated Diagnoses

Conservative Treatment

All associated conditions should be treated during the period of conservative therapy. These include cervical spine diseases, shoulder tendinitis or impingement syndrome, fibromyalgia, and other compression syndromes such as carpal and cubital tunnel syndromes.

Stretching Exercises

Time

A number of exercise programs have been recommended for TOS. Some of the most popular came from the Mayo Clinic in 1956 (1). These exercises involved shoulder shrugging and arm strengthening with light weights with the goal of “lifting” the shoulder up to open the thoracic outlet area. In our experience, and that of many therapists, these are usually unsuccessful in TOS patients. In most cases of neurogenic TOS, the abnormality is in the scalene muscles, and arm and shoulder exercises only aggravate the symptoms.

Nature heals many muscle strains and bruises over time. Conservative therapy for TOS should be given several months of trial before being abandoned.

Treatment

Surgical Treatment Indications Surgery for TOS is the last resort. Surgical treatment of neurogenic TOS should be considered under two sets of

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circumstances. The first is if all of the following indications are met: 1. 2. 3. 4.

adequate conservative therapy has been tried and failed; all associated conditions have been diagnosed and treated; symptoms are interfering with activities of daily living, work, or sleep; and symptoms have been present for at least several months.

The second is in the presence of muscle wasting and neuroelectric abnormalities of proximal ulnar nerve compression, in which case surgical decompression is indicated urgently to prevent further loss of motor function. Choice of Operation Three operations are currently in vogue to treat neurogenic TOS: 1. 2. 3.

first-rib resection; anterior scalenectomy with or without middle scalenectomy; and combined rib resection and scalenectomy in one operation.

The choice of operations is determined by the surgeon’s training and experiences. The senior author (RS) performed transaxillary first-rib resection for several years with a 10% initial failure rate and 20% recurrence rate. Anterior and middle scalenectomy were then performed for several more years with identical results. Finally, combined supraclavicular first-rib resection and anterior and middle scalenectomy were performed over another few years with results about 5% better, but this was not significantly different from the results of either procedure alone (Fig. 77.6). However, during the 1990s further comparison of the results of scalenectomy with and without first-

FIGURE 77.6 Results of three primary operations for TOS using life-table analysis methods. (Reproduced by permission from Sanders RJ, Haug CE. Thoracic outlet syndrome: a common sequella of neck injuries. Philadelphia: JB Lippincott, 1991:182.)

rib resection revealed a consistent 10% to 15% lower failure rate when first-rib resection was added. Therefore, in the late 1990s we changed our operation to combined scalenectomy with first-rib resection through a supraclavicular approach. However, in a few patients in whom supraclavicular rib resection appears technically hazardous for fear of nerve injury, we will perform scalenectomy only. Should recurrence develop, transaxillary first-rib resection can be performed at a later date. Transaxillary first-rib resection is indicated when there is a history of cyanosis and arm swelling, suggesting venous TOS along with neurogenic TOS. In this case, firstrib resection must include the anterior portion of the first rib. This requires either a transaxillary or infraclavicular approach as the anterior part of the rib is inaccessible supraclavicularly.

Surgical Techniques Anterior and Middle Total Scalenectomy The patient is positioned with the back raised 20 to 30° and a donut-shaped pillow is placed under the head so that the neck can be slightly hyperextended. A towel is placed under the shoulder to elevate the clavicle. A 6 cm supraclavicular skin incision is made 2 cm above the clavicle beginning just lateral to the midline (Fig. 77.7A). The platysma muscle is divided and skin flaps are elevated, inferiorly to the clavicle and as high cephalad as possible. The lateral edge of sternocleidomastoid muscle is freed as high as possible (Fig. 77.7B). Incisions made lateral to the sternocleidomastoid muscle do not help exposure and can lead to unnecessary dissection and injury to the supraclavicular nerves. When seen, these nerves should be preserved as their injury can cause postoperative burning pain over the chest wall and shoulder. A bipolar, rather than a unipolar, electric cautery is used to control bleeding and to avoid damage to the many nerves that lie close to small bleeding vessels in the neck. The omohyoid muscle is divided, and the medial half is used to retract the lateral edge of the sternocleidomastoid muscle. This exposes the scalene fat pad, which is carefully divided with a cautery or scissors in a vertical direction about 1 cm lateral to the internal jugular vein (Fig. 77.7C). This avoids most of the lymphatics that will be encountered if the fat pad is taken directly off the internal jugular vein. Should lymphatics be injured, particularly the thoracic duct on the left side, lymph leaks are controlled by ties or metal clips. Frequently a small artery, the transverse cervical, runs transversely at the bottom of the fat pad. It is ligated and divided. Immediately below the artery the phrenic nerve is usually found. At this point, the operation is greatly facilitated by the insertion of a self-retaining retractor (Small Omnitract, designed by Dr Ron Stoney). The phrenic nerve is identified lying on the anterior scalene muscle. The nerve is freed on its medial and lateral sides so it can be rolled easily

Chapter 77 Neurogenic Thoracic Outlet Syndrome

A

B

C

D

E

F

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FIGURE 77.7 (A)–(L) Description of surgical technique of supraclavicular scalenectomy and supraclavicular first-rib resection. See text for details. (Modified from Sanders RJ, Raymer S. The supraclavicular approach to scalenectomy and first rib resection: description of technique. J Vasc Surg 1985;5:751–756.)

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G

H

I

J

K

L

FIGURE 77.7 (continued)

from side to side without traction. A marking suture or vessel loop is not routinely used around the phrenic; rather, it is kept in constant view. The nerve is exposed over 5 to 6 cm. A nerve stimulator is unnecessary except during reoperations when the nerve has scar around it. A double phrenic nerve exists in 13% of the population (7). If present, both phrenic nerve branches are preserved.

The anterior scalene muscle is mobilized medially and laterally down to its first-rib insertion. The subclavian artery is identified below it. The portion of fat pad near the clavicle is either divided or retracted so that the anterior scalene muscle insertion can be visualized on the first rib, where the muscle is divided (Fig. 77.7D). A curved retractor placed over the clavicle is used to protect

Chapter 77 Neurogenic Thoracic Outlet Syndrome

the subclavian vein, which usually is not seen but is located close by and can be injured. The pleura lies immediately behind the muscle, and caution is necessary to avoid opening it here. The divided anterior scalene muscle is dissected off the subclavian artery grasped with a large hemostat, and dissected cephalad, freeing all adhesions to the upper plexus and interdigitating muscle fibers to the middle scalene muscle. The anterior scalene muscle is freed below the phrenic nerve (Fig. 77.7E), and the muscle is then passed cephalad beneath the phrenic and regrasped above the phrenic. Detachment of the muscle from its origin at the transverse processes completes its removal. Brachial plexus neurolysis is performed next by removing all remaining muscle, scar, and bands from the surface of C5, C6, and C7 back to the neural foramina. The bipolar cautery is used to control all small bleeding vessels. Neurolysis is continued by removing the fat and connective tissue lying between C7 and subclavian artery. In 25% to 50% of patients, a scalene minimus muscle is found at this level (4,5,28). When there is no muscle here, there often is a tight fascial band (Fig. 77.7F). This overlies C8 and T1 nerve roots. Once the scalene minimus has been removed, these two nerve rots are plainly seen to join together to form the inferior trunk of the brachial plexus. Middle scalenectomy is performed next by first mobilizing C5 on its lateral edge for 5 to 7 cm (C5 and C6 are often fused to form the superior trunk of the plexus at this point). The middle scalene muscle is dissected on its lateral surface and the long thoracic nerve is sought exiting the muscle about 5 cm cephalad to the first rib and 1 cm deep to C5 (Fig. 77.7G). If the nerve is not here, it probably is lying immediately posterior to C5 and C6. The long thoracic nerve must be identified before proceeding with middle scalenectomy. Once identified, the lateral portion of the middle scalene muscle is dissected to its insertion on the lateral edge of first rib, where it is divided. This point in the operation is often made difficult by an arterial and venous branch of the subclavian (transverse scapular artery and vein). When found, they should immediately be ligated and divided. Exposure of the middle scalene muscle is assisted by gently retracting the lateral nerves of the plexus with a suction tip. If the nerves are tight, mobilizing the neck toward the operating side and elevating the ipsilateral shoulder should loosen them. With the lateral portion gone, the medial portion of the muscle is easier to see and excise. It is divided at its first-rib insertion either from behind C5 and C6, or through the space between C6 and C7, whichever approach is easiest. The cephalic portion of the muscle is divided close to transverse processes. All remaining muscle and connective tissue fibers and bands are excised to completely free the posterior surface of the brachial plexus. Total scalenectomy is now complete, and the operation is concluded by inserting a small suction drain beneath the plexus and approximating the scalene fat pad to its origi-

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nal position above the phrenic nerve. The fat pad is not wrapped around the plexus. The wound is closed with subcutaneous and subcuticular sutures.

Cervical Rib Excision Cervical ribs lie in the midst of the middle scalene muscle (Fig. 77.7H). When present, they are excised, usually piecemeal, with bone rongeurs back to the transverse process and the bone ends are trimmed smooth. Raney and duckbill rongeurs are appropriate for this, but others may be equally effective. Once the cervical rib has been excised, first-rib resection should also be performed as the failure rate is higher when first-rib resection is not done.

Supraclavicular First-rib Resection First-rib resection is performed following total anterior and middle scalenectomy via the same incision. Once both muscles have been excised, an Overholt first-rib periosteal elevator frees the medial and lateral edges of the first rib. A Raney rongeur, or Schumaker rib cutter, then transects the neck of the rib near its transverse process (Fig. 77.7I). The neck of the rib is elevated with the Overholt elevator; and using an index finger beneath the rib, the pleura is pushed away and intercostal muscles are bluntly torn until the rib is free from neck to anterior rib, below the subclavian artery (Fig. 77.7J). The anterior rib is divided with a special Pilling infraclavicular rib cutter designed for this purpose (Fig. 77.7K). The point of division is 2 to 3 cm lateral to the costochondral junction because the more medial rib cannot be reached safely. The now freed rib is then extracted from beneath the plexus (Fig. 77.7L). If removal of more anterior rib is necessary, an infraclavicular incision is added to reach the costal cartilage, or the supraclavicular incision is stretched below the clavicle and the anterior end is excised with rongeurs (29). The final step is to smooth both rib stumps with rongeurs. Wound closure is the same as for scalenectomy.

Transaxillary First-rib Resection First-rib resection without scalenectomy can be performed from below the clavicle or through the axilla. Currently the transaxillary route is more popular and also permits better exposure of the anterior end of the rib. (However, the neck of the rib is best visualized supraclavicularly.) For transaxillary first-rib resection, the patient is positioned in a lateral decubitus position, elevated only 30° to 40° from the table, and the arm is suspended vertically on an IV pole. Both the arm and pole are covered with sterile drapes. A skin incision of 8 to 10 cm is placed in the axilla, 1 to 2 cm below the hairline. Subcutaneous tissue is divided to the latissimus dorsi muscle. The anterior edge of latissimus dorsi is freed for 6 to 8 cm to provide

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working room. Gelpi retractors hold the skin edges open. Dissection proceeds just anterior to latissimus dorsi, going deep until the chest wall is seen. By finger dissection, a tunnel is created medially, following the surface of the chest wall, until the lateral edge of the first rib is identified. This plane goes beneath both pectoralis major and minor muscles without dissecting or identifying either muscle. Two structures encountered in this tunnel are the thoracoepigastric vessels, which are ligated and divided, and the second intercostal brachial cutaneous nerve. The nerve is saved if it can lie out of the way without being stretched. However, if it will be stretched, it is better to divide the nerve and accept an area of anesthesia beneath the arm. If the nerve is injured but not divided, pain and paresthesia can develop, which can be disabling. A long, 2-cm-wide retractor, such as a Simon Heaney or narrow Deaver, is placed under the pectoral muscles and lifted upward. The tip of this retractor is positioned above the second rib to avoid its getting in the way of dissection on the first rib. The lateral edge of the first rib is the initial part encountered. In large patients, finding the first rib may be difficult. Identifying the subclavian vein in the superior part of the incision provides a landmark. Following the vein medially, it first crosses the lateral edge of the first rib then dives behind the anterior corner at the costoclavicular ligament. Rib resection begins by dividing with a scissors or cautery the intercostal muscles beneath the lateral edge of the rib. Care is taken to avoid entering the pleural space. Once 2 to 3 cm of the rib is exposed, the scissors can bluntly dissect a plane under the rib and outside the pleura. When the inner edge of the rib is reached, the rightangled end of an Overholt No. 1 periosteal elevator is inserted beneath the rib and the right angle wrapped around the medial edge. The elevator is then moved anteriorly and posteriorly under the rib, as far as possible, to tear more intercostal muscles in each direction. Remaining intercostals are divided with a scissors, keeping the scissors against the edge of the rib. In dividing posterior intercostals, the long thoracic nerve may be encountered just lateral to the rib. As the nerve is often not seen, by hugging the rib with the scissors, injury to the long thoracic nerve can be avoided. The anterior scalene muscle is identified on top of the rib and divided, taking note of the subclavian artery lying immediately posterior to it. Middle scalene muscle is separated from the upper surface of the posterior part of the rib with a scissors. The T1 nerve root lies near the inner rib edge at the anterior border of the middle scalene muscle and must be avoided. Once both scalenes and intercostal muscles have been divided, the underside of the rib is freed from the pleura with the Overholt No. 1 elevator. A flat elevator, such as a Matson, is used to free the posterior rib from remaining muscle attachments. A rib cutter or a rib shears divides the neck of the rib as far posterior as possible. The large size of the rib cutter prevents it from getting all the way back. The

anterior rib end is divided close to the costochondral junction with a rib shears. The main section of rib is removed. The posterior end is shortened with long thin rongeurs as close to the transverse process as is safe, and can usually be taken to within 1 cm of the transverse process. The anterior end is resected with rongeurs until the shiny surface of the cartilage is seen. Sharp points at the rib ends are trimmed. The lung is expanded and holes in the pleura are sought. A small suction tube is left deep in the wound and brought out through the lateral corner of the skin incision. If there is a hole, the tube is left inside the pleural space. The anethesiologist expands the lung and holds the patient in positive end-expiratory pressure while the wound is closed with subcutaneous and subcuticular sutures. By maintaining positive pressure, air is prevented from entering the pleural opening and a pneumothorax is usually avoided.

Postoperative Care An upright chest x-ray in the recovery room is always obtained. A small pneumothorax is left alone. Large air collections, over 25% of lung volume, are tapped with a plastic needle through the second or third anterior interspace. A chest tube is rarely needed as the air in the chest came through the incision, not through an injury to the lung itself. Following scalenectomy, with or without rib resection, patients are ready for discharge in 1 or 2 days. Passive neck-stretching exercises are begun in the first few postoperative days and are continued daily on a home program for several months. Range-of-motion exercises of the arm are begun within a day or two and are continued until the arm has regained a full range of motion. The suction drain usually removes 50 to 70 mL of serosanguinous fluid in the first 8 to 16 hours, then reduces rapidly. The drain is removed when the drainage is minimal, often on the first postoperative day.

Complications of Surgery Intraoperatively, hemorrhage and nerve injury are the main complications. Subclavian artery damage is rare but major arterial bleeding through the transaxillary route presents a challenge. The order in which to obtain proximal control is by vascular clamp, intravascular balloon, supraclavicular incision, or thoracotomy. Subclavian vein bleeding is more common. If this occurs through the transaxillary approach, the bleeding should be controlled immediately by direct pressure. The first rib usually must be removed while the pressure is maintained against the vein because it is often impossible to position a needle holder to sew the vein with the rib in place. Subclavian vein bleeding from the supraclavicular route may occur from tearing off a small venous branch. Usually bleeding can be controlled with a vascular forceps occluding the venous defect while a fine figure-of-eight suture is placed. If control is difficult, an infraclavicular inci-

Chapter 77 Neurogenic Thoracic Outlet Syndrome

sion, similar to the one used for axillofemoral bypass, will expose the distal vein for control. The vein is then repaired from above. Lymphatic leaks can occur from supraclavicular dissections. This is more common on the left side but can occur on the right as well. If there is postoperative lymph drainage for more than 2 to 3 days, the wound is explored and the lymphatic clipped or tied. Ties around lymphatics can be effective, but if there is any tension while tying, the lymphatic leaks again. Clips are sometimes more effective. Nerve injuries usually occur from excessive traction. Once injured, there is little treatment other than maintaining muscle tone until the nerve recovers. Phrenic nerve paresis occurs in about 6% of scalenectomies (12). Spontaneous recovery is seen in almost all cases, usually within a few weeks, but it can take as long as 18 to 24 months to occur. In most large series, the incidence of permanent plexus injury is under 1%.

Results of Treatment The long-term results of transaxillary first-rib resection, anterior and middle scalenectomy, and the combined operation are similar. The immediate success rate of 90% indicates a 10% error in diagnosis. Over the years, this incidence has not been reduced. After 2 years, using lifetable analysis methods, the success rate drops to 70% (Fig. 77.6), indicating a 20% recurrence rate. After 5 and 10 years, there is only a slight fall in success rate as few recurrences are seen after 2 years. Those that do occur are often the result of another neck injury. A significant variable is the etiology of the TOS. Our follow-ups indicate that the results of patients who develop TOS following non-work accidents or spontaneous onset are 10% to 15% better than patients who develop TOS following work injuries or repetitive stress injuries (10). This differs from another study which found in a 5-year follow-up of first-rib resection that post-trauma patients had a satisfaction rate of 73% compared to nontrauma patients whose satisfaction rate was 82% (31). When removing the first rib through the axilla, it is necessary to divide both anterior and middle scalene muscles at their first-rib insertions. Thus, scalenotomy is an integral part of all first-rib resections. Perhaps the explanation for the similarity in results between first-rib resection and scalenectomy is that the operations have in common the release of the anterior and middle scalene muscles. In an extensive review of the literature between 1947 and 1989, excluding the authors’ patients, results were similar for all operations, except anterior scalenotomy, which was not as good as the others (Table 77.4). However, a review of our results from the early 1990s indicated that supraclavicular scalenectomy with first-rib resection had a 10% to 15% better success rate than supraclavicular scalenectomy without first-rib resection. Nerve decompression operations anywhere in the

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TABLE 77.4 Summary of results of all operations for thoracic outlet syndrome*

Technique Anterior scalenotomy Anterior scalenectomy Transaxillary first rib Supraclavicular first rib Infraclavicular first rib Posterior first rib Transpleural first rib Combined†

No. of operations 241 338 3444 715 44 175 18 94

Good Fair Result Result Failed (%) (%) (%) 57 79 83 83 82 86 75 99

13 9 5 13 9 9

30 12 12 4 9 5 25 1

Reproduced by permission from Sanders RJ, Haug CE. Thoracic outl et syndrome: a common sequella of neck injuries. Philadelphia: JB Lippincott, 1991:179. * Follow-up times are mixed: a few months to a few years—no standard. † Combined is a transaxillary first-rib resection and anterior and middle scalenectomy.

body are followed by scar tissue formation during the healing process. Thoracic outlet operations are no exception. Scar tissue forms regardless of which operation is performed: scalenectomy, first-rib resection, or the combined operation. Failure is more the result of postoperative scarring rather than the choice of operation. Success is a subjective evaluation. Most patients with good results have experienced improvement in their major symptoms, but seldom are they totally relieved. The ability of a patient to return to work following relief of major symptoms depends on the job to which the patient is returning. Although some patients can return to heavy labor and heavy lifting, many cannot. These patients have experienced improvement, but not cure, of their pain and hand paresthesia. Returning to their previous heavy-duty jobs often causes recurrent symptoms. On the other hand, most patients with light-duty jobs can return to them. Therefore, the patient’s ability to return to the same job should not be used as the sole criterion for success. Ability to return to gainful employment is also an important consideration.

Persistence, Recurrence, and Reoperation Persistent symptoms following TOS operations are usually the result of a wrong diagnosis. If the initial operation was first-rib resection, further surgery is most likely to fail. On the other hand, if the initial operation was scalenectomy, and if head and neck symptoms were relieved but the hand symptoms were not, first-rib resection is appropriate at a second operation. Recurrence indicates that there was symptomatic improvement for at least a few months. Recurrence is treated in the same way as the original TOS problem. Conservative treatment is always used first. This includes neck-

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cally, by scalenectomy or first-rib resection, releases pressure from the brachial plexus, thereby relieving extremity symptoms, and also relieving neck pain and occipital headaches.

References

FIGURE 77.8 Results of reoperation for recurrent or persistent TOS. Curves show success rates of primary and secondary (repeat) operations. (Reproduced by permission from Sanders RJ, Haug C, Pearce WH. Recurrent thoracic outlet syndrome. J Vasc Surg 1990;12:396.)

stretching exercises and medication. Failure of conservative therapy after several months is one of the indications for reoperation. The other indications are disabling symptoms and treatment of all other associated conditions first. Surgery for recurrence depends upon which operation was performed the first time. Recurrence following first-rib resection is treated by supraclavicular anterior and middle scalenectomy with neurolysis. Recurrence following scalenectomy is treated by transaxillary first-rib resection. If both rib resection and scalenectomy have already been performed, supraclavicular brachial plexus neurolysis is the preferred procedure. The success rate of operations for recurrence is not as high as that of primary operations. The 5-year life-table improvement rate of 41% to 45% (30,32) indicates that operations for recurrence should be undertaken only after all conservative measures have been tried and failed. There is a place for reoperation, however, and it can improve long-term success rates of primary operations. Expressing the long-term results of initial and recurrent operations on the same population in terms of primary and secondary success rates, the secondary success rate for either rib resection followed by scalenectomy or scalenectomy followed by rib resection was about 85% (30) (Fig. 77.8).

Pathophysiology Putting together the history, symptoms, physical findings, response to scalenectomy, and microscopic changes in the scalene muscles, the following hypothesis is offered to explain neurogenic TOS. Hyperextension neck injuries or repeated small trauma to the neck muscles causes scalene muscle stretching or tearing. This is followed by fibrosis around individual scalene muscle fibers that produces tight, tender scalene muscles. In turn, this causes neck pain, sometimes reduced neck motion, and occipital headaches. The tight muscles then press against the brachial plexus, causing pain and paresthesia in the hand and upper extremity. Dividing the scalene muscles surgi-

1. Peet RM, Hendriksen JD, et al. Thoracic outlet syndrome: evaluation of a therapeutic exercise program. Proc Mayo Clin 1956;31:281–287. 2. Rob CG, Standeven A. Arterial occlusion complicating thoracic outlet compression syndrome. Br Med J 1958;2:709–712. 3. Adson AW. Surgical treatment for symptoms produced by cervical ribs and the scalenus anticus muscle. Surg Gynecol Obstet 1947;85:687–700. 4. Gage M, Parnell H. Scalenus anticus syndrome. Am J Surg 1947:73:252–268. 5. Kirgis RD, Reed AR. Significant anatomic relations in the syndrome of the scalene muscles. Ann Surg 1948;127: 1182–1201. 6. Thomas GI, Jones TW, et al. The middle scalene muscle and its contribution to the TOS. Am J Surg 1983; 145:589–592. 7. Sanders RJ, Roos DR. The surgical anatomy of the scalene triangle. Contemp Surg 1989;35:11–16. 8. Makhoul RG, Machleder HI. Developmental anomalies at the thoracic outlet: an analysis of 200 consecutive cases. J Vasc Surg 1992;16:534–545. 9. Cheng SWK, Reilly LM, et al. Neurogenic thoracic outlet decompression: rationale for sparing the first rib. J Vasc Surg 1993;17:225–226. 10. Sanders RJ, Haug CE. Thoracic outlet syndrome: a common sequella of neck injuries. Philadelphia: JB Lippincott, 1991. 11. Love JG. The scalenus anticus syndrome with and without cervical rib. Proc Mayo Clin 1945;20:65–70. 12. Sanders RJ, Pearce WH. The treatment of thoracic outlet syndrome: a comparison of different operations. J Vasc Surg 1989;10:626–634. 13. Roos DB. New concepts of thoracic outlet syndrome that explain etiology, symptoms, diagnosis, and treatment. Vasc Surg 1979;13:313–321. 14. Machleder HI, Moll F, Verity A. The anterior scalene muscle in thoracic outlet compression syndrome: histochemical and morphometric studies. Arch Surg 1986;121:1141–1144. 15. Sanders RJ, Jackson CGR, et al. Scalene muscle abnormalities in traumatic thoracic outlet syndrome. Am J Surg 1990;159:231–236. 16. Gergoudis R, Barnes RW. Thoracic outlet arterial compression: prevalence in normal persons. Angiology 1980;31:538–541. 17. Warrens A, Heaton JM. Thoracic outlet compression syndrome: the lack of reliability of its clinical assessment. Ann R Coll Surg Engl 1987;69:203–204. 18. Gilliatt RW, Willison RG, et al. Peripheral nerve conduction in patients with a cervical rib and band. Ann Neurol 1978;4:124–129. 19. Kenneally M, Rubenach H, Elvey R. The upper limb tension test: the SLR test of the arm. In: Grant R, ed. Physi-

Chapter 77 Neurogenic Thoracic Outlet Syndrome

20.

21.

22.

23.

24. 25.

cal therapy of the cervical and thoracic spine. New York: Churchill Livingstone, 1988:167–194. Urschel MC Jr, Razzuk MA, et al. Objective diagnosis (ulnar nerve conduction velocity) and current therapy of the thoracic outlet syndrome. Ann Thorac Surg 1971;12:608–620. Glover JL, Worth RM, et al. Evoked responses in the diagnosis of thoracic outlet syndrome. Surgery 1981;89:86–93. Machleder HJ, Moll F, et al. Somatosensory evoked potentials in the assessment of thoracic outlet compression syndrome. J Vasc Surg 1987;6:177–184. Wilbourn AJ. Evidence for conduction delay in thoracic outlet syndrome is challenged. N Engl J Med 1984;310:1052–1053. Gage M. Scalenus anticus syndrome: a diagnostic and confirmatory test. Surgery 1939;5:599–601. Jordan SE, Machleder HI. Diagnosis of thoracic outlet syndrome using electrophysiologically guided anterior scalene muscle blocks. Ann Vasc Surg 1998;12:260–264.

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26. Upton ARM, McComas AJ. The double crush in nerveentrapment syndromes. Lancet 1973;2:359–362. 27. Wood VP, Blondi J. Double-crush nerve compression in thoracic outlet syndrome. J Bone Joint Surg 1990; 72A:85–87. 28. Telford ED, Mottershead S. Pressure at the cervicobrachial junction: an operative and anatomical study. J Bone Joint Surg 1948;30:249–265. 29. Robicsek F, Eastman D. “Above-under” exposure of the first rib: a modified approach for the treatment of thoracic outlet syndrome. Ann Vasc Surg 1997;11:304–306. 30. Sanders RJ, Haug C, Pearce WH. Recurrent thoracic outlet syndrome. J Vasc Surg 1990;12:390–400. 31. Green RM, McNamara J, Ouriel K. Long-term followup after thoracic outlet decompression: an analysis of factors determining outcome. J Vasc Surg 1991;14: 739–746. 32. Cheng SWK, Stoney RJ. Supraclavicular reoperation for neurogenic thoracic outlet syndrome. J Vasc Surg 1994;19:565–572.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction Richard J. Sanders and Michael A. Cooper

Venous thoracic outlet syndrome (TOS) is synonymous with subclavian vein obstruction in much the same way as arterial TOS is synonymous with subclavian artery disease. The cause of arterial TOS is usually a cervical or abnormal first rib; the cause of venous TOS is often a narrow costoclavicular space just proximal to where the subclavian vein joins the innominate vein. Cervical ribs lie too far away from the subclavian vein to cause extrinsic venous compression.

Classification Subclavian vein obstruction may be associated with thrombus, or it may be nonthrombotic. The underlying cause is the same whether or not there is a clot; however, treatment will be different because the thrombus must be treated separately. Once the thrombus has been managed, treating the cause of the obstruction is the same for thrombotic and nonthrombotic obstruction. Etiology may be primary or secondary. Primary venous TOS means that the etiology is obscure. Secondary venous TOS implies that there is a specific recognizable cause for the obstruction.

Thrombotic versus Nonthrombotic Venous Obstruction Subclavian vein obstruction can be produced by extrinsic pressure or intrinsic trauma, either of which can produce

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primary or secondary venous obstruction. Either extrinsic or intrinsic causes can elicit thrombotic or nonthrombotic subclavian vein obstruction, secondary to stenosis of the subclavian vein. Severe enough stenosis causes symptoms of arm pain and swelling. These are the early signs of venous obstruction. If the stenosis progresses, thrombosis may be the next step, with increase in intensity of symptoms. Nonthrombotic obstruction has a gradual insidious onset and may progress slowly or remain a mild chronic problem. The incidence ratio of nonthrombotic to thrombotic cases in reported series of subclavian vein obstruction is close to 50 : 50 (1,2).

Primary versus Secondary Subclavian Vein Thrombosis Currently, the majority of patients with subclavian vein thrombosis have had intrinsic trauma to the vein by the insertion of catheters or pacemaker wires. When the cause is apparent, the term secondary subclavian vein thrombosis is used. Other causes of secondary thrombosis are coagulopathies, cancer and irradiation. The term primary thrombosis is used to indicate that there is no obvious cause for the thrombosis. This condition was first described by Paget in 1875 (3) and von Schrotter in 1884 (4) and was labeled Paget–Schrotter syndrome in 1948 (5). Many patients who suffered acute thrombosis of the subclavian vein had been doing heavy work with their arm, giving rise to the name “effort thrombosis.” These terms, effort thrombosis and Paget–Schrotter’s

Chapter 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction

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FIGURE 78.1 Anatomy of costoclavicular space. (Reproduced by permissim on from Sanders RJ, Haug CE. Subclavian vein obstruction and thoracic outlet syndrome: a review of etiology and management. Ann Vasc Surg 1990;4:397–410.)

syndrome, are synonymous with primary subclavian vein thrombosis.

Anatomy and Etiology Primary subclavian vein thrombosis is caused by a congenitally narrow passage for the subclavian vein at the costoclavicular angle. The costoclavicular ligament and subclavius muscle surround the subclavian vein as it passes between first rib and clavicle to enter the mediastinum (Fig. 78.1). Enlargement of either ligament or muscle, or a narrow angle between the two bones, can extrinsically compress the subclavian vein. Another possible explanation is that the position of the subclavian vein is too medial in these patients compared to the average person. As a result, the vein lies too close to the costoclavicular ligament and is subject to trauma. Arm motion causes repetitive trauma to the vein wall in the tight confines of the costoclavicular space. Intimal injury, thickening, web formation, and stenosis result. The final event is thrombosis, which may occur early or late in the process, or may never occur. Thus the pathology within a narrowed subclavian vein can vary widely, and treatment is dependent on the actual abnormalities found inside or outside the vein. Another interesting cause of subclavian vein obstruction is an anterior-lying phrenic nerve. Normally, the phrenic nerve passes below the clavicle posterior to the subclavian vein, but in three studies anteriorlying phrenic nerves were identified in 5%, 6%, or 7% of anatomic dissections (5–7). This may be a more common cause of subclavian vein obstruction than is realized. The condition is rarely recognized preoperatively because exploration is required for diagnosis (Fig. 78.2). Secondary subclavian vein thrombosis has several causes: intimal damage from devices such as indwelling

FIGURE 78.2 Prevenous phrenic nerve. (Reproduced by permission from Sanders RJ, Haug CE. Subclavian vein obstruction and thoracic outlet syndrome: a review of etiology and management. Ann Vasc Surg 1990;4:397–410.)

catheters or wires; extrinsic pressure from neoplasms, such as Pancoast tumors; and irradiation, which can cause intimal damage from ongoing vasculitis or extrinsic compression from scarring and fibrosis. Other causes of subclavian vein obstruction include congenital bands and ligaments, the pectoralis minor tendon, and thickened valves inside the vein. It is difficult to know whether the valves were congenitally hypertrophied and malformed or became thick in response to extrinsic pressure and trauma. Recently, we have seen two young men with nonthrombotic subclavian vein obstruction due to an anomalous first rib, one in association with exostosis of the second rib.

Clinical Manifestations Side and Gender The right side is more commonly involved in subclavian vein thrombosis than the left. About two-thirds of the reported cases are on the right side (8). One explanation for this is that the right hand is dominant in most people and therefore more likely to be used for strenuous activities which might promote “effort thrombosis.” Another explanation is the differences in anatomy between right and left innominate veins. The junction of right subclavian and innominate veins is a right angle whereas the junction of these two veins on the left side is almost on a straight line. Hemodynamically, the right side has more turbulent flow at this point and, hence, seems more likely to thrombose. More men than women develop subclavian vein obstruction while the reverse is true for the presence of cervical ribs. The reason for this is unknown. It has been suggested that men use their arms for more vigorous activities than do women, which makes men more susceptible to effort thrombosis.

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Symptoms Swelling of the hand and arm, a pressure sensation, and pain are the primary symptoms of subclavian vein obstruction. The arm may feel as if it is “bursting.” The symptoms are the same for thrombotic and nonthrombotic obstruction although the latter has a gradual onset while the former may have an acute or a gradual presentation. Many patients with acute subclavian vein thrombosis have had mild symptoms of pressure and swelling for several months preceding the acute episode but ignored them and did not seek medical attention until severe symptoms suddenly appeared. The mild symptoms probably represent gradual stenosis from repeated trauma. It is only after total occlusion that the milder symptoms are appreciated in retrospect. Physical activity of the arm aggravates the symptoms.

some cases, adduction will show severe compression or total occlusion (Fig. 78.4).

Venous Pressure Venous pressure can be measured at rest, with the arm elevated, and with the shoulders hyperabducted in a military position. The normal venous pressure at rest is 8 to 15 cmH2O. This pressure may double or triple with eleva-

Physical Findings In addition to swelling, physical findings include cyanosis of the hand and arm, and distended veins over the shoulder and chest wall. These findings are worse in the acute phase. They often subside when collateral circulation develops.

Diagnosis Venography The primary diagnostic procedure is subclavian venography. If the vein is totally occluded, single views with the arm at rest will establish a diagnosis (Fig. 78.3). In partial obstruction, dynamic venography is necessary. The vein may appear normal or have minimal stenosis at rest, but elevating the arm to 90°, 180°, hyperabduction or, in

A

B

FIGURE 78.3 Acute subclavian vein occlusion. Venogram with arm resting at side.

FIGURE 78.4 (A) Normal subclavian venogram with arm at side on the asymptomatic side of patient in Figure 78.3. Note that there is mild stenosis that is clinically asymptomatic. (B) With arm raised 90°, vein is 90% occluded.

Chapter 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction

tion or assumption of the military position in normal subjects. In patients with venous obstruction, the pressures may be elevated at rest and more than triple with dynamic maneuvers (9). The value of venous pressures is limited. Abnormal values must still be confirmed by venography because they do not precisely localize or quantitate the venous abnormality. Furthermore, normal resting venous pressures do not rule out partial venous obstruction and venography is still necessary. Their main value may be in providing objective measurements with which to follow the results of treatment. Clinically, we have not used venous pressure measurements for many years.

Duplex Scanning Duplex scanning can accurately identify subclavian venous obstruction although it is sometimes impossible to visualize the subclavian vein at the most likely point of obstruction, between the clavicle and first rib, because the clavicle often interferes with visualization at this point. Duplex scanning can be helpful as a screening device when the vein can be seen. A positive duplex scan is usually followed by venography for confirmation and more precise characterization of the defect.

Magnetic Resonance Angiography The newest diagnostic tool to be used to visualize subclavian vein obstruction is magnetic resonance angiography (MRA) (Fig. 78.5). Currently, the image is not detailed enough to permit planning an operation but, as technology improves, MRA may replace conventional venography.

FIGURE 78.5 Magnetic resonance angiogram, in a 16year-old girl with right-arm pain, cyanosis, and swelling. A 5-cm obstruction (single arrow) is detected in the right subclavian vein; axillary vein (double arrow).

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Treatment Secondary subclavian venous obstruction can usually be treated conservatively with anticoagulants: heparin for several days followed by warfarin for 3 to 6 months. If indwelling catheters are still present, they should be removed. In a few cases, particularly in dialysis patients with a functioning arteriovenous fistula (AVF) in the obstructed arm, symptoms may be severe, interfering with sleep and daily activities. In such cases, removal of the AVF will usually alleviate symptoms. However, if access sites are limited, and it is desirable to retain the AVF, surgical correction of the obstruction is an alternative as is transluminal angioplasty with stent placement. Axillary or brachial–internal jugular bypass may be used to decompress the arm and bypass the obstructed axillarysubclavian vein. Prosthetic grafts, particularly 8-mm expanded polytetrafluoroethylene (ePTFE), work well in this situation, probably better than vein grafts. This is because existing AVFs for dialysis usually require a graft of large capacity to handle large flows (Fig. 78.6). Primary subclavian vein obstruction is usually symptomatic when first seen and requires treatment. How much treatment is necessary depends on the intensity of symptoms and the nature of the obstruction. Treatment of subclavian vein obstruction has three goals which are reached in the following order: 1.

to remove the acute thrombus, when present;

FIGURE 78.6 Dialysis patient with secondary subclavian vein occlusion (single arrow) treated with ePTFE axillojugular vein bypass (double arrow).

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Part X Upper Extremity Conditions

to relieve the extrinsic pressure by decompression of the thoracic outlet; and to eliminate the intrinsic defect.

The Acute Thrombus Acute subclavian vein thrombosis is usually treated with heparin or thrombolysis. Heparin is given for 5 to 7 days until a therapeutic level of warfarin is established. Oral anticoagulation is then continued for 3 to 6 months. Heparin poorly addresses the existing thrombosis; its primary role is to prevent propagation of existing thrombus. However, many patients improve on heparin and warfarin therapy because collateral circulation is protected and recanalization of the thrombus occurs. How often this would have occurred with no therapy has been questioned, but there are no good statistics that compare no treatment with anticoagulant therapy. Thrombolytic therapy has been used for several years. Currently, most cases of primary subclavian vein thrombosis should be considered for thrombolytic therapy. Unlike heparin, thrombolysis actually dissolves clot. However, to be effective in venous thrombosis, the thrombolysin must be infused directly into the clot by imbedding the perfusion catheter in the thrombus. If the catheter cannot be positioned in the clot, lytic therapy is usually unsuccessful. Thrombolysis is most effective in thrombus less than a few days old, but on occasion it can dissolve thrombus that is several weeks to months old. The early success rate of thrombolysis is good, 79% (Table 78.1),

TABLE 78.1 Treatment results for subclavian vein occlusion* (source: reference 8, pp. 247–254) No. of Patients

Success (%)†

Range

Acute clot Heparin Fibrinolysis Surgical thrombectomy

185 82 33

91 (49%) 65 (79%) 31 (94%)

4–100 50–100 75–100

Extrinsic pressure

114

92 (81%)

50–100

23

19 (83%)

0–100

6

5 (83%)

NA

25

24 (96%)

50–100

8

7 (88%)

75–100

7

3 (43%)

0–100

Problem

Intrinsic stenosis

Treatment

First-rib resection Soft-tissue release‡ Claviculectomy Endovenectomy with patch Jugulosubclavian vein bypass with AV fistula Jugulosubclavian vein bypass without AV fistula

* Collected results from the literature. † Most results are subjective; few patients had venograms to confirm patency. Some venograms revealed rethromboses and recanalization. ‡ Soft tissue release: division of costoclavicular ligament, subclavius muscle, and anterior scalene muscle.

but long-term success depends on treatment of the underlying cause. Failure to treat the extrinsic compression on the vein and any intrinsic defect may be followed by recurrent thrombosis. Surgical thrombectomy is the other way of removing thrombus. Its indications are failure of thrombolysis, contraindication of fibrinolytic therapy, or inability to deliver the agent directly into the thrombus, plus persistence of severe symptoms. Although heparin without thrombolytic therapy can be used, many patients will still develop a symptomatic postphlebitic arm, which may be disabling. In patients with intense acute symptoms, surgical thrombectomy, followed by reconstruction of the underlying defect, has a better chance of reducing long-term morbidity than anticoagulant therapy alone. Thrombectomy is performed through an 8- to 12-cm infraclavicular incision 2 to 3 cm below the clavicle. The pectoralis minor tendon is divided at the coracoid process and the costoclavicular ligament is opened medially. The axillosubclavian vein is dissected for 6 to 8 cm and vessel loops are passed around each exposed end for control. The patient is systemically heparinized and the vein opened longitudinally (Fig. 78.7). Thrombectomy is performed distally, using an elastic bandage to squeeze thrombus proximally from the arm into the venotomy. If venous inflow to the axillary vein cannot be accomplished, there is little value in proceeding further. Even if the subclavian vein can be opened, it will reclot if there is no inflow reaching the vein. In this situation, closing the venotomy and maintaining anticoagulation for a few months is the only option. If the distal venous bed is successfully opened, thrombectomy is performed proximally. Once all of the clot is removed, the subclavian vein is sounded with dilators to determine its patency. If there is no backbleeding and a dilator cannot pass into the innominate vein, the subclavian vein is severely narrowed or occluded. The options available at this point are to perform a reconstruction by venous bypass or venous patch angioplasty, or to close the incision and treat the patient with anticoagulants. The last option has a high probability of rethrombosis with chronic disability, and the patient may still require venous reconstruction at a later date. Unfortunately, delaying reconstruction makes the opportunity for the venous inflow to reclot a significant risk.

The Extrinsic Pressure Once the axillosubclavian vein has been opened by thrombolysis, rethrombosis can recur. The incidence of rethrombosis has not been well documented in any large study, but two small studies have noted an incidence of 34% (10) and 27% (11). While some authors have tried to select for surgical decompression only those patients with significant residual stenosis following thrombolysis (11), in our experience this has not been infallible — rethrombosis still occurs in patients whose post-thrombolytic venogram was normal. Since most of the patients with this

Chapter 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction

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FIGURE 78.7 Thrombectomy. (Reproduced by permission from Sanders RJ, Haug CE. Management of subclavian vein obstruction. in Bergan JJ, Kistner LR, eds. Atlas of venous surgery. Philadelphia: WB Saunders, 1992:262.)

A

B

condition are young and healthy, surgery may provide a better long-term chance of a normal arm without further episodes of thrombosis. Therefore, following successful thrombolysis, the underlying cause of the occlusion should be repaired. In most cases, the pathology is extrinsic compression of the subclavian vein at the costoclavicular ligament. This is treated by dividing the costoclavicular ligament and subclavius muscle and resection of the first rib. It is vital to remove the anterior part of the first rib and enough costal cartilage to totally free the subclavian vein (venolysis) (12). First-rib resection can be accomplished through an infraclavicular or transaxillary incision but cannot be done supraclavicularly because the anterior part of the rib is seldom reachable from above the clavicle. Postoperatively, in patients who had experienced recent thrombosis, anticoagulation with warfarin is continued for 3 months to prevent recurrent venous thrombosis. The choice between transaxillary and infraclavicular approaches depends on what else is planned for the operation. If rib resection might involve subclavian vein exploration or reconstruction, the infraclavicular incision provides better access to the subclavian vein. For only rib resection and venolysis without venotomy, the transaxillary approach gives good exposure. Concern has been expressed regarding adequate exposure to remove the posterior portion of the first rib through the infraclavicular approach. Although this can be difficult, we have found that elevating the shoulder lifts the clavicle. This permits retraction of the subclavian vein upward, away from the lateral portion of the first rib, so that the neck of the rib can be removed to within 1 cm of the transverse process (Fig. 78.8). In patients who have combined neurogenic and venous TOS, first-rib resection should treat both conditions. Although supraclavicular scalenectomy can be added to infraclavicular rib resection with venolysis (12), first-rib resection alone may relieve both groups of symptoms. We have reserved supraclavicular scalenectomy for a later

FIGURE 78.8 Postoperative chest x-ray in a large patient following infraclavicular first-rib resection. Note short posterior stump of first rib (arrow).

date should symptoms of neurogenic TOS be incompletely resolved. Timing of first-rib resection is controversial. Most surgeons who have written about this, including the authors, recommend first-rib resection within a few days of thrombolysis (13,14), or resecting it simultaneously with surgical thrombectomy. Another approach has been to anticoagulate for 3 months and then resect the rib only if the patient is symptomatic. In following the latter protocol, more than 70% of the patients in one series underwent operation after 3 months (10). However, in a more recent review of their statistics, the same group has found no difference in results whether or not there is a 3-month delay. Therefore, they now perform first-rib resection during the same hospitalization (15). The rationale for delaying operation was that after thrombolysis the patient is hypercoagulable and elective surgery may lead to rethrombosis of the vein. However, it

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Part X Upper Extremity Conditions

has been noted that rethrombosis occurs when surgery is delayed, as well as when surgery is performed within a few days of thrombolysis. In either case, repeat lytic therapy is indicated and has been successful in lysing the recurrent recent thrombosis. It remains our opinion and experience that first-rib resection and venous repair are best performed immediately after thrombolysis. We have seen several patients in whom delay resulted in rethrombosis that was not treated within a few days. When reconstruction was finally performed, it was difficult or impossible to open the brachial and axillary veins for adequate inflow, or to open the subclavian vein for adequate outflow. If the subclavian vein cannot be opened, first-rib resection is no longer necessary. There is little point in decompressing an already occluded vein. The one exception is if the proximal subclavian vein remains open and receives the cephalic vein collateral. This determination can be made by venogram. A

The Intrinsic Defect Once the vein is open and the extrinsic pressure relieved, venography and symptoms determine the next step. If there is significant stenosis but no symptoms, nothing further is required. If symptoms are present, or develop later, balloon angioplasty can be performed. If balloon angioplasty fails, vein patch angioplasty can be performed at a later date. However, if surgical thrombectomy is required to open the vein, vein patch angioplasty can be performed simultaneously. Vein patch angioplasty, with or without endovenectomy, is indicated if the subclavian vein flows into the innominate but is narrow, webbed, scarred, or contains old thrombus. In most patients, patch grafts, with or without endovenectomy, can be performed through the infraclavicular incision. The success rate for short patches is close to 100%, while it diminishes for longer patches (13). In most patients, vein patch angioplasty can be performed through the infraclavicular incision, but in a few patients it is impossible to obtain adequate exposure of the proximal subclavian vein without opening the mediastinum. A modified mediastinotomy has been described by dividing the sternum vertically down to the first interspace, then transecting the remaining sternum transversely through that interspace. This provides excellent exposure of the innominate and subclavian veins, making patch angioplasty much easier (16). An example of partial clot lysis followed by thrombectomy and vein patch graft is seen in Figure 78.9. Jugulosubclavian vein bypass is used to restore venous flow to the arm when the subclavian vein is totally occluded or patch angioplasty is undesirable. A prerequisite to a successful bypass is adequate inflow into the axillary vein. If the brachial and axillary veins are occluded, it is essential to perform a thrombectomy, even in chronic occlusion, to develop adequate inflow. If inflow cannot

B

FIGURE 78.9 (A) Venogram following partial lysis of clot in same patient as Figure 78.3. (B) postoperative venogram In same patient following infraclavicular first-rib resection, thrombectomy, and vein patch graft with temporary arteriovenous fistula. The dye is thin distal to the fistula (arrow).

be established, a jugulosubclavian bypass should not be attempted. Jugulosubclavian bypass is performed by exposing the axillary vein through an infraclavicular incision as described above for thrombectomy. Adequate inflow is ascertained first and a thrombectomy is done if necessary. The internal jugular vein is exposed through two short transverse incisions, one above the clavicle, the other

Chapter 78 Venous Thoracic Outlet Syndrome or Subclavian Vein Obstruction

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FIGURE 78.10 Jugulosubclavian vein bypass by turning down the internal jugular vein to sew to the axillary vein behind the clavicle. (Reproduced by permission from Sanders RJ, Haug CE. Subclavian vein obstruction and thoracic outlet syndrome: a review of etiology and management. Ann Vasc Surg 1990;4:397–410.)

below the jaw (Fig. 78.10). The internal jugular vein is dissected free as high as possible and suture-ligated near the base of the skull. The caudal end is totally mobilized to the clavicle, passed behind the clavicle, and sewn end-to-side to the axillary vein. Adequate space is obtained to pass the vein behind the clavicle by elevating the shoulder (which lifts up the clavicle) and by transecting the subclavius muscle. If both axillary and subclavian veins are occluded, turning down the jugular vein cannot be used because the jugular vein is too short. However, other venous bypasses can be performed using saphenous vein (17), crossover cephalic vein (18), or a long prosthesis (16). Any of these procedures must be supported by an AVF. Percutaneous balloon angioplasty is an option to treat stenosis in the subclavian vein following successful thrombolysis. However, angioplasty treats the intrinsic venous problem only and does nothing for the extrinsic compression. First-rib resection and venolysis should be performed surgically before angioplasty is attempted. In a series of 21 subclavian vein angioplasties, 12 performed following fibrinolysis without rib resection all failed. In contrast, seven of nine angioplasties performed following extrinsic decompression by first-rib resection were successful (10). A temporary AVF should be created whenever a vein is opened for thrombectomy, endovenectomy, or bypass. Although some venous repairs succeed without a fistula (13), other studies in the lower extremities indicate that the success rate of venous repair is higher if a temporary AVF is employed (19,20). Fistulas can be created by sewing a nearby vein to the axillary artery, by sewing a section of saphenous vein to the axillary artery and employing the distal part as an onlay vein patch when performing endovenectomy, or by using a loop of Teflon-reinforced ePTFE between the axillary artery and vein. The advantage of the prosthetic loop graft is that it is

looped upward toward the skin and left in the subcutaneous tissue. Closure of the fistula is much easier if it is just under the skin incision, a procedure that can be performed under local anesthesia (21). When a piece of vein is used for the AVF, a double loop of polypropylene is left around the fistula, the sutures are brought up into the subcutaneous tissue, and the ends are tagged with a large hemoclip. Closure by tying the suture in about 3 months is usually successful, but we have experienced reopening of the fistula when fat under the tie became necrotic and the suture loosened. Another option to close the fistula is to discharge a coil into it via arterial catheterization.

Results of Treatment The results of various therapies for venous TOS are difficult to evaluate because many of the follow-up reports are based on clinical improvement without venograms to confirm patency of the vein. When venograms have been available in patients with good clinical improvement, they have sometimes revealed an occluded subclavian vein with good collateral circulation or an irregular recanalized subclavian vein. It is not known if the same result would have been possible with no treatment at all. Appreciating the limitations described above, Table 78.1 summarizes the results of different treatments for subclavian vein obstruction. The success with bypass grafts has been greater when an AVF accompanied the repair although the number of cases is small. Half of the patients who received lytic therapy also had first-rib resections. One-third of the patients undergoing first-rib resection had been treated previously with thrombolysis. Thus combination therapy is appropriately becoming more prevalent.

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Management of the Contralateral Side Patients suffering from unilateral axillary–subclavian vein obstruction are at increased risk to develop the same problem on the contralateral side. In routine venography of the asymptomatic side in one series of 34 patients, 53% had evidence of 50% or greater diameter compression and 15% already had contralateral thrombosis (10). In another report, 2 of 21 patients (10%) developed thrombosis on the contralateral side (11). There are not enough data at present to make a definitive recommendation regarding the incidence of thrombosis on the contralateral side. In the two studies cited above, it was 15% and 10%, respectively, in just a few years. Our present policy is to advise patients that they are at increased risk on the opposite side and offer elective prophylactic first-rib resection, although we do not encourage it. Those patients who have had prophylactic rib resections have had no problems. Other patients are being followed without rib resection. Should symptoms develop, rib resection will be recommended.

References 1. Roelson E. So-called traumatic thrombosis of the axillary and subclavian veins. Acta Med Scand 1939;98:589–622. 2. Mercier CP, Branchereau A, et al. Venous thrombosis of the upper limb: effort or compression. J Cardiovasc Surg (Torino) 1973; Spec. No:519–522. 3. Paget J. Clinical lectures and essays. London, 1875. 4. von Schrotter L. Handbuch der alligemeinen Pathologie und Therapie (Nothnagel). Berlin: A. Hirschwald, 1884: 533. Cited by Sampson JJ. Am Heart J 1943;25:313. 5. Hughes ESR. Venous obstruction in the upper extremity. Br J Surg 1948;36:155–163. 6. Schroeder WE, Green FR. Phrenic nerve injuries; report of a case. Anatomical and experimental researches, and critical review of the literature. Am J Med Sci 1902;123:196–220. 7. Hovelacque A, Monod O, et al. Etude anatomique du nerf phrenique pre-veineux. Ann D’Anatomie Path 1936;13:518–522.

8. Sanders RJ, Haug CE. Thoracic outlet syndrome: a common sequella of neck injuries. Philadelphia: JB Lippincott, 1991:233–262. 9. Daskalakis E, Bouhoutsos J. Subclavian and axillary compression of musculoskeletal origin. Br J Surg 1980;67:573–576. 10. Machleder HI. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 1993;17:305–317. 11. Lokanathan R, Salvian AJ, et al. Outcome of thrombolysis and selective thoracic outlet decompression for primary axillary vein thrombosis. J Vasc Surg 2001;33:783–788. 12. Thompson RW, Schneider PA, et al. Circumferential venolysis and paraclavicular thoracic outlet decompression for “effort thrombosis” of the subclavian. J Vasc Surg 1992;16:723–732. 13. Molina EJ. Need for emergency treatment in subclavian vein effort thrombosis. J Am Coll Surg 1995;181:414–420. 14. Roos DB. Discussion. In: Machleder HI. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 1993;17:316–317. 15. Angle N, Gelabert HA, et al. Safety and efficacy of early surgical decompression of the thoracic outlet for PagetSchroetter syndrome. Ann Vasc Surg 2001;15:37–42. 16. Molina JE. A new surgical approach to the innominate and subclavian veins. J Vasc Surg 1998;27:576–581. 17. Rabinowitz R, Goldfarb D. Surgical treatment of axillosubclavian venous thrombosis: a case report. Surgery 1971;70:703–706. 18. Hashmonai M, Schramek A, Farbstein J. Cephalic vein cross-over bypass for subclavian vein thrombosis: a case report. Surgery 1976;80:563–564. 19. Johnson V, Eiseman B. Evaluation of arteriovenous shunt to maintain patency of venous autograft. Am J Surg 1969;118:915–920. 20. Eklof B, Albrechtson U, et al. The temporary arteriovenous fistula in venous reconstructive surgery. Int Angiol 1985;4:455–462. 21. Sanders RJ, Rosales C, Pearce WH. Creation and closure of temporary arteriovenous fistulas for venous reconstruction or thrombectomy: description of technique. J Vasc Surg 1987;6:504–505.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 79 Arterial Thoracic Outlet Syndrome Frank J. Veith and Henry Haimovici

Arterial complications of a thoracic outlet syndrome are much less common than the neurogenic and venous conditions. Their pathophysiology and clinical manifestations are often more complex, and if not recognized early may be potentially serious by threatening the viability of the upper extremity. Their initiating cause is related mainly to subclavian artery compression by congenital cervical ribs, more rarely by anomalous first and second thoracic ribs, and only occasionally by a callus of malunion of a fractured clavicle or rarely a tight anterior scalene muscle.

Historical Background Although cervical ribs and other osseous abnormalities of the thoracic outlet have been reported for over a century as anatomic curiosities, it was not until 1861 that Coote removed a cervical rib that caused pressure on the subclavian and axillary vessels with resulting ischemia of the arm (1). Then, in 1863, Hilton reported a case of thrombosis of the subclavian artery resulting from its compression by an exostosis of the first thoracic rib (2). Other publications appeared subsequently that confirmed the significance of the osseous compression of the subclavian vessels (3–5). Only after the development of roentgenologic identification were cervical ribs and other osseous anomalies increasingly noted. Thus Halsted was able in 1916 to collect from the literature 716 cases of cervical ribs, 360 of which presented symptoms of compression, and, of the latter, 125 presented with vascular symptoms (6).

In 1934, Lewis and Pickering postulated that the vascular changes in the upper extremity were due to traumatic compression of the subclavian artery by the cervical rib, followed by mural thrombosis and embolic manifestations (7). The term “thoracic outlet syndrome” was introduced by Peet et al. (8) in 1956 and popularized in 1958 by Rob and Standeven (9) as “thoracic outlet compression syndrome.” This terminology helped provide a unifying concept of the underlying pathogenesis of the various entities as described in the literature. In 1916, Halsted, in his paper mentioned above, included a tabulation of 27 clinical cases of subclavian aneurysm in association with a cervical rib. In the 1930s, such related vascular complications were being reported with greater frequency, as reflected in Eden’s review of 48 cases (10). In 1956, a collected review of the literature by Schein, Haimovici, and Young dealt with an evaluation of the thromboembolic manifestations on the basis of anatomopathologic criteria in a group of 30 cases (11). In 1958, Rob and Standeven, mentioned above, reported 10 cases of arterial occlusion of the upper extremity associated with the thoracic outlet compression syndrome. Subsequent vascular complications due to cervical ribs continued to emphasize the need for their early recognition and treatment. A better understanding of the surgical management of the compressing structures of the thoracic outlet has thus evolved as reflected in several reports (12–15). The increasing number of cases being reported suggests that vascular complications are most likely more frequent than they seemed to be from the earlier literature.

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Part X Upper Extremity Conditions

Clinical Pathologic Background The majority of patients with cervical rib problems fall into the 21- to 50-year-old age group, with a range between 16 and 66 years of age in our series. Eden, in his review, mentioned the uncommon occurrences of this condition in a 5-year-old child and in a 75-year-old woman. The vast majority of cases occur in young or middle-aged men. Eden noted a reversed ratio of 20 males to 26 females, which may have been due to a possible preponderance of neurologic complications. Most reports indicated that vascular symptoms are more common in the right arm, due usually to the greater number of righthanded individuals. However, in Eden’s series, 24 cases occurred in the left arm, as opposed to 20 in the right. In 70% of cases, the condition is bilateral. The incidence of cervical ribs encountered in routine chest films has been estimated as between 0.5% and 0.7% (16). The vast majority of these patients are asymptomatic. The largest group of symptomatic patients comprises those with impingement upon the brachial plexus by an incomplete cervical rib. Ischemic symptoms are rare. Adson reported vascular symptomatology in 5.6% of his patients (17). These symptoms were manifested as Raynaud’s phenomenon with signs referable to partial intermittent subclavian artery occlusion. The type of cervical rib is of great significance in vascular complications. It has been well established since Gruber’s study that short (type I) and incomplete (type II) ribs produce neurologic complications, while only long or complete ones (type III) are associated with arterial complications (18). In our personal review, every case except one had a complete cervical rib (Fig. 79.1).

The Subclavian Artery In the presence of a complete cervical rib, the supraclavicular course of the subclavian artery is displaced. There is an upward extension of the thorax so that the subclavian artery passes high in the neck as it emerges from the lateral border of the anterior scalene muscle, as it is elevated and usually readily palpable well above the clavicle. Indeed, in all these patients there is a supraclavicular mass represented by the cervical rib at its articulating site with the normal first rib. The artery at this level is occasionally tender. Short described two variants of the course of the subclavian artery (19). In type A, the subclavian artery crosses the first rib medially to its exostosis. Short found that in this type all patients had major vascular symptoms. In type B, the subclavian artery crosses the first rib lateral to the exostosis and the symptoms are neurologic rather than vascular. Short further pointed out that the two groups can be distinguished clinically and that each type has a different prognosis.

FIGURE 79.1 Oblique view of the cervical spine showing a complete right cervical rib. (Reproduced by permission from Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs: surgical considerations. Report of a case and review of the literature. Surgery 1956,40:428–443.)

Extrinsic Compression of Subclavian Artery If the compression of the artery is of short duration, the caliber of the vessel may return to normal following surgical correction of the compression. The prolonged compression of the subclavian artery may lead to: 1.

2. 3.

structural changes of the arterial wall, consisting often of a greatly thickened vessel adherent to the surrounding structures and initial ulceration with platelet thrombi; stenosis at the site of the extravascular compression; often a poststenotic dilatation (Fig. 79.2).

Subclavian Aneurysms Subclavian artery aneurysms were recognized by Halsted as early as 1916, as mentioned above (6). In 27 (21.6%) of the 125 cases, there were subclavian aneurysms. This review led Halsted to reinvestigate the causes of subclavian aneurysm formation and of poststenotic dilation. On the basis of his experiments, he attributed poststenotic dilatation to two chief factors: 1.

to the “whirlpool-like” play of the blood below the site of the constriction; and

Chapter 79 Arterial Thoracic Outlet Syndrome

951

FIGURE 79.2 Algorithm of origin and sequence of clinicopathologic events associated with arterial thoracic outlet syndrome. (Reproduced by permission from Haimovici H. Arterial thromboembolism due to thoracic outlet complications. In: Haimovici H, ed. Vascular surgery, 3rd edn. Norwalk, CT: Appleton & Lange, 1989:842.)

2.

to the lowered blood pressure.

Holman later essentially confirmed the mechanism of the poststenotic dilation by attributing it to mural structural fatigue secondary to the turbulent flow that induces vibrations leading to the histologic changes of the artery (20). Subsequently, few reports dealt with this complication; in 1962 Wellington and Martin could find only 57 such cases. Since that time, however, many more instances of this entity have been diagnosed. On the other hand, a number of observations reported most cases as poststenotic dilations as distinct from aneurysms (21). In some cases it may be difficult to differentiate between the two, especially when the dilated poststenotic lesion is thrombosed. Arbitrarily, a subclavian aneurysm is being defined as an arterial dilation of more than twice the diameter of the uninvolved artery. Based on a series of personal observations, Short stated that “a large number of crippling cases of ischemia of the arm or hand are due to thromboembolic propagation from silent subclavian aneurysms” (19). Thus, of the 12 cases reported by Bertelsen et al., two patients had aneurysmal lesions and two had simple dilations of the subclavian artery (22). On the other hand, Judy and Heyman in 1972 stated that in seven cases no aneurysm or dilation was noted on the arteriographic studies (23). The features in those cases were overwhelmingly those of thromboembolic manifestations (24). The thrombosis in the sac may obscure the aneurysms in the angiograms (25). With the newer techniques of computed tomography (CT) scans and duplex ultrasonography, the aneurysmal presence may be revealed more often by noninvasive procedures than by simple arteriography. In conclusion, postcompression occlusion of the third portion of the subclavian artery may present aneurysmal

formation more often than has been reported in the literature. This would confirm what Halsted produced experimentally and Holman demonstrated later, namely that compression in one area of the arterial tree due to hemodynamic factors results in variable degrees of distal lesions from simple dilation to aneurysm formation. Although some reports in the past failed to mention the diagnosis of aneurysmal dilatations, one may conclude that the thromboembolic complications must be anticipated as part of the arterial damage and aneurysm formation. The thrombotic manifestations originate in the aneurysmal sac and embolize into the distal portion of the upper extremity including the hand, as demonstrated by the observations of Short, Scher and Veith, and others.

Clinical Manifestations Most vascular complications associated with the thoracic outlet take months or years to become apparent or significant. However, when first seen by the physician, patients with these complications usually present with an acute stage of the process. Generally, the clinical picture may go through three phases: prodromal, early ischemic, and severe ischemic.

Prodromal Phase The most common symptoms at onset are largely confined to the fingers and hands and consist of attacks of coldness, numbness, cyanosis or pallor, and pain, especially on exposure to cold. Often these attacks resemble a typical Raynaud’s phenomenon. Sometimes associated neurologic involvement is evidenced by symptoms that are not always easy to distinguish accurately from symptoms of ischemic origin, such as numbness, wasting, and pain.

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The initial manifestations are usually attributed to occlusion of digital or palmar arterioles. The color and temperature changes and response to cold are confined to the acral parts of the limb and often show temporary regression. The natural course of this process, however, consists of episodic and repetitive peripheral microemboli that impart a progressive ischemia to the hand or forearm. Depending on the degree of ischemia, the clinical course may assume either of the following two advanced states.

Early Ischemic Phase The color changes of Raynaud’s phenomenon on exposure to cold become more severe and are usually confined to the involved hand only and sometimes to one finger, most commonly the index finger. Pulsations present in the previous phase disappear first in the digital arterioles and later at the radial and ulnar or even brachial artery. Pain experienced in the arm becomes more pronounced, especially during exercise.

Severe Ischemic Phase Because this process sometimes progresses at a rapid pace, the ischemia may become severe enough to prevent the patient from sleeping at night, especially if the collateral circulation has decreased. Sometimes this phase may be preceded by some episode of trauma, which obviously is only a coincidental event, not uncommonly with medicolegal implications. The usual duration of the entire spectrum of the ischemic manifestations ranges from a few weeks to a few months or longer before the condition becomes critical. When the symptoms worsen, the pain becomes acutely intolerable, and at this point the patient presents himself or herself to the physician. Physical examination usually turns up evidence of a cervical rib in the supraclavicular region. A thrill is palpable and a systolic bruit is audible in most instances. The hand and arm may show evidence of vascular compromise. Blood pressure in that extremity may be decreased or absent; wrist and brachial pulses may be unobtainable. Muscle atrophy may be present not only in the intrinsic muscles of the hand, but also in the thenar or hypothenar regions. In advanced cases, the forearm and the arm musculature may show similar changes. Ulcerations or gangrene of the tips of the fingers, either focal or extensive, may be noted in these advanced cases. In a previously reported review of 30 patients, 11 (36.7%) sustained the loss of a phalanx or a digit, and two (6.7%) required a major upper extremity amputation (11).

Differential Diagnosis Many of the symptoms described in the early stages of the thromboembolic complications associated with the tho-

racic outlet syndrome may mimic symptoms of other lesions, requiring careful differentiation. Among these are carpal tunnel syndrome, cervical root entrapment, cervical arthritis, and a protruded cervical disk, most of which produce severe pain and are often more typical of a neurologic rather than a vascular complication. In the presence of unilateral vascular symptoms, it is necessary to rule out collagen vascular disease, vasospastic syndromes, autoimmune vasculitides, traumatic thrombosis of hand vessels, and actual cardiogenic embolic disease. Unfortunately, quite often identification of the source of microemboli is not directed toward the possible thoracic outlet origin. At the stage of acute vascular manifestations, differential diagnosis may pose less of a problem. Awareness of the potential presence of cervical ribs or anomalies of the osseous structures of the thoracic aperture is essential in recognizing the nature of the disease and in deciding the management of these complications at an early stage.

Diagnostic Tests Routine Roentgenograms Roentgenograms are essential for determining the presence of the following potential conditions: cervical ribs, abnormal transverse process of C7, anomalous first rib, clavicular exostosis or callus from a malunited fracture, or vertebral abnormalities.

Classic Shoulder Girdle Maneuvers Classic shoulder girdle maneuvers are helpful for detecting vascular, neurologic, or neurovascular manifestations of the thoracic outlet syndrome, possibly associated with costoclavicular hyperabduction conditions.

Noninvasive Tests Pulse–volume recording at digital, wrist, forearm, and arm levels may suggest arterial occlusions. The pulse– volume index at various levels may also be of help in assessing the result of treatment and the overall prognosis. Unless associated neurologic signs are present, electrodiagnostic tests are of limited or no value in the diagnostic evaluation of the arterial complications.

Imaging Arteriography Arteriography are recently magnetic resonance imaging (MRI) are the most important diagnostic tools. These help visualize the point of vessel occlusion and may localize emboli in brachial, radial, ulnar, palmar, and digital arteries. Commonly used arteriographic techniques consist of direct radiopaque injection via a catheter inserted into the proximal subclavian artery through the femoral artery (24). Duplex scanning of the involved extremity as well as of the asymptomatic side is also indicated to look for intraluminal thrombus.

Chapter 79 Arterial Thoracic Outlet Syndrome

Treatment The vascular complications associated with the thoracic outlet require prompt attention in every case, whether apparently moderate or frankly severe. Lack of awareness of its potentially serious prognostic significance may lead to irreversible ischemic changes with tissue loss. The type of therapy will depend on the stage of the ischemic manifestations arising from entrapment of the subclavian and the extent of distal arterial lesions. In the absence of threatening ischemia, the thoracic outlet syndrome may be treated by nonsurgical methods if there is no arterial compression. Surgical treatment may include: 1. 2. 3.

decompression of the subclavian artery; repair of the arterial lesions; and management of the associated ischemia of the hand.

Surgical Exposure for Subclavian Artery Decompression Surgical exposure of the thoracic outlet structures usually depends on the type of vascular lesions. The supraclavicular approach, used originally in 1910 by Murphy, is still favored by most vascular surgeons. It provides access not only to the subclavian vessels but also to the cervical rib and almost all of the other structures of the thoracic outlet. However, if the axillary vessels and the first thoracic rib are to be exposed, this approach may be inadequate. The infraclavicular or anterior approach offers access to the first rib and to the distal portion of the subclavian and axillary vessels. This exposure also affords easy evaluation of the potential compressive effects of the pectoralis minor tendon in the hyperabduction syndrome. Combined supraclavicular and infraclavicular approaches, when indicated, offer a logical solution to the exposure of the many structural elements.

953

A claviculectomy, either partial or total, provides exposure for both the supraclavicular and infraclavicular areas. Lord and Rosati found the claviculectomy to offer easy access with favorable results (26), but most surgeons try to avoid this manoever.

Removal of Compressive Structures The compressive structures include the cervical rib, the anterior scalene muscle, the first thoracic rib, and the pectoralis minor tendon. Satisfactory decompression of the subclavian artery can be achieved in the majority of cases only by removal of the cervical rib and scalenectomy. Occasionally associated pectoralis minor tenotomy may be indicated. The excision of the cervical rib in most cases is the first and most important step. It should be done together with the resection of the bony prominence on the first rib if these structures are a primary cause of impingement upon and indentation of the subclavian artery. In the absence of definite compression, resection of the cervical rib may not be necessary (Fig. 79.3). Routine removal of the first thoracic rib through the posterior or transaxillary approach, as favored by Ross and others, is being challenged as a “cure-all” by those dealing primarily with the arterial complications (27). However, some surgeons advocate removal of the cervical and first ribs via a transaxillary approach, although others find this to be a difficult procedure. On the basis of current experience, excision of the first rib should be reserved for patients with proven compression of the subclavian artery directly related to it. Scalenectomy is indicated whenever the subclavian artery is exposed (26). Simple scalenotomy, failing to provide long-term subclavian decompression, is not indicated owing to recurrence of symptoms resulting from scalene muscle reattachment to the first rib and to other structures contributing to the arterial compression (28).

FIGURE 79.3 Operative findings of cervical rib and its relation to subclavian artery thrombosis. Dotted lines indicate site of arterial resection. (Reproduced by permission from Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs: surgical considerations. Report of a case and review of the literature. Surgery 1956,40:428–443.)

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Arterial Reconstruction The subclavian artery, site of origin of the thromboembolic process, should be considered for repair after its decompression. The method used depends on the extent of the mural lesions and the occlusion of its lumen (Fig. 79.4). Simple thrombectomy in advanced lesions is rarely sufficient. A thromboendarterectomy at the level of the compression of the artery, consisting of excision of both the ulcerated intima and thrombus, may be performed (Figs. 79.5 and 79.6). Another, better option is excision of the involved artery with replacement by an interposition graft. Axillary and brachial thromboembolic occlusions, if of long standing, may be difficult or impossible to disobstruct with an embolectomy catheter. A direct approach through a separate exposure is then necessary. An arteriogram is essential to localize the extent of the occlusion

and delineate the outflow distal to the brachial. It is important to distinguish between a brachial occlusion at its origin just proximal to the profunda brachii, and an occlusion at the elbow, where it divides into radial and ulnar arteries. The prognosis appears better with a proximal than with a distal occlusion because disobstruction is easier. Thromboembolectomy or thrombolysis of the proximal brachial may provide adequate flow to the forearm and hand, especially if the distal brachial is patent. Reestablishing patency of the deep brachial artery in the event that the distal brachial thrombus cannot be dislodged is somewhat equivalent to profunda femoris revascularization in the thigh when the superficial femoral is occluded. Should the thromboembolectomy fail, an autogenous vein graft bypass from the subclavian or axillary to the brachial should be considered if possible. Direct repair of the forearm or hand is rarely feasible because of multiple chronic repetitive embolic episodes affecting these distal vessels. These episodes often account for failure to restore normal wrist pulses.

Cervicothoracic Sympathectomy Indications for cervicothoracic sympathectomy may be dictated by the inability to restore arterial patency below the elbow for the reasons stated above. This procedure may be appropriate when there is evidence of hand ischemia of a threatening nature. The procedure is carried out through the supraclavicular exposure used for dealing with the decompressive maneuvers and consists of removal of the distal half of the stellate ganglion and the second and third thoracic ganglia. This provides sympathetic denervation of the forearm and hand. Although it is controversial, some vascular surgeons have found the cervicothoracic sympathectomy to be an important additional step in the overall management of this syndrome.

Results

FIGURE 79.4 Right subclavian axillary arteriogram via transfemoral retrograde thoracic aortogram 5 seconds after contrast material injection. Collateral filling of axillary artery showing several incompletely obstructing thrombi. (Reproduced by permission from Haimovici H. Vascular surgery, 3rd edn. Norwalk, CT: Appleton & Lange, 1989:840–852.)

Management of these arterial lesions has improved thanks to greater awareness of their presence and a prompter combined use of the various methods of decompression and revascularization. The changing concepts of the management of these lesions are reflected in Tables 79.1 through 79.4. Table 79.1 deals with 30 cases evaluated during the period up to 1955. It indicates that most decompressive procedures were cervical rib resections and scalenotomies and were performed in 58% and 42% of the cases, respectively. Arterial repair consisting of arteriotomy for thrombectomy was rarely performed except in combination with a few other procedures. Table 79.2 includes 50 cases during the period between 1956 and 1965. It show greater use of cervical rib resection than that of the first thoracic rib. Scalenotomy alone, excluding its mandatory use with the first thoracic rib resection, was done in 23% of the cases. Arterial repair

Chapter 79 Arterial Thoracic Outlet Syndrome

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FIGURE 79.5 Right arterlographic findings in Figure 79.4 and a left poststenotic dilatation of the left axillary artery seen on left subclavian arteriogram. (Reproduced by permission from Haimovici H. Vascular surgery, 3rd edn. Norwalk, CT: Appleton & Lange, 1989:840–852.)

TABLE 79.1 Management of the cervical rib with arterial complications (1815–1955) No. Decompressive procedures Cervical rib resection Scalenotomy Total

%

17 12 29

58 42

Arterial repair and/or thoracic sympathectomy Arteriotomy 7 Periarterial stripping 1 Dorsal sympathectomy 1 Thrombectomy 1 Resection with graft replacement 1 Total 11

63.6 9.1 9.1 9.1 9.1

Based on data from Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs: surgical considerations. Report of a case and review of the literature. Surgery 1956;40:428.

TABLE 79.2 Management of the cervical rib with arterial complications (1956–1965)

FIGURE 79.6 Surgical specimen consisting of atherosclerotic intima and thrombi removed from third part of subclavian during thromboendarterectomy, recent organized thrombus extending from subclavian into axillary, and old organized thrombi (emboli) of brachial artery. (Reproduced by permission from Haimovici H. Vascular surgery, 3rd edn. Norwalk, CT: Appleton & Lange, 1989:840–852.)

No.

%

Decompressive procedures Cervical rib resection First thoracic rib resection Scalenotomy

15 5 6

57.7 19.2 23.1

Arterial repair and/or thoracic sympathectomy Arterial repair (thrombectomy, thromboembolectomy, excision of subclavian artery with graft replacement) Thoracic sympathectomy

14 13

51.8 48.2

Based on data from Judy KL, Heyman RL. Vascular complications of the thoracic outlet syndrome. Am J Surg 1972;123:521.

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Part X Upper Extremity Conditions

FIGURE 79.7 Algorithm of treatment options for arterial thoracic outlet syndrome. (Reproduced by permission from Sanders RJ, Haug C. Review of arterial thoracic outlet syndrome with a report of five new instances. Surg Gynecol Obstet 1991;173:415–425.)

TABLE 79.3 Management of the cervical rib with arterial complications (1966–1978)

Decompression procedures Cervical rib resection First thoracic rib resection Claviculectomy Scalenotomy Ecostosis of first rib Arterial repair and/or thoracic sympathectomy Thrombectomy Thromboendarterectomy Excision of SCA with graft interposition Embolectomy

TABLE 79.4 Management of the cervical rib with arterial complications (1979–1990)

No.

%

26 14 10 8 1

44.0 23.7 17.0 13.5 1.8

4 7 8 7

52.7 12.3

Based on data from Williams and Carpenter (29), Peet et al. (8), Bertelsen et al. (22), and Banis et al. (31).

was used in only 14 cases and included thrombectomy, thromboembolectomy, and excision of the subclavian artery with graft interposition, while the remaining cases were treated by thoracic sympathectomy either alone or in conjunction with arterial repair. Table 79.3, which includes 50 cases treated between 1966 and 1978, indicates a more aggressive approach to these lesions. It consists of wider application of decompressive procedures associated with more advanced techniques of arterial repair. The results obtained were more gratifying, although perfect revascularization of the limb is always difficult to achieve because of the multiple microembolic and repetitive lesions present distally.

Cervical rib Rudimentary first rib Fracture clavicle/rib No bony abnormality Extrinsic decompression (rib resection, scalenotomy, claviculectomy) Resection or ligation of artery (no repair) End-to-end anastomosis Graft (vein or prosthesis) Repair (often endarterectomy) with or without patch Thrombectomy/embolectomy Dorsal sympathectomy, only treatment No treatment Dorsal sympathectomy as adjuvant treatment Claviculectomy as part of treatment Improved No improvement Amputation Stroke (CVA) Death

No.

%

91 26 4 16 42

66 19 3 12 31

1 36 30 24

1 26 22 18

3 0 0 22

2 0 0 16

30 108 13 4 1 2 (CVA)

22 84 10 3 1 2

Data are from Sanders RJ, Haug C. Review of arterial thoracic outlet syndrome with a report of five new instances. Surg Gynecol Obstet 1991;173:415–425.

In the current era, the concepts and management of arterial thoracic outlet syndrome have greatly improved due to the progress achieved in vascular surgery on the whole. Table 79.4 reflects these improvements. Figure

Chapter 79 Arterial Thoracic Outlet Syndrome

79.7 shows treatment options for arterial thoracic outlet syndrome.

Comments The results of the combined arterial repair and cervicothoracic sympathectomy depend on the collateral network available at the hand and finger levels. If gangrene is present, either of the digits or of the hand, every effort should be made to delay amputation in order to provide time for development of the collateral circulation. A greater awareness of this unusual thromboembolic process associated with the thoracic outlet may lead to an earlier diagnosis with a better outlook for more complete limb salvage.

Conclusion The relatively rare vascular complications resulting from abnormal structures of the thoracic outlet with a potential threat to the viability of the upper limb are still not widely appreciated. Early recognition of the underlying thromboembolic process — the cause of the clinical manifestations — is the key to prevention and appropriate management of these complications.

References 1. Coote H. Exostosis of the left transverse process of the seventh cervical vertebra surrounded by blood vessels and nerves: successful removal. Lancet 1861;1:360. 2. Hilton J. Lectures on rest and pain. London, 1863:179. 3. Murphy JB. The clinical significance of cervical ribs. Surg Gynecol Obstet 1906;3:515–520. 4. Telford ED, Stopford JSB. The vascular complications of the cervical rib. Br J Surg 1931;18:577. 5. Todd TW. The vascular symptoms in “cervical” rib. Lancet 1912;2:362. 6. Halsted WS. An experimental study of circumscribed dilatation of an artery immediately distal to a partially occluding band, and its bearing on the dilatation of the subclavian artery observed in certain cases of cervical rib. J Exp Med 1916;24:271. 7. Lewis T, Pickering GW. Observations upon maladies in which the blood supply to digits ceases intermittently or permanently, and upon bilateral gangrene of digits: observations relevant to so-called “Raynaud’s disease.” Clin Sci 1934;1:327. 8. Peet RM, Hendricksen JD, et al. Thoracic outlet syndrome: evaluation of a therapeutic exercise program. Proc Mayo Clin 1956;31:281. 9. Rob CG, Standeven A. Arterial occlusion complication thoracic outlet compression syndrome. Br Med J 1958;2:709.

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10. Eden KC. The vascular complications of cervical ribs and first rib abnormalities. Br J Surg 1939–1940;27:111. 11. Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs: surgical considerations. Report of a case and review of the literature. Surgery 1956;40:428. 12. Scher LA, Veith FJ, et al. Staging of arterial complications of cervical rib: guidelines for surgical management. Surgery 1984;95:644. 13. Cormier JM, Amrane M, et al. Arterial complications of the thoracic outlet syndrome: fifty-five operative cases. J Vasc Surg 1989;9:778–787. 14. Kieffer E, Jeu-denis P, et al. Complications arterielles du syndrome de la traversee thoraco-brachiale. Traitement chirurgical de 38 cas. Chirurgie 1983;109: 714–722. 15. Sanders RJ, Haug C. Review of arterial thoracic outlet syndrome with a report of five new instances. Surg Gynecol Obstet 1991;173:415–425. 16. White JC, Poppel MH, Adams R. Congenital malformations of the first thoracic rib. Surg Gynecol Obstet 1945;81:643. 17. Adson AW. Surgical treatment for symptoms produced by cervical ribs and the scalenus anticus muscle. Surg Gynecol Obstet 1947;85:687. 18. Gruber W. Ueber die Halsrippen des Menshen mit verglerchendanatomischen Bmerkunger. Mem Acad Sci (St Petersburg) 1969;7:(2). 19. Short DW. The subclavian artery in 16 patients with complete cervical ribs. J Cardiovasc Surg 1975;16:135. 20. Holman EF. The obscure physiology of poststenotic dilatation: its relation to the development of aneurysms. J Thorac Cardiovasc Surg 1954;28:109. 21. Wellington JL. Martin P. Post-stenotic subclavian aneurysms. Angiology 1965;16:566. 22. Bertelsen S, Mathiesen FR, Phlenschlaeger HH. Vascular complications of cervical rib. Scand J Thorac Cardiovas Surg 1968;2:133. 23. Judy KL, Heyman RL. Vascular complications of the thoracic outlet syndrome. Am J Surg 1972;123:521. 24. Haimovici H. Arterial thromboembolism: thoracic outlet complications. In: Haimovici H, ed. Vascular emergencies. New York: Appleton-Century-Crofts, 1982:190. 25. Haimovici H, Caplan LH. Arterial thrombosis complicating the thoracic outlet syndrome: arteriographic considerations. Radiology 1966;87:457. 26. Lord JW Jr, Rosati LM. Thoracic outlet syndromes: clinical symposia. Ciba Found Symp 1971;23:3. 27. Roos D. Thoracic outlet syndromes: update. Am J Surg 1987;154:568–573. 28. Sanders RJ, Monsour JW, et al. Scalenectomy versus first rib resection for treatment of the thoracic outlet syndrome. Surgery 1979;85:109. 29. Williams HT, Carpenter NH. Surgical treatment of the thoracic outlet syndrome. Arch Surg 1978;113:850–852. 30. Mathes SJ, Salam AA. Subclavian artery aneurysm: sequela of thoracic outlet syndrome. Surgery 1974;76:506. 31. Banis JC, Rich N, Whelan TJ. Ischemia of the upper extremity due to noncardiac emboli. Am Surg 1977;134:131.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 80 Arterial Surgery of the Upper Extremity James S.T. Yao

Unlike occlusive disease affecting the lower extremities in which the etiology is either atherosclerotic or embolic, a wide variety of systemic diseases may cause ischemic symptoms of the upper extremity. Because of this, evaluation of upper extremity ischemia and selection of patients for surgery requires a thorough history and a careful physical examination. A good history-taking, including occupational, athletic, pharmacologic, and medical history, helps guide the diagnostic workup. For surgical treatment, the type of procedure depends on the location of the disease and the classification into proximal versus distal lesions. Surgical intervention is often indicated in patients with severe ischemia due to proximal arterial occlusion. Table 80.1 enumerates the causes of upper extremity ischemia.

Symptoms Presenting symptoms of upper extremity ischemia include pain, pallor, coolness, evidence of arterial emboli, and easy fatigue of the forearm after exercise. Arterial emboli can occur as livedo reticularis, petechiae of the skin, or gangrene of the tips of the fingers. Intermittent vasospasm must be distinguished from acrocyanosis, which is characterized by persistent, diffuse cyanosis of the fingers and hands. Easy fatigue or intolerance to exercise of the forearm are usually due to proximal artery lesions.

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Clinical Examination Examination of patients with symptoms of upper extremity ischemia must include the thoracic outlet and the entire upper extremity. Palpation of the supraclavicular region may help detect the presence of a subclavian artery aneurysm or a cervical rib. Auscultation of the subclavian artery and listening for the presence of a bruit during various thoracic outlet maneuvers helps establish the diagnosis of thoracic outlet compression to the artery. Arteries in the upper extremity are accessible to pulse palpation, and a decrease of pulse or absence of a pulse is diagnostic for major artery high-grade stenosis or occlusion. Examination of hand ischemia is not complete unless an Allen’s test is performed (1). The test is done as follows. The examiner stands beside or facing the subject. The radial and ulnar arteries of one wrist are compressed by the examiner’s fingers. The subject is asked to open and close the hand rapidly for 1 minute in order to squeeze blood out of the hand, then to extend the fingers quickly. The radial or the ulnar artery is released, and the hand is observed for capillary refilling and return of color. The test is judged normal if refilling of the hand is complete within a short period (<6 seconds). Any portion of the hand that does not blush is an indication of incomplete continuity of the arch. Hyperextension of the fingers must be avoided because this will give a false-positive result. In addition to the Allen test, examination of the hand must include palpation of the palm for a pulsatile mass. Assessment of patency of the digital arteries by palpation is difficult and unreliable.

Chapter 80 Arterial Surgery of the Upper Extremity TABLE 80.1 Etiology of upper extremity and digital ischemia I.

II.

III.

IV.

V.

VI. VII. VIII.

IX. X.

Atherosclerosis A. Arteriosclerosis obliterans B. Embolization 1. Cardiac 2. Atheromatous emboli Arteritis A. Collagen disease 1. Scleroderma 2. Rheumatoid arteritis 3. Systemic lupus erythematosus 4. Polyarteritis B. Allergic necrotizing arteritis C. Takayasu’s disease (autoimmune disorder) D. Buerger’s syndrome E. Giant cell arteritis Blood dyscrasias A. Cold agglutinins B. Cryoglobulins C. Polycythemia Drug-induced occlusion A. Ergot poisoning B. Drug abuse C. Dopamine-induced ischemia D. Chemotherapeutic agents Occupational trauma A. Vibration syndrome B. Hypothenar hammer syndrome C. Electrical burns D. Pitching a baseball E. Playing a musical instrument Thoracic outlet syndrome Congenital arterial wall defects Trauma A. Iatrogenic catheter injury 1. Cardiac catheterization 2. Arterial blood gas and pressure monitoring 3. Arteriography Renal transplantation and related problems A. Azotemic arteriopathy B. Hemodialysis shunts Aneurysms of the upper extremity

Diagnosis In most instances, the diagnosis of large-artery occlusion is not difficult, and a careful pulse examination will establish the diagnosis. In severe bilateral hand ischemia, a systemic cause of the arterial insufficiency should be sought. The major causes of such ischemia can be identified by serologic testing. Although patients harboring these conditions are seldom candidates for surgical intervention, it is important to establish the proper diagnosis. Recently, antiphospholipid antibody syndrome has been recognized as a distinct clinical entity causing thromboembolic symptoms. Diagnosis of the syndrome can be established by detection of anticardiolipin antibody in the blood. Increased titers of either IgG antibody to cardiolipin (a phospholipid) or IgM titers are diagnostic for this syndrome (2).

959

Noninvasive Tests Several noninvasive tests, including plethysmography and transcutaneous Doppler ultrasound flow detection, are now available for objective evaluation of hand ischemia. Of these techniques, Doppler flow detection is simplest. The Doppler examination of the upper extremity consists of both arterial waveform recording and analysis, and pressure measurements. Bilateral examinations should be performed because many of the diseases affecting the hand are symmetric (3), and often the asymptomatic hand will also have significant disease. Because the axillary and brachial arteries are superficially located, they lend themselves to Doppler examination throughout their entire course in the upper arm. Distal to the elbow, however, arterial signals are more difficult to obtain, and it is not until the wrist that both the radial and ulnar arteries become superficially situated once again. In the hand, the palmar arches are best heard at the midthenar and hypothenar regions. The common digital vessels are heard at the base of the fingers at their division into the proper digital arteries along the shaft of each finger. The waveforms are analyzed for their shape and contour, similar to examination of the lower extremity. For segmental upper extremity pressures, a pneumatic cuff is placed at the upper arm, as routinely used for blood pressure recording. The arm pressure will represent the brachial pressure, which should be within 10 to 20 mmHg of the opposite extremity. A greater difference signifies innominate, subclavian, axillary, or brachial artery stenosis. If brachial artery occlusion is suspected, a pressure cuff may be applied to the forearm and the pressure recorded in a similar manner using the radial artery for signal detection. If there is a pressure drop of 20 to 30 mmHg, this signifies an obstruction distal to the brachial artery. For digital pressure measurement, a 2.5-cm cuff is placed at the base of the finger, and the return of Doppler signals following cuff deflation is monitored at the fingertip. The palmar circulation is assessed by listening over the hypothenar and thenar eminences for the palmar arches. Patency of the palmar arch is assessed by the modified Allen test described by Kamienski and Barnes (4). The Doppler probe is placed over the radial artery while compressing the ulnar artery. Should the waveform be obliterated, the arch is dependent on the ulnar artery for supply. If the pulse remains present, the arch is complete. The procedure is repeated by listening over the ulnar artery while compressing the radial artery. The Allen’s test can be repeated while listening at the base of each digit or along the proper digital vessels of each finger. In some cases, even though the arch appears patent, pulsatile flow will be lost to the digits. The Doppler technique is of particular value to determine palmar arch patency in a patient who is unconscious or uncooperative in performing an Allen’s test. Arterial obstruction distal to the palmar arch is best detected by

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Part X Upper Extremity Conditions FIGURE 80.1 Normal variation of the brachial artery and its major branches. (Reproduced by permission from Bergan JJ, ed. Arterial surgery. New York: Churchill Livingstone, 1984.)

digital pressure measurements. An arterial occlusion distal to the palmar arch is defined by a pressure gradient between the fingers of greater than 15 mmHg or a wrist-to-digit difference of 30 mmHg. These very distal occlusions are caused by emboli, Buerger’s disease, or arteritis. There is good correlation between Doppler criteria and radiographic findings (5).

in 2.6% of cases. Rare anomalies, such as an accessory brachial artery or partially duplicated radial artery, were also identified. Of all arterial patterns of the upper extremity, the palmar arch is subject to most variation (Fig. 80.2). In a study by Coleman and Anson, the superficial arch was found to be complete in 80% of cases (8). In this group, five subgroups were identified:

Arteriography

Type A

Arteriography remains the most conclusive test for diagnosis of upper extremity ischemia, and it must be done if surgery is contemplated. Unless a focal proximal lesion is suggested by physical examination or noninvasive testing, bilateral studies are recommended. The preferred method for arteriography of the upper extremity, including the hand, is transfemoral catheterization of the subclavian and brachial arteries, with selective injection of contrast material (6). The innominate and subclavian arteries must be included in the examination. If thoracic outlet syndrome is suspected, a hyperabduction or external rotation with abduction view is obtained to detect the presence of compression. In addition to establishing a diagnosis, arteriography defines variations of the normal anatomy of the brachial artery and its branches. Such variations are of surgical significance if an operative procedure is contemplated, since normal anatomic variations have been observed in the brachial artery and its branches and in the palmar arch of the hand. The origin of the radial and ulnar vessels has been noted to be variable by McCormack et al. (7). In 750 upper extremity dissections, 139 specimens had high origin of the radial branch (14%), either from the axillary (2%) or midbrachial (12%) artery (Fig. 80.1). High origin of the ulnar artery was seen less frequently, being present

The arch was formed by the ulnar artery and the superficial palmar branch of the radial artery (35.5%). Type B The arch was formed entirely by the ulnar artery (37%). Type C The arch was formed by an enlarged median artery (3%). Type D The arch was formed by the radial, median, and ulnar arteries (1.2%). Type E The arch was formed by the ulnar artery joined by vessel from the deep palmar arch at the base of the thenar eminence. Incomplete arches are present in the remaining 20% of individuals and probably are a major underlying factor in the etiology of digital ischemia (Fig. 80.2). An incomplete arch is defined as one in which the superficial arch does not anastomose with any radial branch and the ulnar artery does not supply the thumb and radial aspects of the index finger. There are four subgroups of incomplete arches (8): Type A

Type B

The superficial palmar branches of both the radial and ulnar arteries supply the palm and fingers but do not anastomose (3.2%). The ulnar artery forms the entire superficial palmar arch but does not supply the thumb or index finger (13.4%).

Chapter 80 Arterial Surgery of the Upper Extremity

B

A

C

FIGURE 80.2 Patterns of normal palmar anatomy. (Reproduced by permission from Coleman SS, Anson BJ. Arterial patterns in the hand based upon a study of 650 specimens. Surg Gynecol Obstet 1961;113:409.)

F

E

G

D

961

H

I

J

Type C

The median artery reaches the hand to supply the digits but does not anastomose with the radial or ulnar arteries, and the median artery supplies a branch to the thumb (3.8%). Type D The radial, median, and ulnar arteries all give origin to the superficial vessels but do not anastomose (1.1%).

Proximal Arterial Lesions Atherosclerosis Atherosclerotic stenosis or occlusion is common in the subclavian artery but less so in the axillary, brachial, and distal arteries. Because of the rich collateral networks of the scapular region, occlusion of the subclavian artery seldom causes severe digital ischemia unless there is associated embolization. Atheromatous embolization to the digital arteries may present with Raynaud’s phenomenon, and the source may be an ulcerating proximal plaque or aneurysm (Fig. 80.3). Proximal subclavian artery occlusion is often associated with the vertebral steal phenomenon. Occlusion of the subclavian artery in the second or third part is less common. Collateral pathways in such instances depend on the site of the occlusion. Atherosclerotic occlusion of the axillary artery is uncommon. Instead, most occlusions of the axillary artery

FIGURE 80.3 Atherosclerotic plaque (arrow) of the subclavian artery in a patient with embolization to fingers.

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Part X Upper Extremity Conditions

are from unrecognized emboli originating from proximal atheromatous plaques or intracardiac thrombi.

Arterial Emboli The upper limbs are the site of acute arterial occlusion in 10% to 20% of acute embolic events (9), and the brachial artery is the most common site (65%) for lodgment of emboli in the upper extremity (10). Diagnosis of embolism of the brachial artery is not difficult. A careful pulse examination, with history and symptoms, usually establishes the diagnosis. Because of this, arteriography in a clear-cut case is seldom needed. A cardiac origin of emboli of the upper limb accounts for over 90% of these cases (10). Myxoma is one other possible source of the emboli (11). Occasionally, arterial emboli may go unnoticed, and the patient will present with recurrent symptoms. In this circumstance, arteriography is helpful in establishing the diagnosis.

Takayasu’s Arteritis Takayasu’s arteritis is a nonspecific inflammatory process of unknown etiology affecting segmentally the aorta and its main branches. Since Takayasu’s description of this disease in 1908 (12), it has been known by many names: pulseless disease, aortic arch syndrome, young female arteritis, and Martorell’s syndrome. In 1977, Ishikawa et al. (13) referred to Takayasu’s disease as occlusive thromboaortopathy to denote the widespread disease process that affects carotid, subclavian, axillary, and pulmonary arteries and the thoracic and abdominal aorta. Because the subclavian-axillary arteries are often involved, it is not unusual for patients to present with upper extremity ischemia. Mishima reported that of 774 operations performed in Japan between 1981 and 1990, 76 cases (9.0%) were for subclavian artery occlusion (14). Classically, the disease affects young women between 10 and 30 years of age, the sex ratio being at least 7 to 1. Though the bulk of cases have been reported in Japan, Takayasu’s arteritis is seen worldwide. The basic pathologic process is panarteritis, probably first affecting the adventitia and vasa vasorum. Later, the media is affected, with a loss of elastic fibers. The intima responds by proliferation, with subsequent thrombosis resulting in stenosis, occlusion, or aneurysm formation. In addition to symptoms referable to the arterial lesions, an acute or chronic nonspecific systemic illness often occurs. The etiology remains obscure, but the current consensus favors a hypersensitivity or autoimmune reaction. Inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein are elevated in these patients. Also, an abnormal HLA gene has been reported in Takayasu’s arteritis (15). Arteriography provides definitive diagnosis. Because of the widespread involvement of various arteries, total aortography has been advocated (13,16). In its most familiar form, the aortic arch and the main trunks are

FIGURE 80.4 Occlusion of innominate artery at left subclavian artery in a patient with Takayasu’s arteritis.

affected (Fig. 80.4), but lesions are also common in the descending thoracic and abdominal aorta. The pulmonary artery was affected in 45% of patients reported by Nasu (17). One of the distinct features of Takayasu’s arteritis is the presence of abundant collateral vessels (see Fig. 80.4). This finding is probably due to the chronicity of the disease. Unlike arteriosclerosis, subclavian occlusion proximal to the vertebral artery is rare. Rich collateral pathways from the subclavian, axillary, and proximal brachial arteries participate in the network.

Giant Cell Arteritis The most frequently recognized clinical features of giant cell arteritis (cranial, temporal, and granulomatous arteritis) result from involvement of cranial arteries. Systemic symptoms, such as malaise and fever, are common in these patients. Although involvement of large arteries by giant cell arteritis is uncommon, it has received some attention (18). Of 248 patients with giant cell arteritis reported by Klein et al., 15 were found to have ischemic symptoms of the upper extremity (18). Of these 15 patients, five had Raynaud’s phenomenon. Characteristic arteriographic findings in these patients included long segments of smooth arterial stenosis alternating with areas of normal or increased caliber; smooth, tapered occlusions; and absence of irregular plaques and ulcerations (Fig. 80.5).

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FIGURE 80.5 Arteriogram in a patient with proven giant cell arteritis. Note the typical tapering appearance of the subclavian artery.

Ergot Poisoning With the introduction of ergotamine tartrate for the treatment of migraine, vascular complications as a result of overdosage have become a diagnostic problem for those who are not familiar with ergot poisoning. The affected arteries may be in the upper extremities or the lower extremities (19,20). Most arterial occlusions may be reversed, if prompt diagnosis of ergot poisoning is made and the medication is discontinued instantly (21). In prolonged ischemia due to ergot poisoning, thrombosis with tissue necrosis may occur. Pharmacologically, ergot compounds produce intense vasoconstriction because of direct stimulation of the a receptors in the vessel wall. The characteristic finding on the arteriogram is intense spasm seen as long, smooth areas of narrowing. This is often bilateral and tends to be symmetric. Occasionally, focal spasm is seen. Other prominent features are the presence of abundant collateral vessels. Although rare, thrombi may be present and are seen as filling defects on the arteriogram. Spasm and narrowing of the affected artery often reverse to normal when ergot drugs are completely withdrawn (Figs. 80.6 and 80.7). Ergot poisoning victims may occasionally benefit from the administration of sodium nitroprusside.

Thoracic Outlet Syndrome Thoracic outlet syndrome consists of neurologic and vascular manifestations. The anatomic boundaries of the thoracic outlet generally correspond to the area traversed by the subclavian artery and vein and the brachial plexus. These structures pass through the interscalene triangle (anterior and medial), with the exception that the subclavian vein lies anterior to the scalene muscle. They then lie

FIGURE 80.6 Arteriogram demonstrating occlusion of the brachial artery in a young woman with ergot poisoning. Note extensive spasm of the brachial artery. (Reproduced by permission from Neiman HL, Yao JST, eds. Angiography of vascular disease. New York: Churchill Livingstone, 1985.)

in the retroclavicular fossa, pass beneath the clavicle, and enter the upper extremity. The subclavian and axillary vessels and brachial plexus can be compressed extrinsically at four sites: 1. 2. 3.

4.

the costoclavicular space; the interscalene triangle; the angle between the insertion of the pectoralis minor muscle and the coracoid process in the axilla; and the humerus head (22).

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Humerus head compression causes not only damage to the third portion of the axillary artery but also aneurysm formation of the circumflex humeral artery (23). These damages have been frequently found in baseball pitchers and other high-performance athletes (23,24). Of these sites, the costoclavicular space, formed by the first thoracic rib and clavicle, is the most common site of compression. Any structure that encroaches upon the thoracic outlet or any process that functionally reduces its dimensions can produce compression of the brachial plexus and underlying vascular structures. Thoracic outlet syndrome may be due to cervical rib, abnormalities of the scalenus anticus muscle, or bony abnormalities of the cervical vertebrae, clavicle, or first rib. Although between 0.5% and 1% of the population have a cervical rib, 10% or fewer of such persons have symptoms of neurovascular compression. The majority of patients with thoracic outlet syndrome present with neurologic rather than ischemic symptoms. Pain is usual and involves the C8 and T1 dermatome. Vascular abnormalities in thoracic outlet syndrome include direct compression of the artery or poststenotic dilation or aneurysm formation with thrombus formation and distal embolization (Figs. 80.8 and 80.9). Raynaud’s phenomenon is not uncommon as an initial complaint, and it is often unilateral.

Radiation Injury

FIGURE 80.7 Repeat arteriogram in the same patient as in Figure 80.6, 10 days after cessation of drug. The brachial artery has returned to normal appearance. (Reproduced by permission from Neiman HL, Yao JST, eds. Angiography of vascular disease. New York: Churchill Livingstone, 1985.)

Irradiation may cause damage not only to small vessels but also to large arteries such as the subclavian (25). Morphologic changes in small arteries have been described by several investigators (26,27). These changes include endothelial proliferation, degeneration of the cells of the media with subsequent cystic medial necrosis, and fibrosis. Most injuries to the arteries present with late manifestations, and for the most part injury to the vasa

FIGURE 80.8 Arteriogram of a patient with thoracic outlet compression syndrome. (A) Neutral position. (B) Hyperabduction. The subclavian artery became stenotic.

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FIGURE 80.10 Arteriogram in a patient with a history of irradiation of the shoulder region. Note the linear web-like defect in the artery. (Reproduced by permission from Neiman HL, Yao JST, eds. Angiography of vascular disease. New York: Churchill Livingstone, 1985.)

FIGURE 80.9 Arteriogram in a patient with cervical rib and hand ischemia, showing aneurysm dilation of the subclavian artery. A filling defect (arrow) is seen in the brachial artery, indicating embolization.

vasorum is present. Fonkalsrud et al. documented these changes by light-electron microscopy (27). Fibrosis of the arterial wall as a result of damage to the vasa vasorum leads to narrowing of the vessel lumen. As stated by Butler et al., there are three stages following irradiation (25). The first is at 5 years following radiation, when most patients present with mural thrombosis. These patients are also found to have multiple digital artery occlusions, presumably due to embolization from the injured subclavian artery (Fig. 80.10). The second stage occurs 10 years after irradiation, when patients present with symptoms caused by fibrotic occlusion of the irradiated vessel. The third stage is much later (20 to 25 years or more following irradiation), when the lesion involves periarterial fibrosis together with accelerated atherosclerosis.

Distal Arterial Lesions Collagen Disease Collagen diseases are a broad category of disorders having in common the finding of generalized connective tissue damage with an increase in the amount of collagen in skin, muscle, tendons, fascia, and viscera. Each of the different types of disease classified under this grouping has prominent, nonspecific, constitutional manifestations, along

with varying patterns of organ involvement. When the characteristic histologic changes of fibrinoid degeneration and intimal thickening occur in the blood vessels, signs of ischemia can occur. In addition, the added insult of vasospasm may adversely contribute to the clinical picture. Collagen disease includes scleroderma, rheumatoid arteritis, systemic lupus erythematosus, polyarteritis nodosa, and dermatomyositis. All these diseases have systemic symptoms, and the diagnosis is made by elevation of erythrocyte sedimentation rate and positive serologic tests.

Buerger’s Disease (Thromboangiitis Obliterans) Raynaud’s disease and Buerger’s disease have met with similar controversy in regard to their being distinct clinical entities. Buerger’s disease was first described by von Winiwarter in 1879. In 1908, Buerger described the disease in Jewish patients who presented with digital gangrene without occlusion of the larger arteries (28). Today it is noted that such patients are invariably heavy smokers. While the disease, if it exists, is more common in the lower extremity, it may also occur in the upper extremity. Recent study has shown impaired endothelium-dependent vasorelaxation as a factor in Buerger’s disease (29). As arteriography became more frequent, patients suspected of having Buerger’s disease were found to have atherosclerosis rather than thromboangiitis obliterans. Similarly, modern investigation in suspected patients often uncovers an underlying connective tissue disorders. At present, the diagnosis of Buerger’s disease depends on histologic examination with involvement not only of arteries but of veins as well. This is manifested clinically as migrating phlebitis. Characteristic arteriographic findings are occlusion of small arteries of the digits, with abundant collaterals

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Mayo Clinic and found that a third of these patients had vascular complications (31). Of 200 patients with polycythemia vera, the arterial complications ranged from cerebrovascular accident to peripheral artery occlusion and also included venous thrombosis in 34% (32). The cause of small artery occlusion is generally thought to be local thrombosis or embolism. Regardless of the cause, acute digital ischemia may occur.

Drug Abuse Drug abuse presents social problems and a wide variety of medical problems. Vascular complications due to drug abuse may be related to local damage to the artery by unsterile needles leading to infection, false aneurysm formation, or arteriovenous fistula. Apart from the systemic effect of various drugs on the arterial system itself, the inadvertent injection of hypertonic solution or powder into the arterial system often causes multiple digital arterial occlusions. Raynaud’s phenomenon following this form of obstruction is not uncommon.

Catheter Injury

FIGURE 80.11 Arteriographic appearance of the hand vasculature in a patient with a history of heavy smoking without collagen disease.

(Fig. 80.11). A characteristic corrugated appearance of the artery proximal to an occlusion is often seen and this finding has been cited as one of the diagnostic findings in Buerger’s disease. However, the corrugated artery may also be seen in other conditions. Not only does the symptomatic hand demonstrate digital artery occlusion, but the asymptomatic hand may show it as well (30).

Blood Dyscrasias Cold agglutinins, cryoglobulin, and polycythemia vera are the most common forms of blood dyscrasias which may be associated with occlusion of the arteries of the legs or hands. In 1903, William Osler first drew attention to vascular complications of polycythemia. Norman and Allen reported their experience with polycythemia at the

With increasing use of diagnostic and therapeutic procedures involving catheterization, damage to the radial or brachial artery has become more common, especially when an incomplete palmar arch is not recognized prior to placement of a catheter in the radial artery (32). Catheterization of the heart or arteriographic examination of the extremities and trunk may result in damage to the brachial artery, which causes thrombosis, embolization, or dissection. Failure to recognize normal anatomic variation of the brachial and hand arterial anatomy may cause puzzling problems. Further, unrecognized injury to the brachial artery following cardiac catheterization may cause exercise pain in the forearm or cold sensitivity of the involved extremity. Arteriographic examination is often needed to clarify the situation. The arteriographic finding is often occlusion of the brachial artery with irregularity of the arterial wall. When there is associated embolization, multiple occlusions of the digital arteries may also be seen. Injuries to the radial artery from blood gas monitoring are not uncommon. Severe ischemia may result if there is incompleteness of the superficial and deep volar arches, and gangrene of the hand has been reported. Arteriography is seldom needed when acute thrombus is recognized and promptly treated. In chronic ischemia, arteriography may be necessary to define the anatomy of the hand, thus allowing consideration of microvascular repair of the artery.

Hypothenar Hammer Syndrome The predisposing factor in the development of hypothenar hammer syndrome is the repetitive use of the palm of the hand in activities that involve pushing, pound-

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FIGURE 80.12 Mechanism of injury to the ulnar artery in hypothenar hammer syndrome. (See text for explanation.)

ing, or twisting (Fig. 80.12). The anatomic location of the ulnar artery in the area of the hypothenar eminence places it in a vulnerable position. When this area is repeatedly traumatized, ulnar or digital artery occlusion or aneurysm formation can result (33).

Azotemic Arteriopathy In chronic renal failure, calcification, such as is seen in Monckeberg’s arteriosclerosis of the lower extremity, may affect the digital arteries of the hand, causing gangrene of the digits. The so-called azotemic arteriopathy (34) is characterized by calcification of the media of the digital arteries, resulting in a pipestem pattern on plain xray film (Fig. 80.13). A similar condition may be observed in patients with longstanding diabetes mellitus.

Aneurysms of Upper Extremity Arteries Common sites for aneurysm formation in the upper extremity are the subclavian artery and the hand. False aneurysm due to trauma, however, may occur along the

FIGURE 80.13 Typical appearance of azotemic arteriopathy in a diabetic patient with renal transplant. All digital arteries are distinctly seen on plain x-ray film. The radial artery also shows heavy calcification. Arteriogram in this patient shows multiple digital artery occlusions.

course of the arterial system in the upper extremity. Innominate artery aneurysm may cause hand ischemia, but this is rare.

Subclavian Artery Aneurysm Aneurysms of the subclavian artery are rare in comparison with other peripheral aneurysms, and most subclavian aneurysms are caused by blunt or penetrating trauma or by thoracic outlet syndrome. In the latter condition, poststenotic dilation is often observed in patients with cervical rib. The incidence of arteriosclerotic aneurysm of the subclavian artery is unknown, but the condition is rare, even in patients with multiple aneurysms. Several authors, however, have reported series of arteriosclerotic subclavian artery aneurysms (35,36), and aneurysm of the anomalous subclavian artery has received attention (38). Other, less common causes of subclavian artery aneurysm

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development of microvascular surgery, most aneurysms are now being treated with vein graft interposition or simply by end-to-end anastomosis.

Treatment Treatment of upper extremity ischemia is strictly according to the etiology. Withdrawal of drugs such as ergot derivatives, dopamine, or chemotherapeutic agents will help reverse ischemia. For patients with collagen disease, treatment must be directed toward the underlying cause and steroid or immunosuppressive treatment may be necessary. Patients with digital artery occlusion without proximal artery lesions are not candidates for surgical intervention. Severe hand ischemia associated with major arterial lesions is the prime indication for arterial reconstructive surgery in the upper extremity. In patients with associated arteritis or autoimmune disease with a high erythrocyte sedimentation rate, the use of a steroid preparation may be necessary. The type of procedure employed varies according to the location of the lesion.

Proximal Artery Occlusion

FIGURE 80.14 Aneurysm of the terminal branch of the ulnar artery in a carpenter with hypothenar hammer syndrome.

are syphilis (38), cystic medial necrosis, congenital defects, and invasion from tuberculous lymphadenitis. Subclavian artery aneurysm may present as a late complication of a Blalock-Taussig anastomosis and may also be a part of an arteriovenous malformation. Subclavian artery aneurysm may cause digital artery occlusion because of embolization from debris or thrombi within the aneurysm.

Aneurysms of the Hand False aneurysms due to penetrating trauma or needle puncture are the most common forms of aneurysm of the hand. Other aneurysms of the hand arteries may be due to occupational trauma with injury to the ulnar artery where it passes across the hook of the hamate bone (Fig. 80.14). Arteriosclerotic aneurysms of the hand are rare and have been reported sporadically (39). The lesions are usually associated with significant arteriosclerotic disease involving other vessels. Either the radial or the ulnar artery may be involved. Arteriography allows examination of the integrity of the volar arch and the collateral pathways. With the

Lesions involving the innominate, subclavian, or axillary artery are best treated by bypass grafting. In selected cases in which the atherosclerotic process, such as ulcerating plaque, is localized, a short-segment endarterectomy with patch may be used. An intrathoracic approach using the thoracic aorta as the origin of the graft is needed if the innominate or proximal subclavian artery is occluded. Long-segment occlusion of the axillary or brachial artery is also best treated by bypass grafting. The use of autogenous vein (saphenous or cephalic) as the bypass conduit is preferred to prosthetic materials. Short segmental stenosis or occlusion of the brachial artery (< 2 cm) is amenable to endarterectomy with vein patch. In extensive occlusion of the forearm arteries, bypass to the ulnar, radial, or interosseous artery using autogenous vein is indicated to relieve severe ischemia. Management of vascular complications of the thoracic outlet syndrome depends on the extent of injury and the mechanism of compression. Damage to the artery such as mural thrombosis, poststenotic dilation, or aneurysm formation must be dealt with by replacement of the injured segment with a short bypass graft. At the same time, the responsible compression structure (cervical rib, anterior scalene muscle) must be removed. If there is no arterial damage but there is evidence of compression, removal of the cervical rib or offending muscle is needed to prevent future assault on the artery. Distal embolization as a result of mural thrombus or thrombosed aneurysm may require distal bypass to relieve severe ischemia. Exposure of Subclavian Artery The skin incision is made 1 cm above and parallel to the clavicle, beginning medially at the sternal head of the ster-

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A

A B

B

C

FIGURE 80.16 (A) Skin incision for axillary to brachial, ulnar, radial artery bypass. (B) Exposure of the axillary artery is greatly facilitated by dividing the pectoris minor muscle at its insertion. (Reproduced by permis-

D

FIGURE 80.15 Exposure of the subclavian artery. (See text for explanation.) (Reproduced by permission from Bergan JJ, Yao JST, eds. Cerebrovascular insufficiency. New York: Grune & Stratton, 1983.)

nocleidomastoid muscle and extending laterally to the midpoint of the clavicle (Fig. 80.15A). The incision is carried through the subcutaneous tissue and platysma muscle to expose the clavicular head of the sternocleidomastoid muscle (Fig. 80.15B). The muscle is then divided parallel to the clavicle using the coagulation mode of the electrocautery, exposing the scalene fat pad. Dissection medially in the scalene fat should identify the anterior scalene muscle and its attachment to the first rib (Fig. 80.15C). Particular care must be given to this dissection, because the phrenic nerve courses along the anterior border of the anterior scalene muscle and must be preserved. The phrenic nerve is mobilized from the anterior scalene muscle and retracted gently with a Silastic sling. The anterior scalene muscle may then be divided close to its junction with the first rib, thus exposing the more proximal portion of the subclavian artery (Fig. 80.15D). It must be remembered that the subclavian vein lies just anterior to the anterior scalene muscle and should be protected during division of the muscle. Also, the thoracic duct, which enters the junction of the left internal jugular vein and the left subclavian

sion from Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

vein, can easily be injured inadvertently at this point in the dissection. At this time, the subclavian artery is skeletonized. Remember that the pleura lies just deep to the vessel. The vertebral artery should be preserved unless it is occluded by atherosclerotic disease. The internal mammary artery and thyrocervical trunk should be preserved, but division of the internal mammary artery increases mobility of the subclavian artery. Vascular control is obtained through the use of Silastic slings on the proximal and distal extent of the subclavian artery, proximal control being obtained as early as possible during the dissection. Branch vessels are controlled by the double-looping of Silastic slings that are placed on mild tension prior to arteriotomy. Exposure of Axillary Artery A horizontal incision is made approximately 6 to 8 cm in length, about two finger-breadths below the clavicle (Fig. 80.16A). This is similar to exposure of the axillary artery for axillary-femoral bypass. The pectoralis major muscle fibers between the clavicular and sternocostal heads are split horizontally, parallel to the skin incision. After division of the pectoralis minor close to its insertion, the axillary artery is exposed easily. Great care must be taken to avoid injury to surrounding structures, such as the axillary vein, which lies inferiorly, and the lateral cord of the brachial plexus, which is located above the artery. Exposure of the axillary artery may be facilitated by dividing the pectoralis nerve (Fig. 80.16B). This procedure causes no motor loss. The lateral thoracic artery must be identi-

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A A

B

FIGURE 80.17 (A) Skin incision for exposure of brachial artery and its trifurcation. (B) The brachial artery is readily identifiable after the sheath of the neurovascular bundle is entered. (Reproduced by permission from Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

B

FIGURE 80.18 The radial and ulnar arteries are often seen beneath the bicipital aponeurosis, which may be divided to facilitate exposure. (Reproduced by permission from Bergan JJ, Yao JST, eds. Operative techniques in vascular surgery. New York: Grune & Stratton, 1980.)

fied and looped with a Silastic tape for control of bleeding during the arteriotomy. After exposure of the axillary artery proximally and distally for about 4 cm, the artery is ready for the bypass procedure. Exposure of Brachial Artery The arm is placed in abduction with the forearm and hand in supination. An incision of 6 to 8 cm is made medially along the posterior border of the biceps muscle (Fig. 80.17A). After medial and lateral retraction of muscle, the brachial artery is identifiable. The sheath of the neurovascular bundle is entered through an avascular area. The artery is normally surrounded by the median nerve and medial cutaneous nerve of the forearm. A 4-cm segment of brachial artery is exposed (Fig. 80.17B), which can be used either to accept a vein graft from the axillary artery or as the proximal supply of a brachial to radial or brachial to ulnar artery bypass. Exposure of Radial, Ulnar, or Interosseous Artery Depending on the nature of the occlusion, the radial or ulnar artery can be exposed and used for bypass at either the elbow or the wrist. At the elbow, the radial or ulnar artery is exposed simply by extending the incision across the elbow joint as depicted in Figure 80.18A. The lacertus fibrosus (bicipital aponeurosis) of the biceps muscle can be retracted laterally to facilitate the exposure of these two major branches. If necessary, the bicipital aponeurosis may be divided. The brachial vein is seen between the artery and the median nerve. The recurrent radial artery, a small branch, may be seen and must be identified for control of backbleeding. Either the ulnar or radial artery may

be used as the recipient for the bypass. If both the ulnar and radial arteries are occluded, the interosseous artery may be used. The common interosseous artery originates from the dorsal lateral surface of the ulnar artery about 2 to 3 cm distal to the brachial bifurcation (Fig. 80.18B). The size of this artery is close to the size of the proximal ulnar artery, and it divides into posterior and anterior branches just proximal to the interosseous membrane (Fig. 80.19). Exposure of the anterior interosseous artery follows the anatomic landmark of the ulnar artery. The anterior interosseous artery is found between the flexor digitorum profundus muscle and the flexor pollicis longus (Fig. 80.20) and is accompanied by the anterior interosseous branch of the median nerve. The latter provides motor regulation to the flexor digitorum profunda and the flexor pollicis longus. The posterior interosseous artery is located on the dorsal aspect of the forearm, and a separate skin incision on the dorsum of the forearm is needed to expose this artery.

Surgical Procedure The patient is placed in supine position with the hand and upper arm positioned at 90° abduction and resting on an arm board. The arm must be draped free in sterile fashion using a stockinette so that an incision on the inner aspect of the upper arm can be made easily, if necessary. This position allows palpation of distal pulses (radial, ulnar, and brachial) to ascertain the success of the operation. Bypass procedures in the upper extremity are normally done with autogenous vein harvested from the

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FIGURE 80.20 Cross-section of forearm shows exposure of the interosseous digitorum profundus. (Reproduced by permission from McCarthy WJ, Flinn WR, et al. Result of bypass grafting for upper limb ischemia. J Vasc Surg 1986;3:741.)

FIGURE 80.19 Anatomy of left forearm. Note relation between the median nerve and the anterior interosseous artery. (Reproduced by permission from McCarthy WJ, Flinn WR, et al. Result of bypass grafting for upper limb ischemia. J Vasc Surg 1986;3:741.)

lower limb. Therefore, one of the lower extremities, including the groin, must be prepared and draped during the procedure. If the saphenous vein is not available, the cephalic vein from the contralateral arm may be used. Expanded polytetrafluoroethylene is used only when no autogenous vein is available. Once the sites for inflow and distal anastomoses are determined, the exposure described above is executed on the appropriate artery. Following this, the saphenous vein is harvested and prepared. The vein is distended with normal saline, and all leaking branches are ligated with 4–0 sutures. The vein is then ready for anastomosis. Tunneling of the bypass graft follows the normal pathway of the artery using a long DeBakey clamp placed subfascially. If necessary, a separate jump incision is made to facilitate passing of the graft. The vein graft is placed in reverse position and passed through the subfascial tunnel. At this point, 5000 U of heparin is given. Anastomosis of vein to artery is often done in end-toside manner using 6–0 Prolene sutures. At the completion of the anastomoses, an electromagnetic flowmeter is used to ascertain the flow value, followed by an intraoperative arteriogram to evaluate the integrity of the distal anastomosis. The latter procedure is done by placing a 20-gauge intra-arterial shunt catheter into the graft. Injection of 20 mL of contrast media is often sufficient to visualize the distal arm and the hand. The hand must be included to allow detailed study of the palmar arch anatomy.

Distal Arterial Lesions This refers to stenosis, occlusion, or aneurysm at the wrist level or in the hand. A short segmental occlusion of either the radial or ulnar artery is best treated by thrombectomy or endarterectomy with vein patch. An aneurysm in the hand is not uncommonly associated with hypothenar hammer syndrome, and the aneurysm can be resected and replaced with either primary end-to-end anastomosis or an interposed vein graft. Recently, Nehler and his colleagues reported 17 successful arterial bypasses distal to the wrist (40). Occlusion distal to the proximal palmar crease is not ordinarily amenable to surgery, but perhaps microvascular repair should be considered.

Results Garrett et al. (41) were the first to report on the use of an autogenous vein bypass for upper extremity ischemia. Subsequently, others have also reported good results with bypass grafting (42–48). In our recent review of upper extremity arterial bypass grafting during a 15-year period, the overall patency rate was 61.2% at 5 years. More proximally placed grafts had better outcomes than distal bypass grafts: 67.5% vs. 41.4% (Fig. 80.21) (49). Unlike lower extremity surgery, major amputation was not required in any case, even after graft occlusion.

Cervical Sympathectomy Like lumbar sympathectomy, cervical sympathectomy is done less and less frequently. This is because of the better understanding of episodic vasospasm and, in particular,

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FIGURE 80.21 Cumulative patency in patients with rest pain and tissue loss compared with that in patients with other symptoms showed no statistical difference.

an improvement in diagnostic techniques. Many patients thought to have Raynaud’s disease have been found to have secondary disease, and sympathectomy is not helpful in patients with collagen disease. As a result, cervical sympathectomy is done only in selected instances. Sympathectomy is indicated in hyperhidrosis and causalgia.

References 1. Allen EV. Thromboangiitis obliterans: methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am J Med 1929;178:237. 2. Love PE, Santoro SA. Antiphospholipid antibodies: anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-SLE disorders Ann Intern Med 1990;112:682–698. 3. Erlandson EE, Forrest ME, et al. Discriminant arteriographic criteria in the management of forearm and hand ischemia. Surgery 1981;90:1025. 4. Kamienski RW, Barnes RW. Critique of the Allen test for continuity of the palmar arch assessed by Doppler ultrasound. Surg Gynecol Obstet 1976;142:861. 5. Yao JST, Gourmos C, Irvine WT. A method for assessing ischemia of the hand and fingers. Surgery 1972;135:373. 6. Yao JST, Bergan JJ, Neiman HL. Arteriography for upper extremity and digital ischemia. In: Neiman HL, Yao JST, eds. Angiography of vascular disease. New York: Churchill Livingstone, 1985;353–419. 7. McCormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns: a study of 750 extremities. Surg Gynecol Obstet 1953;96:43.

8. Coleman SS, Anson BJ. Arterial patterns in the hand based upon a study of 650 specimens. Surg Gynecol Obstet 1961;113:409. 9. Metz P, Sager P. Acute arterial occlusion of the upper limbs: a follow-up study of 31 extremities. Acta Chir Scand 1974;140:195. 10. Savelyev JS, Zatevakhin II, Stepanov NV. Arterial embolism of the upper limbs. Surgery 1977;81:367. 11. Thompson JR, Simmons CR. Arterial embolus: manifestation of unsuspected myxoma. J Am Med Assoc 1974;228:864. 12. Takayasu M. A case with peculiar changes of the central retinal vessels. Acta Soc Ophthalmol Jpn 1908;12:554. 13. Ishikawa K, Serin Y, et al. Occlusive thromboaortopathy (Takayasu’s disease) and allied diseases. In: Proceedings 34th Asian-Pacific Congress Cardiology, vol 1,1964:43. 14. Mishima Y. Leriche Memorial Lecture at 24th World Congress, “Takayasu’s arteritis in Asia.” Cardiovascular Surgery 2001;9:3–10. 15. Numano F, Okawara M, et al. Takayasu’s arteritis. Lancet 2000;356:1023–1025. 16. Lande A, Rosse P. The value of total aortography in the diagnosis of Takayasu’s arteritis. Radiology 1975;114:287. 17. Nasu T. Pathology of pulseless disease: a systematic study and critical review of twenty-one autopsy cases reported in Japan. Angiology 1963;14:225. 18. Klein RG, Hunder CG, et al. Large artery involvement in giant cell (temporal) arteritis. Ann Intern Med 1975;83:806. 19. Kempczinski RF, Buckley CJ, Darling RC. Vascular insufficiency secondary to ergotism. Surgery 1976;79:597. 20. Yao JST, Goodwin DP, Kenyon JR. Case of ergot poisoning. Br Med J 1970;3:86. 21. Fielding JML, Donovan RM, et al. Reversible arteriopathy following an ergotamine overdose in a heavy smoker. Br J Surg 1980;67:247. 22. Rohrer MJ, Cardullo PA, et al. Axillary artery compression and thrombus in throwing athletes. J Vasc Surg 1990;11:761–769. 23. McCarthy WJ, Yao JST, et al. Upper extremity arterial injury in athletes. J Vasc Surg 1989;9:317–327. 24. Durham JR, Yao JST, et al. Arterial injuries in the thoracic outlet syndrome. J Vasc Surg 1995;21:57–70. 25. Butler MJ, Lane RHS, Webster JHH. Irradiation injury to large arteries. Br J Surg 1980;67:341. 26. Moss WT, Brand WN, Battifora H. The heart and blood vessels. In: Radiation oncology, rationale, technique, results. St. Louis: CV Mosby, 1973:248. 27. Fonkalsrud EW, Sanchez M, et al. Serial changes in arterial structure following radiation therapy. Surg Gynecol Obstet 1977;145:395. 28. Buerger L. Thrombo-angiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. Am J Med Sc 1908;136:567. 29. Makita S, Nakamura M, et al. Impaired endotheliumdependent vasorelaxation in peripheral vasculature of patients with thromboangiitis obliterans (Buerger’s disease). Circulation 1996;94(suppl II):II-211–II-215. 30. Hirai M, Shionoya S. Arterial obstruction of the upper limb in Buerger’s disease: its incidence and primary lesion. Br J Surg 1979;66:124. 31. Norman IL, Allen EV. The vascular complications of polycythemia. Am Heart J 1937;13:257.

Chapter 80 Arterial Surgery of the Upper Extremity 32. Rich NM, Hobson RW II, Fedde CW. Vascular trauma secondary to diagnostic and therapeutic procedures. Am J Surg 1974;128:715. 33. Conn J, Bergan JJ, Bell JL. Hypothenar hammer syndrome: posttraumatic digital ischemia. Surgery 1970;68:1122. 34. Conn, KrumLovsky FA, et al. Calciphylaxis: etiology of progressive vascular calcification and gangrene? Ann Surg 1973;177:206. 35. Hobson RW II, Sarkaria J, et al. Atherosclerotic aneurysms of the subclavian artery. Surgery 1979;85:368. 36. Pairolero PC, Walls JT, et al. Subclavian-axillary artery aneurysms. Surgery 1981;90:757. 37. Rodgers BM, Talbert JL, Holenbeck JI. Aneurysm of anomalous subclavian artery: an unusual cause of dysphagia lusoria in childhood. Ann Surg 1978;187:158. 38. Bjork VO. Aneurysm and occlusion of the right subclavian artery. Acta Chir Scand Suppl 1965;356:103. 39. Thorrens S, Trippel OH, Bergan JJ. Arteriosclerotic aneurysms of the hand: excision and restoration of continuity. Arch Surg 1966;92:937. 40. Nehler MR, Dalman RL, et al. Upper extremity arterial bypass distal to the wrist. J Vasc Surg 1992;16:633–642.

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41. Garrett HE, Morris GC, et al. Revascularization of upper extremity with autogenous vein bypass graft. Arch Surg 1965;91:751. 42. Wood PB. Vein-graft bypass in axillary and brachial artery occlusions causing claudication. Br J Surg 1973;60:29. 43. Holleman JH Jr, Hardy JD, et al. Arterial surgery for arm ischemia: a survey of 136 patients. Ann Surg 1980;191:727. 44. Gross WS, Flanigan DP, et al. Chronic upper extremity arterial insufficiency: etiology, manifestations, and operative management. Arch Surg 1978;113:419. 45. Bergqvist D, Ericsson BF, et al. Arterial surgery of the upper extremity. World J Surg 1983;7:786. 46. McNamara MF, Takiki HS, et al. A systematic approach to severe hand ischemia. Surgery 1978;83:1. 47. Welling RE, Cranley JJ, et al. Obliterative arterial disease of the upper extremity. Arch Surg 1981;116:1593. 48. McCarthy WJ, Flinn WR, et al. Result of bypass grafting for upper limb ischemia. J Vasc Surg 1986;3:741. 49. Mesh CL, McCarthy WJ, et al. Upper extremity bypass grafting: a 15-year experience. Arch Surg 1993;128:795–802.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 81 Upper Thoracic Sympathectomy: Conventional Technique Henry Haimovici

Sympathetic denervation of the upper extremity may be achieved by various techniques. In spite of technical improvements, it is well recognized that a lasting denervation of the upper extremity has remained a goal sometimes difficult to achieve (1,2). 䊏

Neuroanatomy of Upper Thoracic Sympathetic Chain The inferior cervical ganglion is commonly fused with the first thoracic ganglion, thus constituting the stellate ganglion. To achieve adequate sympathetic denervation of the upper extremity, removal of the inferior cervical and upper three thoracic segments of the sympathetic trunk is essential. As a result of its ablation, however, a Horner’s syndrome may be produced.

䊏

䊏

䊏

Indications The most common indications for sympathectomy of the upper extremity are as follows: 䊏

Vasospastic syndromes: Raynaud’s disease with disabling symptoms and signs, unyielding to medical management and lasting over 1 to 2 years; Raynaud’s phenomenon secondary to scleroderma. The va-

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sospastic changes of the digits associated with the latter conditions are less amenable to this type of surgery. In hyperhidrosis, when severe enough and disabling, an upper thoracic sympathectomy usually provides excellent results. Organic diseases: Thromboangiitis obliterans, arteriosclerosis obliterans, affecting mostly the lower extremities, may also involve the upper extremities. In advanced cases with ischemic lesions and vasomotor changes in the absence of reconstructive arterial surgery, an upper thoracic sympathectomy may sometimes yield gratifying results. Thoracic outlet syndromes with involvement of the subclavian or axillary arteries, resulting in peripheral emboli, may occasionally be managed by a combined cervical rib resection and an upper thoracic sympathectomy (3,4). Causalgia or causalgia-like syndromes may occasionally benefit from an upper thoracic sympathectomy. Posttraumatic sympathetic dystrophy (Sudeck’s atrophy) with marked osteoporosis, swelling, coldness, sweating, and pain of the hands has been successfully controlled by this procedure.

Operative Techniques The choice of one of the several approaches available depends essentially on which one offers the easiest exposure

Chapter 81 Upper Thoracic Sympathectomy: Conventional Technique

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FlGURE 81.1 Right supraclavicular approach. (A) Position of the patient and line of skin incision. (B) Dotted lines indicate the site of sectioning of the sternocleidomastoid and omohyoid muscles. The external jugular vein is being divided. (C) Anterior scalene muscle is divided along dotted line, care being taken to retract the phrenic nerve medially. (D) Retraction of the subclavian artery downward and the vertebral artery and phrenic nerve medially helps to expose the stellate ganglion. Note the brachial plexus laterally and the pleural dome behind the subclavian artery. (E) Cervicothoracic sympathetic ganglia in their retropleural relation.

B

A

C

D

E

of the sympathetic trunk and carries the least operative risk. The following three approaches have somewhat different indications:

bell-shaped structure, 1.5 to 2.5 cm in length, which is usually a fused single mass of the two ganglia (Fig. 81.1E).

1. 2. 3.

The procedure on the left side is, of course, identical to that on the right, except that the thoracic duct must be identified and retracted out of the field with a thin ribbon retractor (Fig. 81.2). It should be borne in mind that the thoracic duct emerges forward out of the depth of the mediastinum from behind the jugular vein and enters the subclavian just lateral to its junction with the jugular (Fig. 81.2).

the supraclavicular; the anterior transthoracic; and the axillary transthoracic.

Supraclavicular Approach One of the earliest approaches was the supraclavicular (Fig. 81.1). Leriche and Fontaine (5) and Gask and Ross (6) were among its advocates. Right Cervicothoracic Sympathectomy Position of Patient The patient is placed in the supine position with the head turned away from the side of the incision and the neck somewhat hyperextended. The shoulders are elevated by a bolster (Fig. 81.1A).

Left Cervicothoracic Sympathectomy

Pitfalls and Complications Two important pitfalls are most often connected with this approach: 1. 2.

Excision of Cervicothoracic Sympathetic Ganglia The first structure visualized is the stellate ganglion, a dumb-

limited exposure of the dorsal sympathetic nerve, thus allowing only a partial sympathectomy; and difficulties in controlling serious hemorrhage if a large vessel is injured, which may lead in some instances to ischemia of the limb (7).

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Part X Upper Extremity Conditions 䉳 FIGURE 81.2 (A) Position of the patient and line of skin incision in the left supraclavicular area. (B) Exposure of the left stellate ganglion, using an approach similar to that shown in Figure 81.1D. Note position of the thoracic duct.

Complications include injuries to the subclavian artery, thoracic duct, brachial plexus, phrenic nerve, and the pleura. A thoracic duct injury must be carefully ligated to prevent lymphorrhea. Pneumothorax may be easily treated by insertion of a chest tube in some cases. If a Horner’s syndrome occurs, anhidrosis of the affected side of the face and neck will be present in addition to that of the upper extremity, including the upper chest and part of the axilla.

A

Anterior Transthoracic Upper Dorsal Sympathectomy In contrast to the supraclavicular technique, the anterior transthoracic approach (Fig. 81.3) provides direct and easy exposure of the sympathetic chain (8).

B

Position of Patient The patient is placed in the supine position elevated about 15° by a bolster under the scapula. The upper extremity is abducted to 90°, with the forearm anchored to a crossbar.

FIGURE 81.3 Anterior transthoracic approach. (A) Position of the patient, showing the line of incision in the third intercostal space. Left upper extremity is in marked abduction with the forearm supported by a crossbar in a sling. (B) Transection of the pectoralis major and intercostal muscles. (C) Detachment of the third rib after dividing of the costochondral junction. (D) Retraction of the third interspace and exposure of the lung.

A

B

C

D

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This procedure provides excellent access to the sympathetic chain except that, in some instances, the upper part of the stellate ganglion may be difficult to expose.

Transaxillary Approach Atkins, in 1949, was the first to publish the transaxillary technique (9). The operation consists of a transaxillary and transpleural approach to the upper thoracic sympathetic nerve (Figs. 81.5–81.7). Right Transaxillary Sympathectomy The patient is placed in the left lateral prone position, crucial for adequate exposure. The upper arm is abducted to approximately 100°. The arm should be wrapped loosely and secured in place on the arm rest with a bandage. Details of the technique are illustrated in Figure 81.5. Further technical details are shown in Figure 81.6. A

Left Transaxillary Sympathectomy The patient’s position for a left transaxillary sympathectomy (Fig. 81.7C) is similar to that for the right. Technical details are illustrated in Figure 81.7C.

Postoperative Care

B

FIGURE 81.4 (A) Posterior parietal pleura overlying the sympathetic chain is opened. The shaded segment of the ganglionated chain and the position of the clips indicate the segment to be removed (T1 to T5), excluding the lower cervical ganglion. (B) Closure of the chest. Note the chest tube emerging through a stab wound two interspaces below the third in the anterior axillary line.

After a successful upper thoracic sympathectomy with any of the above approaches, the skin of the denervated extremity, as a rule, will become warm and dry almost immediately. In the presence of a Horner’s syndrome, one finds typical signs of myosis, ptosis of the upper eyelid, slight elevation of the lower lid, and anhidrosis of the face and neck on the side of the sympathetic denervation. The patient may be out of bed the day after the operation. Routine chest films for the presence of pleural effusion or pneumothorax are taken. Intercostal pain is usually present postoperatively. This is controlled by analgesics or mild narcotics. The arm may be protected in a sling if pain is due to pulling on the suture line.

Pitfalls and Complications Operative Pitfalls Procedure The pectoralis major and intercostal muscles are divided, and the pleura is opened (Fig. 81.3B). The lung is deflated and depressed downward to permit exposure of the upper posterior aspect of the thoracic wall (Fig. 81.3C and D). The sympathetic chain is dissected free from the chest wall (Fig. 81.4A). The chain is then dissected cephalad toward the upper border of the first rib. As in the previous procedure, handling of the stellate ganglion may raise some difficulty. In order to prevent Horner’s syndrome, partial freeing of the stellate ganglion is advisable.

Injury to intercostal vessels or the azygos vein or the thoracic duct has been dealt with above.

Complications Postsympathectomy Neuralgia This postoperative pain varies from patient to patient. Two types of pain are generally observed: one due to the operative exposure and manipulation of the intercostal nerves, and the other more deep-seated, disappearing or becoming much less pronounced within a few weeks. Gentle handling of the intercostal nerves during the oper-

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Part X Upper Extremity Conditions

A

B

C

D

ation will minimize to a great extent this postoperative pain. Occasional procaine block of intercostal nerves at the posterior origin may control the pain if the usual analgesics fail to do so. Sudomotor Changes Compensatory body sweating may be a complication of sympathetic denervation of the large surface area of the body. This occurs most often in a four-extremity sympathectomy for hyperhidrosis. Usually, after several months, readjustment of the sudomotor activity occurs, consisting of lessening of this hyperhidrosis in the nondenervated skin. Gustatory sweating on half of the face is a common occurrence, especially after bilateral operations. It is associated with eating and is accompanied by tingling and flushing as well as pilomotor changes in the skin. The use of spicy or acid foods or sweets may initiate the complaint. It is more frequently noted whenever a cervicodorsal sympathectomy is performed for hyperhidrosis or Raynaud’s disease. This phenomenon may be delayed, although most often it appears in the first 12 months postoperatively. Treatment of this complication includes the use of ganglionic blocking drugs and, in some cases, excision of any residual stellate ganglion tissue.

FIGURE 81.5 Right transaxillary approach. (A) Position of the patient, line of skin incision, and abduction of the right upper extremity with the forearm supported by a crossbar. (B) Exposure of the serratus anterior muscle and line of incision overlying the third rib. Note the long thoracic and thoracodorsal nerves, the latter along the latissimus dorsi muscle and the former overlying the serratus, posteriorly to the pectoralis major muscle. (C) Retraction of the edges of the divided serratus muscle, and the extraperiosteal mobilization of the third rib. (D) Incision of the anterior parietal pleura and exposure of the lung.

Return of Sympathetic Activity It is well known that a cervicothoracic sympathectomy may sometimes fail to offer permanent denervation to the upper extremity. In the immediate postoperative period, a residual vasospasm is attributable to a hypersensitivity of the denervated arteriolar smooth muscle to epinephrine. This interpretation is based on Cannon’s law of denervation, which states that interruption of the postganglionic fibers results in an increased sensitivity of the neuroeffector cells to circulating epinephrine (10). Although this phenomenon was clearly demonstrated in animal experiments, the physiologic importance in humans appears undoubtedly overstated (11). The return of vasomotor tone, particularly in cases of Raynaud’s disease, may rather be related to inadequate denervation or local digital arteriolar sensitivity to cold, or a combination of the two. Regeneration of the Sympathetic Activity In a preganglionic denervation by the Telford technique (12), regeneration of these fibers was implicated as a factor responsible for the return of the vasomotor tone. However, if this were possible, the reconnection of the preganglionic fibers with the postganglionic neuron still remains difficult to understand, although regeneration of

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A

B

C FIGURE 81.6 (A) Exposure of the posterior parietal pleura and its incision over the underlying sympathetic chain. (B) Excision of the upper thoracic sympathetic ganglionated chain below the inferior cervical ganglion. Note the clips on the rami connecting the chain to the intercostal nerves and other plexuses not shown in the drawing. (C) Details of the upper thoracic sympathetic chain and inferior cervical ganglion.

FIGURE 81.7 (A) Closure of the thoracotomy with pericostal sutures. Note the chest tube through the intercostal space. (B) Closure of the muscle layers. (C) Drawing of the left transaxillary upper thoracic sympathectomy.

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preganglionic fibers does take place in accordance with Waller’s law. In experimental animals, there is indeed evidence for regeneration of preganglionic fibers. Haimovici and Hodes (13) presented evidence for regeneration of certain fibers (adrenal, pupillary) even after removal of the entire sympathetic chain on both sides. Similar findings were reported by other investigators (14). Whether an identical regeneration occurs in humans in the upper extremity and by what mechanism is still a moot question. Among other likely possibilities to account for return of sympathetic activity is the presence of accessory ganglia described by Wrete (15) and Skoog (16). These findings would account for the fact that some degree of residual sweating is always present over some areas. The inescapable fact remains, however, that in a certain number of cases a lasting denervation of the upper extremity is difficult to achieve, for reasons that are equally difficult to interpret. The recurrence may be related to a return of some vascular tone as well as to some technical problems responsible for incompleteness of denervation. The more complex neuroanatomy of the autonomic nervous system at this level may account, at least partially, for the latter fact.

References 1. Kuntz A. Distribution of the sympathetic rami to the brachial plexus. Arch Surg 1927;15:871. 2. White JC, Smithwick RM, et al. The autonomic nervous system: anatomy; physiology and surgical applicaton, 3rd ed. New York: Macmillan, 1941. 3. Schein CJ, Haimovici H, et al. Arterial thrombosis asso-

4.

5. 6.

7.

8. 9.

10. 11.

12. 13.

14.

15

16.

ciated with cervical ribs: surgical considerations. Report of a case and review of the literature. Surgery 1956;40:428. Roos DR. Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 1966;163:354. Leriche R, Fontaine R. Technique de l‘ablation du ganglion étoilé. J Chir 1933;41:353. Gask GE, Ross JP. The surgery of the sympathetic nervous system, 2nd ed. Baltimore: William Wood & Co, 1937. Lord JW. Post-traumatic vascular disorders and upper extremity sympathectomy. Orthop Clin North Am 1970;1:393. Palumbo LT, Lulu DJ. Anterior transthoracic upper dorsal sympathectomy. Arch Surg 1966;92:247. Atkins HJB. Peraxillary approach to the stellate and upper thoracic sympathetic ganglia. Lancet 1949;2:1152. Cannon WB. A law of denervation. Am J Med Sc 1939;198:737. Simeone FA, Felder DA. Observations upon the supersensitivity of denervated digital blood vessels in man. Surgery 1951;30:218. Telford ED. The technique of sympathectomy. Br J Surg 1935;23:448. Haimovici H, Hodes R. Preganglionic nerve regeneration in completely sympathectomized cats. Am J Physiol 1940;128:463. Hinsey JC, Phillips RA, et al. Observations on cats following pre- and postganglionic sympathectomies. Am J Physiol 1939;126:534. Wrete M. Die Entwicklung der intermediären Ganglien béim Menschen. Gegenbauers Morpholjahrb 1935;75:229. Skoog T. Ganglia in the communicating rami of the cervical sympathetic trunk. Lancet 1947;253:457.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 82 Thoracoscopic Sympathectomy P. Michael McFadden and Larry H. Hollier

Thoracic sympathectomy is a procedure designed to interrupt the adrenergic effect of the central nervous system on the upper extremity. The predominant effects of sympathectomy are reduction of vasomotor tone and lowering of peripheral vascular resistance. Surgical removal of the upper thoracic sympathetic chain has demonstrated its clinical effectiveness in the management of a variety of autonomic-mediated disorders of the upper extremity. These disorders include causalgia, reflex sympathetic dystrophy, nonreconstructible arterial insufficiency, hyperhidrosis, cold sensitivity after cold injury, refractory Buerger’s disease, and Raynaud’s phenomenon. Relief of autonomic-mediated pain syndromes and reduction in perspiration are significant clinical effects of sympathectomy. Goetz’s excellent collective review in 1948 provided a historical and physiologic perspective of sympathectomy in cardiovascular disorders (1). Through the parallel evolution of two seemingly unrelated and independent surgical developments — endoscopic surgery and thoracic sympathectomy — thoracoscopic sympathectomy has become the procedure of choice for thoracic sympathectomy (2,3). The first development was a succession of surgical procedures to interrupt the upper thoracic sympathetic chain in treating autonomic-mediated disorders of the upper extremity. Although Jaboulay in 1899 first proposed that sympathectomy might be of value in promoting circulation in the extremities (4), Kotzareff is credited with having performed the first cervical sympathectomy for hyperhidrosis in 1920 (5). An anterior cervical approach to the thoracic sympathetic chain was described

independently by Jonnesco (6) and Brüning (7). A transthoracic approach to the sympathetic chain was first described shortly thereafter by Goetz and Marr in 1944 (8). A variety of effective surgical techniques for thoracic sympathectomy evolved (9–15): 䊏 䊏 䊏 䊏 䊏 䊏 䊏

cervical (supraclavicular) dorsal (posterior) anterior transthoracic extrapleural transthoracic transpleural transaxillary thoracoscopic (video-assisted).

The specific advantages and disadvantages of each of these surgical approaches have been thoroughly reviewed by Roos (16). The birth and development of endoscopy with the introduction of the cystoscope by Bozzini in 1806 (17) was the second important development that subsequently led to the application of diagnostic and therapeutic endoscopic procedures. Thoracoscopy was introduced by Jacobaeus, a Swedish internist, in 1910 (18). He later described pleural operations through the thoracoscope (19). The procedure was essentially limited to diagnostic purposes until improvements in anesthetic techniques and single-lung ventilation provided a stimulus to expand the scope of diagnostic procedures and encourage the therapeutic application of thoracoscopic surgery. Although cauterization of the second thoracic sympathetic ganglion through the thoracoscope was first performed in 1948 (1), thoracoscopic sympathectomy did not become popular

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Part X Upper Extremity Conditions

until the advent of quality video-assisted endoscopic equipment. Owing to the excellent results being obtained with minimal morbidity, the video-assisted thoracoscopic approach to resection of the upper thoracic sympathetic chain has evolved as the procedure of choice for selected conditions affecting the upper extremity.

Indications and Contraindications The indications for thoracoscopic sympathectomy are the same as for open sympathectomy: 䊏 䊏 䊏 䊏 䊏 䊏 䊏

causalgia reflex sympathetic dystrophy nonreconstructible arterial insufficiency hyperhidrosis cold sensitivity after cold injury refractory Buerger’s disease Raynaud’s syndrome.

The preoperative evaluation consists of a thorough history and physical examination. Special emphasis is given to the evaluation of the vascular, neurologic, and musculoskeletal systems. Routine laboratory, radiographic, and electrocardiographic studies are performed. Particular attention is paid to the evaluation of pulmonary function. Sophisticated invasive and noninvasive testing with arteriography, myelography, nerve conduction studies, magnetic resonance imaging, and computed tomography are performed, if indicated, to establish the diagnosis. Once the diagnosis and clinical indication for sympathectomy have been established, a stellate ganglion block is performed to aid in predicting the surgical outcome. Horner’s syndrome induced by this procedure does not itself prove an adequate sympathetic nerve block, but in conjunction with relief of symptoms, it may indicate a reasonable chance for success with sympathectomy. Relative contraindications to thoracoscopic sympathectomy include previous pleural or pulmonary conditions that promote adhesions and obliteration of the pleural space. Conditions such as empyema or previous thoracotomy make access to the pleural space with the thoracoscope difficult, if not impossible. Inability to maintain adequate arterial oxygen saturation with contralateral single-lung ventilation also precludes a thoracoscopic approach. A thoracoscopic procedure is generally discouraged in infants and small children because the thoracic cavity is small, the intracostal space is narrow, and the thoracoscopic instruments are comparatively large. Maintenance of single-lung ventilation is difficult in children because the available double-lumen endotracheal tubes are too large. A thoracoscopic procedure however, may be accomplished by using a bronchial blocker. Sympathectomy for hyperhidrosis is rarely indicated in infants and children. Hyperhidrosis frequently resolves spontaneously after puberty; therefore, a conservative approach is rec-

ommended in children. The increase in the performance of diagnostic procedures and use of invasive monitoring devices in neonatal and pediatric intensive care units may lead to a greater incidence of vasospastic or nonreconstructible vascular problems. Young patients with these disorders may benefit from repeated stellate ganglion blocks or surgical sympathectomy.

Requirements for a Successful Thoracoscopic Sympathectomy To accomplish an adequate sympathectomy of the upper extremity, there are certain essential requirements: a free pleural space, deflation of the lung, and visual identification of the upper thoracic sympathetic chain from the stellate ganglion through the fourth thoracic ganglion. Appropriate instrumentation and the capability of rapid access to the thoracic cavity are imperative. The basic equipment includes a 0º-angle thoracoscope, a videocamera with monitor and videocassette recorder, a light source, appropriate endoscopic grasping instruments, a nerve hook, electrocautery, vascular clips, and instruments for open thoracotomy should it become necessary. Although the majority of thoracoscopic sympathectomy procedures are performed under contralateral single-lung ventilation with the introduction of an ipsilateral pneumothorax, CO2 insufflation may be used to aid in decompression of the ipsilateral lung. If CO2 insufflation is required, abdominal trocars rather than the routine thoracic trocars are necessary to maintain positive-pressure CO2 insufflation. Insufflation pressure should not exceed 8 cmH2O, and the average should approximate 4 cmH2O if this method is used.

Complications The potential complications of thoracoscopic sympathectomy include adverse occurrences that may result from any thoracoscopic procedure and complications specific to sympathectomy. Some general complications include: 䊏 䊏 䊏 䊏 䊏 䊏

䊏

pain arrhythmia hypotension hypercarbia hemorrhage pneumothorax or persistent pulmonary parenchymal air leak Horner’s syndrome

Postoperative pain resulting from irritation of the intercostal nerves at the sites of trocar placement or from the chest tube site is common but usually transient. Antiinflammatory agents, such as indomethacin, have been beneficial and may be initiated by rectal suppository in the early recovery period. Refractory pain unresponsive to

Chapter 82 Thoracoscopic Sympathectomy

oral analgesics and anti-inflammatory agents may be managed by either local intercostal nerve blocks or epidural anesthetic agents. These modalities, however, are rarely required. Thoracoscopic manipulation of the lung and mediastinal structures may result in cardiac arrhythmias. Electrical current from the cautery may initiate atrial or ventricular tachycardia or fibrillation. Sinus tachycardia may occur secondary to CO2 retention when insufflation techniques are used. A mediastinal shift with compromise of venous return to the heart may initiate a reflex sinus tachycardia. Vagal stimulation and air or CO2 embolism with insufflation techniques may lead to bradycardia or asystole. Hypotension may result from mediastinal tamponade, air or CO2 embolization, or hemorrhage. Hypercarbia, which results from CO2 insufflation, can result in hypertension and tachycardia. Hemorrhage from the intracostal vessels may occur at the site of trocar placement. The proximity of the upper thoracic sympathetic chain and the stellate ganglion to the subclavian artery and its many branches places the patient at risk should one of these arteries be injured during dissection of the sympathetic chain. The anatomic location of the subclavian artery, vertebral artery, thyrocervical trunk, and internal mammary artery must be known in order to safely expose the chain. The rami communicantes are often accompanied by small arteries and veins at the level of the intercostal spaces. Precise application of vascular clips to these structures should avoid troublesome hemorrhage. Hemorrhage is often optically magnified when viewed through the video-assisted thoracoscope. Exposure of the thoracic sympathetic chain requires retraction of the lung apex away from the posterior chest wall. Improper instrumentation and the frequent presence of apical blebs or adhesions may result in a parenchymal lung injury and postoperative pneumothorax or persistent air leak. Horner’s syndrome that includes ipsilateral miosis, facial anhidrosis, and ptosis of the eyelid may result if the sympathectomy includes portions of the C7 or C8 cervical sympathetic ganglia. These structures comprise the bulk of the superior portion of the stellate ganglion. Failure to locate the upper thoracic sympathetic chain is rare. However, if pleural conditions obscure the sympathetic chain or if previous extrapleural procedures such as first-rib resection or repeated percutaneous stellate ganglion blocks have resulted in scarring or adhesions, the anatomy of the upper sympathetic chain may be obscured.

Technique Preoperative Preparation The operative procedure and the potential complications of hemorrhage, arrhythmia, hypotension, pneumotho-

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rax, pain, persistent air leak, inability to complete the procedure thoracoscopically, and death are reviewed with the patient. Informed consent is obtained for open thoracotomy as well as thoracoscopic sympathectomy, in the event that an open procedure is necessary. The operation should be performed only by an experienced surgeon who is thoroughly trained in thoracoscopic surgical techniques and capable of surgical management of emergent thoracic complications.

Anesthetic Management Thoracoscopic sympathectomy is usually performed under general double-lumen endotracheal anesthesia. Either a left- or right-sided double-lumen endotracheal tube may be used. A left-sided tube is preferred because it is easier to place and provides greater stability. A single-lumen endotracheal tube with a bronchial blocker may also be used. Bronchial blockers have been less reliable in our experience, as they frequently dislodge and are difficult to reengage. Proper position and function of the endotracheal tube are confirmed by auscultation and fiberoptic bronchoscopy after intubation. The patient is turned to a lateral decubitus position, as for thoracotomy. The position and function of the endotracheal tube are reconfirmed after the patient is positioned. The ability to adequately decompress the lung on the side of the sympathectomy and appropriately ventilate the contralateral lung is essential in attaining surgical exposure of the sympathetic chain. If a bilateral thoracic sympathectomy is planned, the patient is maintained in a supine position with arms abducted and suspended superiorly to expose the upper thorax. The patient is monitored with an arterial line and an oxygen saturation monitor. Long-acting anesthetic agents are avoided to allow immediate extubation at the termination of the procedure. Postoperative pain is rarely a significant problem. Intravenous or oral analgesic agents usually suffice. Occasionally, intercostal nerve blocks or epidural analgesia may be required for significant postoperative pain (20,21).

Surgical Technique Thoracoscopic sympathectomy requires a minimum of three ports for visualization, exposure, and dissection of the sympathetic chain. The lung on the operative side is decompressed by discontinuance of ipsilateral ventilation. An 11.5-mm thoracoport is placed through an incision in the fourth intercostal space at the midaxillary line. A 0° thoracoscope with a videocamera is introduced through this port. The lung and pleural space are thoroughly inspected and evaluated. Additional thoracoports are placed in the third intercostal space at the anterior axillary line and in the fourth intercostal space at the posterior axillary line. Through these ports, thoracoscopic instruments, such as scissors, grasping forceps, dissecting hooks, and cautery and suction devices, are introduced to expose and dissect free the sympathetic chain (Fig. 82.1).

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B

A

FIGURE 82.1 Thoracoscopic sympathectomy performed in a thoracotomy position. (A) Incisions are placed in the third and fourth intercostal spaces in a triangulated fashion. Multiple incisions may be required. (B) The working ports are placed lateral to the video-assisted thoracoscope.

Exposure is best obtained by retraction of the apex of the upper lobe anteriorly and inferiorly. The sympathetic chain is identified as a firm longitudinal white structure beneath the parietal pleura at the junction of the transverse processes of the vertebral spine and the ribs. A complete sympathectomy for upper extremity disorders should include the T2, T3, and T4 thoracic sympathetic ganglia. Controversy still exists as to whether T1 should be included. T1 comprises the lower portion of the stellate ganglion (C7 through T1) (Fig. 82.2). T1 supplies sympathetic innervation to portions of the lower neck and shoulder. The division between T1 and the lower cervical sympathetic ganglion (C7, C8) within the sympathetic ganglion is ill-defined. The lower cervical sympathetic ganglion supplies sympathetic innervation to the ipsilateral face and head. Inclusion of T1 may result in Horner’s syndrome (22). Palumbo proposed that a successful thoracic sympathectomy is possible without resection of the T1 sympathetic ganglion (23). Conditions such as palmar hyperhidrosis or pain syndromes of the distal upper extremity and digits may be addressed with resection of the T2 through T4 sympathectomy chain and ganglia. However, complete resolution of pain syndromes that involve the shoulder or lower neck cannot be anticipated without

FIGURE 82.2 Anatomy of the cervical and thoracic sympathetic ganglia. The first thoracic ganglion (T1) forms the lower portion of the stellate ganglion. Inclusion of T1 in thoracic sympathectomy may potentially result in Horner’s syndrome.

the inclusion of T1. We attempt to include T1 by excising the lower one-fourth to one-third of the stellate ganglion. This conservative approach has not resulted in a permanent Horner’s syndrome in our patients. The parietal pleura overlying the sympathetic chain at the level of the third and fourth rib may be incised with scissors or elevated and divided with a cautery hook. The main sympathetic trunk from the stellate ganglion to the T4 thoracic ganglion is exposed along with the accompanying rami communicantes. Exposure of the stellate ganglion at the level of the first rib must be approached with caution. The stellate ganglion lies in close apposition to the vertebral and thyrocervical branches of the subclavian artery, which may be injured during dissection (Fig. 82.3). The chain is elevated with a grasper or hook while vascular clips are applied to the rami (Fig. 82.4). The rami are divided with scissors, between the main trunk and the clips. Application of vascular clips to the main sympathetic trunk has been discouraged by some because postoperative neuralgia may occur (24). It is our practice to apply clips to the chain distal to the fourth thoracic ganglion and to the lower portion of the stellate ganglion before its transection. The application of clips provides hemostasis and aids in radiographic identification of the superior and inferior extents of the sympathectomy after surgery (Fig. 82.5). Postoperative neuralgia has not been a problem in our experience. Thoracoscopic visualization of the specimen as it is removed is recommended to avoid losing the specimen

Chapter 82 Thoracoscopic Sympathectomy

FIGURE 82.3 Relation of the left thoracic sympathetic chain and ganglia to the vascular and bony structures of the upper thorax. IMA, internal mammary artery.

FIGURE 82.4 The upper thoracic sympathetic chain (T1 through T4) and accompanying rami communicantes are isolated with vascular clips and resected under direct visualization with the video thoracoscope.

within the thoracic cavity should it become dislodged. Meticulous hemostasis of the operative site is accomplished with electric cauterization or application of vascular clips. Histologic confirmation of the sympathetic chain is attained by frozen histologic section before termination of the procedure. A single chest tube is inserted through a thoracoport incision to evacuate the pleural space at termination of the procedure. Some authors have reported

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FIGURE 82.5 Postoperative chest film after thoracoscopic sympathectomy. Metal clips in right superior mediastinum demonstrate the superior and inferior extents of the thoracoscopic sympathectomy in a patient with palmar hyperhidrosis.

satisfactory results without pleural drainage (24). The remaining incisions are closed with absorbable subcutaneous and subcuticular sutures, and bandaged. The patient is returned to the supine position and extubated in the operating room. A postoperative chest x-ray is obtained in the recovery room and the respiratory status is monitored closely. The patient is transferred to a hospital room when appropriate. The chest tube is usually removed on the first postoperative day. Discharge may be anticipated on the second or third postoperative day. Immediate results of the sympathectomy are recorded before the patient’s discharge. Determination of the intermediate and long-term results of sympathectomy requires thorough and periodic postoperative evaluation.

Results The immediate results of thoracoscopic sympathectomy for autonomic-mediated disorders of the upper extremity have been excellent (1,24–27). The intermediate and long-term results of video-assisted thoracoscopic sympathectomy have yet to be determined. Comparison against historical results from open thoracotomy and thoracoscopic sympathetic cryoablation procedures will be re-

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TABLE 82.1 Results of video-assisted thoracoscopic sympathectomy for hyperhidrosis Source (Ref. No.) Adams & Poskitt 1991 (29) Pace et al. 1992 (2) Mack et al. 1992 (25) Edmonson et al. 1992 (30) Krasna et al. 1993 (27)

No. of Patients (No. of Procedures) 13 (25) 1 (2) 1 (1) NS (50) 1 (1)

Results

Horner’s Syndrome

Excellent (one late reourrence) Excellent Excellent Good–excellent Excellent

Not stated (none implied) None 2 (one transient, one permanent)* None None

*Not stated which of six sympathectomies (one for hyperhidrosis) resulted in Horner’s syndrome. NS, not stated.

quired. Experience to date indicates that the results of video-assisted thoracoscopic sympathectomy will equal or surpass those of previous surgical approaches.

Hyperhidrosis Historically, the success rate for the surgical management of palmar hyperhidrosis approaches 85% to 95% at 1 year (24). A review by Drott et al. indicated that excellent and durable results were obtained up to 5 years after thoracoscopic sympathectomy (3). Primary failure of the sympathectomy occurred in only five (1.4%) of 367 patients, and early recurrence was seen in four patients (1.1%). Successful reoperation was accomplished thoracoscopically in eight patients. Fritsch et al. reported durable results over 10 years (28). The majority of sympathectomies in this series were accomplished with thoracoscopic cryoablation rather than excision of the chain and were performed without video-assisted techniques. Results of thoracoscopic management of axillary hyperhidrosis have been less encouraging than for palmar hyperhidrosis. In the series by Kux, 18.6% of patients continued to have axillary hyperhidrosis after thoracic sympathectomy despite excellent resolution of their palmar problem (26). Kux suggested that inclusion of the T5 sympathetic ganglion in the sympathectomy improved the results in axillary hyperhidrosis. Adams and Poskirt observed equally good results for axillary and palmar hyperhidrosis (29). Current reports indicate that excellent results may be anticipated with a video-assisted thoracoscopic approach for both palmar and axillary hyperhidrosis (Table 82.1). These results compare favorably with the excellent results summarized in the review by Drott et al. (3) and report by Lin (31) in which thoracoscopic cryoablation and chemical ablation of the sympathetic chain were accomplished without video-assisted techniques. Gustatory and compensatory sweating of the trunk and lower extremities are occasional side effects of thoracoscopic sympathectomy. Fortunately, these are selflimiting and usually resolve with time (30). Horner’s syndrome is the most distressing and undesirable postoperative complication. Its occurrence following end-

oscopic thoracic sympathectomy is uncommon. In the review by Drott et al. (3), Horner’s syndrome occurred in 17 (1.86%) of 912 patients. Of the 17 patients, 12 (71%) experienced only a transient problem. A permanent Horner’s syndrome occurred in only 0.54% of these patients undergoing endoscopic thoracic sympathectomy for palmar hyperhidrosis.

Reflex Sympathetic Dystrophy and Causalgia Reflex sympathetic dystrophy (RSD) is a post-traumatic pain syndrome that is mediated through the autonomic nervous system. The term causalgia is applied when there has been direct injury to a peripheral nerve. Early intervention and treatment of these conditions are the keys to successful management. Olcott and associates found conservative modalities, including repeated stellate ganglion blocks, analgesic agents, and physical therapy, to be successful in 50% to 70% of their patients with RSD (32). These authors stressed the value of a team approach in the evaluation of post-traumatic pain syndromes because of the difficulty in diagnosis and management of these conditions. Video-assisted thoracoscopic sympathectomy in the treatment of RSD and causalgia is in its infancy. Results with this procedure must be compared with ablative thoracoscopic sympathetic techniques that are not videoassisted and with open surgical sympathectomy. Olcott et al. reported excellent results in 74% of patients, good results in 17%, and poor results in 9% with surgical sympathectomy (32). Patman et al. attained excellent results in 84% of patients, good results in 8.9%, and poor results in 7.1% (33). Mockus et al. reported significant improvement in 94% of their patients (34). Recent reports of video-assisted thoracoscopic techniques for RSD and causalgia have been encouraging (Table 82.2). No mortalities or complications requiring conversion to open thoracotomy have been reported. Early results have been excellent, and the incidence of Horner’s syndrome has been low. The results with video-assisted thoracoscopic sympathectomy for RSD and causalgia, as with other approaches, depend largely on proper selection of the patient.

Chapter 82 Thoracoscopic Sympathectomy

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TABLE 82.2 Results of video-assisted thoracoscopic sympathectomy for reflex sympathetic dystrophy and causalgia Source (Ref. No.)

Procedures

Level

Results

Horner’s Syndrome

Pace et al. 1992 (2) Mack et al. 1992 (25) Krasna et al. 1993 (27)

2 6 (five patients) 1

T2–4 T1–4 T1–4

Significant improvement Excellent and complete in 5 of 6 Excellent

0 2 (one transient, one permanent) 0

Nonreconstructible Peripheral Vascular Disease and Vasospastic Disorders The results of surgical sympathectomy for occlusive vascular disease and vasospastic disorders of the upper extremity have been less reliable. The effects are usually transient and less durable than for hyperhydrosis, reflex sympathetic dystrophy, and causalgia (35,36). Sympathectomy has been performed for limb salvage in patients with obliterative non-reconstructible arterial disease and in combination with arterial repair when ischemic trophic changes are present. The results of sympathectomy have been better for obliterative arterial disease than for vasospastic disorders (37). The report by Kux et al. (38) documented the excellent early results obtained with thoracoscopic sympathectomy that was not video-assisted in 34 patients with vasospastic disorders. However, symptoms recurred in 15 patients (44%) on late follow-up. This temporary effect was reconfirmed by Drott et al. in 12 patients undergoing thoracoscopic cryoablation of the sympathetic chain (3). Distal extremity ulceration, however, healed in the majority of these patients. Bardaxoglou et al. (39) reported favorable results with thoracoscopic chemical sympathectomy in proximal occlusive disease in one patient, distal occlusive disease in three, and Raynaud’s phenomenon in two. In all patients, preexisting signs and symptoms disappeared and trophic changes healed. No recurrences were reported at 6 months. Sympathectomy in Buerger’s disease has had variable results. Modification of predisposing factors and cessation of smoking are the best hope in limiting the effects of this disease. However, sympathectomy is an alternative when the patient does not respond to conservative management (40). Results of thoracoscopic approaches for this condition have not been established.

Connective Tissue Disorders The application of sympathectomy for the management of upper extremity effects of collagen vascular diseases, such as scleroderma, rheumatoid arthritis, lupus erythematosus, and Raynaud’s disease, has been unrewarding. Sympathectomy is ineffective because of the underlying connective tissue pathophysiology in these disorders. Sympathectomy is not recommended in the routine management of collagen vascular disorders.

It is predicted that the less invasive thoracoscopic approach to disorders of the chest will provide financial and resource benefits over open thoracotomy procedures. Landreneau et al. have demonstrated that pain-related morbidity, shoulder dysfunction, and early pulmonary problems were fewer in patients undergoing video-assisted thoracoscopic pulmonary resections when compared with open thoracotomy (41). They demonstrated a lower narcotic requirement and an average 5-day hospital stay, rather than 7.5 days with thoracotomy. The hospital stay for our patients undergoing thoracoscopic sympathectomy averages 2.5 days. A lower morbidity, faster recovery, and conservation of costs and resources have been further benefits of the thoracoscopic surgical approach to thoracic disease.

Conclusion Thoracoscopic sympathectomy has been effective in the management of a variety of autonomic-mediated disorders of the upper extremity. The results of thoracoscopic sympathectomy compare favorably with those of open surgical procedures. Excellent long-term results may be anticipated in more than 90% of patients treated for hyperhidrosis, reflex sympathetic dystrophy, and causalgia. Acceptable results have been observed in patients with nonreconstructible occlusive vascular disease and vasospastic disorders; however, the response may be transient and less durable in patients with vasospastic disorders. Sympathectomy infrequently resolves problems caused by the connective tissue disorders of scleroderma, rheumatoid arthritis, and lupus erythematosus. Thoracoscopic sympathectomy has replaced the more traditional open cervical, dorsal, and transthoracic surgical approaches. The procedure is simple, effective, and minimally invasive. Excellent exposure and visualization are attained with the video-assisted thoracoscope, allowing for a precise sympathectomy. The procedure is attended with minimal postoperative pain and morbidity. Early patient rehabilitation and shorter hospitalization have resulted in lower costs and better utilization of resources. Although the long-term results of video-assisted thoracic sympathectomy remain to be determined, the procedure demonstrates tremendous promise in the management of autonomic-mediated disorders of the upper extremity.

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References 1. Goetz RH. Collective review: the surgical physiology of the sympathetic nervous system with special reference to cardiovascular disorders. Int Abstract Surg 1948;87:417–459. 2. Pace RF. Brown PM, Gutelius JR. Thoracoscopic transthoracic dorsal sympathectomy. Can J Surg 1992;35:509–511. 3. Drott C, Göthberg C, Claes C. Endoscopic procedures of the upper-thoracic sympathetic chain: a review. Arch Surg 1993;128:237–241. 4. Jaboulay M. Le traitment de quelques troubles trophique du pied et de la jambe par la dénudation de l’artére et la distension des nerfs vasculaires. Med Lyon 1899;91:467. 5. Kotzareff A. Resection partielle de tronc sympathetique cervical droit pour hyperhidrose unilaterale. Rev Med Suisse Rom 1920;40:111. 6. Jonnesco T. Le sympathizue cervico-thoracico. Paris: Mason & Cie, 1923. 7. Bruning F Resection of cervical sympathetic nerves. Zentralbl Chir 1923;50:1056–1059. 8. Goetz RH, Marr JAS. Importance of the second thoracic ganglion for sympathetic supply of the upper extremities with a description of 2 new approaches for its removal in cases of vascular surgery. Clin Proc 1944;3:102–114. 9. Kwan ST. The treatment of causalgia by thoracic sympathetic ganglionectomy. Ann Surg 1935;101:222–227. 10. Atkins HJB. Sympathectomy by the axillary approach. Lancet 1954;1:538–539. 11. Carry TP, Henry AK. Anterior transcostal access to upper parts of thoracic sympathetic chain. Ir J Med Sci 1949;Oct:757–761. 12. Palumbo LT. Anterior transthoracic approach for upper extremity thoracic sympathectomy. Arch Surg 1956;72:659–666. 13. Kirtley JA, Riddell DH, et al. Cervicothoracic sympathectomy in neurovascular abnormalities of the upper extremities: experiences in 76 patients with 104 sympathectomies. Ann Surg 1967;165:869–879. 14. Smithwick RH. Modified dorsal sympathectomy for vascular spasm (Raynaud’s disease) of upper extremity: preliminary report. Ann Surg 1936;104:339–350. 15. Kleinert HE, Cook FW, Kutz JE. Neurovascular disorders of the upper extremity treated by transaxillary sympathectomy. Arch Surg 1965;90:612–616. 16. Roos DB. Sympathectomy for the upper extremities: anatomy, indications and techniques. In: Rutherford RB, ed. Vascular surgery. Philadelphia: WB Saunders, 1977:623–628. 17. Bozzini P. Der Lichleiter oder Beschreibank einer einfachen Vorrichtung und inhern Anwendung surer/echtung innerer Hohlen und Wischenraume des lebenden animalischen Korpers. Weimar, Germany, 1907. 18. Jacobaeus HC. Possibility of the use of the cystoscope for the investigation of serous cavities. Munch Med Wochenschr 1910;57:2090–2092. 19. Jacobaeus HC. Endopleural operations by means of a thoracoscope. Beitr Klin Tuberk 1915;35:1. 20. Weiss SJ, Cheung AT. Anesthesia for thoracoscopic surgery. In: Kaiser LR, Daniel TM, eds. Thoracoscopic surgery. Boston: Little, Brown, 1993:17–36.

21. Kraenzler EJ, Hearn CJ. Anesthesia for video-assisted thoracoscopy. Semin Thorac Cardiovasc Surg 1993;5(4):321–326. 22. Mack MJ. Thoracoscopy and its role in mediastinal disease and sympathectomy. Semin Thorac Cardiovasc Surg 1993;5:332–336. 23. Palumbo LT. Upper dorsal sympathectomy without Horner’s syndrome. Arch Surg 1955;71:743–751. 24. Hazelrigg SR, Mack MJ. Surgery for anatomic disorders. In: Kaiser LR, Daniel TM, eds. Thorascopic surgery. Boston: Little, Brown, 1993:189–202. 25. Mack MJ, Aronoff RJ, et al. Present role of thoracoscopy in the diagnosis and treatment of diseases of the chest. Ann Thorac Surg l992;54:403–409. 26. Kux M. Thoracic endoscopic sympathectomy in palmar and axillary hyperhidrosis. Arch Surg 1978;113:264–266. 27. Krasna MJ, Flowers J, Morvick R. Thoracoscopic sympathectomy. Surg Laparosc Endosc 1993;3:391–394. 28. Fritsch A, Kokoschka R, Mach K. Ergebnisse der thorakoskopischen Sympathektomie bei: Hyperhidrosis der oberen Extremität. Wien Klin Wochenschr 1975;87:548–550. 29. Adams DCR, Poskitt KR. Surgical management of primary hyperhidrosis [letter]. Br J Surg 1991;78:1019–1020. 30. Edmonson RA, Banerjee AK, Rennie JA. Endoscopic transthoracic sympathectomy in the treatment of hyperhidrosis. Ann Surg 1992;15:289–293. 31. Lin CC. Extended thoracoscopic T2 sympathectomy in treatment of hyperhidrosis: experience with 130 consecutive cases. J Laproendosc Surg 1992;2:1–6. 32. Olcott C IV, Eltherington LG, et al. Reflex sympathetic dystrophy: the surgeon’s role in management. J Vasc Surg 1991;14:488–495. 33. Patman RD, Thompson JE, Persson AV. Management of post-traumatic pain syndromes: report of 113 cases. Ann Surg 1973;177:780–787. 34. Mockus MB, Rutherford RB, et al. Sympathectomy for causalgia: patient selection and long-term results. Arch Surg 1987;122:668–672. 35. Manart FD, Sadler TR Jr, et al. Upper dorsal sympathectomy. Am J Surg 1985;150:762–766. 36. Varennes L, Violet F, et al. Indications et resultats de la sympathectomie thoracique dans les syndromes vasculaires de membre superieur. Lyon Chir 1985;3:181–183. 37. van de Wal HJ, Skotnicki SH, et al. Thoracic sympathectomy as a therapy for upper extremity ischemia: a longterm follow-up study. Thorac Cardio Vasc Surg 1985;33:181–187. 38. Kux M, Fritsch A., et al. Endoscopic thoracic sympathectomy for the treatment of Raynaud’s phenomenon and disease. Eur Surg Res 1976;8:32–33. 39. Bardaxoglou E, Reigner B, et al. Transthoracic endoscopy for upper thoracic chemical sympathectomy. Am Vasc Surg 1992;6:390–392. 40. de Takats G. Analysis of results following sympathectomy for peripheral vascular disease Am J Surg 1940;47(1):78–86. 41. Landreneau RJ, Hazelrigg SR, et al. Postoperative painrelated morbidity: video-assisted thoracic surgery versus thoracotomy. Ann Thorac Surg 1993;56:1285–1289.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART XI Arteriovenous Malformation

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 83 Arteriovenous Fistulas and Vascular Malformations Peter Gloviczki, Audra A. Noel, and Larry H. Hollier

The development of abnormal communications between the arterial and venous system has been the center of interest of surgeons for over two centuries. Depending on the amount of shunted blood that bypasses the capillary circulation, these lesions may be asymptomatic or may have local effects on the surrounding tissues. Arteriovenous fistulas may also have serious consequences for the distal circulation, may cause irreversible pathologic changes in the proximal blood vessels, and in rare cases of large central shunts they may result in profound circulatory and metabolic alterations. Arteriovenous fistulas can be acquired or congenital. While the term arteriovenous malformation (AVM) has been used to describe all congenital vascular malformations, the term is confusing, since not all malformations have abnormal arteriovenous shunting. Therefore, malformations of the vascular system will be discussed in this chapter under the term vascular malformations (VMs). The term AVM will be reserved for those VMs which have clinical or radiographic evidence of arteriovenous shunting.

Historical Note Guido Guidi (1500–1559), surgeon of the emperor Francis I, is credited with describing the first patient with an AVM, who had pulsating varices (so-called “cirsoid aneurysm”) of the head (1). As early as 1757, William Hunter described a patient with a traumatic arteriovenous fistula (2) and a detailed

analysis of two cases was published in 1764 (3). He not only recognized the characteristic thrill and bruit (which disappeared after compressing the proximal artery or the fistula) but also noted the tortuosity and dilation of the artery proximal to the “aneurysm by anastomosis,” as well as the pulsating, distended superficial vein and a decreased distal arterial pulsation. Early attempts to cure the fistula with ligation of the proximal artery frequently resulted in gangrene of the extremity (4), but already, in 1843, Norris reported on treatment of an arteriovenous fistula by double arterial ligation (5). The typical “bradycardiac sign,” the slowing of the heart rate after compression of the arteriovenous communication, was described first by Nicoladoni in a patient with an AVM (6), and 15 years later, in 1890, by Branham in a patient with acquired arteriovenous fistula (7). The pathophysiology of arteriovenous fistula was remarkably well documented as early as 1937 by Emile Holman (8). Experiences from World War II (9), the Korean conflict (10), and, most important, the Vietnam War (11) gave us important information about correct management of traumatic arteriovenous fistulas. Our knowledge of malformations with and without arteriovenous communications (Fig. 83.1) is based primarily on the work of Reid (12), Holman (8), de Takats (13), and Coursley et al. (14). Malan and Puglionisi, in landmark articles, summarized the state of the art of congenital angiodysplasias of the extremities (15), and Szilagyi et al. gave us a usable clinical classification and guidelines for management of these lesions (16,17).

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Acquired arteriovenous fistulas are most frequently caused by penetrating injuries; in wartime these are usually due to flying fragments or gunshot wounds (9–11), whereas among civilian injuries the cause is frequently gunshot or stab wounds and fractures (21,22). Iatrogenic arteriovenous fistulas have been reported after diagnostic or therapeutic catheterization, lumbar laminectomy, orthopedic procedures, percutaneous biopsies of organs (e.g., kidney or liver), embolectomy with Fogarty balloon catheters, and as a result of mass ligation of artery and vein after splenectomy or nephrectomy (23–40). Tumors such as hypernephromas or metastases from thyroid carcinomas may also contain arteriovenous fistulas. Spontaneous major intra-abdominal arteriovenous fistulas may develop in patients with atherosclerotic or mycotic aortoiliac aneurysmal disease (41,42). Aortocaval fistulas due to abdominal aortic aneurysms and arteriovenous fistulas, the latter created surgically for hemodialysis, as an adjunct to improve patency of distal arterial bypasses or venous grafts, or as a treatment option for venous thrombosis, are discussed elsewhere in this book.

Pathophysiology

FIGURE 83.1 Artist’s conception of an arteriovenous malformation (“cirsoid aneurysm”) of the hand. (Reproduced from Breschet G. Mémoire sur les aneurysms. Mem Acad Med (Paris) 1833;3:101, by permission of the journal.)

Superselective arterial catheterization was another major advancement; it helped us to classify the lesions and also to treat AVMs (18,19). Belov reported on a useful classification of VMs, based on a consensus meeting at the seventh meeting of the International Workshop on Vascular Malformations in Hamburg, in 1988 (20).

Etiology Arteriovenous fistulas may be congenital or acquired. As mentioned before, the term VMs is the most appropriate term to use for all vascular malformations, independent of the amount of blood, shunted through arteriovenous communications. These VMs are not true tumors and represent only an “anomalous development of the primitive vascular system” (13).

According to Holman (43), all circulatory changes that occur as a result of congenital or acquired arteriovenous fistula can be explained by a basic hemodynamic principle: “Blood, like flowing water, has an inherent and natural tendency to follow the path of least resistance.” The arteriovenous fistula is an abnormal connection between a high-pressure, high-resistance arterial system and low-pressure, low-resistance, high-capacity venous system. Because of the low resistance, blood preferentially flows through the fistula rather than through the normal capillary bed. Pressure in the artery distal to the fistula decreases; the distal venous pressure increases. These hemodynamic changes lead to the development of increased arterial and venous collateral circulation around the fistula (Fig. 83.2). As a result of increased circulating blood volume, there is a progressive dilation of the entire circulatory system proximal to the fistula; although cardiac enlargement and venous distention may reverse after fistula closure, irreversible ectasia and aneurysm formation in the arteries proximal to chronic fistulas may develop. The amount of blood shunted depends on the diameter and type of the fistula and its proximity to the heart. While many VMs are asymptomatic or cause cosmetic problems or local effects only, the natural history of most traumatic arteriovenous fistulas is continuous increase in size, and increase in the volume of shunted blood. As a consequence, total blood volume, heart rate, cardiac index, stroke volume, and left atrial and pulmonary artery pressures increase and cardiac failure may develop. The natural history of iatrogenic arteriovenous fistulas,

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

993

FIGURE 83.2 Anatomic and hemodynamic changes due to an arteriovenous fistula.

caused by femoral catheterization, is more benign and many may close spontaneously (25,27). If a significant chronic shunt is closed by external compression, there is an immediate rise in systolic blood pressure, and as a vagal response on the stimulation of baroreceptors in the aorta and cerebral arteries, bradycardia almost instantaneously develops. Cardiac output decreases, and if the closure of the shunt is definitive, total blood volume contracts to normal within a few days. The metabolic changes that occur as a result of high central shunt have been studied by Davis et al. (44) and by Epstein and Ferguson (45). It is presumed that the increased venous pressure and the decreased mean arterial pressure, due to the wide pulse pressure, result in decreased renal plasma flow and decreased glomerular filtration rate. As a response, the juxtaglomerular apparatus increases production of aldosterone through the renin–angiotensin system, which subsequently results in increased sodium and water reabsorption and an increase in total plasma volume. The oliguria or anuria that is present in large central shunts can be reversed by closure of the fistula, which produces diuresis, decreases aldosterone secretion, and, within a few days, restores plasma volume to normal levels.

Acquired Arteriovenous Fistulas Incidence and Distribution Since the diagnosis of an arteriovenous fistula has frequently been made years after the injury, it is difficult to define the true incidence of this lesion. In a review of the literature until 1914, Callander, a student of Halsted, found 447 arteriovenous fistulas and only three of those were congenital (46). Of 7500 vascular injuries, 262 patients had arteriovenous fistulas, according to the Vietnam Vascular Registry, which gives an incidence of about 3.5% (11). An almost equal number of patients had

FIGURE 83.3 Distribution of traumatic arteriovenous fistulas.

false arterial aneurysms (3.9%). The incidence of arteriovenous fistula in civilian vascular injuries was similar: 6 (2.3%) of 256 injuries in a review by Patman et al. (21) and 7 (3.6%) of 192 patients in a review by Sirinek et al. (47). Traumatic fistula is most frequent in the lower extremity; in the five largest series of acquired artenovenous fistulas, over 50% were traumatic fistulas (Fig. 83.3) (9–11,21,48). Of 70 arteriovenous fistulas due to injuries in civilian patients, 13% occurred in the neck between the carotid artery and jugular vein, 12% were carotid– cavernous fistulas, and 17% occurred in the femoral vessels (22). Within the abdomen, renal arteriovenous fistula is the most frequent, followed by hepatic lesions. The incidence of arteriovenous fistula following catheter trauma varies depending on the size of the catheter and on the use of postprocedural anticoagulation or thrombolytic therapy. In a review from the Emory University Hospital, Oweida et al. reported on eight femoral arteriovenous fistulas that developed following 4988 percutaneous transluminal coronary angioplasty procedures with an incidence of 0.16% (24). A similar incidence of 0.11% was observed by Kim et al. in a study of 13,203

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many as 45% of the cases. Distal pulses were decreased in only 11% of 70 cases reported by Kollmeyer et al. (22), and none of the techniques with acute fistulas had a positive Branham–Nicoladoni sign. Although penetrating trauma is the most important cause of arteriovenous fistula, blunt trauma in civilian injuries is a definite etiologic factor. Basilar skull fracture with cranial bruit is pathognomonic of carotid–cavernous fistula. These patients may have pulsatile headache, vision changes, pulsatile exophthalmos, and conjunctival engorgement (51).

Diagnosis

FIGURE 83.4 Possible anatomic variations of acquired arteriovenous fistulas.

transfemoral diagnostic and therapeutic cardiac catheterizations (26). The anatomy of the arteriovenous fistula is determined by the site of arterial and venous injury and by the chronicity of the lesion (Fig. 83.4). False aneurysm develops shortly after the injury as a persisting pulsatile hematoma with arterial and venous connection or as a result of injury to the vessel wall in the proximity of the arteriovenous fistula. Chronic true arterial and venous aneurysms are direct consequences of local and systemic hemodynamic factors, which include increased circulating blood volume, high fistula flow, and increased intravascular pressure, as discussed earlier. The incidence of associated arterial and venous aneurysms ranged from 20% to 60% (49,50).

Clinical Data The clinical presentation of a patient with an acquired arteriovenous fistula is usually typical. There is a palpable thrill and a systolic–diastolic machine-like murmur; there may be a pulsatile mass; the superficial veins are distended; the peripheral arterial pulse may be diminished; and there is evidence of penetrating injury or fracture in the proximity of major blood vessels. In acute arteriovenous fistulas, the clinical picture is not always characteristic, and a bruit can be absent in as

In patients with chronic arteriovenous fistula, the diagnosis almost always can be made on the basis of history and physical examination alone. Apart from the bruit and thrill, signs of chronic venous stasis, including ulceration, pigmentation, edema, varicosity, and induration, with increased skin temperature at the level of and proximal to the fistula, and signs and symptoms of cardiac failure are clues to the diagnosis. In longstanding arteriovenous fistulas, if they were present before closure of the epiphyseal plates, the development of bony hypertrophy with elongation of the extremity has been reported (52). In some patients with chronic fistulas, there is frank aneurysm formation in the arteries proximal to the fistula. As a rare complication of a chronic arteriovenous fistula, subacute bacterial endocarditis may develop. Patients who have large central shunts, such as an aortocaval fistula, usually have a dramatic presentation, with acute congestive cardiac failure, abdominal bruit, and wide pulse pressure associated with lower extremity ischemia and edema (41). In spontaneous iliac arteriovenous fistula, venous stasis or arterial ischemia or both are localized to the affected extremity only (42). Noninvasive diagnostic techniques may be necessary to evaluate small arteriovenous fistulas and to determine the amount of shunting and the degree of peripheral ischemia as a result of the “distal” steal. Segmental limb systolic pressure measurements, pulse–volume recording, Doppler examinations, and duplex scanning are the most valuable diagnostic tools; these tools have been evaluated by Sumner (53) and by Rutherford (54) and are discussed in more detail elsewhere in this book. Segmental limb systolic pressure measurements reveal an elevated systolic pressure proximal to a significant arteriovenous fistula; the pressure may be normal or decreased distal to the lesion compared with the healthy contralateral extremity. Pulse–volume recordings are elevated proximal to the fistula and show a sharper systolic peak, with a decreased or absent anacrotic notch. Decreased pulse volume may or may not be recorded distally. Doppler examination is a useful noninvasive diagnostic technique. In the proximal artery, it reveals an abnormal velocity waveform with forward diastolic flow instead of a normal triphasic arterial flow. The increase in

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

end-diastolic velocity is proportionate to the decrease in peripheral resistance caused by the arterioovenous fistula. In the proximal veins the Doppler study may reveal a pulsatile flow pattern. Color flow duplex scanning is the most valuable noninvasive diagnostic test to identify an arteriovenous fistula. We use an Acuson 128 color-flow duplex ultrasound (Acuson, Inc., Mountain View, CA) with a 5- or 7.5-MHz linear array probe. Color flow duplex ultrasonography combines real-time B-mode ultrasound images with pulsed Doppler spectral analysis. By combining the anatomic imaging with hemodynamic data in the artery and the vein, duplex scanning offers a distinct advantage over any of the noninvasive diagnostic tests. Because it is noninvasive, it can be repeated and is suitable to follow nonoperative management (27). Measurement of venous oxygen saturation on the affected extremity proximal to the fistula shows elevated values compared with samples taken from veins in other parts of the body. Serial angiography performed with percutaneous catheterization through the femoral or brachial artery is the best and most definitive diagnostic test that delineates anatomy and, as a functional study, gives information on the hemodynamics of the fistula. Angiography not only localizes the fistula but also reveals arterial and venous aneurysmal changes and may document venous valvular incompetence distal to the fistula. Because the diagnosis of an acute traumatic arteriovenous fistula could be missed in 45% of the cases on the basis of physical examination alone (22), angiography, or in selected cases duplex scanning, is recommended for every patient with stable hemodynamics who has penetrating injury next to major blood vessels. The advantages of other imaging modalities, such as contrast-enhanced computed tomographic angiography with three-dimensional reconstructions, cinefluoroscopy and the advantages of duplex scanning and intravascular ultrasound (IVUS) have been discussed by White et al. (55).

Treatment and Results Disconnection of the arteriovenous fistula and reconstruction of a normal circulation are needed in most patients with large traumatic arteriovenous fistulas. Spontaneous cure of small acquired arteriovenous fistulas has been reported (22). In patients with iatrogenic fistula developing after femoral catheterization, spontaneous closure has been observed. Rivers et al. followed nine arteriovenous fistulas following cardiac catheterization (27). Six resolved spontaneously while three remained asymptomatic during a follow-up period that extended up to 20 months after injury. Others such as Oweida et al. suggest aggressive management of most fistulas (24). In those patients who develop arteriovenous fistula following kidney biopsy, spontaneous closure is usual rather than the exception (37). The majority of acquired arteri-

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FIGURE 83.5 Options of surgical treatment for acquired arteriovenous fistulas.

ovenous fistulas, however, are progressive and require treatment. Hunterian ligation of the artery proximal to the fistula is of historic interest only and should not be used. Quadruple ligation in cases of small distal vessels is still practiced and is acceptable only in distal vessels if the collateral circulation is adequate to prevent distal ischemia. Figure 83.5 depicts the various possibilities of open surgical reconstruction. In spite of an attempt to reconstruct both artery and vein after injury, arterial ligation was still the primary treatment in 52% of 558 patients who had arteriovenous fistula or false aneurysms, according to the Vietnam Vascular Registry. End-to-end anastomosis was performed in 25%, vein graft in 10%, and lateral suture in 7% of the arterial repairs. Venous ligation was used in 52% and suture repair in 30% of the cases (11). Of 233 patients with traumatic arteriovenous fistula, Linder (50) reported the use of lateral suture repair after division of the fistula in 67% of the cases. Of 70 arteriovenous fistulas due to civilian injuries, 40% were treated with primary arterial repair by the Parkland group (21). If lateral repair or end-to-end anastomosis cannot be done, our choice of graft material is the contralateral saphenous vein. Although under exceptional circumstances ligation of major veins can be

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performed without major consequence or can even be lifesaving for the patient with hemorrhage due to major abdominal trauma, every attempt should be made to reconstruct three important veins: the suprarenal inferior vena cava, the common femoral vein, and the popliteal vein. Prosthetic grafts for popliteal vein replacement have almost uniformly been unsuccessful; therefore contralateral saphenous vein should be used whenever it is necessary. The use of a spiral vein graft is an excellent way to reconstruct short segments of large-caliber veins (56). The results of surgical treatment of acquired arterionovenous fistulas are universally good. The overall mortality rate for 558 arteriovenous fistulas and false aneurysms in the Vietnam Vascular Registry was 1.8%, with a morbidity rate of 6.3% and an amputation rate of 1.7% (11). Linder reported a cure rate of 96% with only four amputations, which were necessary after quadruple ligation of the vessels (50). The complication rate from major intra-abdominal arteriovenous fistulas is more significant because of sudden circulatory overload and an increased risk of pulmonary embolization. A review of 73 collected cases reported an overall mortality rate of 30% and a morbidity rate of 32% (41). With the development of techniques of endovascular grafting, the surgical treatment of traumatic arteriovenous fistulas will undoubtedly change in the future. Mann et al. used a percutaneously placed stent–graft to repair a femoral arteriovenous fistula (56). Marin et al. (58) and later White et al. also reported on successful cases of stent–graft treatment of traumatic arteriovenous fistulas (55). Embolization is not as widely used as a treatment option in VMs with arteriovenous shunting. However, in certain types of acquired fistulas, especially in the region of the head and neck, in abdominal viscera, or in fistulas after pelvic fractures, embolization has become an important treatment either alone or as an adjunctive form of surgical treatment (22). Because the fistula is almost always a single large connection between artery and vein, embolizing particles usually must be larger than those used to obstruct congenital fistulas: detachable balloons, coils, or muscle fragments are used primarily. With detachable balloons alone, Debrun et al. (59) could preserve internal carotid blood flow in 59% of the cases with traumatic carotid–cavernous fistulas. The technique reported by Kollmeyer et al. (22) seems more successful; in high carotid–cavernous fistulas, embolization was preceded by extracranial-intracranial bypass: of six patients treated this way, only one had a transient neurologic deficit. Iatrogenic arteriovenous fistulas in the subclavian region were effectively treated by endovascular occlusion using detachable balloons (60). The safety and efficacy of transcatheter embolization in the nonsurgical management of vascular injuries was reported by Levey et al. (61). These authors treated traumatic arteriovenous fistulas in the axilla and shoulder using either Gianturco coils or

Hilal wires, with or without gelatin sponge or autologous clot. Ultrasound-guided compression treatment of iatrogenic femoral artery injuries was first reported in 1991 by Fellmeth et al. (62). Although this technique is more useful for the treatment of pseudoaneurysms, successful closure of arteriovenous fistulas has also been reported (28). While most catheter-related femoral arteriovenous fistulas can be managed conservatively (27) or by ultrasoundguided compression (28,62), surgical treatment in these patients still may be needed for those who have cardiovascular compromise, associated increasing hemorrhage, or large fistula in spite of attempts at ultrasound-guided compression treatment (63,64).

Arteriovenous Fistula after Lumbar Laminectomy Arteriovenous fistulas after lumber laminectomy were reported first by Linton and White (30) in 1945, and the topic was extensively reviewed recently by others (31–34). The cause of the arteriovenous fistula is usually the bone rongeur, which penetrates the anterior spinal ligament, most frequently at the level of L4 to L5, and injures the right common iliac artery and right or left common iliac vein. Arteriovenous fistulas at the L3 to L4 and L5 to 5–1 levels have also been reported. Because of retroperitoneal tamponade of the bleeding, this complication usually becomes evident in the postoperative course, sometimes months or even years after the injury. Lower extremity edema, fatigue, signs of congestive heart failure, and systolic–diastolic murmur are clues to the diagnosis, but aortography is recommended to precisely define anatomy and plan surgical correction. Division of the fistula, venorrhaphy, and direct arterial repair are usually possible. It is sometimes necessary to divide the right common iliac artery to gain better access to the venous repair. Prosthetic graft placement is seldom required, but in rare infected cases the use of in situ autologous material or extra-anatomic prosthetic arterial grafting may be needed.

Arteriovenous Fistula after Nephrectomy The first arteriovenous fistula after nephrectomy was described in 1934 by Hollingsworth (35) and by 1984 only 50 cases had been reported (36). The cause is most frequently the mass ligature of artery and vein, transfixing suture, or local infection. Symptoms, such as pain, palpable mass, elevated blood pressure, and cardiac failure, may develop anywhere from 6 months to 36 years after the operation. An audible bruit at the site of nephrectomy strongly suggests the diagnosis, which is definitively confirmed by angiography. Separate ligature of the artery or vein or transcatheter embolization is the treatment of choice (65).

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

Arteriovenous Fistula after Embolectomy with Fogarty Balloon Catheter Since the first report of an arteriovenous fistula as a complication of the Fogarty embolectomy catheter was made by Lord et al. in 1968 (38), 18 cases had been collected in the literature up to 1985 (39). The number of unreported cases must be much higher, and Schweitzer et al. concluded that 10% of the complications by Fogarty catheters are arteriovenous fistulas (40). Most of the true arteriovenous fistulas develop distal to the knee, but carotid–cavernous fistulas also have been reported. The causes may be: 1. 2. 3. 4.

catheters of inadequate size; diseased vessels with atherosclerotic plaques; faulty surgical technique; or multiple attempts to extract emboli, especially in cases of “late” embolectomy.

Although some publications have suggested leaving the arteriovenous fistulas to improve patency, significant arteriovenous fistula should be repaired. The routine use of intraoperative angiogram after embolectomy is recommended.

Vascular Malformations Similar to acquired arteriovenous fistulas, VMs frequently have abnormal communications between the arterial and venous system. As mentioned before, however, the true characteristics of VMs is not arteriovenous shunting but the abnormal development of one or several segments of the vascular system, the arteries, veins, capillaries, or lymphatic vessels. These lesions are the result of faulty development of the blood vessels, and the arteriovenous connections, when present, are almost invariably multiple. Progression is mostly the result of hemodynamic factors, and tumor-like behavior with endothelial proliferations, as emphasized in a pioneer article by Mullikan and Glowacki, is not characteristic (66). VMs are usually present at birth, although signs and symptoms may become manifest only later in life. Hereditary transmission is rare, of 840 cases with vascular malformations (angyodysplasias), Malan et al. found only seven patients with familial inheritance (67). The large spectrum of clinical presentations explains why so many different names (arteriovenous hemangioma, arteriovenous aneurysm, arteriovenous fistula, cirsoid aneurysm, serpentine aneurysm) and syndromes (Parkes-Weber, Klippel–Trénaunay, Rendu–Osler–Weber) (Table 83.1) have been attached to these lesions.

Classifications There have been few areas in medicine in which so much confusion and controversy have existed than in the field of

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vascular malformations. A plethora of classifications has been suggested, some of those based simply on external appearance of the lesions and on resemblance to fruits, fish, birds, or insects (68). The most valuable classification systems have been based on morphologic features (15,69), embryologic development (16,17), endothelial characteristics and cell biology (66), hemodynamics, and angiographic appearance (70,71) or a combination of these (20). Vascular malformations or angiodysplasias include developmental abnormalities of the arterial, capillary, venous, or lymphatic system. In the case of AVM, which are malformations with arteriovenous shunting, the pathologic vasculature is mixed arteriovenous. Secondary morphologic changes in the feeding arteries and draining veins are the result of hemodynamic factors and depend primarily on the amount of blood shunted through the abnormal vessels. Malan and Puglionisi (15) divided the VMs into: 1. 2.

truncular arteriovenous fistulas, local or diffuse, more or less active; and arteriovenous angiomas, single, polycentric or diffuse, more or less active.

On the basis of morphologic variations, further subgroups such as single truncular, plexiform, aneurysmal, or circumscribed were distinguished. The classification of Szilagyi et al. (16,17) is simpler and is based primarily on the development of the vascular system. Studies by Woollard (72) first shed light on the stages of embryologic development: 1. 2. 3.

the capillary network stage, which is an undifferentiated interlacing network of primitive blood lakes; the retiform stage, when separation of primitive arterial and venous channels develops; and the stage of gross differentiation with the appearance of mature vascular stems.

Although Szilagyi named them hemangiomas, these are capillary or cavernous vascular malformations, developmental abnormalities of the capillary network stage (Fig. 83.6). It is in the retiform stage that arrest in the development results in congenital arteriovenous communications. Depending on the size of the abnormal communicating vessels and whether or not angiography could demonstrate the exact site of arteriovenous connections, this group has been further subdivided into microfistulous and macrofistulous arteriovenous fistulas. Abnormal development of stage 3 results in persistence of anomalous vascular channels. Studies of Mulliken et al. (66,73) gave important information on the endothelial characteristics and cell biology of congenital vascular lesions. These authors reserve the term “hemangioma” for those lesions that clinically undergo growth and usually resolution and in the proliferative phase show endothelial hyperplasia; the term VM

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TABLE 83.1 Clinical syndromes associated with congenital vascular malformation Syndrome

Inheritance

Type

Location

Characteristic Features

Treatment

Prognosis

Parkes-Weber

No

AVM (intraosseal or close to epiphyseal plate) Port-wine stain

Extremity Pelvis

Observation Elastic support Embolization + excision

Deep diffuse lesions have poor prognosis

Klippel–Trénaunay

No

No or low-shunt AVM Venous or lymphatic VM Port-wine stain

Extremities Pelvis Trunk

Elastic support Seldom: epiphyseal stapling, or selective excision of varicose veins

Usually good

Rendu–Osler–Weber (hereditary hemorrhagic telangiectasia)

Autosomal dominant

Punctate angioma Telangiectasia AVM

Transfusions Embolization vs. laser treatment + excision

Good if bleeding can be controlled and no CNS manifestations

Sturge–Weber (encephalotrigeminal angiomatosis)

No

Port-wine stains

Skin Mucous membrane GI tract Liver Lungs Kidney Brain Spinal cord Trigeminal area Leptomeninges Choroid Oral mucosa

Soft tissue and bony hypertrophy Varicosity (atypical) Capillary and highflow, high-shunt AVM Soft tissue and bony hypertrophy Varicosities (lateral lumbar to foot pattern) Capillary or venous vascular malformation/ lymphatic malformation Epistasis Hematemesis, melena Hematuria Hepatomegaly Neurologic symptoms

Anticonvulsants Neurosurgical procedur

Guarded Depends on intracranial lesion

Von Hippel-Lindau (oculocerebellar hemangioblastomatosis) Blue rubber bleb nevus

Autosomal dominant

Hemangioma

Retina Cerebellum

Excision of cysts

Autosomal dominant

Cavernous venous hemangioma

Transfusions Electrocoagulation Excision

Depends on intracranial lesion Depends on CNS and GI involvement

Kasabach-Merritt

Autosomal dominant

Large cavernous hemangiomas

Skin GI tract Spleen Liver CNS Trunk Extremity

Convulsions Hemiplegia Ocular deformities Mental retardation Glaucoma Intracerebral calcification Cysts in cerebellum, pancreas, liver, adrenals, kidneys Bluish, compressible rubbery lesions GI bleeding,anemia

Compression Transfusion of blood, platelets

Death from hemorrhage or infection

Maffucci (dyschondroplasia with vascular hamartoma)

Probably autosomal dominant

AVM Cavernous hemangioma Lymphangioma

Fingers Toes Extremity Viscera

Thrombocytopenia Hemorrhage Anemia Ecchymosis Purpura Enchondromas Spontaneous fractures Deformed, shorter shorter extremity extremity Vitiligo

Orthopedic management

Chance of malignancy 20%

(like port-wine stains and arteriovenous, venous, or lymphatic malformations) is used for clinically and cellularly adynamic lesions. As opposed to VMs, hemangiomas in the proliferative phase incorporate [3H]thymidine and also have an increased mast cell count (74). The classification of Forbes, May, and Jackson (71), from the Mayo Clinic, is based on hemodynamics and an-

giographic appearance. Its advantages are that it is simple and it has practical clinical value because, with the clinical picture, it helps to determine treatment and prognosis. Depending on the amount of shunted blood, high- and low-shunt lesions are distinguished, and the size of the lesion is determined by the volume of blood that enters the feeding vessels. High-shunt lesions correspond with

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

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TABLE 83.2 Classification of vascular malformations

A

Blood Vessel

Anatomic Area

Abnormality

Arterial

Truncular

Venous

Extratruncular Truncular

Agenesis, aplasia, hypoplasia, dilation, aneurysm Limited, infiltrating Agenesis, aplasia, hypoplasia, dilation, aneurysm (with or without valvular agenesis or dysplasia) Limited, infiltrating Superficial, deep Limited, infiltrating Aplasia, hypoplasia, obstruction, dilation Limited, infiltrating Arterial/venous, venous/ lymphatic, etc. Limited, infiltrating

Lymphatic

Extratruncular Truncular Extratruncular Truncular

Mixed

Extratruncular Truncular

Arteriovenous

Extratruncular

B

C FIGURE 83.6 (A) Capillary arteriovenous malformation. (B) Microfistulous arteriovenous fistulas. (C) Macrofistulous arteriovenous fistulas.

macrofistulous arteriovenous VMs whereas hemangiomas are obviously low-shunt lesions. Between these two extremes a whole spectrum of malformations can be found. The most complete and useful classification is the 1988 Hamburg classification (20), with some modifications as presented recently by Lee (75). Based largely on Lee’s modifications, we made additional changes and propose the classification currently used by our group at the Mayo Clinic (Table 83.2). Malformation is first classified by the predominant vascular defect (e.g., arterial, venous, arteriovenous, lymphatic, or mixed); then, it is further classified to truncular or extratruncular form depending on the embryonal stage when developmental arrest occurred. Our further discussion is limited to two main groups of VMs: first, to those lesions that have clinical or angiographic evidence of arteriovenous communications and, based on the Hamburg classification, belong to malformations with arteriovenous shunting (Parkes-Weber-type malformations). The second group we discuss includes patients with predominantly mixed, venous, capillary, and lymphatic malformations, and those with Klippel– Trénaunay syndrome (76,77,81,82). It should be remem-

FIGURE 83.7 Anatomic distribution of congenital arteriovenous malformations in 185 patients. (Reproduced from Schwartz RS, Osmundson PJ, Hollier LH. Treatment and prognosis in congenital arteriovenous malformation of the extremity. Phlebology 1986;1:171, by permission of John Libbey & Co.)

bered that over 70% of congenital arteriovenous fistulas are mixed vascular malformations that include capillary, venous, and lymphatic elements as well (17).

Malformations with Arteriovenous Shunting Location Although VMs with arteriovenous shunting (arteriovenous malformations or AVMs) can occur almost anywhere in the body, lesions involving the lower extremity are the most frequent (Fig. 83.7). After the extremities, head and neck lesions have the second highest prevalence.

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FIGURE 83.8 Symptoms of 185 patients with congenital arteriovenous malformations of the pelvis and extremities. (Reproduced from Schwartz RS, Osmundson PJ, Hollier LH. Treatment and prognosis in congenital arteriovenous malformation of the extremity. Phlebology 1986;1:171, by permission of John Libbey & Co.)

FIGURE 83.9 Physical findings of 185 patients with congenital arteriovenous malformations of the pelvis and extremities. (Reproduced from Schwartz RS, Osmundson PJ, Hollier LH. Treatment and prognosis in congenital arteriovenous malformation of the extremity. Phlebology 1986;1:171, by permission of John Libbey & Co.)

AVMs in this area are divided into two groups: intra-axial (branches of the internal carotid artery and basilar arteries supplying brain tissue) and extra-axial (branches of external carotid artery and those branches of the internal carotid and basilar arteries that supply nonbrain tissue such as dura, bone, or muscle) (19). This distinction is important because the lesions in the two groups are managed differently. AVMs of the spinal cord may have dramatic presentations. Pelvic lesions can be serious management problems, and lesions involving the viscera (lung, gastrointestinal tract, kidneys, and liver) can produce significant symptoms. Lesions in the lung can have either pulmonary arterial or, rarely, systemic blood supply.

Clinical Data In a Mayo Clinic study of 185 patients with AVMs of the extremities and pelvis, with arteriovenous shunting, there were 100 female and 85 male patients (78). The median age of the patients when the first lesion was noted was 1.9 years, but the median age at the onset of symptoms was 11 years. No data are available on the natural history because many patients with asymptomatic small lesions never seek medical help. The mean interval between the appearance of the first lesion and the time the first medical examination was done was 12.7 years (median 16.6 years). The most frequent presenting problem was skin discoloration (43%), followed by pain (37%), a palpable mass (35%), and limb hypertrophy (34%). Of these patients 27% had distended superficial veins, and less than 1% of the patients were completely asymptomatic at the time when medical examination was performed at the Mayo Clinic (Fig. 83.8). The most frequent abnormality found on physical examination was a vascular malformation, described as “hemangioma” (34%), usually as “capillary type” (Fig. 83.9). An audible bruit was present in 26% of the 185 patients; ulceration (Fig. 83.10) and skin necrosis were relatively frequent (20%). Increased skin temperature at the

FIGURE 83.10 Persisting ulcer of dorsum of left foot of 22-year-old woman due to arteriovenous malformation. Repeated embolization and several attempts at skin grafting failed to heal the ulcer.

level of the lesion, decreased distal pulses, pulsatile veins, and edema of the extremity — with other symptoms of venous hypertension, hyperhydrosis, and hypertrichosis — were additional findings. The development of soft tissue and bony hypertrophy in association with congenital arteriovenous fistulas, first described by F. Parkes-Weber (79,80) as “hemangiectatic hypertrophy” in 1907 and again in 1918, is still not well understood. Holman’s hypothesis that increased arterial flow in the area of the epiphyseal plates is the cause of the overgrowth is hardly acceptable, because nutritive flow in

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arteriovenous fistulas is always diminished (21). Venous stasis is another explanation because longer limbs are also seen in Klippel–Trénaunay syndrome (81,82), in which significant arteriovenous shunting is not present. There is some experimental evidence from a small number of animals that venous stasis alone causes bony hypertrophy (83,84). A tissue growth factor or a complex anomaly in the development of mesenchymal tissue are further possible explanations. The significance of skeletal changes has been emphasized by Boyd et al. (85): bony alterations occurred in 34% of 224 vascular malformations, in contrast with only 1% of 356 hemangiomas. The clinical presentation of AVMs in the head and neck region is determined by the location of the lesion. Occipital dural malformations may be associated with headache, bruit, and seizures; cavernous sinus lesions are associated with retinopathy and vision loss; facial AVMs usually cause cosmetic deformity, mass effect, or bleeding in the tongue or floor of the mouth (19). Congenital AVMs in the pelvis are more rare than the acquired lesions (86,87). They may be silent for a long time and be discovered only incidentally during a pelvic examination or computed tomographic (CT) scan, or during a laparotomy done for other reasons. Some lesions may cause compression, whereas others may result in vaginal bleeding.

Diagnosis The diagnosis of a congenital AVM can usually be made by history and physical examination. Confirmation is generally by CT scanning, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), or, if treatment is planned, by angiography. Noninvasive studies, such as pulse–volume recording, sequential limb systolic measurements, Doppler examination, and duplex scanning, may be useful to diagnose microfistulous lowshunt lesions (Fig. 83.11) (88). Contrast echocardiography can detect the appearance of indocyanine green on the venous side, after intra-arterial injection, and the test is useful to determine residual shunts after surgical excision (87,89). Colored duplex scanning is performed in all cases of AVMs on the limbs in our practice to define flow patterns and diagnose venous anatomy and arterial flow in the venous system. Radionuclide scanning of 99mTc-labeled human albumin can be used to estimate the amount of shunted blood. The labeled 35-mm spheres are injected first into the main feeding artery and then into the vein; radioactivity above the lungs is measured with a gamma camera. Whereas, after venous injection, 100% of the isotope is trapped in the lung, the percentage of radioactivity after arterial injection depends on the arteriovenous shunt flow, which in normal individuals without anesthesia should not exceed 3% (46). This test is able to estimate local and systemic hemodynamic effects of the arteriovenous shunt and is suitable to monitor the progression of the disease. These noninvasive examinations, however do not replace angiography, CT, or MRI.

FIGURE 83.11 Arteriogram of left foot, indicating two areas of angiomas (arrows) on lateral side, one at proximal end near ankle and the other at base of fifth toe. (A) Posterotibial arterial pulse wave is distinctly different from those of arteriovenous shunt waves. (B and C) Doppler ultrasonographic recordings were obtained with probe placed on two angiomatous masses and represented pulsatile waves with contours characteristic of arteriovenous shunts. (Reproduced from Haimovici H, Sprayregen S. Arch Surg 1986,121:1065, by permission of the American Medical Association.)

Angiography Considerable progress has been made in the field of angiography since 6 December 1933, when Horton and Ghormley (90) first injected 10 mL of thorium oxide (Thorotrast) into the brachial artery of a man to visualize a congenital arteriovenous fistula of the hand. Angiography, complemented by CT with intravenously administered contrast medium or MRI, is still the most important diagnostic test that should be done before an invasive treatment plan is designed. The arteriography is performed with the Seldinger technique, usually through the femoral artery, and selective or superselective catheterization and injections are performed. With angiography, the size of the feeding arteries can be measured and the size of the arteriovenous shunts

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(2 mm in large shunts, 100 to 200 mm in small shunts) can be estimated with acceptable accuracy on the basis of appearance time of contrast medium in the vein (71). The flow volume is determined by the size and rate of opacification of the feeding arteries, whereas the shunt volume can be estimated by the time and appearance of contrast medium in the veins. On the basis of data from Szilagyi et al. (17) in 1964, in 40% of congenital AVMs the site of shunting cannot be determined with angiography. With the help of superselective angiography of multiple feeding vessels and rapid filming, today this number is probably lower. There are still, however, a considerable number of lesions in which angiography gives only indirect evidence of shunting: early venous filling, increased afferent arterial flow, decreased opacification of the distal arterial tree, pooling of the contrast medium in the area of the fistula, and tortuosity and dilation of the afferent arteries. In these cases, the diagnosis can be supported further by ultrasonography (88), CT, MRI, or MRA. Computed Tomography In recent years, CT has made the diagnostic evaluation of patients with congenital AVMs more complete. It delineates the relation of the lesion to the surrounding tissue. Enhanced with intravenously administered contrast medium, CT provides even better separation of these vascular lesions from adjacent normal tissue. Soft tissue and bone hypertrophy can be accurately documented. Although MRI has gained increasing popularity, CT scan, with three-dimensional reconstruction, because of its easy availability, is still an important diagnostic test in these patients.

FIGURE 83.12 Arteriovenous malformation of ankle with serpiginous vessels (arrow) clearly seen on partial saturation sagittal magnetic resonance image. (Reproduced by permission from Berquist TH. Bone and soft tissue tumors. In Berquist TH, ed. Magnetic resonance of the musculoskeletal svstem. New York: Raven Press, 1987:85–108.)

Magnetic Resonance Imaging and Angiography MRI and MRA with the use of gadolinium offers several advantages over other diagnostic modalities and has become the main technique to diagnose and follow congenital AVMs (71,91–93). MRI delineates the relation of AVMs to muscle groups, fascial planes, nerves, and tendons, and detects invasion of bone. For MRA, iodinated contrast is not needed and gadolinium is used for enhancement. No radiation is used, and both sagittal and longitudinal planes can be visualized (Figs. 83.12 and 83.13). MRI and MRA became the most important diagnostic test in our practice for AVMs.

Treatment and Results Many congenital AVMs are asymptomatic or have minimal symptoms and require observation only. Because of obvious limitations in the complete cure of these lesions, unless they are small and can be excised in toto, it is irresponsible to treat silent and asymptomatic lesions, because any intervention may frequently produce further growth. It is equally important, however, to do everything possible to treat obviously enlarging lesions before significant overgrowth of the extremity or severe disfigurement

FIGURE 83.13 Vascular malformation of the forearm. (A) Computed tomographic scan with contrast medium shows numerous contrast-filled vessels in forearm. (B and C) Axial magnetic resonance images demonstrate irregular high-intensity lesion with multiple vessels. (Reproduced by permission from Berquist TH. Bone and soft tissue tumors. In: Berquist TH, ed. Magnetic resonance of the musculoskeletal system. New York: Raven Press, 1987:85–108.)

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Nonsurgical Treatment

FIGURE 83.14 A 33-year-old man who required right hip disarticulation for extensive lower extremity arteriovenous malformation. (A) His 12-cm abdominal aortic aneurysm was repaired with a straight aortoleft common iliac Dacron graft. (B) Chest radiograph showing cardiomegaly with pulmonary venous hypertension.

of the patient develops. In addition, complications of AVMs, such as bleeding, infection, critical distal ischemia, disabling pain, tissue necrosis, and ulcers, need treatment. In rare cases, treatment is indicated because of congestive heart failure, and, in some, secondary aneurysmal changes of the proximal feeding arteries need repair to avoid rupture (Fig. 83.14). Management of any significant AVM requires teamwork and consultation with the radiologist and the vascular, plastic, or orthopedic surgeon.

Elastic compression, in the form of elastic stocking or garment, is not curative, but it is useful in extremity lesions, not only to compress the hemangioma or the distended superficial veins, but also to give more protection to the extremity to avoid trauma to these vascularized vulnerable lesions. Laser treatment has become popular for treatment of vascular malformations. The main types in use are the argon, carbon dioxide, and neodymium:yttrium aluminum garnet (Nd:YAG) lasers. The argon and the Nd:YAG lasers can be used with a flexible endoscope. The Nd:YAG laser, which is used in the treatment of 95% of gastrointestinal lesions, has a deeper penetration and, in contrast to the argon beam, it is not absorbed in the red spectrum and can penetrate blood clot over the vascular malformations. Argon lasers are primarily used for portwine stains (94), which are special intradermal capillary malformations, usually in the area of the distribution of the trigeminal nerve or on the lateral aspect of the thigh in patients with Klippel–Trénaunay syndrome (82). Most of the patients, usually adults with purple, well-vascularized lesions, benefit from argon laser treatment, although unacceptable scarring was reported to occur in 5% to 24% of the cases (68). With the introduction of the yellow light lasers, scarring is observed less frequently. The flashlamppumped pulsed dye laser seems to be a safe and effective treatment to treat port-wine stain capillary malformations in infants and in children (96). The benefit of treatment of port-wine stains using the yellow light from a copper vapor laser was confirmed by Pickering et al. (97). These authors also concurred that the occurrence of scarring, hyperpigmentation, and hypopigmentation was low in comparison with previous studies. Cryotherapy and electrolysis have no proven value in the treatment of AVMs and should be abandoned. Sclerotherapy can be effectively used in selected lowshunt lesions with the injection of 3% sodium tetradecyl sulfate directly into the lesion (71). Small amounts of the drug (0.5 to 2.0 mL) are injected during one session after blood has been emptied from the lesion either by aspiration with the syringe or by elevation of the extremity. Compression treatment is necessary after sclerotherapy. The indications for this form of treatment are limited, and it should not be used with high-shunt lesions. Embolization with percutaneous catheterization has become an important treatment option for AVMs, used alone or in combination with surgical treatment (Figs. 83.15–83.18) (18,19,38,47,49,71,94–104). It requires careful planning, special knowledge of anatomy of the blood vessels, and a radiologist or neuroradiologist who is well trained in selective and superselective catheterization. Congenital AVMs are frequently supplied by several arteries; therefore, catheterization through more than one main artery may be necessary. The aim of the embolization is to stop abnormal shunting at the precapillary or capillary level. Occlusion of the main arterial trunk is a se-

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Part XI Arteriovenous Malformation

FIGURE 83.15 (A) Large macrofistulous arteriovenous malformation of right thigh of 37-year-old man who had three previous attempts at surgical excision. (B) surgical excision and then embolizatlon with 3-mm woolly-tailed coils and Ivalon particles were performed. Angiogram 5 months later shows good result with minimal arteriovenous shunting.

rious error because it makes the AVM inaccessible for further embolization while allowing the AVM to open new distal collateral vessels. The material used for embolization should therefore be small enough to reach the capillary level but larger than the size of the fistula to avoid pulmonary embolization. Embolizing materials are divided into two groups: temporary and permanent. Temporary materials such as blood clot, gelatin sponge, or microfibrillar collagen are usually used for preoperative embolization to decrease operative blood loss, are usually little risk to normal tissues, and dissolve within a few days or weeks. Permanent materials used are silicone spheres, polyvinyl alcohol particles, stainless steel coils, or for large fistulas, detachable balloons. Liquid such as absolute alcohol or bucrylate are also used, although bucrylate has become less popular because of a presumed carcinogenic effect. Silicon spheres can be accurately sized, but the disadvantage is that a large-diameter catheter is required for

FIGURE 83.16 Occipital dural arteriovenous malformation with peripheral drainage. (A) Carotid angiogram demonstrates rapid shunting along dura into sigmoid sinus and jugular vein. (B) Subselective occipital artery catheterization reveals four penetrating muscular branches that supply malformation. (C) Postembolization angiogram shows occlusion of malformation and preservation of normal arterial trunk vessels. (Reproduced by permission from Forbes G, Earnest F IV, et al. Therapeutic embolization angiography for extra-axial lesions in the head. Mayo Clin Proc 1986;61:427.)

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

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FIGURE 83.17 (A) High-flow arteriovenous malformation. (B) Clinical impression confirmed by right carotid angiography that shows extensive supply from external system. (C) Appearance after embolization. (D) Resection of malformation 48 hours after embolization by using Karapandzic technique of reconstruction. (E) Lesion excised. (F) Reconstruction of lip and chin. (G) Postoperative result. (H) Function of lips. (Reproduced by permission from Forbes G, May GR, Jackson IT. Vascular anomalies in children. In: Jackson IT, Mustarde J, eds. Plastic surgery in infancy and childhood. New York: Churchill Livingstone, 1988:691–710.)

FIGURE 83.18 (A) Angiogram of high-flow arteriovenous malformation of shoulder in child. Lesion is supplied by humeral circumflex arteries. (B) Postembolization with blood clot; most of arteries are occluded. Lesion was resected 24 hours after embolization. (Reproduced by permission from Forbes G, May GR, Jackson IT. Vascular anomalies in children. In: Jackson IT, Mustarde J, eds. Plastic surgery in infancy and childhood. New York: Churchill Livingstone, 1988:691–710.)

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Part XI Arteriovenous Malformation FIGURE 83.19 (A) High-flow arteriovenous malformation involving the left arm and hand of a 26-yearold woman. (B) Left arm arteriogram reveals extensive arteriovenous malformation with involvement of the bone and soft tissue. (C) Selective injection of the deep brachial artery reveals involvement of the interosseous branches of the humerus as well. (D) The large arteriovenous fistula in the medullary cavity of the humerus was embolized using more than 13 coils and three strands of No. 2–0 silk sutures. Almost complete occlusion of the arteriovenous fistula in the humerus was noted. (Courtesy of A W. Stanson, Mayo Clinic and Foundation.)

A

C

B

D

delivery. The advantages of polyvinyl alcohol foam (Ivalon) are that 1) a smaller catheter can be used and 2) after embolization the size of the particles increases up to 10 times. The particles are injected in the form of a liquid slurry by using a mixture of contrast medium and warm saline solution containing the foam particles, ranging from 100 mm to 1mm in diameter (19). Stainless steel coils with tufted Dacron are adequate to occlude large vessels (Fig. 83.19). Thrombosis, which is enhanced by using the tufted Dacron, can also be augmented by injecting thrombotic materials in addition to the coils. Embolization is performed in one or, if necessary, in several stages with a continuous fluoroscopically monitored flow-delivery technique using a single-lumen, nontapered catheter, described by Kerber (98) in 1977, to avoid reflux and poor deposition. Complications can be decreased by careful selection of the embolizing material and embolization technique and by a thorough knowledge of vascular anatomy. Al-

though certain arteries, such as branches of the hypogastric artery, branches of the profunda femoris artery, or certain muscle branches, are ideal for embolization, embolic occlusion of distal arteries of the extremities may, unfortunately, lead to tissue loss or gangrene. Forbes et al. (19) reported on 31 therapeutic embolizations of 23 patients with extra-axial vascular malformations of the head. Of the nine patients with AVMs, embolization in seven produced excellent results: the degree of obstruction was 80% or more. Two patients with high-shunt flow needed combined radiologic–surgical treatment. Beneficial effect from embolization in cases of pelvic congenital AVMs (99–102) or extremity lesions (100,102) has been reported as well. Jacobowitz et al. (104) from the New York Hospital recently reported long-term follow-up of transcatheter embolization therapy in symptomatic complex pelvic AVMs in 35 patients. The most common presenting symptoms was abdominal pain (59%); 44% had a palpable pulsation or thrill; 27% had hemorrhage; and 18% had

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

congestive heart failure. A total of 89% had arteriovenous shunting. The patients required a mean of 2.4 embolization procedures (range, 1 to 11 procedures) over a mean period of 23.3 months (range, 1 to 144 months), using rapidly polymerizing acrylic adhesives most frequently. More than one procedure was performed in 20 patients (53%). Adjunctive surgical procedures were performed subsequent to embolization therapy only in five patients (15%). A total of 83% of patients were asymptomatic or significantly improved at a mean follow-up of 84 months (range, 1 to 204 months). The authors concluded that transcatheter embolization is currently the treatment of choice for symptomatic pelvic AVMs and that surgical ligation of large proximal feeding vessels should be avoided, since it prevents multiple embolization, if needed in the future. Surgical Treatment It is imperative to emphasize again that ligation of the proximal feeding vessel alone has no place in the treatment of AVMs. It will invariably lead to the development of collateral circulation, and it impedes radiologic embolization as a form of treatment of these lesions. Direct feeding arteries should be ligated only in those rare cases in which immediate complete resection of a localized AVM is possible. The presence of an AVM alone does not mandate aggressive treatment. This conservative attitude is clearly reflected in the study of Gomes and Bernatz (105) from the Mayo Clinic: of 80 patients with congenital AVMs of the extremities, surgical excision was attempted in only 10. If surgical treatment is indicated because of rare cosmetic reasons, sudden progression, involvement of adjacent important structures, limb ischemia, disabling pain, ulceration of the skin, repeated infection, or bleeding, or rarely congestive heart failure, it should be most carefully planned. In our present practice, embolization with or without an attempt at complete surgical resection seems to be the best treatment option. Embolization can be repeated if necessary if the main feeding vessels are left intact. If excision is contemplated, we avoid staging and make every attempt to perform a resection as complete as possible at one stage. In general, in only about 20% of all AVMs can curative resection be performed (106). If the lesion is on the extremity, a proximal tourniquet significantly decreases blood loss. Meticulous hemostasis during the procedure is imperative. The use of the cell-saver for autotransfusion in these patients has become routine. Cardiopulmonary bypass, temporary circulatory arrest, and hypothermia have been used for excision of large AVMs (107). Intraoperative Doppler echocardiography has been a useful adjunct to determine the extent of these tumors and to localize the feeding vessels (108). With the technique of careful serial ligation of all branches of major extremity arteries and veins to interrupt feeding vessels to the AVMs, Volimar and Stalker (69) reported an improvement in 19 of 21 cases of extremity AVMs, and only two patients needed amputations. We combine this technique

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with attempts at complete resection, even if large defects are made which need reconstruction with axial or arterialized flaps. The overall experience is, unfortunately, that extensive lesions cannot be excised for cure in the majority of cases. Szilagyi (106) reported poor results in five of eight patients with deep diffuse AVMs who underwent an attempt at surgical resection. Surgery helped in only one patient, and the result was clearly worse in five. Trout et al. (109) attempted surgical treatment of four lower extremity AVMs, two of which required amputations. In our retrospective study (78), symptomatic patients with surgical excision seemed to do better; probably because of the larger number of localized lesions than in those treated conservatively. The surgical group of 82 patients included 18 patients who required amputations at various levels of the extremity. Many of these amputations, however, meant cure for the patients and saved them from the long-term morbidity of repeated procedures. Figure 83.20 summarizes our current concept of management of AVMs.

Visceral Arteriovenous Malformations As a result of improvement in diagnostic techniques, especially in selective cardiac and superior mesenteric catheterizations, there has been an increased recognition of the importance and frequency of gastrointestinal AVMs. The lesions classified as type I by Moore et al. (110) are probably acquired submucosal AVMs, which develop in elderly patients with valvular heart disease or severe atherosclerosis and are usually located in the terminal ileum, cecum, or ascending colon. The type II lesions are, however, true congenital AVMs and occur mostly in the upper portion of the small bowel in younger patients. The type III lesions are punctate angiomas, which are the gastrointestinal manifestations of hereditary hemorrhagic telangiectasia (Rendu–Osler–Weber syndrome). Selective or superselective angiography with magnification is frequently necessary to visualize the lesions, which produce the so-called tram-track sign, the simultaneous opacification of the feeding artery and the draining vein. Embolization, endoscopic treatment, and surgical excisions are the options if bleeding does not cease after correction of coagulation abnormalities and transfusion. Embolization, if done, should be performed with extreme caution and with superselective catheterization only — bowel necrosis is a definite possibility (102). For this reason, endoscopic treatment, with monopolar or bipolar electrocoagulation, heater probe, and especially photocoagulation with the Nd:YAG laser; has gained increasing popularity. The YAG laser produces thermal destruction of the vascular tissue, even in the submucosa, and produces mucosal ulceration that needs several weeks to heal. It is an effective way, however, to stop bleeding from vascular malformations, although rebleeding rates as high as 25% have been reported. In a series of 59 patients treated

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Part XI Arteriovenous Malformation FIGURE 83.20 Management of peripheral congenital arteriovenous malformations. (Adapted from

Clinical evaluation Noninvasive tests Magnetic resonance imaging

Diffuse extensive

Discrete localized

Arteriography

Rutherford RB. In St. Belov DA, Loose JW, eds. Periodica Angiologica 16, Vascular Malformations. Hamburg, Germany: Einhorn-Presse Verlag, 1989:64.)

High flow

Hemorrhage? Critical ischemia? Disabling pain? Ulceration?

Yes

Low flow

No

Elastic support Elevation

Arteriogram with embolization and with or without surgical excision or amputation Surgical excision for specific indications

with the laser, two cecal perforations required hemicolectomy (111). Surgical excision, if the lesion is clearly identified on angiogram, is usually effective (110). Intraoperative identification of the mucosal AVM may be facilitated by transillumination. Recurrent bleeding, usually from other malformations, can be as frequent as 10% (112). Renal AVMs, which are usually located beneath the mucosa of the renal collective system, may result in hematuria or flank pain or may be an incidental finding during renal arteriography done for other purposes. Massive bleeding from renal AVM during pregnancy has been reported (113). Transcatheter embolization is the treatment for symptomatic lesions. If it is unsuccessful, partial or sometimes total nephrectomy is necessary. Hepatic or splenic AVMs are extremely rare and may be manifestations of hereditary hemorrhagic telangiectasia (Rendu–Osler–Weber syndrome) (114). Jaundice, significant hepatomegaly, and high shunt volume with cardiac failure have been reported. If the lesions are symptomatic, excision and embolization are the treatment options. Pulmonary AVMs have an almost 40% chance of being associated with hereditary hemorrhagic telangiec-

tasia. The most frequent symptoms are dyspnea, palpitation, and hemoptysis; 60% of the patients have an audible bruit (115). Cyanosis and clubbing are additional findings. Patients with hereditary hemorrhagic telangiectasia usually have multiple fistulas. There is an increased rate of fistula growth and increased frequency of complications, especially cerebrovascular accidents. Angiography confirms multiplicity and identifies blood supply. Surgical excision gives good results and is indicated if the patient is symptomatic and if a single fistula is associated with hereditary telangiectasia and, in rare cases, with systemic blood supply (115). Multiple bilateral AVMs with hereditary telangiectasia, managed with staged bilateral thoracotomies, have been reported (116). Patients with multiple bilateral lesions can be effectively treated with embolization with detachable balloons, as reported by Barth et al. (103).

Klippel–Trénaunay Syndrome One of the best-known vascular malformations, Klippel–Trénaunay syndrome (KTS) affects predominantly veins, capillaries, and the lymphatic system (76,77,81,82,117–123). It is a complex malformation

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

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FIGURE 83.21 (A) 19-year-old man with a large incompetent lateral embryonic vein extending from the ankle to the saphenofemoral junction. (B) Same patient is allowed to stand for 5 minutes, and the veins are marked with ink pen before vein stripping and avulsion of varicosities. (With permission from Noel AA, Gloviczki P, et al. Surgical treatment of venous malformations in Klippel–Trénaunay syndrome. J Vasc Surg 2000;32:840–847.)

A

B

that may affect the lower or upper extremities or, less commonly, may involve the trunk, head, or neck. The three main components of KTS are varicosities and venous malformations, capillary malformations (port-wine stains), and hypertrophy of the soft tissue and bone (Figs. 83.21A and B and 83.22). Lymphatic abnormality is frequent in this mixed type of VM, affecting veins, capillaries, and lymphatics. Frequently, venous drainage is abnormal because of persistent embryonic veins, agenesis, hypoplasia, valvular incompetence, or aneurysms of deep veins (Fig 83.23). KTS is caused by developmental mesodermal abnormality, affecting blood vessels, bone, and soft tissue. Clinically significant arteriovenous shunting is not detected. The mesodermal abnormality may be regulated by angiogenesis and vasculogenesis factors such as vascular endothelial growth factor (VEGF). The effect of hemodynamic factors on limb hypertrophy is not confirmed and it is very likely less significant than previously thought. Our opinion remains that soft tissue and bony hypertrophy are not direct consequences of venous stasis in these patients. Patients need treatment of symptomatic varicosity or advanced chronic venous insufficiency, caused by valvular incompetence and, less frequently, by venous occlusion. Most cases are sporadic and very few cases within the same family have been reported (126). In a report of 14 patients from Spain, paternal and maternal age and the number of pregnancies were related to the prevalence of KTS, which suggested a variably expressed autosomal dominant inheritance (127). In most cases, the limb hypertrophy, port-wine stains and even varicosity is present at birth or in the first few years of life. In 252 patients with KTS reported from our

FIGURE 83.22 Port-wine stain (capillary malformation) on affected extremity of patient with KTS. Note large lateral embryonic vein of the thigh (arrow). (With permission from Noel AA, Gloviczki P, et al. Surgical treatment of venous malformations in Klippel–Trénaunay syndrome. J Vasc Surg 2000;32:840–847.)

institution, 98% had capillary malformations, 72% had varicosities or VMs, and 67% had limb hypertrophy (123). Of these 252 patients, 63% had all three features of KTS. Digital anomalies, such as syndactyly, macro-

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Part XI Arteriovenous Malformation

FIGURE 83.23 Ascending phlebogram in a 19-year-old man confirms large lateral embryonic vein with multiple varicosities (arrow) and a phlebectasia (double arrows) of the popliteal vein with band-like narrowing. (With permission from Noel AA, Gloviczki P, et al. Surgical treatment of venous malformations in Klippel–Trénaunay syndrome. J Vasc Surg 2000;32:840–847.)

dactyly, polydactyly, and hip dysplasia have been reported in up to 29% of patients with KTS (123). Clinical symptoms are related to the extent and location of the hypertrophy and VMs, which may vary from mild varicosities to massively enlarged limbs or truncal involvement. Treatment is usually conservative and includes elastic compression, frequent leg elevation, laser treatment of port-wine stains, and physical therapy for treatment of lymphedema, with manual massage or intermittent compression pumps. In a recent publication, we reported results of surgical treatment in 20 patients with KTS. Surgery is rarely needed, since this group represented 6.9% of 290 patients with KTS we have followed during the past decade. All 20 patients (100%) had varicose veins or VMs. Pain was the most common complaint, which was present in 16 patients (80%), followed by swelling in 15 (75%) and bleeding in 8 (40%). Stripping of large lateral veins, avulsion,

and excision of varicosities or VMs were performed on all limbs. Three patients required staged resections. The release of entrapped popliteal veins, popliteal–saphenous bypass graft, excision of persistent sciatic vein, and open and endoscopic perforator vein ligations were additional procedures performed. Two patients (12%) had hematomas that required evacuation. No patients had caval filter placement; none had postoperative deep venous thrombosis or pulmonary embolus. The mean follow-up was 64 months and all patients reported initial improvement. Varicosities recurred in 10 patients (50%), an ulcer did not heal in one, and a new ulcer developed in another. Three patients underwent reoperation for recurrent varicosities. Lee et al. have advocated absolute alcohol sclerotherapy for patients with venous malformations, some of these belonging to KTS (75). Excellent results were reported recently in a group of 30 patients with predominantly venous malformations, who underwent 98 sessions of multistage therapy with direct puncture technique. After a mean follow-up of 10 months, improvement was reported in 96% of the patients. Major to minor acute complications developed during the procedure in 27% of the patients, or 16% of the sessions, and included ischemic bullae, tissue fibrosis, deep venous thrombosis, pulmonary embolism, peripheral nerve palsy, and temporary pulmonary hypertension. All complications were successfully managed with full recovery except one case of permanent peroneal nerve palsy. No recurrence was detected. The introduction and initial success of polydochanol foam sclerotherapy for varicose veins (126–128) holds promise for effective treatment of many of the venous and low-shunt arteriovenous malformations.

Conclusion Because of local effects and systemic hemodynamic consequences, the majority of traumatic arteriovenous fistulas require treatment. Surgical repair of acquired fistulas is rewarding and usually curative. Endovascular techniques have been used increasingly and with good results. A significant number of vascular malformations have arteriovenous shunting, and transcatheter embolization of these with or without surgical excision has improved results, especially in the region of the head and neck, pelvis, and certain forms of visceral malformations. The laser has gained increasing popularity in treating cutaneous vascular lesions. Large high-shunt extremity malformations, in spite of the combined radiologic–surgical management, are difficult to control, and in some (fortunately rare) cases amputation is the only alternative. The management of most patients with KTS continues to be nonoperative, but those patients with patent deep veins can be considered for excision of symptomatic varicose veins and VMs. Although the recurrence rate is high, clinical improvement is significant, and reoperations can be performed if

Chapter 83 Arteriovenous Fistulas and Vascular Malformations

needed. Patients with symptomatic venous malformations can be considered for sclerotherapy.

References 1. Virchow R. Pathologie des tumeurs: cours professé à l’Université de Berlin, vol 4. Paris: Germer-Bailliére, 1876:169. 2. Hunter W. The history of an aneurysm of the aorta, with some remarks on aneurysms in general. Med Observations Inquiries 1757;1:323. 3. Hunter W. Further observations upon a particular species of aneurysm. Med Observations Inquiries 1764:2:390. 4. Breichet G. Mémoire sur les anéurysmes. Mem Acad Med (Paris) 1833;3:101. 5. Norris G. Varicose aneurism at the bend of the arm: ligature of the artery above and below the sac; secondary hemorrhages with a return of the aneurismal thrill on the tenth day; cure. Am J Med Sci 1843;5:28. 6. Nicoladoni C. Phlebarteriectasie der rechten oberen Extremität. Arch Kim Chir 1875;18:252. 7. Branham HH. Aneurismal varix of the femoral artery and vein following a gunshot wound. Int J Surg 1890; 3:250. 8. Holman E. Arteriovenous aneurysm: abnormal communications between the arterial and venous circulations. New York: Macmillan, 1937. 9. Shumacker HB Jr, Carter KL. Arteriovenous fistulas and arterial aneurysms in military personnel. Surgery 1946;20:9. 10. Hughes CW, Jahnke EJ Jr. The surgery of traumatic arteriovenous fistulas and aneurysms: a five-year follow-up study of 215 lesions. Ann Surg 1958;148:790. 11. Rich NM, Hobson RW II, Collins GJ Jr. Traumatic arteriovenous fistulas and false aneurysms: a review of 558 lesions. Surgery 1975;78:817. 12. Reid MR. Studies on abnormal arteriovenous communications, acquired and congenital: I. Report of a series of cases. Arch Surg 1925;10:601. 13. de Takats G. Vascular anomalies of the extremities: report of five cases. Surg Gynecol Obstet 1932;55: 227. 14. Coursley G, Ivins JC, Barker NW. Congenital arteriovenous fistulas in the extremities: an analysis of sixty-nine cases. Angiology 1956;7:201. 15. Malan E, Puglionisi A. Congenital angiodysplasias of the extremities. (Note I: Generalities and classification; venous dysplasias.) (Note II: Arterial. arterial and venous, and haemolymphatic dysplasias.) J Cardiovasc Surg 1964;5:87; 1965;6:255. 16. Szilagyi DE, Elliott JP, et al. Peripheral congenital arteriovenous fistulas. Surgery 1965;57:61. 17. Szilagyi DE, Smith RF, et al. Congenital arteriovenous anomalies of the limbs. Arch Surg 1976;111:423. 18. Natali J, Merland JJ. Superselective arteriography and therapeutic embolisation for vascular malformations (angiodysplasias). J Cardiovasc Surg (Torino) 1976;17:465. 19. Forbes G, Earnest F IV et al. Therapeutic emboluation angiography for extra-axial lesions in the head. Mayo Clin Proc 1986;61:427.

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20. Belov DA. Classification of congenital vascular defects. Int Angiol 1990;9(3):141–146. 21. Patman RD, Poulos E, Shires GT. The management of civilian arterial injuries. Surg Gynecol Obstet 1964;118:725. 22. Kollmeyer KR, Runt JL, et al. Acute and chronic traumatic arteriovenous fistulae in civilians: epidemiology and treatment. Arch Surg 1981;116:697. 23. Lamar R, Berg R, Rama K. Femoral arteriovenous fistula as a complication of percutaneous transluminal coronary angioplasty: a report of five cases. Am Surg 1990;56:702–706. 24. Oweida SW, Roubin GS, et al. Postcatheterization vascular complications associated with percutaneous transluminal coronary angioplasty. J Vasc Surg 1990;12:310–315. 25. McCann RL, Schwartz LB, Pieper KS. Vascular complications of cardiac catheterization. J Vasc Surg 1991; 14:375–381. 26. Kim D, Orron DE, et al. Role of superficial femoral artery puncture in the development of pseudoaneurysm and arteriovenous fistula complicating percutaneous transfemoral cardiac catheterization. Cathet Cardiovasc Diagn 1991;25:91–97. 27. Rivers SP Lee ES, et al. Successful conservative management of iatrogenic femoral arterial trauma. Ann Vasc Surg 1992;6:45–49. 28. Feld R, Patton GM, et al. Treatment of iatrogenic femoral artery injuries with ultrasound-guided compression. J Vasc Surg 1992;16:832–840. 29. Kent KC, McArdle CR, et al. A prospective study of the clinical outcome of femoral pseudoaneurysms and arteriovenous fistulas induced by arterial puncture. J Vasc Surg 1993;17:125–131. 30. Linton RR, White PD. Arteriovenous fistula between the right common iliac artery and the inferior vena cava: report of a case of its occurrence following an operation for a ruptured intervertebral disk with cure by operation. Arch Surg 1945;50:6. 31. Quigley TM, Stoney RJ. Arteriovenous fistula following lumbar laminectomy: the anatomy defined. J Vasc Surg 1985;2:828. 32. Christensen C, Bank A. Arteriovenous fistula complicating lumbar disc surgery. Case report. Eur J Surg 1991;157:145–146. 33. Sande E, Myhre HO, et al. Vascular complications of lumbar disc surgery. Case report. Eur J Surg 1991;157:141–143. 34. Machado-Atias I, Fornes O, et al. Iliac arteriovenous fistula due to spinal disk surgery causes severe hemodynamic repercussion with pulmonary hypertension. Texas Heart Inst J 1993;20:60–65 (discussion 65). 35. Hollingsworth EW. Arteriovenous fistula of the renal vessels. Am J Med Sci 1934;188:399. 36. Dzsinich C, Szabó, et al. Arteriovenous fistula after partial nephrectomy: successful surgical repair: report of a case. Thorac Cardiovasc Surg 1984;32:325. 37. Mono RP, Dunn EJ, Wright CB. Renal arteriovenous fistulas: a review of etiology, diagnosis, and management. Surgery 1986;99:114. 38. Lord RSA, Ehrenfeld WK, Wylie EJ. Arterial injury from the Fogarty catheter. Med J Aust 1968;2:70. 39. Shifrin EG, Anner H, et al. Arterio-venous fistula in the

1012

40.

41.

42. 43. 44.

45.

46.

47.

48.

49.

50. 51. 52.

53.

54.

55.

56.

57.

58.

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lower limb in consequence of Fogarty balloon catheter embolectomy: case report and review of the literature. J Cardiovasc Surg (Torino) 1985;26:310. Schweitzer DL, Aguam AS, Wilder JR. Complications encountered during arterial embolectomy with the Fogarty balloon catheter: report of a case and review of the literature. Vasc Surg 1976;10:144. McAuley CE, Peitzman AB, et al. The syndrome of spontaneous iliac arteriovenous fistula: a distinct clinical and pathophysiologic entity. Surgery 1986;99:373. Davis PM, Gloviczki P, et al. Aorto-caval and ilio-iliac arteriovenous fistulae. Am J Surg 1998;176;115–118. Holman E. Abnormal arteriovenous communications. Springfield, IL: Charles C Thomas, 1968. Davis JO, Urquhart J, et al. Hypersecretion of aldosterone in dogs with a chronic aortid–caval fistula and high output heart failure. Circ Res 1964;14:471. Epstein FR, Ferguson TB. The effect of formation of an arteriovenous fistula upon blood volume. J Clin Invest 1955;34:434. Callander CL. Study of arterio-venous fistula with an analysis of 447 cases. Johns Hopkins Hosp Rep 1920;19:259. Sirinek KR, Gaskill HV III, et al. Exclusion angiography for patients with possible vascular injuries of the extremities: a better use of trauma center resources. Surgery 1983;94:598. Vollmar J, Krumhaar D. Surgical experience with 200 traumatic arteriovenous fistulae. In: Hiertonn T; Rybeck B, eds. Symposium on traumatic arterial lesions, Uppsala. Stockholm: Försvarets forskningsanstalt, 1968. Shumacker RB Jr, Wayson EF. Spontaneous cure of aneurysms and arteriovenous fistulas, with some notes on intrasaccular thrombosis. Am J Surg 1950;79:532. Linder F. Acquired arterio-venous fistulas: report of 223 operated cases. Ann Chir Gynaecol 1985;74:1. Harris AE, McMenamin PG. Carotid artery-cavernous sinus fistula. Arch Otolaryngol 1984; 110:618. Janes JM, Jennings WK Jr. Effect of induced arteriovenous fistula on leg length: 10-year observations. Proc Staff Meeting Mayo Clin 1961;36:1. Sumner DS. Diagnostic evaluation of arteriovenous fistulas. In: Rutherford RB, ed. Vascular surgery, 2nd ed. Philadelphia: WB Saunders, 1984. Rutherford RB. Noninvasive testing in the diagnosis and assessment of arteriovenous fistula. In: Bernstein EF, ed. Noninvasive diagnostic techniques in vascular disease, 3rd ed. St Louis: CV Mosby, 1985:666–679. White RA, Donayre CE, et al. Preliminary clinical outcome and imaging criterion for endovascular prosthesis development in high-risk patients who have aortoiliac and traumatic arterial lesions. J Vasc Surg 1996;24:556–571. Gloviczki P, Pairolero PC, et al. Reconstruction of large veins for nonmalignant venous occlusive disease. J Vasc Surg 1992;16:750–761. Mann ML, Veith FJ, et al. Percutaneous transfemoral insertion of a stented graft to repair a traumatic femoral arteriovenous fistula. J Vasc Surg 1993;18:299–302. Marin ML, Veith FJ, et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg 1994;20:466–473.

59. Debrun G, Lacour P, et al. Treatment of 54 traumatic carotid–cavernous fistulas. J Neurosurg 1981;55:678. 60. Herbreteau D, Aymard A, et al. Endovascular treatment of arteriovenous fistulas arising from branches of the subclavian artery. J Vasc Interv Radiol 1993:4:237–240. 61. Levey DS, Teitelbaum GP, et al. Safety and efficacy of transcatheter embolization of axillary and shoulder arterial injuries. J Vasc Interv Radiol 1991;2:99–104. 62. Fellmeth BD, Roberts AC, et al. Postangiographic femoral artery injuries: nonsurgical repair with ultrasound guided compression. Radiology 1991:178:671–675. 63. Oweida SW, Roubin GS, et al. Postcatheterization vascular complications associated with percutaneous transluminal coronary angioplasty. J Vasc Surg 1990;12:310–315. 64. Lin PH, Dodson TF, et al. Surgical intervention for complications caused by femoral artery catheterization in pediatric patients. J Vasc Surg 2001;34:1071–1078. 65. Robinson DL, Teitelbaum GP, et al. Transcatheter embolization of an aortocaval fistula caused by residual renal artery stump from previous nephrectomy: a case report. J Vasc Surg 1993;17:794–797. 66. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982;69:412. 67. Malan E, Sala A, Tardito E. Arteriovenous fistulas. In: Haimovici H, ed. Vascular surgery: principles and techniques, 2nd ed. Norwalk, CT: Appleton-CenturyCrofts, 1984:777–794. 68. Rohrich RJ, Spicer TE. Hemangiomas and vascular malformations/lymphedema. Selected Readings Plast Surg 1986;4:1. 69. Vollmar JF, Stalker CG. The surgical treatment of congenital arterio-venous fistulas in the extremities. J Cardiovasc Surg (Torino) 1976;17:340. 70. Merland JJ, Riche MC, et al. Classification actuelle des malformations vasculaires. Ann Chir Plast 1980;25:105. 71. Forbes G, May GR, Jackson IT. Vascular anomalies in children. In: Jackson IT, Mustarde J, eds. Plastic surgery in infancy and childhood. New York: Churchill Livingstone, 1988:691–710. 72. Woollard RH. The development of the principal arterial stems in the forelimb of the pig. In: Carnegie Institution of Washington: Contributions to embryology, vol 14, No.70. Publication No. 277. Washington, DC: Carnegie Institution of Washington, 1992:139–154. 73. Mulliken JB, Zetter BR, Folkman J. In vitro characteristics of endothelium from hemangiomas and vascular malformations. Surgery 1982;92:348. 74. Glowacki J, Mulliken JB. Mast cells in hemangiomas and vascular malformations. Pediatrics 1982;70:48. 75. Lee BB, Kim I, et al. New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation. J Vasc Surg 2002;33:764–772. 76. Eifert S, Villavicencio JL, et al. Prevalence of deep venous anomalies in congenital vascular malformations of venous predominance. J Vasc Surg 2000;31:462–471. 77. Noel AA, Gloviczki P, et al. Surgical treatment of venous malformations in Klippel–Trénaunay syndrome. J Vasc Surg 2000;32:840–847.

Chapter 83 Arteriovenous Fistulas and Vascular Malformations 78. Schwartz RS, Osmundson PJ, Rollier LH. Treatment and prognosis in congenital arteriovenous malformation of the extremity. Phlebology 1986;1:171. 79. Weber FP. Angioma-formation in connection with hypertrophy of limbs and hemi-hypertrophy. Br J Dermatol 1907;19:231. 80. Weber FP. Haemangiectatic hypertrophy of limbs: congenital phlebarteriectasis and so-called congenital varicose veins. Br J Child Dis 1918;15:13. 81. Gloviczki P, Hollier LR, et al. Surgical implications of Klippel–Trénaunay syndrome. Ann Surg 1983;197:353. 82. Gloviczki P, Stanson AW, et al. Klippel–Trénaunay syndrome: the risks and benefits of vascular interventions. Surgery 1991;110:469–479. 83. Servelle M. Stase veineuse et croissance osseuse. Bull Acad Natl Med 1948;132:471. 84. Hutchison WJ, Burdeaux BD Jr. The influence of stasis on bone growth. Surg Gynecol Obstet 1954;99:413. 85. Boyd JB, Mulliken JB, et al. Skeletal changes associated with vascular malformations. Plast Reconstr Surg 1984;74:789. 86. Decker DG, Fish CR, Juergens JL. Arteriovenous fistulas of the female pelvis: a diagnostic problem. Obstet Gynecol 1968;31:799. 87. Pritchard DA, Maloney JD, et al. Surgical treatment of congenital pelvic arteriovenous malformation. Mayo Clin Proc 1978;53:607. 88. Haimovici H, Sprayregen S. Congenital microarteriovenous shunts: angiographic and Doppler ultrasonographic identification. Arch Surg 1986;121:1065. 89. Pritchard DA, Maloney JD, et al. Peripheral arteriovenous fistula: detection by contrast echocardiography. Mayo Clin Proc 1977;52:186. 90. Horton BT, Ghormley RK. Congenital arteriovenous fistulae of the extremities visualized by arteriography. Surg Gynecol Obstet 1935;60:978. 91. Amparo EG, Higgins CB, Hricak H. Primary diagnosis of abdominal arteriovenous fistula by MR imaging. J Comput Assist Tomogr 1984;8:1140. 92. Berquist TH. Bone and soft tissue tumors. In: Berquist TH, ed. Magnetic resonance of the musculoskeletal system. New York: Raven Press, 1987:85–108. 93. Pearce WR, Rutherford RB, et al. Nuclear magnetic resonance imaging: its diagnostic value in patients with congenital vascular malformations of the limbs. J Vasc Surg 1988;8:764–770. 94. Noe JM, Barsky SH, et al. Port wine stains and the response to argon laser therapy: successful treatment and the predictive role of color, age, and biopsy. Plast Reconstr Surg 1980;65:130. 95. Achauer BM, Vander-Kam VM. Vascular lesions. Clin Plast Surg 1993;20:43–51. 96. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of port-wine stains (capillary malformation) with the flashlamp-pumped pulsed dye laser. J Pediatr 1993; 122:71–77. 97. Pickering JW, Walker EP, et al. Copper vapour laser treatment of port-wine stains and other vascular malformations. Br J Plast Surg 1990;43:273–282. 98. Kerber CW. Catheter therapy: fluoroscopic monitoring of deliberate embolic occlusion. Radiology 1977;125:538. 99. Kaufman SL, Kumar AAJ, et al. Transcatheter emboliza-

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tion in the management of congenital arteriovenous malformations. Radiology 1980;137:21. 100. Widlus DM, Murray RR, et al. Congenital arteriovenous malformations: tailored embolotherapy. Radiology 1988;169:511–516. 101. Van Poppel H, Claes H, et al. Intraarterial embolization in combination with surgery in the management of congenital pelvic arteriovenous malformation. Urol Radiol 1988;10:89–91. 102. Gomes AS, Mali WI, Oppenheim WL. Embolization therapy in the management of congenital arteriovenous malformations. Radiology 1982;144:41. 103. Barth KR, White RI Jr, et al. Embolotherapy of pulmonary arteriovenous malformations with detachable balloons. Radiology 1982;142:599. 104. Jacobowitz GR, Rosen RJ, et al. Transcatheter embolization of complex pelvic vascular malformations: results and long-term follow-up. J Vasc Surg 2001;33:51–55. 105. Gomes MMR, Bernatz PE. Arteriovenous fistulas: a review and ten-year experience at the Mayo Clinic. Mayo Clin Proc 1970;45:81. 106. Szilagyi DE. Vascular malformations (with special emphasis on peripheral arteriovenous lesions). In: Moore W, ed. Vascular surgery: a comprehensive review, 2nd edn. New York: Grune & Stratton, 1986:773–790. 107. Fowl RJ, Kempczinski RF, et al. Management of a complex, posttraumatic, pelvic arteriovenous fistula with the use of cardiopulmonary bypass: case report and review of the literature. J Vasc Surg 1987;6:257–261. 108. Cormier JM, Laurian C, et al. Traitement chirurgical des fistules artério-veineuses congénitales des membres sous contrôle ultrasonographique. Chirurgie 1981;107:424. 109. Trout RH III, McAllister RA Jr, et al. Vascular malformations. Surgery 1985;97:36. 110. Moore JD, Thompson NW, et al. Arteriovenous malformations of the gastrointestinal tract. Arch Surg 1976;111:381. 111. Rutgeerts P, Van Gompel F, et al. Long-term results of treatment of vascular malformations of the gastrointestinal tract by neodymium:YAG laser photocoagulation. Gut 1985;26:586. 112. Richardson JD, Max MH, et al. Bleeding vascular malformations of the intestine. Surgery 1978;84:430. 113. Klimberg I, Wilson J, et al. Hemorrhage from congenital renal arteriovenous malformation in pregnancy. Urology 1984;23:381. 114. Burckhardt D, Stalder GA, et al. Hyperdynamic circulatory state due to Osler-Weber-Rendu disease with intrahepatic arteriovenous fistulas. Am Heart J 1973;85:797. 115. Dines DE, Arms RA, et al. Pulmonary arteriovenous fistulas. Mayo Clin Proc 1974;49:460. 116. Brown SE, Wright PW, et al. Staged bilateral thoracotomies for multiple pulmonary arteriovenous malformations complicating hereditary hemorrhagic telangiectasia. J Thorac Cardiovasc Surg 1982;83:285. 117. Klippel M, Trénaunay P. Du naevus variquex osteohypertrophique. Archives of General Medicine (Paris) 1900;3:641–72. 118. Servelle M. Klippel and Trénaunay’s syndrome: 768 operated cases. Ann Surg 1985;201:365–373. 119. Baskerville PA, Ackroyd JS, et al. The Klippel–Trénaunay syndrome: clinical, radiological and haemodynamic features and management. Br J Surg 1985;72:232–236.

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120. Lindenauer SM. The Klippel–Trénaunay syndrome: varicosity, hypertrophy and hemangioma with no arteriovenous fistula. Ann Surg 1965;162:303–313. 121. Villavicencio JL. Congenital vascular malformations of venous predominance: Klippel–Trénaunay syndrome. In: Raju S, Villavicencio JL, eds. Surgical management of venous disease. 1st edn. Baltimore: Williams & Wilkins, 1997;445–461. 122. Baskerville PA, Ackroyd JS, Browse NL. The etiology of the Klippel–Trénaunay syndrome. Ann Surg 1985;202:624–627. 123. Jacob AG, Driscoll DJ, et al. Klippel–Trénaunay syndrome: spectrum and management. Mayo Clin Proc 1998;73:28–36. 124. Eifet S, Villavicencio JL, et al. Prevalence of deep venous anomalies in congenital vascular malformations of venous predominance. J Vasc Surg 2000;31:462–471.

125. Lorda-Sanchex I, Prieto L, et al. Increased parental age and number of pregnancies in Klippel–Trénaunay-Weber syndrome. Ann Hum Genet 1998;62:235–239. 126. Frullini A, Cavezzi A. Sclerosing foam in the treatment of varicose veins and telangiectases: history and analysis of safety and complications. Dermatol Surg 2002;28:11–15. 127. Tessari L, Cavezzi A, Frullini A. Preliminary experience with a new sclerosing foam in the treatment of varicose veins. Dermatol Surg 2001;27:58–60. 128. Cabrera Garrido JR, Cabrera Garcia-Olmedo JR, Garcia-Olmedo Dominiguez MA. Extending the limits of sclerotherapy: new sclerosing agents. (in French.) Phlebologie 1997;50:181–188.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 84 Vascular Access for Dialysis Harry Schanzer and Andres Schanzer

The introduction of hemodialysis as a treatment for renal failure represents one of the significant medical developments of the twentieth century. The use of this technique has changed the fate of tens of thousands of patients. Initially, and because of limitations in the techniques of access to the circulation, it was only used in patients suffering from acute renal failure. With the development of new modalities of angioaccess that allowed for repetitive and long-term dialysis, treatment was extended to patients with end-stage renal disease. The refinements of hemodialysis, together with legislation passed in 1972 that made it available to practically all residents of the United States, produced an exponential growth in the population being maintained with this therapeutic modality. In 1970, there were approximately 2500 patients maintained on hemodialysis in the United States. By 1996, over 170,000 patients were being treated with hemodialysis (1). This large population requires, as an essential part of its treatment, specialized surgical care. In fact, access surgery has become one of the most common procedures performed by vascular surgeons. Its apparent simplicity can be misleading. Often, these patients can pose problems that are very challenging and difficult to solve. Excellent technique and very sound judgment are essential for a successful long-term dialysis treatment. After all, the angioaccess is literally the lifeline of these patients.

Historical Background The origins of hemodialysis can be traced to the days of the German occupation of the Netherlands, during World War II. There, in 1943, Dr Willem J. Kolff developed the first artificial kidney (2). This machine consisted of a large

container filled with the dialysis fluid, and a wooden rotating drum, with cellophane tubing going around it. The patient’s blood circulated through the cellophane tubing, and the drum was made to rotate, interfacing the blood with the dialyzing fluid. In order to connect the patient to this machine, the cannulation of both an artery and a vein was necessary. The number of dialysis treatments to be done, therefore, was limited to the number of sites that could have these vessels sacrificed. Because of these limitations, dialysis was used only in cases of acute renal failure, in which a few treatments would buy time for the kidney to recover. In the next 17 years, despite the development of more sophisticated machines, the use of this technique continued to be limited and its results were rather disappointing. The development of the external shunt by Quinton et al. in 1960 broke this impasse (3). This modality of angioaccess allowed for repetitive dialysis and opened the field of chronic dialysis. Initially, these external shunts were made of Teflon. Because of the rigid nature of this material, trauma of the cannulated vessels with joint movement reduced the life expectancy of these shunts. The replacement of Teflon by silicone in the manufacturing of the tubes, leaving only the tips to be introduced in the vessel made out of Teflon, greatly improved their function. Still, even with excellent nursing care, it was difficult to achieve patencies beyond 3 to 6 months. Thrombosis and infection were quite common. These limitations further stimulated the search for new modalities. In 1966, Dr Appel, a surgeon working at the Bronx VA Hospital, thought of using a surgically produced arteriovenous (AV) fistula as a source of access to dialysis. His nephrology colleagues, Drs Brescia and Cimino, received this idea enthusiastically. Human trials met with immedi-

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ate success (4). This fistula allowed for long-term repetitive dialysis with low morbidity. Clearly, it became the procedure of choice for chronic dialysis, and this has not changed till this day. In order to construct an AV fistula, a suitable artery and vein have to be in proximity. Unfortunately, this anatomic configuration was not always present in these sick patients. The most common problem was absence of a good vein. A natural solution to this problem was to interpose an autologous or synthetic tube graft between an artery and a vein. This was the origin of the graft AV fistula. Many different materials were tried as tube grafts. This access provided good function for chronic dialysis, but its complication rate was significantly higher than that of the AV fistulas. Both AV fistula and graft AV fistula had, as a limitation, the need for a period of “maturation” or “incorporation” of the graft of approximately 1 to 4 weeks. During this time, the access could not be safely used. If the patient required immediate dialysis, a different modality, satisfactory for acute dialysis, had to be obtained. In the early days, the external Silastic shunt was extensively used for that purpose. If the patient was extremely uremic, had hyperkalemia, severe acidosis, or fluid overload and was in need of immediate dialysis, an external shunt was first inserted and at a subsequent occasion a definite chronic access (AV fistula or graft AV fistula) was placed. The limitations inherent in the use of the external shunt (frequent infections, bleeding, short patency, and sacrifice of arteries) led Shaldon in the early 1960s to the development of techniques of immediate dialysis through percutaneous cannulation of large veins using the Seldinger technique (5). He used a single-lumen catheter through the femoral vein. This catheter was removed after each dialysis. In later years, this technique was refined: early rigid Teflon catheters were changed for softer materials less traumatic to the vessels such as silicone. A single lumen was modified to double lumen, affording more efficient dialysis (6). The advances of this technique are such that it has become the primary angioaccess procedure for immediate dialysis. Several catheters are available on the market. The Shiley catheter is a Silastic double-lumen catheter that is implanted percutaneously through the subclavian or internal jugular vein. This catheter can be left in place for about 3 weeks (it can be implanted through the femoral vein, but the high incidence of deep-vein thrombosis makes this position unwarranted). The Permcath is a similar double-lumen catheter with a Dacron cuff that is preferentially placed percutaneously through the internal jugular vein. The Dacron cuff elicits fibrosis around it, providing a barrier to the propagation of infection from the skin to the tunnel. This allows long-term placement of this indwelling catheter. It can remain in position for 1 month to, occasionally, several years. Femoral catheters can be placed intermittently at each dialysis. These tech-

TABLE 84.1 Indications for prolonged venous access Parenteral nutrition and drug therapy Hyperemesis gravidarum Inflammatory bowel disease Gastroparesis Pancreatitis Cystic fibrosis Short bowel syndrome Heparin (heart valves, deep vein thrombosis) Antibiotics (bacterial endocarditis, osteomyelitis) Chemotherapeutic agents for malignancy Magnesium sulfate Lack of peripheral access Previous intravenous drug abuse Previous prolonged chemotherapy Hemodialysis

niques have relegated the external shunt to an historical role. Table 84.1 lists indications for prolonged venous access, including dialysis.

Prerequisites for a Dialysis Angioaccess The following are prerequisites for adequate dialysis angioaccess: 1.

2.

3. 4.

It has to be able to provide a minimum of 200 mL per minute of blood to flow through the dialysis machine and has to accept a similar volume for return. Lower flows make dialysis inefficient. It has to be easily cannulated. It is not sufficient to have a good thrill in an AV fistula. The vein has to be superficial, so that needle cannulation can be done safely and easily. In the case of acute access, it must allow immediate use after implantation. In the case of chronic access, it has to allow for repetitive cannulation (i.e., three times per week), and have long-term patency and low rate of complications.

Techniques for Angioaccess Angioaccess techniques can be classified into acute temporary and chronic procedures, depending on how soon after placement they can be used and on their longevity. Techniques for acute temporary access are the external shunt and the large-vein catheter. Table 84.2 lists the features of various types of central venous catheter. Chronic angioaccess is achieved by means of an autogenous AV fistula or a graft AV fistula.

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TABLE 84.2 Central venous catheter types Short-term

Long-term

Implantable

Location Duration Venous site

Transcutaneous < 2 weeks Peripheral Pedal Saphenous Femoral

Subcutaneous Months or years Same as central long-term Huber point needle required of access to reservoir

Material

Polyethylene, polyurethane, vinyl chloride, silicone No cuff Varies Difficult access Dislodgement of catheter Decreased patient mobility Open

Transcutaneous > 4 weeks Central Subclavian External Jugular Internal jugular Cephalic Facial Saphenous Femoral Silicone

Cuff Lumen Indication Risks or benefits Tip

Dacron Chronic illness

Single or double Chronic illness Increased patient mobility

Groshong valve

Acute Temporary Angioaccess External Shunt The external shunt first described by Quinton et al. in 1960 (4) is rarely used today. It is indicated only for the rare occasion where a hemofiltration procedure is required. The tubes used for this procedure are made of silicone, with the tips that enter the vessels made out of Teflon and available in different sizes (to fit a specific vessel size). The procedure is performed under local anesthesia. A site with an adequate artery that can be sacrificed and a good vein is identified. Usually, this will be the ankle (with anterior tibial or posterior tibial arteries and the saphenous vein) or the wrist (with radial artery and cephalic or antecubital vein). One tube is placed in the artery and another in the vein. For cannulation, both artery and vein are ligated distally, and the Teflon tip has to be introduced with care, avoiding damage and dissection of the intima. The tubes have different loops that allow for good stabilization in the subcutaneous plane. They are brought out through stab wounds and connected externally with a special Teflon tube (“connector”). Nonabsorbable ties are used to fix the catheter to the vessels, and anchoring stitches are placed at the exit site. Adhesive tape is placed at the connecting site to prevent accidental separation of both tubes (Fig. 84.1). At each dialysis, the arterial and venous tubes are separated and then connected to the arterial and venous line of the hemodialysis machine. At the end of the procedure, the tubes are reconnected, allowing blood to flow from artery to vein. For the safe, effective, and long-term function of this shunt, devoted nursing care is essential. The exit sites have to be kept clean, and antiseptic ointment must be applied after each use. The connection between arterial and

FIGURE 84.1 External shunt placed at the ankle level. The arterial tube has been connected to the anterior tibial artery and the venous tube to the saphenous vein. To prevent accidental separation of both tubes, an adhesive tape has been placed at the connection.

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venous tubes has to be taped at all times to avoid accidental separation with the potential for fatal bleeding. The silicone tubes have to be handled gently, especially when clamped, to avoid cracks. Complications common to these accesses are thrombosis, infection, bleeding, and skin erosion by the tubes. Thrombosis early after placement of the shunt is usually due to a technical surgical problem or inadequate vessels. Late thrombosis is usually due to intimal hyperplasia, most commonly at the venous site. Thrombectomy can be done by injection–aspiration of the tubes with heparinized saline solution, by passing small Fogarty catheters if the tubes are straight, or by infusion of fibrinolytic agents in the tubes. At times, when these maneuvers are not successful, placement of a tube in a new vein is necessary. Infection and skin erosion usually require withdrawal of the shunt. The process of shunt removal is simple and can be done in the office or at the bedside. As a first step, it is occluded by clamping it for 24 hours. This allows for a stable clot to obliterate the lumen of the end vessels. With this accomplished, using local anesthesia, gentle continued traction is exerted on each cannula, until the tie holding the tube to the vessel extrudes. This is divided and the remaining portion of the cannula comes out easily. Very rarely, arterial bleeding occurs or a small segment of cannula breaks and remains buried in the subcutaneous tissue. For bleeding, compression with elastic bandages for another 24 hours usually suffices. If bleeding is persistent, a cutdown of the vessel and direct ligation is required. For the foreign body, reopening of the wound and extraction is performed.

Large-vein Catheters The use of double-lumen catheters with the tip placed in a large vein allows for withdrawal of adequate amounts of blood to pass through the dialyzer and return of the treated blood with low rates of recirculation (less than 20%) (6). These catheters can be used for single treatments or in an indwelling fashion. Single puncture is used mainly in the femoral vein. A catheter is inserted using the Seldinger technique and is removed at the end of the procedure. This technique is relatively safe and allows for immediate dialysis for a few weeks. Its negative aspects are poor acceptability to patients, the increased labor required of nephrologists, and the occasional hematoma that can result, especially when the femoral artery is accidentally punctured. Two kinds of indwelling catheters, noncuffed catheters and tunneled cuffed catheters, are available on the market (Fig. 84.2). Both of them currently are manufactured from soft silicone and have a double lumen. The noncuffed catheters are placed using the Seldinger technique, preferentially in the internal jugular vein. Because of the high rate of central vein thrombosis, a subclavian vein approach should be used only when an internal jugular approach is not feasible. The tip of the catheter is positioned at the level of the caval–atrial junction or right

FIGURE 84.2 The percutaneous indwelling doublelumen venous catheter is placed using the Seldinger technique. The double-lumen indwelling catheter with Dacron cuff is placed percutaneously, through a peel-out sheath. The Dacron cuff is invaded by fibroblasts, sealing the tunnel and decreasing the Incidence of infection. This characteristic provides the tube with the potential for prolonged use.

atrium. These catheters can also be placed into the femoral vein. The high incidence of deep-vein thrombophlebitis and the danger of pulmonary emboli make this location undesirable. These catheters usually can be used for approximately 3 weeks. The main problems encountered are infection at the entrance site and thrombosis. Exchanging a nonworking catheter for a new one over a guidewire can prolong continuous use at a given site. The double-lumen indwelling catheter with a Dacron cuff has the advantage of significantly decreasing the incidence of tunnel infection. The cuff, placed in the subcutaneous tunnel, is invaded by fibroblasts, thereby sealing the tunnel from the exit wound. This property enables it to be used for 1 month to several years. Occasionally, patients with end-stage renal dialysis who cannot have chronic accesses constructed or who are hemodynamically unstable can survive for a long time with chronic dialysis through these tubes. Implantation is preferentially done percutaneously. Cutdown insertion can be done, but it often results in eventual thrombosis of the vein. This precludes future use of this site. In the percutaneous technique, the internal jugular vein is accessed with an 18-gauge needle, preferentially under ultrasound guidance. A guidewire is placed through the needle and once this is accomplished the needle is removed. The catheter is introduced through a stab wound in the prepectoral area, allowing the Dacron cuff to be positioned in the tunnel, 2 cm from the exit wound. A peel-out sheath-dilator is passed over the guidewire, and the catheter is introduced through the sheath. With

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catheter in place, the peel-out sheath is removed. The location of the tip in the superior vena cava or right atrium is confirmed fluoroscopically. An anchoring stitch is placed at the exit site to prevent extrusion of the Dacron cuff from the tunnel. Easy forceful aspiration of blood with a 20-mL syringe ensures good positioning of the tip. At the end of the procedure, in order to prevent thrombosis, 2 mL of saline containing 2500 units of heparin is injected into each lumen. In August 2000, the FDA approved a new device that combines the double-catheter technique and two subcutaneous ports (Lifesite‚, Vasca, Inc.). This access can be used immediately after implantation and has the potential for long-term use (7)). Ongoing studies with long-term follow-ups will determine its utility as an access. At the present moment, its main indication is in patients that have used all sites for chronic access and are being dialyzed through tunneled cuffed catheters.

TABLE 84.3 Complications of central venous catheters

Complications

catheters). Because of the rich collateral of the venous circulation in that area, obstruction of the vein commonly is asymptomatic. When present, symptoms can manifest as mild swelling of the affected extremity, evidence of subcutaneous collateral veins, florid superior vena cava syndrome, or signs and symptoms of pulmonary emboli. The true frequency of central venous thrombosis has been estimated by several studies to be approximately 30% (8,9). Thrombosis of a subclavian vein often will eliminate the affected extremity as a later source of chronic access for dialysis. Treatment of this condition consists of removal of the catheter and anticoagulation. In very symptomatic cases, local thrombolytic therapy can be effective and is indicated.

Occlusion This is a common complication. Usually it is due to a break in the technique of heparin priming at the conclusion of dialysis or to a prolonged period of catheter nonuse without heparin priming. This can be prevented by infusing heparin solution (2500 units in 2 mL per lumen) every other day if the catheter is not being used. If the thrombus is recent, it can often be dissolved with fibrinolytic therapy. If this is unsuccessful, the catheter can be exchanged for a new one using an over-guidewire technique and a peel-out sheath. Infection Of the various complications that can affect this angioaccess modality, infection by bacteria or fungi is the most serious one. In the vast majority, the infection results from invasion of the catheter track by skin organisms (Staphylococcus aureus and Staphylococcus epidermidis). Infection in the tunnel can eventually invade the lumen of the vein. Mild infection at the exit site occasionally can be treated successfully with local drainage and proper antibiotic coverage. If the infection extends to the tunnel, treatment usually will require removal of the catheter. The patient with sepsis who does not have any evident focus of infection and has an access catheter poses a difficult problem. If the sepsis persists after short-term antibiotic treatment, removal of the catheter becomes necessary. Very often, the infection has seeded the catheter and its removal results in cure.

Immediate

Delayed

Insertion failure Malposition Air embolism Catheter embolism Cardiac arrhythmia Pneumothorax Hemothorax Hydrothorax/chylothorax Tracheal/esophageal injury Femoral nerve injury Brachial plexus injury Phrenic nerve injury Vagus nerve injury Recurrent laryngeal nerve injury Stellate ganglion injury

Venous thrombosis Pulmonary embolism Superior vena caval syndrome Venous stenosis Arteriovenous fistula Arterial pseudoaneurysm Catheter thrombosis Catheter dislodgement/breakage Catheter-related infection Endocarditis Cardiac perforation Cardiac tamponade Suppurative thrombophlebitis Clavicular osteomyelitis Recurrent

Technique for Removal of Indwelling Dacron Cuff Catheters This procedure is simple and can be done in an office setting. In order to prevent an air embolism, the patient has to be placed in a supine horizontal position. The skin is cleaned with antimicrobial solution, the anchoring stitch is removed, and the exit site is infiltrated with local anesthesia. Using mild traction and blunt clamp dissection, the Dacron cuff is freed from the surrounding tissue. Once this is accomplished, the catheter is removed and the patient is asked to sit while applying compression on the neck site. After a few minutes, the bleeding stops. The exit wound is left open to close secondarily.

Chronic Angioaccess

Central Venous Thrombosis Catheter-induced thrombosis of the internal jugular, subclavian, innominate, or superior vena cava are much more frequent occurrences than generally appreciated (see Table 84.3 for complications of central venous

Autogenous Arteriovenous Fistula The peripheral subcutaneous AV fistula, first performed by Appel in 1965 and reported in 1966 by Brescia et al. (4), represented a giant step in the development of dialysis

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as a means of maintenance therapy for patients with endstage renal disease. Its durability and low complication rate overcame the many problems of the external shunt, and the AV fistula remains the preferred access for chronic hemodialysis. A relatively high rate of early failure (10% to 15%) owing to poor blood vessels, excessive dehydration, or outflow obstruction is outweighed by an excellent long-term patency rate of about 78% at 3 years (10,11). In a successful fistula, the vein receiving the increased blood flow is arterialized (its lumen is enlarged and the wall is thickened). This allows for repeated and multiple punctures and provides enough flow for adequate dialysis. Good planning is essential. Because it may take 3 to 8 weeks for the vein to become adequate for dialysis, the nephrologist should refer the patient for surgery as soon as it is certain that dialysis will be needed in the near future (creatinine clearance < 25 mL/min, serum creatinine > 4 mg/dL). This will obviate the need for extra procedures required for acute dialysis. Careful examination of the upper extremity is essential for the creation of a successful fistula. The quality of the arterial circulation should be well established. The quality of the pulse at the radial and ulnar arteries at the wrist has to be adequate. The Allen test should demonstrate good collateral circulation. Examination of the veins is of paramount importance. A tourniquet is applied above the elbow and veins are evaluated for size and continuity. A good cephalic vein at the wrist level occluded at midportion in the forearm is useless for AV fistula creation. Simple percussion usually is enough to determine continuous patency of the vein. Duplex scanning examination is extremely useful in planning a vascular access. This venous mapping should be done whenever availability of vein for AV fistula is in doubt. The advantage of autologous AV fistula over graft AV fistulas is such that this extra effort is well justified. The preferred site for AV fistula creation is from the radial artery to the cephalic vein at the wrist level. Some authors have reported excellent results anastomosing the same vessels in the anatomic snuff box (12). In patients with poor cephalic veins in the forearm and a good antecubital or cephalic vein at the elbow, with a cephalic vein superficially located in the upper arm, an AV fistula at the elbow level will provide satisfactory access (13). The use of the ulnar artery and the basilic vein can occasionally be successful (14). The problem with this location is that the arterialized vein runs in the medial posterior aspect of the forearm, and this requires the patient to have the arm uncomfortably positioned during dialysis. Very often, because of its inaccessibility to intravenous therapy, the basilic vein in the upper arm is of very good quality. This vein runs deep under the fascia, and in order to be useful for dialysis access, it needs to be superficialized and anastomosed end-to-side to the brachial artery. This basilic vein transposition AV fistula technique has given excellent results, with 1-year patency rates varying from 55% to 70% (15,16). The radiocephalic Brecia–Cimino AV fistula is done under local anesthesia. Loupe magnification is essential

FIGURE 84.3 Brescia–Cimino AV fistuIa. The preferred place for construction of this fistula is the wrist, between the radial artery and cephalic vein. If this site is not adequate, it can be done at the brachiocephalic or ulnar–basilic area. The anastomosis is performed in an end-to-side fashion with running suture. The posterior wall is done first, from inside the lumen.

for a good technical result. We prefer a small longitudinal incision in the skin between the artery and the vein. Good mobilization of both vessels for proper approximation without kinking is very important. We routinely perform a proximal end-of-vein to side-of-artery anastomosis. Because of the potential problems of distal venous hypertension, we have abandoned the originally described side-to-side technique. A 1-cm arteriotomy and venotomy are performed. Prior to performing the anastomosis, a small catheter is introduced through the vein; irrigation without resistance must be obtained. The anastomosis is performed with running No. 6–0 nonabsorbable suture. The posterior wall is done first, from inside the lumen (Fig. 84.3). Before completing the anterior anastomosis, coronary dilators (up to No. 3) are passed through both the vein and artery to release spasm. After removing the clamps, a thrill in the vein has to be felt. Presence of a pulse in the vein indicates inadequate outflow. Absence of thrill or pulse indicates poor inflow to the fistula. Both these findings are predictors of fistula failure, and the potential problem should be corrected before ending the procedure. The wound is closed in layers with interrupted absorbable sutures for the subcutaneous tissue and staples for the skin.

Complications of Autogenous Arteriovenous Fistula Fistula Thrombosis This is the most common AV fistula complication. Early thrombosis after surgical construction is usually due to

Chapter 84 Vascular Access for Dialysis

error in technique or judgment. Common problems include inadequate anastomosis, kinking of the vein just proximal to the anastomosis, or undetected occlusion of venous outflow. An inadequate arterial inflow due to proximal arterial disease can also produce early failure. Simple thrombectomy of the fistula, without correcting the primary problem that produced the failure, will inevitably result in rethrombosis. Late occlusion is due most commonly to progressive stenosis at the anastomosis site or in the vein as it leaves the anastomosis, secondary to intimal hyperplasia. Another common cause of venous stenosis is fibrosis of the vein in an area that has been traumatized by repeated needle punctures. This problem usually can be corrected by placing a new AV fistula just proximal to the area of stenosis. This can be done as long as the vein remains patent. Prevention of fistula thrombosis by correcting the underlying problem before the occlusion occurs gives a much better result in terms of prolongation of fistula function. The presence of a lesion that threatens its patency should be suspected if one of the following findings is present: decrease in the intensity and duration of the thrill, presence of pulsation that has replaced a well-established thrill, decrease in the blood flow obtainable in the dialysis machine during dialysis. Recirculation studies in native AV fistulas can be very sensitive in recognizing impending failure (recirculation of over 10% should raise great concern on fistula viability). Duplex ultrasound or fistula angiogram are the tests of choice for confirming that a threatening lesion is present. Because recognition and correction of impending fistula failure is so important for prolonging a fistula’s life, a committee of the National Kidney Foundation (NKF DOQI) recently recommended that dialysis units establish a surveillance system that includes weekly palpation of thrill of the fistula, monthly access flow measurement (ultrasound dilution, conductance dilution, thermal dilution or duplex flow measurement) and monthly measurements of recirculation. Fistulas showing abnormal values or trends should be evaluated with a fistulogram. Hand Edema This is a rare complication of AV fistula. Usually, it occurs late in the course of AV fistula and is due to distal venous hypertension secondary to obstruction of the outflow vein with persistence of flow in the distal vein. Often, venous tributaries that have dilated and become incompetent perfuse retrograde towards the hand, producing capillary hypertension. If this problem is not treated, development of a classic chronic venous stasis syndrome of the hand with edema, pigmentation, and ulceration can occur (Fig. 84.4). Treatment is simple and consists of repair of the fistula outflow or, if not possible, ligation of the fistula. A dramatic and immediate improvement occurs after performing this correction. Aneurysm Formation Aneurysmal dilatation of the vein is common in AV fistulas (Fig. 84.5). The high-pressure flow in a vein weakened

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FIGURE 84.4 Chronic venous stasis of the hand as a complication of venous hypertension in a patient with a Brescia–Cimino AV fistula. This was due to obstruction of the cephalic vein proximal to the fistula. Notice the characteristic swelling, pigmentation, and skin ulcerations.

FIGURE 84.5 Aneurysmal dilation of a Brescia–Cimino AV fistula. There is a small area of erosion in the covering skin.

by repeated punctures is responsible for this abnormality. This complication produces few symptoms or potential problems. The main problem is an unappealing cosmetic appearance. An aneurysmatic fistula can continue providing excellent hemodialysis access for many years. Correction by excision or exclusion should be attempted only if there if erosion of the covering skin or significant progressive growth. Infection Primary infection of the wound is extremely rare. If it occurs, it has to be treated aggressively because it poses the potential danger of anastomotic breakdown and massive bleeding. Superficial erythema and cellulitis can be treated with intravenous antibiotics. The presence of frank pus

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FIGURE 84.7 Secondary places for graft AV fistula. These locations are used when the primary places are unavailable. Shown here are the upper arm loop graft between the axillary artery and axillary vein (A), the cross-axillary artery to axillary vein bridge (B), the bridge between the axillary artery and jugular vein (C), the axillary artery to iliac vein graft (D), and the thigh loop between the superficial femoral artery and proximal saphenous vein (E). FIGURE 84.6 Primary places for graft AV fistulas. The most common locations are the upper arm, with a straight graft between the brachial artery and the axillary vein (B) and the forearm, with a loop between the brachial artery and the antecubital vein (A).

involving the anastomosis requires open drainage and ligation of the fistula (proximal and distal arterial ligation). Late infections are usually due to a break in the aseptic technique used during cannulation of the fistula. Because there is no foreign body, it usually responds well to drainage and antibiotic therapy. Hand Ischemia Symptoms and signs of arterial insufficiency in the distal extremity after AV fistula are rare (about 1%). Its clinical presentation, pathophysiology, and treatment will be discussed extensively in the section below on graft AV fistulas.

Graft Arteriovenous Fistula When access for chronic hemodialysis is required and an AV fistula cannot be constructed because of inadequate vein or poor distal arterial supply, a graft AV fistula is necessary. In this procedure, a vascular graft is placed between an artery and a vein. The cannulation is performed in the vascular graft. The most common locations used for this procedure are the forearm, with a loop graft between the brachial artery and the antecubital vein, and the upper arm, bridging the brachial artery to the axillary vein (Fig. 84.6). The

straight graft AV fistula from radial artery to antecubital vein, advocated by some as the first choice, has in our experience given very poor results and we do not use it. When the primary sites become unavailable (Fig. 84.7), a graft AV fistula can be done in reverse fashion in the upper arm (axillary artery to branchial or antecubital vein) or looped from the axillary artery to the axillary vein. A modality that has had good results in our hands is the bridge from axillary artery to the internal or external jugular vein, with the graft going around the shoulder. More desperate alternatives are the cross-sternal bridge AV fistula from axillary artery to axillary vein and from axillary artery to external iliac vein. Grafts located in the groin, looped between the superficial femoral artery and proximal saphenous vein, are very dangerous in our experience. Infection is a common complication in that area and, should it occur, it can place the limb and occasionally the life of the patient in serious jeopardy (17). For this reason, we use this location only as a last resort. Materials that have been used for the graft include autogenous saphenous vein (18,19), bovine heterograft (18,20), umbilical vein (21,22), Dacron (23,24), and expanded polytetrafluoroethylene (ePTFE) (25–27). After more than 20 years of usage, ePTFE has clearly become the preferred material. It is simple to use and easy to reexplore and repair, it tolerates infection relatively well, and its results are superior to those with the other materials (18).

Chapter 84 Vascular Access for Dialysis

Technique of the Graft Arteriovenous Fistula The procedure is performed under local anesthesia. A single intravenous dose of antibiotic (cephalosporin) is given at the initiation of surgery. The artery and vein to be used are exposed through separate incisions if distant or through a single incision if contiguous. The vein is ligated distally and a longitudinal venotomy of 1 to 2 cm is performed. A 6-mm ePTFE is anastomosed to this vein in end-to-side fashion using continuous No. 6–0 nonabsorbable vascular suture. With a tubular tunneler, a very superficial tunnel is made, connecting both incisions, and the graft is brought through it. A superficial location of the graft is essential for easy cannulation. After clamping the artery, a 1-cm arteriotomy is performed and the arterial end of the graft is anastomosed in an end-to-side fashion to the artery, also with continuous No. 6–0 nonabsorbable vascular suture. After removal of the clamps, pressure at the site of the anastomosis is applied for 5 minutes. This time is usually sufficient for the needle-hole bleeding to stop. A thrill at the site of the arterial anastomosis has to be felt. The thrill can be quite faint if the artery is very narrow. Its palpation, nevertheless, is a good prognostic sign. Wounds are closed in two layers, using absorbable interrupted stitches for the subcutaneous tissue and staples for the skin. It is very important to close the subcutaneous tissue, as it is not unusual to have small separations at the skin edges. The closed subcutaneous tissue prevents exposure of the foreign material. Optimal timing for the initial cannulation of these grafts is 2 weeks. This allows for operative pain and edema to subside and for the graft to be incorporated into the surrounding tissue. Early cannulation is possible if performed with extreme care and proficiency, but the potential for development of perigraft hematoma and subsequent graft failure is significantly increased.

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TABLE 84.4 Complications of arterial catheters Hematoma Hemorrhage Catheter occlusion Catheter dislocation Infection Embolism Ischemic injury Thrombosis Pseudoaneurysm Arteriovenous fistula

Complications of Graft Arteriovenous Fistulas Reported 1-year patency rates for graft AV fistulas vary from 65% to 75% (18,28). This significant attrition in the life of these accesses is due to the varying and frequent complications that they sustain. The treatment of these complications is challenging and requires sound judgment, creativity, and technical proficiency. The goal of good long-term patency can be achieved only by properly treating the expected complications. Table 84.4 lists the complications of arterial catheters. Thrombosis This is the most common complication of graft AV fistula. Systemic causes such as hypotension and hypercoagulability can produce thrombosis at any time in the life of the access. Early thrombosis usually is due to technical errors in the performance of the access (poor anastomosis, kink-

FIGURE 84.8 Fistula angiogram of a patient with high pressures in the dialysis returning line, recirculation values of 20% and blood flow of 450 mL/min. Observe marked stenosis of the vein starting at the point of the anastomosis.

ing of the graft, poor inflow or outflow). In a well-established access, over 90% of thromboses are due to stenosis at the venous anastomosis site and occasionally to stenosis of the vein several centimeters beyond the anastomosis, secondary to intimal hyperplasia (29–31) (Fig. 84.8). Stenosis of the arterial anastomosis or graft defects due to the trauma produced by multiple punctures are less common. Successful treatment must include correction of the original defect that caused the thrombosis. Simple

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Part XI Arteriovenous Malformation

at 3-month intervals. Reported results in comparative studies of surgical versus percutaneous thrombectomy show similar technical success and long-term patency rates (30,34–37). It is our opinion that, at this time, the choice depends on specific center preferences and available support. It has been conclusively demonstrated that prospective monitoring of AV grafts for hemodynamically significant stenosis, when combined with correction, improves patency and decreases the incidence of thrombosis. Furthermore, correction of the offending lesion before thrombosis occurs, either with surgery or with percutaneous angioplasty, produces higher rates of graft survival than corrections done in an already thrombosed graft (38–42). As with AV fistulas, regular palpation, access flow measurements, and assessment of recirculation play a role in preventing thrombosis. Quantification of dynamic and static venous pressures is an indirect measurement of flow that is useful in predicting a graft in danger of thrombosis. These parameters should be evaluated at frequent and repeated intervals. Both abnormally low absolute values or an abnormal trend indicating decreased flow mandate angiographic evaluation. FIGURE 84.9 Correction of the graft venous stenosis. This can be accomplished by interposing a new segment of graft between the original graft distal to the venous anastomosis and the vein proximal to the stenotic segment, by placing a patch at the stenotic area, or by performing balloon angioplasty.

thrombectomy is successful only if a correctable systemic defect is identified and rectified. Until recently, open surgical thrombectomy using Fogarty catheters was the only technique available. Our surgical approach consists of exposing the graft near the venous anastomosis. At that point, catheter thrombectomy is performed and the venous anastomosis is evaluated with operative angiography. The demonstration of stenosis by angiography makes correction of the defect imperative (Fig. 84.9). If there is enough proximal vein, a graft interposition is performed. Otherwise, patch angioplasty is carried out. If the problem is identified at the arterial anastomosis or in the graft itself, proper correction will prolong the life of the access. More recently, a variety of mechanical devices and pharmacologic thrombolysis have been developed that allow for thrombectomy of grafts to be performed percutaneously (31). When using percutaneous declotting techniques, venous stenosis can be corrected using balloon angioplasty (32,33) or surgery. When central venous stenosis is present (subclavian or innominate vein), balloon angioplasty is the procedure of choice. In these cases, if the balloon dilatation is not able to overcome the stenosis, or if the stenosis recurs in less than 3 months, endovascular stents are placed. The incidence of recurrence of central vein stenosis is very high, and in order to extend the life of these grafts, close follow-up is recommended with repeated fistulograms

Swelling Early postoperative swelling is a very common finding following creation of a graft AV fistula. It results from venous hypertension and as collaterals develop and outflow improves, it rapidly disappears. Elevating the arm and reassuring the patient are usually enough. Persistence of very severe swelling suggests obstruction of a major outflow vein (axillary-subclavian-innominate vein). A fistula angiogram will document this clinical impression. This condition can be treated by extending the graft to a vein beyond the obstruction (i.e., internal jugular vein in case of subclavian obstruction), by primary balloon angioplasty, by balloon angioplasty plus stenting, or by ligating the graft. Late swelling is usually due to central vein (axillary, subclavian, or innominate vein) stenosis or obstruction (Fig. 84.10). In this particular situation, the causative factor is intimal hyperplasia that results from either the turbulent flow draining the graft AV fistula or trauma to the vein wall induced by long-term indwelling catheters. The clinical presentation can vary from simple swelling to advanced changes of chronic venous stasis with pigmentation, indurated swelling, and ulcerations. Diagnosis is supported by the presence of venous collaterals around the shoulder and is documented by fistula angiography. Treatment again consists of extension of the graft to an unobstructed vein, balloon angioplasty alone or with stenting, or access ligation. Infection This is a serious and potentially lethal complication of access surgery. In graft AV fistula in particular, the presence of foreign material makes the complication even more difficult to treat. The infection can result from a breakdown in sterility during surgery or as a consequence of poor

Chapter 84 Vascular Access for Dialysis

1025

FIGURE 84.11 Perigraft seroma. Observe the mass in the distal part of this brachial artery to axillary vein graft AV fistula, close to the arterial anastomosis. FIGURE 84.10 Fistula angiogram of a patient with severe arm swelling developed 3 years after construction of a brachial artery to axillary vein graft AV fistula. There is marked stenosis in the proximal subclavian vein.

are required. Infected wounds are left open to close by secondary intention. Aneurysms

sterile technique during cannulation. Agents most commonly responsible are skin pathogens (S. aureus, S. epidermidis). The surgical wound infection can be superficial or deep. The former can be treated successfully with aggressive local treatment (debridement of all infected and necrotic tissue and systemic antibiotics). If the infection is deep, involves the graft, and occurs soon after surgery (i.e., the graft is not well incorporated yet), treatment requires opening of the wound, debridement, systemic antibiotics, and excision of the whole graft with ligation of the artery. In the upper extremity, because of rich collaterals, ligation of the artery is usually innocuous and does not require revascularization. Prevention of this complication with preoperative prophylactic antibiotics is very important. Needle puncture infection usually presents as an abscess in the area of cannulation. If the infection is localized, graft salvage can be attempted. This can be accomplished by first treating the local infection with drainage and systemic antibiotics. It is not unusual during the drainage to find bleeding through the graft needle hole. This procedure therefore should be done in an operating room setting and the bleeding controlled with a local stitch. Once the infection is controlled, usually after a few days, excision of the involved segment and interposition of a new segment placed through a clean and new tunnel is done. If the infection is more extensive and cannot be controlled as described above, drainage, segmental excision of the involved graft, debridement of necrotic tissue, and systemic antibiotics

True aneurysms of the graft itself were occasionally seen with bovine heterografts and umbilical veins. With ePTFE, only pseudoaneurysms, most commonly originating from needle punctures, are seen. When small and not infected, they can be repaired by placing a simple stitch closing the defect. If larger, they may need resection of the defective graft and interposition of a new segment. Seroma Perigraft seroma is a relatively rare complication of synthetic vascular prostheses (Fig. 84.11). Treatment is difficult and is often unsuccessful. The pathology consists of an enlarging sterile fluid collection around the prosthetic graft. In graft AV fistulas, it always occurs in the proximity of the arterial anastomosis. When the graft is exposed at that point, active transudation of serum-like fluid can be observed. The etiology is unclear. Various mechanisms have been proposed, ranging from changes of the graft itself that induce increased transmural permeability (changes in the matrix produced by exposure to high pressure, or modification in superficial tension by contact with detergents, subcutaneous fat, or denucleation) (43–46) to biological alterations in the host (circulatory factors, inhibition of fibroblast) (47,48). Therapy by repeated percutaneous aspiration, open drainage with excision of the pseudocapsule, injections of irritants, and collagen powder infiltration have all failed. Some successes have been reported with injection of fibrin glue into the leaking graft (49). In our hands, resection of the pseudocapsule, excision of the failing segment of graft, and replacement with a new segment that goes through a new tunnel have given

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Part XI Arteriovenous Malformation

the best results. Recently, we have had promising results by replacing the segment of transudating ePTFE graft with a segment of Dacron graft. Cardiac Failure This is a common manifestation of large traumatic AV fistulas. The higher venous return to the heart increases cardiac output, eventually leading to cardiomegaly and congestive heart failure. It has been estimated that heart failure occurs when 20% to 50% of the cardiac output is shunted through the fistula (50). As Brescia-Cimino AV fistulas have blood flows of about 300 mL per minute and graft AV fistulas, when constructed with 6-mm-diameter grafts, have outputs of 700 to 1000 mL per minute (51), they rarely produce cardiac failure. A decreasing pulse rate with fistula compression (Braham sign) supports the diagnosis of congestive heart failure secondary to the fistula. Treatment consists of decreasing the flow by stenosing the fistula at its outflow (banding), or ligating the AV connection and constructing a new access with lower flow. Ischemia Upper extremity ischemia related to the presence of a subcutaneous AV fistula or a bridge AV fistula is a relatively infrequent but potentially devastating complication (Fig. 84.12). Mild presentation characterized by coldness, numbness, and pain during dialysis occurs in about 10% of all cases. Usually it is self-correcting and the symptoms reverse completely in a few weeks (52). More severe ischemia, necessitating treatment, has been reported to occur in about 1% of patients with AV fistulas (most commonly, when performed at the elbow level between the brachial artery and antecubital vein) and about 2.7% to 4.3% of patients with graft AV fistulas (53–57). The majority of patients affected by this condition have diabetes and severe obstructive disease of the arteries distal to the brachial artery. Symptoms can occur immediately after construction of the arterial venous connection or later after operation. In our experience, severe ischemia requiring surgical correction became manifested very early after construction of the fistula in over three-quarters of the patients. In the remaining quarter, the ischemia occurred between 5 months and 5 years after access surgery. A great deal has been written concerning the importance of a careful preoperative evaluation of the circulatory status and the collateral potential of the limb, as a way of predicting and preventing ischemia. In our experience, however, even the best of physical examinations cannot ensure an accurate prediction of which arms are at risk. It is, therefore, of the utmost importance to be able to recognize the existence of ischemia in a timely manner, and if severe, initiate immediate treatment. The pathophysiologic basis of these ischemic complications has been discussed in detail by Barnes (58). The low-pressure system present at the outflow side of the arteriovenous connection induces a reversal of flow in the portion of the artery distal to the fistula. This alteration in

FIGURE 84.12 Severe ischemia with gangrenous changes in the third finger, in a diabetic patient with a brachial-to-cephalic AV fistula constructed 2 years earlier.

the direction of flow is referred to as “steal,” and, when it is of sufficient magnitude and cannot be compensated by collateral flow, it results in ischemic manifestations. This is particularly likely to occur in diabetic individuals, who often have diffuse arterial occlusive disease. Hemodynamic studies directly measuring the direction and amount of blood flow in the different components of the fistula, have demonstrated that “steal” occurs in 73% of AV fistulas and 91% of graft AV fistulas (51). If the ischemic manifestations are severe and the viability of the limb is threatened, surgical treatment is required. Several techniques have been utilized for this purpose. The simplest and most direct means of treating the ischemic steal is the ligation of the outflow of the fistula. This instantaneously reverses the steal and improves distal perfusion. The obvious drawback of this technique is that the angioaccess is lost. Another widely used technique is the so-called “banding.” It consists of producing a stenosis in the outflow portion of the AV fistula or graft AV fistula, close to the anastomosis. Many variations of banding, all intended to produce a narrowing and conse-

Chapter 84 Vascular Access for Dialysis

quent flow reduction, have been reported (59–63). Several manufacturers produce grafts designed to prevent steal phenomena. These grafts are tapered, and the narrowest portion is intended to be anastomosed to the artery. The rationale for this design is based on the concept that steal will be prevented by increasing the resistance at the outflow of the fistula. The practical problem of banding techniques or of using tapered grafts stems from the difficulty in establishing the precise degree of stenosis required for elimination of the steal while still allowing a flow sufficient to sustain patency of the fistula. In our experience, thrombosis of the access is common, even if the amount of narrowing is determined with careful hemodynamic measurements (direct flow measurements or digital plethysmography). The explanation for this discouraging fact is that, at the level of “critical stenosis” that results from the banding procedure, a minimal further reduction in fistula flow, produced for example by mild hypotension, can induce thrombosis of the graft. Another technique that is being used is elongation of the graft AV fistula (64). The purpose of this procedure is also to increase peripheral resistance of the fistula outflow, and it has the same difficulties as banding. A recently described technique (65), presented as a solution for early steal after brachial artery to axillary vein graft AV fistula, is the use of a branch of the axillary artery for inflow and the brachial vein for outflow. The explanation proposed for the success of this technique was that the reduced amount of flow delivered by the axillary branch, prevented ischemic steal. In similar circumstances, we have used the axillary artery itself as inflow source with comparable results. Our explanation for the success of this technique is that the axillary artery is very rich in collateral circulation and this overcomes the steal. In 1988, we reported a new technique that consists of ligation of the artery just distal to the takeoff of the AV fistula or graft AV fistula and an arterial bypass from the artery proximal to the takeoff of the arterial venous connection to the artery distal to the ligation (66) (Fig. 84.13). The purpose of the ligation of the artery distal to the AV fistula/bridge AV fistula is to eliminate reversal of flow. The addition of the arterial bypass provides the distal vascular bed with normal perfusion pressure and flow. This technique has been named “DRIL” (distal revascularization interval ligation) and has given excellent results, with immediate reversal of the ischemic condition while maintaining function of the access (67). In our view, it is the procedure of choice for the correction of AV fistula- or graft AV fistula-induced ischemic steal.

Conclusion Vascular access procedures are the lifeline of patients with end-stage renal disease maintained on hemodialysis. The function of the access will greatly determine the quality of life that this patient population will enjoy. As is clear from this review, there are many access pro-

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FIGURE 84.13 Correction of ischemic steal by arterial ligation and bypass (DRIL procedure). The artery is ligated just distal to the takeoff of the fistula connection and an arterial bypass is created between the artery proximal to the takeoff of the fistula or graft AV fistula and the artery distal to the ligation.

cedures, each of them with its indications and contraindications, benefits and disadvantages. The process of deciding what access should be provided to a particular patient has to be the result of teamwork. Adequate timing for the referral to access surgery is the responsibility of the nephrologist. The nephrologist has to discuss with the surgeon, who has done a complete preoperative evaluation, which access is best fitted for a particular patient. The input of the hemodialysis nurse, technician, and social worker will help determine which modality of treatment will benefit the patient most (peritoneal dialysis, hemodialysis). The patient is a very important member of this decision team, and therefore his or her education is essential for this purpose. Complications of these accesses are common, many times serious, and usually difficult to treat. For successful therapy, the surgeon has to be knowledgeable in the management of vascular complications and have excellent judgment. From this review, it can also be concluded that no individual angioaccess is perfect and fits all needs. Acute

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accesses usually have a short lifespan and cannot be used chronically. Chronic access cannot be used immediately with safety. This field, therefore, is open to innovation. New indwelling catheters, development of new graft materials, and the control of intimal hyperplasia are certainly important problems that are waiting to be solved. With those in the field keeping an open mind and avoiding tunnel vision, new ways to establish contact between the patient and the machine will be established.

References 1. USRDS. Excerpts from the United States Renal Data System 1998 Annual Data Report. Incidence and prevalence of ESRD. Am J Kidney Dis 1998;32(suppl 1):S38S49. 2. Kolff WJ, Berk HT, et al. The artificial kidney: a dialyzer with a great area. Acta Med Scand 1944;117:121. 3. Quinton WE, Dillard DH, Scribner BH. Cannulation of blood vessels for prolonged hemodialysis. Trans Am Soc Artif Intern Organs 1960;6:104. 4. Brescia MJ, Cimino JE, et al. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med 1966;275:1089. 5. Shaldon S, Chiandussi L, Higgs B. Hemodialysis by percutaneous catheterization of the femoral artery and vein with regional heparinization. Lancet 1961;2:857. 6. Schanzer H, Kaplan S, et al. Double silicone rubber indwelling venous catheters: a new modality for hemoaccess. Arch Surg 1986;121:229–232. 7. Beathard GA, Posen GA. Initial clinical results with the LifeSite hemodialysis access system. Kidney Int 2000;58(5):2221–2227. 8. Horattas MC, Wright DJ, et al. Changing concepts of deep venous thrombosis of the upper extremity. Report of a series and review of the literature. Surgery 1988;104:561–567. 9. Ryan JA, Abel RM, et al. Catheter complications in total parenteral nutrition: a prospective study of 200 consecutive patients. N Engl J Med 1974;290:757. 10. Haimovici H, Steinman C, Caplan L. Role of arteriovenous anastomoses in vascular diseases of the lower extremity. Ann Surg 1966;164(6):990. 11. Mandel S, Martin P, et al. Vascular access in a university transplant and dialysis program. Arch Surg 1977;112:1375. 12. Bunalumi U, Civalleri D, et al. Utilization of the “anatomical snuff box” for vascular access in hemodialysis. In: Koostra G, Journing PJG, eds. Vascular access. Boston: MTP Press, 1983:15–20. 13. Kinnaert P, Moris C. Arteriovenous fistula at the elbow for maintenance hemodialysis. In: Koostra C, Journing PJG, eds. Access surgery. Boston: MTP Press, 1983:25–29. 14. Kinnaert P, Vereerstraeten D, et al. Ulnar arteriovenous fistula for maintenance hemodialysis. Br J Surg 1971;58:641. 15. Rivers, SP, Scher LA, et al. Basilic vein transposition: an underused autologous alternative to prosthetic dialysis angioaccess. J Vasc Surg 1993;18:391–397.

16. Ascher E, Hingoran A, et al. The value and limitations of the arm cephalic and basilic vein for arteriovenous access. Ann Vasc Surg 2001;15(1):89–97. 17. Morgan PA, Knight CD, et al. Femoral triangle sepsis in dialysis patients. Ann Surg 1980;191:460. 18. Haimov M, Burrows L, et al. Alternatives for vascular access for hemodialysis: experience with autogenous saphenous vein autografts and bovine heterografts. Surgery 1974;75:447. 19. May J, Tiller D, et al. Saphenous vein arteriovenous fistula in regular dialysis treatment. N Engl J Med 1969;280:770. 20. Haimov M, Burrows L, et al. Experience with arterial substitutes in the construction of vascular access for hemodialysis. J Cardiovasc Surg 1980;21:149. 21. Dardik H, Ibrahim IM, Dardik I. Arteriovenous fistulas constructed with modified human umbilical cord vein graft. Arch Surg 1976;111:60. 22. Mindich BI, Silverman MJ, et al. Umbilical cord vein fistula for vascular access in hemodialysis. Trans Am Soc Artif Intern Organs 1975;21:273. 23. Flores L, Dunn I, et al. Dacron arteriovenous shunts for vascular access in hemodialysis. Trans Am Soc Artif Intern Organs 1973;19:33. 24. Burdick JI, Scott W, Cosimi AB. Experience with Dacron graft arteriovenous fistulas for dialysis access. Ann Surg 1978;198:262. 25. Gross CJ, Hayes JF. PTFE grafts arteriovenous fistulas for hemodialysis access. Am J Surg 1979; 45: 748. 26. Haimov M. Vascular access for hemodialysis. Surg Gynecol Obstet 1975;141:691. 27. Haimov M. Clinical experience with the expanded polytetrafluoroethylene vascular prosthesis. Angiology 1978;29:1. 28. Oakes D, Ma M, et al. A three year experience using modified bovine arterial heterografts for vascular access in patients requiring hemodialysis. Ann Surg 1978;187(4):423. 29. Valji K, Bookstein JJ, et al. Pulse-spray pharmacomechanical thrombolysis of thrombosed hemodialysis access grafts: long-term experience and comparison of original and current techniques. Am J Roentgenol 1995;164:1495–1500. 30. Beathard GA. Mechanical versus pharmacomechanical thrombolysis for the treatment of thrombosed dialysis access grafts. Kidney Int 1994;45:1401– 1406. 31. Trerotola SO, Lund GB, et al. Thrombosed dialysis access grafts: percutaneous mechanical declotting without urokinase. Radiology 1995;191:721–726. 32. Beathard GA. Percutaneous transvenous angioplasty in the treatment of vascular access stenosis. Kidney Int 1992;42:1390–1397. 33. Schwab SJ, Saeed M, et al. Transluminal angioplasty of venous stenoses in polytetrafluoroethylene vascular access grafts. Kidney Int 1987;32:395–398. 34. Sands JJ, Miranda CL. Prolongation of hemodialysis access survival with elective revision. Clin Nephrol 1995;44:334–337. 35. Schuman E, Quinn S, et al. Thrombolysis versus thrombectomy for occluded hemodialysis grafts. Am J Surg 1994;167:473–476.

Chapter 84 Vascular Access for Dialysis 36. Summers S, Drazan K, Gomes A. Urokinase therapy for thrombosed hemodialysis grafts. Surg Gyncol Obstet 1993;176: 534–538. 37. Schwartz CL, McBrayer CV, et al. Thrombosed hemodialysis grafts: comparison of treatment with transluminal angioplasty and surgical revision. Radiology 1995;194:337–341. 38. Besarab A, Sullivan KL, et al. Utility of intra-access pressure monitoring in detecting and correcting venous outlet stenosis prior to thrombosis. Kidney Int 1995;47:1364–1373. 39. Palder SB, Kirkman RL, et al. Vascular access for hemodialysis: patency rates and results of revision. Ann Surg 1985;202:235–239. 40. Etheredge EE, Haid SD, et al. Salvage operations for malfunctioning polytetrafluoroethylene hemodialysis access grafts. Surgery 1983;94:464–470. 41. Beathard GA. Percutaneous angioplasty for the treatment of venous stenosis: a nephrologist’s view. Semin Dial 1995;8:166–170. 42. Burger H, Zijlstra JJ, et al. Percutaneous transluminal angioplasty improves longevity in fistulae and shunts for hemodialysis. Nephrol Dial Transplant 1990;5:608–611. 43. Bolton W, Cannon J. Seroma formation associated with PTFE vascular grafts used as arteriovenous fistulae. Dialysis Transplant 1981;10:60–63. 44. LeBlanc J, Albus R, et al. Serous fluid leakage: a complication following the modified Blalock-Taussig shunt. J Thorac Cardiovasc Surg 1984;88:259–262. 45. Blumenberg RM, Gelfand M, Dale W. Perigraft seromas complicating arterial grafts. Surgery 1985;97:192–203. 46. Buche M, Schoevaerdts JC, et al. Perigraft seroma following axillofemoral bypass: report of three cases. Ann Vasc Surg 1986;1:374–377. 47. Ahn S, Machleder H, et al. Pathogenesis of perigraft seroma: evidence of a humoral fibroblast inhibitor. Surg Forum 1986;37:460–461. 48. Sladen J, Mandl M, et al. Fibroblast inhibition: a new and treatable cause of prosthetic graft failure. Am J Surg 1985;149:588–590. 49. Maitland A, Williams W, et al. A method of treating serous fluid leak from a polytetrafluoroethylene Blalock Taussig shunt. J Cardiovasc Surg 1985; 90:791–793. 50. Bosanac P, Bilder B, et al. Post-permanent access neuropathy. Trans Am Soc Artif Intern Organs 1977;23:612. 51. Kwun KB, Schanzer H, et al. Hemodyoamic evaluation of angioaccess procedures for hemodialysis. Vasc Surg 1979;13:170–177.

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52. Schanzer H, Schwartz M, et al. Treatment of ischemia due to “steal” by arteriovenous fistula with distal artery ligation and revascularization. J Vasc Surg 1988;7:770–773. 53. Duncan H, Ferguson L, Fans I. Incidence of the radial steal syndrome in patients with Brescia fistula for hemodialysis: its clinical significance. J Vasc Surg 1986;4:144–147. 54. Haimov W, Burrows L, et al. Experience with arterial substitutes in the construction of vascular access for hemodialysis. J Cardiovasc Surg 1980;21:149–154. 55. Porter JA, Sharp WV, Walsh EJ. Complications of vascular access in a dialysis population. Curr Surg 1985;42:298–300. 56. Zibari GB, Rohr MS, et al. Complications from permanent hemodialysis vascular access. Surgery 1988;104:681–686. 57. Winsett OF, Wolma FJ. Complications of vascular access for hemodialysis. South Med J 1985;78:513–517. 58. Barnes RW. Hemodynamics for the vascular surgeon. Arch Surg 1980;115:216–223. 59. Corry RJ, Natvarlal PP, West JC. Surgical management of complications of vascular access for hemodialysis. Surg Gynecol Obstet 1980;51:49–54. 60. Drasler WJ, Wilson GJ, et al. Venturi grafts for hemodialysis access. ASAIO Trans 1990;36:M753–760. 61. Khalil IM, Livingston DH. The management of steal syndrome occurring after access for dialysis. J Vasc Surg 1988;7:572–573. 62. Mattson WJ. Recognition and treatment of vascular steal secondary to hemodialysis prostheses. Am J Surg 1987;154:198–201. 63. West JC, Bertsch DJ, et al. Arterial insufficiency in hemodialysis access procedures: correction by “banding” technique. Transplant Proc 1991;23:1838–1840. 64. West JC, Evans RD, et al. Arterial insufficiency in hemodialysis access procedures: reconstruction by an interposition polytetrafluoroethylene graft conduit. Am J Surg 1987;153:300–301. 65. Jendrisak, MD, Anderson CB. Vascular access in patients with arterial insufficiency. Ann Surg 1990;212(2):187– 193. 66. Schanzer H, Skladany M, Haimov M. Treatment of angioaccess-induced ischemia by revascularization. J Vasc Surg 1992;16(6):861–866. 67. Schanzer H, Skladany M, et al. Ischemia following angioaccess surgery. In: Current Critical Problems in Vascular Surgery, Vol 7, Quality Medical Publishing, 1996;484–486.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 85 Portal Hypertension James D. Eason and John C. Bowen

The management of variceal bleeding from portal hypertension has changed dramatically over the last decade. New pharmacologic agents and improvement in endoscopic techniques have greatly improved the prognosis for acute bleeding as well as the prevention of recurrent bleeding episodes. The advent of transjugular intrahepatic portosystemic shunts (TIPS) has largely replaced emergency surgery and become effective management for refractory ascites as well as variceal bleeding for some patients. The success of orthotopic liver transplantation (OLT) as the only potential cure for end-stage liver disease has redefined the goal in management of portal hypertension. No longer is the end point merely the prevention of the complications of cirrhosis, but rather replacement of the diseased liver. However, OLT is limited by the availability of donor organs and recurrence of disease in some instances. Surgical portosystemic shunts and other surgical procedures have therefore maintained an important place in the repertoire of available therapy for variceal bleeding.

Historical Background Massive hemorrhage was first identified as a complication of esophageal varices in 1839. During the nineteenth century and the early part of the twentieth century, the venous abnormalities in cirrhotic patients were attributed to the diseased spleen. The concept of Banti’s syndrome, described as hypersplenism with thrombocytopenia and leukopenia, was introduced by Guido Banti, the Italian clinician (1). Eppinger, a prominent German physician, introduced splenectomy for management of Banti’s syndrome, which achieved great popularity in the 1920s. Although portal pressure had been measured in animals

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in 1896, the term “portal hypertension” did not appear in the medical literature until 1930 (2–4). In 1937, portal pressure was measured in humans via water manometry during abdominal surgery (5). These studies showed that increased portal and splenic pulp pressures existed in Banti’s syndrome. The various interpretations of the role of splenomegaly in the etiology and pathophysiology of portal hypertension during this period led to the widespread use of splenectomy and devascularization procedures. End-to-side portocaval shunting was first described by Eck in 1877. Whipple and his colleagues at Columbia Presbyterian Hospital introduced this procedure into clinical practice in 1945 (6). Their initial success in controlling variceal bleeding by connecting the portal and caval venous systems was a promising step in the surgical management of portal hypertension. Over the next two decades, however, randomized controlled trials demonstrated that total portal diversion dramatically increased the incidence of encephalopathy and accelerated liver failure. These observations led Warren and his colleagues to introduce the distal splenorenal shunt, reported in 1967 as a selective shunt designed to maintain perfusion of the hepatic parenchyma by portal blood flow from the splanchnic bed while selectively decompressing the portal venous drainage of the esophagus and stomach (7). Sclerotherapy had been abandoned after its introduction in 1939 but regained popularity in the 1970s with the advent of fiberoptic endoscopes (8). Sclerotherapy began to rapidly supplant shunt procedures in the initial management of the acute bleeding episode, and in the prevention of recurrent hemorrhage. Vasopressin was first used to manage acute variceal bleeding in the 1950s (9). Pharmacotherapy, using beta-blockers, for the prevention

Chapter 85 Portal Hypertension

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of recurrent variceal bleeding was introduced in 1981 by LeBrec and coworkers (10). Stimulated by initial success, pharmacotherapy became an area of intense clinical interest in the treatment of portal hypertension. Somatostatin and its analog octreotide were introduced for the management of acute bleeding episodes in the 1990s (11). Dr Starzl pioneered liver transplantation in the mid1960s as an option for end-stage liver disease. Advances in immunosuppression, preservation, and surgical techniques have led to the success of liver transplantation as the treatment of choice for patients with portal hypertension and advanced liver disease (12). More recently, the transjugular intrahepatic portosystemic shunt (TIPS), first described by Rosch et al. in 1969, has become established therapy for acute hemorrhage and as a bridge to OLT (13).

Anatomy and Pathophysiology The portal vein is formed by the confluence of the splenic vein and superior mesenteric vein posterior to the head of the pancreas. The inferior mesenteric vein contributes to the portal vein flow by joining the splenic or superior mesenteric vein or occasionally directly into the splenomesenteric junction. The portal vein courses posterior to the first portion of the duodenum where it receives flow from the right gastroepiploic vein and the coronary vein on its way to the liver. Pancreatic and cystic branches empty into the main portal proximal to the bifurcation at the porta hepatis. Multiple splanchnic and systemic collaterals exist which may become enlarged in portal hypertension (Fig. 85.1). The intrahepatic portal vein anatomy is defined by Couinaud’s segmental division of the liver (14). Couinaud’s system divides the liver into eight distinct segments according to the distribution of the portal triad structures and hepatic venous drainage. Segment I is the caudate lobe, segments II and III comprise the left lateral segment, and segment IV is the portion of the left lobe medial to the falciform ligament and to the left of Cantlies’ line which courses along the anteroposterior plane from the gallbladder fossa to the vena cava. This line divides the left lobe segments I–IV from the right lobe segments V–VIII. Segments V and VIII are the anterior segments of the right lobe and segments VI and VII form the posterior right lobe. Caudate branches are the first branches to the liver, usually arising from the left portal vein. The left portal vein gives branches to segment IV and segments II and III of the left lateral segment. The right portal vein divides into an anterior branch, which supplies segments V and VIII and a posterior branch, which supplies segments VI and VII. Hepatic venous drainage consists of the right hepatic vein draining the right lobe, the middle hepatic vein draining portions of the right lobe and segment IV of the left lobe, and the left hepatic vein which drains part of segment IV and segments II and III. The caudate veins usually drain directly into the vena cava. In addition, there

FIGURE 85.1 Portal–systemic collateral pathways. SVC, superior vena cava; IVC, inferior vena cava.

may be an accessory hepatic vein draining the posterior inferior aspect of the right lobe. Hepatic blood flow averages 1500 mL/min, twothirds of which comes from the portal vein, with the remainder coming from the hepatic artery. This blood flow is approximately 25% of the cardiac output. The oxygen supply to the liver is equally supplied by the portal vein and hepatic artery. Portal venous volume is indirectly regulated by vasoconstriction and vasodilation of the splanchnic arterial bed. Portal venous pressure (P) is directly related to blood flow (Q) and resistance (R) through the liver as described by Ohm’s law: P = QR. Portal hypertension is caused primarily by increased resistance at the presinusoidal, sinusoidal, or postsinusoidal level, while increased flow through a hyperdynamic splanchnic system plays a significant role as well (Fig. 85.2). The balance between the potent vasoconstrictor endothelin-1 and the potent vasodilator nitric oxide may be important in initiation of increased intrahepatic resistance. Endothelin-1 is important in hepatic sinusoidal contractility, thereby increasing intrahepatic vascular resistance (15,16,17). In

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Part XI Arteriovenous Malformation FIGURE 85.2 Etiology of portal hypertension according to site of resistance.

later stages of liver disease, fibrosis and the progression to cirrhosis are responsible for the tremendous intrahepatic resistance leading to varices. Nitric oxide appears to be the primary factor responsible for the systemic hyperdynamic circulatory response in cirrhosis. Portosystemic collaterals form varices after being subjected to prolonged portal hypertension. The pressure gradient required to form varices is approximately 12 mmHg although some patients may not form varices until the gradient is much higher (16,18). This gradient is measured as the difference between hepatic venous wedged pressure and free hepatic venous pressure. Normally, this gradient is 5 mmHg or less. Bleeding from varices is determined by both physical and clinical factors. Physical factors include elasticity of the vessel and variceal wall tension (T) determined by transmural pressure (TP), the vessel radius (R) and wall thickness (w) according to Frank’s modification of Laplace’s law: (T = [TP ¥ R]/w). (16) The distal esophageal veins are very superficial and lack support from surrounding tissues, thus predisposing them to variceal formation and bleeding.

Etiology The most common etiology of portal hypertension is cirrhosis from alcohol and viral hepatitis in the United States and most Western countries. Cirrhosis from these conditions, as well as biliary cirrhosis, causes sinusoidal portal hypertension secondary to fibrosis and scarring of the perisinusoidal tissue. Schistosomiasis remains the most common cause of portal hypertension worldwide, which is presinusoidal in location. Another cause of presinusoidal portal hypertension is primary portal vein thrombosis, which may be associated with normal liver function. The prototype of postsinusoidal portal hypertension is Budd–Chiari syndrome caused by hepatic vein thrombosis or stenosis, venoocclusive disease or vena

cava stenosis or thrombosis. Primary portal vein thrombosis and Budd–Chiari syndrome are frequently associated with a hypercoagulable state or autoimmune connective tissue disorders. Portal vein thrombosis is also seen in children or young adults with a history of umbilical vascular access as a neonate. Another spectrum of liver disease characterized by portal hypertension with wellpreserved hepatic function is polycystic disease including congenital hepatic fibrosis and nodular regenerative hyperplasia (NRH). Infiltrative diseases such as reticulosis, sarcoidosis, and myelofibrosis also cause presinusoidal portal hypertension.

Evaluation of the Patient In assessing the patient with portal hypertension, it is important to try to determine the etiology and severity of liver disease along with portal and mesenteric venous anatomy and the presence and severity of varices. Evaluation of the patient with portal hypertension begins with a detailed history for risk factors for liver disease. Alcohol abuse, previous transfusions, intravenous drug use, and tattoos are risk factors for liver disease. In addition, the history should focus on environmental or occupational exposure or medications as well as family history and history of any biliary disease or autoimmune disorders. Recent travel to Africa, Asia, or Middle Eastern countries where parasitic liver diseases are common may be pertinent. Along with risk factors for liver disease, the history should elicit any symptoms or signs, which the patient or family members may have noticed. Jaundice, confusion, fluid retention, hematemesis, or melena are obvious symptoms which may be noticed. Sleep disturbance, easy bruising, and fatigue are more subtle findings that may indicate significant liver disease. Physical examination of these patients may reveal scleral icterus, spider angiomas,

Chapter 85 Portal Hypertension

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TABLE 85.1 Child–Turcotte–Pugh (CTP) classification Parameter

1 point

2 points 3 points

Encephalopathy grade Ascites Albumin Prothrombin time Bilirubin in cirrhosis Bilirubin in cholestatic disease

None Absent >3.5 <4 <2 <4

1–2 Slight 2.8–3.5 4–6 2–3 4–10

3–4 Moderate <2.8 >6 >3 >10

CTP class A = 5–6 points, class B = 7–9 points, class C ≥ 10 points.

TABLE 85.2 MELD score Multiplication Factor

Parameter

10 ¥ 0.378 ¥ 1.120 ¥ MELD score

[0.957 loge (creatinine)] Loge (bilirubin mg/dL) Loge (INR) Sum

INR = international normalized ratio of prothrombin time.

palmar erythema, gynecomastia, splenomegaly, or peripheral edema. Signs of advanced liver disease including jaundice, ascites, caput medusa, asterixis, or encephalopathy signify a greater risk of variceal bleeding, with a poorer prognosis. Laboratory tests are important in determining the severity of liver disease as well as clinical factors, which may increase the risk of bleeding. The Child–Pugh classification system (Table 85.1) stratifies patients into risk categories based on the level of serum bilirubin, albumin, and INR, and the degree of ascites and encephalopathy (19,20). More recently, the Mayo endstage liver disease or model for end-stage liver disease (MELD) score (Table 85.2) was determined to accurately predict survival of patients undergoing TIPS (20). This scoring system is now being used to stratify patients awaiting liver transplantation according to mortality risk on the waiting list. The MELD system considers only serum bilirubin, INR, and serum creatinine. Another standard laboratory test which should be done is a complete blood count to determine anemia and the degree of leukopenia and thrombocytopenia, which are caused by chronic malnutrition, bone marrow suppression, and hypersplenism. The serum ammonia level is an important marker for encephalopathy. Serologic markers for viral hepatitis and HIV should also be determined. Serum alpha-fetoprotein is a useful marker for hepatocellular carcinoma, which is common in alcoholic liver disease and viral hepatitis. The incidence of hepatocellular carcinoma has been reported to be greater than onethird of patients with hepatitis C cirrhosis undergoing liver transplantation (21). Patients with Budd–Chiari syndrome or primary portal vein thrombosis should be evaluated for a hypercoagulable state (22). The best noninvasive evaluation of portal venous

FIGURE 85.3 Power Doppler scan of 8-mm PTFE mesocaval shunt. (Courtesy of Laurie Troxclair, RDMS, RVT.)

anatomy is Doppler ultrasound. Ultrasonography should be able to identify the presence of portal vein, superior mesenteric vein, and splenic vein flow as well as ascites, liver and spleen size, and the presence of liver masses. Any patient with evidence of liver disease or portal hypertension should undergo screening esophagogastroduodenoscopy to determine the presence and severity of varices. Bleeding from esophageal varices represents the greatest risk of death in these patients.

Radiographic Evaluation The gold standards for evaluation of portal hypertension have been the hepatic venogram with pressure measurements and the celiac and superior mesenteric arteriogram with portal venous phase. The venogram details anatomy of the hepatic veins and vena cava while wedged hepatic vein pressures give an accurate determination of the severity of portal hypertension. Hepatic venogram and vena cavagram are essential in diagnosis and management of Budd–Chiari syndrome. Celiac and superior mesenteric arteriogram with venous phase gives detailed anatomy of arterial and venous flow to the liver. Improving techniques in Doppler ultrasonography have been very accurate in our experience in delineating portal vein, splenic vein, and superior mesenteric vein patency and direction of flow prior to liver transplantation and portosystemic shunting. Doppler ultrasound is also used routinely in our institution in the postoperative evaluation of shunt patency in both mesocaval and distal splenorenal shunts, as well as portal vein, hepatic vein and hepatic artery integrity following transplantation (Fig. 85.3). The use of Doppler ultrasound in these situations is extremely valuable because of the coexistence of renal disease, which may be worsened by angiography. Magnetic resonance angiography is also a useful tool in portal vein evaluation although it

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Part XI Arteriovenous Malformation

cannot be used in patients with a TIPS procedure (23). Computed tomography (CT) is another important radiologic tool in evaluating the patient with cirrhosis and portal hypertension. CT can accurately determine the presence of masses suspicious for hepatocellular carcinoma (HCC), which frequently coexist in patients with cirrhosis and portal hypertension. The presence of HCC is an important determinant in whether a patient may be a candidate for shunting or transplantation. CT can also determine the size of the liver and the presence of ascites. Helical CT scanning and triple-phase scans have increased the sensitivity in identifying small hepatic lesions and identifying portal vein anatomy. These scans employ rapid scanning techniques and non-contrast CT along with arterial phase and venous phase scanning.

Complications The greatest risk of death in patients with cirrhosis is uncontrollable variceal hemorrhage. Gastroesophageal variceal bleeding is the most common presentation of portal hypertension occurring in approximately 30% of patients with cirrhosis (24). Initial bleeding episodes are fatal in up to 30% of cases, and the incidence of rebleeding in survivors approaches 70% (16). Ascites is another common finding in patients with portal hypertension and is caused by a combination of hypoalbuminemia in conjunction with portal hypertension. Ascites is usually a manifestation of advanced liver disease, but may be present in portal hypertension from other causes. Sampling of the ascites is an important diagnostic tool to determine the presence of spontaneous bacterial peritonitis (SBP) and to determine the concentration of albumin in the fluid. A white blood cell count greater than 250 cells/mm3 signifies infection of the ascites. Longstanding liver disease with portal hypertension may also result in hepatorenal syndrome and hepatopulmonary syndrome or pulmonary artery hypertension. Encephalopathy is a result of both portosystemic shunting and hepatocellular dysfunction.

Management of Variceal Bleeding The management of esophageal varices and bleeding can be divided into three strategies: prophylaxis of initial bleeding, control of acute bleeding, and prevention of recurrent bleeding. Prophylaxis against first bleeding is critical because of the high incidence of bleeding in patients with cirrhosis and the poor prognosis associated with first bleeding episodes. The clinical predictors of bleeding are continued alcohol use and advanced liver disease by Child-Pugh classification (16). Endoscopic findings of large varices and the presence of red wale markings correlate highly with an increased risk of bleeding (25). Increasing hepatic venous pressure gradient is a reliable predictor of bleeding in patients with cirrhosis, but is invasive and

not commonly performed. Thrombocytopenia may be useful in predicting the presence of large varices and increased risk of bleeding (26). The primary methods used in the prophylaxis of initial bleeding episodes are pharmacologic therapy and endoscopic therapy. The principal objective with pharmacologic therapy is to reduce portal vein pressure. Vasoconstrictors, principally beta-blockers, are used to reduce collateral portal venous flow. Vasodilators such as nitrates and alpha-blockers have also been used in an attempt to decrease intrahepatic vascular resistance. Beta-blockers have proven efficacy in reducing splanchnic blood flow, portal pressure, and gastroesophageal collateral blood flow. Propranolol and nadolol are the primary beta-blockers in clinical use, because of their demonstrated benefit in controlled trials of a 40–50% reduction in the risk of bleeding (16,26). These agents are preferred because of their nonselective activity of blockade of b1-adrenergic receptors, which causes splanchnic vasoconstriction by unopposed alpha-adrenergic activity as well as elimination of b2-mediated vasodilation. The goal of beta-blockade is a 20% reduction of portal pressure or a decrease in the hepatic venous pressure gradient to less than 12 mmHg. However, clinical measurements of achieving a reduction in heart rate to 55 beats per minute or 25% of baseline are the most commonly used parameters. Isosorbide mononitrate is the primary nitrate, which has been used to reduce portal hypertension. The use of this agent in conjunction with propranolol or nadolol has been shown to reduce the risk of bleeding over beta-blockers alone, however it is poorly tolerated because of the potential to accentuate the vasodilatory hemodynamics typical of cirrhosis (27). Prazosin has also been used in conjunction with propranolol with a similar reduction in hepatic venous pressure gradient, but an associated increase in fluid retention as with isosorbide mononitrate. Endoscopy is an essential diagnostic tool for management of portal hypertension and varices. Sclerotherapy and band ligation of varices have been used extensively in the management of acute variceal bleeding and recently for prophylaxis of bleeding. Band ligation has become a common method to eradicate varices in patients at risk for bleeding. Two recent randomized trials demonstrated a lower risk of spontaneous bleeding with band ligation in patients with high-risk varices (28,29). Sclerotherapy, while effective, has no advantage over band ligation in prophylaxis and may be associated with a higher risk of serious complications including death. Recent trials have demonstrated a benefit of banding over propranolol in preventing bleeding (30). One important tenet with band ligation is the necessity of repeat endoscopy to eradicate varices for effective prophylaxis (27). Combination pharmacologic therapy and endoscopic therapy, or sclerotherapy with band ligation, are attractive ideas for prophylaxis but have not been proven to have any benefit over any of these methods alone (27). Surgery has no role in the prophylaxis of bleeding at this time. Previous studies evaluating prophylactic

Chapter 85 Portal Hypertension

surgery have demonstrated that bleeding can be effectively prevented; however, liver failure may be accelerated, resulting in a higher mortality rate (31). In addition, unnecessary surgery may complicate future liver transplantation in these patients.

Management of Acute Bleeding Acute variceal bleeding is the most common and most lethal complication of portal hypertension. The management of the acutely bleeding patient requires a multidisciplinary approach in which pharmacologic therapy, balloon tamponade, endoscopic therapy, radiologic intervention, and surgical shunting may all play a role. The initial presentation of a patient with bleeding varices determines the course of action and guides further diagnostic and therapeutic intervention. The rate of bleeding needs to be determined immediately and aggressive resuscitation initiated. In the presence of severe hematemesis or mental status changes associated with bleeding, the patient should be intubated for airway protection. A nasogastric tube should be inserted to determine the presence of active bleeding, estimate the quantity of bleeding and lavage the blood and clot. Large-bore intravenous access needs to be obtained rapidly for volume resuscitation and replacement of blood and coagulation factors. Once the patient has been resuscitated and lavaged, endoscopy should be performed. Sclerotherapy is able to stop bleeding in 80 to 90% of cases of acute variceal hemorrhage (16). Endoscopic variceal band ligation is equally effective in controlling initial bleeding although it is associated with a higher recurrence of varices (32,33). Pharmacologic therapy with vasopressin or somatostatin or one of its synthetic analogs (octreotide or vapreotide) should be instituted immediately. Octreotide is effective in stopping hemorrhage in 80% of patients and is equivalent to vasopressin and endoscopic therapy (16). Terlipressin is a synthetic analog of vasopressin, which is equally effective in controlling bleeding, with fewer systemic and splanchnic side effects; however, it is currently unavailable in the United States (16). Somatostatin or its analogs should be considered the pharmacologic therapy of choice for control of acute variceal hemorrhage because of their efficacy and safety profile. Combination therapy with octreotide or vapreotide with endoscopic sclerotherapy or band ligation results in improvement in control of bleeding and reduced transfusion requirements (16,27). The management of bleeding, gastric varices from portal hypertensive gastropathy is more problematic. Conventional sclerotherapy or variceal band ligation is ineffective for gastric variceal bleeding. Endoscopic injection of gastric varices with N-butyl-2-cyanoacrylate has proven efficacy, as has a detachable mini-snare in small, uncontrolled trials (16,27). Balloon tamponade with a Sengstaken-Blakemore tube may be necessary for uncontrollable hemorrhage. This technique is effective in achieving hemostasis in a majority of cases; however, it is limited by the necessity

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to decompress the balloon to prevent ischemia of the gastroesophageal junction. Decompression of the balloon frequently results in recurrent bleeding, which makes balloon tamponade only useful as a temporary adjunct to more definitive therapy (34). Transjugular intrahepatic portosystemic shunts (TIPS) have significantly changed the role of emergency surgical shunting for control of variceal bleeding. The success rate of TIPS for controlling acute bleeding episodes approaches 100% (16). TIPS should now be considered the treatment of choice in patients with variceal hemorrhage that cannot be controlled by pharmacologic and endoscopic maneuvers. The incidence of rebleeding following emergency TIPS is approximately 15% with primary 1-year patency rates around 75%, which improves to up to 95% following revision of stenotic shunts (35). Patients with advanced liver disease who are classified as a Child-Pugh class C have a high mortality rate following TIPS and should be considered for urgent liver transplantation if they are candidates. The MELD score is used to predict mortality following TIPS and should be applied to determine the urgency of transplantation (20). TIPS have been monumental as a rescue procedure for refractory bleeding and allowing patients to survive until transplantation. In addition, TIPS is effective for the management of gastric variceal bleeding as well as esophageal variceal bleeding (16). TIPS also allow elective surgical shunting in Child’s A or B patients after recovery from the initial bleeding episode (36). There have been successful TIPS performed in the presence of cavernous transformation of the portal vein, as well as in venoocclusive disease and Budd–Chiari disease (37–39). TIPS can also be used for acute bleeding in pediatric patients (40). Emergency surgical portosystemic shunting is only rarely indicated now, with the success of current medical and interventional therapy (41). The exceptional patient with refractory bleeding, which cannot be controlled by TIPS, or with portal vein thrombosis should be considered for emergency liver transplantation, with emergency portosystemic shunting reserved for those who are not candidates for transplantation or for whom a donor is not quickly available. End-to-side portocaval shunting is the classical surgical shunt used in the emergency setting. Patients with portal vein thrombosis or severe ascites should undergo a side-to-side shunt, mesocaval shunt, or proximal splenorenal shunt with splenectomy. An emergency distal splenorenal shunt may also be used in appropriately selected patients with a large splenic vein and minimal or controlled ascites. The mortality rate for emergency surgical shunt procedures is between 20 and 55% and correlates most closely with the severity of liver disease. Death following emergency shunt procedures is usually secondary to encephalopathy or progressive liver failure. Splenectomy is the treatment of choice and is usually curative for isolated gastric varices associated with splenic vein thrombosis.

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Prevention of Recurrent Bleeding The incidence of recurrent bleeding after an initial variceal hemorrhage has been reported to be as high as 70%. Prevention of recurrent bleeding should be individualized to each patient, with the ultimate goal being maintaining optimum health until transplantation can be performed. The determinant of the need for liver transplantation is the severity of liver disease by the Child–Pugh score and MELD criteria. Patients with severe liver disease should be managed through pharmacologic and endoscopic therapy, or TIPS in refractory cases or in patients with severe ascites or who are poor surgical candidates. Patients with compensated liver disease (Child’s A or B) are probably best suited for elective surgical shunt procedures (42). A recent matched comparison of 20 Child’s class A or B patients undergoing surgical shunt with 20 class A or B patients undergoing TIPS revealed decreased 30-day mortality and rebleeding rates in the surgical shunt group (42). Prospective randomized trials have demonstrated an advantage to surgical shunting over medical or endoscopic therapy with low mortality when patients and choice of shunt procedure are properly selected (43). The choice of surgical shunt performed depends on the associated manifestations of liver disease as well as the specific patient’s anatomy (Fig. 85.4). A selective shunt, specifically the distal splenorenal shunt (DSRS), is the best option for most patients. The DSRS preserves portal blood flow and therefore has a low incidence of hepatic encephalopathy and maintains stability of liver function. The incidence of hepatic encephalopathy is 5% to 15% following DSRS versus 15% to 40% for nonselective shunts or TIPS (43–47). In a recent series of 81 patients presenting to a transplant center with variceal bleeding who subsequently underwent DSRS, recurrent bleeding occurred in 6.8% and encephalopathy occurred in 14.9% (44). All patients were Child’s A or B and operative mortality was 6%. Long-term survival was 74% at 5 years without transplantation, demonstrating a benefit in selective shunting for compensated cirrhotics to delay the need for transplantation. Other series have reported lower rates of encephalopathy (43,47). Although a more favorable outcome in transplantation has been determined by some centers following TIPS over DSRS, TIPS is best reserved for those patients with more severe liver disease (48). Recurrent bleeding and mortality following DSRS should be 5% to 10% when performed in Child’s A or B patients. Patients with ascites or portal vein thrombosis are best suited for a mesocaval shunt or proximal splenorenal shunt (49). DSRS in these patients may exacerbate the ascites by eliminating mesenteric venous outflow through the splenic vein. Occasionally, a side-to-side portocaval shunt may be required as in Budd–Chiari syndrome but, in most patients, hilar dissection should be avoided to minimize the difficulty of future transplantation. In patients with Budd–Chiari syndrome, early side-

to-side portocaval shunting may halt the progression to cirrhosis (50).

Surgical Techniques The type of incision used depends on the type of shunt anticipated. Portocaval shunts or splenorenal shunts are usually performed through a right or left subcostal incision or chevron incision. These incisions can later be incorporated into a transplant incision. A midline incision may be used as an alternative and is the most appropriate incision for a mesocaval shunt.

Distal Splenorenal Shunt The distal splenorenal shunt (Fig. 85.5) begins with entrance into the lesser sac by dividing the lesser omentum to visualize the pancreas. The gastroepiploic vein should be ligated close to its entrance into the superior mesenteric or portal vein just inferior to the pylorus and superior to the pancreas. The splenocolic ligament should be divided to improve exposure and eliminate collaterals from the colon to the spleen. The peritoneum along the lower border of the pancreas is opened and the pancreas is fully mobilized along its inferior border using cautery and ligatures for any large vessels. The inferior mesenteric vein is identified at this point and traced to its entrance into the splenic or superior mesenteric vein where it is ligated and divided. The pancreas is gently retracted superiorly to expose the splenic vein posteriorly. All pancreatic branches should be carefully ligated with 4–0 or finer silk ligatures. Dividing these pancreatic veins allows complete mobilization of the splenic vein and helps prevent the “pancreatic siphon” effect, which may result in recurrent varices and decreased portal flow in alcoholic liver disease. At this point, the left gastric or coronary vein should be ligated and divided. The renal vein is identified by dissecting the retroperitoneal tissue immediately posterior to the pancreas and to the left of the superior mesenteric artery. This dissection is accomplished with cautery and ligation of large vessels or lymphatics. The adrenal vein is identified and ligated and divided, while the gonadal vein is maintained as an outflow tract. The renal vein should be mobilized sufficiently to allow a Satinsky clamp to be placed anteriorly without tearing the vein or its branches. The original approach to the splenic vein described by Warren and colleagues was through the gastrocolic omentum and the lesser sac. After the splenic vein dissection was complete, the renal vein was approached from beneath the mesocolon as in abdominal aortic surgery. An alternative approach to simplify this procedure is to approach both the splenic vein and left renal vein at the ligament of Treitz through a midline incision (51). In this approach, the pancreas is elevated in order to dissect the splenic vein from its posterior aspect. The left renal vein is then identified and dissected free of its retroperitoneal

FIGURE 85.4 Algorithm for shunt procedures and transplantation. PV, portal vein; DSRS, distal splenorenal shunt; TIPS, transjugular intrahepatic portosystemic shunt.

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FIGURE 85.6 Mesocaval shunt with 8-mm ringed PTFE graft. IVC, inferior vena cava; SMV, superior mesenteric vein. FIGURE 85.5 Distal splenorenal shunt. Portal venous pressure is maintained while gastroesophageal venous pressure is relieved. IVC, inferior vena cava.

Mesocaval Shunt

attachments, including division of the left adrenal and gonadal veins for further mobilization if necessary. This approach simplifies the dissection and reduces operative time. Once the renal vein has been mobilized, and the splenic vein has been circumferentially mobilized and disconnected from pancreatic branches, a small vascular clamp is placed across the splenic vein approximately 1 cm proximal to the junction with the superior mesenteric vein. The splenic vein is then sharply divided leaving about 1 cm of vein proximal to the clamp. This remnant is then oversewn with a running 5–0 Prolene suture and the clamp is removed. It is important not to encroach upon the superior mesenteric vein as portal vein thrombosis may occur. Next, the left renal vein is clamped and a venotomy made in the anterosuperior wall. The splenic vein is trimmed to prevent kinking and is then sewn to the renal vein using a running 5–0 Prolene suture. The vein is flushed with heparin prior to completion of the anastomosis. Once the clamps are removed, flow should go briskly from the splenic vein to the renal vein and should be confirmed by a Doppler probe. Meticulous hemostasis is essential as postoperative bleeding with hypotension may cause decompensated liver failure. Before the patient is discharged from the hospital, it is important to confirm shunt patency and flow. Doppler ultrasound is used in our institution with excellent sensitivity and specificity. Arteriogram is rarely required and should be avoided if possible, because many of these patients have associated renal insufficiency.

The mesocaval shunt (Fig. 85.6) is an important alternative to distal splenorenal shunt for some patients. A mesocaval shunt is the procedure of choice in a patient with portal vein thrombosis or in a patient with uncontrolled ascites in whom a surgical shunt is deemed necessary (49,52). Mesocaval shunts are nonselective shunts; however, a shunt diameter of 8 mm or less maintains portal flow with a low incidence of encephalopathy. A midline incision is used to gain access to the superior mesenteric vein and the infrarenal vena cava. The right colon is mobilized medially to gain exposure to the vena cava as well as the posterior aspect of the superior mesenteric vein. The duodenum must be retracted cephalad, however a complete Kocher maneuver is rarely necessary. The right gonadal vein is ligated and divided at its junction with the vena cava to avoid traction injury to this vein. The gonadal vein also frequently empties at the site to be used for anastomosis. The areolar tissue surrounding the vena cava is divided only to the extent necessary to place a Satinsky clamp safely. Identification of the superior mesenteric vein is best performed by an anterior approach at the base of the transverse mesocolon to the right of the superior mesenteric artery. Once the vein is identified, circumferential dissection to expose the posterior aspect is performed. The posterior side of the vein is used for the anastomosis to prevent kinking of the prosthetic graft. After the superior mesenteric vein is exposed, a Satinsky clamp is placed on the vena cava below the confluence of the left renal vein. A venotomy is made with an 11-blade scalpel and extended using Potts’ scissors. A ringed PTFE 8-mm graft cut at an angle is used as the conduit. The venotomy is flushed with heparin solution and the graft is

Chapter 85 Portal Hypertension

sutured to the vena cava in an end-to-side fashion using a running 5–0 Prolene suture. The graft is then filled with heparin solution and clamped so that the vena cava clamp can be removed to restore caval flow. A smaller Satinsky clamp is then placed on the posterior aspect of the superior mesenteric vein and a venotomy is made, again using an 11-blade scalpel, and extending the venotomy using Potts’ scissors. The graft is cut to an appropriate length to prevent kinking and to prevent compression against the third portion of the duodenum. The superior mesenteric venous anastomosis to the graft is then performed using a running 5–0 Prolene suture begun cephalad, with the left side of the anastomosis accomplished from the inside of the vein which is tied to a second suture on the caudad end of the venotomy. The right side of the anastomosis is then performed from outside the vein. The clamps are then removed and the graft should immediately fill with blood. Patency and flow direction can be confirmed using a Doppler probe and sequentially compressing the cephalad and caudad ends of the superior mesenteric vein and vena cava. Once hemostasis is assured, the patient should be systemically anticoagulated with heparin followed by coumadin. Prior to discharge, flow is confirmed using Doppler ultrasonography. Diuretic therapy with furosemide with or without spironolactone is used to prevent ascites formation.

Portocaval Shunts Portocaval shunts (Fig. 85.7) were historically used as the primary surgical management of acute variceal hemorrhage. Portocaval shunts are performed either end-toside, in which case the hepatic end of the portal vein is oversewn, or side-to-side allowing continuation of portal flow (Figs. 85.5 and 85.7) These operations have essentially been replaced in the management of emergency bleeding by TIPS, although in select patients they may still be necessary. The end-to-side portocaval shunt is the procedure of choice for Budd–Chiari syndrome if detected early before cirrhosis is established. Portocaval shunts are performed through a right subcostal incision or a chevron incision. The dissection should proceed from the right side, beginning with mobilization of the hepatic flexure of the colon. There may be large collateral veins through the hepatic flexure that must be ligated. The round ligament is divided and the falciform ligament is divided to gain exposure to the porta hepatis. A self-retaining retractor is placed to retract the colon and duodenum inferiorly and the liver and gallbladder superiorly. The gallbladder can be manually decompressed but cholecystectomy should be avoided because of infectious risk. Dissection into the porta hepatis is initiated from the right and posterior to the common bile duct. Care should be taken to identify a replaced right hepatic artery, which would lie posterior to the bile duct if present. The neural and lymphatic tissue lateral and posterior to the bile duct and portal vein is ligated and divided to decrease bleeding and ascites leak. The gastrohepatic

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FIGURE 85.7 Side-to-side portocaval shunt. IVC, inferior vena cava.

ligament is partially divided to gain access to the left side of the portal vein. The lymphatics on the left are divided as well, taking care not to injure the left or proper hepatic artery. The coronary vein and right gastric vein should be ligated to aid in mobilizing the portal vein and in preventing recurrent varices. The gastroepiploic vein should also be ligated to prevent recurrent variceal bleeding. Likewise on the right side, pancreatic branches may be divided to mobilize the vein. There is usually no need to dissect anteriorly in the porta hepatitis. The portal vein should be exposed from the confluence of the superior mesenteric vein and splenic vein to just proximal to the bifurcation in the porta hepatis in order to perform a tension-free anastomosis. After the portal vein has been fully mobilized, the infrahepatic vena cava is exposed by incising the overlying peritoneum inferior to the caudate lobe using electrocautery. Some of the short hepatic veins draining the caudate lobe may have to be divided to expose the vena cava. The first and second portions of the duodenum are reflected to expose the vena cava from the renal veins to the caudate lobe anteriorly and laterally. The vena cava exposure must be sufficient to allow placement of a Satinsky clamp anterolaterally above the renal veins. Before the anastomosis is performed, it is important to measure the portal vein pressure and vena cava pressure using a 20-gauge needle connected to a manometer. Once exposure of the portal vein and vena cava is complete, the hepatic arteries and bile duct are retracted anteriorly and to the right using a vessel loop. For an end-to-side portocaval shunt, the portal vein is clamped with a small vascular clamp distal to the confluence of the superior mesenteric vein and splenic vein and approximately 1 cm proximal to the por-

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tal vein bifurcation. The portal vein is transected, leaving a 1-cm cuff of vein on the clamp which is oversewn with a 4–0 Prolene suture. The vena cava Satinsky clamp is then applied and a venotomy made in the vena cava anteriorly using an 11-blade scalpel and Potts’ scissors. The portal vein end is cut at an angle to prevent kinking and the anastomosis is performed using a 4–0 Prolene suture placed at the cephalad and caudad ends of the venotomy. The left side of the anastomosis is accomplished from inside the vein beginning cephalad and running caudad where the suture is tied. The right side of the anastomosis is performed by running the cephalad suture outside the vein and tying to the inferior suture. The portal vein clamp is then removed followed by the cava clamp. Flow is confirmed using a Doppler probe and the portal vein pressure is measure using needle manometry. A side-to-side portocaval shunt is performed in a similar fashion except that a single small Satinsky clamp is placed on the portal vein at a point, which can be approximated to the vena cava. The anastomosis performed in this instance should be performed in identical fashion with an 8 to 10 mm diameter in order to maintain hepatic portal perfusion. If there is too much tension to allow anastomosis of the portal vein to the vena cava directly, an H-graft may be performed using an 8-mm diameter reinforced PTFE graft. If a graft is used, the graft is beveled and sewn to the portal vein first, sewing the left side from within and the right side from outside using a 5–0 suture. The vena cava anastomosis is then performed sewing the left side from within and the right side from the outside. The graft is flushed with heparin and systemic anticoagulation is used once the variceal bleeding is stopped. The principal advantages of a side-to-side portocaval shunt are in maintaining hepatic perfusion and decreasing hepatic encephalopathy.

Budd–Chiari Syndrome Budd–Chiari syndrome (BCS) is caused by outflow obstruction of the hepatic veins or vena cava near the ostia of the hepatic veins. This syndrome, described by Budd in 1845 and Chiari in 1899, produces intense congestion of the liver resulting in hepatomegaly ascites and portal hypertension. There is usually a history of some predisposing factor such as autoimmune disorders, hypercoagulable states, connective tissue disorders, hematologic disorders, infections, or neoplasm. The incidence appears to be increasing and is associated with oral contraceptive use. Venoocclusive disease is similar in presentation but is characterized by obliteration of the sublobular branches of the hepatic veins. Venoocclusive disease is usually associated with toxin exposure or following antineoplastic chemotherapy or bone marrow transplantation. The course of BCS can be a fulminant process with liver failure progressing over a few weeks to a few months, or it may take a more chronic course over months to years with findings consistent with cirrhosis. Abdominal distention

is the most consistent finding in all patients, and is associated with hepatomegaly and ascites. Once the diagnosis of BCS is suspected, hepatic venography should be performed to ascertain the degree and level of obstruction and to determine the venous gradient across the obstruction as well as hepatic venous wedge pressure if possible. In some cases, interventional techniques such as dilation of the vena cava or TIPS may be indicated. A liver biopsy is essential to determine the extent of liver damage. Cirrhosis usually develops within 3 months if left untreated. Therapy for BCS involves all aspects of medical, endoscopic, interventional, and surgical management of portal hypertension. The primary determinant of which definitive therapeutic approach is indicated is the liver biopsy. In the early stages of BCS before cirrhosis occurs, a side-to-side portocaval shunt may prevent the progression to cirrhosis and eliminate associated symptoms (50). In patients with vena cava stenosis, a mesoatrial shunt may halt the progression of disease, although radiologic dilation and stenting may be effective and should be attempted if technically feasible (50,53,54). A recent series in England demonstrated relief of obstruction in 14 of 18 patients undergoing hepatic vein or vena cava dilation in conjunction with thrombolysis and stenting in some patients (54). This approach may be useful in up to 35% of patients presenting with BCS, although repeated dilations are frequently necessary. We have had success in our institution with interventional balloon dilation of suprahepatic vena cava stenosis without stenting. Liver histology normalized and symptoms abated after successive dilations performed at 4-week intervals over 3 months. Acute variceal hemorrhage may be controlled using TIPS in patients with BCS or venoocclusive disease (38,39). Patients with fulminant hepatic failure, a failed shunt procedure, or those who have developed cirrhosis should be evaluated for possible liver transplantation. Long-term anticoagulation should be used following shunting or liver transplantation for BCS.

Portal Hypertension in Children Children presenting with signs and symptoms of portal hypertension usually have presinusoidal obstruction due to portal vein thrombosis or atresia (55,56). Frequently there is a history of umbilical vein catheterization, transfusion, or omphalitis. The most common intrahepatic causes of portal hypertension in children are congenital hepatic fibrosis and cirrhosis from biliary atresia, cystic fibrosis, a1-antitrypsin deficiency, and autoimmune or viral hepatitis. Variceal bleeding is a common presentation of portal hypertension in children. The evaluation of a child with variceal bleeding should begin with endoscopy and ultrasonography of the portal vein. The management of bleeding varices is analogous to that in adults utilizing pharmacotherapy, endoscopic banding and

Chapter 85 Portal Hypertension

sclerotherapy, TIPS, surgical shunting, and liver transplantation. The type of shunt performed in children may differ from adults in the situation with portal vein thrombosis. A mesocaval shunt or proximal splenorenal shunt is the preferred shunt, however the J shunt devised by Clatworthy, in which the IVC is divided and anastomosed to the superior mesenteric vein in an end-to-side fashion, has been our preferred approach for small children. This procedure has a low incidence of thrombosis and is well tolerated in infants. A proximal splenorenal shunt is an effective alternative in children with portal vein thrombosis and may be preferred in larger children. A distal splenorenal shunt is feasible in children with a patent portal vein and cirrhosis and can be performed in vessels 1 cm in diameter. Portocaval shunting may be indicated in isolated cases (57). Surgical shunting has been shown to have a demonstrable reduction in splenic size and splenic pulp pressure in patients with noncirrhotic portal hypertension and portal vein obstruction (58). TIPS is successful in controlling acute bleeding and should be implemented in children awaiting transplantation (40,55). Acute bleeding in a child is an indication for urgent transplantation.

Devascularization and Esophageal Transection Surgical shunting is not possible in some patients because of extensive portal and mesenteric venous thrombosis. In these rare instances, esophageal devascularization and transection may be the only option to prevent recurrent variceal bleeding. Sugiura and Futagawa described a technique in 1973 whereby the distal esophagus and proximal stomach are devascularized, combined with stapled esophageal transection and splenectomy (Fig. 85.8). This procedure requires thoracic and abdominal incisions performed 4 to 6 weeks apart. Modifications of this procedure utilizing a left subcostal incision, splenectomy, and paraesophagogastric devascularization with esophageal transection using a circular stapler have had similar success. These procedures have a high operative morbidity and mortality and with advancements in nonsurgical therapy are rarely indicated.

Liver Transplantation The only potential cure for portal hypertension and endstage liver disease is liver transplantation. Any patient with manifestations of portal hypertension and liver disease should be managed in such a way as to potentiate transplantation. Liver transplantation was initially sought only as a treatment of last resort for moribund patients and was associated with tremendous blood loss and long operative times. Technical advances such as elimination of venovenous bypass and elimination of biliary

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stenting have streamlined the operation in our experience with mean operative time of 4 hours and median blood transfusion requirements of 7 units. Advances in immunosuppressive therapy have resulted in 1-year survival rates of 90%. The principal limitation to liver transplantation is the shortage of donor organs. There are currently over 17,000 patients on the liver waiting list with approximately 4500 liver transplants performed yearly in the US. Living donor liver transplantation utilizing the right lobe in adults or left lateral segment in children has become a successful method to increase the number of donor organs available. Split-liver transplantation using the right lobe of a cadaveric organ for an adult and left lateral segment for a child is another method being used to increase the number of donor organs. Currently liver allocation is based on Pugh’s modification of the Child–Turcotte classification. The MELD score is undergoing final validation before implementation and is based on the premise that mortality following portosystemic shunting is determined by the degree of liver disease. Although the MELD score does not directly consider symptoms of portal hypertension, it does consider renal insufficiency, which is associated with severe portal hypertension in cirrhotics. Because of the shortage of donor organs and allocation to those patients with end-stage liver disease, it is even more important to utilize every means available to manage portal hypertensive bleeding. While surgical shunting has been performed less frequently in recent years, a resurgence in appropriate shunting procedures is in order for managing variceal bleeding in well compensated cirrhotics.

References 1. Banti G. La splenomegalia con cirrosi epatica. Sperimentale 1894;48:407. 2. Hallion L, Francois-Franck CA. Recherches experimentales executees a l’aide d’un nouvel appareil volumetrique sur l’innervation vaso-motrice intestinale. Arch Physiol Norm Pathol (Paris) 1896;8:493–508. 3. McIndoe AH. Vascular lesions of portal cirrhosis. Arch Pathol Lab Med 1928;5:23–42. 4. McMichael J. Portal circulation: action of adrenaline and pituitary pressor extract. J Physiol (Lond) 1932;75:241–263. 5. Thompson WP, Caughey JL, et al. Splenic vein pressure in congestive splenomegaly (Banti’s syndrome). J Clin Invest 1937;16:571–572. 6. Rikkers LF. Surgical complications of cirrhosis and portal hypertension. In Sabiston DC, ed. Textbook of Surgery, 14th edn. Philadelphia, PA: WB Saunders, 1991:1020. 7. Warren WD, Zeppa R, Fomon JJ. Selective transsplenic decompression of gastroesophageal varices by distal splenorenal shunt. Ann Surg 1967;166:437–455. 8. Crafoord C, Frenckner P. New surgical treatment of varicose veins of the oesophagus. Acta Otolaryngol (Stockh) 1939; 27:422–429.

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9. Merigan TC, Plotkin GR, Davidson CS. Effect of intravenously administered posterior pituitary extract on hemorrhage from bleeding esophageal varices: a controlled evaluation. N Engl J Med 1962;266:134–135. 10. LeBrec D, Poynard T, et al. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study. N Engl J Med 1981;305:1371–1374. 11. Burroughs AK, McCormick PA, et al. Randomised double-blind placebo controlled trial of somatostatin for variceal bleeding: emergency control and prevention of early variceal rebleeding. Gastroenterology 1990;99:1388–1395. 12. Starzl TE, Groth GG, et al. Orthotopic homotransplantation of the human liver. Ann Surg 1968;168:392–415. 13. Rosch J, Hanafee WN, Snow H. Transjugular portal venography and radiological portosystemic shunt: an experimental study. Radiology 1969;92:1112–1114. 14. Blumgart LH, Hann LE. Surgical and radiologic anatomy of the liver and biliary tract. In: Blumgart LH, ed. Surgery of the Liver and Biliary Tract, 3rd edn. Vol 1. Edinburgh, UK: WB Saunders, 2000:3–33. 15. Mathie RT, Wheatley AM. Liver blood flow: physiology, measurement and clinical relevance. In: Blumgart LH, ed. Surgery of the Liver and Biliary Tract, 3rd edn. Vol 1. Edinburgh, UK: WB Saunders, 2000:85–107. 16. Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med 2001;345:9:669–681. 17. Nolte W, Ehrenreich H, et al. Systemic and splanchnic endothelin-1 plasma levels in liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS). Liver 2000;20:60–65. 18. Garcia-Tsao G, Groszman RJ, et al. Portal pressure, presence of gastroesophageal varices and variceal bleeding. Hepatology 1985;5:419–424. 19. Child CG. The Liver and Portal Hypertension. Philadelphia, PA: WB Saunders, 1964:4. 20. Wiesner RH, McDiarmid SV, et al. MELD and PELD: application of survival models to liver allocation. Liver Trans 2001;7:7:567–580. 21. Dick D, Loss JE Jr, et al. Increasing incidence of hepatocellular carcinoma in patients with hepatitis C cirrhosis undergoing liver transplantation. Hepatology 2000;32(4):261A. 22. Fisher NC, Wilde JT, et al. Deficiency of natural anticoagulant proteins C, S, and antithrombin in portal vein thrombosis: a secondary phenomenon? Gut 2000;46:534–539. 23. Leyendecker JR, Rivera E Jr, et al. MR angiography of the portal venous system: techniques, interpretation, and applications. Radiographics 1997;17(6):1425–1443. 24. D’Amico G, Pagliaro L, Bosch J. The treatment of portal hypertension: a meta-analytic review. Hepatology 1995;22:332–354. 25. The North Italian Endoscopic Club for the Study and Treatment of Esophageal Varices. Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver and esophageal varices: a prospective multicenter study. N Engl J Med 1988;319:983–989. 26. Schepis F, Camma C, Niceforo D. Which patients with cirrhosis should undergo endoscopic screening for esophageal varices detection? Hepatology 2001;33:333–338.

27. Binmoeller KF, Borsatto R. Variceal bleeding and portal hypertension. Endoscopy 2000;32(3):189–199. 28. Lo GH, Lai KH, et al. Emergency banding ligation versus sclerotherapy for the control of active bleeding from esophageal varices. Hepatology 1997;25:1101–1104. 29. Stiegmann GV, Goff JS, et al. Endoscopic sclerotherapy as compared with endoscopic ligation for bleeding esophageal varices. N Engl J Med 1992;326:1527–1532. 30. Sarin SK, Guptan RK, et al. A randomized controlled trial of endoscopic variceal band ligation for primary prophylaxis of variceal bleeding. Eur J Gastroenterol Hepatol 1996;8:337–342. 31. Grace ND. Prevention of initial variceal hemorrhage. Gastroent Clin N Am 1992;21:149–161. 32. Lay CS, Tsai Y, et al. Endoscopic variceal ligation in prophylaxis of first variceal bleeding in cirrhotic patients with high-risk esophageal varices. Hepatology 1997;25:1346–1350. 33. Sarin SK, Lamba GS, et al. Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding. N Engl J Med 1999;340:988– 993. 34. Moreto M, Zaballa M, et al. A randomized trial of tamponade or sclerotherapy as immediate treatment for bleeding esophageal varices. Surg Gynecol Obstet 1988;167:331–334. 35. Fillmore DJ, Miller FJ, et al. Transjugular intrahepatic portosystemic shunt: midterm clinical and angiographic follow-up. J Vasc Intervent Radiol 1996;7:255–261. 36. Selim N, Fendley MJ, et al. Conversion of failed transjugular intrahepatic portosystemic shunt to distal splenorenal shunt in patients with Child A or B cirrhosis. Ann Surg 1998;227:4:600–603. 37. Kawamata H, Kumazaki T, et al. Transjugular intrahepatic portosystemic shunt in a patient with cavernomatous portal vein occlusion. Cardiovasc Intervent Radiol 2000;23(2):145–149. 38. Azoulay D, Castaing D, et al. Transjugular intrahepatic portosystemic shunt (TIPS) for severe veno-occlusive disease of the liver following bone marrow transplantation. Bone Marrow Trans 2000;25:987–992. 39. Michl P, Bilzer M, et al. Successful treatment of chronic Budd–Chiari syndrome with a transjugular intrahepatic portosystemic shunt. J Hepatol 2000;32:516–520. 40. Johnson SP, Leyendecker JR, et al. Transjugular portosystemic shunts in pediatric patients awaiting liver transplantation. Transplantation 1996;62(8):1178–1181. 41. Rikkers LF, Jin G. Emergency shunt: role in the present management of variceal bleeding. Arch Surg 1995;130:472–477. 42. Helton WS, Maves R, et al. Transjugular intrahepatic portosystemic shunt vs surgical shunt in good-risk cirrhotic patients. Arch Surg 2001;136:17–20. 43. Orozco H, Mercado MA, et al. A comparative study of the elective treatment of variceal hemorrhage with betablockers, transendoscopic sclerotherapy, and surgery: a prospective, controlled, and randomized trial during 10 years. Ann Surg 2000;232(2):216–219. 44. Jenkins RL, Gedaly R, et al. Distal splenorenal shunt: role, indications, and utility in the era of liver transplantation. Arch Surg 1999;134:416–420.

Chapter 85 Portal Hypertension 45. Orozco H, Mercado MA, et al. Selective shunts for portal hypertension: current role of a 21-year experience. Liver Transpl Surg 1997;3(5):475–480. 46. Henderson JM. Selective shunts in the 1990s. Liver Transpl Surg 1997;3(5):552–555. 47. Becker YT, Reed G, et al. The role of elective operation in the treatment of portal hypertension. Am Surg 1996;62:171–177. 48. Abouljoud MS, Levy MF, et al. A comparison of treatment with transjugular intrahepatic portosystemic shunt or distal splenorenal shunt in the management of variceal bleeding prior to liver transplantation. Transplantation 1995;59(2):226–229. 49. Rikkers LF. The changing spectrum of treatment for variceal bleeding. Ann Surg 1998;228(4):536–546. 50. Orloff MJ, Girard B. Long-term results of treatment of Budd–Chiari syndrome by side-to-side portacaval shunt. Surg Gynecol Obstet 1989;168:33–41. 51. Bowen JC, Vauthey JN, et al. Long-term results after distal splenorenal shunt. Dig Surg 1988;5:201–206. 52. Mercado MA, Morales-Linares JC, et al. Distal splenorenal shunt versus 10-mm low-diameter mesocaval shunt for variceal hemorrhage. Am J Surg 1996;171:591– 595. 53. Olzinski AT, Sanyal AJ. Treating Budd–Chiari syndrome: making rational choices from a myriad of options. J Clin Gastroenterol 2000;30(2):155–161. 54. Griffith JF, Mahmoud AEA, et al. Radiological intervention in Budd–Chiari syndrome: techniques and outcome in 18 patients. Clin Radiol 1996;51:775–784.

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55. Bismuth H, Fecteau AH. Portal hypertension in children. In: Blumgart LH, ed. Surgery of the Liver and Biliary Tract, 2001;2:1907–1915. 56. Goh DW, Myers NA. Portal hypertension in children: the changing spectrum. J Pediatr Surg 1994;29:688–691. 57. Corbeel L, Lierde SV, Jaeken J. Long-term follow-up of portacaval shunt in glycogen storage disease type 1B. Eur J Pediatr 2000;159:268–272. 58. Sharma BC, Singh RP, et al. Portal vein hypertension: effect of shunt surgery on spleen size, portal pressure and oesophageal varices in patients with non-cirrhotic portal hypertension. J Gastro Hepatol 1997;12:582–584. 59. Fleet M, Stanley AJ, et al. Transjugular intrahepatic portosystemic stent shunt placement in a patient with cystic fibrosis complicated by portal hypertension. Clin Radiol 2000;55:236–247. 60. Tajiri T, Onda M, et al. Comparison of the long-term results of distal splenorenal shunt and esophageal transection for the treatment of esophageal varices. Hepato-Gastroenterol, 2000;47:1619–1621. 61. Kanaya S, Katoh H. Long-term evaluation of distal splenorenal shunt with splenopancreatic and gastric disconnection. Surgery 1995;118(1):29–35. 62. Jin G, Rikkers LF. Transabdominal esophagogastric devascularization as treatment for variceal hemorrhage. Surgery 1996;120(4):641–649. 63. Eason JD, Loss GE, et al. Steroid-free liver transplantation using rabbit antithymocyte globulin induction: results of a prospective randomized trial. Liver Transpl 2001;7(8):693–697.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART XII Venous and Lymphatic Surgery

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 86 Clinical Application of Objective Testing in Venous Insufficiency John J. Bergan and Warner P. Bundens

Venous insufficiency manifests itself in different ways. Its appearance varies from simple telangiectatic blemishes to severe chronic leg ulcer in an edematous, pigmented leg. Symptoms also vary from the essentially asymptomatic limb to that with disabling post-exercise pain. Manifestations of venous insufficiency include various conditions such as telangiectasias, varicose veins, and axial incompetence. These are easily treated. In contrast, venous insufficiency may be refractory to treatment as in the severely damaged post-thrombotic limb which manifests segmental occlusion in combination with universal reflux. Desirability of accurate, objective testing which can quantitate venous insufficiency and guide effective therapy is obvious. Much progress has been made toward this end. Most of this progress has occurred since the last edition of this textbook. There has been perfection of noninvasive testing as well as improved imaging. It is the objective of this chapter to furnish a perspective on this progress.

Essential Background Earliest tests of venous pathophysiology, including the Trendelenburg and Perthes tests, assisted in defining the importance of venous reflux and obstruction. However, in recent years, when assessed by objective techniques, they have proven to be unreliable, misleading, and even impossible to perform (1). Venous pressure measurements in the static state and in the post-exercise condition also contributed knowledge

about venous physiology and pathophysiology (2). Because of their objectivity, they became the standard against which other methods of investigation were tested (3). In practice, post-exercise venous pressure recovery time using tourniquet obstruction of superficial venous flow assisted in separating patients with pure superficial venous reflux from those with deep venous insufficiency. This proved to be a theoretical advance as pressure measurements were invasive, nonrepeatable, and could not be used in screening. A variety of noninvasive tests became available and were proposed to substitute for various pressure determinations in quantitation of venous insufficiency (4). These included photoplethysmography (PPG) (5), mercury strain-gauge plethysmography (6), Doppler testing (7), and ascending (8) and descending phlebography (9). These imaging techniques gave anatomic information which could be used in patient evaluation and in planning therapy. The three plethysmographic techniques of assessing venous function, photoplethysmography, mercury strain gauge plethysmography, and light reflection rheography (10) were especially appealing to investigators. They could be, and were, compared to the standard venous pressure recovery time, were noninvasive, and purported to separate superficial from deep venous incompetence. In practice, these indirect techniques, dependent upon tourniquet efficacy, proved inaccurate and therefore inadequate. Photoplethysmography was shown to correlate only with visible skin changes (11). Though it was proven to detect venous dysfunction (12), it was not specific in identifying

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precise vein segment dysfunction nor pathologic process. Therefore, the photoplethysmographic examination proved to be sensitive but it had poor specificity.

CEAP Classification An international ad hoc committee of the American Venous Forum developed the CEAP classification for chronic venous disease in 1994. The goal was to stratify clinical levels of venous insufficiency. The four categories selected for classification were: clinical state (C), etiology (E), anatomy (A), and pathophysiology (P). The CEAP classification (13) has been endorsed worldwide despite its acknowledged deficiencies. It has been adopted as a standard in many clinics in Europe, Asia, and South America and is considered the only modern method for reporting data in the United States.

Diagnostic Approach The first step in evaluating a patient with chronic venous disease is to establish his clinical class. The next is to correlate the symptoms. These place the limb being examined into one of the classes shown in Table 86.1. The patient’s clinical class will dictate need for further evaluation. In patients with telangiectasias (class 1), the evaluation can be limited to a physical examination and evaluation of the superficial venous system with a hand-held continuous-wave Doppler. Patients with symptomatic class 2 varicosities and class 4, 5, and 6 skin changes require a duplex venous reflux examination because surgical intervention is indicated. Recalcitrant cases may require more extensive imaging studies to detect venous occlusive disease. Physiologic testing can be relegated to documentation rather than to diagnosis, and phlebography done only when venous reconstruction is contemplated.

function but only crudely indicated directions in specific care. For example, the PPG examination, in which an above-knee tourniquet normalized venous refill time, suggested reflux through the long saphenous system, while refill time normalization with a below-knee tourniquet suggested short saphenous venous incompetence. Such testing did not take into consideration reflux into the long saphenous system originating in sites away from the saphenofemoral junction such as the below-knee tributary veins. The continuous-wave Doppler instrument proved to be an advance toward more specific identification of segmental reflux (14). It could identify long saphenous reflux of nonjunctional origin and could identify limbs in which stasis symptoms and visible varicosities were of nonsaphenous origin (15). However, the continuouswave Doppler could not isolate reflux in individual veins, one from another. It detects velocity of blood flow from any vein lying in the path of the ultrasound beam (16). At femoral level, for example, detected reflux might have as its origin the femoral vein, the saphenous vein, a venous anomaly, or a duplicated long saphenous vein. Duplex technology has markedly changed evaluation of venous function (Fig. 86.1). The B-mode ultrasound component allows imaging of the superficial and deep veins (17). Then venous flow can be assessed by observation of the intraluminal moving echoes produced by red blood cell microaggregates (18). Flow toward and away from the heart can be color coded to allow more rapid vessel identification as well as presence or absence of pathologic reflux flow. Venous valves can be identified, their leaflets often seen as normal, shortened, thickened, nonfunctional, or functional. Duplex patient examination is most frequently done for detection of deep venous thrombosis. Because in this

Duplex Assessment of Venous Reflux Prior to noninvasive imaging of the lower extremity venous system, testing methods detected altered venous

TABLE 86.1 CEAP clinical classification (modified from reference 5) Class 0 Class 1 Class 2 Class 3 Class 4 Class 5 Class 6

No visible or palpable signs of venous insufficiency Telangiectasias and/or reticular varicosities Varicose veins Edema Hyperpigmentation, dermatitis Healed venous ulceration Open venous ulceration

A suffix “A” or “S” is added to designate asymptomatic or symptomatic status of the limb. No suffix is needed for classes 4, 5, and 6.

FIGURE 86.1 Doppler duplex examination allows clear visualization of venous structures such as this beginning venous aneurysm, an eccentric blowout just distal to an incompetent valve.

Chapter 86 Clinical Application of Objective Testing in Venous Insufficiency

examination the patient is supine, a common error occurs in duplex venous examination for reflux. In the supine subject, the venous valves are open in a floating position. Even where there is no flow, the valves remain open. Valve closure requires a reversal of flow with a pressure gradient which is higher proximally than distally. In the supine individual, manual compression proximally does not reliably produce the requisite pressure gradient and sufficient flow velocity (30 cm/s) in a distal direction to effect valve closure. While a Valsalva maneuver can close proximal valves such as the iliofemoral, distal valve closure of the popliteal and crural levels is not accomplished. Thus, venous valve function cannot be assessed reliably in a supine individual.

Reflux Examination Development The Valsalva maneuver is time-honored in examinations for venous reflux. However, experience teaches that a competent valve in the iliofemoral axis negates the examination of inducing reverse flow at distal levels. Therefore, in developing a standardized test of venous reflux applicable to a wide variety of patients with varying severity of venous insufficiency, it has been necessary to utilize release of distal compression as a stimulus for reflux.

Quantitative Measurement of Venous Reflux During 1989, two reports confirmed the possibility of standardizing tests of venous valve reflux by duplex scanning (19,20). The University of Washington group studied patients in the supine and standing positions (19). The group from the Irvine Laboratory at St Mary’s Hospital, London, examined patients in the standing position and compared results with ambulatory venous pressure measurements (20). Both groups used duplex scanning and pneumatic cuffs capable of rapid inflation and deflation. The Washington group used a 24-cm thigh cuff, a 12-cm calf cuff, and a 7-cm foot cuff. The London group used a 10-cm calf cuff. The sites examined included the common femoral vein, the superficial femoral vein, the deep femoral vein, the posterior tibial vein midway between knee and ankle (the posterior tibial vein at the ankle for the Washington group), and saphenofemoral and saphenopopliteal junctions (the medial aspect of the leg for the London group). Both groups used a standard pressure of 100 mmHg in the calf cuff to produce cephalad flow, and recordings were made during deflation and for 4 seconds after deflation. Duplex scanning allows measurement of the diameter of the vessel in longitudinal and cross-sectional views. The Doppler sample volume is adjusted to insonate the whole lumen of the vessel (wall to wall); the cross-sectional area of the vessel is calculated by the system software. The time average velocity of the whole duration of reflux is calculated from the Fast-Fourier spectrum of the reflux when

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the angle of insonation and diameter of the vessel are known. Peak reflux velocity is obtained by placing the cursor at the point of peak reflux. Calculation is performed by system software. The Washington group pointed out that new duplex testing requires comparison with a standard, previously acceptable test in order to achieve utility. However, in assessing venous reflux, the historically important tests such as descending phlebography and recording of ambulatory venous pressures are themselves flawed. In descending phlebography, presence of a competent valve in the proximal system prevents evaluation of distal areas. Furthermore, examination in the upright position, as required by descending phlebography, is hampered by a higher specific gravity of the contrast media compared with blood. In addition, the examinations are not usually done after calf muscle pump contraction. Ambulatory venous pressure measurements are flawed by the presence of deep venous obstruction at any level. Also, as indicated previously, use of tourniquets during precise measurement recording fails to differentiate accurately deep, superficial, and perforator incompetence. Although the St Mary’s group described the taking of ambulatory venous pressure measurements and the performance of ascending phlebography, they failed to correlate these precisely with quantification of venous reflux. On the other hand, they did verify the reproducibility of the technique by studying seven legs six times on the same day. Also, in patients with severe venous stasis, separation of patients with liposclerosis and/or ulceration from those without was demonstrated by flow at peak reflux. Reflux greater than 10 mL/s correlated with severe skin and subcutaneous changes. Further, the St Mary’s studies showed that perforator vein reflux was important, but it was not possible to quantify this flow because of the irregular course of perforating veins and their location in the leg, which prevented use of a pneumatic cuff.

The Examination Stand As examination of the patient with varicose veins and suspected venous reflux requires that the patient be standing, an examination stand has been designed and manufactured. The characteristics of this stand are as follows: examination platform 18 ¥ 12 inches, platform height 18.5 inches, height of handrail, 48 inches, and height of each step 6 inches (Fig. 86.2B). In practice, the vascular sonographer can sit on the top step or a separate stool while the patient stands and the non-weightbearing limb is examined. It is recommended that the terms long saphenous vein (LSV) and short saphenous vein (SSV) be used rather than greater saphenous vein (GSV) and lesser saphenous vein (LSV) to avoid confusion. Similarly, the term superficial femoral vein should be replaced by the term femoral vein (21).

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FIGURE 86.2 The examination stand as illustrated allows the sonographer to be seated, work at eye level, and perform the examination without assistance.

TABLE 86.2 Interrogation points in the venous reflux examination Common femoral vein Femoral vein Upper third Distal third Popliteal vein Gastrocnemius (sural) veins Saphenofemoral junction* Saphenous vein, above the knee Saphenous vein, below the knee Saphenopopliteal junction† Mode of termination, short saphenous vein *Record diameter of the refluxing long saphenous vein.

†Record distance from floor.

Examination Protocol The protocol includes interrogation of specific points as listed in Table 86.2. The patient is examined in an upright position when leg veins are maximally dilated. The full length of the axial venous system from ankle to groin is examined. The extremity is scanned with the probe in a transverse position which allows identification of specific named veins and their relation to other limb structures. The veins are scanned by moving the probe up and down along their course. Double segments, sites of tributary confluence, and large perforating veins as well as their deep venous connections are identified. Varicose veins are often arranged in multiple parallel channels. It is a waste of time to follow reflux into all of the varicose clusters because these are obvious to the treating physician. The patient is standing free of lower extremity clothing from the waist down except for non-constricting underwear (Fig. 86.3). Of particular importance is instruction to the patient to inform the ultrasonographer of any lightness, faint feelings, dizziness, or nausea. These

FIGURE 86.3 With the patient standing, the nonweightbearing extremity is examined by the seated sonographer. The miniaturized ultrasound unit in this photo is enhanced by a large monitoring screen.

symptoms seem to be associated with the overall atmosphere of the room and the presence of Doppler velocity signals. These symptoms appear less in patients when the examination itself is performed silently. If such tendency to fainting because of vagovagal reflux is encountered, the examination may need to be modified with the patient in the semi-upright but lying position. The miniaturized ultrasound unit has greatly enhanced the ease of scanning as the instrumentation is lightweight and easily movable (Fig. 86.4). It is positioned close to the sonographer and best resolution is obtained using the soft tissue setting. This gives best edge definition to the vessels and soft tissues being scanned. The augmentation of flow (distal compression) should be done sharply, quickly, and aggressively and pressure applied to the calf to activate the gastrocnemius and soleus pump. The probe should be angled to provide a 60º or less insonation angle when using the color or pulsed-wave Doppler. Examination should include both lower extremities initially. The CEAP class of each limb should be recorded (Table 86.1). Post-treatment examinations may be targeted to a single extremity or a single area of an extremity. The search for perforating veins should be done in cases of severe chronic venous insufficiency (CVI) with hyperpigmentation, lipodermatosclerosis, healed or open ulcer. The search for perforators need not be done only in patients with venous insufficiency without skin changes at the ankle. Terms in common use in addition to the long saphenous vein and short saphenous vein are Cockett I, II, III

Chapter 86 Clinical Application of Objective Testing in Venous Insufficiency

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FIGURE 86.5 In this transverse ultrasound scan, the skin is uppermost. The hyperechoic superficial fascia and deep fascia surround the saphenous vein and define the saphenous compartment.

FIGURE 86.4 The miniaturized ultrasound unit shown here is highly portable for use in the office, clinic, operating room, and vascular laboratory.

perforating veins, 24-cm perforating vein, Boyd perforating vein, and intersaphenous communicating vein. Other veins can be referred to as unnamed. Perforating veins are defined as those veins which course from the subcutaneous tissue through deep fascia to anastomose with one of the named deep venous structures. Communicating veins are those which anastomose with one another within a single anatomic plane. The long saphenous vein is identified by its relationship to the deep and superficial fascia which ensheathe it, anchoring it to the deep fascia and forming the saphenous compartment (Fig. 86.5). This was first described by Thomson in 1979 (22). High-resolution B-mode ultrasound imaging of the superficial fascia in the transverse plane has shown this to be strongly ultrasound reflective, giving a characteristic image of the saphenous vein called the “saphenous eye” (23). The saphenous eye is a constant marker, clearly demonstrable in transverse sections of the medial aspect of the thigh. This differentiates the saphenous vein from varicose tributaries and other superficial veins. Casual examination of the thigh will often reveal an elongated, dilated vein which is considered to be the long saphenous vein. This opinion is refuted by ultrasound scanning using the anatomical markers of the saphenous eye (24,25). Venous reflux can be elicited manually by squeezing calf muscles, by the Valsalva maneuver, or by pneumatic tourniquet release. In Szendro’s study, standing subjects were examined and manual compression of calf muscles followed by sudden release was used to assess reflux

FIGURE 86.6 This ultrasound scan shows venous reflux using a Valsalva maneuver and reveals vein wall irregularities of old thrombus.

(26). Normal healthy limbs had a duration of reflux of less than 0.5 s. Sarin’s group, using manual calf compression in the standing position showed duration of reflux in limbs with significant venous reflux to exceed 0.5 s in both the deep and the superficial veins (27). van Bemmelen’s study found similar duration of reflux in 95% of the limbs examined (20) and Araki’s study found that there was no difference between pneumatic tourniquet release and manual compression and release (Fig. 86.6) (27). As pneumatic tourniquet release is cumbersome and requires two vascular sonographers, the manual compression and release method has become very attractive. If saphenofemoral reflux of > 0.5 s duration is present, the diameter of the saphenous vein is recorded 2.5 cm distal to the saphenofemoral junction. Present saphenous ablation technology with radiofrequency energy is limited to saphenous veins < 1.2 cm in diameter (29). If saphenopopliteal reflux is

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identified, the type of short saphenous termination is described and the height of the saphenopopliteal junction is recorded. As indicated above, the transverse viewing is used for most of the examination as it gives the best overall view of vessels that are being examined. In the standing patient, longitudinal scanning can be difficult and unnecessarily taxing. A centimeter scale on the vertical supports of the examination stand or a tape measure can be used to indicate significant parts of the examination (30). The examination continues distally along the long saphenous vein, checking for reflux with distal augmentation. Reflux frequently ends in the region of the knee. The point in which reflux stops is noted in centimeters measured from the floor. The femoral vein, formerly termed the superficial femoral vein, is checked for reflux and vein wall irregularities at mid-thigh. The posterior examination is also done on the nonweightbearing lower extremity and the examination begins at the saphenopopliteal junction with special attention being paid to reflux in the popliteal vein, the saphenopopliteal junction, and the gastrocnemius (sural) veins (31). Valsalva may be used to stimulate reflux as well as distal augmentation and release. Valsalva-induced reflux is halted by competent proximal valves. The short saphenous vein is followed from its retromalleolar position on the lateral aspect of the ankle proximally to the saphenopopliteal junction and augmentation maneuvers are used every few centimeters. The termination of the short saphenous vein is noted and if the vein terminates proximally in the vein of Giacomini in the femoropopliteal vein or otherwise, a specific check is made for a connection to the popliteal vein. If the short saphenous vein is refluxing, measurement of the dis-

tance of the saphenopopliteal junction from the floor is recorded. Comparison of venous diameters in refluxing and nonrefluxing veins is shown in Table 86.3. The search for incompetent perforating veins is done only in limbs with chronic venous insufficiency manifested by hyperpigmentation, atrophie blanche, woody edema, scars from healed ulceration, or actual open ulcers. Incompetent perforating veins in limbs without CVI are associated with varicose veins and are controlled by varicose phlebectomy. Identification of perforating veins in the lower extremity can be difficult even for the experienced sonographer. In the calf, there are major groups of medial and lateral perforating veins (32). Five clusters of medial perforating veins are consistent in their location. These connect the posterior arch vein system with the posterior tibial veins. The first three are referred to as the Cockett I, II, and III perforating veins. The 24-cm perforator carries no special name but the highest anteromedial perforating veins is called the Boyd perforator. Localization of these medial perforators is important because they are responsible for nearly 40% of incompetent perforating veins. Lateral calf perforating veins are much more difficult to visualize with duplex ultrasound. In contrast to medial perforating veins, these perforating veins tend to vary in location. In the proximal lateral aspect of the calf, there are two perforating veins that connect the short saphenous vein to the soleal or gastrocnemius vein(s). In the distal lateral aspect of the calf there exist two perforating veins approximately 5 and 12 cm above the os calcis. Once a perforating vein is identified, manual compression can be used to determine reflux. Manual compression is to be applied above and below the transducer.

TABLE 86.3 Comparison of vein diameters in limbs with and without venous reflux No Reflux

Reflux

Vein

n

Diameter (cm)

n

Diameter (cm)

p-Value

Total population CFV LSV POP SSV

202 116 212 215

1.28 (0.25) 0.58 (0.15) 0.88 (0.19) 0.45 (0.14)

57 111 50 48

1.40 (0.31) 0.76 (0.25) 0.89 (0.24) 0.57 (0.22)

0.008 <0.001 >0.30 (NS) <0.001

Females CFV LSV POP SSV

161 84 168 173

1.22 (0.22) 0.57 (0.14) 0.86 (0.18) 0.43 (0.12)

30 83 24 20

1.22 (0.27) 0.75 (0.23) 0.74 (0.18) 0.53 (0.20)

>0.30 (NS) <0.001 0.003 0.036

41 32 44 42

1.52 (0.21) 0.61 (0.17) 0.93 (0.21) 0.53 (0.18)

27 28 26 28

1.60 (0.20) 0.81 (0.31) 1.03 (0.20) 0.60 (0.24)

Males CFV LSV POP SSV Results expressed as mean (SD).

CFV, common femoral vein; LSV, long saphenous vein; POP, popliteal vein; SSV, short saphenous vein; NS, not significant.

0.14 (NS) 0.005 0.061 (NS) 0.228 (NS)

Chapter 86 Clinical Application of Objective Testing in Venous Insufficiency

Relationship of the pressure to the perforator will determine whether there is superficial-to-deep venous blood flow which is physiologically normal. Venous blood flow during pressure from above suggests perforator outflow.

Office Practice The combination of miniaturized ultrasound equipment and an examination stand have considerably simplified the venous reflux examination. The ultrasonographer can perform the entire examination while sitting and can manipulate the equipment and perform stimulus to venous flow without need for a second ultrasonographer (Fig. 86.3). Notation of significant vein diameters and location of anomalous anatomy, perforating veins, and the saphenopopliteal confluence are easily done during the examination. This eliminates the need to resort to memory. Primary varicose veins frequently arise from a normal deep venous system and these connections can be identified by using the technique described above. Although the examination as detailed above appears to be time consuming, it can be done in 30 minutes. It is essential that the ultrasonographer establish good rapport with the responsible surgeon as communication regarding details of the examination are as important as notes taken and the checkpoints recorded. There is a distinct challenge for the vascular sonographer to perform a detailed and relevant venous examination. This requires knowledge of the anatomy of the major veins and their anomalies as well as knowledge of the nomenclature of the relevant veins. A visit to the operating room for increased knowledge of the surgical procedures assists the ultrasonographer to emphasize important portions of the examination. The surgical procedure will be enhanced by knowledge passed by the ultrasonographer to the surgeon as the two comprise a true team to accomplish the best in patient care. The interrogation points selected for the venous reflux examination are based on clinical experience. In Table 86.2, the important interrogation points of reflux in the superficial and deep venous systems are indicated. Presence or absence of reflux should be a part of the ultrasonographer’s report. These serve only as minimal guidelines because the interested ultrasonographer will trace out duplicated veins and note reflux in major tributaries such as the anterolateral tributary and the posteromedial tributary to the saphenofemoral junction. The common femoral vein may reflux directly into the saphenous vein but this is not true deep venous reflux. The femoral vein is interrogated in its upper, middle, and distal third of the positions in the thigh, looking for evidence of previous deep venous thrombosis. The popliteal vein may reflux directly into the short saphenous vein and, similarly, this is not true deep venous reflux. The gastrocnemius veins may be the only veins in the popliteal fossa which are refluxing. In the proximal thigh, if saphenofemoral junction reflux is absent, there may be reflux in tributaries such as the posteromedial tributary or, more frequently, the anterolateral tributary. This will give the appearance of

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saphenofemoral reflux if care is not taken in identifying each of the tributaries. If there is no reflux at the saphenofemoral junction but varicose veins are present, the most common origin of reflux is the mid-thigh Hunterian perforating veins which may produce reflux in the distal saphenous vein. Similarly, if there is no reflux at the saphenofemoral junction nor at the saphenous vein above the knee, saphenous vein varicosities may originate because of reflux from a Boyd perforating vein in the anteromedial aspect of the calf. Finally, recording the areas of segmental reflux in the short saphenous vein may define the exact surgery to be done to correct this abnormal reflux.

Validation of Duplex Testing As each new method of clinical testing becomes available, it should be evaluated and compared to existing examinations. Shanik’s group evaluated color-coded duplex examination of venous reflux and compared this to continuous-wave Doppler study (33). Eighty-two limbs in 41 patients (35 women) were examined. The patients were studied supine, head elevated 30°, and then standing. The Parks 5-MHz continuous-wave Doppler probe was used and results compared with identical examinations using a 5-MHz linear array probe. The reflux stimulus was a Valsalva forced expiration. Duplex examination with the patients supine and standing correctly identified 50 incompetent and 32 competent saphenofemoral junctions. Continuous-wave Doppler failed to detect four incompetent junctions (8%) and incorrectly diagnosed incompetence in eight junctions (25%). Examinations using continuous-wave Doppler with the patient standing were similar. Incompetence was not detected in four junctions, and incompetence was diagnosed in seven competent junctions. Although the Valsalva maneuver provided an inconstant stimulus, duplex study results with the patients supine and standing proved identical. The continuouswave Doppler studies were at variance with these. Masuda and Kistner studied 25 limbs in 20 patients, comparing duplex study to ascending and descending phlebography (34). Duplex study was done with a 5-MHz probe and with the patients (16 men, four women) supine with head elevated 10° to 15°. The forced expiration, nonquantified Valsalva maneuver was utilized as the reflux stimulus. Descending phlebography was done with the patient in the 60°, semi-erect position and with a Valsalva reflux stimulus. Grading of reflux was consonant with previously described descending phlebography grading but modified to allow duplex comparison. Duplex, grade I, was reflux confined to the common femoral vein, grade II reflux in the superficial femoral and/or profunda femoris vein in the presence of popliteal vein competence, grade III reflux included findings of grade II but with popliteal re-

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Part XII Venous and Lymphatic Surgery

flux also, and grade III included limbs with full-length reflux to tibial veins. Duplex evaluation of reflux less than 0.5 s correlated with phlebographic reflux in 94 of 105 segments (sensitivity 90%). No reflux, or reflux less than 0.4 s duration, correlated with phlebographic competence in 32 of 38 segments (specificity 84%). A total of 17 discrepancies were identified among the 143 total segments studied for an accuracy of 88%. The largest proportion of these were in the phlebographically competent group, in which 6 of 38 segments showed a duration of reflux greater than 0.5 s but less than 2 s. Among 105 segments with phlebographic reflux, 11 showed a reflux duration less than 0.5 s. Most of these were in the tibial segment. When these were eliminated from consideration, sensitivity was 93% and specificity 87%. Kistner was able to inspect valve function surgically in eight vein segments. Surgical findings verified phlebographic findings but in one superficial femoral vein segment, duplex examination failed to detect valvular incompetence. The duplex studies were performed with only 15% of reverse Trendelenburg position, however (35). Rosfors in Stockholm has investigated the utility of a number of tests of venous function (36). The extent of deep venous reflux was evaluated with descending phlebography and duplex scanning in 23 extremities. During a Valsalva stimulation of reflux, there was agreement in 15 of 23 extremities. Five limbs with reflux to low thigh (grade II) were underestimated by duplex. In two limbs, severe incompetence was found by duplex but, on phlebograms, the incompetence was only moderate. The study was flawed by the fact that duplex examinations were performed with the patient sitting, knees bent, and feet supported. Flow stimulus was provided by distal manual compression. Despite these flaws, Rosfors concluded: “the present results indicate clearly that conventional phlebographic studies are less useful than noninvasive techniques for functional evaluation of CVI.” Neglen and Raju also compared duplex reflux evaluation to phlebography (37). In this important study, the duplex technique of van Bemmelen was compared with the descending phlebography technique of Kistner in 56 lower extremities. In 19 limbs, findings of phlebography and ultrasonography were completely discordant. Eight limbs had severe reflux by ultrasonography but no reflux below the popliteal on descending phlebography. The authors speculated that “the Valsalva method used in descending phlebography may be less effective in delineating reflux in postthrombotic limbs than the calf compression method used with ultrasonography.”

Duplex Determination of Patterns of Venous Reflux In Newcastle, England, Lees and Lambert studied patients referred to a specialist vein clinic (38). Three hundred limbs were studied in 153 individuals, including 20 chosen as normal controls.

Quantitation of reflux was not attempted. However, presence or absence of reflux in vein segments was determined using a 5-MHz pulsed Doppler probe with the patients scanned in a standing position. Cephalad flow was induced by active contraction of calf muscle and by passive compression. Reflux, if present, followed the relaxation of calf muscle or release of compression. For examination of veins in the thigh, passive compression was attained by rapid inflation to 140 mmHg of a 5-cmdiameter pneumatic tourniquet placed on the widest circumference of the calf. In the 20 normal control limbs in individuals with no symptoms or signs of venous disease, 15 limbs had no venous reflux, two had isolated medial perforating vein reflux in thigh or calf, and three showed segmental superficial reflux. In patients with venous disease, 57 limbs opposite to the limb with venous disease were studied. These limbs were clinically normal but 27 had reflux in one or more segments on duplex testing. In limbs with more advanced venous insufficiency, reflux was prominent. In those limbs with skin changes, 57% showed superficial reflux without deep vein incompetence. In limbs with ulceration, 52% showed superficial reflux without deep incompetence. However, 77% of ulcerated limbs with superficial incompetence also had associated gastrocnemius or medial perforating vein incompetence. This study is very important in that it shows superficial vein incompetence is important in the etiology of skin changes of chronic venous insufficiency. Limbs with such changes show an increased incidence of deep vein incompetence when compared to those without skin changes, and there is a higher incidence of perforating vein reflux in limbs with advanced changes. The very high incidence of superficial reflux, whether isolated or combined with reflux in the perforating or gastrocnemius veins, suggests that many patients with chronic venous insufficiency can be offered surgical treatment, thus underscoring the clinical importance of duplex venous testing in patients with venous insufficiency.

Valve Incompetence in Limbs With Venous Ulceration Menzoian’s group at Boston University studied 95 extremities in 78 patients with high-resolution duplex ultrasound (39). A variety of reflux stimuli were used, including Valsalva, proximal and distal manual compression, and Valsalva by having the patient blow up a rubber examination glove. Patients were examined in a 60º upright position but most of the study was conducted with the patient supine. All of the extremities had venous ulcers and 19% of these exhibited only superficial and perforator incompetence. An additional 16.8% showed only superficial incompetence so that the total number of limbs with ulcer that demonstrated superficial incompetence which could be corrected by surgery was 35%. Only 2.1% of limbs showed deep system incompetence alone, and only an ad-

Chapter 86 Clinical Application of Objective Testing in Venous Insufficiency

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ditional 4.2% showed deep system and perforator incompetence. Thus, only 6.3% of limbs exhibited reflux which would be difficult to correct. Interestingly, an additional 8.4% of limbs showed only perforator incompetence without superficial or deep component. Thus, the duplex examination suggested that a large pecentage of the limbs could be corrected by surgical intervention using ablative superficial techniques. The late Dr Michael Hume, in commenting on this presentation, said: “we are entering a new era with duplex ultrasonography as part of the evaluation of chronic venous insufficiency.” He said further that “. . . individual physiologic testing must precede the selection of an operation designed to control venous insufficiency.”

more frequent (43). Using the duplex venous reflux examination described above, it was found that in women without femoral venous reflux, only 20% exhibit popliteal venous reflux but that in women with femoral venous reflux, 42% have popliteal reflux as well. Similar findings have been found in men. Limbs without femoral reflux exhibit popliteal venous reflux in 20% of cases. However, in limbs with femoral reflux, 65% exhibit popliteal venous reflux. When two levels of venous reflux are present in the same limb, the clinical grade of venous insufficiency is more severe. The distal popliteal vein is larger, has greater area, and larger volume of reflux flow. Further studies have shown that the presence of distal venous reflux has no effect on proximal venous hemodynamics.

Correction of Deep Venous Reflux By Superficial Venous Stripping

Hemodynamic Testing

Availability of duplex technology has allowed preoperative and postoperative evaluation of patients having various forms of venous surgery (40). We were able to identify 29 limbs in 21 patients in which long saphenous reflux was present and surgery was indicated. All of these limbs also demonstrated superficial femoral vein reflux when the examination was done using the tourniquet deflation technique described above. The surgery performed was outpatient groin-to-knee saphenous inversion stripping, removing the saphenous vein to knee level. Stab avulsion of varicose tributary veins removed perforator incompetence as well. In 27 of 29 limbs with preoperative femoral reflux, that reflux was abolished by long saphenous stripping. In two limbs, associated popliteal venous reflux was present and was also abolished by the superficial venous stripping. Improvement of the deep venous hemodynamics by ablation of superficial reflux supports a reflux circuit theory of venous overload. Such deep venous overload was described in 1970 by Reinhard Fischer (41). He noted in a phlebographic study increased diameters of the deep venous system accompanying superficial venous reflux. As indicated above, we have noted an increased diameter of deep veins which correlated with the presence of reflux. The increased volume of blood flow caused by saphenous reflux and diverted by re-entry through perforating veins has been found to elongate and kink the femoral and popliteal veins as well as the femoropopliteal junction (42). It would be logical to suppose that ablation of such a reflux circuit by superficial vein removal would correct the deep venous volume overload and allow diminution of diameter of veins, thus producing valvular competence.

Proximal Reflux Affects Distal Deep Venous Function Observations from our laboratory have revealed that when proximal venous reflux is present, distal reflux is

In the past, hemodynamic testing by measurement of venous pressure in a dorsal foot vein during various maneuvers to stimulate venous blood flow was taken as a gold standard. Pressure at rest and pressure at the end of ten tiptoe movements, as well as refilling time to baseline, were recorded. It is an invasive test and cannot easily be repeated nor used for screening purposes. It is a global assessment of limb function and does not interrogate specific veins. Therefore, it cannot be used in planning precise therapy. It is classified as a research tool. Because detection of hemodynamically important venous occlusion is so difficult, the arm/foot pressure differential has been devised by Raju of Jackson, Mississippi (44). The method consists of recording venous pressure in a vein of the foot and in the hand simultaneously while the patient is supine. The measurements are repeated during a reactive hyperemia of the lower extremity. Using these, Raju has defined grades of venous obstruction. This technique, much as ambulatory venous pressure, is a global measure of hemodynamic function. It detects proximal occlusion more reliably than any other method. The only exception is direct visualization of obstruction by phlebography but such demonstration does not define hemodynamic importance. This method is also invasive and requires two venipunctures, but does aid in selecting patients for venous disobliteration and venoplasty and/or venous stenting. Plethysmography is another form of hemodynamic testing. Three names are given to the technique of photoplethysmography. These are photoplethysmography, light reflection rheography, and digital photoplethysmography. All of these detect local changes in blood content of tissues in the skin. They can be looked at as a step forward from the recording of ambulatory venous pressure, and these techniques became popular because of their noninvasiveness. Each test records reflected infrared light from the subepidermal venous pool. Emptying of that pool during tiptoe exercises and refilling time can be recorded. Computer technology allows self-standardization to determine amplitude of flow as well as time-related parameters.

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FIGURE 86.7 These typical air plethysmography (APG) tracings illustrate the normal and postthrombotic situation. The maneuvers are similar to those obtained in determining ambulatory venous pressure and in photoplethysmography (PPG). Reading from left to right: As the subject arises from the supine position, venous volume increases to complete filling or baseline. Tiptoe maneuvers empty the normal venous system. The system fills again slowly in the normal situation and more rapidly in the post-thrombotic state when filling is from reflux rather than pure arterial inflow. The 10-tiptoe maneuver is designed to empty, as completely as possible, the venous system of the calf and more clearly shows the slow filling of the normal situation, where venous filling is accomplished by arterial inflow alone and no reflux is present. On the other hand, in the post-thrombotic state, with deep venous reflux, the refilling is much more rapid. As the subject assumes the supine position once again, venous volume of the leg is diminished below the standing baseline.

In practice, the PPG filling time is determined before and after occlusion of the superficial veins by tourniquet. However, a number of factors enter to obscure the accuracy of the determinations. For example, the refill time which is determined by plethysmography depends on several physical factors including the size of the reservoir to be filled and the diameter of the veins in which reflux occurs. A long refill time may be observed when reflux occurs in small-diameter veins. The photoplethysmographic tests are useful for screening and remain popular because they are noninvasive. Air plethysmography deserves a separate mention because it has been extensively used in the recent past (45,46). It uses a circumferential plastic wrap on the limb and the quantity of volume can be standardized so that measurement of venous reflux in milliliters per second can be ascertained. Venous outflow can be measured and the ejection fraction of a single calf muscle contraction determined. Unfortunately, in contrast with duplex scanning, abnormalities in individual veins cannot be determined. Thus the technique proves useful in clinical research but not in selecting therapy for an individual patient (Fig. 86.7).

Conclusion Clinical application of duplex technology allows individual patient evaluation for prescription of precise therapy. Such examinations also reveal additional knowledge

about venous pathophysiology and the effects of venous surgery on residual venous hemodynamics.

References 1. Nicolaides A, Christopoulos D, Vasdekis S. Progress in investigation of chronic venous insufficiency. Ann Vasc Surg 1989; 3:278–292. 2. Pollack AA, Wood EH. Venous pressure in the saphenous vein at the ankle in man during exercise and changes in posture. J Appl Physiol 1949; 1:649–662. 3. Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg 1986; 10:919–924. 4. Yao JST, Flinn WR, et al. The role of noninvasive testing in the evaluation of chronic venous problems. World J Surg 1986; 10:911–918. 5. Abramowitz HB, Queral LA, et al. Use of photoplethysmography in the assessment of venous insufficiency: a comparison with venous pressure measurements. Surgery 1979; 86:434–439. 6. Barnes RW, Collicott RE, et al. Noninvasive quantitation of venous reflux in the postphlebitic syndrome. Surg Gynecol Obstet 1973; 136:769–776. 7. Tibbs DJ, Fletcher EWL. Direction of flow in superficial veins as a guide to venous disorders in lower limbs. Surgery 1983; 93:758–766. 8. Lea Thomas M. Phlebography of the Lower Limb. Scotland: Churchill Livingston, 1982. 9. Herman RJ, Neiman HL, Yao JST. Descending venography: a method of evaluating lower limb

Chapter 86 Clinical Application of Objective Testing in Venous Insufficiency

10. 11.

12.

13.

14. 15.

16.

17.

18.

19.

20.

21.

22.

23.

24. 25. 26.

27.

28.

29.

extremity valvular function. Radiology 1980; 137: 63–69. Neuman HAM, Boersma IDS. Light reflection rheography. J Dermatol Surg Oncol 1992; 18:425–430. van Bemmelen PS, van Ramshorst B, Eikelboom BC. Photoplethysmography reexamined: lack of correlation with duplex scanning. Surgery 1992; 112:544–548. Sarin S, Shields DA, et al. Photoplethysmography: a valuable noninvasive tool in the assessment of venous dysfunction? J Vasc Surg 1992; 16:154–162. Beebe WG, Bergan JJ, Bergqvist D, et al. Classification of chronic venous disease of the lower extremities: A consensus statement. Eur J Vasc Endovasc Surg 1996; 12:487–492. Miller SS, Grossman JA, Foote PV. The ultrasonic detection of perforating veins. Br J Surg 1975; 58:872–874. Hoare MC, Royle JP. Doppler ultrasound detection of saphenofemoral and saphenopopliteal incompetence and operative venography to ensure precise saphenopopliteal ligation. Aust NZ J Surg 1984; 54:49–53. Bergan JJ, Moulton SL, et al. Patient selection for surgery of varicose veins using venous reflux quantitation. In: Veith FJ, ed. Current Critical Problems in Vascular Surgery 4. St Louis: Quality Medical Publishers, 1992. Rollins DL, Semrow ML, et al. Use of ultrasonic venography in the evaluation of venous valve function. Am J Surg 1987; 154:189–191. Sigel B, Machi S, et al. Red cell aggregation as a cause of blood flow echogenicity. Radiology 1983; 148: 799– 806. van Bemmelen PS, Bedford G, et al. Quantitative segmental evaluation of venous valvular reflux with ultrasound scanning. J Vasc Surg 1989; 10:425–431. Vasdekis SN, Clarke GH, Nicolaides AN. Quantification of venous reflux by means of duplex scanning. J Vasc Surg 1989; 10:670–677. Browse NL, Burnand KG, Lea Thomas M. Diseases of the Veins: Pathology, Diagnosis, and Treatment. Great Britain: Edward Arnold Publishers, 1988:478. Thomson H. The surgical anatomy of the superficial and perforating veins of the lower limb. Ann R Coll Surg Engl 1979; 61:198–203. Zamboni P. La chirurgia conservativa del sistema venoso superficiale. Faenza: Gruppo Editoriale Faenza Editrice 1996; 3–9. Caggiati A. Fascial relationship of the long saphenous vein. Circulation 1999; 100:2547–2549. Caggiati A. The saphenous compartments. Surg Radiol Anat 1999; 21:29–34. Szendro G, Nicolaides AN, et al. Duplex scanning in the assessment of deep venous incompetence. J Vasc Surg 1986; 4:237–242. Sarin S, Sommerville K, et al. Duplex ultrasonography for assessment of venous valvular function of the lower limb. Br J Surg 1994; 81:1591–1595. Araki CT, Back TL, et al. Refinements in the ultrasonic detection of popliteal vein reflux. J Vasc Surg 1993; 18:742–748. Pichot O, Sessa C, et al. Role of duplex imaging in en-

30.

31.

32.

33.

34.

35. 36.

37.

38.

39.

40.

41.

42.

43.

44. 45.

46.

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dovenous obliteration for primary venous insufficiency. J Endovasc Ther 2000; 7:451–459. Mekenas L, Bergan JJ. Venous reflux examination: technique using miniaturized ultrasound scanning. J Vasc Tech 2002; 26:139–146. Payne SPK, London NJM, et al. Investigation and significance of short saphenous vein incompetence. Ann Royal Coll Surg 1993; 75:354–357. Delis KT, Ibeguna V, et al. Prevalence and distribution of incompetent perforating veins in chronic venous insufficiency. J Vasc Surg 1998; 28:815–825. Grouden MC, Stanley ST, et al. Triplex imaging of the saphenofemoral junction is the test of choice in patients with primary varicose veins. J Vasc Tech 1993; 17:131–133. Masuda EM, Kistner RL. Prospective comparison of duplex scanning and descending venography in the assessment of venous insufficiency. Am J Surg 1992; 164:254–259. Kistner RL, Ferris EB, et al. A method of performing descending phlebography. J Vasc Surg 1986; 4:464–468. Rosfors S. A methodological study of venous valvular insufficiency and musculovenous pump function of the lower leg. Phlebology 1992; 7:12–19. Neglen P, Raju S. A comparison between descending phlebography and duplex doppler investigations in the evaluation of reflux in chronic venous insufficiency: a challenge to phlebography as the “gold standard.” J Vasc Surg 1992; 16:687–693. Lees TA, Lambert D. Patterns of venous reflux in limbs with skin changes associated with chronic venous insufficiency. Br J Surg 1993; 80:725–728. Hanrahan LM, Araki CT, et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991; 13:805–812. Walsh JC, Bergan JJ, et al. Femoral venous reflux is abolished by greater saphenous stripping. Ann Vasc Surg 1993; 1994; 8:566–570. Fischer H, Siebrecht H. Das Kaliber der tiefen Unterschenkelvenen bei der primaren Varicose und beim postthrombotischen Syndrome (Eine phlebographische Studie). Der Hautarzt 1970; 5:205–211. Hach W, Schirmers U, Becker L. Veranderungen der tiefen Lietvenen bei einer Stammverikose der V. saphena magna. In: Muller-Wiefel H, ed. Mikrozirkulation and Blutrheologic. Baden Baden: Witzstock, 1980. Walsh JC, Bergan JJ, et al. Proximal reflux adversely affects distal venous function. Vasc Surg 1996; 30: 89–96. Neglen P, Raju S. Detection of outflow in chronic venous insufficiency. J Vasc Surg 1993; 17:583–589. McDaniel HB, Marston WA, et al. Recurrence of chronic venous ulcers on the basis of clinical, etiologic, anatomic, and pathophysiologic criteria and air plethysmography. J Vasc Surg 2002; 35:723–728. Marston WA. PPG, APG, duplex: Which noninvasive tests are most appropriate for the management of patients with chronic venous insufficiency? Semin Vasc Surg 2002; 15:13–20.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 87 Varicose Veins Mark D. lafrati and Thomas F. O’Donnell, Jr.

Varicose veins and their treatment have been commented upon since antiquity (1). Although the surgical treatment of ligation and stripping of the greater saphenous veins has been fairly standard for nearly the last 100 years (2), more recent studies have questioned this approach (3–5). It is the purpose of this chapter to review the pathophysiology, diagnosis, and surgical treatment of varicose veins. Data on the actual incidence and prevalence of varicose veins are conflicting. During the 1930s to 1960s, several large studies reported that the prevalence of varicose veins roughly averaged 2% in the general population (6–8); one study found that the prevalence in women was approximately two to four times that in men (9). The weakness of these surveys lies in their questionnaire format. In 1978 Widmer reported data from a defined population of factory workers (10). Surprisingly, he found a higher incidence of varicose veins in men (5.2%) than in women (3.2%), with the overall incidence of varicose veins being 4.2%. A clear association of varicose veins with advanced age has been shown, with one study reporting a fivefold increased prevalence of varicose veins in the elderly (11). In addition a strong familial predisposition was shown in 43% to 90% of patients with either varicose or telangiectatic veins (10,12,13). Most recently a large cross-sectional survey was carried out in the city of Edinburgh. Men and women aged 18 to 64 years were selected randomly from 12 general practices. In 1566 subjects examined, the age-adjusted prevalence of trunk varices was 40% in men and 32% in women. This sex difference was mostly a result of higher prevalence of mild trunk varices in men. More than 80% of all subjects had mild hyphenweb and reticular varices. The prevalence of all categories of varices increased with age. No relation was found with social class. In contrast with the findings in most older

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studies, chronic venous insufficiency and mild varicose veins were more common in men than women (14).

Pathophysiology Conflicting theories exist as to the etiology of varicose veins (15–17). Valvular incompetence and venous hypertension have in the past been considered primary processes of varicosis. The classic theory of descending valve incompetence has the support of famous physicians dating back to Trendelenburg (18) and Harvey. The Edinburgh vein study demonstrated that, while segmental venous reflux can be identified in patients without varices, superficial and mixed reflux increases in subjects with more severe varices (19). While there is a clear link between venous hypertension and varicose veins, pressure alone seems to be an insufficient causal agent. When normal veins are subjected to high intraluminal pressure they become hypertrophied. Thus veins that are used for arterial bypass become ‘‘arterialized” and have a thickened wall. The veins of patients with a varicose condition dilate rather than hypertrophy. Such defects could explain lateral blowouts, fusiform varicosities between competent valves, spontaneous resolution of peripartum varicosities, and the reason why in situ saphenous vein bypass grafts with the valves lysed do not dilate (16). Recent data suggest that intrinsic abnormalities of the veins lead to dilation with subsequent insufficiency (20,21). Light and electron microscopy of varicose vein segments revealed a degeneration of cellular organization that was distinctly different from normal veins. These structural abnormalities identified by light and electron microscopy include vacuolated endothelium with pyknotic nuclei (22), thin-

Chapter 87 Varicose Veins

ning and disorganization of the smooth muscle layer (16,20), fibrous degeneration of the media (16), and swelling and helical splitting of collagen fibers. Muscle cells were found to be separated by collagenous infiltrates which, it is suggested, prevent them from acting as a whole to maintain venous tone in response to postural, environmental, and hormonal influences (16). The distribution of wall degeneration is not uniform. Some segments may be thickened and fibrotic while others are aneurysmal. Morphologic and histochemical studies have emphasized altered content of elastin, collagen, and smooth muscle in superficial leg veins obtained from patients with primary varicosities (16,20,23). Thulesius et al. have shown that isolated segments of vein obtained from patients with primary and secondary varicose veins had a reduced ability to contract in response to norepinephrine, serotonin, histamine, and passive stretch (24). Lowell et al. demonstrated that, in primary varicose veins, endothelium-independent relaxation produced by nitrous oxide was diminished by 86% compared with that in controls, protein content was decreased, and endothelial content was increased. These data suggest that both endothelial and smooth muscle function is impaired in vein segments removed from patients with primary varicosities. Similar functional, biochemical, and structural changes were seen not only in varicose tributaries but also in nonvaricose saphenous veins from the same patient. These findings support the hypothesis that abnormalities within the venous wall that affect both smooth muscle and endothelial cells exist before, and perhaps contribute to, the formation of varicosities (25). While the triggers and mechanisms operative in compromising vein walls and valves remains unclear, an inflammatory process may be an early participant. Indicators of inflammatory processes include: elevation of endothelial permeability; attachment of circulating leukocytes to the endothelium; infiltration of monocytes, lymphocytes, and mast cells into the connective tissue; and development of fibrotic tissue infiltrates and several molecular markers, such as growth factor or membrane adhesion molecule generation (26). Plasma from patients with venous disease activates monocytes by an undefined pathway (27). Many of these markers are already detectable at early stages of chronic venous insufficiency (CVI) and may be involved in the development of primary venous valve dysfunction. Among several possible mechanisms (hypoxia, humoral stimulation), a shift in fluid shear stress from normal physiologic levels and endothelial distension under the influence of elevated venous pressure may serve as trigger mechanisms for inflammation (26,28).

Anatomy of the Superficial Venous System Chronic venous insufficiency has been traditionally classified on the basis of anatomy, function, and clinical

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severity. The anatomic classification of CVI is important because it links the location of CVI with its subsequent clinical management. CVI may affect the superficial venous system at three levels of depths (Fig. 87.1). 1.

2.

3.

First, the subcuticular venules, at the most superficial level, comprise an extensive network of small veins that are visible just beneath the skin. In the earliest form of CVI affecting the superficial system, these vessels are quite readily recognized, particularly below the medial malleolus, and produce the “ankle flare sign.” At the second level within the subcutaneous tissues lie veins of a larger caliber, which are tributaries of the main superficial venous trunks. These veins elongate and dilate in association with valvular incompetence within them or within the main trunks of the greater or lesser saphenous veins. At the third level, the deepest layer resting directly on the deep fascia, are found the main superficial venous trunks comprising the greater (long) and lesser (short) saphenous veins.

The anatomy of the greater saphenous vein has been better defined owing to the interest shown in the in situ

FIGURE 87.1 Superficial venous system and its tributaries can be divided into three depths. On the most superficial level, the first level, are the subcuticular venules, which are a network of small veins. At the middle level, or second level, lie the tributaries of the main superficial venous trunks, which commonly elongate and produce varicosities. At the third, or deepest layer, rest the main superficial venous trunk, i.e., the saphenous system.

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femoral-popliteal-tibial bypass. Both duplex scanning studies and ascending phlebography have defined the anatomic variations and will be discussed subsequently (29). The greater saphenous vein arises anterior to the medial malleolus and courses obliquely and posteriorly as it crosses the anteromedial surface of the tibia (Fig. 87.2). At or below the knee joint, the posterior arch vein joins it. As the main saphenous trunk continues in a slightly more superficial plane around the knee joint, the anterior vein of the leg merges with it. The long saphenous vein then courses cephalad on top of the deep fascia to join the common femoral vein at the foramen ovale. In the upper third of the thigh the anterolateral and posteromedial veins of the thigh enter the saphenous vein. The long saphenous vein may be a complete double system or a branching double system between the knee and the foramen ovale, which is of obvious importance for ligation and stripping procedures. In the calf, a solitary vein was found in only 65% of cases. Duplex scanning studies suggest that these variations may be more common than previously realized. Kupinski and the Albany group have recorded their experience with duplex evaluation of the greater saphenous vein in nearly 1500 limbs (30). This evaluation was divided between approximately 1200 greater saphenous and 470 lesser saphenous examinations, which were carried out preparatory to infrainguinal bypass. At the thigh level in 60% of the limbs, the greater saphenous vein had a sin-

gle medial dominant system, while a branching double system was observed in nearly 20%, a complete double system in 10%, and a closed-loop system in another 10%. Of interest was a single lateral dominant system in another 8%. At the calf level, a greater proportion of limbs had a single venous system—65%. The remaining proportion had a double system. In nearly 90% of the limbs, the greater saphenous vein at the calf level was anterior dominant. There was considerable variability in the number and location of branch veins. Several surgeons have pointed out that the saphenous vein is like Neptune’s trident as it branches both at the upper thigh and knee joint. The lesser saphenous vein begins posterior to the lateral malleolus and courses cephalad lateral to the Achilles tendon (Fig. 87.3). This vein takes on a midline position lying on the deep fascia at the junction of the lower and middle thirds of the calf. In the upper third of the calf, the lesser saphenous penetrates the deep fascia and proceeds into the popliteal space between the heads of the gastrocnemius muscles. In well over one-half of the cases, the lesser saphenous vein enters the popliteal vein above the level of the knee joint. By contrast, in roughly one-third of limbs the lesser saphenous vein may join with the long saphenous vein or even with the deep muscular veins in

FIGURE 87.2 Anatomy of the greater saphenous vein. The greater saphenous has an anterior and a posterior branch at the thigh level that runs in a plane more superficial to the main trunk. At the knee, the saphenous trifurcates like Neptune’s trident into both an anterior and posterior branch.

FIGURE 87.3 Anatomy of the lesser saphenous vein. The lesser saphenous vein may communicate with the greater saphenous located medially as shown. This vein originates posterior to the lateral malleolus and courses proximally to the popliteal, in the majority of cases above the popliteal crease.

Chapter 87 Varicose Veins

the upper thigh. Rarely, the lesser saphenous may merge with the deep veins of the calf or the long saphenous vein in the upper third of the leg.

Perforating Veins Perforating veins connect the superficial to the deep venous system (31). The term “communicating vein” is reserved for veins which connect veins within the same system (32). In contrast to the superficial branches, the perforating veins demonstrate more consistency in location. As shown in a previous study by our group, in which direct observation at the time of subfascial vein legation was carried out, incompetent perforating veins were most commonly observed about 5 to 10 cm above the medial malleolus (33). In the normal limb, the perforating veins permit the unidirectional flow of blood from the superficial to the deep venous systems through a set of one-way valves (Fig. 87.4). Perforating veins are either direct, permitting the superficial venous system to communicate di-

FIGURE 87.4 Anatomy of the perforating or communicating veins. (A) This view of the medial aspect of the lower leg shows the anterior branch, the saphenous vein, and the main saphenous trunk, which originates anterior to the medial malleolus, and the posterior arch vein, which connects with major communicating veins. (B) The medial communicating veins as they penetrate the fascia and enter the posterior tibial veins. The lateral communicating veins enter the peroneal vein higher up.

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rectly with the main deep veins, or indirect, such that they connect with the deep veins by way of a muscular vein. The direct perforating veins are relatively constant in anatomic location whereas the indirect perforators are irregularly distributed (31,33–35). There are four groups of perforating veins in the leg: those of the foot, medial and lateral calf, and the thigh. Foot perforators directly connect the deep veins (dorsalis pedis and tarsal) with the superficial veins of the foot. These perforators either have no valves or have valves directing blood from deep to superficial (36,37). The medial calf veins are clinically most significant. Cadaver studies have identified 7–20 medial calf perforating veins with slightly more than half being direct perforators. In our experience, the lower perforator (Cockett I) is located posterior and inferior to the medial malleolus just over the posterior tibial vein (33). This is usually the smallest of the three perforating veins. The Cockett II and III perforating veins are typically located 7 to 9 cm and 10–12 cm above the medial malleolus, posterior to the tibia. These perforators connect the posterior arch vein or other tributaries of the saphenous vein directly with the posterior tibial vein (35) (Fig. 87.5). A fourth group of medial calf perforating veins is located 1–2 cm posterior to the medial edge of the tibia. These paratibial perforating veins are clustered in three groups 18–32 cm from the medial maleolus. Less than half of these perforators make direct connections from the saphenous trunk to the poste-

FIGURE 87.5 The four common areas for medial incompetent communicating veins (circles); the course of the saphenous vein (dashed line); and the customary incision for an open (Linton) subfascial ligation, which is placed over these veins (solid line).

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rior tibial veins, with the majority connecting indirectly. Although all medial calf perforating veins pass from the deep posterior compartment to the subcutaneous space, only approximately 62% traverse the superficial posterior compartment (35) (Fig. 87.6). This anatomic finding has significant surgical implications since the initial exposure in subfascial endoscopic perforator ligation reveals only the superficial posterior compartment. Identification of the remaining perforating veins requires paratibial fasciotomy. The Boyd perforator is found just below the knee joint, and it communicates between the main trunk or tributaries of the saphenous and the tibial or popliteal veins (38). On the lateral aspect of the calf, perforating veins are located in three groups. In the proximal posterior lateral calf, perforating veins connect tributaries of the lesser saphenous vein with muscular sinuses or the connecting veins which feed the deep veins. More distally on the posterior lateral aspect are peroneal perforators. Anterior lateral perforators drain tributaries of the greater saphenous to the anterior tibial veins (39). In the thigh there are fewer perforating veins; however, they can be clinically very important. The Dodd and Hunterian perforators usually are within Hunter’s canal and communicate between the superficial femoral vein or popliteal vein and the long saphenous vein either directly or indirectly (32).

Diagnosis Clinical Presentation The principal symptoms produced by varicose veins are a cosmetically displeasing appearance, ankle swelling, calf pain, and, in the more advanced forms, cutaneous pigmentation, lipodermatosclerosis, and eczema. Ulceration is an unusual end-stage result from simple varicose veins. Superficial phlebitis and hemorrhage from the vein are less frequently encountered.

Symptoms Venous Dilation With involvement of the superficial venous system, the most common first symptoms in addition to mild edema may be cosmetically displeasing dilated superficial varicosities. Initially the venous dilation may be most apparent in the dependent portion of the limb, particularly on the inner aspect of the lower calf. The patient may observe dilation of small veins underneath the medial malleolus, the so-called ankle flare sign, which is pathognomonic of chronic venous insufficiency. The veins will become most prominent following prolonged standing. In women, ve-

FIGURE 87.6 Compartments and medial veins of the leg. Cross-sections at level of Cockett II (A), Cocket III (B), “24 cm” (C), and more proximal paratibial (D) PVs. GSV, greater saphenous vein; PAV, posterior arch vein; PTVs, posterior tibial veins; SPC, superficial posterior compartment; CII, Cockett II, CIII, Cockett III; PTP, paratibial perforator. (Reproduced with permission by Mozes G, Gloviczki P, et al. J Vasc Surg 1996;24:800–808.)

A

B

C

D

Chapter 87 Varicose Veins

nous dilation may also occur at the time of menses. With progression of CVI, the veins become more tortuous and larger, and the patient will note their appearance in the proximal portion of the limb. Although some mild varicosities may develop in women during adolescence, they usually progress rapidly in size and number during pregnancy. With each successive pregnancy, the number and diameter of these varicosities usually increase. Swelling Edema is an early symptom of venous disease. The patient usually notes that the swelling is mild and limited to the area just above the shoe line around the malleolae. This edema usually resolves with bedrest, particularly after the limb has been elevated. In the early phases of CVI the distribution of the edema is limited to the malleolar area but, with more advanced varicose veins, the edema may progress up to the midcalf level. Unlike the location of swelling associated with lymphedema, the metatarsal area is usually spared in the early phases of CVI. Initially, the edema may be pitting, however, with chronic edema formation, subcutaneous fibrosis occurs, so that the edema may fail to pit. While it has been taught that only lymphedema fails to pit, the critical factor that determines pitting is the degree of subcutaneous fibrosis, irrespective of a venous or lymphatic cause (40). Leg Pain Several types of pain are associated commonly with CVI. The most frequent type is limb heaviness or ache that occurs after prolonged standing. The pain is usually felt over the calf area and, as opposed to the calf pain associated with arterial insufficiency, walking may ease the calf ache associated with CVI. Patients may also experience pain along the course of dilated varicose veins after prolonged standing, which is probably the result of venous stasis within the varicosity and distention of the vein wall. Lying down, particularly with elevation of the limb, relieves limb heaviness within a short period of time. The aching sensation may be worse in warm humid weather or for women during their menses because both conditions are associated with greater salt and water retention, which worsens the edema. Patients with deep venous valvular incompetence may note the sudden development of leg heaviness upon standing. Our patients have described it as similar to the sensation of water being poured into the leg and filling it up. After standing for a while, this sensation may be followed by a bursting type of heaviness in the calf, which can be quite incapacitating. Concomitant superficial venous incompetence is the rule. Cutaneous infection, secondary to dermatitis, can produce pain in the limb with CVI, but this pain is related to the primary process rather than to actual venous involvement. Cutaneous Manifestations Finally, the patient may observe skin pigmentary changes, usually characterized by brownish hemosiderin deposits

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in the skin. The patient describes the skin discoloration as embarrassing—as if “I didn’t wash the area” or “it looks like dirt.” Not infrequently, the eczematous dermatitis associated with advanced CVI may prompt referral to a skin specialist for treatment. In general, such skin changes are manifestations of longstanding venous insufficiency. Patients with an antecedent episode of superficial thrombophlebitis will note serpiginous pigmentation along the course of the affected vein.

Physical Examination The physical examination of the limb in a patient with chronic venous insufficiency may play a more important role in guiding therapy than in the patient with arterial insufficiency. The patient should be examined standing, preferably on a stool or bench. The use of an incandescent lamp is quite helpful in allowing the varicosities to cast shadows. The four traditional stages of the physical examination, inspection, palpation, percussion, and auscultation, are followed in succession, with particular emphasis on the first two steps. The patient’s limb is inspected in a standing position. Specially prepared anatomic diagrams of the lower extremity for CVI are helpful in making clinical notations. The presence of the ankle venous flare underneath the medial malleolus is one of the first signs of CVI. Telangiectases are defined as dilated intradermal venules less than 1 mm in size. Reticular veins are dilated, nonpalpable, subdermal veins 4 mm in size or less. Varicose veins are defined as dilated palpable subcutaneous veins generally larger than 4 mm (41). Edema indicates more functionally advanced venous disease. Limb girths should be measured at specific anatomic points to document objectively the extent of edema. The presence of skin pigmentary changes, particularly in the supramalleolar area, denotes severe CVI and should be described. An associated scaling dermatitis may be present. The location of a venous ulcer is charted on the diagram, and the size and depth of the ulcer as well as the degree of granulation tissue should be described. Venous ulcers usually occur over the gaiter area (medial supramalleolar area), the site of the lower three major perforating veins, and also the area that is under the influence of maximal hydrostatic pressure. As opposed to arterial ulcers, venous ulcers are superficial and rarely penetrate through the fascia. The location of incisions from previous venous surgery should be sought anterior to the medial malleolus, in the inguinal area, or over the perforating vein area. Finally, the distribution of dilated superficial veins should be charted. The limb is next palpated. The compliance of the subcutaneous tissue edema is assessed. The limb with more advanced CVI will feel woody and resilient to palpation. The skin temperature is felt, and an increased temperature

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may indicate underlying cellulitis. Because some veins will not be readily visible in patients with moderate obesity, palpation may be the best method to locate dilated superficial varicosities of the thigh and calf. In the calf region, palpation of circular defects in the subcutaneous tissue usually indicates the site of incompetent dilated perforating veins (33). Lubricating the skin with gel facilitates palpation for fascial defects. These sites should be marked on the skin if the examination is done before surgery or should be noted on the diagram in terms of distance from the malleolus.

Tourniquet Tests Tourniquet tests, originally developed by Brody and subsequently modified by Trendelenburg (18), have two purposes: 1. 2.

to determine the level of valvular incompetence in the superficial system; and to ascertain whether deep venous system involvement is present.

The patient should be in a supine position with the limb elevated for at least a minute before starting the examina-

tion. This maneuver empties the veins by reducing venous congestion in the superficial venous system. Tourniquets are then placed at the upper thigh, lower thigh, calf, and upper ankle. The patient then stands. If the superficial veins of the calf segment fill, perforating vein incompetence is usually present. The tourniquets are then removed from the bottom upward (Fig. 87.7). If removing the ankle tourniquet fills the superficial venous system, perforating vein incompetence is suspected. If after removal of the below-knee tourniquet the lesser saphenous system fills, then lesser saphenous incompetence is most likely. Next, the above-knee tourniquet is removed to assess the competence of the Hunter’s canal perforator. Finally, if the superficial venous system remains empty, then the highthigh tourniquet is removed to detect saphenofemoral incompetence. Further information may be obtained by varying the sequence of tourniquet removal and exercising the patient. In addition to the tourniquet tests of perforator incompetence, digital control of the perforating veins can be carried out. The fingers are placed over the sites of the perforating veins, and the limb is elevated to decompress the superficial venous system. The patient then stands, and the fingers are removed from the perforating veins individually, as if one were playing notes on the keyboard of

FIGURE 87.7 (A) Trendelenburg test. Tourniquets are placed around the upper thigh and knee levels to demonstrate both lesser and greater saphenous incompetence. Right: the lower tourniquet has been removed, demonstrating an incompetent lesser saphenous vein. (B) Trendelenburg test for greater saphenous insufficiency. The dilated greater saphenous system (left) before elevation on application of tourniquet. Following removal of a tourniquet below the fossa ovalis, the superficial venous system fills promptly owing to an incompetent saphenofemoral valve.

Chapter 87 Varicose Veins

a piano. Veins will bulge at the sites of incompetent perforators as the fingertip is removed.

TABLE 87.1 Classification of chronic lower extremity venous disease ( reference 41) C

Auscultation Arteriovenous fistulas, although an unusual occurrence, can be associated with the development of prominent lower extremity varicosities. Auscultation over the varicosities will usually reveal a continuous murmur. A pulsatile arterial component will be heard if a Doppler probe is placed over the varicose veins. There also will be increased skin temperature.

Venous Imaging Studies While a thorough physical examination reveals a wealth of useful clinical information, vascular imaging techniques can be extremely helpful in the management of venous diseases. Available studies may be broadly divided into physiologic and anatomic examinations, although there is significant overlap in the data. Phlebography and duplex scanning provide detailed anatomic information which allows for vein mapping, perforator mapping, identification of occlusions, and evaluation of segmental vein valve reflux. Physiologic data may be obtained by a variety of plethysmographic techniques. A comprehensive discussion of vascular imaging techniques is beyond the scope of this chapter. We find duplex scanning with measurement of segmental valve closure times by the rapid cuff deflation technique (42) to be very useful in planning routine surgical intervention. Phlebography is reserved for more complex cases such as those requiring vein valve transplant or multiple re-do procedures. We find plethysmography useful primarily as a research tool, allowing us to quantify the hemodynamic effects of our interventions.

Classification of Chronic Venous Insufficiency Interpretation and communication of data relating to venous disease has historically been hampered by the lack of uniform reporting standards in venous disease. The Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery improved this situation with the publication of Reporting Standards in Venous Disease in 1988 (43). These guidelines for reporting on venous disease were subsequently refined and expanded at an international consensus conference on chronic venous disease held under the auspices of the American Venous Forum (41). Limbs with chronic venous disease are classified according to clinical signs (C), etiology (E), anatomic distribution (A), and pathophysiologic condition (P), as depicted in Tables 87.1–87.3. By using this scheme, communication between providers and in the medical literature can be much more precise and uniform than was previously possible. For instance, a patient with

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E A P

Clinical signs (grade 0–6), supplemented by (A) for asymptomatic and (S) for symptomatic presentation Etiologic classification (congenital, primary, secondary) Anatomic distribution (superficial, deep, or perforator, alone or in combination) Pathophysiologic dysfunction (reflux or obstruction, alone or in combination)

TABLE 87.2 Clinical classification of chronic lower extremity venous disease ( reference 41) Class 0 Class 1 Class 2 Class 3 Class 4 Class 5 Class 6

No visible or palpable signs of venous disease Telangiectases, reticular veins, malleolar flare Varicose veins Edema without skin changes Skin changes ascribed to venous disease (e.g., pigmentation, venous eczema, and lipodermatosclerosis) Skin changes as defined above with healed ulceration Skin changes as defined above with active ulceration

TABLE 87.3 Segmental localization of chronic lower extremity venous disease ( reference 41) Superficial veins (AS1–5) 1 Telangiectasias/reticular veins Greater (long) saphenous vein 2 Above-knee 3 Below-knee 4 Lesser (short) saphenous vein 5 Nonsaphenous Deep veins (AD6–16) 6 Inferior vena cava Iliac 7 Common 8 Internal 9 External 10 Pelvic: gonadal, broad ligament, femoral 11 Common 12 Deep 13 Superficial 14 Popliteal 15 Tibial (anterior, posterior or peroneal) 16 Muscular (gastrointestinal, soleal, other) Perforating veins (AP17,18) 17 Thigh 18 Calf

an active ulcer, who developed varices at age 40, with no history of thrombosis, found to have reflux at the saphenofemoral junction and popliteal vein only would be denoted as C6EpAS2D14PR. In addition to the CEAP classification, the reporting standards also include numeric grading schemes for disease severity, risk factors, and outcome criteria.

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Nonsurgical Treatment The most common therapies for lower extremity venous disorders are rest, elevation, and compression. Compression therapy dates back to at least the eighth century BC when the prophet Isaiah (ch. 1 v. 6) refers to medically treated bandages. In 1676, Weisman introduced a laced stocking crafted from dog skin used in the treatment of venous ulcers (44). Compression stockings and wraps have become more sophisticated in their materials and constructions, allowing graded compression and better fit; however, the principle has remained. Compression therapy remains a mainstay in the management of venous disorders. Pharmacologic therapy for venous disease in the United States has been largely confined to anticoagulant and anti-inflammatory treatments for thrombotic complications, pain medications as needed, and antibiotics when infections are present. A number of agents are being investigated. The most promising are micronized purified flavonoid fractions. This venotropic drug has been shown to increase venous tone and improve lymphatic drainage. These agents (Dalfon 500) are available in Europe and have been used extensively. Randomized, double-blind, placebo-controlled trials have demonstrated decreased edema, improved trancutaneous oxygen tension, stasis dermatitis, and possibly ulcer healing (44,45).

Surgical Treatment Before surgery, the varicose tributaries of the greater and lesser saphenous veins are marked with an indelible pen. This is best done with the patient in a standing position and with a light that casts a shadow to define the veins. Palpation is helpful for patients with an abundance of subcutaneous fat when the examiner cannot directly visualize tributaries.

Operative Procedure The choice of anesthesia is individualized with reference to the patient’s general medical condition and planned surgery. Spinal, epidural, general, and local anesthesia have all been effectively employed. A wooden T-extension off the end of the table permits abduction of the limb. In addition, a pillow-covered Mayo stand may be helpful to elevate the limb so that the posteromedial calf veins become accessible. Iodine-based antiseptic solution is used to paint the limb. To avoid wiping off the marks identifying the branch veins, only the inguinal area is scrubbed and then subsequently painted. In applying the drapes, care should be paid to coverage of the perineal area. A towel folded in thirds followed by an elastic impermeable barrier will wall off this section. The foot can be encased in a large glove because it can be placed over half of the foot, or alternatively in a Lahey bag. If the foot is in the field it

should be scrubbed with an iodine-based solution prior to double application of iodine-based paint.

Exposure of the Greater Saphenous Vein In contrast to some descriptions of this segment of the procedure, we prefer to make the skin incision transversally above the inguinal crease. A small incision can be made starting over the femoral artery and continuing laterally above the inguinal crease for approximately 5 cm. In obese patients this skin incision will be longer. There are several advantages to placement of the skin incision in this area: 1. 2. 3.

it is cosmetically pleasing because it is above most bathingsuit lines; the incision is under minimal tension; and it places the incision over the usual location of the saphenofemoral junction.

The incision is deepened through Camper’s and Scarpa’s fascia. At this point a Gelpe retractor can be used to retract the tissue. In addition, a small right-angle retractor is required to demonstrate the various branches of the saphenous vein. In general, from three to five branches are identified and ligated with No. 3–0 silk (Fig. 87.8). Starting at 12 o’clock, the superficial epigastric vein runs vertically in the subcutaneous tissue to join the saphenous vein, while at 3 o’clock the deep external pudendal vein is encountered at the level of the saphenofemoral function or deeper. The superficial circumflex iliac vein joins the saphenous at 9 o’clock. Although constant in number, these tributaries are quite variable in the location where they join the saphenous vein. The posteromedial and anterolateral branches of the saphenous vein usually rejoin the greater saphenous vein. They should be identified if enlarged for separate stripping. The saphenofemoral junction should be dissected circumferentially, encircling the greater saphenous vein with a vessel loop and placing it on traction to facilitate the dissection. Inadvertent injury to the superficial external pudendal artery can lead to troublesome bleeding. Although it usually lies deep to the saphenous vein on the deep fascia, in one-third of cases it may cross superficial to the vein. At this time, care should be taken to identify the deep external pudendal vein that issues directly from the saphenous or femoral vein in a medial direction at the region of the saphenofemoral valve. This tributary can feed vulvar varices, and if flush ligation of the saphenous is not performed, it may be missed. The saphenous vein is then ligated flush with the common femoral vein. The distal saphenous vein is then identified at the knee. Stripping to the knee rather than the ankle reduces the risk of saphenous nerve injury, since the saphenous nerve typically joins the saphenous vein in the mid- to upper calf. If the vein cannot be palpated at the knee, then continuous wave Doppler or duplex scanning will identify it. The saphenous vein is dissected through a

Chapter 87 Varicose Veins

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FIGURE 87.9 Avulsion of branch varicosities through small stab incisions.

FIGURE 87.8 Of the three to five branches at the proximal end of the greater saphenous vein, the superficial epigastric vein, superficial external pudendal vein, medial saphenous vein, greater saphenous vein, and deep pudendal vein are depicted.

small incision using blunt dissection. The trunk is carefully separated from the saphenous nerve if present, so that injury to this nerve is avoided. The distal segment of the saphenous vein is then tied with white polyglycolic suture. This suture is preferred because it does not show through the skin and is less likely to “spit” than black silk. With traction on the distal tie, a transverse venotomy is made with a No. 11 blade. A small snap is inserted into the lumen to dilate the vein and then a disposable plastic stripper (Codman) is inserted and passed up the vein proximally. The passage of the stripper along the limb is identified and marked with a marking pen so that its relation to previously placed marks over the branch varices can be noted. The stripper will jiggle the snap on the divided saphenous vein in the proximal inguinal incision,

which provides confirmation that the greater saphenous trunk has been identified. Attention is then directed toward the avulsion of small tributary varices that have been marked preoperatively. Small 3-mm transverse incisions are made along the Laniers lines. A crochet hook or fine snap can be used to tease the veins out. The veins are then divided between two small snaps and by means of fine Iris scissors are dissected free of subcutaneous tissue (Fig. 87.9). By sequentially tugging on the branches and with sharp dissection, a long segment of the branch vein can be isolated. Countertraction with a skin hook on the skin edge is essential. More traction can be placed on the vein if it is twisted. The vein is then avulsed. Larger veins are controlled with a fine absorbable clip. At the completion of the branch avulsions, the greater saphenous vein is slowly stripped from groin to knee (above to below), which direction has been shown to decrease saphenous nerve injury. Tight compression is applied to the thigh area with folded towels as the vein is stripped. In patients with large greater saphenous trunks, a hemovac drain can be attached to the end of the stripper with a No. 4–0 silk and released when the drain has traversed most of the tunnel. The drain is then brought out through a counter-incision. To further decrease delayed hemorrhage in the tract of the greater saphenous vein, a rolled absorbent pad is included in the elastic bandage wrap. The small incisions for the branch varices are sutured with one buried No. 5–0 subcuticular suture. Sterile strips are then applied. The inguinal wound is irrigated, and clot is manually milked out of the saphenousstripping tract. The inguinal wound is closed in two layers

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to the subcutaneous tissue. A continuous subcuticular suture approximates the skin and sterile strips are applied.

New Surgical Procedures Subfascial endoscopic perforator surgery Robert Linton emphasized the significance of incompetent perforating veins and developed a technique for perforator ligation utilizing a long medial calf incision (31). However, despite refinements in technique, significant wound complications have limited acceptance of perforator ligation. In recent years, endoscopic techniques for perforator ligation have been developed (46–48). Using video scopes, these less invasive approaches use incisions in the upper calf to gain access to lower calf perforating veins, thereby avoiding incisions in the underprivileged or lipodermatosclerotic tissues in order to minimize wound complications. Subfascial endoscopic perforator surgery (SEPS) has been shown to be technically feasible, with minimal perioperative morbidity and short hospital stays (49,50). Pierik et al. reported a prospective randomized trial in which 39 patients with medial leg venous ulcers and incompetent perforating veins underwent correction of superficial and perforator vein reflux. Patients were randomized to either endoscopic or traditional open perforator ligation. They found no difference in ulcer healing rates at four months (85% vs. 90%) or recurrence at 21 months (none). However 53% in the open group had wound infections compared with none with SEPS (51). While SEPS is generally safe and effective we find that Cockett I or inframaleolar perforating veins are not well addressed by this technique. Further caution must be exercised when performing paratibial fasciotomy for deep posterior compartment exposure to safeguard the posterior tibial neurovascular bundle. Finally, the overall importance of ligating incompetent perforating veins is not universally accepted and awaits investigation in a prospective randomized trial. Endovenous Obliteration Endovascular therapies have become very prevalent in the management of arterial diseases but have a much more limited role in venous disease. The possibility of ablating the saphenous vein or repairing venous reflux without the discomfort and morbidity of open surgical procedures is enticing. Two devices were evaluated in a multicenter European study. The Closure catheter applied resistive heating over long vein lengths to cause maximum wall contraction for permanent obliteration; the Restore catheter induced a short subvalvular constriction to improve the competence of mobile but nonmeeting leaflets. Closure treatment caused acute obliteration in 141 (93%) of 151 limbs; Restore treatment, shrinking one or more valves, acutely reduced reflux to less than 1 second in 41 (60%) of 68 limbs. Closure treatments were associated with early recanalization (6%), paresthesias (thigh, 9%; leg, 51%; p < 0.001), three skin burns, and three deep-vein

thrombus extensions, with one embolism. Restore treatments were thrombogenic (16%) despite prophylactic anticoagulation, and treated valves enlarged over 6 weeks, becoming less competent. At 6 months, 87% of 53 Closure patients were class 0 or 1, 75% were symptom-free, and 96% of 55 treated limbs were completely free of reflux. Fourteen of 31 Restore patients (45%) had no symptoms, but 55% were class 2 or lower and only 19% had less than 1 second reflux (52). The poor results from the Restore device eliminated it from consideration. Further evaluation of the Closure device was conducted in 301 patients in Europe and the United States. They reported initial success in 96% of cases and at 4.9 months follow-up 7.2% of initially obliterated saphenous veins were recanalized. Paresthesias were noted in 15% of treatments confined to the thigh and 30% of limbs when extended to the ankle. Skin burns were reported in eight patients (53). This group further analyzed their data and concluded that endovenous ablation is equally efficacious with or without extended saphenofemoral ligation (54). Because of the significant incidence of paresthesias, vein recanalization, and deep venous thrombosis combined with the new complication of thermal skin injury and the lack of long-term follow-up, we do not currently employ this technique. Powered Phlebectomy Another new surgical technique utilizes transillumination, subcutaneous infiltration of tumescent anesthesia with hydrodissection, and a powered phlebectomy catheter to extract multiple branch varices through limited incisions. This technique may be applied to tributary disease but not the main trunk of the saphenous vein. Proponents of the technique anticipate fewer incisions and more complete excision of varices because of the enhanced visualization resulting from transillumination. They further suggest that, in difficult extremities, with lipodermatosclerosis or prior liposuction, the remote location of the incisions is a benefit. Data on this technique is extremely limited. Spitz et al. reported their experience in 59 limbs. Their operative time ranged from 23 to 58 min and incisions per limb averaged 5.7 compared with 17 in their historical control group of hook phlebectomies. Total complications including cellulitis, excessive bruising or swelling totaled 6.8%. They also noted favorable cosmetic results (55). Once again, additional data is required for this technique prior to general acceptance. Perforate–Invaginate Stripping Perforate–invaginate (PIN) stripping is a technique for invaginating the saphenous vein during stripping. This technique using a rigid stripper was published by Oesch in 1993 (56). Since the vein is stripped from within its lumen there may be a smaller subcutaneous tunnel created. Proponents of this technique claim diminished hematoma, neuralgia, incision size, and cost (57). This technique has been tested in only one prospective randomized trial from the UK. Burkin et al. randomized 80 patients with saphenous vein reflux to either conventional stripping or PIN

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Chapter 87 Varicose Veins

stripping with all other techniques equally applied. They found no difference in operative time, percentage of vein stripped, or area of bruising (58). However, in selfreported quality-of-life indices, PIN stripping conveyed an advantage in the EQ global quality-of-life score (59).

Results of Surgery Flush ligation and stripping of the greater saphenous vein (GSV), as advocated by Myers nearly 50 years ago (60), has been the accepted standard of management for symptomatic varicose veins. However, since this procedure removes one of the most valuable conduits for arterial bypass, and results in significant saphenous nerve injury, thigh hematomas, and discomfort, many have argued for preservation of the GSV (3,5). Selective preservation of the GSV has been shown to reduce significantly the incidence of nerve injury from 23% to 50% to less than 5% (5,61,62). Furthermore, one can expect less hematoma formation and a more rapid recovery in patients following only branch vein avulsion (63). However, abundant data from prospective randomized trials indicate that a uniform policy of GSV preservation is associated with an unacceptably high rate of recurrent reflux and varicosities. Table 87.4 shows the results of six prospective randomized trials which in aggregate showed that GSV stripping reduced recurrence of both reflux and varicosities from 50% or greater to 26% to 28% in limbs followed for 2 to 5 years. These data have appropriately led may investigators to declare that stripping should be routine for primary GSV disease (64). Despite this compelling data supporting a universal policy of GSV stripping rather than high ligation, there may still be a role for selective GSV preservation in carefully evaluated patients with branch varices associated with normal saphenous veins. Large has shown that the recurrence rate for patients who underwent venous surgery with preservation of normal saphenous veins did not differ significantly from that for those in whom the GSV was stripped (3). He found a recurrence rate of only 10.5% at 3 years in those patients

with GSV preservation. One problem in Large’s study was that only clinical tests for the diagnosis of GSV incompetence were used. Koyano and Shukichi used Doppler ultrasound to select patients for limited stripping operations. Using the manual calf compression technique, 337 limbs with primary varicose veins were examined. They identified 80 limbs with isolated branch disease compared with 189 with GSV incompetence. By employing limited stripping operations they reduced saphenous nerve injury from 27% to 5% and sural nerve injury from 20% to 0%. No significant difference was noted in recurrence rates between patients undergoing selective stripping operations and those subjected to groin-to-ankle stripping of the GSV (5). We believe that the literature supports the concept that preservation of the GSV is a goal worth pursuing. The successful application of this technique, however, is predicated on our ability to assess GSV competence and to locate incompetent perforating veins. In the assessment of GSV competence we have shown that physical examination and photoplethysmography are 100% specific but have poor sensitivity (43% and 24% respectively) (65). Van Bemmelen also noted the poor sensitivity of plethysmography for venous insufficiency when compared with duplex scanning (66). He concluded: “these results do not warrant the continued use of photoplethysmography for surgical decision making in patients with suspected venous insufficiency.” Color flow duplex ultrasound has been validated as a sensitive and specific tool for the assessment of venous insufficiency (42,67,68). Our 1992 study showed that the degree of reflux on descending phlebography was accurately predicted by duplex valve closure times at both the superficial femoral and popliteal vein levels (67). Neglen has presented evidence that segmental color flow duplex scanning accurately reflects the degree and distribution of venous reflux with findings similar to our study (68). He suggested further that duplex scanning may be even more useful than descending venography because of the highly accurate information and noninvasive nature of duplex scanning with the rapid cuff deflation technique (42). It has been accepted as the gold

TABLE 87.4 Results of surgery for varicose veins Limbs Undergoing Saphenectomy Author (reference) Jakobsen (69) Munn (70) Hammarsten (71) Sarin (72) Neglen (73) Rutgers (74) Dwerryhouse (64) Aggregate

Follow-up (months)

Recurrent Reflux

36 30–42 52

— — —

21 60 36 60 21–60

Recurrent Varices

Nerve Injury

Limbs Undergoing GSV preservation Recurrent RefluxVarices

Recurrent Injury

Nerve

16/158 (10%) 21/57 (37%) 3/24 (12.5%)

— 19/57 (33%) —

— — —

56/162 (35%) 34/57 (60%) 2/18 (11%)

— 9/57 (16%) —

21/43 (49%) — 10/69 (14%) 15/52 (29%)

15/43 (35%) 30/74 (41%) 27/69 (39%) 11/52 (21%)

— 7/74 (9%) 27/69 (39%) —

38/46 (83%) — 34/73 (47%) 41/58 (71%)

38/46 (83%) 53/63 (84%) 44/73 (60%) 8/58 (14%)

0/63 0/73

56/161 (35%)

123/477 (26%)

113/177 (64%)

235/477 (49%)

53/200 (26.5%)

— — 9/193 (5%)

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Hunterian perforators allows one to verify that the stripping will ablate these vessels. The current state of knowledge in venous diseases suggest that the practitioner be well versed in physical examination skills, various noninvasive and invasive vascular studies, and interventions including medications, compression therapy, sclerotherapy, and surgery. There are many emerging therapies, which may eventually prove to be valuable adjuncts. It is clear that a thoughtful approach to diagnosis and treatment of the patient with venous disease is rewarded with improved and durable results.

References

FIGURE 87.10 This algorithm selects varicose vein patients with functionally normal greater saphenous veins for preservation of the GSV. Duplex examination is performed according to the rapid deflation technique of van Bemmelen (see reference 42).

standard for venous disease at our institution. The use of duplex examination in conjunction with Valsalva maneuvers as used in Koyano’s study is to be avoided because the presence of competent proximal valves can result in falsenegative results distally. Moreover, the Valsalva maneuver fails to develop sufficient reversal of venous flow to produce supravalvular pressure changes that cause consistent valve closure (42). Use of the Valsalva maneuver in the selection of patients for GSV preservation would result in some cases of unrecognized saphenofemoral junction incompetence, which could lead one to inappropriately preserve the GSV and result in a predicable recurrence. We developed an algorithm to identify those patients who would most likely benefit from a policy of selective GSV preservation (65), while minimizing unnecessary testing (Fig. 87.10). Patients with varicose veins would be examined clinically. If a diagnosis of GSV incompetence can be made on clinical grounds, then no further testing is required and the patient would proceed with the ligation and stripping operation. If the diagnosis of GSV incompetence cannot be made clinically, then the patient would undergo duplex scanning. The GSV would be stripped if it were found to be incompetent. Physical examination as the initial screening test for GSV incompetence reduces by one-third the number of duplex scanning studies ordered without compromising operative decision making. Plethysmography has no role in this algorithm. When GSV stripping is indicated it should generally be limited to the knee or upper calf level. This minimizes risk of damage to the saphenous nerve while consistently interrupting the Hunterian perforators. Given the frequency of duplicated saphenous systems, preoperative marking of incompetent

1. Wood. Works of Hippocrates. Vol. 2. New York: The Genuine Wood Co., 1886. 2. Mayo C. Treatment of varicose veins. Surg Gynec Obst 1906; 2:385–392. 3. Large J. Surgical treatment of saphenous varices with preservation of the main great trunk. J Vasc Surg 1985; 2:886–892. 4. Kistner RL, Ferris E, et al. The evolving management of varicose veins. Straub clinic experience. Postgrad Med 1986; 80:51–53, 56–59. 5. Koyano K, Shukichi S. Selective stripping operation based on doppler ultrasound findings for primary varicose veins of the lower extremities. Surgery 1988; 103:615–619. 6. National Health Survey 1935–1936. Washington, DC: US Department of Health, Education, and Welfare, 1938. 7. Logan W, Brooke E. Studies on medical and population subjects, No 12. The survey of sickness. London: General Register Office, 1957. 8. The sickness survey of Denmark. Copenhagen: The committee on Danish national morbidity survey, 1960. 9. Bobek K, Cajzl L, et al. Study on the incidence of phlebologic diseases and the influence of some etiologic factors. Phlebology 1966; 19:217–230. 10. Widmer L. Prevalence and sociomedical importance— observations in 4529 apparently healthy persons, from Basle III study. In: Peripheral venous disorders. Huber: Bern Haus, 1978. 11. Madar G, Widmer L. Varicose veins and chronic venous insufficiency: disorder or disease? A critical epidemiological review. Vasa 1986; 15:126–134. 12. Sadick NS. Treatment of varicose and telangiectatic leg veins with hypertonic saline: a comparative study of heparin and saline. J Dermatol Surg Oncol 1990; 16:24–28. 13. Duffy D. Small vessel sclerotherapy: an overview. Adv Dermatol 1988; 3:221–242. 14. Evans CJ, Fowkes FG, et al. Prevalence of varicose veins and chronic venous insufficiency in men and women in the general population: Edinburgh vein study. J Epidemiol Community Health 1999; 53:149–153. 15. Crotty T. The roles of turbulence and vasa vasorum in the aetiology of varicose veins. Med Hypotheses 1991; 34:41–48. 16. Rose S, Ahmed A. Some thoughts on the aetiology of varicose veins. J Cardiovasc Surg 1986; 1986:534–543.

Chapter 87 Varicose Veins 17. Ludbrook J. Valvular defect in primary varicose veins: cause or effect? Lancet 1963; 2:1289–1292. 18. Trendelenburg F. Uber die Unterbindung der Vena Saphena magna bei unterschenkel Varicen. Beitrag Z Clin Chir 1891; 7:195–205. 19. Allan P, Bradbury A, et al. Patterns of reflux and severity of varicose veins in the general population: Edinburgh vein study. Eur J Vasc Endovasc Surg 2000; 20:470–477. 20. Bouissou H, Julian M. Vein morphology. Phlebology 1988; 3:1–11. 21. Psaila J, Melhuish J. Viscoelastic properties and collagen content of the long saphenous vein in normal and varicose veins. Br J Surg 1989; 76:37–40. 22. Thulesius O, Ugaily-Thulesius L, et al. The varicose saphenous vein, functional and ultrastructural studies, with special reference to smooth muscle. Phlebology 1988; 3:89–95. 23. Pascale K. Geometry of varicose vein segments. Biomed Tech 1991; 36:145–148. 24. Thulesius O, Said S, et al. Endothelial mediated enhancement of noradrenaline induced vasoconstriction in normal and varicose veins. Clin Physiol 1991; 11:153–159. 25. Lowell L, Gloviczki P, Miller V. In vitro evaluation of endothelial and smooth muscle function of primary varicose veins. J Vasc Surg 1992; 16:679–686. 26. Schmid-Schonbein GW, Takase S, Bergan JJ. New advances in the understanding of the pathophysiology of chronic venous insufficiency. Angiology 2001; 52(Suppl 1):S27–34. 27. Takase S, Schmid-Schonbein G, Bergan JJ. Leukocyte activation in patients with venous insufficiency. J Vasc Surg 1999; 30:148–156. 28. Takase S, Bergan JJ, Schmid-Schonbein G. Expression of adhesion molecules and cytokines on saphenous veins in chronic venous insufficiency. Ann Vasc Surg 2000; 14:427–435. 29. Leather R, Kupinski A. A preoperative evaluation of the saphenous vein as a suitable graft. Semin Vasc Surg 1988; 1:51. 30. Kupinski A, Evans S, et al. Ultrasonic characterization of the saphenous vein. Cardiovasc Surg 1993; 1:513–517. 31. Linton R. The communicating veins of the lower leg and the operative technique for their ligation. Ann Surg 1938; 107:582–593. 32. May R. Nomenclature of the surgically most important connecting veins. In: May R, Partsh H, Staubesand J, eds. Perforating veins. Baltimore: Urban & Schwarzenberg, 1981:13–18. 33. O’Donnell T, Burnand K, et al. Doppler examination vs clinical and phlebographic detection of the location of incompetent perforating veins. Arch Surg 1977; 112:31–35. 34. Cockett F, Jones D. The ankle blow-out syndrome: a new approach to the varicose ulcer problem. Lancet 1953; 1:17–23. 35. Mozes G, Gloviczki P, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996; 24:800–808. 36. Kuster G, Lofgren EP, Hollinshead WH. Anatomy of the veins of the foot. Surg Gynec Obst 1968; 127: 817–823. 37. Mozes G, Gloviczki P, et al. Surgical anatomy of perforating veins. In: Gloviczki P, Bergan JJ, eds. Atlas of endo-

38. 39. 40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

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scopic perforator vein surgery. London: Springer, 1998:17–28. Boyd AM. Discussion on primary treatment of varicose veins. Proc Royal Soc Med 1948; 41:633–639. Hollinshead WH. Anatomy for surgeons: the back and limbs. Vol. 3. New York: Harper & Row, 1969:617–807. O’Donnell T, Shepard A. Chronic venous insufficiency. In: Jarret F, Hirsh J, eds. Vascular surgery of the lower extremity. St. Louis: CV Mosby, 1985. Porter J, Moneta G. Reporting standards in venous disease: an update. International Consensus Committee on Chronic Venous Disease. J Vasc Surg 1995; 21: 635–645. van Bemmelen P, Bedford G, et al. Quantitative segmental evaluation of venous valvular reflux and duplex ultrasound scanning. J Vasc Surg 1989; 10:425–431. Reporting standards in venous disease. Prepared by the Subcommittee on Reporting Standards in Venous Disease, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 1988; 8:172–181. Partsch H, Stemmer R. Compression therapy of the extremities. Paris: Editions Phlebologiques Francaises, 2001. Smith PD. Micronized purified flavonoid fraction and the treatment of chronic venous insufficiency: microcirculatory mechanisms. Microcirculation 2000; 7:S35–40. Jugenheimer M. Die endoskopische subfaziale Perforansvenendissektion im Behandlungskonzept der primaeren Varikosis. Medizinische Klinik 1992; 87:289–292. Glovicizki P, Cambria R, et al. Surgical technique and preliminary results of endoscopic subfascial division of perforating veins. J Vasc Surg 1996; 23:517–523. O’Donnell T. Surgical treatment of incompetent communicating veins. In: Bergan J, Kistner R, eds. Atlas of Venous Surgery. Philadephia: WB Saunders, 1992: 111–124. Iafrati M, Bergan J, et al. Chronic venous insufficiency and the SEPS procedure. Denver, CO: Education Design Inc., 1997. Gloviczki P, Bergan JJ, et al. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American subfascial endoscopic perforator surgery registry. The North American Study Group. J Vasc Surg 1999; 29:489–502. Pierik E, van Urk H, et al. Endoscopic versus open subfascial division of incompetent perforating veins in the treatment of venous leg ulceration: a randomized trial. J Vasc Surg 1997; 26:1049–1054. Manfrini S, Gasbarro V, et al. Endovenous management of saphenous vein reflux. Endovenous Reflux Management Study Group. Br J Surg 1992; 79:889–893. Chandler J, Pichot O, et al. Treatment of primary venous insufficiency by endovenous saphenous vein obliteration. Vasc Surg 2000; 34:201–214. Chandler J, Pichot O, et al. Defining the role of extended saphenofemoral junction ligation: a prospective comparative study. J Vasc Surg 2000; 32:941–953. Spitz G, Braxton J, Bergan JJ. Outpatient varicose vein surgery with transilluminated powered phlebectomy. Vasc Surg 2000; 34:547–555.

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56. Oesch A. Pin stripping : a novel method of atraumatic stripping. Phlebology 1993; 4:171–173. 57. Goren G, Yellin A. Invaginated axial saphenectomy by a semirigid stripper: perforate-invaginate stripping. J Vasc Surg 1994; 20:970–977. 58. Durkin M, Turton E, et al. A prospective randomized trial of PIN versus conventional stripping in varicose vein surgery. Ann R Coll Surg Engl 1999; 81:171–174. 59. Durkin M, Turton E, et al. Long saphenous vein stripping and quality of life: a randomized trial. Eur J Vasc Endovasc Surg 2001; 21:545–549. 60. Myers T. Results and techniques of stripping operation for varicose veins. J Am Med Assoc 1957; 2:889. 61. Holme K, Matzen M, et al. Partial or total stripping of the great saphenous vein: 5-year recurrence frequency of neural complications after partial and total stripping of the great saphenous vein. Ugeskr Laeger 1996; 158:405–408. 62. Wellwood J, Cox S, et al. Sensory changes following stripping of the long saphenous vein. J Cardiovasc Surg 1975; 16:123–124. 63. Khan B, Khan S, et al. Prospective randomized trial comparing sequential avulsion with stripping of the long saphenous vein. Br J Surg 1996; 83: 1559–1562. 64. Dwerryhouse S, Davies B, et al. Stripping the long saphenous vein reduces the rate of reoperation for recurrent varicose veins: five-year results of a randomized trial. J Vasc Surg 1999; 29:589–592. 65. Iafrati M, O’Donnell T, et al. Clinical exam, duplex ultrasound, and plethysmography for varicose veins. Phlebology 1994; 9:114–118.

66. van Bemmelen PS, van Ramshorst B, Eikelboom BC. Photoplethysmography reexamined: lack of correlation with duplex scanning. Surgery 1992; 112:544–548. 67. Welch H, Faliakou E, et al. Comparison of descending phlebography with quantitative photoplethysmography, air plethysmography, and duplex quantitative valve closure time in assessing deep venous reflux. J Vasc Surg 1992; 16:913–919. 68. Neglen P, Seshardi R. A comparison between descending phlebography and duplex Doppler investigation in the evaluation of reflux in chronic venous insufficiency: a challenge to phlebography as the “gold standard.” J Vasc Surg 1992;16:687–193. 69. Jakobsen B. The value of different forms of treatment for varicose veins. Br J Surg 1979; 66:182–184. 70. Munn S, Morton J, et al. To strip or not to strip the long saphenous vein? A varicose veins trial. Br J Surg 1981; 68:426–428. 71. Hammarsten J, Pedersen P, et al. Long saphenous vein saving surgery for varicose veins: a long-term follow-up. Eur J Vasc Surg 1990; 4:361–364. 72. Sarin S, Scurr J, Coleridge Smith P. Stripping of the long saphenous vein in the treatment of primary varicose veins. Br J Surg 1994; 81:1455–1458. 73. Neglen P, Einarsson E, Eklof B. The functional long-term value of different types of treatment for saphenous vein incompetence. J Cardiovasc Surg (Torino) 1993; 34:295–301. 74. Rutgers P, Kitslaar P. Randomized trial of stripping versus high ligation combined with sclerotherapy in the treatment of the incompetent greater saphenous vein. Am J Surg 1994; 168:311–315.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 88 Superficial Thrombophlebitis Anil Hingorani and Enrico Ascher

Although superficial venous thrombophlebitis (SVT) is a relatively common disorder with a significant incidence of recurrence and has potential morbidity from extension and pulmonary embolism, it has been considered the stepchild of deep vein thrombosis (DVT) and received limited attention in the literature. It has been reported that acute SVT occurs in approximately 125,000 people in the United States each year (1). However, the actual incidence of SVT is most likely far greater as these reported statistics may be outdated and many cases go unreported. Traditional teaching suggests that SVT is a self-limiting process of little consequence and small risk, leading some physicians to dismiss these patients with the clinical diagnosis of SVT and to treat them with “benign neglect.” In an attempt to dispel this misconception, this chapter will examine the more current data regarding SVT and its treatment.

Clinical Presentation Approximately 35% to 46% of patients diagnosed with SVT are males with an average age of 54 years old, while the average age for females is about 58 years old (2,3). The most frequent predisposing risk factor for SVT is the presence of varicose veins, which occurs in 62% of patients. Others factors associated with SVT include: age >60 years old, obesity, tobacco use, and history of deep venous thrombosis (DVT) or SVT. Factors associated with extension of SVT include age > 60 years old, male sex and history of DVT. The physical diagnosis of superficial thrombophlebitis is based on the presence of erythema and

tenderness in the distribution of the superficial veins with the thrombosis identified by a palpable cord. Pain and warmth are clinically evident and significant swelling may be present even without DVT. From time to time, a patient may present with erythema, pain and tenderness as a streak along the leg, with a duplex ultrasound scan revealing no DVT or SVT. In these patients, the diagnosis of cellutitis or lymphangitis needs to be considered.

Etiology The tenet that blood flow changes, changes in the vessel walls, and changes in the characteristics of the flow of blood, as propounded by Virchow over 100 years ago, play a role in the etiology of thrombosis, is recognized. While stasis and trauma of the endothelium have been cited as a cause of SVT, a hypercoagulable state associated with SVT has largely been unexplored. Furthermore, since the DVT which occurs in association with SVT is often found to be noncontiguous with the SVT (2,3), the presumed mechanism of DVT by direct extension of thrombosis from the superficial venous system to the deep venous system needs to be questioned, and systemic factors in the pathophysiology of SVT should be explored. In order to determine whether a hypercoagulable state contributes to the development of SVT, the prevalence of deficient levels of anticoagulants were measured in a population of patients with acute SVT (4). A group of 29 patients with SVT were entered into the study. All patients had duplex ultrasound scans performed on both the superficial and deep venous systems. Patients solely

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with SVT were treated with nonsteroidal anti-inflammatory drugs while those with DVT were treated with heparin and warfarin. All patients had a coagulation profile performed that included: 1. 2. 3. 4. 5.

protein C antigen and activity; activated protein C (APC) resistance; protein S antigen and activity; antithrombin III (AT III); and lupus-type anticoagulant.

Of the 29, 12 patients (41%) were found to have abnormal results consistent with a hypercoagulable state. Five patients (38%) with combined SVT and DVT and seven patients (44%) with SVT alone were found to be hypercoagulable. Four patients had decreased levels of AT III only and four patients had APC resistance identified. One patient had decreased protein C and protein S, and three patients had deficiencies of AT III, protein C, and protein S. The most prevalent anticoagulant deficiency was AT III. Furthermore, in a subsequent separate set of data examining patients with recurrent SVT, anticardiolipin antibodies were detected in 33% of patients (5). These findings suggest that patients with SVT are at an increased risk of having an underlying hypercoagulable state.

Pathology While a great deal of literature exists describing the various changes that take place in the leukocyte–vessel wall interactions, cytokines/chemokines, and various other factors involved with the development and resolution of DVT, data concerning the changes involved with SVT seem to be lacking. Although some authors have theorized that the underlying pathology of SVT may be analogous with DVT, to date, this viewpoint remains largely unsupported.

Trauma The most common source of trauma associated with SVT is an intravenous cannula. This SVT may result in erythema, warmth, and tenderness along its course. Treatment starts with removal of the cannula and warm compresses. The resultant lump may persist for months notwithstanding this treatment.

Suppurative SVT Suppurative SVT (SSVT) is also associated with the use of an intravenous cannula; however, SSVT may be lethal due to its association with septicemia. The associated signs and symptoms of SSVT include pus at an intravenous site, fever, leukocytosis, and local intense pain (6). Treatment begins with removal of the foreign body and intravenous antibiotics. Excision of the vein is rarely needed to clear infection.

Migratory Thrombophlebitis Migratory thrombophlebitis was first described by Jadioux in 1845 (7) as an entity characterized by repeated thrombosis developing in superficial veins at varying sites, but most commonly in the lower extremity. This entity may be associated with carcinoma and may precede diagnosis of the carcinoma by several years. Consequently, a workup for occult malignancy may, in fact, be warranted when the diagnosis of migratory thrombophlebitis is made.

Mondor’s Disease Mondor’s disease is defined as thrombophlebitis of the thoracoepigastic vein of the breast and chest wall. It is thought to be associated with breast carcinoma or hypercoagulable state, although cases have been reported with no identifiable cause (8). Recently, the term has also been applied to SVT of the dorsal vein of the penis (9). Treatment consists of conservative measures with warm compresses and nonsteroidal anti-inflammatories.

Lesser Saphenous SVT While the bulk of attention has been focused on SVT of the greater saphenous vein, SVT of the lesser saphenous vein is also of clinical import. Lesser saphenous vein SVT may progress into popliteal DVT. In a group of 56 patients with lesser saphenous vein SVT, 16% suffered from pulmonary embolism or DVT (2). Therefore, it is crucial that patients with lesser saphenous vein SVT be treated similarly to those diagnosed with greater saphenous vein SVT, employing the same careful duplex examination, followup, and anticoagulation or ligation if the SVT approaches the popliteal vein.

Superficial Thrombophlebitis with Varicose Veins It has been reported that only 3% to 20% of SVT patients with varicose veins will develop DVT, compared with 44–60% without varicose veins (10,11,22). Therefore, it appears that patients with varicose veins may have a different pathophysiology compared with those without varicose veins. However, in a more recent study, no increased incidence of DVT or pulmonary embolism was noted when comparing patients with and without varicose veins in the 186 SVT patients identified (2). Consequently, the question of whether the SVT patients with and without associated varicose veins should be thought of as separate classifications remains undecided. However, addressing those patients with SVT involving varicose veins is essential. This type of SVT may remain localized to the cluster of tributary varicosities or may, from time to time, extend into the greater saphenous vein (2). SVT of varicose veins themselves may occur without antecedent trauma. SVT is frequently found in

Chapter 88 Superficial Thrombophlebitis

varicose veins surrounding venous stasis ulcers. This diagnosis should be confirmed by duplex ultrasound scan as the degree of the SVT may be much greater than that based solely on clinical examination. Treatment consists of conservative therapy with warm compresses and nonsteroidal anti-inflammatory agents.

Upper Extremity SVT Although very little appears in the literature, upper extremity SVT is believed to be the result of intravenous cannulation and infusion of caustic substances that damage the endothelium. Interestingly, the extension of upper extremity SVT into upper extremity DVT or pulmonary embolism is a very rare occurrence compared with lower extremity SVT (12). Initial treatment of upper extremity SVT is catheter removal followed by conservative measures, such as warm compresses and nonsteroidal antiinflammatory medications.

Diagnosis It is supposed by a few authors that SVT is a benign common process that requires no further workup unless symptoms fail to resolve quickly on their own (13). This is despite the findings that indicate DVT associated with SVT may not be clinically apparent (2). Duplex ultrasound scanning has become the initial test of choice for the diagnosis of DVT and the evaluation of SVT since first introduced by Talbot in 1982. The availability of reliable duplex ultrasonography of the deep and superficial venous systems has made routine determination of the location and incidence of DVT in association with SVT accurate and practical. Furthermore, the extent of involvement of the deep and superficial systems can be more accurately assessed utilizing this modality as routine clinical examination may not be able to precisely evaluate the proximal extent of involvement of the deep or superficial systems. Duplex ultrasound imaging also offers the advantages of being inexpensive, noninvasive, and can be repeated for follow-up examination. As venography may contribute to the onset of phlebitis and duplex imaging affords an accurate diagnosis, venography is not recommended. Duplex imaging of patients with SVT has revealed the concomitant DVT to range from 5% to 40% (2,14–16,23). It is important to note that up to 25% of these patients’ DVTs may not be contiguous with the SVT or may even be in the contralateral lower extremity (2).

Treatment The location of the SVT determines the course of treatment. The therapy may be altered should the SVT involve tributaries of the greater saphenous vein, distal greater saphenous vein, or greater saphenous vein of the proximal

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thigh. Traditional treatment for SVT localized in tributaries of the greater saphenous vein and the distal greater saphenous vein has consisted of ambulation, warm soaks, and nonsteroidal antiinflammatory agents (1,17,18). Surgical excision may play a role in the rare case of recurrent bouts of thrombophlebitis in spite of maximal medical management. However, this type of management does not address the possibilities of clot extension or attendant DVT associated with proximal greater saphenous vein SVT. The progression of isolated superficial venous thrombosis to DVT has been evaluated (19). In one study, patients with thrombosis isolated to the superficial veins with no evidence of deep venous involvement by duplex ultrasound examination were assessed by follow-up duplex ultrasonography to determine the incidence of disease progression into the deep veins of the lower extremities. Initial and follow-up duplex scans evaluated the femoropopliteal and deep calf veins in their entirety, with follow-up studies performed at an average of 6.3 days. A total of 263 patients were identified with isolated superficial venous thrombosis. Of these, 30 (11%) patients had documented progression to deep venous involvement. The most common site of deep vein involvement was the progression of disease from the greater saphenous vein in the thigh into the common femoral vein (21 patients), with 18 of these extensions noted to be nonocclusive and 12 having a free-floating component. Three patients had extended above-knee saphenous vein thrombi through thigh perforators to occlude the femoral vein in the thigh. Three patients had extended below-knee saphenous SVT into the popliteal vein and three patients had extended below-knee thrombi into the tibioperoneal veins with calf perforators. At the time of the follow-up examination, all 30 patients were being treated without anticoagulation. As a result of this type of experience, we recommend repeat duplex scanning for SVT of the greater or lesser saphenous vein after 48 hours to assess for progression (20). For SVT within 1 cm of the saphenofemoral junction, management with high saphenous ligation with or without saphenous vein stripping has been suggested to be the treatment of choice due to the recognized potential for extension into the deep system and embolization (21–24). In a series of 43 patients who underwent ligation of the saphenofemoral junction with and without local common femoral vein thrombectomy and stripping of the GSV, only two patients were found with postoperative contralateral DVT, one of whom had a pulmonary embolism (3). A total of 86% of the patients were discharged within 3 days. Four patients developed a wound cellulitis and were treated with antibiotics. One patient had a wound hematoma requiring no treatment. While satisfactory results were noted in these instances, several issues still remain unresolved. The question of whether or not to strip the GSV in addition to high ligation is not clearly addressed, although these patients do seem to experience less

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pain once the SVT is removed. Ligation was initially proposed to avert the development of deep venous thrombosis by preventing extension via the saphenofemoral junction. Since issues of noncontiguous DVT and post-ligation DVT with pulmonary embolism are not addressed by this therapy, alternative treatment options need to be explored. A prospective nonrandomized study was conducted to evaluate the efficacy of a nonoperative approach of anticoagulation therapy to manage saphenofemoral junction thrombophlebitis (SFJT) (22). Over a 2-year period between January 1993 and January 1995, 20 consecutive patients with SFJT were entered into the study. These patients were hospitalized and given a full course of heparin treatment. Duplex ultrasonography was performed before admission, both to establish the diagnosis and to evaluate the deep venous system; 2 to 4 days after admission, a follow-up duplex ultrasound scan was performed to assess resolution of SFJT and to reexamine the deep venous system. Patients with SFJT alone and resolution of SFJT as documented by duplex ultrasound scans were maintained on warfarin for 6 weeks. Those patients with SFJT and DVT were maintained on warfarin for 6 months. The incidence of concurrent DVT and its location were noted. The efficacy of anticoagulation therapy was evaluated by measuring SFJT resolution, recurrent episodes of SFJT, and occurrence of pulmonary embolism. A 40% incidence (8 of 20 patients) of concurrent DVT with SFJT was found. Of these eight patients, four had unilateral DVT, two had bilateral DVT, and two had development of DVT with anticoagulation. DVT was contiguous with SFJT in five patients and noncontiguous in three patients. Seven out of 13 duplex ultrasound scans obtained at 2 to 8 months’ follow-up demonstrated partial resolution of SFJT, five had complete resolution, and one demonstrated no resolution. There were no episodes of pulmonary embolism, zero recurrences, and no anticoagulation complications at maximum follow-up of 14 months. Anticoagulation therapy to manage SFJT was effective in achieving resolution, preventing recurrence, and preventing pulmonary embolism within the followup period. The high incidence of DVT associated with SFJT suggests that careful evaluation of the deep venous system during the course of management is necessary (25). It should be noted that the short-term effect of anticoagulation on progression to DVT or long-term effect on local recurrence of SVT had not been evaluated. When comparing these two types of therapy, one group suggested that high ligation for SFJT would be more cost effective than systemic anticoagulation for 6 months (3). The question as to whether patients with SVT need to be treated for a 6-month period remains uncertain. Our treatment course of anticoagulation spans a period of 6 weeks and, over the last 10 years, we have noted no incidence of pulmonary embolism or complications of anticoagulation. Furthermore, significant cost savings could be realized if the low-molecular-weight heparins are used in an outpatient setting instead of unfractionated intravenous heparin. In addition, since the surgical options

do not address the hypercoagulable state of these patients and may create injury to the endothelium at the saphenofemoral junction, the surgical options seem to be less appealing, at least on a theoretical basis. This issue of anticoagulation versus surgical therapy was addressed in a prospective study consisting of 444 patients randomized to six different treatment plans (compression only, early surgery (with and without stripping), low-dose subcutaneous heparin, low-molecular-weight heparin, and oral anticoagulant treatment) in the management of superficial thrombophlebitis (26). Patients presenting with SVT and large varicose veins without any suspected or documented systemic disorder were included in this study. The criteria for inclusion were as follows: venous incompetence (by duplex); a tender, indurated cord along a superficial vein; and redness and heat in the affected area. Exclusion criteria were obesity, cardiovascular or neoplastic diseases, non-ambulatory status, bone/ joint disease, problems requiring immobilization, age >70 years, and patients with superficial thrombophlebitis without varicose veins. Color duplex ultrasound scans were used to detect concomitant DVT and to evaluate the extension or reduction of SVT at 3 and 6 months. The incidence of SVT extension was higher in the elastic compression and in the saphenous ligation groups (p < 0.05) after 3 and 6 months. There was no significant difference in DVT incidence at 3 months among the treatment groups. Stripping of the affected veins was associated with the lowest incidence of thrombus extension. The cost for compression solely was found to be the lowest, and the treatment arm including low-molecular-weight heparin was found to be the most expensive. The highest social cost (lost working days, inactivity) was observed in subjects treated with stockings alone. However, careful examination reveals that the results of this study are difficult to evaluate, as the details of the treatment protocols were not specifically identified. Furthermore, the exclusion criteria would eliminate many of the patients diagnosed with SVT in a clinical practice and the inclusion of almost any patient presenting with SVT, regardless of its location, makes the remaining groups quite variable. In an attempt to further clarify some of these issues, one group attempted to perform a metaanalysis of surgical versus medical therapy for isolated above knee SVT. However, a formal meta-analysis was not possible due to the paucity of comparable data between the two groups. This review suggested that medical management with anticoagulants is somewhat superior for minimizing complications and preventing subsequent DVT and pulmonary embolism. Ligation with stripping allows superior symptomatic relief from pain (27). Based on these data, the authors suggest that anticoagulation is appropriate in patients without contraindication. Although proximal greater saphenous vein SVT occurs not infrequently, the best treatment regimen based on its underlying pathophysiology and resolution rate remains controversial. More recent investigations do offer

Chapter 88 Superficial Thrombophlebitis

some guidelines; however, care should be exercised by the physician in diagnosing SVT to avoid the complications that may ensue due to the nature of the SVT. Further examination of the unresolved issues involving SVT is fundamental.

References 1. DeWeese MS. Nonoperative treatment of acute superficial thrombophlebitis and deep femoral venous thrombosis. In: Ernst CB, Stanley JC, eds. Current therapy in vascular surgery. Philadelphia: BC Decker Inc. 1991; 952–960. 2. Lutter KS, Kerr TM, et al. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery 1991;110:42–46. 3. Lohr JM, McDevitt DT, et al. Operative management of greater saphenous thrombophlebitis involving the saphenofemoral junction. Am J Surg 1992; 164: 269–275. 4. Hanson JN, Ascher E, et al. Saphenous vein thrombophlebitis (SVT): a deceptively benign disease. J Vasc Surg 1998; 27:677–680. 5. de Godoy JM, Batigalia F, Braile DM. Superficial thrombophlebitis and anticardiolipin antibodies: report of association. Angiology 2001; 52:127–129. 6. Hammond JS, Varas R, Ward CG. Suppurative thrombophlebitis: a new look at a continuing problem. South Med J 1988; 81:969–971. 7. Glasser ST. Principles of Peripheral Vascular Surgery. Philadelphia: FA Davis, 1959. 8. Mayor M, Buron I, et al. Mondor’s disease. Int J Dermatol 2000; 39:922–925. 9. Sasso F, Gulino G, et al. Penile Mondors’ disease: an underestimated pathology. Br J Urol 1996; 77:729–732. 10. Bergqvist D, Jaroszewski H. Deep vein thrombosis in patients with superficial thrombophlebitis of the leg. Br Med J 1986; 292:658–659. 11. Prountjos P, Bastounis E, et al. Superficial venous thrombosis of the lower extremities co-existing with deep venous thrombosis: a phlebographic study on 57 cases. Int Angiol 1991; 10:263–265. 12. Sassu GP, Chisholm CD, et al. A rare etiology for pulmonary embolism: basilic vein thrombosis. J Emerg Med 1990; 8:45–49.

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13. Cunningham et al. (eds) Section XIII. Medical and Surgical Complication in Pregnancy. Williams Obstetrics, 20th edn. Stamford CT: Appleton & Lange, 1997;1112. 14. Talbot SR. Use of real-time imaging in identifying deep venous obstruction: a preliminary report. Bruit 1982; 6:41–42. 15. Skillman JJ, Kent KC, et al. Simultaneous occurrence of superficial and deep thrombophlebitis in the lower extremity. J Vasc Surg, 1990; 11:818–823. 16. Jorgensen JO, Hanel KC, et al. The incidence of deep venous thrombosis in patients with superficial thrombophlebitis of the lower limbs. J Vasc Surg 1993; 18:70–73. 17. Ludbrook J, Jamieson GG. Disorders of veins. In: Sabiston DC Jr, ed. Textbook of surgery. 12th edn. Philadelphia: WB Saunders, 1981:1808–1827. 18. Hobbs JT. Superficial thrombophlebitis. In: Hobbs JT, editor. The treatment of venous disorders. Philadelphia: JB Lippincott, 1977; 414–427. 19. Chengelis DL, Bendick PJ, et al. Progression of superficial venous thrombosis to deep vein thrombosis. J Vasc Surg 1996; 24:745–749. 20. Blumenberg RM, Barton E, et al. Occult deep venous thrombosis complicating superficial thrombophlebitis. J Vasc Surg 1998; 27:338–343. 21. Husni EA, Williams WA. Superficial thrombophlebitis of lower limbs. Surgery 1982; 91:70–73. 22. Lofgren EP, Lofgren KA. The surgical treatment of superficial thrombophlebitis. Surgery 1981; 90:49–54. 23. Gjores JE. Surgical therapy of ascending thrombophlebitis in the saphenous system. Angiology 1962; 13:241–243. 24. Plate G, Eklof B, et al. Deep venous thrombosis, pulmonary embolism and acute surgery in thrombophlebitis of the long saphenous vein. Acta Chir Scand 1985; 151:241–244. 25. Ascer E, Lorensen E, et al. Preliminary results of a nonoperative approach to saphenofemoral junction thrombophlebitis. J Vasc Surg 1995; 22:616–621. 26. Belcaro G, Nicolaides AN, et al. Superficial thrombophlebitis of the legs: a randomized, controlled, follow-up study. Angiology 1999; 50:523–529. 27. Sullivan V, Denk PM, et al. Ligation versus anticoagulation: treatment of above-knee superficial thrombophlebitis not involving the deep venous system. J Am Coll Surg 2001; 193:556–562.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 89 Acute Deep Vein Thrombosis Anthony J. Comerota

Etiology

Hypercoagulability

Venous thromboembolism is a major cause of morbidity in the surgical patient. Pulmonary embolism remains a frequent and often preventable cause of postoperative mortality and the acute and long-term consequences of lower extremity deep vein thrombosis (DVT) add significant morbidity. A recent 25-year epidemiologic study demonstrated that, although the incidence of pulmonary embolism has decreased, the incidence of DVT is unchanged for men and is increasing for older women (1). Because age is a known risk factor for venous thromboembolic disease, the overall number of patients suffering venous thromboembolic complications will likely increase as our aged population increases.

The effect of hypercoagulable states and the existence of stasis has been summarized by Stead (6). An increased risk for thrombosis is associated with an increase in procoagulant activity in the plasma, including increases in platelet count and adhesiveness, changes in the coagulation cascade and endogenous fibrinolytic activity (7). Additionally, deficiencies of antithrombin III, protein C, and protein S, as well as the presence of the lupus anticoagulant, indicate either primary or secondary hypercoagulable states that are induced by operative procedures. A hypercoagulable state and stasis are well accepted in the etiologic theories of postoperative DVT. The role of venous injury in initiating thrombus formation, however, has received a little attention over the years. Few would argue that direct vein wall injury either at the operative site or by penetrating or blunt trauma would lead to thrombus formation. As one examines the current problem, it is clear that the distant veins are not directly damaged by most surgical operations, yet are the most common sites of postoperative DVT.

Stasis It is well accepted that surgical patients suffer periods of prolonged venous stasis in their lower extremities. This has been demonstrated radiographically (2), with femoral vein blood flow measurements (3) and with radioisotopic techniques (4). The soleal sinuses (within the valve cusps) may have the most profound stasis, and an autopsy study (5) showed this location to be the principal site of venous thrombosis. It is logical that reduced velocity of venous return prolongs the contact time of activated platelets and clotting factors with the vein wall, thereby permitting thrombus formation. Stasis alone, however, has not been shown to be closely related to DVT, and other factors appear to be necessary.

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Vein Wall (Endothelial) Injury To study the possibility that venous endothelial damage in veins distant from the operative site would occur, animal models have been developed evaluating both abdominal operations (8) and total hip operations (9). Following the surgical procedure, canine jugular veins were excised after the animals were perfusion-fixed to study the venous endothelium in a vein distant from the site of the operation

Chapter 89 Acute Deep Vein Thrombosis

(Fig. 89.1). Endothelial damage occurred after abdominal operations, and more serious endothelial damage was found after total hip replacement. These endothelial lesions occurred as multiple micro-tears within the valve cusps, usually at the junction of small side branches to the

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main vein (Fig. 89.2). These lesions extended through the endothelium and through the basement membrane, exposing subendothelial collagen, which is a potent thrombogenic substance. Such lesions serve as a nidus for thrombus formation, and the observation that damage is

FIGURE 89.1 Scanning electron micrograft of the intimal surface of the jugular vein of a dog that was anesthetized, but not operated (N). The osteum of a side-branch is centered with a valve (v) visualized. Both lowpower (A) and high-power (B) magnification demonstrate an intact endothelial monolayer without evidence of damage.

FIGURE 89.2 Scanning electron micrograft of a jugular vein of a dog that underwent total hip arthroplasty (OP) and had significant operative venodilation. Under low-power magnification (A), an endothelial tear (t) is located within a valve cusp (v). With progressively higher magnification, it appears that the endothelial damage occurred as a stretching (tearing) mechanism. The damage extends through the endothelium and basement membrane, exposing highly thrombogenic subendothelial collagen (B). The adherence of red blood cells, white blood cells, and platelets and the early production of fibrin strands are evident in the area of damage.

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occurring within valve cusps fits with the early observations in humans that the valve cusp was the site of origin of DVT. Because this appeared to be a tearing injury, it was theorized that operative venodilation might be responsible for the initiation of the damage. Venous diameter was then monitored in the animal model during operations, and it was found that operative venodilation beyond a certain critical point correlated with an increased incidence of venous lesions. Interestingly, the incidence of endothelial lesions in dogs that showed no dilation of the jugular vein was the same as that in the anesthetized nonoperated control animals. Examination of the endothelium of jugular and femoral veins indicated that the more severe the operative venodilation the greater the number of microtears that were observed. When examining the femoral veins in animals undergoing total hip replacement, it was evident that the femoral vein on the operated side sustained more endothelial injury, which is likely to be the result of the local concentration of vasoactive amines generated in the wound. These observations suggest that blood-borne substances are produced by operative trauma and released at the operative site, gaining entry into the bloodstream through capillaries and lymphatics, and then circulating throughout the body. Such substances may have an effect on platelets and leukocytes as well as altering the function of endothelium and having a direct effect (or indirect effect through mediators) on vascular smooth muscle. This concept was evaluated in humans (10) when the cephalic vein of patients who underwent total hip operation was monitored with continuous intraoperative ultrasound and all patients had postoperative ascending phlebography. The patients were randomly assigned to receive either the venotonic agent dihydroergotamine plus heparin or placebo preoperatively and during the postoperative period. This study was then extended to include patients undergoing total knee replacement (11). The findings indicated that dilation of the cephalic vein beyond a critical point correlated with the subsequent development of venographically proven DVT. The concept that vasoactive mediators are generated at the site of an operation and circulate in the bloodstream to cause vasodilation of distant veins is confirmed by the fact that patients undergoing total hip operations demonstrate operative venodilation and frequently develop contralateral lower extremity DVT (10). The patients undergoing total knee operation (with an intraoperative tourniquet applied to the thigh) do not develop operative venodilation, although they frequently develop postoperative DVT (11). The postoperative DVT in total knee replacement patients, however, occurs on the operated side and rarely occurs in the contralateral leg. There is substantial clinical evidence supporting the importance of operative venodilation as a cause of postoperative DVT, especially when studies evaluating prophylaxis are integrated. Observations by Kakkar and colleagues (12), the multicenter trial committee (13), and Biesaw and associates (14) have

shown that the addition of a venotonic agent, dihydroergotamine, to low-dose unfractionated heparin significantly improves the efficacy of DVT prophylaxis. It now appears that the triad proposed by Virchow (15) more than 150 years ago remains valid. Stasis and hypercoagulability occur in operated patients, and it now appears that venous endothelial damage is likely to occur in many patients, especially those undergoing larger, more serious operations. Measures designed to alter hypercoagulability, reduce stasis, and possibly modify the mediators involved with the products of tissue injury should reduce the incidence and severity of postoperative venous thromboembolic complications.

Diagnosis DVT remains a common and serious medical condition, frequently complicating the recovery of surgical patients with recognized (or unrecognized) risk factors. More than 1 million patients with DVT are diagnosed in the United States annually, resulting in approximately 50,000 to 200,000 deaths from pulmonary emboli (16,17). The predilection for blood clots to form in the veins of the lower extremities has not been fully explained, although by investigating the pathophysiology of postoperative DVT, some light has been shed on this aspect (9,10). A number of well-defined patient populations and high risk factors have been identified (18). Pulmonary embolism remains the major early complication of DVT. The postthrombotic syndrome is a costly and morbid long-term complication of DVT, resulting from venous valvular damage and persistent luminal obstruction (19,20). The risk for both pulmonary embolism and post-thrombotic syndrome escalates in patients with recurrent DVT. Because recurrent DVT is more likely to occur in patients inadequately treated (21), the necessity for an accurate diagnosis becomes apparent. An accurate evaluation of the patient at high risk for or suspected of having DVT can be challenging. Although some physicians rely solely on a single diagnostic test, others integrate imaging of the venous system with elements of the physiology of clot formation and lysis in their diagnostic approach (22,23). New imaging techniques allow the evaluation of the peripheral venous system, which was previously unavailable (24). This chapter focuses on the current approach to the diagnosis of DVT, incorporating valuable diagnostic techniques to arrive at the most reliable evaluation of the patient. Descriptions of the available diagnostic techniques for DVT have been covered in previous chapters. Certain elements of the various diagnostic methods are reviewed here to place the techniques into proper clinical prospective.

Clinical Assessment It has been accepted that an objective diagnosis of DVT is mandatory because clinical evaluation is inaccurate (25).

Chapter 89 Acute Deep Vein Thrombosis

Unfortunately, this observation has spawned an attitude that clinical assessment is never of value in these patients. This is unfortunate since clinical features can be used to classify patients with symptoms suggesting DVT and to improve diagnostic strategies. Such patients can be categorized as having either a high or low probability of DVT before diagnostic testing. Studies have shown that by categorizing the patient’s pretest probability of DVT into low, moderate, or high likelihood, diagnostic precision can be improved (26). Investigators demonstrated that the use of a model of clinical probability of DVT combined with common femoral and popliteal vein compression ultrasound decreased the number of false-positive and false-negative diagnoses using ascending phlebography as the definitive diagnostic test. They found that patients in whom there was a high clinical suspicion of DVT have an 85% chance of having phlebographically proven DVT. They also suggested that the patients with low pretest probability and negative noninvasive tests do not require treatment or additional testing, and those with a high pretest probability and a positive noninvasive test can be treated. In patients with discordant clinical assessment (pretest probability) and diagnostic tests, additional evaluation is necessary. This approach parallels that of the PIOPED investigators who demonstrated the value of clinical assessment of a patient with suspected pulmonary embolism (27).

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physiologic tests for venous obstruction proved reasonably reliable for identifying those with proximal DVT. These changes in venous physiology and the clinical presentation of symptomatic DVT are based upon the acute thrombus causing enough obstruction of the deep venous system to alter the hemodynamics of venous return. Physiologic tests are unreliable in high-risk but symptom-free patients (33). Since many of these symptom-free patients have nonocclusive thrombus, the physiologic parameters monitored were not sensitive enough to demonstrate abnormalities (and there is not enough venous obstruction to cause symptoms). Therefore, unacceptably low sensitivities were observed.

Venous Duplex Imaging Venous duplex imaging is the mainstay in the diagnosis of DVT. It has excellent diagnostic accuracy in patients with clinically suspected DVT (33,34). Some centers have good results in high-risk symptom-free patients (34), whereas other have reported poor sensitivity in symptom-free patients in surveillance programs (35). Venous duplex imaging is more accurate than indirect physiologic tests for DVT (34,36) and has essentially replaced them for the initial screening of patients, and is the definitive diagnostic study for DVT in most medical centers.

Magnetic Resonance Venography Phlebography Ascending contrast phlebography has been regarded for years as the diagnostic standard for lower extremity DVT. Because of the numerous disadvantages of phlebography and the improved results with venous duplex ultrasonography, ascending phlebography is used infrequently for the diagnosis of acute DVT. Opinions expressing the value of phlebography are generally inflated and based on evaluation of selected patients. Phlebograms used for prior reports were frequently chosen after the phlebogram was completed and the films judged to be of good quality, rather than entering the diagnostic matrix at the “point of need.” In our experience and that of others, ascending phlebography cannot be completed in 20% to 40% of the patients in whom it is requested (28,29). In patients who have successful venous access for contrast injection, goodquality biplane visualization of the lower leg is usually achieved; however, inadequate evaluation of the proximal venous system is common (29).

Indirect Physiologic Studies Physiologic studies have been used to evaluate the deep venous system as an indirect method of diagnosing DVT, assuming that reduction of maximal venous outflow (impedance plethysmography) (21,30), phasic respiratory volume change, or abnormal augmentation maneuvers (phleborheography) (31,32) were the consequences of acute DVT. In patients with clinically suspected DVT,

Magnetic resonance venography (MRV) has demonstrated excellent sensitivity in the diagnosis of proximal venous thrombosis when compared with ascending phlebography (24). Availability, cost, metallic implants, and claustrophobia limit its application. The true value of MRV is likely to be found in patients with pelvic and vena caval thrombosis, in whom traditional diagnostic studies are inadequate. Improvements in technique, the use of a 1.5 tesla magnet, intravenous gadolinium and time invested in post-processing will increase the utility of this valuable technique.

Blood Tests Since the 1980s, the use of blood tests has been investigated to assist with the diagnosis of acute DVT. Attempts were made to identify reliable markers that might indicate the presence of acute clot. Breakdown products of fibrinogen generated during clot formation as well as breakdown products of complexed fibrin generated during physiologic fibrinolysis have been studied (37,38). Prothrombin fragment and fibrinopeptides A and B are sensitive byproducts of clot formation, but have not been found to be clinically useful. D-dimer is a degradation product resulting from fibrinolysis of complexed fibrin (fibrin acted upon by factor XIII), which has proved useful in evaluating patients with suspected DVT. Although D-dimer levels are elevated in postoperative and acutely ill patients (39), a negative D-dimer test in patients with suspected DVT

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has a high negative predictive value (22,40). The conventional enzyme-linked immunosorbent assay (ELISA) is the best for D-dimer analysis; however, it is costly, time consuming, and not practical for clinical use (38,40). A number of rapid assays have been evaluated and have demonstrated results comparable to the ELISA assay (22,23), indicating that the D-dimer blood test can be performed quickly and reliably enough to be used clinically. Although an elevated D-dimer cannot be used to make treatment decisions, a normal D-dimer reliably excludes DVT. Ginsberg and associates (22) showed that a normal D-dimer had a negative predictive value of 97% and, in the subgroup of patients with a low pretest likelihood of DVT, the negative predictive value of a normal D-dimer level was 99.4%.

Management of Acute Deep Venous Thrombosis The management of patients with acute DVT has changed considerably during the past 5 years and continues to evolve. Physicians who are involved in the management of patients with venous thromboembolic disorders understand that not all venous thrombosis is the same. The location of the DVT, the associated comorbidities and risk factors, as well as patient presentation all factor into the therapeutic recommendation. There has been an important evolution to outpatient care and many patients with acute DVT are managed in an ambulatory outpatient setting. Specific anticoagulants are covered in previous chapters; however, pertinent details will be reviewed to emphasize certain aspects of patient care. Although DVT refers to blood clot formation in veins anywhere in the body, this chapter will focus on venous thrombosis of the lower extremity. Proper treatment of acute DVT can have a major impact on outcome, both over the short and long term. Numerous studies have emphasized the importance of early therapeutic anticoagulation and the potential benefits of the newer low-molecular-weight heparins (LMWHs). Newer anticoagulants such as parenteral pentasaccharides and oral thrombin inhibitors are being evaluated in clinical trials and will likely offer improved treatment alternatives in many patients. Patients with extensive DVT (iliofemoral DVT) stand to benefit from a treatment strategy which removes the clot, such as catheter-directed thrombolysis or venous thrombectomy followed by effective anticoagulation, and these treatment modalities will be integrated into an overall management strategy for patients with iliofemoral DVT.

Caveats of Anticoagulation The purpose of early anticoagulation with heparin compounds is to interrupt ongoing thrombosis, whereas the goal of longer-term oral anticoagulation with warfarin

compounds is prophylactic, aimed at preventing recurrent, acute venous thrombosis. It is generally accepted that a heparin level of 0.2 IU/mL or higher is required to effectively inhibit thrombin formation and interrupt ongoing venous thrombosis (41–44). Animal and human studies point to a plasma heparin level of 0.2 to 0.4 IU/mL as the target for effectiveness (41–44), with heparin requirements being the greatest during the first few days of treatment of acute DVT. The most widely used test for monitoring heparin therapy is the APTT, which is a general coagulation test but does not directly reflect plasma heparin levels (45,46). Several studies have shown that an APTT of >1.5 times the control level generally correlates to a plasma heparin level of 0.2 IU/mL (47). A number of clinical trials suggested that the risk of recurrent venous thromboembolism was related to the heparin dose itself (48–50), and that clinical recurrence was unusual if the patient was given a heparin dose of at least 1250 U/h (47). This most likely reflects the fact that this heparin dose is associated with effective therapeutic anticoagulation, rather than indicate a specific “heparin dose threshold.” Oral anticoagulation with warfarin compounds is used to protect patients from recurrent venous thrombosis over the long term. These compounds act by inhibiting the synthesis of four vitamin-K-dependent clotting factors—II, VII, IX and X—as well as at least two vitamin-Kdependent anticoagulant factors, proteins C and S. Since protein C has relatively rapid plasma kinetics, reducing effective protein C levels with a large loading dose of warfarin may tip the hemostatic balance toward coagulation rather than anticoagulation during the first 24 to 48 h of therapy. Therefore, the need for effective initial anticoagulation with heparin becomes evident. Since reductions of factors X and II are required for effective long-term anticoagulation with warfarin compounds, and since these factors have a long half-life, a 4- to 7-day overlap of warfarin with heparin is required. The early introduction of warfarin on day 1 of treatment limits the total duration of heparin therapy to 4 to 6 days in most patients. This improves efficiency, reduces cost, and minimizes the incidence of heparin-induced thrombocytopenia.

Heparin Effective anticoagulation prevents clot propagation and allows the body’s endogenous fibrinolytic system the opportunity to reduce thrombus burden and recanalize the thrombosed vein. The biologic half-life of unfractionated heparin does not follow simple first-order kinetics. Increasing doses of heparin disproportionately prolongs the half-life, whereas a large thrombus burden reduces the half-life, therefore the dose–response relationship is not linear (51,52). In general, a half-life of 1.5 to 2 h is often observed. Heparin is bound by platelets (51), vascular endothelium (52), and antithrombin III (53) and is neutralized by platelet factor 4 (54) and other plasma proteins such as histadine-rich glycoprotein and vitronectin.

Chapter 89 Acute Deep Vein Thrombosis

Therapeutic initial anticoagulation is important to reduce future venous thromboembolic events. Inadequate (subtherapeutic) anticoagulation is associated with significantly higher recurrent thromboembolic events. Randomized trials have shown a 15-fold increase in recurrent DVT when early anticoagulation with unfractionated heparin fell below therapeutic levels (55,56). Since these recurrences occur months later, it is not intuitively evident to treating physicians that inadequate early anticoagulation is responsible for the recurrent DVT. Early aggressive anticoagulation, maintaining the activated partial thromboplastin time (APTT) > 100, is associated with significantly fewer recurrent thromboembolic complications. If the patient does not have associated comorbidities for bleeding, there should be no increased risk of bleeding since the duration of supratherapeutic anticoagulation is relatively short. Unfortunately, oral anticoagulation alone without initial and concomitant heparin anticoagulation is associated with a significantly higher rate of recurrent venous thrombosis (56). This relationship undoubtedly is the result of subtherapeutic anticoagulation early in the course of therapy exacerbated by warfarin-induced protein C deficiency producing a relative procoagulant state. Audits of heparin anticoagulation demonstrate that many patients continue to be inadequately treated (57,58). Investigators have confirmed that a prescriptive approach to heparin administration is more effective than the subjective, individual approach attempted by many clinicians (59). An example of this prescriptive approach (using unfractionated heparin) is described in Table 89.1. When ordering heparin anticoagulation for acute DVT in the absence of comorbidities for bleeding, I prescribe a 10,000 IU bolus intravenously followed by 2000 IU/h and check the APTT at least 8 hours after the bolus, with the goal of maintaining the APTT > 100 s. This level of anticoagulation is required for only 4 to 5 days, at which time the heparin is discontinued since oral anticoagulation is now therapeutic [if the international normalized ratio (INR) > 2.0]. Using the prescriptive approach

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summarized in Table 89.1 is another good option. However, in patients with comorbidities for bleeding, one also must be cautious of potential bleeding complications. Heparin-induced thrombocytopenia (HIT) is a wellrecognized complication of heparin therapy caused by heparin-specific immunoglobulin G (IgG) antibodies generated against heparin–PF4 complexes (60). The immune complexes, which interact with the Fc receptor on the platelet, stimulate platelet activation and aggregation, and increase thrombin generation. HIT is usually recognized 5 to 10 days after heparin therapy is initiated. However, an abrupt fall in platelet count can occur with a recent heparin exposure (within 3 months) (61). HIT is reported in 2% to 8% of patients receiving heparin and is more common with bovine heparin than with porcine heparin. HIT is an antigen–antibody immunologic response which is not dose related. HIT antibody seroconversion has been reported in 8% to 17% of patients receiving UFH; however, thrombotic complications occur only in patients whose platelet counts drop. Platelet counts should be monitored in all patients receiving heparin, regardless of the route of administration or the dose prescribed. If initial heparin therapy is limited to 7 days or less, the frequency of HIT is less than 1%. In general, the platelet count should be checked between days 3 and 5. If heparin is administered for longer periods, another platelet count should be checked between days 7 and 10 and another at day 14. HIT is unusual after 14 days of heparin therapy, although thrombotic complications of HIT can develop up to 1 month after heparin is discontinued. A drop in platelet count by more that 30% indicates a high likelihood of HIT, therefore heparin should be discontinued and alternative antithrombotic therapy initiated.

Oral Anticoagulation As mentioned, warfarin compounds inhibit the vitamin K-dependent clotting factors II, VII, IX, and X. Warfarin compounds do not have an immediate effect on the coagulation system because the normal clotting factors that

TABLE 89.1 A prescriptive approach to intravenous heparin therapy: a titration nomogram for activated thromboplastin time Intravenous Infusion APTT*

Rate Change (mL/h)

Dose Change (units/24 h)†‡

£45 46–54 55–85 86–110 >110

+6 +3 0 -3 -6

+5780 +2880 0 -2280 -5760

Action Repeat APTT in 4 to 6 h Repeat APPT in 4 to 6 h None§ Stop heparin in 1 h; repeat APTT 4–6 h after restarting heparin Stop heparin sodium for 1 h; repeat APTT 4–6 h after restarting heparin

*Activated partial thromboplastin time. †Heparin sodium concentration, 20,000 units/500 mL = 40 units/mL. ‡With the use of Actin-Fs thromboplastin reagent (Dade, Mississauga, Ontario). §

During the first 24 hours repeat APTT in 4–6 h. Thereafter, the APTT will be determined once daily, unless subtherapeutic.

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exist in the circulation must be cleared. Warfarin compounds generally require 4 to 5 days of administration to achieve an adequate reduction in clotting factors to reach a therapeutic prolongation of the prothrombin time, therefore patients should be treated with heparin until this effect occurs. Primary anticoagulation with warfarin compounds alone is associated with an unacceptably high rate of recurrent venous thromboembolic complications (56). The appropriate intensity of oral anticoagulation has been identified by prospective studies which demonstrated that a prothrombin time of 1.5 times control or an international normalized ratio (INR) of 2.0 to 3.0 is as effective at preventing recurrent thromboembolic events as higher levels of anticoagulation, but is associated with significantly fewer bleeding complications. A target INR of 2.5 is therefore appropriate. Monitoring oral anticoagulation has been critically evaluated, and the INR is now the standard by which all patients should be followed. Because prothrombin time ratios have shown great variability depending on the thromboplastin used, adopting the INR as a therapeutic end point has standardized therapy and improved safety. The major complication of oral anticoagulation is bleeding, which often correlates with the degree of anticoagulation as predicted by the prothrombin time. A nonhemorrhagic complication is skin necrosis, which has been associated with a heterozygote protein-C deficiency and malignancy. Warfarin compounds cross the placenta and can produce teratogenic effects that have been characterized as “warfarin embryopathy.” This consists of nasal hypoplasia and/or stippled epiphyses, which occur after exposure to oral anticoagulants during the first trimester of pregnancy. Other central nervous system abnormalities can occur after exposure during any trimester. Neonatal bleeding is a potential risk, especially at the time of delivery because of the trauma of passage through the birth canal. Because heparin compounds do not cross the placenta, there is no risk of congenital defects or increased risk of neonatal bleeding. All women of childbearing potential taking warfarin compounds should avoid pregnancy. If anticoagulation is indicated during pregnancy,

subcutaneous heparin or low-molecular-weight heparin (LMWH) is recommended.

Low-molecular-weight Heparin LMWHs function by inhibiting factor Xa activity and factor IIa activity, with relatively more anti-Xa activity (2 : 1 to 4 : 1). LMWH preparations have a longer plasma halflife (4 to 4.5 h) than unfractionated heparin and a significantly higher plasma level following subcutaneous injection (80% to 90% vs. 20%) as a result of their improved bioavailability (62). LMWHs have less variability in anticoagulant response to a fixed dose. Because of their pharmacokinetic properties, they obtain a stable and sustained anticoagulant effect when administered subcutaneously once or twice daily, and laboratory monitoring is not necessary. LMWHs also have the advantage of a decreased incidence of HIT (approximately one-tenth that of unfractionated heparin) since there is less interaction with platelets and platelet factor 4 (PF4). Prolonged therapy with LMWHs is associated with less risk of osteoporosis compared to unfractionated heparin, due to less interaction with osteoclasts. LMWHs are approved in the United States for DVT prophylaxis in general surgery and orthopedic patients, for treatment of acute DVT and pulmonary emboli, and for prevention of ischemic complications of unstable angina and non-Q-wave myocardial infarction. The evidence that these newer anticoagulants are safe and effective for treating acute DVT is impressive. Table 89.2 reviews a meta-analysis of randomized trials evaluating treatment of acute DVT with a fixed dose (weight adjusted) of LMWH given subcutaneously compared with adjusted dose unfractionated heparin given intravenously (63). The incidence rates of recurrent symptomatic venous thromboembolism, venographic thrombus resolution, major bleeding complications, and mortality are listed. Subcutaneous injection of LMWH compounds once or twice daily without laboratory monitoring is an important advance in the management of acute DVT. Because of the ease of administration and the fact that laboratory monitoring is not necessary, outpatient therapy for acute

TABLE 89.2 Anticoagulation: low-molecular-weight heparin for treatment of acute deep venous thrombosis: a meta-analysis of prosective, randomized trials (from reference 63)

Symptomatic VTE* Venographic change Improved Worse Major bleed Mortality *Venous thromboembolism.

Unfractionated Heparin

Low-molecular-weight Heparin

Risk Reduction (%)

p-Value

6.6% (36/546)

3.1% (17/540)

53

<0.01

52% (261/500) 12% (58/500) 2.8% (21/759) 7.1% (39/546)

63% (312/492) 6% (29/492) 0.8% (6/753) 3.9% (21/540)

— — 68 47

< 0.001 <0.005 <0.04

Chapter 89 Acute Deep Vein Thrombosis

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DVT has become routine in patients who do not require hospitalization for other illnesses. The LMWH formulations approved for treatment are enoxaparin (Lovenox) and tinzaparin (Innohep). It is likely that other LMWH compounds will be approved for this indication in the future. Patients treated for acute DVT without pulmonary embolism should receive subcutaneous enoxaparin 1 mg/kg every 12 hours or 1.5 mg/kg every 24 hours. Alternatively, tinzaparin can be used at a dose of 175 IU/kg/24 h. LMWH is continued for 4 to 5 days during which time a warfarin compound is given; LMWH is discontinued when the INR is > 2.0.

Treatment Strategies The treatment strategies that follow are recommendations based upon the level and extent of venous thrombosis. These recommendations are based on the known natural history of acute DVT and the recognized benefits of therapy according to current treatment modalities.

Calf Vein Thrombosis Venous thrombosis limited to the calf veins is an important clinical issue; however, treatment remains controversial. Isolated calf vein thrombi often do not cause major sequelae and do not place the patient at high risk for pulmonary embolism. However, calf vein thrombi can embolize and propagation into the larger proximal veins increases the risk for pulmonary embolism and the post-thrombotic syndrome. Whether patients are symptomatic or asymptomatic and whether the calf vein thrombi are found incidentally on screening examinations of high-risk inpatients or in symptomatic outpatients further complicates the clinical question. Several studies which followed patients with isolated calf vein thrombosis found propagation rates as high as 30% in postoperative and hospitalized patients. Early propagation was found in 10% of symptomatic patients. If not treated with therapeutic anticoagulation, recurrent venous thromboembolic complications have been observed in up to 30% of patients with isolated calf DVT (64,65). Considering these results, treatment of patients with calf vein thrombosis appears to be indicated, especially if their thromboembolic risk continues or if the cause of their DVT has not been identified and eliminated (Fig. 89.3). Outpatients with symptomatic calf DVT and inpatients with ongoing thromboembolic risk should benefit from 6 weeks to 3 months of anticoagulation. If patients are not anticoagulated because of an increased risk of bleeding, they should be monitored with venous duplex imaging at 5- to 7-day intervals for 10 to 14 days or until their high-risk period has passed and they have returned to full ambulation. If extension into the proximal venous system is demonstrated, patients are then reevaluated for definitive therapy.

FIGURE 89.3 Algorithm for the management of patients with calf vein thrombosis.

Femoral–Popliteal Venous Thrombosis Since up to 40% of patients with proximal DVT have asymptomatic pulmonary embolism, a ventilation–perfusion (V/Q) scan should be considered part of the initial evaluation of patients with proximal DVT (66). However, routine V/Q scans are often difficult to justify in today’s climate of cost containment, although V/Q scan findings may be of practical value in the management of the patient with subsequent pleuritic symptoms who is therapeutically anticoagulated. Approximately 25% of patients with initially asymptomatic pulmonary embolism develop new signs or symptoms of pulmonary embolism during anticoagulation (usually pleuritic chest discomfort) and these new symptoms are often interpreted as failure of anticoagulation unless the physician is aware that the patient had prior documentation of a V/Q mismatch. A repeat lung scan that fails to identify new perfusion defects indicates that the symptoms are a consequence of the prior pulmonary embolism; therefore, the patient is not a treatment failure and caval filtration is not indicated. DVT involving the femoral vein of the thigh and popliteal veins is the most common form necessitating therapy. Anticoagulation is standard therapy, but it does not actively eliminate thrombus from the deep venous system. However, effective anticoagulation allows physiologic fibrinolysis to recanalize occluded veins. Furthermore, even in the absence of recanalization, morbidity may be minimal if thrombus is limited to the femoral vein in the thigh. It has been shown that ligation of the femoral vein below the origin of the profunda femoris causes minimal morbidity (67), since most patients have adequate venous collateral drainage around a mid-thigh obstruction. In light of these observations, early effective anticoagulation is the preferred treatment. Immediate treatment consists of either intravenous unfractionated heparin (for inpatients) or subcutaneous LMWHs for outpatients (and many inpatients). If intravenous unfractionated heparin is chosen, supratherapeutic anticoagulation for the first 3 to 4 days of therapy is my preferred approach rather than monitored anticoagulation (in patients without comorbidities for bleeding).

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Supratherapeutic heparin anticoagulation (PTT > 100 s) for 3 to 5 days is not associated with additional bleeding complications in the absence of comorbidites for bleeding (68). At therapeutic concentrations of unfractionated heparin, two-thirds of the administered dose has no anticoagulant activity. However, at higher heparin concentrations (supratherapeutic levels), both high-affinity and low-affinity heparin molecules catalyze the antithrombin effect of a second plasma protein, heparin cofactor II (69). Oral anticoagulation is started immediately and continued over the long term, maintaining an INR of 2.0 to 3.0. Patients are allowed to ambulate normally. The appropriate duration of anticoagulation continues to be investigated, however, one year of anticoagulation appears more effective than shorter courses of therapy (70), suggesting that one year should be the minimum. Longer therapy should be considered for patients with extensive DVT and those who have persistent venous obstruction on repeat duplex imaging after a 1-year course of therapy. There may be the occasional patient who has pronounced symptoms of pain and swelling with femoralpopliteal DVT who would benefit from thrombolysis. This occurs most often when the thrombus extends through the femoral and popliteal veins and involves the confluence of the popliteal vein draining the calf veins. In this instance, catheter-directed thrombolysis can be beneficial (Fig. 89.4). Patients who have cancer, anticardiolipin antibodies, antithrombin deficiency, and those who have recurrent venous thromboembolic events should be considered for lifelong anticoagulation. Maintaining the INR in the range of 2.0 to 3.0 with a target of 2.5 is associated with a low risk of bleeding complications, yet patients are effectively protected from recurrent thrombosis (71). Patients who present with recurrent DVT are evaluated for an underlying malignancy and hypercoagulable state and are treated indefinitely with oral anticoagulation. Recurrent DVT in cancer patients is best managed with long-term

FIGURE 89.4 Basic algorithm for the management of patients with iliofemoral deep vein thrombosis.

LMWH, as warfarin compounds are often ineffective and associated with increased bleeding complications (72–74). LMWHs have become the preferred initial treatment for most patients with acute DVT (71). Weight-adjusted subcutaneous injection of 1 mg/kg of enoxaparin every 12 hours or 1.5 mg/kg daily, or tinzaparin at 175 IU/kg daily are recommended. Treatment is continued until the patient has received oral anticoagulants for 4 days or longer and the INR is therapeutic. Because LMWHs are given subcutaneously and do not require monitoring, hospitalization is not mandatory for safe, effective treatment. An initial hospitalization of 24 hours may be advisable for instruction and education of the patient and for planning the logistics of ongoing care. Although femoral vein ligation (below the profunda) has been abandoned as primary treatment for DVT in patients with thrombus located in the thigh and distally, this option still may be useful in selected patients who cannot receive anticoagulant treatment. Superficial femoral vein ligation is effective in preventing pulmonary embolism and propagation into the more proximal venous system in patients with thrombus limited to the ipsilateral infraprofunda venous system. Interestingly, the long-term postthrombotic sequelae are modest in these patients (75), which reinforces the importance of preserving drainage through the profunda femoris vein. Patients with proximal vein thrombosis who have an absolute contraindication to anticoagulation and those who have had pulmonary embolism while therapeutically anticoagulated are best managed with vena caval filtration. Percutaneous placement of a vena cava filter is safe and effective (76–78). If the indication for caval filtration is failure rather than a contraindication to anticoagulation, anticoagulation should be continued after filter placement to treat the primary process, DVT.

Iliofemoral Venous Thrombosis Iliofemoral DVT is the most extensive form of acute disease. These patients experience the most severe acute symptoms, which are followed by the most severe postthrombotic sequelae (79,80). Removing the thrombus from the iliofemoral venous system significantly improves short- and long-term venous function and reduces postthrombotic morbidity (81–83). Therefore, active individuals who present with iliofemoral DVT should be offered a strategy of thrombus removal, correction of an underlying iliac vein stenosis (if present) followed by effective anticoagulation. The primary goals of treating patients with iliofemoral DVT should be to prevent pulmonary emboli and eliminate the acute thrombotic and chronic postthrombotic morbidity. These goals can be achieved if the clot is eliminated from the iliofemoral venous system, unobstructed venous drainage is restored to the vena cava, and rethrombosis is avoided. Two treatment options offer the potential to achieve these goals (Fig. 89.4): catheterdirected thrombolysis and venous thrombectomy.

Chapter 89 Acute Deep Vein Thrombosis

In patients without contraindications to thrombolysis, catheter-directed thrombolysis is preferred using multiside-hole catheters which are positioned into the thrombus, usually via an ipsilateral popliteal vein or posterior tibial vein puncture (achieved under ultrasound guidance). The largest number of patients treated have received urokinase, in doses of 250,000 to 500,000 bolus and 250,000 to 350,000 U/h. Since urokinase has been removed from the market, recombinant tissue plasminogen activator (rtPA) or reteplase (occasionally in combination with abciximab) have been used. A bolus dose of 4 to 8 mg of rtPA is infused into the clot, depending upon overall thrombus burden. The bolus is followed by a 2 to 4 mg/h infusion. Dilution of the rtPA into larger volumes of saline (1 mg in 50 mL) appears to be an important improvement in technique. Larger infusion volumes appear to saturate the thrombus with the plasminogen activator more completely, resulting in more rapid lysis. When reteplase is used as the plasminogen activator, it is infused at 1 to 2 units per hour. Abciximab has been added to reteplace on occasion, used in a dose of 0.25 mg/kg bolus followed by a 12-hour infusion at 0.125 mg/kg/min. While there may be an advantage to intrathrombus infusion of abciximab, it is not yet known whether the catheter-directed, intrathrombus infusion is more effective than systemic, intravenous infusion, or whether abciximab combined with tPA is better than tPA alone. Thrombus resolution is followed by repeat phlebography at 6- to 12-h intervals. If the catheters are appropriately positioned, lysis is achieved in the majority of patients, usually within 24 h. A stenotic lesion in the iliac vein is commonly observed and must be corrected, usually with balloon angioplasty and stenting. Although vena caval filters are not routinely used as part of this catheterdirected approach, patients who have free-floating thrombus in their vena cava should be considered for caval filtration before catheter-directed thrombolysis. If catheters cannot be positioned into the occluded iliofemoral segment, or if contraindication to thrombolysis exists, an iliofemoral venous thrombectomy is performed (see Chapter 92). If patients are not operative candidates, and cannot be treated with catheter-directed thrombolysis, supratherapeutic heparin (maintaining the PTT > 100 s) with leg elevation and effective long leg compression is recommended, followed by long-term oral anticoagulation.

Heparin-Induced Thrombocytopenia Heparin-induced thrombocytopenia (HIT) is also known as heparin-associated thrombocytopenia and white-clot syndrome. It is an IgG-mediated adverse drug reaction, which in its most serious form is associated with new thrombotic events (HITT) caused by platelet and coagulation system activation (84). HIT is observed more commonly with bovine heparin than with porcine heparin.

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The reaction is not a dose-related phenomenon, and it occurs in approximately 3% to 8% of patients treated with unfractionated heparin. In patients without previous exposure to heparin, IgG seroconversion usually occurs 5 to 10 days after heparin was begun. If a patient was recently exposed to heparin (within 2 to 3 months) and is given heparin again, an immediate fall in platelet count (and thrombosis) can occur and HIT should be suspected. In this case, the abrupt fall in platelet count is indicative of preexisting heparin antibodies. In contrast, in the patient in whom heparin exposure is remote or who has not been exposed to heparin, an early fall in platelet count is generally the result of factors other than HIT. Studies have indicated that up to 8% of patients receiving unfractionated heparin develop HIT antibodies; however, only patients who exhibit thrombocytopenia are at increased risk for thrombosis. Recent studies have shown that approximately 38% to 50% who had serologically confirmed HIT developed a clinically relevant thrombosis (HITT) within 30 days (85,86). Although most series of HIT do not report such a high thrombotic complication rate, these observations underscore the importance of continuing appropriate anticoagulation (usually with a direct thrombin inhibitor) in patients with documented HIT. In the early experience in the management of patients with HIT, heparin was immediately discontinued and warfarin compounds were prescribed. Some patients developed progressive thrombosis and others with lower extremity DVT progressed to venous gangrene (87–89). It became evident that warfarin could worsen the early thrombotic complications of HIT. Thrombin generation is an important part of the pathogenesis of HITT, and protein C levels are important in downregulating thrombin generation, particularly in the small blood vessels. Warfarin rapidly reduces protein C levels, thereby allowing progressive thrombin generation, especially in the small subcutaneous venules. Therefore, HIT should be regarded as a major risk factor for warfarin-induced venous limb gangrene because of the significant increase in thrombin generation. It follows that warfarin should not be given to patients with documented HIT early in their course of therapy, at least until the patient is anticoagulated by direct thrombin inhibitors and the platelet count has returned to normal. Once the diagnosis of HIT has been made and heparin has been discontinued, three treatment options are available. Danaparoid is a mixture of low-molecular-weight polysaccharides (glycosaminoglycan), consisting mainly of heparan sulfate and dermatan sulfate, which has a molecular weight of approximately 6,000 Da (90). Danaparoid is an indirect thrombin inhibitor acting by inhibition of factor Xa. It does not prolong the APTT. Although Danaparoid has been used successfully in many patients with HIT (90–92), cross-reactivity with HIT antibodies occurs in 20% to 40% of patients (93). Although the clinical significance of this cross-reactivity is uncertain, many clinicians prefer to use alternative treatment.

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Argatroban is an anticoagulant, which is a synthetic peptide acting as a rapid and reversible direct thrombin inhibitor, which is approved for patients with HIT. Argatroban does not cross-react with heparin. It is metabolized by the liver and has a half-life of approximately 40 min (93). Argatroban is given intravenously at a dose of 2 mg/kg/min and is titrated to the APTT. Since the prothrombin time is also affected, conversion to oral anticoagulation can be difficult. Recombinant hirudin (lepirudin) is approved for treating HIT in the United States (94). Lepirudin is a 6980-Da protein that directly inhibits thrombin and is one of the most potent thrombin inhibitors currently available. Because HIT is considered a hypercoagulable state, drugs with antithrombin activity are important in the appropriate treatment of these patients. Compared with historical controls, lepirudin reduces new thromboembolic complications by 50% or more in patients with HIT. Lepirudin is available under the trade name Refludan. It is administered intravenously with the bolus of 0.4 mg/kg and a continuous infusion of 0.15 mg/kg/h. The APTT is monitored with a target of 1.5 to 2.5 times normal. When the platelet count returns to normal, the patient can be slowly restarted on warfarin and anticoagulated accordingly. Platelet-inhibiting agents have a potential therapeutic role in HIT, but do not reduce thrombin generation. Platelet inhibition appears to be an appropriate adjunctive therapy which I use routinely, especially in patients at risk for arterial thrombosis.

References 1. Silverstein MD, Heit JA, et al. Trends in the in incidence of deep vein thrombosis and pulmonary embolism: A 25-year-old population-based study. Arch Intern Med 1998;158:585–593. 2. Almen T, Nylander G. Serial phlebography of the normal lower leg during muscular contraction and relaxation. Acta Radiol 1961;57:264. 3. Clark C, Cotton LT. Blood flow in deep veins of the legs: recording technique and evaluation of methods to increase flow during operation. Br J Surg 1968;55:211. 4. Nicolaides AN, Kakkar VV, Renney JTG. The soleal sinuses and stasis. Br J Surg 1971;58:307. 5. Gibbs NM. Venous thrombosis of the lower limb with particular reference to Bedrest. Br J Med 1957;45:209. 6. Stead RB. The hypercoagulable state. In Goldhaber SZ, ed. Pulmonary Embolism and Deep Venous Thrombosis. Philadelphia: WB Saunders, 1985;161. 7. Hirsh J, Barlow GH, et al. Diagnosis of prethrombotic state in surgical patients. Contemp Surg 1980;16:65. 8. Schaub RG, Lynch PR, Steward GJ. The response of canine veins to three types of abdominal surgery: a scanning and transmission electron microscope study. Surgery 1978;83:411. 9. Stewart GJ, Alburger PD, et al. Total hip replacement induces injury to remote veins in a canine model. J Bone Joint Surg 1983;65:97.

10. Comerota AJ, Stewart GJ, et al. Operative venodilation: a previously unsuspected factor in the cause of postoperative deep vein thrombosis. Surgery 1989;106:301. 11. Stewart GJ, Lachman JW, et al. Intraoperative venous dilation and subsequent development of deep vein thrombosis in patients undergoing total hip or total knee replacement. Ultrasound Med Biol 1990;16:133. 12. Kakkar VV, Stamatakis JD, et al. Prophylaxis for postoperative deep vein thrombosis: synergistic effect of heparin and dihydroergotamine. J Am Med Assoc 1979;241: 39. 13. The Multicenter Trial Committee: Dihydroergotamine/heparin prophylaxis of postoperative deep vein thrombosis. J Am Med Assoc 1984;251: 2960. 14. Biesaw NE, Comerota AJ, et al. Dihydroergotaine/ heparin in the prevention of deep vein thrombosis after total hip replacement. J Bone Joint Surg 1988; 70-A:2. 15. Virchow R. Neuer Fall von todlicher Emboli der Lungenarterie. Arch Pathol Anat 1856;10:225. 16. Anderson FA Jr, Wheeler HB, et al. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism: The Worchester DVT Study. Arch Intern Med 1991;151:933. 17. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975;17:257. 18. Hirsh J, Hull RD. Pathogenesis of venous thromboembolism and clinical risk factors. In: Hirsh H, Hull RD, eds. Venous Thromboembolism: Natural History, Diagnosis and Management. Boca Raton, FL: CRC Press, 1987;5. 19. Johnson BF, Manzo RA, et al. Relationship between changes in the deep venous system and the development of the post-thrombotic syndrome after an acute episode of lower limb deep vein thrombosis: a one-to-six year followup. J Vasc Surg 1995;21:307–313. 20. Shull KC, Nicolaides AN, et al. Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg 1979;114:1304–1308. 21. Hull RD, Raskob GE, et al. Continuous intravenous heparin compared with intermittent subcutaneous heparin in the initial treatment of proximal-vein thrombosis. N Engl J Med 1986;315:1109–1113. 22. Ginsberg JS, Keaton C, et al. The use of D-dimer testing and impedance plethysmographic examination in patients with clinical indications of deep vein thrombosis. Arch Intern Med 1997;157:1077. 23. Scarano L, Bernardi E, et al. Accuracy of two newly described D-dimer tests in patients with suspected deep venous thrombosis. Thromb Res 1997;86:93. 24. Carpenter JP, Holland GA, et al. Magnetic reasonance venography for detection of deep venous thrombus: comparison with contrast venography and duplex Doppler ultrasonography. J Vasc Surg 1993;18:734. 25. Cranley JJ, Canos AJ, Sull WJ. The diagnosis of deep venous thrombosis: fallibility of clinical symptoms and signs. Arch Surg 1976;III:34. 26. Wells PS, Hirsh J, et al. Accuracy of clinical assessment of deep-vein thrombosis. Lancet 1995;345:1326–1330. 27. The PIOPED Investigators. Value of the ventilation/ perfusion scan in acute pulmonary embolism: results

Chapter 89 Acute Deep Vein Thrombosis

28.

29.

30.

31. 32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). J Am Med Assoc 1990;268:2753. Bergqvist D. Efficacy and safety of enoxaparin versus unfractionated heparin for randomized multicentre trial with venographic assessment. Br J Surg 1997;84:1099. Comerota AJ, White JV, Katz ML. Diagnostic methods for deep vein thrombosis: venous Doppler examination, phleborheography, iodine-125 fibrinogen uptake and phlebography. Am J Surg 1985;150:14. Hull RD, Hirsh H, et al. Diagnostic efficacy of impedance plethysmography for clinically suspected deep vein thrombosis: a randomized trial. Ann Intern Med 1985;102:21. Comerota AJ, Cranley JJ, et al. Phleborheography: results of a ten-year experience. Surgery 1982;91:573. Cranley JJ, Canos AJ, et al. Phleborheographic technique for diagnosis of deep vein thrombosis of the lower extremities. Surg Gynecol Obstet 1975;141:331. Comerota AJ, Katz ML, et al. The comparative value of noninvasive testing for diagnosis and surveillance of deep venous thrombosis. J Vasc Surg 1988;7:40. Comerota AJ, Katz ML, et al. Venous duplex imaging: Should it replace hemodynamic tests for deep venous thrombosis? Vasc Surg 1990;11:53. Ginsberg JS, Caco CC, et al. Venous thrombosis in patients who have undergone major hip or knee surgery: detection with compression US and impedance plethysmography. Radiology 1991;181:651. Heijboer H, Buller HR, et al. A comparison of realtime compression ultrasonography with impedance plethysmography for the diagnosis of deep vein thrombosis in symptomatic outpatients. N Engl J Med 1993;329: 1365. Bauer JJ. Surgical management of primary and recurrent varicose veins. In: Gloviczki JST, ed. Handbook of Venous Disorders: Guidelines of the American Venous Forum. Vol. 1. London: Chapman & Hall, 1996;394–415. Boneu B, Bes G, et al. D-dimers, thrombin antithrombin III complexes and prothrombin fragments 1 + 2: diagnosis value of clinically suspected deep vein thrombosis. Thromb Haemost 1991;65:28. Rowbotham BJ, Carrol P, et al. Measurement of crosslinked fibrin derivatives: use in the diagnosis of venous thrombosis. Throm Haemost 1987;57:59. Bounameaux H, De Moerloose P, et al. Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview. Thromb Haemost 1994;71:1. Gitel SN, Wessler S. The antithrombotic effects of warfarin and heparin following infusion of tissue thromboplastin in rabbits: clinical implication. J Lab Clin Med 1979;94:481–488. Wessler S, Reimer L, et al. Serum-induced thrombosis: studies of its induction and evolution under controlled conditions in vivo. Circulation 1959;20:264–274. Chui HM, Hirsh J, et al. Relationship between the anticoagulant and antithrombotic effects of heparin in experimental venous thrombosis. Blood 1977;49: 171–184. Morris TA, Marsh JJ, et al. Antibodies against the fibrin B-chain amino terminus detect active canine venous thrombi. Circulation 1997;96:3173-3179.

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45. Poller L, Tomson JM, Yee KF. Heparin and partial thomboplastin time: an international survey. Br J Haematol 1980;44:161–165. 46. Triplett DA, Harris CS, Koepke JA. The effect of heparin on the activated partial thromboplastin time. Am J Clin Pathol 1978;70:556–559. 47. Hull RD, Raskob GE, et al. Relation between the time to achieve the lower limit of the APTT therapeutic range and recurrent venous thromboembolism during heparin treatment for deep vein thrombosis. Arch Intern Med 1997;157:2562–2568. 48. Wester JP, de Valk HW, et al. Risk factors for bleeding during treatment of acute venous thromboembolism. Thromb Haemost 1996;76:682–688. 49. Anand S, Ginsberg JS, et al. The relation between the activated partial thromboplastin time response and recurrence in patients with venous thrombosis treated with continuous intravenous heparin. Arch Intern Med 1996;156:1677–1681. 50. Anand SS, Bates S, et al. Recurrent venous thrombosis and heparin therapy: an evaluation of the importance of early activated partial thromboplastin times. Arch Intern Med 1999;159:2029–2032. 51. de Swart CAM, Nijmeyer B, et al. Kinetics of intravenously administered heparin in normal humans. Blood 1982;60;1251. 52. Olsson P, Lagergren H, Ek, S. The elimination from plasma of intravenous heparin: an experimental study on dogs and humans. Acta Med Scand 1963;173: 619. 53. Glimelius B, Busch C, Hook M. Binding of heparin on the surface of cultured human endothelial cells. Throm Res 1978;12:773. 54. Rosenberg RD. The heparin-antithrombin system: a natural anticoagulation mechanism. In: Colman RW, Hirsh J, Marder VJ, Salzman EW, eds. Hemostasis and Thrombosis: Basic Principles and Clinical Practice, 2nd edn. Philadelphia: JB Lippincott, 1987;1373–1392. 55. Hull RD, Raskob GE, et al. Continuous intravenous heparin compared with intermittent subcutaneous heparin in the initial treatment of proximal-vein thrombosis. N Engl J Med 1986;315:1109. 56. Brandjes DPM, Buller HR, et al. Comparative trial of heparin and oral anticoagulants in the initial treatment of proximal deep vein thrombosis. N Engl J Med 1992;327:1485. 57. Wheeler AP, Jaquiss RD, Newman JH. Physician practices in the treatment of pulmonary embolism and deep vein thrombosis. Arch Intern Med 1988;148:1321–1325. 58. Hull RD, Raskob GE, et al. Optimal therapeutic level of heparin therapy in patients with venous thrombosis. Arch Intern Med 1992;152:1589–1595. 59. Raschke RA, Reilly BM, et al. The weight-based heparin dosing nomogram compared with a ‘standard care’ nomogram: a randomized controlled trial. Ann Intern Med 1993;119:874–881. 60. Greinacher A. Antigen generation in heparin-associated thrombocytopenia: the nonimmunologic type and the immunologic type are closely linked in their pathogenesis. Semin Throm Hemost 1995;21:106–116. 61. Warkentin TE, Levine MN, et al. Heparin-induced thrombocytopenia in patients treated with low-

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62.

63.

64. 65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78. 79.

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molecular-weight heparin or unfractionated heparin. N Engl J Med 1995;332:1330–1335. Bara L, Billaud E, et al. Comparative pharmocokinetics of low-molecular-weight heparin (PK 10169) and unfractionated heparin after intravenous and subcutaneous administration. Throm Res 1985;39;631–636. Lensing AWA, Prins MN, et al. Treatment of deep venous thrombosis with low-molecular-weight heparins: a meta analysis. Arch Intern Med 1995;155,601–607. Lohr JM, James KV, et al. Calf vein thrombi are not a benign finding. Am J Surg 1995;170:86–90. Philbrick JT, Becker DM. Calf vein thrombosis: a wolf in sheep’s clothing? Arch Intern Med 1988;148:2131–2138. Monreal M, Barroso RJ, et al. Asymptomatic pulmonary embolism in patients with deep vein thrombosis: Is it useful to take a lung scan to rule out this condition? J Cardiovasc Surg 1989;30:104–107. Masuda EM, Kistner RL, Ferris EB 3rd. Long-term effects of superficial femoral vein ligation: thirteen-year followup. J Vasc Surg 1992;16:741–749. Conti S, Daschbach J, Blaisdell FW. A comparison of high dose versus conventional dose heparin therapy for deep vein thrombosis. Surgery 1982;92: 972–976. Tollefsen DM, Majerus DW, Blank MK. Heparin Cofactor II: purification and properties of a heparin-dependent inhibitor of thrombin in human plasma. J. Biol Chem 1982;247:2162–2169. Kearon C, Gent M, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 1999;342:955–960. Hyers TM, Agnelli G, et al. Anti-thrombotic therapy for venous thromboembolic disease. Chest 1002;119:1765–1935. Calligaro KD, Bergen WS, et al. Thromboembolic complications in patients with advanced cancer: anticoagulation versus Greenfield filter placement. Ann Vasc Surg 1991;5(2):186. Cohen JR, Tenenbaum N, Citron M. Greenfield filter as primary therapy for deep venous thrombosis and/or pulmonary embolism in patients with cancer. Surgery 1991;109(1):12. Whitney BA, Kerstein MD. Thrombocytopenia and cancer. Use of the Kim-Ray Greenfield filter to prevent thromboembolism. South Med J 1987;80:1246. Masuda EM, Kistner RL, Ferris EB. Long-term effects of superficial femoral vein ligation: thirteen-year followup. J Vasc Surg 1992;16:741. Greenfield LJ, Rutherford RB. Recommended reporting standards for vena caval filter placement and patient followup: Vena Caval Filter Consensus Conference. J Vasc Interv Radiol 1999;10:1013–1019. JA, Jones BT. The Greenfield filter as the primary means of therapy in venous thrombembolic disease. Surg Gynecol Obstet 1991;172:253–292. Leach TA, Pastena JA, et al. Surgical prophylaxis for pulmonary embolism. Am Surg 1994;60:292–295. O’Donnell TF, Browne NL, et al. The socioeconomic

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83.

84.

85.

86.

87.

88.

89.

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effects of an iliofemoral venous thrombosis. J Surg Res 1977;22:483. Akesson H, Brudin L, et al. Venous function assessed during a 5-year period after iliofemoral venous thrombosis treated with anticoagulation. Eur J Vasc Surg 1990:4:43–48. Plate G, Einarsson E, et al. Thrombectomy with temporary arteriovenous fistula in acute iliofemoral venous thrombosis. J Vasc Surg 1984;1:867. Plate G, Akesson H, et al. Long-term results in venous thrombectomy combined with a temporary arteriovenous fistula. Eur J Vas Surg 1990:4:483–489. Comerota AJ, Aldridge SC, et al. A strategy of aggressive regional therapy for acute iliofemoral venous thrombosis with contemporary venous thrombectomy or catheterdirected thrombolysis. J Vasc Surg 1994;20:244–254. Warkentin TE, Chong BH, Greinacher A. Heparin-induced thrombocytopenia: towards consensus. Thromb Haemost 1998;79:1–7. Warkentin TE, Kelton JG. A 14-year study of heparininduced thrombocytopenia. Am J Med 1996;101: 502–507. Wallis DE, Quintos R, et al. Safety of warfarin anticoagulation in patients with heparin-induced thrombocytopenia. Chest 1999;116:1333–1338. Warkentin TE, Elevathil LJ, et al. The pathogenesis of venous limb gangrene associated with heparin-induced thrombocytopenia. Ann Intern Med 1997;127:804–812. Warkentin TE, Sikov WM, Lillicrap DP. Multicentric warfarin-induced skin necrosis complicating heparininduced thrombocytopenia. Am J Hematol 1999;62: 44–48. Warkentin TE. Heparin-induced thrombocytomapenia: IgG-mediated platelet activation, platelet microparticle generation, and altered procoagulant/anticoagulant balance in the pathogenesis of thrombosis and venous limb gangrene complicating heparin-induced thrombocytopenia. Tranfus Med Rev 1996;10:249–258. Magnani HN. Heparin-induced thrombocytopenia (HIT): an overview of 230 patients treated with Orgaran (Org 10172). Thromb Haemost 1993;70:546–61. Warkentin TE. Danaparoid (Orgaran) for the treatment of heparin-induced thrombocytopenia (HIT) and thrombosis: effects on in vivo thrombin and cross-linked fibrin generation and evaluation of the clinical significance of in vitro cross-reactivity (XR) of Danaparoid for HIT-IgG. Blood 1996;88(Suppl. 1):626a. Lewis BE, Wallis DE, Matthai W, for the ARG-911 Study Investigators. Argatroban provides effective and safe anticoagulation in patients with heparin-induced thrombocytopenia: a prospective, historical controlled study. J Am Coll Cardiol 2000:35(Suppl.A):266A (Abstract 832–2). Warkentin TE, Chong BH, Greinacher A. Heparin-induced thrombocytopenia: towards consensus. Throm Haemost 1998;79:1–7. Greinacher A, Volpel H, et al. Recombinant hirudin (lepirudin) provides safe and effective anticoagulation in patients with heparin-induced thrombocytopenia: a prospective study. Circulation 1999;99:73–80.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 90 Acute Upper Extremity Deep Vein Thrombosis Anil Hingorani and Enrico Ascher

It is widely believed that upper extremity deep vein thrombosis (UEDVT) is a benign, nonlethal disease that affects most frequently the younger male population (1–4). Several reports have emphasized the extremely low incidence of pulmonary embolism associated with UEDVT while underscoring the importance of long-term arm disability caused by obstruction or recanalization of the axillary–subclavian vein segment (1,3,5). Accordingly, recent publications have focused on aggressive diagnostic and treatment protocols that have included infusion of thrombolytic agents, balloon angioplasties, stent placement, and thoracic outlet decompression (6–8). This notion is sustained by the paucity of data regarding UEDVT. Many of the prior studies had very small numbers of patients, ranging from 12 to 30 patients (9–14). Conversely, little has been written regarding the management of patients in whom UEDVT developed during hospitalization. This is somewhat surprising since this entity appears to be more often diagnosed in a hospital setting than in an outpatient clinic. There are three obvious reasons that may account for the increased incidence of inpatient UEDVT: 1. 2. 3.

the widespread use of long-term intravenous catheters; the more liberal use of duplex scans; and the increased awareness of this condition by the intensivist, the clinician, and the surgeon.

Since these patients usually have an underlying pathology that may compound the thrombotic process, they may require different or modified approaches to treatment.

To further investigate the natural history of UEDVT, as well as the patient characteristics and associated complications, we reviewed data obtained from 170 patients referred to the service over 5 years and compared the incidence of pulmonary embolism and the rate of mortality in the presence of UEDVT between inpatients and outpatients.

Upper Extremity Deep Vein Thrombosis A total of 605 patients underwent duplex ultrasonography to rule out UEDVT at our institution over a 5-year period. A total of 170 patients were positive for UEDVT by duplex scanning. The indications for these 170 duplex examinations were either upper extremity swelling (95%) or as part of the workup for pulmonary embolism (5%). There were 103 females (61%) and 67 males (39%) with ages ranging from 9 to 101 years old (mean 68 ± 17 years). In all, 152 patients (89%) were diagnosed while admitted to the hospital, and 18 patients (11%) were diagnosed in the outpatient clinic. Risk factors included presence of a central venous catheter or pacemaker in 110 patients (65%), malignancy in 63 patients (37%), concomitant lower extremity deep venous thrombosis (LEDVT) in 19 patients (11%) and prior history of LEDVT in 18 patients (11%). Of the 170 patients, 56 patients (33%) had multiple risk factors while 36 patients (21%) had no obvious risk factor. The 1-month and 3-month mortality rates for the entire group were 16% and 34% respectively. Those

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patients with concomitant LEDVT, with age greater than or equal to 75 years old, and not treated with anticoagulation had a significantly higher 1-month mortality. Patients diagnosed in the outpatient setting were statistically younger and had a lower 3-month mortality rate than the patients diagnosed as inpatients. In the inpatient group, 12 patients (8%) experienced pulmonary emboli documented by ventilation/perfusion scan. No patient in the group diagnosed with UEDVT as an outpatient was documented to have had a pulmonary embolism. All patients were followed for between 0 and 49 months (mean 13 ± 1 month). No swelling of the affected arm was observed in 145 patients (94%), with four patients complaining of mild intermittent swelling (2%) and seven reporting significant swelling (4%). Contrary to previous reports, these findings suggest that UEDVT is associated with a low incidence of postthrombotic upper extremity swelling but a noteworthy incidence of pulmonary embolism and rate of mortality. However, how do these data compare to LEDVT? The following data help to establish the fact that UEDVT is a more serious entity than previously reported and should be managed as aggressively as LEDVT.

Comparison of Upper and Lower Extremity DVT In an attempt to justify this concept, we reviewed the records of 52 such patients admitted to our institution during an 18-month period. In addition, we compared the result to those obtained from the analysis of 430 patients with LEDVT admitted during the same period. Pulmonary embolism was documented by ventilation–perfusion lung scan in 9 of 52 patients (17%) with UEDVT and 33 of 430 patients (8%) with LEDVT (p < 0.05). Of the UEDVT patients, 25 (48%) died within 6 months of the diagnosis of UEDVT. Conversely, 14 patients (13%) in the LEDVT group died within 6 months of the diagnosis of LEDVT (p < 0.0002). Contrary to previous reports, this study suggests that UEDVT is indeed associated with a higher morbidity and mortality as compared to LEDVT and that UEDVT has been and remains an under-recognized predictor of morbidity and mortality. To further investigate this high mortality associated with UEDVT, we analyzed the mortality of various subgroups of patients with UEDVT. The precise cause of this high mortality did not become readily apparent as none of these various subgroups was associated with a remarkable increase in mortality above that of UEDVT patients in general. However, the higher mortality of the subgroups of UEDVT patients with increased age, central venous catheters, concomitant LEDVT, and lack of anticoagulation suggests that the UEDVT patients with multiple medical problems who are acutely ill with multisystem organ dysfunction may partially account for the

high mortality associated with UEDVT. Furthermore, a comparison of patients diagnosed with UEDVT as inpatients and outpatients demonstrated that the UEDVT patients diagnosed as inpatients tended to be of advanced age, have more pulmonary emboli, and have a higher associated mortality. This comparison implies that the high mortality associated with UEDVT may be reflective of the increased age and complexity of the underlying medical problems with which UEDVT patients are now presenting.

Placement of Superior Vena Cava Filters Consequently, we have tried to systemically anticoagulate these patients with UEDVT by means of a 3- to 6-month course of heparin and warfarin. However, treatment for those patients found to have an UEDVT who have contraindications to anticoagulation therapy or who suffer a pulmonary embolism despite adequate anticoagulation has not been well addressed in the literature. We propose that these patients would benefit from the placement of a superior vena cava (SVC) filter (15–19) (Fig. 90.1). Our previously reported experience on SVC filters demonstrated the clinical feasibility of the placement of Greenfield filters (GF) in the SVC (15). Nevertheless, there is scant follow-up examining a large series of patients undergoing placement of SVC filters in the literature. Issues concerning long-term efficacy, SVC thrombosis, migration of the filter, and perforation of the SVC have not been addressed. Based on our recent experience, we investigated the values and limitations of the placement of SVC filtration devices in the acute setting (20). During a 78-month period, we placed SVC-GF in 72 patients with UEDVT in whom anticoagulation was either deemed contraindicated (n = 67) or proven ineffective in preventing recurrent PE (n = 4) or extension of the thrombus (n = 1). There were 25 males (35%) and 47 females (65%) ranging in age from 25 to 99 years (mean 74 years). Follow-up ranged from 10 days to 78 months (mean 7.8 months). Sequential chest roentgenograms revealed no filter migration or displacement in 26 patients. Of the 72 patients, 34 (47%) died in the hospital of causes unrelated to the SVC filter or recurrent thromboembolism (mean time to death 20 days). Follow-up of the surviving 38 patients ranged from 1 month to 78 months (mean 22 months), with none of these patients presenting with any evidence of pulmonary embolism. One SVC-GF was incorrectly discharged into the innominate vein and left in place. This vein remains patent 2 months after insertion without evidence of filter migration. One of the most striking features of this series was the extremely high rate of mortality in these patients. Similarly, an earlier report found a survival rate of only 48% at 6 months. While it is difficult to analyze the factors

Chapter 90 Acute Upper Extremity Deep Vein Thrombosis

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FIGURE 90.1 Example of SVC-GF. Left: Chest radiograph in November 1995. Arrow marks SVC-GF. Right: Same patient’s chest radiograph in Februrary 2002. Note no apparent change in location of filter despite multiple interval placements of short- and longterm venous catheters.

contributing to the high mortality associated with UEDVT, from a prior review of UEDVT patients (8) we were able to conclude that clinically evident pulmonary embolism did not seem to contribute to this high mortality, whereas the underlying severity of the comorbid medical problems, such as multi-organ system dysfunction, sepsis, metastatic carcinoma, etc., may play a role in these findings. However, this analysis failed to identify a subset of the population with a very limited life expectancy in whom the SVC filter placement would have little benefit. This may have been secondary to the relatively small number of patients in each subgroup. Nevertheless, due to the difficulty in justifying placement of a SVC filter in a moribund patient, and appreciating the high mortality associated with UEDVT, we have attempted to limit the use of SVC filter to patients with an expected life expectancy greater than 1 month, fully realizing that prediction of life expectancy by any measure can be extremely inaccurate. These retrospective data suggest that the elderly patients with multiple comorbid factors with multi-organ system dysfunction (acute respiratory failure, cardiogenic shock, fulminant sepsis, acute renal failure, etc.) at the end of a protracted intensive care stay would be the type of patient in whom limiting the placement of an SVC filter due to minimal expected benefit might be entertained. We believe that insertion of SVC-GFs is a safe, efficacious, and feasible therapy and may prevent recurrent thromboembolism in patients with UEDVT who are refractory to anticoagulation therapy or have contraindications to anticoagulation. There have been no major complications related to the procedure, and a similar rate of complications to IVC filter placement can be expected (21). On intermediate follow-up, there remains no clinical evidence of recurrent pulmonary embolism or SVC thrombosis after SVC filter placement in our cohort of patients. Of course, certain precautions need to be taken to avoid the pitfalls of SVC filter placement, and further data need to be collected to properly assess which patients are candidates for the procedure. However, the overall efficacy and safety of filters placed in the SVC seems to justify further investigation.

Hypercoagulable States Associated with UEDVT In 1856, Virchow wrote the original paper describing the etiology of deep venous thrombosis (DVT) as a combination of factors involving stasis, endothelial damage, and hypercoagulable states. Since that time, further work has examined the roles of venous compression, varicosities, venous flow dynamics, and inflammation in etiology of lower extremity deep venous thrombosis (LEDVT) (22–24). Recently, much attention had been focused on the role of hypercoagulable states in the etiology of LEDVT (25–29). Conversely, while factors such as neoplasm, insertion of central venous catheter, congestive heart failure, and thoracic outlet syndrome (30) have been thought to play a role in the development of upper extremity deep venous thrombosis (UEDVT), surprisingly little information is available on the role of hypercoagulable states in the etiology of UEDVT (31,32). In our prior review of UEDVT in 170 patients, we noted that a significant number (n = 36) (21%) of patients did not have central venous catheters, neoplasm, congestive heart failure, known history of a hypercoagulable state, or local inflammation (33). In addition, we noted that 26% of these patients with UEDVT had either a history of LEDVT, a concomitant LEDVT or LEDVT after the diagnosis of UEDVT was made. Finally, we cite that not all patients with neoplasm and central venous catheter suffer UEDVT. These findings suggest that other unidentified systemic factors may play a role in the etiology of UEDVT. Thus, we prospectively investigated the prevalence of a hypercoagulable state in patients with UEDVT (34). A group of 52 patients who presented with UEDVT at our institution during a 10-month period underwent a hematological profile consisting of activated protein C (APC) resistance, antithrombin III (ATIII) level and activity, factor V mutation (arginine 506 to glycine), protein C level and activity, protein S level and activity, factors II and X activity, lupus anticoagulant, and cardiolipin antibody. This represented 68% (52/76) of the total number of

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patients in whom the diagnosis of UEDVT was made by duplex ultrasonography during this time period. The ages ranged from 9 to 97 (mean 63 years). There were 22 males and 30 females; 25 patients (48%) had a central venous line in place, 4 patients (8%) had a pacemaker, 14 patients (27%) had a history of neoplasm, and 7 patients (13%) had concomitant LEDVT. Of the 52 patients studied, 29 (56%) were found to have a hypercoagulable state; 16 patients (30%) had an ATIII deficiency, 6 patients (11%) had APC resistance due to a factor V mutation, 4 patients (8%) had antibodies to cardiolipin, 2 patients (4%) had low protein S activity, and 1 patient (2%) had low protein C activity and antigen. Of the 52 patients, 11 (21%) died during the study. Of the remaining 41 patients, 29 (71%) agreed to have their blood tests repeated twice. Of these 29 patients, 17 (58%) were found to have a hypercoagulable state, 8 patients (28%) had an ATIII deficiency, 5 patients (17%) had APC resistance due to a factor V mutation, and three patients (10%) had antibodies to cardiolipin. One patient (3%) had low protein C activity and antigen. Thus, we conclude that a hypercoagulable state may be an under-recognized and unappreciated contributing factor in the development of UEDVT. Conversely, recent investigators have suggested that UEDVT does not seem to be associated with a hypercoagulable state compared with LEDVT (35,36). However, it should be noted that these studies were comprised of very few patients, with limited testing performed and no follow-up examination to confirm the positive results. Furthermore, many of these patients were outpatients with a much younger mean age. On the other hand, another group of investigators has confirmed the association between a hypercoagulable state and UEDVT (37).

Combined UEDVT and LEDVT While these reported data largely suggested that the underlying medical condition of the UEDVT patient may be more severe compared with that of the LEDVT patient, many specific questions remained unanswered. In an attempt to further explore this issue, we examined the subset of patients with combined UEDVT and LEDVT and compared these patients to patients with UEDVT alone (38). During a 3-year period, 21 patients presented to our institution with both LEDVT and UEDVT (group 1). During the same time period, 144 patients were diagnosed with UEDVT alone (group 2). The diagnosis was confirmed by duplex scanning in all patients. In group 1, there were 14 women (67%) and 7 men (23%), with ages which ranged from 25 to 97 years old [mean 73 years old ± 17 years (SD)]. In group 2, there were 84 females (58%) and 60 males (42%), with ages ranging from 9 to 101 years old [mean 67 ± 17 years (SD)]. Differences in age and sex between the two groups were not statistically significant.

In group 1, systemic anticoagulation was implemented in 17 patients (81%). Two patients (9.5%) required placement of SVC and IVC filters due to contraindication to anticoagulation. One patient did not receive anticoagulation, and one patient was started on only aspirin. Treatment in group 2 consisted of systemic anticoagulation in 94 patients (65%). Treatment of the balance of patients consisted of aspirin in three patients (2%) and no anticoagulation in 31 patients (19%); 16 patients (11%) underwent placement of a SVC filter either due to failure of anticoagulation to prevent pulmonary embolism (two patients) or contraindication to anticoagulation (14 patients). Pulmonary emboli were documented by ventilation/perfusion lung scan in two patients (9.5%) in group 1 and in 16 patients (11%) in group 2. In the first group, 8 of the 21 patients (38%) died within 1 month of the diagnosis of UEDVT, and 11 of 21 patients (52%) died within 2 months of the diagnosis of UEDVT. In the second group, 20 of 144 patients (14%) died within 1 month of the diagnosis of UEDVT and 38 of 144 patients (26%) died within 2 months of diagnosis (p < 0.02). Our findings indicate that patients with both UEDVT and LEDVT have a higher mortality than patients with UEDVT alone. As the risk for pulmonary embolism is similar in both groups, we conjecture that the severity of medical illness in patients with both UEDVT and LEDVT may be a contributing factor to this higher mortality rate. Based on these findings, we hypothesize that the severe physiologic derangements in these extremely ill patients may be accompanied by additional hematological or venous changes that may contribute to the development of multifocal DVT. Under this hypothesis, the more severe the underlying medical condition, the more likely the patient is to develop these changes that lead to DVT. While this is not a new concept, the exact nature of these changes has not been well elucidated (39,40). It has been our experience that patients with both UEDVT and LEDVT have among the highest mortality associated with DVT. Despite the analysis that the data is subjected to including admission and discharge diagnoses, we have yet to identify factors causing this increased mortality (1,41). Upon review of these patient profiles and the causes of death in these patient populations, it was noted that the patients often had multi-system organ dysfunction consisting of cardiac, pulmonary, renal, and infectious complications. While multi-system organ dysfunction has been associated with a high mortality, this did not seem to be able to account for the increased mortality alone, as many of the patients who died during the study did not have this syndrome or were not in the intensive care unit. This may have been due to the small number of patients in the respective groups. Based on stepwise regression analysis, it appears that age and whether or not the patient received an anticoagulant primarily drive the probability of death within 30 days. The impact of LEDVT may be driven by age in that this group tended to be older (p = 0.09). When mortality is

Chapter 90 Acute Upper Extremity Deep Vein Thrombosis

adjusted for age, presence of LEDVT does not appear to be significant; however, the use of anticoagulants does still appear significant. Conversely, as this was a retrospective review with small numbers of patients, the statistical analysis of risk factors associated with mortality is of limited value. Furthermore, since the clinicians had decided which patients were to undergo examination of the lower extremities, it is possible that some of the patients in group 2 may have had concomitant LEDVT. The decision by the primary care physician not to give anticoagulant treatment to a set of patients may have also introduced a source of bias, as they may have more reluctant to administer anticoagulants to the extremely ill patients. This may have led to the patients with more severe underlying illness not receiving anticoagulant treatment. Nonetheless, these results relate that patients with concomitant UEDVT and LEDVT have a high associated mortality, and that further investigation is indeed warranted.

8.

9. 10.

11.

12.

13.

14.

Conclusions UEDVT is associated with a significant incidence of pulmonary embolism and mortality as compared to LEDVT. The patients’ overall profile suggests that their underlying medical conditions may contribute to their high mortality. While systemic anticoagulation should be used as firstline therapy for UEDVT for a period of 3–6 months, when it is contraindicated or has failed, placement of a SVC filter should be considered. In conclusion, UEDVT is a more serious entity than previously reported and should be managed as aggressively as LEDVT. However, more extensive study and follow-up is required before these beliefs can be considered proven.

15.

16.

17.

18.

19.

20.

References 1. Tilney NL, Griffiths HJG, Edward EA. Natural history of major venous thrombosis of the upper extremity. Arch Surg 1977; 101:792–296. 2. Prescott SM, Tikoff G. Deep venous thrombosis of the upper extremity: a reappraisal. Circ 1951; 59:350–355. 3. Gloviczki P, Kazmier F, Hollier L. Axillary-subclavian venous occlusion: the morbidity of a non lethal disease. J Vasc Surg 1986; 4:333–337. 4. Painter TD, Karpf M. Deep venous thrombosis of the upper extremity: five years experience at a university hospital. Angiology 1984; 35(11):743–749. 5. Donayre CE, White GH, et al. Pathogenesis determines late morbidity of axillosubclavian vein thrombosis. Am Surg 1986; 152:179–184. 6. Machleder H. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 1993; 17:305–317. 7. Cohen GS, Braunstein L, et al. Effort thrombosis: effective treatment with vascular stent after unrelieved venous

21.

22.

23.

24.

25.

26.

27.

1095

stenosis following a surgical release procedure. Cardiovasc Intervent Radiol 1996; 1:37–39. Grassi CJ, Bettmann MA. Effort thrombosis: role of interventional therapy. Cardiovasc Intervent Radiol 1990; 13:317–322. Cohen JR, Dubin M. Deep venous thrombosis of the upper extremity. NY State J Med 1988; 88:177–179. Horattas MC, Wright DJ, et al. Changing concept of deep venous thrombosis of the upper extremity: report of a series and review of the literature. Surgery 1988; 104:561–567. Shattil SJ. Diagnosis and treatment of recurrent venous thromboembolism. Med Clin North Am 1984; 68:577–601. Monreal M, Lafoz E, et al. Upper extremity deep venous thrombosis and pulmonary embolism: a prospective study. Chest 1991; 99:280–283. Adams JT, DeWeese JA. “Effort” thrombosis of the axillary and subclavian veins. J Trauma 1971; 11:923–930. Campbell DV, et al. Axillary, subclavian and brachiocephalic vein obstruction. Surg 1977; 82: 816–826. Ascer E, Gennaro M, et al. Superior vena caval Greenfield filter: indications, techniques, and results. J Vasc Surg 1996; 23:498–503. Ascher E, Hingorani A, et al. Superior vena cava Greenfield filters: indications, techniques and intermediate results. J Endovasc Surg 1999; 6(4):365–369. Hoffman MJ, Greenfield. Central venous septic thrombosis managed by superior vena cava Greenfield filter and venous thrombectomy: a case report. J Vasc Surg 1986; 4:606–611. Pais SO, Orchis DF, Mirvis SE. Superior vena caval placement of Kimray-Greenfield filter. Radiology 1987; 165:385–386. Quang DB, Chartier MB, et al. Mise en place du filtre de Greenfield dans la veine cave superiure (letter). Presse Med 1985; 24:1388–1344. Ascher E, Hingorani A, et al. Lessons learned from a 6-year clinical experience with superior vena cava Greenfield filters. J Vasc Surg 2000; 32:881–887. Greenfield LJ, Proctor MC, et al. Extended evaluation of the titanium Greenfield vena caval filter. J Vasc Surg 1994; 20:458–464. Berquist D. Postoperative thrombo-embolism: frequency, etiology, prophylaxis. New York : SpringerVerlag, 1983. Markel A, Manzo RA, et al. Valvular reflux after deep vein thrombosis: incidence and time of occurrence. J Vasc Surg 1992; 15:377–384. Prandoni P, Lensing AW, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996; 125:1–7. Svensson PJ, DahlbÂack B. Resistance to activated protein C as a basis for venous thrombosis. N Engl J Med 1994; 330:517–522. Heijboer H, Brandjes DP, et al. Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis. N Engl J Med 1990; 323:1512–1516. Pabinger I, Brâucker S, et al. Hereditary deficiency of antithrombin III, protein C and protein S: prevalence in patients with a history of venous thrombosis and criteria

1096

28.

29.

30.

31. 32. 33.

34.

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for rational patient screening. Blood Coagul Fibrinolysis 1992; 3:547–553. Khamashta MA, Cuadrado MJ, et al. The management of thrombosis in the antiphospholipid-antibody syndrome [see comments]. N Engl J Med 1995; 332:993–997. Heijboer H, Brandjes DP, et al. Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis N Engl J Med 1990; 323:1512–1516. Demeter SL, Pritchard JS, et al. Upper extremity thrombosis: etiology and prognosis. Angiology 1982; 33:743–755. Pradnoni P, Polistena P, et al. Upper extremity deep venous thrombosis. Arch Int Med 1997; 157:57–62. Haire WD. Arm vein thrombosis. Clin Chest Med 1995; 16:341–351. Hingorani A, Ascher E, et al. Upper extremity versus lower extremity deep venous thrombosis. Ann Surg 1997; 174:214–217. Hingorani A, Ascher E, et al. Upper extremity deep venous thrombosis: an underrecognized manifestation of a hypercoagulable state. Ann Vasc Surg 2000; 14(5):421–426.

35. Ruggeri M, Castaman G, et al. Low prevalence of thrombophilic coagulation defects in patients with deep vein thrombosis of the upper limbs. Blood Coagul Fibrinolysis 1997; 8:191–194. 36. Martinelli I, Cattaneo M, et al. Risk factors for deep venous thrombosis of the upper extremities. Ann Intern Med 1997; 126:707–711. 37. Prandoni P, Polistena P, et al. Upper-extremity deep vein thrombosis: risk factors, diagnosis, and complications. Arch Intern Med 1997; 157:57–62. 38. Hingorani A, Ascher E, et al. Combined upper and lower extremity deep venous thrombosis. Cardiovasc Surg 2001; 9:472–477. 39. Lowe GD, Haverkate F, et al. Prediction of deep vein thrombosis after elective hip replacement surgery by preoperative clinical and haemostatic variables: The ECAT DVT Study. European Concerted Action on Thrombosis. Thromb Haemost 1999; 81:879–886. 40. Comerota AJ, Stewart GJ. Venous tone regulatory mechanisms: What’s new? Int Angiol 1995; 14:1–7. 41. Hingorani A, Ascher E, et al. Upper extremity deep venous thrombosis and its impact on morbidity and mortality in a hospital based population. J Vasc Surg 1997; 26:853–856.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 91 Venous Interruption Lazar J. Greenfield and Mary C. Proctor

Complications of Venous Thrombosis and Prophylaxis Post-thrombotic syndrome and pulmonary embolism are the major complications of venous thrombosis. Smith et al. found pulmonary embolism to be the most frequent fatal pulmonary disorder among adults who are autopsied (1). Pulmonary embolism accounts for 142,000 to 200,000 deaths in the United States annually, with another 300,000 nonfatal cases reported (2,3). These rates have not improved with time. Pulmonary embolism is also the major contributing cause of mortality in 9% to 18% of autopsied patients (1,4). However, ante-mortem diagnosis is uncommon. In order to reduce the mortality associated with pulmonary embolism, rapid diagnosis and appropriate treatment are necessary since 11% of patients die within the first hour, and another 13% die subsequently. Among those patients who survive the first pulmonary embolism, 30% will develop recurrent disease, which is fatal in 18%. The majority of thromboemboli originate in the lower extremities (90% to 95%) with the remaining 5% to 10% developing from cardiac or upper extremity sources. With the use of permanent indwelling subclavian venous access catheters, this percentage is increasing (5,6). Previously, it was felt that significant embolism from calf vein thrombosis was rare, but now it is recognized that 50% to 65% of pulmonary emboli originate below the inguinal ligament, often from involvement of the calf and soleal veins (7–9). Two major consensus conferences on prophylaxis of thromboembolism have identified major risk factors contributing to formation of deep venous thrombosis (DVT).

These include the reason for admission as well as preexisting patient variables (10–12) (Table 91.1).

Pulmonary Embolism Clinical signs and symptoms of thromboembolism include chest pain, dyspnea, tachypnea, rales and accentuated P2, hemoptysis, collapse, sweats, alterations in arterial blood gas values, hypotension, and tachycardia. However, these signs and symptoms lack sensitivity and specificity, leading to misdiagnosis in 50% of cases. Goodall and Greenfield found that the combination of hypoxemia and hypocarbia strongly suggested pulmonary embolism, especially when the pH was normal or alkaline, while Stein et al. found the combination of dyspnea and hypoxia in a patient with a normal chest radiograph occurred more often (13,14). In studying a group of 117 patients with pulmonary embolism but no history or evidence of preexisting cardiac or pulmonary disease, Stein identified a group of signs and symptoms that were frequently present (15) (Table 91.2). When these signs are present in a patient who is at risk for thromboembolic disease, with or without evidence of DVT, further diagnostic evaluation is required. Diagnosis begins with the chest radiograph. The major objective is to rule out other disorders causing respiratory distress, such as pneumothorax, aspiration, congestive heart failure, or pneumonia. Pleural effusion pulmonary infiltrate, atelectasis, and elevated hemidiaphragm are commonly associated with but not specific for pulmonary embolism (Table 91.3). Westermark’s sign of segmental or lobar perfusion loss has been considered a hallmark of pulmonary embolism, but it is rare (13) and neither sensitive nor specific (15,16). The chest radi-

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TABLE 91.1 Risk factors for thromboembolic disease reported in consensus conference reports (data from references 10 and 11) Increasing age Prior DVT/embolism Thrombophilias Birth control pills Pregnancy Obesity Varicose veins Malignancy Stroke Postpartum Immobilization Sepsis Stasis Trauma or operation >2 h

TABLE 91.3 Chest radiograph findings in patients with and without pulmonary embolism reported in both the Goodall & Greenfield and PIOPED studies (data from references 13 and 18) Findings

Atelectasis Effusion Elevated diaphragm Cardiomegaly Westermark’s sign Pulmonary edema

Goodall (n = 71)

PIOPED* (n = 365)

PE (%)

No PE (%)

PE (%)

No PE (%)

5 10 5

16 24 4

68 48 24

48 31 19

30 5

14 2

12 7

11 1

5

8

4

13

*This group of PIOPED patients had no prior history of pulmonary or cardiac disease.

TABLE 91.2 Presenting signs and symptoms in documented pulmonary embolism reported in both the UPET and PIOPED studies (data from references 17 and 18) UPET (%)

PIOPED* (%)

Symptoms Dyspnea Pleural pain Cough Hemoptysis

81 72 54 34

73 66 37 13

Signs Tachypnea Rales Increased P2 Tachycardia Fever S3S4 Sweating Phlebitis/DVT Cyanosis

88 53 53 43 42 34 34 33 18

70† 51 23 30† 7† 27 11 11 1

*This group of PIOPED patients had no prior history of pulmonary or cardiac disease. †Differences may be due to the definitions of these terms.

ograph is most useful as an adjunct to the interpretation of the ventilation–perfusion (V/Q) lung scan. The V/Q lung scan is a noninvasive technique for the diagnosis of pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED) confirmed that a high-probability scan is indicative of pulmonary embolism and low-probability scans can virtually rule out pulmonary embolism (18) Intermediate probability readings are inadequate for making a diagnosis. These scans offer the advantages of being less expensive than angiography, less resource intensive, and more easily repeated. With the ability to detect emboli in vessels as small as 1 to 2 mm, pulmonary angiography is the diagnostic standard for pulmonary embolism. However, the technique is demanding. Optimal studies require several projections,

selective and subselective injections, and careful attention to detail (19). In major medical centers, morbidity and mortality are very low, and physicians should not hesitate to order arteriography when results from lung scans, laboratory tests, and clinical judgment are indeterminate. Spiral CT scans of the chest can also be used for diagnosis of PE. This test offers another noninvasive method of diagnosis that is both safe and effective. While there is ongoing discussion regarding the sensitivity of this test in the more distal branches of the pulmonary artery, it is accurate out to the third level. Diagnosis is based on the direct visualization of intraluminal clots: partial filling defects, complete filling defects, “railway track” signs, and mural defects (20,21). A second PIOPED study is in progress to compare spiral CT to V/Q scans and pulmonary angiography.

Historical Background Early attempts to prevent pulmonary embolism involved ligation or plication of the inferior vena cava (IVC) (22). They were effective in preventing pulmonary embolism but were associated with a high rate of mortality, recurrent pulmonary embolism, and chronic venous insufficiency (23,24). Later, external caval clip devices were developed that reduced morbidity and mortality but the procedure required general anesthesia in these critically ill patients. Intraluminal devices were introduced during the 1960s and were inserted under local anesthesia, thus providing mechanical protection from pulmonary embolism but with an improved risk–benefit profile. Early devices totally occluded the IVC but were removed when the risk had resolved. Nonremovable intraluminal filters soon replaced the temporary devices. Initially, the procedure was performed on moribund patients too compromised to withstand laparotomy. Intraluminal filters were used only

Chapter 91 Venous Interruption

in extreme situations because of concern for possible filter migration. Over time, vena caval filters have replaced ligation and extraluminal interruption as the preferred method of preventing pulmonary embolism in patients who require mechanical intervention. This change was due to several factors, including the introduction of the conical-shaped Greenfield filter in 1972 (25). It provided a high level of protection from pulmonary embolism while maintaining caval flow. Tadavarthy et al. modified the placement technique in 1984 (24), with percutaneous insertion of the Greenfield filter over a wire through a dilated track using the Seldinger technique. Although these procedures were successful, there was a high rate of insertion-site thrombosis (33–41%), hematoma, and reports of arteriovenous fistulas (26,27). This led to the development of IVC filters with a smaller profile (28). As evidence of the safety and efficacy of vena caval filters has accumulated, the indications for their use have been expanded.

Indications for Mechanical Protection Most patients with pulmonary embolism are effectively managed by anticoagulation with heparin and warfarin; however, a proportion of patients require caval interruption. The most frequent indications are contraindication to anticoagulation (38%), recurrent pulmonary embolism despite adequate anticoagulation (27%), complication of anticoagulation (17%), following pulmonary embolectomy (3%), and for prophylaxis (17%) (29). These indications have been broadened at many institutions to include a more liberal definition of prophylaxis that can encompass patients without venous thrombosis. We continue to reserve prophylactic placement for the following situations: chronic pulmonary hypertension, major DVT in a patient with severe respiratory impairment, free-floating thrombus in the iliofemoral system or vena cava, significant traumatic injuries in patients who can not be anticoagulated, or a history of DVT in patients undergoing surgical procedures at high risk for pulmonary embolism (30). Some have adopted a more liberal policy and use prophylactic filters for patients with an ongoing risk of pulmonary embolism such as oncology patients and those with paraplegia or quadriplegia.

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but ultrasound imaging can provide the same level of assurance. These methods have been found to be at least as accurate as contrast venography. Because they are performed at the bedside, they are safer for the patient, do not require exposure to radiation or contrast agents, and do not require nursing personnel to move critically ill patients to the radiology department.

Greenfield Vena Cava Filter The conical design of the Greenfield filter provides a maximal entrapment area while preserving blood flow (Fig. 91.1). The geometry of the cone permits filling to 70% of depth while maintaining 51% of the crosssectional area open. More than 80% of the depth must be filled before flow is decreased (33) (Fig. 91.2). Spacing among the six limbs ensures trapping of all emboli larger than 3 mm. The filter was initially inserted by means of a femoral or internal jugular venotomy but this approach has been replaced by percutaneous techniques. No deaths have been reported during placement of the Greenfield filter. Because of the construction of the hooks and fixation within the caval wall, migration has not occurred after the filter is deployed and fixed to the caval wall. It is not uncommon to note a gradual 0- to 18-mm difference in filter position relative to underlying bony structures on serial radiographs, but these are most often due to radiologic measurement error or respiratory fluctuation. The tip of the filter hook may rarely penetrate the vena caval wall. When this occurs, the exposed metal is incorporated in a fibrous cap that protects adjacent structures (34). Mor-

Preplacement Assessment Vena caval imaging is necessary prior to filter placement in order to evaluate the patency of the IVC, to identify any caval anomalies, to calculate the diameter of the vessel, and to determine the correct level for deployment. The contrast venacavogram remains the gold standard for this assessment although bedside placement of filters using ultrasound guidance with either external or intravascular ultrasound has become more widely accepted (31,32). Fluoroscopy is commonly used to monitor placement

FIGURE 91.1 Greenfield filter. Left: Side view with recurved hooks at the end of each limb for secure fixation to the vena cava wall. Right: End-on view showing axial filtering pattern. (Reproduced by permission from Stewart JR, Greenfield LJ. Surg Clin North Am 1982;62(3):412.)

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bidity in our series has been limited to one instance of hematuria, which resolved after discontinuing warfarin, and one case of filter misplacement in an iliac vein involving the obturator nerve, requiring filter removal after referral from another institution (25). Filter misplacement occurred in 4% of patients early in the experience and has decreased with the routine use of a guiding sheath for the titanium filter and a guidewire with the stainless steel. Because of the documented longterm patency rate of 96% (29), filters mistakenly placed in the renal vein or other tributaries contributed no morbidity. In women of childbearing age, those with renal transplants, or patients with malignant tumors or thrombus within the IVC or renal vein, use of suprarenally positioned Greenfield filters has become accepted (35–40). Approximately 15% of new or more severe venous sequelae that develop long-term can be attributed to recurrent DVT and are not correlated with filter patency. The longterm recurrent pulmonary embolism rate is 3.8% over a 20-year follow-up period, with a 1.9% incidence of fatal embolism (41).

FIGURE 91.2 The conical design of the Greenfield filter allows maximal trapping area while maintaining blood flow within the vena cava, accounting for the high rate of caval patency.

Economics The ability to insert filters percutaneously at the time of cavography or angiography led to the development of filters with a reduced delivery profile. Percutaneous insertion reduced placement cost by 58% and bedside placement has resulted in further savings (42). A second factor in reducing the cost of filter placement is the trend toward ultrasound-guided bedside placement. The economic advantages include the lower cost of ultrasound compared to contrast venography, the absence of charges for the radiology suite and the savings in staffing as the patient does not have to be moved from the unit.

Bird’s Nest Filter One of the first systems designed for percutaneous placement was the Bird’s Nest filter (Cook, Bloomington, IN) developed by Gianturco and Roehm in 1980 (43) and finally approved by the FDA in 1989. It consists of four thin strands of stainless-steel wire attached to a pair of shortangled hooks to achieve fixation by penetration of wall of the IVC. It is delivered through a 12-Fr. insertion system (Fig. 91.3). The preformed curved wires produce a fine criss-crossing network similar in appearance to a bird’s nest. This device has undergone hook modifications to correct problems with proximal migration. However, migration continues to occur and occasionally results in massive thromboembolism (44). Most recently, the deployment system has undergone modification to facilitate separation of the filter from the carrier system. Vesely et al. (45) described several technical problems associated with this device including difficulty placing the device in a short infrarenal IVC segment requiring placement of the lower strut in the iliac vein, kinking of the sheath when the iliac vein is acutely angled, filter wire prolapse with potentially impaired clot trapping ability, and difficult filter release (before modification). Although the device has been on the market for several years, relatively limited follow-up data are available. In the one large series of more than 440 patients, evaluation was conducted through telephone calls and subjective questionnaires. Rates of recurrent pulmonary embolism, caval occlusion, and insertion-site thrombosis are grossly underestimated using these techniques. Caval occlusion occurred in 19% of the 37 patients who underwent objective evaluation (46–48). FIGURE 91.3 The bird’s nest filter takes it name from the characteristic maze of wires arranged within a 7-cm segment of the inferior vena cava.

Chapter 91 Venous Interruption

Vena Tech Filter In 1988, Ricco et al. reported the results from a multicenter prospective trial of the “LGM” filter, better known in the United States as the Vena Tech Filter. It is a stamped, six-legged, cone-shaped design made of stainless steel and cobalt that ensures resistance to corrosion and requires a 12-Fr. insertion system (Fig. 91.4). In this well-designed study, Ricco et al. found a 2% incidence of recurrent pulmonary embolism, 93% rate of caval patency, incomplete opening of the filter in eight patients, tilting in 8%, and migration in 14%. One case of migration led to recurrent pulmonary embolism (49). Grassi (50) questioned the advantage of the barbed side rails on malpositioning. Incomplete opening also occurs with this device. Millward et al. followed a group of 64 patients who had LGM filters (51). The IVC thrombosis rate was 22%, raising concern regarding patency after placement. The authors express concern about placing this device in young persons with long life expectancy. Most recent data demonstrate an increasing rate of filter thrombosis as time has increased. Crochet found a thrombosis rate greater than 30% at 9 years (52). The stabilizing bars have undergone modifica-

FIGURE 91.4 The Vena Tech filter has the same cone shape as the Greenfield design but adds the stabilizer bars intended to improve stability after deployment.

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tion, as has the delivery system, but no current data are available since these changes have been made. In the summer of 2001, a revised version of the LGM filter was approved by the FDA. This device retains the conical design and use of side rails for stabilization of the device within the IVC. The profile of this filter has been reduced to a 9-Fr. outer diameter. It is manufactured of the same material as the previous device but is constructed from thin, round wire as compared to the flat, wide wire of the previous device. At this time, little information about its performance is available but it appears to have incorporated changes that should improve its long-term patency.

Simon Nitinol Filter The Simon nitinol filter was initially developed in 1977, went to clinical trial in 1985, and received FDA approval in 1990. It is a two-tiered design of a nickel titanium alloy, with thermal memory allowing it to be straightened during cold storage then regain its shape after deployment at body temperature. The lower level is a six-legged conical design with petal-shaped upper dome (Fig. 91.5). It has a

FIGURE 91.5 The Simon nitinol filter has a dual capture mechanism: a petal-shaped dome at the proximal end and six limbs arranged as a cone on the distal end.

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9-Fr. insertion system, allowing antecubital access when no other route is available (53). Results from the clinical trial reveal a 4% incidence of recurrent embolism, a caval patency rate of 81%, and a low incidence of migration (1.2%) and penetration (0.6%). McCowan et al. reported 14 months of experience with 16 patients and found caval penetration in five, caval thrombus in four, migration in one, and leg fracture in two. No significant clinical sequelae developed, but the authors feel that further clinical follow-up is needed (54). The design of this device has been shown to reduce flow in a vena cava model when a thrombus has been trapped. The stagnant area behind the thrombus becomes a site of new occlusive thrombus, as demonstrated in an animal model (55). It appears that the double-tiered trapping surface presents a significant liability with respect to caval patency and clot resolution. A redesigned nitinol filter has been introduced to the European market and is currently awaiting FDA approval. While it has a new profile, it still retains a second trapping level and long-term follow-up studies will be needed to determine patency and efficacy rates. The proposed advantage of this system is its potential for removal; however, this has not yet been evaluated.

Titanium Greenfield Filter In 1990, Greenfield et al. (56) reported the initial clinical experience with a reduced-profile Greenfield filter manufactured from titanium that allowed for percutaneous placement through a 14-Fr. sheath (Fig. 91.6). Although it functioned well as a filter (recurrent pulmonary embolism 4%), there were problems with distal migration and caval penetration in 30% of the 30 patients 30 days after placement. The hook configuration of this filter was redesigned, and a prospective multicenter clinical trial was undertaken (57). The rate of recurrent embolism was 3% in this series of 181 placements. The incidence of movement was 11%, and caval penetration was seen in only one patient. Leg asymmetry was noted in 10 cases (5.4%) but was able to be corrected by catheter manipulation. Recurrent pulmonary embolism was not associated with the occurrence of asymmetry. Additional in vivo study of the effect of asymmetry on clot-trapping ability supported this conclusion (58). A longer-term report was published in 1994 which demonstrated the incidence of recurrent pulmonary embolism to be 3.5% and a caval patency rate of 99% (59).

Percutaneous Stainless-steel Greenfield Filter The most recent Greenfield filter is similar in design to the titanium filter but is manufactured of stainless steel. It has an opening at the apex to allow passage of a guidewire to secure delivery and facilitate positioning of the filter. Additionally, two of the filter hooks are directed in a down-

FIGURE 91.6 The titanium version of the Greenfield filter shares the conical design of the original Greenfield filter but is delivered through a 12-Fr. delivery system to allow for percutaneous insertion.

ward direction to improve fixation within the vena cava (60). The efficacy of this device is similar to the titanium filter in all respects. The long-term experience indicates a recurrent pulmonary embolism rate of 2.6% and a caval patency rate of 98% (61). This device has the additional benefit of a flexible delivery system that facilitates passage through the left femoral vein when necessary.

Cordis TrapEase Filter One of the newest devices to reach the market is the TrapEase filter distributed by Johnson & Johnson (Fig. 91.7). It received FDA approval during 2000 based upon its similarity to previously approved devices. The device is manufactured of nitinol and is laser-cut from a single piece of material. It appears as two cones attached at the bases with an apex at each end. Minimal data are available for this device as it underwent clinical testing in Europe prior to release in the US. Several factors remain to be evaluated in a larger experience. The design has two trapping surfaces which have been previously shown to be associated with higher rates of caval thrombosis. The limbs are also flat wire, broader than all others except the Vena Tech. This has been associated with increased caval wall thick-

Chapter 91 Venous Interruption

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FIGURE 91.7 The Cordis TrapEase filter is manufactured of broad wire with a double trapping surface. These factors may reduce filter patency following capture of a significant thrombus.

ening (55). Hemodynamic testing has shown several areas of stasis and turbulence when clots are captured against the wall of the cava and, in animal studies, these regions were associated with dense fibrin webbing that occluded flow. It appears that this has also occurred in humans based on the large number of occlusive events reported to the FDA since release of this filter (CDRH MAUDE Database listing of adverse events found on the FDA website— http://www.fda.gov/cdrh/maude.html). These findings suggest one of the inherent problems with the current practice of granting approval of new devices based on an assumed equivalence to an existing device. The TrapEase filter design appears sufficiently different from existing devices that a more extensive evaluation would have been appropriate.

Optional Vena Caval Filters There has been a renewed interest in filters that offer the option of removal at a future time, confirming the cyclical nature of the field. This is especially attractive to trauma surgeons who would like the protection offered by a filter but are hesitant about leaving a permanent device in young patients who have 50 or more years of life expectancy. None of the filters has been on the market long enough to provide data about long-term outcomes. Filter removal is conceptually straightforward and FDA approval is being sought for at least two devices: the Tulip Filter developed by the Cook company and the previously mentioned nitinol device. Unlike temporary filters that must be removed within a short period of time, an optional filter must be designed as carefully as a permanent device as it may never be removed. The design must also

lend itself to nontraumatic retrieval. Several factors must be considered before deciding to use an optional filter. First, is the patient’s risk of thromboembolism truly time limited and is the duration of the risk period known? If this question can be addressed, then the next issue that needs to be understood is the length of the window when the device can be safely removed. This currently ranges between 2 and 6 weeks. The final issue relates to the status of the filter at the time of removal and what will happen if it contains thrombus. The underlying premise is that a vena caval filter poses risk to the patient over time but this has not been observed in long-term follow-up of the Greenfield filter. Early studies have shown that relatively few optional filters are ever removed but, as experience with these devices increases, this will likely change (62,63). Although no randomized studies have been conducted, efforts are being made to compile experience through a multicenter registry (64,65).

Conclusion Intraluminal vena caval filter devices have replaced extraluminal devices because they provide the same effective protection against recurrent pulmonary embolism without the added morbidity and mortality associated with general anesthesia and laparotomy. Furthermore, percutaneous placement of these devices at the time of cavography or angiography has become the most cost-effective technique. The Greenfield vena caval filter remains the most widely used device and the only one with demonstrated long-term patency when placed above the renal veins (39). As new devices are introduced, consistent, ob-

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jective evaluation of safety and long-term efficacy is essential. As interventional radiologists assume more of the responsibility for placing vena caval filters, it is important that they also ensure the continuity of care for recipients, whether they conduct the follow-up themselves or refer patients to their primary care-givers. Routine follow-up of patients with filters is supported by a recent consensus conference of both surgeons and radiologists (66). Study of caval interruption techniques has taught us that ease of placement is important, but it is far more important that vena caval filters provide durable protection from venous thromboembolism while maintaining long-term patency of the IVC.

References 1. Smith G, Dammin G, Dexter L. Postmortem arteriographic studies of the human lung in pulmonary embolization. J Am Med Assoc 1964;188:143–151. 2. Coon W. Venous thromboembolism: prevalence, risk factors, and prevention. Clin Chest Med 1984;5(3):391–401. 3. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Progr Cardiovasc Dis 1975;17:259–270. 4. Havig O. Deep vein thrombosis and pulmonary embolism: an autopsy study with multiple regression analysis of possible risk factors. Acta Chirurg Scand 1977;478 (suppl 1):120. 5. Starkhammar H, Bengtsson M, Morales O. Fibrin sleeve formation after long-term brachial catheterisation with an implantable port device: a prospective venographic study. Eur J Surg 1992;158:481–484. 6. Wechsler RJ, Spirn P, et al. Thrombosis and infection caused by thoracic venous catheters: pathogenesis and imaging findings. Am J Roentgenol 1993;160:467–471. 7. Svendsen E, Karwinski B. Prevalence of pulmonary embolism at necropsy in patients with cancer. J Clin Pathol 1989;42:805–809. 8. Lohr JM, Kerr TM, et al. Lower extremity calf thrombosis: to treat or not to treat. J Vasc Surg 1991;14:618–623. 9. Thomas M, Solis G. The phlebographic distribution of deep venous thrombosis in the calf and its relevance to duplex ultrasound. Phlebology 1992;7:64–66. 10. THRIFT Consensus Group. Risk of and prophylaxis for venous thromboembolism in hospital patients. Br Med J 1992;305:567–574. 11. European Consensus Statement. Prevention of venos thromboembolism. Int Angiol 1992;11(3):151–159. 12. Tapson VF. Prophylaxis for deep venous thrombosis: the ACCP antithrombotic statement, revisited. Chest 1998;113(3):844. 13. Goodall R, Greenfield LJ. Clinical correlations in the diagnosis of pulmonary embolism. Ann Surg 1980;191:219–223. 14. Stein PD, Alavi A, et al. Usefulness of noninvasive diagnostic tools for diagnosis of acute pulmonary embolism in patients with a normal chest radiograph. Am J Cardiol 1991;67(13):1117–1120. 15. Stein PD, Terrin ML, et al. Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-

16.

17. 18.

19.

20.

21.

22. 23. 24.

25.

26.

27.

28.

29.

30. 31.

32.

33.

34.

35.

36.

existing cardiac or pulmonary disease. Chest 1991;100:598–603. Greenspan RH, Ravin C, et al. Accuracy of the chest radiograph in diagnosis of pulmonary embolism. Invest Radiol 1982;17:539–543. Urokinase Pulmonary Embolism Trial. A national cooperative study. Circulation 1973;48 (suppl 2]). Tilyou S. PIOPED (prospective investigation in pulmonary embolism diagnosis) study compares lung scans and pulmonary arteriography. J Nucl Med 1989;39(3):279–280. Alderson P, Martin E. Pulmonary embolism: diagnosis with multiple imaging modalities. Radiology 1987;164(2):297–312. Remy-Jardin M, Remy J. Spiral CT angiography of the pulmonary circulation. Radiology 1999;212(3):615–636. van Erkel AR, van Rossum AB, et al. Spiral CT angiography for suspected pulmonary embolism: a cost-effective analysis. Acad Radiol 1999;6(1):72–74. Homans J. Deep venous thrombosis in the lower limb. Surg Gynec Obstet 1944;79:70. Dale W. Ligation of the inferior vena cava for thromboembolism. Surgery 1958;43(1):24–44. Bernstein EF. The place of venous interruption in the treatment of pulmonary thromboembolism. In: Moser KM, Stein M, eds. Pulmonary Thromboembolism. St.Louis,Mo: Mosby-Yearbook, 1973;312–323. Greenfield LJ, Zocco J, et al. Clinical experience with the Kim-Ray Greenfield vena caval filter. Ann Surg 1977;185(6):692–698. Kantor A, Glanz S, et al. Percutaneous insertion of the Kimray-Greenfield filter: incidence of femoral vein thrombosis. Am J Roentgenol 1987;149(4): 1065–1066. Pais SO, Mirvis S, De Orchis D. Percutaneous insertion of the Kimray-Greenfield filter: technical considerations and problems. Radiology 1987;165:377–381. Molgaard CP, Yucel EK, et al. Access-site thrombosis after placement of inferior vena cava filters with 12-14-F delivery sheaths. Radiology 1992;185:257–261. Greenfield LJ, Peyton R. Greenfield vena caval filter experience: late results in 156 patients. Arch Surg 1981;116:1451–1456. Proctor MC. Indications for filter placement. Semin Vasc Surg 2000;13(3):194–198. Matsumura JS, Morasch MD. Filter placement by ultrasound technique at the bedside. Semin Vasc Surg 2000;13(3):199–203. Sing RF, Smith CH, et al. Preliminary results of bedside inferior vena cava filter placement: safe and costeffective. Chest 1998;114:315–316. Elkins R, McCurdy J, et al. Clinical results with an extracaval prosthesis and description of a new intracaval filter. J Oklahoma State Med Assoc 1973;66:53–59. Proctor MC, Greenfield LJ, et al. Assessment of apparent vena caval penetration by the Greenfield filter. J Endovasc Surg 1998;5:251–258. Stewart J, Peyton W, et al. Clinical results of suprarenal placement of the Greenfield vena cava filter. Surgery 1982;92(1):1–4. Rosenthal D, Gershon C, Rudderman R. Renal cell carcinoma invading the inferior vena cava: the use of the

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37.

38. 39.

40. 41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

Greenfield filter to prevent tumor emboli during nephrectomy. J Urol 1985;134:126–127. Orsini R, Jarrell B. Suprarenal placement of vena caval filters: indications, techniques, and results. J Vasc Surg 1984;1:125–135. Jarrell B, Szentpetery S, et al. Greenfield filter in renal transplant patients. Arch Surg 1981;116:930–932. Greenfield LJ, Cho KJ, et al. Late results of suprarenal Greenfield vena cava filter placement. Arch Surg 1992;127:969–973. Greenfield LJ, Proctor MC. Suprarenal filter placement. J Vasc Surg 1998;28(3):432–438. Greenfield LJ, Proctor MC. Twenty-year clinical experience with the Greenfield filter. Cardiovascular Surgery 1995;3(2):199–205. Hye R, Mitchell A, et al. Analysis of the transition to percutaneous placement of Greenfield filters. Arch Surg 1990;125(12):1550–1553. Gianturco C, Anderson JH, Wallace S. A new vena cava filter: experimental animal evaluation. Radiology 1980;137:835–837. Rogoff PA, Hilgenberg AD, et al. Cephalic migration of the bird’s nest inferior vena caval filter: report of two cases. Radiology 1992;184:819–822. Vesely T, Darcy M, et al. Technical problems associated with placement of the bird’s nest inferior vena cava filter. Am J Roentgenol 1992;158(4):875–880. Hicks M, Middleton W, et al. Prevalence of local venous thrombosis after transfemoral placement of a bird’s nest vena caval filter. J Vasc Intervent Radiol 1990;1:63–68. Wojtowycz MM, Stoehr T, et al. The bird’s nest inferior vena caval filter: review of a single-center experience. J Vasc Intervent Radiol 1997;8(2):171–179. Nicholson AA, Ettles DF, et al. Long-term follow-up of the bird’s nest IVC filter. Clin Radiol 1999;54(11):759–764. Ricco JB, Crochet D, et al. Percutaneous transvenous caval interruption with the “LGM” filter: early results of a multicenter trial. Ann Vasc Surg 1988;2:242–247. Grassi CJ. Inferior vena caval filters: analysis of five currently available devices. Am J Roentgenol 1991;156:813–821. Millward SF, Peterson RA, et al. LGM (Vena Tech) vena cava filter: clinical experience in 64 patients. J Vasc Intervent Radiol 1991;2:429–433. Crochet DP, Brunel P, et al. Long-term follow-up of Vena

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

65.

66.

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Tech-LGM filter: predictors and frequency of caval occlusion. J Vasc Intervent Radiol 1999;10:137–142. Kim D, Schlam B, et al. Insertion of the Simon nitinol caval filter: value of the antecubital vein approach. Am J Roentgenol 1991;157:521–522. McCowan TC, Ferris EJ, et al. Complications of the nitinol vena caval filter. J Vasc Intervent Radiol 1992;3:401–408. Proctor MC, Cho KJ, Greenfield LJ. In vivo evaluation of vena caval filters: can function be linked to design characteristics? Cardiovasc Intervent Radiol 2000;23(6):460–465. Greenfield LJ, Cho KJ, Tauscher J. Limitations of percutaneous insertion of Greenfield filters. J Cardiovasc Surg 1990;31(3):344–350. Greenfield LJ, Cho KJ, et al. Results of a multicenter study of the modified hook titanium Greenfield filter. J Vasc Surg 1991;14:253–257. Greenfield LJ, Proctor MC. Experimental embolic capture by asymmetric Greenfield filters. J Vasc Surg 1992;16(3):436–444. Greenfield LJ, Proctor MC, et al. Extended evaluation of the titanium Greenfield vena caval filter. J Vasc Surg 1994;20:458–465. Cho KJ, Greenfield LJ, et al. Evaluation of a new percutaneous stainless steel Greenfield filter. J Vasc Intervent Radiol 1997;8:181–187. Greenfield LJ, Proctor MC. The percutaneous Greenfield filter: outcomes and practice patterns. J Vasc Surg 2000;32(5):888–893. Millward SF, Bhargava A, et al. Gunther tulip filter: preliminary clinical experience with retrieval. J Vasc Intervent Radiol 2000;11(1):75–82. Hull RD, Pineo GF, Stein P. Heparin and low-molecularweight heparin therapy for venous thromboembolism: the twilight of anticoagulant monitoring. Int Angiol 1998;17(4):213–224. Reekers JA. Current practice of temporary vena cava filter insertion: a multicenter registry. J Vasc Intervent Radiol 2000;11:1363–1364. Lorch H, Welger D, et al. Current practice of temporary vena cava filter insertion: a multicenter registry. J Vascular Intervent Radiol 2000;11(1):83–88. Bonn J, Cho KJ, et al. Recommended reporting standards for vena caval filter placement and patient follow-up. J Vasc Surg 1999;30(3):573–579.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 92 Contemporary Venous Thrombectomy Anthony J. Comerota

The rationale for venous thrombectomy is based upon: 1. 2. 3. 4.

an understanding of the underlying pathophysiology of the post-thrombotic syndrome; knowledge of the natural history of acute DVT; the contemporary experience of iliofemoral venous thrombectomy; and the results of a prospective randomized trial of venous thrombectomy plus arteriovenous fistula vs. standard anticoagulation.

The premise for the benefit of venous thrombectomy is that the post-thrombotic syndrome can be significantly reduced or avoided by eliminating thrombus from the deep venous system. This premise is supported by an understanding of the underlying pathophysiology of the post-thrombotic syndrome. Ambulatory venous hypertension is the underlying pathophysiology of the postthrombotic syndrome, and the main components of ambulatory venous hypertension are obstruction of the venous lumen and valvular dysfunction (1–3). Obstruction is a relative phenomenon, not “all or nothing” (4). Since the pathophysiology of the post-thrombotic syndrome is defined during exercise, attempting to measure the hemodynamic importance of obstruction in the patient who is supine with the leg elevated may confer inaccurate information (5). It has long been recognized that noninvasive techniques such as maximal venous outflow are insensitive to quantifying degrees of obstruction and indeed can mislead the examiner entirely (Fig. 92.1). Clinical studies have shown that patients with combined obstruction and valvular incompetence have the highest

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ambulatory venous pressure and suffer with the most severe post-thrombotic syndrome (2,3). Therefore, it is reasonable to conclude that eliminating obstruction from the deep venous system will reduce the severity of the postthrombotic syndrome and possibly avoid it altogether if valvular function can be maintained. Natural history studies have demonstrated that, when endogenous fibrinolysis is efficient and removes thrombus from the involved vein, valvular function can be preserved (6). Such observations support a management strategy designed to remove thrombus from the deep venous system, especially in those patients who have extensive deep venous thrombosis (7). Such a management strategy is supported by the natural history studies indicating that patients with iliofemoral venous thrombosis generally suffer the most severe post-thrombotic sequelae (8–10). Recent experience has demonstrated that patients undergoing iliofemoral venous thrombectomy can be treated safely and effectively (11–13). A large, prospective randomized trial with patients followed for 6 months, 5 years, and 10 years demonstrated that iliofemoral venous thrombectomy offers a significantly better outcome compared to anticoagulation alone (14–16). Despite the overwhelming amount of information supporting venous thrombectomy (Tables 92.1 and 92.2), most contemporary vascular surgeons are reluctant to perform the procedure on patients who might benefit. Hopefully, by understanding that the principles of venous thrombectomy are essentially similar to those of arterial thrombectomy (remove all thrombus, correct the underlying cause of the occlusion and provide optimal pharmocologic management to reduce the risk of rethrombosis), vascular

Chapter 92 Contemporary Venous Thrombectomy

A

1107

FIGURE 92.1 Ascending phlebography in a patient with a postthrombotic syndrome following extensive DVT 15 years earlier (A). Phlebogram demonstrates recanalization of the femoral vein with phlebographic findings consistent with chronic venous disease. A maximal venous outflow test was performed, which demonstrated normal venous outflow with no evidence of “obstruction.” The patient underwent a classic Linton procedure with ligation and division of the femoral vein below the common femoral–profunda junction. A cross-section of the femoral vein in the thigh (B) demonstrates substantial luminal obstruction and multiple recanalization channels.

B

TABLE 92.1 Venous thrombectomy with arteriovenous fistula: long-term iliac vein patency (modified from reference 11 with permission) Author/Year (ref.)

No.

Plate et al. 1984* (14) Piquet et al. 1985 (17) Einarsson et al. 1986 (13) Vollmar 1986 (18) Juhan et al. 1987* (12) Torngren & Swedenborg 1988 (19) Rasmussen et al. 1990 (20) Eklof & Kistner 1996 (11) Neglen et al. 1991 (21)

31 57 58 93 36 54 24 77 34

Total

464

Follow-up (Months)

Patent Iliac Vein (%)

6 39 10 53 48 19 20 48 24

76 80 61 82 93 54 88 75 88

26 (mean)

75 (mean)

*Later reports excluded from analysis to avoid duplication of numbers.

TABLE 92.2 Venous thrombectomy with arteriovenous fistula: long-term valve competence of femoral-popliteal venous segment (modified from reference 11 with permission) Author/Year (ref.) Plate et al. 1984 (14) Einarsson et al. 1986 (13) Ganger et al. 1989 (22) Neglen et al. 1991 (21) Kniemeyer et al. 1992 (23) Juhan et al. 1997 (24) Total

No. 31 53 17 37 37 77 252

surgeons will become more comfortable with this procedure, which can offer enormous long-term benefit to patients who would otherwise face life-long postthrombotic morbidity.

Historical Perspective Although Lawen (25) was the first to report operative venous thrombectomy with restoration of venous patency, it

Follow-up (Months)

Competence (%)

6 10 91 24 55 60

52 42 82 56 84 80

41 (mean)

65 (mean)

was not until Mahorner reported his early results that enthusiasm began to develop for this technique (26–28). Haller and Abrams (29) reported an 85% patency rate in patients operated on within 10 days of the onset of thrombosis, with 81% of the survivors having “normal legs” without post-thrombotic swelling. Reports such as these were enthusiastically received because of the excellent initial patency without severe post-thrombotic sequelae. The early results reported by Haller and Abrams are even more impressive considering they did not have a balloon

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Part XII Venous and Lymphatic Surgery

catheter at their disposal, but rather used irrigation and suction techniques during the operative procedure. However, subsequent reports indicated higher rates of rethrombosis (30) and failure to prevent post-thrombotic sequelae despite a patent vein because valve competency had been destroyed (30,31). An important report which followed was that of Lansing and Davis (31), commenting on the 5-year follow-up of patients originally described by Haller and Abrams. They reported that 94% of those followed had sufficient edema and stasis changes to require elastic stockings and leg elevation. In addition, all patients who underwent long-term follow-up phlebography were found to have incompetent valves. Lansing and Davis also pointed out that two of the three postoperative deaths (in 34 patients) were from pulmonary embolism and that there was a 30% wound complication rate, an average transfusion requirement of 1000 ml, and a mean hospital stay of 12 days. It is probably not reasonable to expect that similar complications of operative thrombectomy would be observed today in light of the marked advances in all aspects of patient care and the substantial improvements in vascular surgical techniques. The report by Lansing and Davis suffered from a potential selection bias because it is likely that patients with the worst results were the most heavily represented. The patients reported in their follow-up represented only 50% of those initially operated upon, and venographic documentation was achieved in even fewer. Additionally, since the follow-up phlebograms are performed in the supine position, valve function cannot be accurately evaluated. Nevertheless, this and other critical appraisals, plus the emergence of thrombolysis soon relegated venous thrombectomy in most medical centers to the status of a procedure that was of historical interest only. Subsequent reports of successful thrombectomy from European centers have been ignored by surgeons in the United States despite Eklof and Kistner’s (11) efforts to renew enthusiasm in the technique by summarizing the large contemporary European experience which showed favorable results (23).

Contemporary Results The long-term benefits of venous thrombectomy depend upon its ability to achieve and maintain proximal venous patency and preserve valvular function. These are influenced by the initial technical success and of course by the avoidance of rethrombosis. Proper patient selection and attention to technical details of the operation have an important influence on initial success rates. Pooled data from a number of contemporary reports on iliofemoral venous thrombectomy indicate that long-term patency (2 years or more) is approximately 70% to 80% (Table 92.1) and femoropopliteal valve competence is preserved in approximately 60% to 70% (Table 92.2).

The Scandinavian investigators who completed the large prospective randomized trial comparing iliofemoral venous thrombectomy with standard anticoagulation demonstrated complete iliofemoral patency without significant defects in 76% of the thrombectomy patients at 6 months compared to 35% of the patients treated with anticoagulation alone (14). When they evaluated the infrainguinal venous segment, twice as many thrombectomy patients had patent femoropopliteal segments (52% vs. 26%), and valve reflux was demonstrated in four times as many anticoagulated patients (37% vs. 9%). A total of 42% of the operated patients were asymptomatic at 6 months compared with only 7% in the anticoagulated group. Plate and coworkers (15) reevaluated the randomized patients at 5 years. Radionucleotide phlebography showed patency in 76% in the surgical group compared to 20% in the anticoagulation group. Long-term venous function was also elevated. When the results of reflux, obstruction, and calf muscle pump function were considered together, 39% of the operated patients had normal venous function, compared with 19% of the anticoagulated patients. A total of 55% of those operated upon were free of post-thrombotic symptoms, compared with 27% of those randomized to anticoagulation alone. The same investigators reported the 10-year followup of these patients and demonstrated that 83% of the surgical group compared to 41% of the medical group had a patent iliac venous segment (16). Severe reflux was more common in the medical group compared to the surgical group. The clinical classification (CEAP class) was significantly better in the surgical group, with 38% of the operated patients falling into CEAP 0 class, compared with 12% of the medical group. A strategy of thrombus removal and correction of underlying lesions has been instituted at Temple University Hospital with 28 patients having venous thrombectomy (Fig. 92.2). A good to excellent clinical result has been observed in 21 patients. (Fig. 92.3) These patients had minimal postoperative morbidity with edema easily controlled with compression stockings (if edema existed at all). Two patients had a fair outcome. Both had chronic venous occlusion of the femoral vein in the thigh and were operated upon for acute iliac vein thrombosis. Their postoperative edema reverted back to the degree to which it was present preoperatively. Four patients had a poor outcome and one patient died during the postoperative period. The death occurred in a patient who required evacuation of the retroperitoneal hematoma, which occurred following successful catheter-directed thrombolysis and iliac vein angioplasty and stenting. During anticoagulation, the patient developed a retroperitoneal hematoma and the anticoagulation was discontinued. Rethrombosis of the iliofemoral venous system occurred. A venous thrombectomy and arteriovenous fistula was performed at the time of the hematoma evacuation. While the lower extremity complications were minimal postoperatively, the patient went on to progressive respiratory failure and succumbed during the postoperative period.

Chapter 92 Contemporary Venous Thrombectomy

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vena caval thrombosis. This patient was not treated with anticoagulants because of metastatic cancer to the brain. In all other patients, I have not found the need to close the arteriovenous fistula as it causes no problem. The arteriovenous fistula anastomosis should be small, approximately 3.5 to 4 mm. Since many of these patients develop neointimal fibroplasia, the volume of blood flow through the fistula decreases over time.

Technique of Venous Thrombectomy

FIGURE 92.2 Detailed algorithm for the management of patients with iliofemoral venous thrombosis.

Rethrombosis occurred in three other patients. Each had metastatic cancer with acute thrombosis superimposed upon chronic venous thrombotic disease. One patient could not receive any anticoagulation due to brain metastases. Wound complications with venous thrombectomy occurred predominantly in patients who had an unsuccessful procedure. Wound complications occurred in 18%, and most were associated with ongoing iliofemoral venous obstruction causing persistent venous hypertension and increased lymphatic flow with the resultant lymphatic hypertension. Wound problems associated with persistent lymphatic drainage occur more commonly in obese patients. A rethrombosis rate of approximately 15% has been reported. The rethrombosis rate has fallen since an associated arteriovenous fistula has been constructed. However, in those series reporting early rethrombosis, there is no mention of the status of the iliofemoral venous system and whether unobstructed venous drainage into the vena cava was achieved. In my experience, no patient in whom unobstructed venous drainage was documented has suffered rethrombosis. Eklof and Kistner (11) have recommended that the associated arteriovenous fistula be closed approximately 6 weeks after the venous thrombectomy. Closure of the arteriovenous fistula is accompanied by rethrombosis in approximately 15% of patients. I have closed only one arteriovenous fistula, in a patient who developed recurrent

During the past two decades, the technique of venous thrombectomy has been refined and improved. Most of the principles of successful venous thrombectomy follow those established for patients undergoing arterial reconstruction for acute arterial occlusion. There are a number of important technical modifications which have evolved, beginning with the accurate preoperative definition of the extent of the thrombus, both proximally and distally. Presently, the proximal extent of the thrombus is defined by contralateral iliocavography; however, magnetic resonance venography with gadolinium or spiral computerized tomography may obviate the invasive procedure in some patients. During the operation, completion phlebography/fluoroscopy is performed to ensure the adequacy of venous thrombectomy. Correction of an underlying venous stenosis with balloon angioplasty and stenting, if necessary, or cross-pubic venous bypass (Fig. 92.4) is performed if residual iliac vein obstruction persists. Construction of an arteriovenous fistula and immediate and prolonged therapeutic anticoagulation are important. The more recent modifications, which include balloon catheter thrombectomy with suprarenal caval balloon occlusion for nonocclusive caval clot (Fig. 92.5), infrainguinal venous thrombectomy, and early postoperative anticoagulation through a catheter in the posterior tibial vein, further improve outcome. The details of contemporary venous thrombectomy are described below, divided into preoperative, operative and postoperative care.

Preoperative Care 1. 2.

3.

4.

Draw blood for full hypercoagulable evaluation and send specimen for type and crossmatch. The full extent of thrombosis must be defined. Contralateral iliocaval phlebography is most frequenty used to define the proximal extent of the thrombus. Venous duplex imaging accurately defines the extent of infrainguinal venous thrombosis. Therapeutic anticoagulation with heparin is begun and continued throughout the procedure and postoperatively. Vena caval filtration is generally not necessary. An exception may be those patients with nonocclusive thrombus in the vena cava. However, these patients

A

B

C

FIGURE 92.3 Technique of venous thrombectomy with arteriovenous fistula. Preoperative ascending phlebogram of a young woman developing phlegmasia cerulea dolens 6 days after spinal reconstruction for scoliosis. All named veins of the left leg above (A) and below (B, C) the inguinal ligament are thrombosed. Through a longitudinal femoral incision, the common femoral, saphenous, and femoral veins are exposed. A transverse venotomy is made in the common femoral vein (single arrow) which is packed with thrombus (D). Within a short time, thrombus begins to extrude from the venotomy (double arrow) because of high distal venous pressure (E). The leg is raised and a rubber bandage is tightly wrapped from the foot to the upper thigh to remove as much clot as possible from the infrainguinal venous system (F). After passage of a No. 10 venous thrombectomy catheter to remove the proximal thrombus, the extensive amount of thrombus retrieved is appreciated (G). Completion phlebography demonstrates a patent iliofemoral venous system without residual thrombus (H). A small (3.5 to 4 mm) arteriovenous fistula (I) (single arrow) is constructed by sewing the end of the transected saphenous vein to the side of the superficial femoral artery. Photograph taken at the 2-year follow-up visit (J). The patient has mild, intermittent swelling which is easily controlled with low pressure compression stockings.

Chapter 92 Contemporary Venous Thrombectomy

1111

FIGURE 92.3 (continued)

5.

recently have been managed with balloon occlusion of the proximal vena cava at the time of balloon catheter thrombectomy. The protective vena cava balloon is positioned during preoperative iliocavography, using fluoroscopic guidance. The balloon is left deflated until the time of thrombus extraction. Prepare the operating room for fluoroscopy and/or radiography. Prepare to use an autotransfusion device.

Operative Care 6. 7.

FIGURE 92.4 Schematic of a cross-pubic venous bypass with a 10-mm externally supported PTFE graft, with an associated arteriovenous fistula.

General anesthesia is preferred. Perform a longitudinal inguinal incision, with exposure and control of the common femoral vein, femoral vein, saphenofemoral junction, and profunda femoris vein. 8. Perform a longitudinal venotomy about the level of the saphenofemoral junction. The exact location of the venotomy depends upon the extent of thrombosis. 9. Perform the infrainguinal venous thrombectomy first. Evaluate and exsanguinate the leg with a rubber bandage and milk leg clot from below. 10. If infrainguinal clot persists, cut down on the posterior tibial vein and perform an infrainguinal venous thrombectomy. Pass a No. 3 Fogarty balloon catheter from below upward to exit from the common femoral venotomy. Then slide the stem of plastic intravenous catheter (14 gauge) halfway onto the No. 3 Fogarty balloon catheter and slide a No. 4 Fogarty balloon catheter into the other end. Apply pressure to the two balloons and guide the No. 4 Fogarty balloon catheter distally through venous valves to the level of the posterior venotomy. Perform the infrainguinal venous thrombectomy with a No. 4 Fogarty balloon catheter. Repeat catheter passage as required, usually until no further thrombus is extracted.

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12.

13.

14.

15.

16.

FIGURE 92.5 In a patient with phlegmasia cerulea dolens, pretreatment iliocavalogram (A) demonstrates nonocclusive thrombus extending from the left common iliac vein into the distal vena cava. Under fluoroscopy, a balloon catheter is positioned in the suprarenal vena cava and inflated (B) during iliocaval venous thrombectomy.

17.

18. 11. Following the infrainguinal balloon catheter thrombectomy, vigorously flush the infrainguinal venous system with saline to hydraulically force residual thrombus (which can be considerable) by

placing a No. 16 red rubber nasogastric tube into the proximal posterior tibial vein and flushing with a bulb syringe. After applying a vascular clamp below the femoral venotomy, fill the infrainguinal venous system with a plasminogen activator solution, using approximately 500,000 units of urokinase or 4 to 6 mg of rtPA in 150 to 200 ml saline. Allow the plasminogen activator solution to dwell in the infrainguinal venous system for the remainder of procedure. If the infrainguinal venous thrombectomy is not successful due to chronic thrombus in femoral vein, ligate the femoral vein below the profunda and ensure patency of the profunda by direct thrombectomy, if required. Ligate the distal posterior tibial vein and fix an infusion catheter (pediatric nasogastric tube) in the proximal posterior tibial vein for heparin infusion (and follow-up phlebogram). The catheter should exit the leg through a small exit wound adjacent to the incision. This catheter will be used for postoperative heparin anticoagulation, which ensures maximal heparin concentration in the affected venous segment. Pass a No. 8 or No. 10 venous thrombectomy catheter part way into iliac vein for several passes before advancing into the vena cava. Perform the proximal thrombectomy under fluoroscopy with contrast in the balloon, especially if a caval filter is present. The anesthesiologist should apply positive end-expiratory pressure during the iliocaval thrombectomy. After completing the iliofemoral thrombectomy, evaluate the iliofemoral system with intraoperative phlebography/fluoroscopy, to ensure unobstructed venous drainage into the vena cava. Correct any underlying iliac vein stenosis with balloon angioplasty, using a stent if venous recoil occurs. If iliac vein patency cannot be restored with catheterbased techniques, a cross-pubic venous bypass with a 10 mm externally supported PTFE graft plus arteriovenous fistula should be constructed (Fig. 92.4). Construct an end-to-side arteriovenous fistula with the saphenous vein or a large proximal branch of the saphenous vein to the superficial femoral artery. The anastomosis should be approximately 3.5 to 4 mm. (Frequently, the proximal saphenous vein requires thrombectomy to restore patency prior to the arteriovenous fistula.) Wrap a piece of PTFE or silastic around the saphenous arteriovenous fistula and loop monofilament (permanent) suture material around the PTFE and the clip end, leaving it in the subcutaenous tissue. This will guide future dissection in the event that closure of the arteriovenous fistula becomes necessary. Measure femoral vein pressure before and after the arteriovenous fistula is opened. If the femoral pressure increases when the arteriovenous fistula is opened, re-evaluate the proximal iliac vein for residual stenosis or obstruction and be sure to cor-

Chapter 92 Contemporary Venous Thrombectomy TABLE 92.3 Venous thrombectomy: comparison of old and contemporary techniques

Pretreatment phlebography Venous thrombectomy catheter Operative fluoroscopy/ phlebography Correct iliac vein stenosis Arteriovenous fistula Infrainguinal thrombectomy Full postoperative anticoagulation IPC postoperative

Old

Contemporary

Occasionally No

Always Yes

No

Yes

No No No Occasionally

Yes Yes Yes Yes

No

Yes

rect the lesion. If the pressure remains elevated, constrict the arteriovenous fistula to decrease flow and normalize pressure. 19. If there appears to be excessive serous fluid in wound, place a No. 7 Jackson–Pratt drain (or other similar closed suction drain) in wound to evacuate blood and serous fluid. Exit drain through separate puncture site adjacent to incision. 20. Close wound with mulilayered, running absorbable sutures to achieve a hemostatic and lymphostatic wound closure.

Postoperative Care 21. Continue full postoperative anticoagulation with unfractionated heparin through the catheter placed in the posterior tibial vein. Begin oral anticoagulation when the patient resumes oral intake. Continue oral anticoagulation for at least 1 year. 22. Apply external pneumatic compression garments postoperatively. 23. Complete the evaluation for an underlying thrombophilia or other cause for patient’s iliofemoral DVT; however, do not discontinue anticoagulation for this reason alone.

Conclusion The patients with iliofemoral deep venous thrombosis should routinely be considered for a management strategy designed to remove thrombus from the iliofemoral ve nous system in order to reduce the severe post-thrombotic morbidity. The initial approach of catheter-directed thrombolysis is used in patients who have no contraindication to lytic therapy. In patients who have a contraindication to lytic therapy, venous thrombectomy should be performed in patients presenting within 7 to 10 days. For patients who are poor operative candidates, those with longstanding (>10 days) venous thrombosis, and patients who are critically ill or bedridden, anticoagulation is generally recommended.

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Contemporary venous thrombectomy has substantially improved the early and long-term results of the initially reported procedure. The major technical differences are listed in Table 92.3. Recent reports of those performing venous thrombectomy and the long-term results of a large randomized trial confirm significant benefit compared to anticoagulation alone. Therefore, vascular surgeons should include contemporary venous thrombectomy as part of their routine operative armamentarium.

References 1. Nicolaides AN, Schull K, et al. Ambulatory venous pressure: new information. In: Nicolaides AN, Yao JST, eds. Investigation of Vascular Disorders. New York: Churchill Livingstone. 1981;488–494. 2. Shull KC, Nicolaides AN, et al. Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg 1979;114:1304–1306. 3. Johnson BF, Manzo RA, et al. Relationship between changes in the deep venous system and the development of the post-thrombotic syndrome after an acute episode of lower limb deep vein thrombosis: a oneto-one six-year followup. J Vasc Surg 1995;21: 307–313. 4. Comerota AJ. The myths, mystique and misconceptions of venous disease. J Vasc Surg 2001;34:765–773. 5. Comerota AJ, Katz ML, et al. Venous duplex imaging: should it replace hemodynamic tests for DVT? J Vasc Surg 1990;11:53–61. 6. Meissner MH, Manzo RA, et al. Deep vein insufficiency: the relationship between lysis and subsequent reflux. J Vasc Surg 1993;18:596–602. 7. Comerota AJ, Aldridge SC, et al. A strategy of aggressive regional therapy for acute iliofemoral venous thrombosis with temporary thrombectomy and/or catheter-directed thrombolysis. J Vasc Surg 1994;20:244–254. 8. O’Donnell F, Browse NL, et al. The socioeconomic effects of an iliofemoral venous thrombosis. J Surg Res 1997;22:483–488. 9. Mavor GE, Galloway JMD. Iliofemoral venous thrombosis. Br J Surg 1969;56:43–59. 10. Hill SL, Martin D, Evans P. Massive vein thrombosis of the extremities. Am J Surg 1989;158:131–135. 11. Eklof B, Kistner RL. Is there a role for thrombectomy in iliofemoral venous thrombosis? Semin Vas Surg 1996;9(1):34–35. 12. Juhan C, Cornillon B, et al. Patency after iliofemoral and iliocaval venous thrombectomy. Ann Vasc Surg 1987;1:529–533. 13. Einarsson E, Albrechtsson U, Eklof B. Thrombectomy and temporary AV-fistula in iliofemoral vein thrombosis: technical considerations and early results. Angiol 1986;5:65–72. 14. Plate G, Einarsson E, Ohlin P, et al. Thrombectomy with temporary arteriovenous fistula: the treatment of choice in acute iliofemoral venous thrombosis. J Vasc Surg 1984;1:867–876. 15. Plate G, Akesson H, et al. Long-term results of venous thrombectomy combined with a temporary arteriovenous fistula. Eur J Vasc Surg 1990;4:483–489.

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16. Plate G, Eklof B, et al. Venous thrombectomy for iliofemoral vein thrombosis: 10 year results of a prospective randomized study. Eur J Vasc Endovasc Surg 1997;14:367–374. 17. Piquet P, Tournigand P, et al. Traitement chirurgical des thromboses ilio-caves: exigences et resultats. In Kieffer E, ed. Chirurgie de la veine cave inferieure et de ses branches. Paris, Expansion Scientifique Francaise, 1985;210–216. 18. Vollmar JF. Advances in reconstructive venous surgery. Int Angiol 1986;5:117–129. 19. Torngren S, Swedenborg J. Thrombectomy and temporary arteriovenous fistula for iliofemoral venous thrombosis. Int Angiol 1988;7:14–18. 20. Ramussen A, Mogensen K, et al. Acute iliofemoral venous thrombosis: twenty-six cases treated with thrombectomy, temporary arteriovenous fistula and anticoagulants. Ugeskr Laeger 1990;152:2928–2930. 21. Neglen P, al-Hassan HK, et al. Iliofemoral venous thrombectomy followed by percutaneous closure of the temporary arteriovenous fistula. Surg 1991;110:493–499. 22. Ganger KH, Nachbur BH, et al. Surgical thrombectomy venous conservative treatment for deep venous thrombosis: functional comparison of long-term results. Eur J Vas Surg 1989;3:529–538.

23. Kniemeyer HW, Sandmann W, et al. Thrombectomy with AV fistula: the better alternative to prevent recurrent pulmonary embolism. American Venous Forum 4th Annual Meeting, Coronado, CA, February 1992; 26–28. 24. Juhan CM, Alimi YS, et al. Late results of iliofemoral venous thrombectomy. J Vasc Surg 1997;25:417–422. 25. Lawen A. Uber Thrombektomie bei Venenthrombose und Arteriospasmus. Zentralbi Chir 1937;64: 961–968. 26. Mahorner H. New management for thrombosis of deep veins of extremities. Am Surg 1954;20:487–498. 27. Mahorner H, Castleberry JW, Coleman WO. Attempts to restore function in major veins which are the site of massive thrombosis. Ann Surg 1957;146:510–522. 28. Mahorner H. Results of surgical operations for venous thrombosis. Surg Gynec Obstet 1969;129:66–70. 29. Haller JAJ, Abrams BL. Use of thrombectomy in the treatment of acute iliofemoral venous thrombosis in forty-five patients. Ann Surg 1963;158:561–569. 30. Karp RB, Wylie EJ. Recurrent thrombosis after iliofemoral venous thrombectomy. Surg Forum 1966;17:147. 31. Lansing AM, Davis WM. Five-year follow-up study of iliofemoral venous thrombectomy. Ann Surg 1968;168: 620–628.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 93 Endoscopic Subfascial Ligation of Perforating Veins Manju Kalra and Peter Gloviczki

Incompetent perforating veins were observed in patients with venous ulceration more than a century ago by John Gay (1), but surgical interruption of these veins to prevent ulceration was suggested first by Linton in only 1938 (2). Linton attributed a key role to perforator vein incompetence in the pathomechanism of venous ulceration, an idea embraced later by Cockett (3,4), Dodd (5,6), and several other investigators (7–13). This assumption was based on the premise that surgical interruption of perforating veins would prevent the abnormal transmission of elevated venous pressure, generated in the deep venous system during walking, to the superficial venous system. In the mid-twentieth century, perforator ligation was adopted by many surgeons as the panacea to heal venous ulcers. However, a high incidence of wound complications following subfascial perforator ligation, coupled with conflicting long-term results reported by various investigators, led to virtual abandonment of the procedure during the 1980s (14,15). In the light of these results several investigators attempted to modify Linton’s original operation, which required long skin incisions. Less invasive surgical techniques included the use of shorter skin incisions (3–5,7,10,11), long posterior incision away from damaged skin (16,17), multiple medial skin crease incisions (18), and blind avulsion of the perforators with a shearing instrument (19). In the mid-1980s, Hauer developed a technique that enabled incompetent perforating veins to be ligated under direct vision through small incisions situated far away from areas of ulcerated or damaged skin (20). This technique was rapidly adopted and

refined by several groups, and in recent years subfascial endoscopic perforator vein surgery (SEPS) has emerged as an effective minimally invasive technique to interrupt perforating veins (21–31). In this chapter we will review the surgical anatomy of the perforating veins and discuss available evidence supporting the role of perforators in chronic venous disease. We will describe surgical indications and preoperative evaluation of patients and present the currently used open and endoscopic surgical techniques for interruption of perforators. Finally, we will review data in the literature on efficacy of perforator vein interruption.

Surgical Anatomy of Perforating Veins Perforating veins connect the superficial to the deep venous system, either directly to the main axial veins (direct perforators) or indirectly to muscular tributaries or soleal venous sinuses (indirect perforators). The term “communicating” veins refers to interconnecting veins within the same system. In normal limbs, unidirectional flow in calf and thigh perforators, from the great and small saphenous systems towards the deep veins, is assured by venous valves. Perforating veins of the foot, on the other hand, are valveless and paradoxically direct flow from the deep to the superficial venous system (32–34). In the mid- and distal calf the most important direct medial perforators do not originate directly from the

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FIGURE 93.2 Superficial and perforating veins in the medial side of the leg. (From Mozes G, Gloviczki P, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996;24:800–808.)

FIGURE 93.1 Anatomy of medial superficial and perforating veins of the leg. (From Mozes G, Gloviczki P, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996;24:800–808.)

great saphenous vein (Fig. 93.1). This finding was first noted by John Gay in 1866 in a clinical case with venous ulcers, where he demonstrated the posterior arch vein and three perforating veins (1). This observation is extremely important as stripping of the great saphenous vein will not affect flow through incompetent medial calf perforators. The most significant calf perforators, termed the Cockett perforators, connect the posterior arch vein (Leonardo’s vein) (Fig. 93.1) to the paired posterior tibial veins. In some patients the posterior arch veins are not well developed, and other posterior tributaries of the great saphenous vein are connected instead through perforators to the deep system. Three groups of Cockett perforators have been identified. The Cockett I perforator is located posterior to the medial malleolus and may be difficult to reach endoscopically. The Cockett II and III perforators are located 7 to 9 cm and 10 to 12 cm proximal to the lower border of the medial malleolus, respectively (Fig. 93.2) (33). All are found in “Linton’s lane,” 2 to 4 cm posterior to the medial edge of the tibia (34–36). Mozes et al., during anatomic dissections, identified an

average of 14 medial calf perforating veins (direct and indirect) per limb, with a range of seven to 22 veins. However, only three of these were greater than 2 mm in diameter, in concordance with the earlier clinical descriptions of Linton and Cockett, and the fact that only three to five clinically significant incompetent perforators are found in most patients (22). The greatest concentration of perforating veins were located at 25 to 33 cm above the ankle, followed by 7 to 13 cm, findings consistent with Linton’s original description of frequent veins at the junction of the middle and lower third of the leg (2,33). Based on duplex scanning and surgical findings, Pierik et al. and O’Donnell et al. reported about half of all calf perforators occurring 11 to 20 cm and 10 to 15 cm above the medial malleolus respectively, with another 10% to 20% situated in the 20 to 25 cm region (35). The next group of clinically relevant perforating veins are the paratibial perforators which connect the great saphenous vein and its tributaries to the posterior tibial and popliteal veins. Mozes et al. described their anatomy in detail by performing corrosion cast studies in 40 normal limbs from 20 cadavers (33). The paratibial perforators are found in three groups, all located 1 to 2 cm posterior to the medial tibial border. They are located 18 to 22 cm, 23 to 27 cm, and 28 to 32 cm from the inferior border of the medial malleolus (Fig. 93.1). The 18 to 22 cm group corresponds to the “24 centimeter” perforator described by Sherman, who used the sole of the foot as his point of reference (34). There are three additional direct perforating veins that connect the great saphenous vein to the popliteal and superficial femoral veins. Boyd’s perforator, just distal to the knee, connects the greater saphenous vein to the popliteal vein (33). Dodd’s and Hunterian perforators are located in the thigh and connect the great saphenous vein to the proximal popliteal or the femoral veins (Fig. 93.1). Boyd’s perforator may be reached endoscopically, while stripping of the great saphenous vein will interrupt the drainage of Dodd’s and Hunterian perforators, except in 8% of patients with a duplicated saphenous system. Certain anatomic considerations specific to the endoscopic interruption of medial calf perforators need to be

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

emphasized. In cadaver dissections, Mozes et al. noted that only 63% of all medial perforators were directly accessible from the superficial posterior compartment (33). Based on clinical reports, only 32% of Cockett II, 84% of Cockett III, and 43% of lower paratibial perforating veins are accessible from the superficial posterior compartment (37), a significant consideration since majority of incompetent perforators occur at the Cockett II/III level. This is an important observation, since major incompetent perforators will be missed during surgery if dissection is limited to the superficial posterior compartment. Two additional areas that require exploration are the deep posterior compartment, and the intermuscular septum in Linton’ lane, that can be a duplication of the deep fascia. The paratibial and the Cockett veins can be found under the fascia of the deep posterior compartment, while the Cockett II/III veins can also be located within the intermuscular septum (Fig. 93.3). A deceiving anatomic variation of the Cockett II perforator can be a division with a posterior branch directed towards the soleus muscle. While this posterior division is easily visible when it penetrates the superficial posterior compartment, the more important anterior division is hidden by the intermuscular septum or by the deep posterior fascia and it may be missed. Therefore, 68% of Cockett II and16% of Cockett III perforators are hidden by a septum or fascia that needs to be divided during endoscopic surgery, otherwise major perforators will be left behind (33). Distally in the subfas-

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cial space, the Cockett I perforator usually cannot be visualized or reached because of its retromalleolar position. In the calf, anterior and lateral perforators are also found, and in patients with lateral ulceration these veins have clinical significance. The anterior perforators connect tributaries of the great and small saphenous veins directly to the anterior tibial veins. The lateral perforating veins consist of both direct and indirect perforators. In the distal calf, the small saphenous vein is connected by direct perforators to the peroneal veins (Bassi’s perforator). The indirect perforators connect tributaries of the small saphenous vein to either the muscular venous sinuses or the gastrocnemius or soleus veins before entering the deep axial system. The largest indirect muscular perforators are referred to as the soleus and gastrocnemius points.

Pathophysiology Although the pathophysiology of chronic venous insufficiency (CVI) at the cellular level remains controversial, most authors agree that venous hypertension in the erect position and during ambulation is the most important factor responsible for the development of skin changes and venous ulcerations. The relationship between venous ulceration and ambulatory venous pressure was first described by Beecher et al. in 1931 (38). Subsequent studies have confirmed that ambulatory venous pressure has not

FIGURE 93.3 Compartments and medial veins of the leg. Cross-sections are at the levels of (A) Cockett II, (B) Cockett III, (C) “24 cm”, and (D) proximal paratibial perforating veins. GSV, greater saphenous vein; PAV, posterior arch vein; PTVs, posterior tibial veins; SPC, superficial posterior compartment; CII, Cockett II; CIII, Cockett III; PTP, paratibial perforator. (From Mozes G, Gloviczki P, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996;24:800–808.)

A

C

B

D

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only diagnostic but also prognostic significance in CVI (39–42). High ambulatory venous pressure may be due to primary valvular incompetence (PVI) in superficial, deep and/or perforator veins, or it may be the result of a previous deep venous thrombosis (DVT). Deep venous incompetence (DVI) is initially compensated for by the calf muscle pump, but eventually results in secondary incompetence of valves in perforating veins, and transmission of pressure from the deep to the superficial veins, a fact that was first suggested by Homans (43) and documented by Linton (2).

Hemodynamic Abnormalities in Limbs with Venous Ulceration Reflux of blood due to primary or post-thrombotic valvular incompetence coupled with calf muscle pump failure is the most frequent cause of CVI and venous ulceration. While severe isolated incompetence of the superficial system may also lead to sufficiently high ambulatory pressures and the development of ulcers, evidence is increasing that the majority of patients with venous ulcers have multi-system (superficial, deep and/or perforator) incompetence, involving at least two of the three venous systems (31,44–47). DVI has been reported to occur in a significant number of patients (21% to 80%) in large surgical series of venous ulcers (Table 93.1) (44,48,49). Incompetent calf perforators in conjunction with superficial or deep reflux have been reported in 66% of limbs with venous ulceration, and occur more frequently in limbs with complications (48,50). A duplex ultrasound study in 91 limbs with venous ulcerations from Boston University revealed isolated superficial vein incompetence (SVI) in only17% and perforator vein incompetence (PVI) in 63% of limbs (47). Similarly, a 60% incidence of perforator incompetence in ulcer patients was demonstrated by duplex scanning by Lees and Lambert (51), and a 56% incidence by Labrapoulos et al. (46). It is extremely important to ob-

tain an accurate assessment of the underlying pathophysiology in every patient, not only to aid in treatment planning, but also to evaluate and compare results.

Hemodynamic Significance of Incompetent Perforators While few doubt today that incompetent perforators occur in at least two-thirds of patients with venous ulcerations, the contribution of incompetent perforators to the hemodynamic derangement in limbs with CVI remains a topic of debate (52,53). Cockett coined the term “ankle blow-out syndrome” to differentiate perforator incompetence from the usually more benign isolated saphenous incompetence (3,54). Indeed, perforator vein incompetence can raise pressures in the supramalleolar network well above 100 mmHg during calf muscle contraction, a phenomenon best described by Negus using the analogy of a “broken bellows” (11). Experiments of Bjordal confirmed a net outward flow of 60 mL/min through incompetent perforating veins (55). Skin changes and venous ulcers almost always develop in the gaiter area of the leg (the area between the distal edge of the soleus muscle and the ankle), where large incompetent medial perforating veins are located, underscoring their importance. The task of documenting the hemodynamic significance of incompetent perforators is difficult, since isolated perforator vein incompetence in CVI is rare (46), and because incompetent perforators have been observed even in normal limbs; in one study 21% of normal limbs had outward flow in perforating veins (56). However, in a study using Doppler ultrasound and ambulatory venous pressure measurements to assess functional significance of incompetent perforating veins, Zukowski and Nicolaides found that 70% of incompetent perforators were of moderate or major hemodynamic significance (56). Other authors have also repeatedly demonstrated a correlation between the number and size

TABLE 93.I Distribution of valvular incompetence in patients with advanced chronic venous disease No. of Limbs

Superficial incompetence (%)

Perforator incompetence (%)

Deep vein incompetence (%)

Superficial + Perforator (%)

Sup erficial + Perforator + Deep No. (%)

52 77 60 25 91 213 25 59 120 96 120 146

3 (6) 0 (0) 0 (0) 0 (0) 16 (17) 0 (0) 3 (12) 0 (0) 48 (40) 15 (16) 26 (22) 0 (0)

20 (38) 0 (0) 5 (8) 0 (0) 8 (8) 8 (4) 0 (0) 0 (0) 6 (5) 2 (2) 1 (1) 7 (5)

4 (8) 0 (0) 20 (33) 2 (8) 2 (2) 47 (22) 3 (12) 19 (32) 10 (8) 7 (8) 5 (4) 0 (0)

11 (21) 35 (46) 17 (28) 3 (12) 18 (19) 83 (39) 10 (40) 31 (53) 31 (26) 25 (26) 23 (19) 66 (45)

14 (27) 42 (54) 18 (30) 20 (80) 47 (49) 75 (35) 9 (36) 9 (15) 25 (21) 47 (49) 65 (54) 73 (50)

1084

111 (10)

57 (5)

119 (11)

353 (32)

444 (41)

Author, Year (ref.) Schanzer & Pierce 1982 (10) Negus & Friedgood 1983 (11) Sethia & Darke 1984 (54) van Bemmelen et al. 1991 (49) Hanrahan et al. 1991 (47) Darke & Penfold 1992 (91) Lees & Lambert 1993 (92) Shami et al. 1993 (93) van Rij et al. 1994 (44) Myers et al. 1995 (48) Labropoulos et al. 1996 (94) Gloviczki et al. 1999 (29) Total no. of limbs (%)

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

of incompetent perforating veins detected by duplex ultrasonography, and the severity of CVI (45,58,59). In addition to confirming these findings, in contrast to previously published data, Sarin et al. failed to confirm perforator incompetence in 106 normal volunteers (56). Recently, Delis et al. quantified perforator incompetence based on diameter, flow velocities and volume flow, and stressed that incompetent perforators sustain further hemodynamic impairment in the presence of deep reflux (60).

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TABLE 93.2 Diagnostic tests to identify the sites of incompetent perforating veins

Test Physical examination (ref. 35) Continuous wave Doppler ultrasonography (ref. 35) Ascending phlebography (ref. 35) Duplex scanning (ref. 23)

Sensitivity (%)

Specificity (%)

60 62

0 4

60 79

50 100

Indications for Perforator Interruption The presence of incompetent perforators in patients with advanced CVI (clinical classes 4 to 6) constitutes the indication for surgical treatment in a fit patient. While most authors doing open perforator ligation prefer to operate only on patients with healed ulcerations, a clean, granulating open ulcer is not a contraindication for the SEPS procedure. Contraindications include associated chronic arterial occlusive disease, infected ulcer, morbid obesity, and nonambulatory or high-risk patient. Diabetes, renal failure, liver failure, or ulcers in patients with rheumatoid arthritis or scleroderma are relative contraindications. Presence of deep venous obstruction at the level of the popliteal vein or higher on preoperative imaging is also a relative contraindication. Patients with extensive skin changes, circumferential large ulcers, recent deep venous thrombosis, severe lymphedema, or large legs may not be suitable candidates. SEPS has been performed for recurrent disease after previous perforator interruption; however, it is technically more demanding in this situation. Limbs with lateral ulcerations should be managed by open interruption of lateral or posterior perforators where appropriate.

Preoperative Evaluation Preoperative evaluation includes imaging studies to evaluate the superficial, deep, and perforating veins for incompetence and /or obstruction, and to guide the operative intervention. Duplex scanning has 100% specificity and the highest sensitivity of all diagnostic tests to predict the sites of incompetent perforating veins (Table 93.2) (23,35). All candidates for SEPS in our practice undergo duplex ultrasonography of the deep, superficial, and perforator systems (61), and sites of incompetent perforators are marked on the skin (Fig. 93.4). Perforator mapping, a time-consuming test, is done the day before surgery and the sites of incompetent perforators are marked with a nonerasable marker. Duplex scanning is performed with the patient on a tilted examining table with the affected extremity in a near upright non-weightbearing position. Perforator incompetence is defined by retrograde (outward) flow lasting longer than 0.3 s or longer than ante-

FIGURE 93.4 Color Doppler and spectral tracing of an enlarged incompetent perforating vein. Spectral analysis demonstrates bidirectional flow (arrow). (From Gloviczki P, Lewis BD, et al. Preoperative evaluation of chronic venous insufficiency with Duplex scanning and venography. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998:81–91 with permission.)

grade flow during the relaxation phase after release of manual compression (61). Ascending and descending phlebography is reserved for patients with underlying occlusive disease or recurrent ulceration after perforator division, in whom deep venous reconstruction is being considered. In addition to duplex scanning, a functional study such as strain-gauge or air plethysmography may be performed before and after surgery to quantitate the degree of incompetence, identify abnormalities in calf muscle pump function, aid in the exclusion of outflow obstruction, and assess hemodynamic results of surgical intervention (13,30).

Surgical Techniques Open Technique of Perforator Interruption Linton’s radical operation of subfascial ligation (2) which included long medial, anterolateral, and posterolateral calf incisions was soon abandoned because of wound complications. In a subsequent report published in 1953,

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Linton advocated only a long medial incision from the ankle to the knee to interrupt all medial and posterior perforating veins (39). His operation also included stripping of the greater and small saphenous veins, and excision of portion of the deep fascia. (His suggestion to interrupt axial reflux by ligation of the superficial femoral vein is of historic interest only.) Wound complications caused by the incision made in the lipodermatosclerotic skin were still frequent and hospitalization was prolonged. Several other authors proposed modifications to Linton’s open procedure to limit wound complications. Cockett advocated ligation of the perforating veins above the deep fascia, a technique distinctly different from the Linton operation (3). The importance of ligating the perforating veins subfascially was emphasized by Sherman, as the perforating veins branch extensively once they penetrate the deep fascia (34). Modifications included the use of shorter medial incisions or a more posteriorly placed stocking seam type incision (4,16,17). DePalma observed good results using multiple, parallel bipedicled flaps placed along skin lines to access and ligate the perforating veins above or below the fascia (Fig. 93.5) (18). The operation was combined with saphenous stripping, ulcer excision, and skin grafting. The concept of ablating incompetent perforating veins from a site remote from diseased skin was first intro-

duced by Edwards in 1976 (19). He designed a device called the phlebotome which is inserted through a medial incision just distal to the knee, deep to the fascia, and advanced to the level of the medial malleolus (Fig. 93.6). Resistance is felt as perforators are engaged and subsequently disrupted with the leading edge. Other authors have subsequently reported successful application of this device, passed either in the subfascial or extrafascial planes (62). Interruption of perforators through stab wounds and hook avulsion is another possibility, and accuracy of this blind technique improves with preoperative duplex scanning and perforator mapping. Sclerotherapy of perforating veins and suture ligation of perforators without making skin incisions are among other reported techniques. The classic papers of Linton (2,39) and Cockett (3,6) reported benefit from open perforator ligation, and this was supported later by data from several other investigators (7,10,11,64,66). In the larger series, ulcer recurrence ranged from 0% to 55% and averaged 22% (Table 93.3) (9,11,14,65–68). The significant drawback of open perforator ligation was a high rate of wound complications in most series, ranging from 12% to 53%, and averaging 24% (Table 93.3). Further controversy over the efficacy of this operation emerged when Burnand et al. reported a 55% ulcer recurrence rate in their patients, with 100% recurrence in a subset of 23 patients with post-thrombotic syndrome (14). Although this data is compelling evidence against perforating vein ablation, an often overlooked fact is that ulcer recurrence in the other subset of patients in the same study, those without post-thrombotic damage of the deep veins, was only 6%.

FIGURE 93.5 Linton operation modified by DePalma. Note the extent of the area which is dissected as shown in the shaded inset. Also note the submalleolar skin line incisions. (From DePalma RG. Surgical therapy for

FIGURE 93.6 Excision and dissection of a deep ulcer before extrafascial shearing operation. The submalleolar incisions allow division of the retromalleolar perforator. (From DePalma RG. Surgical therapy for venous

venous stasis. Surgery 1974;76:910–917, with permission.)

stasis. Surgery 1974;76:910–917, with permission.)

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

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TABLE 93.3 Clinical results of open perforator interruption for the treatment of advanced chronic venous disease

Author, Year (ref.)

No. of Limbs Treated

No. of Limbs with Ulcer

Silver et al. 1971 (7) Thurston & Williams 1973 (8) Bowen 1975 (9) Burnand et al. 1976 (14) Negus & Friedgood 1983 (11) Wilkinson & Maclaren 1986 (68) Cikrit et al. 1988 (12) Bradbury et al. 1993 (13) Pierik et al. 1997 (24)

31 102 71 41 108 108 32 53 19

19 0 8 0 108 0 30 0 19

Total no. of limbs (%)

565 (100)

184 (33)

Wound Complications (%)

Ulcer Healing (%)

4 (14) 12 (12) 31 (44) — 24 (22) 26 (24) 6 (19) — 10 (53) 113/468 (24)

— † — † 91 (84) † 30 (100) † 17 (90) 138/157 (88)

Ulcer Recurrence* (%) — (10) 11 (13) 24 (34) 24 (55) 16 (15) 3 (7) 5 (19) 14 (26) 0 (0) 97/443 (22)

Mean Follow-up (years) 1–15 3.3 4.5 — 3.7 6.0 4.0 5.0 1.8 —

*Recurrence calculated where data available and percentage accounts for patients lost to follow-up. †Only class 5 (healed ulcer) patients admitted in study.

Techniques of Subfascial Endoscopic Perforator Vein Surgery First introduced by Hauer in 1985, using endoscopic instruments interruption of incompetent, perforators may now be performed through small ports placed remotely from the active ulcer or area of skin discoloration (20–22,69–71). Since its introduction, two main techniques for SEPS have been developed. The first, practiced mostly in Europe, is a refinement of the original work of Hauer (20) by Fischer and Satter (25,72,73), with further development by Bergan (21,75) and by Wittens and Pierik (23,24,75). In the early development of the “single port” technique, available light sources such as mediastinoscopes and bronchoscopes were used. With time, a specially designed instrument was devised which uses a single scope with channels for the camera and working instruments, which sometimes makes visualization and dissection in the same plane difficult (Fig. 93.7). Recent developments in instrumentation for this technique now allow for carbon dioxide insufflation into the subfascial plane. The second technique, using instrumentation from laparoscopic surgery, was introduced in the United States by O’Donnell (76) and developed simultaneously by our group at the Mayo Clinic (28) and Conrad in Australia (27). This technique, the “two port” technique, employs one port for the camera and a separate port for instrumentation, thereby making it easier to work in the limited subfascial space. First, the limb is exsanguinated with an Esmarque bandage and a thigh tourniquet is inflated to 300 mmHg to provide a bloodless field (Fig. 93.8A). A 10mm endoscopic port is next placed in the medial aspect of the calf 10 cm distal to the tibial tuberosity, proximal to the diseased skin. Balloon dissection is routinely used to widen the subfascial space and facilitate access after port placement (Fig. 93.8B) (77). The distal 5-mm port is now placed halfway between the first port and the ankle (about 10 to 12 cm apart), under direct visualization with the

FIGURE 93.7 Olympus endoscope for the subfascial perforating vein interruption. The scope can be used with or without carbon dioxide insufflation. It has an 85° field of view and the outer sheath is either 16 or 22 mm in diameter. The working channel is 6 ¥ 8.5 mm, with a working length of 20 cm. (From Bergan JJ, Ballard JL, Sparks S. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London, Springer-Verlag, 1998:1 41–149, with permission.)

camera (Fig. 93.8C). Carbon dioxide is insufflated into the subfascial space and pressure is maintained around 30 mmHg to improve visualization and access to the perforators. Using laparoscopic scissors inserted through the second port, the remaining loose connective tissue between the calf muscles and the superficial fascia is sharply divided. The subfascial space is widely explored from the medial border of the tibia to the posterior midline, and down to the level of the ankle. All perforators encountered are divided either with the harmonic scalpel, electrocautery, or sharply between clips (Fig. 93.8D). A paratibial fasciotomy is next made by incising the fascia of the posterior deep compartment close to the tibia, to avoid any injury to the posterior tibial vessels and the tibial nerve (Fig.

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A

B

C

D

FIGURE 93.8 Two-port technique of SEPS. (A) A thigh tourniquet inflated to 300mmHg is used to create a bloodless field. (B) Balloon dissection is used to widen the subfascial space. (C) SEPS is performed using two ports: a 10-mm camera port and a 5- or 10-mm distal port inserted under video control. Carbon dioxide is insufflated through the camera port into the subfascial space to a pressure of 30mmHg to improve visualization and access to perforators. (D) The subfascial space is widely explored from the medial border of the tibia to the posterior midline and down to the level of the ankle, and all perforators are interrupted using clips or harmonic scalpel. (E) A paratibial fasciotomy is routinely performed to identify perforators in the deep posterior compartment. (From Gloviczki P, Canton LG, et al. Subfascial endoscopic E

93.8E). The Cockett II and Cockett III perforators are located frequently within an intermuscular septum, and this has to be incised before identification and division of the perforators can be accomplished. The medial insertion of the soleus muscle on the tibia may also have to be exposed to visualize proximal paratibial perforators. By rotating the ports cephalad and continuing the dissection up to the level of the knee, the more proximal perforators can also be divided. While the paratibial fasciotomy can aid in distal exposure, reaching the retromalleolar Cockett I perforator endoscopically is usually not possible, and if incompetent, may require a separate small incision over it to gain direct exposure. After completion of the endoscopic portion of the

perforator vein surgery with gas insufflation. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998:125–138, with permission.)

procedure, the instruments and ports are removed, the caron dioxide is manually expressed from the limb, and the tourniquet is deflated; 20 mL of 0.5% marcain solution is instilled into the subfascial space for postoperative pain control. Stab avulsion of varicosities in addition to high ligation and stripping of the great and/or small saphenous vein, if incompetent, is performed. The wounds are closed and the limb is elevated and wrapped with an elastic bandage. Elevation is maintained at 30∞ postoperatively for 3 hours, after which walking is permitted. Unlike the in-hospital stay after an open Linton procedure, this is an outpatient procedure and patients are discharged the same day or next morning following overnight observation.

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

Efficacy of Subfascial Endoscopic Perforator Vein Surgery Clinical Results In the absence of prospective, randomized trials there is no level I evidence to support the performance of SEPS in patients with advanced CVI and venous ulcers. In fact, there is no convincing evidence that surgical treatment is superior to medical management. Presently, prospective, randomized multicenter trials are being designed in North America as well as in Europe. Until results of such studies are available one can only draw on the experience of investigators in the field, and retrospective as well as prospective data from single institutions.

1123

Encouraging early results with SEPS were reported by several authors and ulcers healed satisfactorily after elimination of both superficial and perforator reflux (22,69,70,74). In fact, patients with combined deep, perforator, and superficial incompetence exhibited accelerated healing and improved venous hemodynamics after ablation of the incompetent superficial and perforator systems without intervention to the deep veins (Figs. 93.9 and 93.10) (78,79). Experience with SEPS continues to grow and results from several centers are available and summarized in Table 93.4. Unfortunately, reporting of results has not been very uniform and several important clinical variables make analysis of results difficult. Many series have not adequately documented the pathophysiology of venous disease, and only the most recent publications FIGURE 93.9 (A) Thirty-six-year-old male with post-thrombotic ulcer right ankle, before endoscopic division of six medial perforating veins. (B) Photograph of the same leg 10 months later shows healed ulcer. (From Gloviczki P, Canton LG, et al. Subfascial endoscopic perforator vein surgery with gas insufflation. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London, Springer-Verlag, 1998:125–138, with permission.)

A

B

FIGURE 93.10 (A) Right leg of a 64-yearold male with a 2-year history of ulcer and severe post-thrombotic syndrome. (B) Postoperative picture at 6 weeks shows healed ulcer and incisions following SEPS, stripping, and avulsion of varicose veins. Three years later the patient is asymptomatic, does not use elastic stockings, and has had no ulcer recurrence. (From Gloviczki P, Canton LG, et al. Subfascial endoscopic perforator vein surgery with gas insufflation. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London, Springer-Verlag, 1998:125–138, with permission.)

A

B

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TABLE 93.4 Clinical results of SEPS for the treatment of advanced chronic venous disease

Author, Year (ref.)

No. of Limbs Treated

No of Limbs With Ulcer*

Concomitant Saphenous Ablation No. (%)

Wound Complications No. (%)

Ulcer Healing No. (%)

Ulcer Recurrence† No. (%)

Mean Follow-up (Months)

Jugenheimer & Junginger 1992 (26) Pierik et al. 1995 (69) Bergan et al. 1996 (21) Wolters et al. 1996 (95) Padberg et al. 1996 (78) Pierik et al. 1997 (96) Rhodes et al. 1998 (30) Gloviczki et al. 1999 (29) Illig et al. 1999 (88) Nelzen 2000 (84)

103

17

97 (94)

3 (3)

16 (94)

0 (0)

40 31 27 11 20 57 146 30 149

16 15 27 0 20 22 101 19 36

4 (10) 31 (100) 0 (0) 11 (100) 14 (70) 41 (72) 86 (59) — 132 (89)

3 (8) 3 (10) 2 (7) — 0 (0) 3 (5) 9 (6) — 11 (7)

16 (100) 15 (100) 26 (96) ‡ 17 (85) 22 (100) 85 (84) 17 (89) 32 (89)

1 (2.5) (0) 2 (8) 0 (0) 0 (0) 5 (12) 26 (21) 4 (15) 3 (5)

46 — 12–24 16 21 17 24 9 32

Total no. of limbs (%)

614 (100)

273 (44)

416/567 (73)

34/556 (6)

41/392 (10)

—

246/273 (90)

27

*Only class 6 (active ulcer) patients are included. †Recurrence calculated for class 5 and 6 limbs only, where data available and percentage accounts for patients lost to follow-up. ‡Only class 5 (healed ulcer) patients were admitted in this study.

use the CEAP classification scheme proposed by the International Consensus Committee on Chronic Venous Disease (80,81). Lack of details regarding the technique of SEPS, especially the performance of a paratibial fasciotomy, and insufficient extended follow-up in significant numbers of patients makes it difficult to accurately predict ulcer recurrence. Despite these limitations valuable insight can be gained from the growing literature. The safety and early efficacy of SEPS has been established in several studies (22,28,69,79), and it yields a much lower wound complication rate than that observed after traditional open surgical techniques (22,24,36). In a noncontrolled trial that compared 37 SEPS procedures to 30 antedated open perforator ligations, SEPS resulted in lower calf wound morbidity, shorter hospital stay, and comparable short-term ulcer healing (82). A single prospective, randomized study by Pierik et al. in 39 patients reported wound complications in 53% of patients undergoing open perforator ligation versus 0% in the SEPS group, with no ulcer recurrence in either group over a mean follow-up of 21 months (24). In a subsequent communication 4 years later, the authors reported long-term follow-up in these patients. Ulcer recurrence in the open perforator ligation group (22%) was not significantly different from that in the SEPS group (12%) in this small patient cohort (83). These data support the use of SEPS rather than open ligation, yet do not address the role of SEPS in the management of advanced CVI and venous ulceration. The relative safety of SEPS was further confirmed in the early report of the North American (NASEPS) registry (22). The uniformity of evaluation and reporting of results from 17 centers in North America emphasize the reliability and significance of results of this study. The study included 146 patients, 101 of whom had active ulcers (C6), and 21 of whom had healed ulcers at the time of op-

eration. Deep venous incompetence (DVI) was present in 72% of patients, and 54 (38%) patients had postthrombotic syndrome (PT). Concomitant superficial venous surgery was performed in 71% of patients. Wound complication rate was 6%, and one deep venous thrombosis occurred at 2 months after surgery The mid-term (24 months) results of the NASEPS registry demonstrated an 88% cumulative ulcer healing rate at 1 year (29). The median time to ulcer healing was 54 days. Cumulative rate of ulcer recurrence was significant: 16% at 1 year, 28% at 2 years. While the observed recurrence rates in the NASEPS registry were high, they still compare favorably to results of nonoperative management (Table 93.5). In the largest series from a single institution, Nelzen et al. reported on prospectively collected data from 149 SEPS procedures in 138 patients (84). There were 36 limbs with active ulcers (C6), 31 with healed ulcers (C5), 34 with skin changes (C4), and 48 with varicose veins (C3). Surprisingly, deep venous insufficiency was present in only 7% of limbs. Combined saphenous vein surgery was performed in 89% of limbs. There were no serious complications, wound infection occurred in 7%, and delayed wound healing in 15%. During a median follow-up of 32 months, 32 of 36 ulcers healed, more than half (19/36) within 1 month. Three ulcers recurred, one of which subsequently healed during follow-up. At a median follow-up of 7 months following surgery, 91% of patients were satisfied with the results of the operation. A recent study analyzed extended results in 103 consecutive SEPS procedures performed at the Mayo Clinic over a 7-year period (85). There were 42 class 6 limbs, 34 class 5 limbs and 24 class 4 limbs. Thirty procedures were performed in post-thrombotic (PT) limbs. Concomitant superficial reflux ablation was performed in 74 limbs (72%); saphenous vein stripping had been previously performed in 29 (28%). Deep venous incompetence was

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

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TABLE 93.5 Ulcer recurrence or new ulceration following medical treatment

Author, Year (ref.)

No. of Limbs Treated

No. of Limbs With Ulcer

Anning 1956 (64) Monk & Sarkany 1982 (98) Kitahama et al. 1982 (99) Negus 1985 (100) Mayberry et al. 1991 (101) Erickson 1995 (102) DePalma & Kowallek 1996 (103) Samson & Showalter 1996 (104)

100 83 65 25 113 99 11 53

100 83 59 0 113 99 11 53

Total

549 (100)

518/549 (94)

Ulcer Recurrence (%)* 59 (59) 58 (69) 8 (14) 17 (68) 24 (33) 52 (58) 11 (100) 23 (43) 241/488 (52)

Mean Follow-up (Months) 64 12 12 — 30 10 24 28 27

*Percentage accounts for patients lost to follow-up.

present in 89% of limbs; 13% had venous outflow obstruction on plethysmography. Of 42 ulcers 38 healed with a median time to ulcer healing of 35 days; all 4 ulcers that failed to heal were in PT limbs. On life-table analysis 90-day and 1-year cumulative ulcer healing rates were 80% and 90%, respectively. During mean follow-up of 3.25 years, nine ulcers recurred (12.5%) and five patients developed new ulcers (one bilaterally, 8.3%), for an overall crude ulcer recurrence rate of 15/72 (20.8%). On lifetable analysis 1-year, 3-year, and 5-year cumulative ulcer recurrence rates were 4%, 20%, and 27%.

Defining the Role of SEPS in Ulcer Healing Since concomitant ablation of superficial reflux is often performed at the same time as SEPS, clinical benefit attributed directly to perforator interruption has been difficult to assess. It must be pointed out that majority (over twothirds) of patients reported in the above studies underwent concomitant saphenous vein stripping and branch varicosity avulsion (Table 93.4), making it impossible to ascertain how much clinical improvement can be attributed to the addition of SEPS. The NASEPS registry demonstrated improved ulcer healing in limbs that underwent SEPS with saphenous vein stripping, compared with limbs that underwent SEPS alone: 3- and 12-month cumulative ulcer healing rates of 76% and 100% compared with 45% and 83% (p < 0.01) respectively (29). Ulcer recurrence was not significantly different among the two groups. We attempted to study this in our recent analysis of 103 limbs (85). Ulcer healing was significantly delayed in limbs undergoing SEPS alone, compared with limbs that underwent SEPS with superficial reflux ablation; 90day cumulative ulcer healing rates were 49% and 90% respectively (p = 0.02). Cumulative ulcer recurrence at 5 years was also higher in limbs that underwent SEPS alone (53%), compared with those undergoing SEPS with superficial reflux ablation (19%) (p = 0.01, Fig. 93.11). However, the number of limbs in the SEPS alone group was considerably smaller, and there was a relative predominance of post-thrombotic limbs in this group; 44% compared with 25% in limbs undergoing SEPS with

A

B FIGURE 93.11 (A) Cumulative ulcer healing based on the extent of venous surgery: 11 limbs following SEPS alone and 31 limbs following SEPS with saphenous vein stripping. (B) Cumulative ulcer recurrence based on extent of venous surgery: 16 limbs following SEPS alone and 56 limbs following SEPS with saphenous vein stripping.

saphenous vein stripping. All 29 limbs undergoing SEPS alone had previously undergone saphenous vein ligation and stripping, and had recurrent or persistent ulcers, automatically placing them in a higher risk category and creating a selection bias. The question regarding the absolute benefit of SEPS will not be answered until such time that patients can be prospectively randomized to undergo

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saphenous vein stripping alone, or saphenous vein stripping with SEPS.

Results in Post-thrombotic Syndrome Another group of patients generating significant controversy is those with post-thrombotic syndrome. In all the above communications, limbs with post-thrombotic syndrome fared poorly compared with limbs with primary valvular incompetence (PVI). Cumulative ulcer recurrence in the first Mayo Clinic series was 60% compared with 0% at 3 years in PT and PVI limbs, respectively, and 46% compared with 20% at 2 years in the NASEPS registry (p < 0.05) (29,86). The nine post-thrombotic limbs with components of deep vein obstruction fared particularly poorly, with failure to heal ulcers in four limbs, and ulcer recurrence in the remaining five. The results of the recent Mayo Clinic series, which comprised a larger group of patients with longer follow-up, support this earlier observation (86). All ulcers in limbs with PVI healed; all four ulcers that did not heal were in post-thrombotic limbs. However, on life-table analysis, ulcer healing in post-thrombotic limbs was not significantly different from that in limbs with PVI, with 90-day cumulative ulcer healing rates of 72% compared with 87%, respectively (p = 0.35). Cumulative 5-year ulcer recurrence in post-thrombotic limbs was 56% compared with 15% in limbs with PVI (p = 0.001, Fig. 9.12). However, in-spite of the high ulcer recurrence rate, patients with post-thrombotic syndrome had marked symptomatic improvement, with significant improvement in the clinical scores following SEPS and superficial reflux ablation (9.5 to 3, Fig. 93.13). In addition, recurrent ulcers were small, superficial, single more often than multiple, and healed easily with conservative management.

p = 0.35

A p = 0.001

B FIGURE 93.12 (A) Cumulative ulcer healing based on the etiology of chronic venous insufficiency: 23 limbs with primary valvular incompetence and 19 limbs with post-thrombotic syndrome. The dotted line represents SEM > 10%. (B) Cumulative ulcer recurrence based on the etiology of chronic venous insufficiency: 51 limbs with primary valvular incompetence and 21 limbs with post-thrombotic syndrome. The dotted line represents SEM > 10%.

Hemodynamic Results Several investigators have attempted to evaluate hemodynamic improvement following superficial reflux ablation and perforator ligation, in an attempt to provide early, objective evidence of the efficacy of surgery and thereby predict long-term results. In 1972, Bjordal et al. showed normalization of direct venous pressures on occlusion of the greater saphenous vein alone in patients with PVI, but not following occlusion of large perforating veins alone (55). They were unable to demonstrate normalization of ambulatory venous hypertension on similar maneuvers in patients with post-thrombotic syndrome. Akesson et al. studied venous hemodynamics by foot volumetry, occlusion plethysmography, and ambulatory foot venous pressure measurements in patients with recurrent ulcers. Deep venous involvement was diagnosed in 85% of limbs on ascending venography. Following saphenous vein ligation and stripping, ambulatory foot venous pressure decreased from 82 to 69 mmHg (p < 0.01), but there was no further hemodynamic improvement following perforator ligation performed 3 months later (87).

FIGURE 93.13 Preoperative and postoperative clinical scores based on the etiology of chronic venous insufficiency: 73 limbs with primary valvular incompetence and 30 limbs with post-thrombotic syndrome.

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins

While most studies, including the NASEPS registry, lacked sufficient hemodynamic data to support the clinical results, functional improvement after perforator interruption has been reported. Bradbury et al. used foot volumetry and duplex scanning to assess hemodynamic improvement after saphenous and perforator ligation in 43 patients with recurrent ulcers (13). Expulsion fraction and half-refilling time (T50) improved significantly after surgery in the 34 patients with no ulcer recurrence at 66 months. Recent air plethysmographic studies by Padberg et al. have documented persistent hemodynamic improvement up to 2 years following perforator ligation with concomitant correction of superficial reflux (78). Illig et al. reported a slight improvement in venous refill time, and a significantly greater number of normal studies on photoplethysmography, following 30 SEPS procedures with superficial reflux ablation in 28 patients (88). Rhodes et al. studied hemodynamic consequences of incompetent perforator vein interruption, using strain gauge plethysmography to assess calf muscle pump function, venous incompetence, and outflow obstruction before and within 6 months following SEPS (30). Both calf muscle pump function and the degree of venous incompetence improved significantly following SEPS, with or without superficial reflux ablation. The improvement in venous incompetence (measured by refill rate), correlated strongly with clinical improvement. A similar significant improvement in calf muscle pump function and the degree of venous incompetence was seen in the subgroup of patients with DVI (n = 24). The etiology of deep venous incompetence was PVI in 17 limbs, and post-thrombotic syndrome in seven limbs. As with clinical improvement, the hemodynamic benefit as a direct consequence of perforator ligation was not evident. In the subset of patients that underwent SEPS alone (n = 7), without concomitant superficial reflux ablation, a significant improvement in hemodynamic status could not be demonstrated. This was most likely due to both the small number of patients in this group, and the relative predominance of post-thrombotic limbs. It is also logical to assume that perforator interruption alone would result in a lesser hemodynamic improvement than perforator interruption with concomitant superficial reflux ablation. Patients with PVI demonstrate significantly better hemodynamic improvement, compared with PT limbs (29,30). Proebstle et al., using light reflection rheography before and 8 weeks following SEPS, had very similar results to the Mayo Clinic series, showing significant improvement in limbs with PVI (89). Similar to findings of Burnand et al. (15) and Stacey et al. (90), neither we nor the University of Ulm group were able to show significant hemodynamic improvement in post-thrombotic patients. It is important to note, however, that the number of patients studied in this subgroup has been low, less than 15 in all reported studies (89,90). The overall benefits in these patients are clearly not of the same magnitude as in those with PVI.

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Conclusion Existing data in the literature at the present time lack answers to several questions about the optimal treatment of patients with advanced CVI and especially venous ulcers. Our knowledge about the efficacy and applicability of SEPS is far from complete, and the need for prospective, randomized studies comparing saphenous vein stripping alone to saphenous vein stripping with SEPS has been expressed by many investigators in the field. Based on our data, and that of the NASEPS registry, patients who benefit from SEPS are those with ulcers due to primary valvular incompetence of the superficial and perforatoring veins, with or without deep venous incompetence. These patients are good candidates for SEPS, and derive maximum benefit in terms of accelerated ulcer healing and an estimated 80% to 90% chance of freedom from ulcer recurrence in the long term. Despite subjective symptomatic and objective clinical score improvement, the role of SEPS continues to be controversial in patients with postthrombotic syndrome, as only 50% of patients can be predicted to be free from ulcer recurrence in the long term. Patients with ulcer recurrence following SEPS should undergo duplex scanning to exclude recurrent or persistent perforators. If these are found to be incompetent, repeat SEPS is warranted. If there is no perforator incompetence, they should be considered for deep venous reconstruction.

References 1. Gay J. Lettsonian Lectures 1867. Varicose Disease of the Lower Extremities. London: Churchill, 1868. 2. Linton RR. The operative treatment of varicose veins and ulcers, based upon a classification of these lesions. Ann Surg 1938;107:582–593. 3. Cockett FB, Jones BD. The ankle blow-out syndrome: a new approach to the varicose ulcer problem. Lancet 1953;i:17–23. 4. Cockett FB. The pathology and treatment of venous ulcers of the leg. Br J Surg 1956;44:260–278. 5. Dodd H. The diagnosis and ligation of incompetent perforating veins. Ann R Coll Surg Engl 1964;34:186–196. 6. Dodd H, Cockett FR. The management of venous ulcers. In: The Pathology and Surgery of the Vein of the Lower Limbs. New York: Churchill-Livingstone, 1976; 269–296. 7. Silver D, Gleysteen JJ, et al. Surgical treatment of the refractory postphlebitic ulcer. Arch Surg 1971;103: 554–560. 8. Thurston OG, Williams HT. Chronic venous insufficiency of the lower extremity. Pathogenesis and surgical treatment. Arch Surg 1973;106:537–539. 9. Bowen FH. Subfascial ligation of the perforating leg veins to treat post-thrombophlebitic syndrome. Am Surg 1975;41:148–151. 10. Schanzer H, Peirce EC. A rational approach to surgery of the chronic venous statis syndrome. Ann Surg 1982;195: 25–29.

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11. Negus D, Friedgood A. The effective management of venous ulceration. Br J Surg 1983;70:623–627. 12. Cikrit DF, Nichols WK, Silver D. Surgical management of refractory venous stasis ulceration. J Vasc Surg 1988; 7:473–478. 13. Bradbury AW, Stonebridge PA, et al. Foot volumetry and duplex ultrasonography after saphenous and subfascial perforating vein ligation for recurrent venous ulceration. Br J Surg 1993;80:845–848. 14. Burnand K, Thomas ML, et al. Relation between postphlebitic changes in the deep veins and results of surgical treatment of venous ulcers. Lancet 1976;1:936–938. 15. Burnand KG, O’Donnell TFJ, et al. The relative importance of incompetent communicating veins in the production of varicose veins and venous ulcers. Surgery 1977;82:9–14. 16. Rob CG. Surgery of the vascular system. Univ Minn Vascular Symposium, 1972;272. 17. Lim RCJ, Blaisdell FW, et al. Subfascial ligation of perforating veins in recurrent stasis ulceration. Am J Surg 1970;119:246–249. 18. DePalma RG. Surgical therapy for venous stasis: results of a modified Linton operation. Am J Surg 1979;137: 810–813. 19. Edwards JM. Shearing operation for incompetent perforating veins. Br J Surg 1976;63:885–886. 20. Hauer G. [Endoscopic subfascial discussion of perforating veins: preliminary report]. [German]. Vasa 1985;14:59–61. 21. Bergan JJ, Murray J, Greason K. Subfascial endoscopic perforator vein surgery: a preliminary report. Ann Vasc Surg 1996;10:211–219. 22. Gloviczki P, Bergan JJ, et al. Safety, feasibility, and early efficacy of subfascial endoscopic perforator surgery: a preliminary report from the North American registry. J Vasc Surg 1997;25:94–105. 23. Pierik EG, Toonder IM, et al. Validation of duplex ultrasonography in detecting competent and incompetent perforating veins in patients with venous ulceration of the lower leg. J Vasc Surg 1997;26:49–52. 24. Pierik EG, van Urk H, et al. Endoscopic versus open subfascial division of incompetent perforating veins in the treatment of venous leg ulceration: a randomized trial. J Vasc Surg 1997;26:1049–1054. 25. Fischer R. Surgical treatment of varicose veins: endoscopic treatment of incompetent Cockett veins. Phlebologie 1989;1040–1041. 26. Jugenheimer M, Junginger T. Endoscopic subfascial sectioning of incompetent perforating veins in treatment of primary varicosis. World J Surg 1992;16:971–975. 27. Conrad, P. Endoscopic exploration of the subfascial space of the lower leg with perforator interruption using laparoscopic equipment: a preliminary report. Phlebology 1994;9:154–157. 28. Gloviczki P, Cambria RA, et al. Surgical technique and preliminary results of endoscopic subfascial division of perforating veins. J Vasc Surg 1996;23:517–523. 29. Gloviczki P, Bergan JJ, et al. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American subfascial endoscopic perforator surgery registry. The North American Study Group. J Vasc Surg 1999;29: 489–502.

30. Rhodes JM, Gloviczki P, et al. Endoscopic perforator vein division with ablation of superficial reflux improves venous hemodynamics. J Vasc Surg 1998;28:839–847. 31. Rhodes JM, Gloviczki P, et al. Factors affecting clinical outcome following endoscopic perforator vein ablation. J Vasc Surg 1998;176:162–167. 32. Lofgren EP, Myers TT, et al. The venous valves of the foot and ankle. Surg Gynecol Obstet 1968;127: 289–290. 33. Mozes G, Gloviczki P, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996;24:800–808. 34. Sherman RS. Varicose veins: further findings based on anatomic and surgical dissections. Ann Surg 1949;130: 218–232. 35. O’Donnell TFJ, Burnand KG, et al. Doppler examination vs clinical and phlebographic detection of the location of incompetent perforating veins: a prospective study. Arch Surg 1977;112:31–35. 36. Negus D. Leg ulcers: a practical approach to management, 2nd edn. Oxford: Butterworth-Heinemann, 1995;3–10. 37. O’Donnell TF Jr. Surgery for incompetent perforating veins at the turn of the milennium. In: Current techniques in vascular surgery. Yao JST, Pearce WH, eds. New York, London: McGraw Hill, 2001;487–515. 38. Beecher HK, Field ME, Krogh A. The effect of walking on the venous pressure at the ankle. Skand Arch F Physiol 1936;73:133–140. 39. Linton RR. The post-thrombotic ulceration of the lower extremity: its etiology and surgical treatment. Ann Surg 1953;138:415–432. 40. De Camp PT, Schramee RJ, Roy CJ, et al. Ambulatory venous pressure determinations in postphlebotic and related syndromes. Surgery 1951;29:44–52. 41. Warren R, White D. Venous pressures in the saphenous system in normal, varicose and post-phlebitic extremities. Surgery 1948;26:435–441. 42. Nicolaides AN, Hussein MK, et al. The relation of venous ulceration with ambulatory venous pressure measurements. J Vasc Surg 1993;17:414–419. 43. Homans J. The operative treatment of varicose veins and ulcers, based upon a classification of these lesions. Surg Gynecol Obstet 1916;22:143–158. 44. van Rij AM, Solomon C, Christie R. Anatomic and physiologic characteristics of venous ulceration. J Vasc Surg 1994;20:759–764. 45. Labropoulos N, Mansour MA, et al. New insights into perforator vein incompetence. Eur J Vasc Endovasc Surg 1999;18:228–234. 46. Labropoulos N, Leon M, et al. Venous hemodynamic abnormalities in patients with leg ulceration. Am J Surg 1995;169:572–574. 47. Hanrahan LM, Araki CT, et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991;13:805–812. 48. Myers KA, Ziegenbein RW, et al. Duplex ultrasonography scanning for chronic venous disease: patterns of venous reflux. J Vasc Surg 1995;21:605–612. 49. van Bemmelen PS, Bedford G, et al. Status of the valves in the superficial and deep venous system in chronic venous disease. Surgery 1991;109:730–734.

Chapter 93 Endoscopic Subfascial Ligation of Perforating Veins 50. Darke SG, Penfold C. Venous ulceration and saphenous ligation. Eur J Vasc Surg 1992;6:4–9. 51. Lees TA, Lambert D. Patterns of venous reflux in limbs with skin changes associated with chronic venous insufficiency. Br J Surg 1993;80:725–728. 52. Coleridge SP. Calf perforating veins: time for an objective appraisal? (editorial). Phlebology 1996;11:135–136. 53. Gloviczki P. Endoscopic perforator vein surgery: Does it work? (editorial). Vasc Surg 1998;32:303–305. 54. Sethia KK, Darke SG. Long saphenous incompetence as a cause of venous ulceration. Br J Surg 1984;71:754–755. 55. Bjordal RI. Circulation patterns in incompetent perforating veins of the calf in venous dysfunction. In: Perforating Veins. May R, Partsch J, Staubesand J, eds. Baltimore MD: Urban & Schwarzenberg, 1981;77–78. 56. Sarin S, Scurr JH, Smith PD. Medial calf perforators in venous disease: the significance of outward flow. J Vasc Surg 1992;16:40–46. 57. Zukowski AJ, Nicolaides AN, et al. Haemodynamic significance of incompetent calf perforating veins [see comments]. Br J Surg 1991;78:625–629. 58. Sandri JL, Barros FS, et al. Diameter–reflux relationship in perforating veins of patients with varicose veins. J Vasc Surg 1999;30:867–874. 59. Stuart WP, Adam DJ, et al. The relationship between the number, competence, and diameter of medial calf perforating veins and the clinical status in healthy subjects and patients with lower-limb venous disease. J Vasc Surg 2000;32:138–143. 60. Delis KT, Husmann M, et al. In situ hemodynamics of perforating veins in chronic venous insufficiency. J Vasc Surg 2001;33:773–782. 61. Gloviczki P, Lewis BD, et al. Preoperative evaluation of chronic venous insufficiency with Duplex scanning and venography. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: SpringerVerlag, 1998;81–91. 62. DePalma, R. G. Linton’s operation and modification of the open techniques. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998;107–113. 63. Anning ST. Leg ulcers: the results of treatment. Angiology 1956;7:505–516. 64. DePalma RG. Surgical therapy for venous stasis. Surgery 1974;76:910–917. 65. Cikrit DF, Nichols WK, Silver D. Surgical management of refractory venous stasis ulceration. J Vasc Surg 1988;7:473–478. 66. Johnson WC, O’Hara ET, et al. Venous stasis ulceration: effectiveness of subfascial ligation. Arch Surg 1985;120:797–800. 67. Robison JG, Elliott BM, Kaplan AJ. Limitations of subfascial ligation for refractory chronic venous stasis ulceration. Ann Vasc Surg 1992;6:9–14. 68. Wilkinson GEJ, Maclaren IF. Long term review of procedures for venous perforator insufficiency. Surg Gynecol Obstet 1986;163:117–120. 69. Pierik EGJM, Wittens CHA, van Urk H. Subfascial endoscopic ligation in the treatment of incompetent perforator veins. Eur J Vasc Endovasc Surg 1995;5:38–41. 70. Sparks SR, Ballard JL, et al. Early benefits of subfascial endoscopic perforator surgery (SEPS) in healing venous ulcers. Ann Vasc Surg 1997;11:367–373.

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71. Wittens CH, Pierik RG, van Urk H. The surgical treatment of incompetent perforating veins. [Review] [63 refs]. Eur J Vasc Endovasc Surg 1995;9:19–23. 72. Fischer R, Sattler G, Vanderpuye R. [Endoscopic treatment of perforating veins: current data]. [French]. Phlebologie 1993;46:701–707. 73. Fischer R, Schwahn-Schreiber C, Sattler G. Conclusions of a consensus conference on subfascial endoscopy of perforating veins in the medial lower leg. Vasc Surg 1998;32:339–347. 74. Bergan JJ, Ballard JL, Sparks S. Subfascial endoscopic perforator surgery: the open technique. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998;141–149. 75. Wittens CHA. Comparison of open Linton operation with subfascial endoscopic perforator vein surgery. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998; 177–185. 76. O’Donnell TF. Surgical treatment of incompetent communicating veins. In: Atlas of Venous Surgery. Philadelphia PA: WB Saunders, 2000;111–124. 77. Allen RC, Tawes RL, et al. Endoscopic perforator vein surgery: creation of a subfascial space. In: Atlas of Endoscopic Perforator Vein Surgery. Gloviczki P, Bergan JJ, eds. London: Springer-Verlag, 1998;153–162. 78. Padberg FTJ, Pappas PJ, et al. Hemodynamic and clinical improvement after superficial vein ablation in primary combined venous insufficiency with ulceration [see comments]. J Vasc Surg 1996;24:711–718. 79. Murray JD, Bergan JJ, Riffenburgh RH. Development of open-scope subfascial perforating vein surgery: lessons learned from the first 67 patients. Ann Vasc Surg 1999;199(13):372–377. 80. Porter JM, Moneta GL. Reporting standards in venous disease: an update. International Consensus Committee on Chronic Venous Disease [see comments]. J Vasc Surg 1995;21:635–645. 81. Nicolaides, A. N., Bergan JJ, et al. and the American Venous Forum Consensus Committee. Classification and grading of chronic venous disease in the lower limbs: a consensus statement. In: Handbook of Venous Disorders. London: Chapman & Hall, 1996;652–660. 82. Stuart WP, Adam DJ, et al. Subfascial endoscopic perforator surgery is associated with significantly less morbidity and shorter hospital stay than open operation (Linton’s procedure) [see comments]. Br J Surg 1997;84:1364–1365. 83. Sybrandy JE, van Gent WB, et al. Endoscopic versus open subfascial division of incompetent perforating veins in the treatment of venous leg ulceration: long-term followup. J Vasc Surg 2001;33:1028–1032. 84. Nelzen O. Prospective study of safety, patient satisfaction and leg ulcer healing following saphenous and subfascial endoscopic perforator surgery. [see comments.] Br J Surg 2000;87:86–91. 85. Kalra M, Gloviczki P,et al. Subfascial endoscopic perforator vein surgery in patients with post-thrombotic venous insufficiency: Is it justified? Vasc Endovasc Surg 2002;36:41–50. 86. Rhodes JM, Gloviczki P, et al. Factors affecting clinical outcome following endoscopic perforator vein ablation. Am J Surg 1998;176:162–167.

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87. Akesson H, Brudin L, et al. Does the correction of insufficient superficial and perforating veins improve venous function in patients with deep venous insufficiency? Phlebology 1990;5:113–123. 88. Illig KA, Shortell CK, et al. Photoplethysmography and calf muscle pump function after subfascial endoscopic perforator ligation. [see comments.] J Vasc Surg 1999;30:1067–1076. 89. Proebstle TM, Weisel G, et al. Light reflection rheography and clinical course of patients with advanced venous disease before and after endoscopic subfascial division of perforating veins. Dermatol Surg 1998;24:771–776. 90. Stacey MC, Burnand KG, et al. Calf pump function in patients with healed venous ulcers is not improved by surgery to the communicating veins or by elastic stockings. Br J Surg 1988;75:436–439. 91. Darke SG, Penfold C. Venous ulceration and saphenous ligation. Eur J Vasc Surg 1992;6:4–9. 92. Lees TA, Lambert D. Patterns of venous reflux in limbs with skin changes associated with chronic venous insufficiency. Br J Surg 1993;80:725–728. 93. Shami SK, Sarin S, et al. Venous ulcers and the superficial venous system. [see comments.] J Vasc Surg 1993;17:487–490. 94. Labropoulos N, Delis K, et al. The role of the distribution and anatomic extent of reflux in the development of signs and symptoms in chronic venous insufficiency. J Vasc Surg 1996;23:504–510.

95. Wolters U, Schmit-Rixen T, et al. Endoscopic dissection of incompetent perforating veins in the treatment of chronic venous leg ulcers. Vasc Surg 1996;30: 481–487. 96. Pierik EG, van Urk H, Wittens CH. Efficacy of subfascial endoscopy in eradicating perforating veins of the lower leg and its relation with venous ulcer healing. J Vasc Surg 1997;26:255–259. 97. Monk BE, Sarkany I. Outcome of treatment of venous stasis ulcers. Clin Exper Dermatol 1982;7:397–400. 98. Kitahama A, Elliott LF, et al. Leg ulcer. Conservative management or surgical treatment? J Am Med Assoc 1982;247:197–199. 99. Negus D. Prevention and treatment of venous ulceration. Ann R Coll Surg Engl 1985;67:144–148. 100. Mayberry JC, Moneta GL, et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery 1991;109:575–581. 101. Erickson CA. Healing of venous ulcers in an ambulatory care program: the role of chronic venous insufficiency and patient compliance. J Vasc Surg 1995;22:629– 636. 102. DePalma RG, Kowallek DL. Venous ulceration: a crossover study from nonoperative to operative treatment. J Vasc Surg 1996;24:788–792. 103. Samson RH, Showalter DP. Stockings and the prevention of recurrent venous ulcers. Dermatol Surg 1996;22:373–376.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 94 Venous Reconstruction in Post-thrombotic Syndrome Seshadri Raju

Post-thrombotic syndrome is a significant cause of chronic disability in the adult population. Because the clinical syndrome is slow to evolve, with years or even decades elapsing before onset of symptoms, its potential seriousness as a disabling complication is often not fully appreciated during the initial onset of deep venous thrombosis. Recurrent thrombosis is common, and multiple bouts often precede full expression of post-thrombotic malsequelae. Because few studies of sufficiently long duration are available, the precise incidence of post-thrombotic syndrome is unknown. Short-term studies (1) indicate that two-thirds of the patients may already suffer from post-thrombotic symptoms within 4 years after the initial onset of thrombosis. The incidence of venous stasis ulceration is variably estimated to be about 3% to 5%, but pain and swelling are important and often disabling components of post-thrombotic syndrome and their prevalence far exceeds that of stasis skin changes. Conservative regimens, with their heavy emphasis on leg elevation and compressive stockings, are often restrictive and frequently provide only temporary relief to the patient with full-blown post-thrombotic syndrome. Noncompliance with compressive stockings is very high (2). Promising new surgical approaches have recently become available to correct obstruction and/or reflux components of post-thrombotic syndrome.

Pathophysiology It is now known that as many as 30% to 50% of patients with clinical features indistinguishable from post-

thrombotic syndrome may in fact have “primary” valve reflux of nonthrombotic etiology (3). In some patients, “primary” valve reflux may be complicated by incidence of distal venous thrombosis from reflux stasis (4). Significant fibrosis often develops at valve stations with “primary” reflux that may be indistinguishable from the phlebitis that develops around post-thrombotic valves (5). The combination of symptoms and signs collectively known as post-thrombotic syndrome results from variable underlying pathology ranging from reflux to obstruction, or often a combination. The eventual pathology probably depends on the extent of initial thrombosis and the degree of subsequent clot resolution that takes place. These factors are quite variable among patients. Serial duplex studies indicate that clot resolution is typically rapid, with half of affected limbs showing recanalization by 90 days (1). Delayed clot resolution and rethrombosis appear to be significant risk factors for the development of postthrombotic syndrome (6). Valvular reflux was already evident in 69% of affected limbs following recanalization of venous segments at 12 months (1). Valve reflux occurs not only in segments directly involved in the thrombotic process, but also in uninvolved segments (7). The process of recanalization and collateralization is often incomplete after iliac vein thrombosis. Residual iliac obstructive lesions are found in a significant proportion of patients with post-thrombotic syndrome (8). In contrast, chronic outflow obstruction is usually not a significant factor in cases of femoropopliteal vein thrombosis without iliac involvement. This is largely due to collateral enlargement of the profunda femoris vein, which assumes

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A

D

B

C

E

FIGURE 94.2 Pathology of post-thrombotic valve. The degree of valve damage is variable. (A) Destroyed valve cusp. (B) Perforated cusp. (C) “Frozen” and thickened valve cusp. (D) Adherent valve cusp with some thickening. (E) Redundant and refluxive valve indistinguishable in appearance from “primary valve reflux.” (From Raju S. In: Mosby-Yearbook: Current Therapy in Vascular Surgery, 3rd edn. Ernst CB, Stanley JC, eds. 1994.)

FIGURE 94.1 Axial transformation of deep femoral vein through large profunda–popliteal connection. Major portion of superficial femoral vein except for distal portion is occluded. (From Raju S, Easterwood L, et al. Saphenectomy in the presence of chronic venous obstruction. Surgery 1998;123:637–644.)

the size and course of the native femoral vein (axial transformation) and is easily mistaken for it (Fig. 94.1) (9). Reflux at the dilated profunda femoris valve is, however, often associated with stasis skin changes including ulceration. Crural vein thrombi usually resolve and, with rare exceptions, do not lead to high-grade venous obstruction. Patients with previous venous thrombosis at or below the knee level usually evince only mild symptoms or may even be totally asymptomatic (8). The combination of symptoms generically defined as post-thrombotic syndrome thus derives from variable underlying pathology, ranging from residual obstruction particularly in the iliac venous segment and postthrombotic reflux commonly in the femoral venous segments. Often, a mixture of these features is present. The reflux abnormality may be due to damage/destruction of axial valves (Fig. 94.2) or to development of collateral reflux. Femoral valves adjacent to the thrombus may escape destruction but may become secondarily incompetent due to constriction and foreshortening of the valve station from periphlebitis (Fig. 94.3). The secondary refluxive

FIGURE 94.3 A possible mechanism for the production of valve redundancy and reflux in post-thrombotic valve stations. Valve station fibrosis may lead to luminal constriction resulting in “secondary” valve leaflet redundance and reflux. Foreshortening of the valve station may lead to widening of the commissural valve angle, contributing further to development of reflux. (From Raju S, Fredericks RK, et al. Venous valve station changes in “primary” and postthrombotic reflux: an analysis of 149 cases. Ann Vasc Surg 2000;14:193–199.)

valves are redundant, similar to “primary” reflux, except the valve station is smaller and constricted. Collateral reflux may result from dilation or thrombotic valve destruction in tributary collaterals (profunda femoris), or reversal of flow direction (transpelvic and prepubic collaterals); valves may be altogether absent in venous collaterals that develop de novo. Post-thrombotic dysfunction

Chapter 94 Venous Reconstruction in Post-thrombotic Syndrome

of the calf venous pump mechanism is frequently present; reduced capacitance from residual thrombus and diminished ejection fraction from compliance changes may compound the reflux and obstructive abnormalities described (10).

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prisingly normal in appearance, and the post-thrombotic etiology may be evident only on venography or duplex examination.

Investigation Clinical Features As may be expected from the variable underlying pathophysiology, patients with post-thrombotic syndrome display a wide spectrum of symptoms ranging from mild to severe. The fortunate patient may evince nothing more than mild calf discomfort with little functional disability, while the patient with the more severe form may be completely disabled with a combination of pain, swelling, and stasis skin changes including frank ulceration. Swelling is more often associated with an obstructive component, and stasis skin changes are frequently the result of the refluxive abnormality. Patients may transit from initial painful swelling to later stasis skin changes, corresponding with the evolution of initial thrombotic obstruction to post-thrombotic reflux as recanalization and collateralization proceed apace. Venous claudication associated with elevation of ambulatory venous pressure beyond resting levels due to extensive post-thrombotic venous obstruction is distinctly uncommon, although this interesting clinical presentation was the focus of considerable attention in the early literature. Symptoms of post-thrombotic syndrome may wax and wane, with acute exacerbation due to recurrent thrombosis, onset of cellulitis in the edematous extremity, or the occurrence of painful inflammatory changes around an indolent stasis ulcer resulting from invasive pathogens. In some patients, no such identifiable cause for episodic worsening of symptoms may be found, and acute decompensation of the calf venous pump mechanism from unknown causes must be assumed. Physical findings on examination are variable, with edema and stasis skin changes; dilated secondary varicosities also may be present. A minority of patients have calf pain as the dominant symptom with no other overt manifestations of venous insufficiency. The affected extremity may be sur-

A rational approach to the treatment of the post-thrombotic syndrome necessitates accurate identification of the underlying hemodynamic abnormality. Except in extreme cases of venous obstruction presenting as phlegmasia, it is generally impossible to differentiate venous obstruction from reflux, based on physical examination alone. Appropriate laboratory investigation is therefore mandatory; ambulatory venous hypertension cannot differentiate between reflux and obstruction. It does provide a global index of post-thrombotic calf pump dysfunction and is a convenient tool to monitor surgical outcome. Resting arm–foot venous pressure differential in the supine patient combined with abnormal elevation of foot venous pressure following induced hyperemia provides a method (8) of diagnosing and grading venous obstruction. Recent clinical experience with venous stents indicates that even this method may not be adequately sensitive. Measurement of outflow fractions with occlusion plethysmography is unreliable and may not be specific. Regional post-thrombotic changes below the inguinal ligament are often detectable on duplex examination. However, ascending venography is generally preferred to define post-thrombotic changes in the lower extremity as it provides a greater composite view. Transfemoral venography is often required to obtain adequate visualization of the iliac venous segments (11). Because of the propensity of iliac vein lesions to predominate in the anteroposterior plane, limited or localized lesions may escape detection by single plane venography. Uniformly diffuse narrowing of the iliac veins is not uncommon and may escape notice because of the absence of collaterals. Post-thrombotic webs and membranous strictures may be masked by flooding of the contrast over the lesions. Intravascular ultrasound examination (IVUS) is a reliable tool to assess the iliac venous segment in suspected cases (Fig. 94.4) (11). Ascending venography is notoriously un-

FIGURE 94.4 Normal appearance of transfemoral venogram in a patient who had a tight (>90%) stenosis detected by IVUS. (From Raju S, Owen S, et al. Reversal of abnormal lymphoscintigraphy after venous stenting. J Vasc Surg 2001;34:780, fig. 1.)

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plications (i.e., cellulitis, ulcer infections, or recurrent thrombosis) should be considered for surgical correction. Younger patients in the working population are preferred candidates for a surgical approach. Gratifying results may be obtained in a highly selected group of older patients who are unable to maintain leg elevation or apply compression devices due to frailty, arthritis or other comorbid conditions. Conservative therapy can be a challenge in these elderly patients with massive ulceration. Surgical intervention allows for easier management of elderly patients living alone or under conditions of sparse nursing resources. Stasis skin changes are often the main indications for surgical intervention. However, it should not be forgotten that other components of post-thrombotic syndrome, such as pain, swelling, recurrent cellulitis, or recurrent phlebitis can be quite disabling even in the absence of stasis skin changes. When resistant to conservative therapy, this group of patients are also suitable surgical candidates. FIGURE 94.5 Venographic appearances of “wiped out” deep system with the saphenous vein functioning as the sole outflow source (left). This is often spurious as descending venogram shows an extensive deep venous network in the same limb (right). If the saphenous vein is refluxive, saphenectomy can be safely performed in this type of case.

reliable (12) to assess the functional capacity of collaterals. Large contrast-filled collaterals may be functionally inadequate due to the presence of kinks, strictures, or valves impeding flow. Some functionally adequate collaterals may not be visualized at all with contrast due to dye dilution, abnormal flow patterns, and regional pressure variations. A venographic appearance that is frequently encountered in post-thrombotic limbs is shown (Fig. 94.5, left). The deep system in the leg and thigh does not visualize and the saphenous vein is the apparent sole outflow source. That the entire limb flow including deep muscle flow should rest on such flimsy collateral is conceptually untenable although radiologists often provide this interpretation in such cases. Profuse deep collaterals can be demonstrated by descending venography in these cases (Fig. 94.5, right). Reflux may be qualitatively assessed by duplex scanning and descending phlebography. Because duplex scanning cannot adequately quantify collateral reflux, a more global test for reflux, such as air plethysmography, is recommended in post-thrombotic cases. When valve reconstruction is contemplated, descending venography is invaluable in identifying valve station location and morphology.

Indications for Surgery and Selection of Patients Patients who have failed conservative therapy due to ineffectiveness or intolerance, or who develop recurrent com-

Venous Obstruction The advent of venous stent technology has had a major impact on the management of post-thrombotic syndrome in general and venous obstruction in particular (13). Placement of iliac venous stent is an outpatient procedure, has low risk, excellent patency, and impressive symptom resolution; it does not preclude later open veno-venous bypass surgery or valve reconstruction if the stent were to fail. For these reasons, iliac venous stent placement has all but replaced traditional veno-venous bypass procedures in our institution despite the relatively short duration of stent experience. Moreover it was noted that iliac vein stent placement resulted in significant healing of venous stasis ulceration (62% actuarial at 24 months), even though the reflux component was not corrected. Venous stent placement has become the initial choice of treatment in the entire group of patients with post-thrombotic syndrome, including those with stasis skin changes, when iliac-caval obstruction is shown to be present by IVUS examination.

Stent Placement Technique Access to the iliac venous segment is obtained percutaneously via the ipsilateral femoral vein under ultrasound guidance (14). The presence of treatable stenosis should be confirmed by an IVUS examination. The stenotic lesion is dilated with a 14-mm or 16-mm balloon followed by placement of self-expanding stent of same size. Stent placement is carried out routinely as recoil invariably occurs without it. For lesions involving the common iliac vein it is important to extend the stent well into the vena cava as a stenosis at the iliac-caval junction invariably develops otherwise (Fig. 94.6). Contralateral iliac flow is not compromised from this practice even in instances of stent

Chapter 94 Venous Reconstruction in Post-thrombotic Syndrome

thrombosis. All stenotic lesions should be adequately treated by stent(s) with extension of the stent below the inguinal ligament into the common femoral vein if necessary, without leaving residual lesions or short skip areas. Crossing the inguinal crease by the flexible stent has not posed a problem with patency rates. The procedure is done under minimal heparinization, with daily aspirin afterwards. Warfarin may be indicated in hypercoagulable patients or in cases of recurrent thrombosis. Stent patency and clinical results are shown in Figures 94.7 and 94.8 and in Tables 94.1. and 94.2.

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Valve Reconstruction Valve reconstruction is reserved for patients who are symptomatic from significant post-thrombotic reflux or patients with combined obstruction/reflux who did not respond to initial stent procedure. The great majority are patients with stasis dermatitis or ulceration.

Technique Valvuloplasty A direct valvuloplasty procedure (15) may be possible in a surprisingly large proportion of patients because the femoral valve survived the thrombotic process. These are either cases where “primary” reflux at the femoral valve resulted in distal thrombosis or an initially competent femoral valve later became secondarily refluxive from restrictive wall changes (Fig. 94.3). Direct valvuloplasty may also apply to valves that become incompetent from dilation in the axially transformed profunda femoris vein (Fig. 94.1). A variety of valvuloplasty techniques is now available. The transcommissural technique preferred by the author is shown in Figure 94.9. Axillary Vein Transfer

FIGURE 94.6 Preoperative and postoperative venograms showing correction of iliac venous stenosis by a long 16-mm stent. (From Raju S, Owen S et al. Reversal of abnormal lymphoscintigraphy after venous stenting. J Vasc Surg 2001;34:782, fig. 2A.)

When the valve structure is destroyed beyond direct repair, the axillary valve transfer technique can be used to restore competency to the venous segment. The technique is shown in Figure 94.10. Surprisingly, even trabeculated veins can be reconstructed using this technique with some modifications (Fig. 94.11). The actuarial ulcer healing rate after valve reconstruction in post-thrombotic limbs in our institution is 61% at 5years. This is very similar to the results in “primary” valve reflux (p = ns). There was no difference between direct valvuloplasty and axillary vein transfer techniques. Surprisingly similar results were obtained with axillary vein transfer in trabeculated veins. Perrin

FIGURE 94.7 Actuarial patency rates (primary and primary assisted/secondary) of iliac venous stents. Limbs at risk at each interval for the two categories are shown in the lower panel. (From Raju S, Owen S, et al. Clinical impact of iliac vein stenting in the management of chronic venous insufficiency. J Vasc Surg 2002;35:10, fig. 1.)

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Part XII Venous and Lymphatic Surgery FIGURE 94.8 Actuarial ulcer-free interval following stent placement. Limbs at risk at each interval are shown at the lower panel. (From Raju S, Owen S et al. Clinical impact of iliac vein stenting in the management of chronic venous insufficiency. J Vasc Surg 2002;35:11, fig. 2.)

TABLE 94.1 Improvement in swelling after stent placement Parameter

Grade†

Pre-stent

Post-stent

Objective swelling

0 (no swelling) 1–3 (swelling) Median (range) 0–3† Median (range)

36/297 = 12%

124/264 = 47%** 1 [0–3)*** n = 62 1 (0–4)***

Subjective swelling

2 (0–3) n = 62 2 (0–4)

A

†Subjective swelling: grade 0 = none, grade 1 = late evening, grade 2 = midday, grade 3 = morning swelling. Objective swelling: grade 0 = none, grade 1 = pitting, grade 2 = ankle edema, grade 3 = gross. **p < 0.01; ***p < 0.001.

TABLE 94.2 Level of pain before and after stent placement Pain Severity Limbs with no pain Limbs with pain Pain level 0–10† 4 (0–9) 0 (0–10)***

Pre-stent

Post-stent

49/291 = 17% Median (range)

185/261 = 71%*** Median (range)

†See text for description of pain level. ***p < 0.001.

(16) has reported 62% actuarial ulcer healing at 5 years. In post-thrombotic limbs nearly identical to our results.

Ancillary Procedures

B FIGURE 94.9 Technique of transcommissural valvuloplasty: transluminal sutures along valve attachment lines are used to simultaneously tighten redundant valve cusps and bring them closer together for better apposition. (From Raju S, Berry MA et al. Transcommissural valvuloplasty: technique and results. J Vasc Surg 2000;32: 969–976.)

with femoral valve reconstruction to correct reflux. No malsequelae were observed despite the saphenous vein appearing as the sole outflow tract in several cases (Fig. 94.5.)

Saphenectomy

Perforator Interruption

Significant saphenous reflux (secondary varix) may be present in post-thrombotic limbs. Saphenectomy can be performed safely (17) in such limbs, either alone or

Intermediate-term results with the endoscopic perforator interruption (SEPS) appears to be inferior in postthrombotic limbs (18).

Chapter 94 Venous Reconstruction in Post-thrombotic Syndrome

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FIGURE 94.10 Technique of axillary vein transfer. The valve should be inserted under optimal tension without torsion. The shallow axillary valves are easily susceptible to malcoaptation and reflux due to technical deficiencies such as torsion or excessive or inadequate tension (inset). A prosthetic sleeve is placed around the transferred axillary valve to prevent late dilation. (From Raju S, Hardy JD. Technical options in venous valve reconstruction. Am J Surg 1997;173:301–307.)

FIGURE 94.11 Axillary vein transfer can be performed in trabeculated veins after excising the synechiae to create a single lumen for anastomosis. Surprisingly good patency and ulcer healing can be achieved with this technique even in these difficult limbs. (From Raju S, Neglen P et al. Axillary vein transfer in trabeculated postthrombotic veins. J Vasc Surg 1999;29:1050–1064.)

References 1. Markel A, Manzo RA, et al. Valvular reflux after deep vein thrombosis: incidence and time of occurrence. J Vasc Surg 1992;15:377–384.

2. Mayberry JC, Moneta GL, et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery 1991;109(5):575–581. 3. Kistner RL. Surgical repair of the incompetent femoral vein valve. Arch Surg 1975;110:1336–1342. 4. Raju S. Venous insufficiency of the lower limb and stasis ulceration: changing concepts and management. Ann Surg 1983;197:688. 5. Raju S, Fredericks RK, et al. Venous valve station changes in “primary” and post-thrombotic reflux: an analysis of 149 cases. Ann Vasc Surg 2000;14: 193–199. 6. Meissner MH, Manzo RA, et al. Deep venous insufficiency: the relationship between lysis and subsequent reflux. J Vasc Surg 1993;18:596–608. 7. Caps MT, Manzo RA, et al. Venous valvular reflux in veins not involved at the time of acute deep vein thrombosis. J Vasc Surg. 1995;22(5):524–531. 8. Raju S, Fredericks R. Venous obstruction: an analysis of 137 cases with hemodynamic, venographic, and clinical correlations. J Vasc Surg 1991;14:305–313. 9. Raju S, Fountain T, et al. Axial transformation of the profunda femoris vein. J Vasc Surg 1998;27:651–659. 10. Raju S, Neglén P, et al. Ambulatory venous hypertension: component analysis in 373 limbs. Vasc Surg 1999;33:257–267. 11. Neglen P, Raju S. Intravascular ultrasound (IVUS) evaluation of the obstructed vein. J Vasc Surg 2002;35:694–700. 12. Raju S. A pressure based technique for the detection of acute and chronic venous obstruction. Phlebology 1988;3:207. 13. Raju S, Owen S Jr, Neglen P. The clinical impact of iliac venous stents in the management of chronic venous insufficiency. J Vasc Surg 2002;35:8–15. 14. Neglen P, Berry MA. Raju S. Endovascular surgery in the treatment of chronic primary and post-thrombotic iliac vein obstruction. Eur J Vasc Endovasc Surg 2000;20:560–571.

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15. Raju S, Hardy JD. Technical options in venous valve reconstruction. Am J Surg 1997;173:301–307. 16. Perrin M. Reconstructive surgery for deep venous reflux: a report on 144 cases. Cardiovasc Surg 2000;8:246–255. 17. Raju S, Easterwood L, et al. Saphenectomy in the presence of chronic venous obstruction. Surgery 1998;126(6):637–644.

18. Gloviczki P, Bergan JJ, et al. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American subfascial endoscopic perforator surgery registry. The North American Study Group. J Vasc Surg 1999;29(3): 489–502.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene Henry Haimovici

Blood clots suddenly blocking veins of an extremity and causing gangrene remained an unknown vascular entity for a long time. Indeed, such a combination of vascular factors was considered incompatible with the prevailing knowledge that only blockage of arterial blood supply to tissues could induce gangrene. Yet early in 1937 in my own experience, I learned that this could also occur under special circumstances in acute thrombosis of veins. Indeed, venous blockage with gangrene was not generally known in 1937 at the time of my first observations of this possibility. I first became aware of such a case during my last year of residency training in surgery at the Hôtel Dieu in Marseilles. This story and its associated circumstances are the tale of a serendipitous observation that led to unsuspected concepts of the pathogenesis of acute venous thrombosis with correlative clinical aspects and new surgical management (see below).

peared to be a need for a more appropriate definition of the terminology based on the pathogenic process of this entity. Ischemia of the tissues was the outstanding common denominator that led me in the early 1960s to propose for this entity the comprehensive term of ischemic venous thrombosis (IVT), subdivided into two distinct clinical stages, for which two of the already widely used terms were retained and defined: 1. 2.

phlegmasia cerulea dolens (PCD), a reversible stage; and venous gangrene, an irreversible stage.

The fundamental difference between the two forms is a matter of extent of the underlying venous occlusion, their clinical course, and their ultimate prognosis. Early recognition and treatment of PCD is of the utmost importance if gangrene is to be prevented. Herein lies the significance of this classification into two stages.

Definition of Terms Venous-induced gangrenous manifestations, in spite of persistent patency of the adjacent arterial tree, may pose difficult diagnostic and therapeutic problems at times. Earlier terms used to define this condition were often inadequate, and at times misleading, such as pseudoembolic phlebitis, acute massive venous occlusion, and thrombophlebitis with spasm and gangrene. There ap-

Historical Background Historically, the possibility of this notion was recognized as early as 1593 by Fabricius Hildanus, who mentioned it as sometimes associated with venous thrombosis. During the eighteenth and nineteenth centuries, this condition was the subject of sporadic case reports, primarily based

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on autopsy findings. Despite a number of subsequent contributions, the idea that ischemia can be induced by acute venous thrombosis was not readily accepted. This condition was experimentally reproduced in the 1930s, solely by extensive occlusion of the venous channels, in an attempt to provide a pathogenic basis for this entity. Consequently, this condition gained some clinical attention and significance. It was in 1938 that the term phlegmasia cerulea dolens was introduced in associating venous gangrene with deep venous thrombosis. Despite accumulating subsequent information, the severe form of venous thrombosis was poorly or incorrectly differentiated from the common form of deep venous thrombosis and was often mistaken for other vascular disorders as well (see below, Differential Diagnosis). Considering the above, it appears that IVT is probably not so uncommon as was generally believed. The incidences of the two stages are different. It is important to emphasize that 82% of cases were due to PCD and only 18% to venous gangrene (see Table 95.1). Prompt and appropriate treatment of the PCD stage may have prevented the gangrene.

FIGURE 95.1 Etiology: site and distribution of phlegmasia cerulea dolens in 175 patients with 189 extremities involved (left) and of venous gangrene in 158 patients with 199 extremities involved (right).

Etiology The etiologic factors of IVC were described in 1971 (Fig. 95.1) in a study of 175 patients with 189 PCD extremities and 158 patients with 199 extremities involved with venous gangrene. The etiology of IVT is not different from that of common deep venous thrombosis (DVT) except that it occurs more frequently. The most common etiologic factors in both groups are mostly a postoperative state or neoplastic disease. A postoperative state was noted in 24.8% of PCD cases and in only 13.3% of venous gangrene cases. It appears, therefore, that about one in seven patients with PCD and one in four patients with venous gangrene had an underlying visceral malignancy. In PCD, the lower extremities were involved in 95.4% of cases and the upper extremities in only 4.6% (Fig. 95.2; Table 95.1). In unilateral cases, the left lower extremity was affected four times as often as the right. Bilateral involvement occurred in only 6.2% of cases. In venous gangrene, by contrast, the left lower extremity was affected only slightly more than the right (left 56%, right 46%). In addition, there were more bilateral cases of venous gangrene than PCD. Analysis of the data shows that venous thrombosis is more extensive in venous gangrene than in PCD, indicating the highest index of thrombogenicity in this type of venous disease.

Clinical Manifestations Phlegmasia Cerulea Dolens The syndrome of this form of acute circulatory disturbance (often preceded by a typical phlegmasia alba

FIGURE 95.2 Distribution and extent of gangrene involving the lower and upper extremities. Note the relatively high incidence of distal and localized gangrene of the toes and fingers.

dolens) includes the classic triad of edema, cyanosis, and pain, hence the term phlegmasia cerulea dolens. Pain is usually severe and always present. Cyanosis is pathognomonic and is as striking as the severity of the pain. The edema, occasionally absent at its inception, is generally characteristic, having a hard, woody, or rubbery consistency. After a few days, cutaneous blebs or bullae may appear. Peripheral arterial pulses, pedal or wrist, at the initial stage may be felt in only one-half of the cases. Arteriography and mostly noninvasive tests are helpful in disclosing

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Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene TABLE 95.1 Incidence of ischemic venous thrombosis relative to overall deep venous thrombosis IVT Study Anlyan & Hart 1957 Devambez 1960 Fogarty et al. 1963 Fontaine et al. 1965 Natali & Tricot 1982 Le Bideau-Gouiran 1983 Haimovici 1983 Total

PCD

VG

No. of DVT

No.

%

No.

%

No.

%

453 589 655 300 117 185 610

19 31 11 32 5 35 62

4.2 5.2 1.7 10.7 4.3 18 9 10.1

17 29 8 32 5 29 40

89.4 93.5 72.9 100.0 100.0 82.9 64.5

2 2 3 — — 6 22

10.6 6.5 27.1 — — 17.1 35.5

2909

195

6.4

160

86.0

35

14.0

DVT, deep venous thrombosis; IVT, ischemic venous thrombosis; PCD, phlegmasia cerulea dolens; VG, venous gangrene.

FIGURE 95.3 Incidence of pulmonary embolism in ischemic venous thrombosis.

the patency of the arterial tree. Phlebography, on the other hand, may disclose extensive venous thrombosis, often up to and including the iliac veins and inferior vena cava. Circulatory collapse or hypovolemic shock from excessive fluid loss occurs in most cases because of entrapment in the involved extremity of 3 to 5 L of fluid. Pulmonary embolism is a frequent complication of PCD, seen in approximately 14.9% of nonfatal cases and 3.4% of fatal cases (Fig. 95.3). This is in contrast to its greater frequency in cases of venous gangrene. Immediate recognition and treatment of PCD are essential for preventing progression to gangrene.

Venous Gangrene The clinical picture of an IVT resulting in gangrene proceed through three different phases: 1) phlegmasia alba dolens, 2) phlegmasia cerulea dolens, and 3) gangrene. Phlegmasia alba dolens will often precede by a few days the blue thrombophlebitis and venous gangrene, although in certain cases it may fail to appear or may pass unnoticed. Phlegmasia cerulea dolens is present in all instances. All peripheral pulses at the initial stage are palpable in more than half the cases. As in simple PCD, circulatory collapse is noted in many instances (21.5%) of IVT. Multiple venous occlusions involving two or more extremities

are most characteristic. In addition, about one in four patients also has uncomplicated venous thrombosis, either as phlegmasia alba dolens or as phlegmasia cerulea dolens, affecting other extremities. Gangrene usually develops within 4 to 8 days after the onset of the ischemic signs. This gap between the two phases affords early recognition of the symptoms and treatment to prevent gangrene. The extent of the gangrene varies. In most patients, the gangrenous lesions are limited to the toes or foot. Rarely, they affect the leg or even the thigh, in which case the incidence of pulmonary embolism is greater, ranging from 19.0% in nonfatal cases of venous gangrene to 22.1% in fatal cases.

Clinicopathologic Patterns of Ischemic Thrombosis Patterns of Lower Extremity Clinical, phlebographic, and operative findings, as well as postmortem examination, indicate that several patterns are associated with the two types of IVT of the lower extremities. In PCD there are essentially three patterns: 1) iliofemoral, 2) femoropopliteotibial, and 3) a combined form. Characteristic in each of the three types is patency of a number of major and collateral veins at the root of the extremity, thus providing escape pathways for venous return and potential reversibility of the ischemic syndrome. In venous gangrene there are essentially two patterns: 1) complete occlusion of the femoroiliocaval axis but with patency of the popliteotibial veins, and 2) complete or nearly complete occlusion of the entire venous system of the extremity, including both superficial and deep channels. Figures 95.2 and 95.4 depict the pattern of venous occlusion leading to venous gangrene.

Patterns of Upper Extremity The anatomicopathologic patterns in the upper extremity are not so well defined as those in the lower extremity. The

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A

B

C

FIGURE 95.4 (A) Incipient gangrene of the toes with marked cyanosis of the right foot. (B) Extent of gangrenous lesions of the plantar surface, sites of skin incisions for the fasciotomies performed earlier for decompression of a swollen foot. (C) Healing of the foot after self-amputation of toes and spontaneous separation of the adjacent necrotic skin 3 months after onset of the gangrene.

clinical findings and the severity of the venous thrombosis do not always correlate with the extent of gangrene. The patterns based on the presence of 1) phlegmasia cerulea dolens and 2) gangrenous lesions best express this correlation of the various findings. First Group: Phlegmasia Cerulea Dolens Only Of the 175 patients with 189 PCD cases, only four patients had associated upper extremity involvement. One involved the right side, and three the left side. The causes of the three cases were 1) influenza, 2) hypertensive cardiovascular disease, and 3) breast carcinoma with metastases in a 67-year-old woman. Second Group: Gangrene of Upper Extremity Of these 158 patients with gangrene of 199 lower extremities, 21 displayed upper extremity gangrenous lesions, and five displayed only simple PCD or phlegmasia alba dolens. The extent of upper extremity involvement to be correlated with the extent of venous thrombosis is as follows: 1. 2.

Discoloration of the skin may involve the hand, the forearm, or the entire arm. The gangrenous lesions may involve the fingers alone, the fingers and hands, the hand and forearm, or the entire arm.

The thrombosed veins of the upper extremity affected thrombotic lesions of the subclavian axillary veins with extensive gangrenous lesions of the hand and forearm.

Pathophysiology The hypercoagulable state appears to be the initiating factor of IVT, followed by a sequence of pathophysiologic events (Fig. 95.5). A number of hematologic components have been implicated in the pathogenesis of hypercoagulability but are not always well documented. Most of the evidence is based on observations of allied conditions of venous thrombosis. A fibrinolytic system that is defective owing to low levels of plasminogen activators and to the liberation of thromboplastic substances from an undetectable source, often a tumor, has been postulated as one cause. Other more specific factors present a series of complex interrelated reactions that involve the plasma coagulation mechanism. Of these, antithrombin deficiency has been suggested as a cause of unexplained thrombosis in vascular surgery. In addition, heparin-induced platelet aggregation may be a cause of unexplained thrombosis in some patients. But the chief contributing factors revealed in a recent study of unexplained thrombosis, primarily venous thrombosis, are related to the low activity level of antithrombin II (heparin cofactor activity), or antithrombin III, or both. Antithrombin III deficiency is inherited and rarely causes clinically manifest thrombosis during the second decade of life. The thrombotic episodes related to antithrombin III are initiated by such predisposing factors as surgery, childbirth, and infection. Another important aspect of coagulation is the role of proteins designated C and S. Protein C is a vitamin K-

Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene

FIGURE 95.5 Sequence of pathophysiologic events in the pathogenesis of ischemic venous thrombosis.

dependent plasma proenzyme produced in the liver. Thrombin is the only known circulating enzyme capable of activating protein C. Activated protein C (APC) inactivates factors Va and VIIIa and thus interferes with the activation of factor X. Protein C deficiency is hereditary and is transmitted as an autosomal dominant trait. Patients with protein C deficiency are at risk of recurring thromboembolism. These patients are usually treated with warfarin. However, they should receive heparin for the first few days of warfarin therapy because protein C levels are depressed more rapidly than are the coagulation factor levels. The full expression of the anticoagulant potential of APC is dependent on the availability of a second glycoprotein known as protein S. Protein S acts as a cofactor protein with APC in the inactivation of factor Xa. Deficiencies of protein S are also inherited as an autosomal dominant trait. These factors of coagulation mechanism are mentioned particularly in relation to venous thrombosis leading to PCD and venous gangrene. Venous thrombosis associated with PCD and venous gangrene massively affects the deep as well as the superficial veins. Its link

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to warfarin in this situation is depletion of protein C and protein S. Their vitamin-K-dependent synthesis is blocked, thereby tipping the hematologic coagulation– anticoagulation scale toward thrombosis. These various factors and their interdependence may play a significant role in the coagulation or hypercoagulable state that initiates the venous thrombosis leading to venous gangrene. So far, few studies have been carried out in which these factors were used as criteria for the development and severity of the thrombogenic factors. Besides the antithrombin II and III deficiencies and the deficiencies of proteins C and S, heparin-induced thrombocytopenia can be an inciting or complicating factor in IVT. Cryoglobulinemia and polycythemia are also found in patients with the massive venous thrombosis that occurs in PCD and venous gangrene. In addition to these hematologic factors, some patients displayed disseminated intravascular coagulation based on laboratory findings. Thus, in addition to the preceding factors, there are strictly hematologic aspects of coagulation that complicate the underlying thrombosis in PCD and venous gangrene. All combined lead to the hypercoagulable state, which has been poorly defined in the past. Some studies have provided a more coherent understanding of what the hypercoagulable state is: a process in which factors of different natures combine to produce this thrombogenic entity (see Towne et al., 1979, 1981; Haimovici and Bergan, 1987). It is important to point out that all these factors do not act individually to produce the thrombotic result. Several of these factors act at one time. They are usually associated with precipitating factors such as trauma, infection, intravenous infusion, and especially a number of lifethreatening illnesses such as those that constitute low cardiac output, sepsis, congestive heart failure, and many of the other elements enumerated in the etiology of this condition. If antithrombin deficiencies are recognized early, thrombosis could be prevented by long-term use of warfarin (Coumadin). It is claimed that warfarin or sodium warfarin, if maintained indefinitely, may elevate antithrombin III levels in some patients. It is obvious from the uncertainty about some aspects of thrombogenesis and its treatment that further experience is necessary before a definitive understanding of the underlying mechanism of the hypercoagulable state can be achieved.

Hemodynamics of Venous Blockage The extensive blockage of venous return causes the interstitial or extravascular fluid retention reflected by massive edema and marked increase in tissue pressure. After 8 hours of massive venous occlusion, there is a rise in tissue pressure of 38 mmHg on the affected side compared with 3 mmHg on the control side. The critical closure of arterial flow occurs mostly in complete blockage. It is in these cases that the Burton principle may account for the capillary stasis leading to is-

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chemia. Another consequence of the aforementioned physiopathologic events is a marked entrapment of blood owing to excessive fluid loss in the extravascular compartment of the involved extremity. This leads to hypovolemic shock. The quantity of trapped fluid in the swollen limb has been estimated to range from 3 to 5 L. As a corollary, the average control hematocrit rises considerably, increasing to about 53%. Vasomotor changes affecting the veins and arteries may also play a role, but such changes have been variously interpreted by clinicians and experimentalists alike. The most commonly encountered vasomotor change is a spasm in the major arteries adjacent to the thrombosed veins, primarily seen during their exposure in the femoral vessels. Vasospasm appears more pronounced in PCD than in venous gangrene cases. Total or near total venous occlusions immediately produce a rise in venous pressure that corresponds to the mean arterial pressure. Concomitantly, the blood flow falls to zero level. Arterial blood pressure and visible arterial pulsations remain normal for a number of hours. Experimentally these changes have been shown to peak in a 6-hour period. After 12 hours of occlusion, the pulse and arterial pressure distal to the occlusion usually disappear. These experimental hemodynamic data confirm the possibility of reversing the ischemic phenomena within 6 to 12 hours. In the clinical setting it may take slightly longer for the ischemic changes, depending on their extent, to become irreversible, a factor to bear in mind in the management of some cases.

Diagnosis The clinical picture of both forms of IVT offers, at onset, the characteristic association of venous and arterial manifestations. Therefore a differential diagnosis from other vascular conditions may have to be made in the presence of either PCD or venous gangrene. For example, internal hemorrhage, myocardial infarction, pulmonary embolism, or traumatic injuries can cause acute peripheral circulatory failure, so common in PCD. To diagnose venous gangrene there must be thrombophlebitis without arterial occlusion. Arteriography is helpful in differentiating venous from arterial gangrene. Other difficult diagnoses are acute infectious diabetic gangrene, gangrene complicating acute prolonged vascular collapse, and embolic gangrene. At onset it may be difficult, if not impossible, to predict whether the ischemic manifestations in a case of PCD are reversible or will continue to progress toward necrosis of the tissues (Figs. 95.6 and 95.7).

Differential Diagnosis As Table 95.2 indicates, the need for differential diagnosis arises from three major clinical findings. Most of the con-

FIGURE 95.6 Gangrene of the left foot and the lateral aspect of the leg up to the knee, with a patchy area of discoloration above the knee. The entire extremity is massively swollen.

ditions mentioned in Table 95.2 are discussed and need not be repeated here. In recent years, however, skin necrosis secondary to anticoagulant therapy has raised difficult problems in diagnosis. Because it is secondary to anticoagulants, drugs universally used in the management of vascular diseases, a special discussion of its differential diagnosis is unwarranted. One of the entities from which it should be differentiated is venous gangrene. A number of European authors, and in recent years a few American investigators as well as surgeons dealing with these problems, have pointed out this little-known complication. Unawareness of the exact pathogenesis of venous gangrene of the extremities has often led to misdiagnosis. In 1961, Feder and Auerbach described “purple toes” as an uncommon complication of oral coumarin drug therapy. They presented six cases with cutaneous vascular lesions occurring 3 to 8 weeks after anticoagulant therapy with coumarin derivatives had been initiated. These were differentiated from other dermatologic effects that have been observed in the course of anticoagulant therapy. The mechanisms ascribed to the production of the cutaneous vascular lesions were direct capillary and cellular damage and vasodilation. Of course, because these lesions appeared 3 to 8 weeks after initiation of the anticoagulant therapy, doubts arose as to whether this mechanism alone would explain this phenomenon. It is possible that another effect on the blood-clotting mechanism is present but has not been isolated. In 1965, Nalbandian et al. reviewed the literature and gave an excellent description of these complications. In their experience, this appeared to be a rare complication of coumarin-congener anticoagulant therapy characterized by a sequence of skin lesions such as petechiae, ecchymoses, and hemorrhagic infarcts. These lesions occur in random sites and have been well documented for several years in the European literature. The

Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene

A

C

B

D

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FIGURE 95.7 Cross-sections of the blood vessels in the case of venous gangrene shown in Figure 95.4. The crosssections are through the following vessels: popliteal (A), posterior (B), anterior tibial (C), and dorsalis pedis (D). The veins are all thrombosed, whereas the arteries are all patent.

TABLE 95.2 Differential diagnosis Phlegmasia cerulea dolens Reflex arteriospasm Acute inflammatory lymphedema Acute peripheral circulatory failure Peripheral arterial embolism Concomitant acute arterial and venous occlusion Venous gangrene Palpable pulses Acute infectious gangrene Gangrene complicating vascular collapse Digital gangrene due to endarteritis Nonpalpable pulses Embolic gangrene Gangrene due to acute arterial thrombosis Gangrene due to mixed arterial and venous occlusions Skin necrosis associated with anticoagulant therapy

lesions appear between the third and the tenth day of anticoagulant therapy, 90% occurring within the third to the sixth day. These alarming lesions were associated only with the use of coumarin-congeners, dicumarol being involved most frequently. Heparin had never been impli-

cated before 1979. Nalbandian et al. (1965) suggested as a possible mechanism a toxic action of the coumarincongeners, which would occur at the dermovascular loop, precisely at the junction of the capillary and the precapillary arteriole. The stage of hemorrhagic infarct that is actually a gangrenous lesion correlates with the thrombosis of the venules resulting from stasis immediately distal to the dermovascular loop. The authors recognize that many aspects remain unresolved and therefore feel that more pathophysiologic studies are indicated to understand more accurately its mechanism.

Warfarin-Induced Skin Necrosis and Venous Gangrene of the Extremities Induction of skin necrosis by warfarin (Coumadin) is rare. Its recognition has emerged slowly in the literature in recent decades. It is characterized by its unique affinity for skin and subcutaneous tissue. Lesions are found in areas where abundant subcutaneous tissue is present, such as breasts, buttocks, abdominal wall, anterior surface of the thighs, and exceptionally in the legs or arms. Furthermore, characteristically these lesions are localized in small areas. Pathologically, arteries in the skin and subcuta-

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neous tissue are spared, whereas the capillaries and venules, and occasionally the subcutaneous veins, are selectively occluded. Hemorrhage originating from the capillaries leads to necrosis of connective and fatty tissue. In its extreme manifestations the Coumadin-induced lesion is a hemorrhagic infarct of the skin and subcutaneous tissue. Warfarin-induced skin necrosis may mimic other skin conditions and may be confused with other entities. Thus a few studies have appeared in which the clinical and pathologic features of venous gangrene resulting from PCD were mistaken for warfarin-induced necrosis. Under these circumstances, warfarin may be erroneously implicated as the cause of the skin lesions and of extensive venous gangrene of the extremities. Such lack of precision in diagnosis may have serious therapeutic consequences. Should such a case also involve a medicolegal question, the consequences of mistaken diagnosis could become financially catastrophic (Fig. 95.8).

It is important to strongly emphasize that these two conditions are fundamentally, pathologically, and pathogenetically different. Massive thrombosis of all the veins of the extremity is the key to the differential diagnosis. This can be confirmed by ultrasound scanning in vivo, by examination of the amputated limb, or by autopsy. The presence of thrombosed major and small veins and patency of the arterial system are a sine qua non of the diagnosis of venous gangrene.

Heparin-Induced Necrosis and Thrombotic complications For many years, warfarin was the only anticoagulant thought capable of inducing skin necrosis. Since 1968, however, cases in which heparin induced similar skin complications as well as thrombotic vascular lesions have been reported. In 1978 Wu reported hyperaggregability of platelets

FIGURE 95.8 (A) Venogram of the left leg disclosing multiple areas of thrombosis in the calf veins of a patient with phlegmasia cerulea dolens. (B) Extension of the calf thrombosis in the popliteal and superficial femoral veins. (C) Venogram obtained 9 days after onset of the process shows patency of the leg and thigh veins with the exception of a small defect in the popliteal area. The patient remained edema-free throughout the 7-year observation.

Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene

and thrombosis in patients in whom thrombocytopenia was present. The same year Weismann and Robin reported on arterial embolism occurring during systemic heparin therapy. Roberts et al. investigated this problem in more detail and in 1973 reported thrombocytopenia with thrombotic and hemorrhagic manifestations associated with the use of heparin. Later, in 1977, the same investigators reported on eight cases with thrombotichemorrhagic complications associated with heparininduced thrombocytopenia. As a result, clinical papers on this subject sounded the warning that not only warfarin but also heparin can induce necrotic as well as hemorrhagic thrombotic skin lesions. The heparin-induced lesions are initiated by thrombocytopenia, followed by platelet aggregation, a fact that White et al. (1979) found in patients in vitro. The same mechanism was assumed to happen in vivo by platelet aggregation, followed by intravascular thrombosis.

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Fibrinolytics The two major fibrinolytic agents currently used are streptokinase and urokinase. In a few controlled multicenter clinical trials, these agents were found to be effective in the management of deep venous thrombosis and pulmonary embolism. Fibrinolysis is indicated only for established thrombophlebitis and should not be used for prophylaxis. Best results may be obtained in relatively fresh thrombi of not more than a week’s duration. Management of Underlying Disease Many patients with ischemic venous thrombosis suffer from serious visceral conditions, such as neoplastic diseases, postoperative situations, and infections or metabolic diseases. Treatment of these conditions must be undertaken concurrently or whenever possible or indicated.

Surgical Management

Although management may vary according to the clinical findings of PCD or venous gangrene, a number of objectives are nevertheless common to both. In order of priority, conditions to which one must direct immediate attention are the following.

From the preceding review of medical management, especially the use of anticoagulants and fibrinolytic therapy, it is obvious that under certain circumstances the venous thrombi are difficult to resolve. Venous thrombectomy is then indicated. Indications for venous thrombectomy upon which there is most general agreement are:

1.

1.

Treatment

2. 3. 4. 5. 6.

combating the venous stasis (edema) by maximum limb elevation; relieving shock by appropriate blood volume replacement; starting intravenous heparin; treating angiospasm; treating concurrently underlying conditions if feasible; assessing the extent of gangrene.

Medical Management Elevation of the Extremity Elevation of the extremity as the first step is essential and can be maintained until the ischemic and venous stasis subside substantially or completely. Maximum elevation is applicable not only in PCD but also in patients with venous gangrene. The reduction in edema is greater in the former than in the latter. Circulatory collapse or hypovolemic shock may be due to excessive entrapment of blood in the involved extremity. Fluid and cell replacements are urgently needed. Anticoagulants and Plasma Expanders In PCD, heparin is the optimal anticoagulant for preventing further propagation of thrombosis, especially when it is used concomitantly with elevation of the extremity. Some patients may show complete resolution of the thrombi in the context of this combined treatment.

2. 3. 4.

phlegmasia cerulea dolens, especially if conservative management failed within 24 to 72 hours; recurrent pulmonary embolism; floating thrombi in the iliocaval axis as determined phlebographically (Fig. 95.9); and rapidly progressive thrombosis in any type of acute femoroiliocaval thrombosis.

This procedure, by removing the thrombus, carries a three-fold salvage role: 1. 2. 3.

it prevents further extension of the thrombosis that could cause gangrene of the limb; it removes the source of pulmonary embolism, frequently fatal in this condition; and it forestalls a serious post-thrombotic syndrome with the well-known dreaded sequelae.

Venous Thrombectomy Comprehensive thrombectomy of proximal and distal venous channels, iliac and popliteotibial veins, is paramount for complete success of the procedure. Fresh thrombi less than 24 to 48 h old offer the best chance for removal from the venous system. In contrast, thrombi 72 to 96 h hold or more adhere to the venous wall and cannot be pulled out with balloon catheters. Radiologic control during thrombectomy may be helpful in visualizing the exact position of possible residual thrombi. Use of an intraoperative image intensifier has been advocated by some as a means of simplifying this evaluation.

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Hutschenreiter (1980), strong proponents of this procedure, in a series of 42 cases with arteriovenous fistula, achieved patency in 83.8% of cases, but without arteriovenous fistula in only 61.5% of 13 cases. Delin et al. (1982) reported similar success with arteriovenous fistula in 85% of their cases. The arteriovenous procedure as an adjunct in arterial or venous diseases for enhancing blood flow is not entirely new. Its protective value in maintaining patency of veins after thrombectomy needs further study to confirm the above successful results. Inferior Vena Cava Interruption

FIGURE 95.9 Phlegmasia cerulea dolens. Inferior venacavogram showing a floating thrombus. On the right, enlargement of the left picture, showing greater detail of the thrombus curling up above the renal veins. A transfemoral thrombectomy of the inferior vena cava was carried out in addition to ligation of ovarian veins because of pelvic pathology.

Vollmar and Hutschenreiter (1980) have recommended routine use of intraoperative vascular endoscopy. Although a relatively simple procedure in the hands of experienced technicians, endoscopy would seem superior to venous angiography. According to Vollmar, it is helpful in the diagnosis of a venous spur, which is frequently seen in recurrent occlusions. Distal Tree Clearance The distal tree may be difficult or impossible to clear in the presence of old organized thrombi. If, on the other hand, the distal thrombi appear to be recent, thrombectomy and thrombolytic measures are helpful. Indeed, streptokinase may be delivered directly to its site of action to avoid systemic side effects. However, successful results could be obtained in certain cases with systemic administration of streptokinase. Control of the results should be obtained by intraoperative phlebography. Postoperative anticoagulation, in addition to fibrinolysis, is highly recommended in these cases. Role of Temporary Arteriovenous Fistula Concomitant temporary arteriovenous fistula is being advocated by a few European surgeons. Vollmar and

As an isolated surgical procedure, this is rarely used except to prevent further pulmonary embolism. Following thrombectomy, if in doubt about the possibility of pulmonary embolism from a peripheral venous tree, it may be necessary. Intraluminal interruption is preferable. The intraluminal method is indicated when the abdominal operation appears contraindicated. Use of Greenfield techniques is most advantageous. One word of caution against complete ligation: interruption of IVC alone without thrombectomy may in itself induce an ischemic syndrome. Our own method of stenosing ligation is by far easier, safer, and more expeditious. A few points concerning this technique are illustrated in Figure 95.10. Fasciotomy There is little doubt that, in the presence of massive venous thrombosis with corresponding increased subcutaneous subfascial edema, a fasciotomy is mandatory for relieving the compression of the various structures involved. It usually restores the caliber of major arteries, reestablishes capillary flow, and decompresses the muscles, which may be on the verge of severe ischemia or necrosis. In recent years the therapeutic potential of fasciotomy has been fully appreciated in PCD, as well as in other vascular conditions. The procedure used in such instances results in relief of the ischemic manifestations and therefore should be recommended widely. In contrast to the technique applied in arterial cases, in PCD the incisions should be wider and carried out not only below but also above the knee, both medially and laterally when necessary. Only in this way can one hope to decompress rapidly the various structures and prevent the impending severe ischemia. Amputations Venous gangrene is usually limited to the distal part of the extremity and mostly to the skin and sometimes the subcutaneous tissue. It rarely extends to the subfascial region and muscle layers, but the possibility that it can should always be considered along with lymphangitis and cellulitis. With or without superimposed infection, most cases of venous gangrene are of the moist variety because of the presence of edema, although dry necrosis is not incompatible

Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene

A

1149

with venous gangrene. The line of demarcation usually takes several weeks. If the infection is prevented or controlled, the necrotic process, which is mostly superficial, appears to be self-limiting. In contrast, spreading of the infection to the deep tissues may lead to loss of the extremity despite patent arteries. Mortality risks are quite high in this group of patients (22.6%). In a series of 75 patients I reviewed, 17 died after the procedure; most of these deaths occurred in aboveknee amputations (13 of 17). A large number of these patients had superficial lesions and could be treated conservatively. It is noteworthy that 20 of the 58 survivors had such lesions, and many of these required only local debridement and skin grafting. It should again be underscored that venous gangrene is usually superficial and more limited than arterial gangrene. Prevention of infection is essential to avoid major loss of tissue. Demarcation of the necrotic areas and their spontaneous eliminations may thus occur.

Prognosis Local and systemic factors, alone or in combination, determine the prognosis concerning both the limb and life of the patient. Analysis of the clinicopathologic data has disclosed that the outcome of this disease is vastly different in the two forms of ischemic thrombophlebitis. Factors that dominate the prognosis are: 1. 2. 3.

local factors, the presence or absence of gangrene; systemic factors, shock, pulmonary embolism, and the underlying disease; and therapeutic factors, the method of treatment and the speed with which it is applied.

In PCD, the overall recovery rate in the entire group of treated and untreated patients reported earlier was 84% (Fig. 95.11). The 16% mortality was related primarily to systemic factors.

B

FIGURE 95.10 (A) Stenosing ligation of inferior vena cava. Note that the ligation is carried out around the tip of a Kelly clamp, and when it is completed the residual vena cava lumen is slightly more than the thickness of the tip of the clamp. (B) An inferior venacavogram of a case in which a stenosing ligation was carried out in a patient in whom repeated pulmonary emboli could not be controlled by intravenous heparin over a period of several weeks. Note the ligation below a lumbar vein, with development of collateral circulation around the ligation. No further pulmonary emboli were noted after this interruption. The patient died 2 months later, and examination of the specimen showed complete clearance of thrombi in the distal veins. (Reproduced by permission from Haimovici H. Vascular emergencies. New York: Appleton-Century-Crofts, 1982.)

FIGURE 95.11 Overall prognosis in all cases of ischemic venous thrombosis, both treated and untreated.

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Circulatory collapse in the reported series was present in 28% of the cases, but from the available data it is difficult to determine whether this condition contributed significantly to fatal outcome. It would appear that in most cases, when adequate treatment was applied in time, circulatory collapse could be reversed. By contrast, the fatal pulmonary emboli that occurred in 3.4% of the patients and the underlying disease were by far the two most important causes of immediate death. Although neoplastic lesions associated with PCD were present in 15.4% of the cases, only about one-third of these patients died shortly after onset of the acute venous thrombosis. Death occurring some time after the acute venous thrombosis has subsided is obviously attributable to the underlying disease rather than to the vascular lesion. Treatment addressed primarily to reversing shock and providing supporting measures is essential at the onset of this condition. Lack of treatment resulted in 10 deaths among the 11 patients in this series. In venous gangrene, in contrast to PCD, the presence of gangrene, especially if it is extensive and associated with infection, represents a serious local factor that may play a significant role in the fatal outcome for the patient. The overall mortality rate associated with venous gangrene was 42%. Patients with bilateral lower extremity gangrene with or without amputation had a 71% mortality rate, associated systemic factors obviously contributing to this high incidence. Circulatory collapse was present in 21.5% of the cases. As in the preceding group, it is difficult to determine from the available data the extent to which the presence of shock could be held responsible for the fatal outcome of these patients. Most significant were two major factors: pulmonarv embolism and neoplastic disease. Fatal pulmonary emboli were reported in 22.1% of patients in the neoplastic disease group. The various conditions—multiple gangrenous lesions, severe shock, pulmonary emboli, and terminal neoplastic diseases—are most often combined in cases with a fatal outcome. The immediate prognosis, however, can be favorably influenced if adequate and prompt treatment is applied. Failure to do so in 18 cases resulted in 15 deaths (83%), as compared with a 36.4% mortality rate for the treated patients. These data clearly indicate that the prognosis in cases of venous gangrene is extremely severe, as opposed to the prognosis with PCD, in which the outcome is more favorable.

Conclusion From the above data, it is clear that there is a fundamental difference between PCD and venous gangrene in their respective survival rates. With better understanding of the two clinical forms, of the pathogenesis of this unusual entity, and of its immediate treatment, a substantial improvement can be achieved in the prognosis concerning both limb salvage and survival of the patient.

Bibliography Andriopoulos A, Wirsing I, Botticher R. Results of iliofemoral venous thrombectomy after acute thrombosis: report on 165 cases. J Cardiovasc Surg 1982;23:123. Anlyan WC, Hart D. Special problems in venous thromboembolism. Ann Surg 1957;146:499. Audier M, Haimovici H. Les gangrenes des membres d’origine veineuse. Presse Med 1938;46:1403. Brockman SK, Vasco JS. Observations on the pathophysiology and treatment of phlegmasia cerulea dolens with special reference to thrombectomy. Am J Surg 1965;109:485. Bulow S, Sager P. Venous gangrene. Acta Chir Scand 1975;141: 272. Burton AC. On the physical equilibrium of small blood vessels Am J Physiol 1951;164:319. DeBakey ME, Ochsner A. Phlegmasia cerulea dolens and gangrene associated with thrombophlebitis. Surgery 1949;26: 16. Decoulx P, Bastien P. Gangrene par spasme arteriel au cours d’une plebite. Ann Anat Phathol 1939;16:353. Delin A, Swedenborg J, et al. Thrombectomy and arteriovenous fistula for iliofemoral venous thrombosis in fertile women. Surg Gynecol Obstet 1982;154:69. Devambez J. Trente et une phlebites bleues: deux amputations pour gangrene. Phlebologie 1960;13:187. DeWeese JA, Adams JT. Iliofemoral venous thrombectomy. In: Haimovici H, ed. Vascular surgery. Norwalk, CT: Appleton-Century-Crofts, 1984:1007. Fabricius Hildanus G. De Gangraena et Sphacelo. Cologne, 1593. Feder W, Auerbach R. “Purple toes”: an uncommon sequela of oral Coumadin drug therapy. Ann Intern Med 1961; 55:911. Fogarty TJ, Cranley JJ, et al. Surgical management of phlegmasia cerulea dolens. Arch Surg 1963;86:256. Fontaine R, de Sousa Pereira A. Obliterations et resections veineuses experimentales: contribution a l’etude de la circulation collaterale veineuse. Rev Chir (Paris) 1937;75:161. Fontaine R, Kieny R, et al. Contribution a l’etude clinique et therapeutique de la phlegmatia coerulea dolens (phlebit bleue). A propose de 32 observations personneles. Lyon Chir 1965;61:321. Gregoire R. Le phlebite bleue (phlegmatia caerulea dolens). Presse Med 1938;46:1313. Goto H, Wada N, et al. Iliofemoral venous thrombectomy: follow-up studies of 88 patients. Surgery 1980;21: 341. Haimovici H. Gangrene of the extremities of venous origin: review of the literature with case reports. Circulation 1950:225. Haimovici H. Ischemic forms of venous thrombosis. Heart Bull 1967;16:101. Haimovici H. Ischemic forms of venous thrombosis: phlegmasia cerulea dolens, venous gangrene. Springfield, IL: Charles C Thomas, 1971. Haimovici H. Ischemic venous thrombosis. In: Haimovici H, ed. Vascular emergencies. Norwalk, CT: AppletonCentury-Crofts, 1982:589. Haimovici H. The ischemic forms of venous thrombosis. J Cardiovase Surg (suppl Philadelphia Congress 1965) 1966; 7:164.

Chapter 95 Ischemic Venous Thrombosis: Phlegmasia Cerulea Dolens and Venous Gangrene Haimovici H, Bergan JJ. Coumadin-induced skin necrosis versus venous gangrene of the extremities (editorial). J Vasc Surg 1987;5(4):655. Le Bideau-Gouiran G. Etude de 35 cas de phlebites ischemiques operees. Phlebologie 1983;36:101. Magendie J, Tingaud R. Phlebite a forme pseudoembolique (phlebite bleue de Gregoire). Bordeaux Chir 1945; 3(4):112. Minar E, Ehringer H, et al. Klinische, funktionelle, und morphologische Spatergebnisse nach venoser Thrombektomie. VASA 1983;12:346. Moreau P, Chevalier JM, et at. Thrombectomie veineuse pour thrombose aigue femoro-ilio-cave. Nouv Presse Med 1981;10:3159. Nachbur B, Beck EA, Senn A. Can the results of treatment of deep venous thrombosis be improved by combining surgical thrombectomy with regional fibrinolysis? J Cardiovasc Surg 1980;21:347. Nalbandian RM, Masler IJ, et al. Petechiae, ecchymoses and necrosis of skin induced by coumarin congeneres. J Am Med Assoc 1965;192:603. Natali J, Tricot JF. Place de la chirurgie dans le traitement des phlebites aigues des membres inferieurs. Phlebologie 1982;35:187. Partsch H, Weidinger P, et al. Funktionelle Spatergebnisse nach Thrombecktomie, Fibrinolyse und konservativer Therapie von Bein-Beckenvenenthrombosen. VASA 1980;9:53. Perlow S, Killian ST, et al. Shock following venous occlusions of a leg. Am J Physiol 1941;134:755. Raithel D, Sohnlein B. Die venose Thrombektomie-Technik und Ergebnisse. VASA 1981;10:119. Rhodes GR, Dixon RH, Silver D. Heparin induced thrombocytopenia: eight cases with thrombotic-hemorrhagic complications. Ann Surg 1977;186:752. Rhodes GR, Dixon RH, Silver D. Heparin induced thrombocytopenia with thrombotic and hemorrhagic manifestations. Surg Gynecol Obstet 1973;136:409. Roberts B, Rosato FE, Rosato EF. Heparin: a cause of arterial emboli? Surgery 1964;55:803. Smith BM, Shield GW, et al. Venous gangrene of the upper extremity. Ann Surg 1985;201:511. Stallworth JM, Najib A, et al. Phlegmasia cerulea dolens: an experimental study. Ann Surg 1967;165:860. Steinman C, Alpert J, Haimovici H. Inferior vena cava bypass grafts: an experimental evaluation of a temporary arteriovenous fistula on their long-term patency. Arch Surg 1966;93:747. Towne JB, Bernhard VM, et al. Antithtombin deficiency: a cause of unexplained thrombosis in vascular surgery. Surgery 1981;89(b):735. Towne JB, Bernhard VM, et al. White clot syndrome. Arch Surg 1979;114:372.

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Valici A, Isman H, et al. Thrombose aigue femoro-ilio-cave en gerontologie, Thrombectomie veineuse avec amplificateur de brillance. Nouv Presse Med 1981;11:1421. Veal JR, Dugan TJ, et al. Acute massive venous occlusion of the lower extremities. Surgery 1951;29:355. Vollmar JF, Hutschenreiter Temporary arteriovenous fistulas. In: Pelvic and abdominal veins: progress in diagnostics and therapy. Princeton, NJ: Excerpta Medica, 1980. Weismann RE, Robin RW. Arterial embolism occurring during systemic heparin therapy. Arch Surg 1958:76:219. White PW, Sadd JR, Nensel RE. Thrombotic complications of heparin therapy. Ann Surg 1979;190:595. Wu KK. Platelet hyperaggregability and thrombosis in patients with thrombocythemia. Ann Intern Med 1978;88:7. Zimmermann R, Mori H, Harenberg J. Urokinase-behandlung der phlegmasia coerulea dolens. Dtsch Med Wochenschr 1979;104:1563.

Selected Reading Battey PM, Salam AA. Surgery 1985;97(5);618–620. The association for close monitoring of platelet counts in patients undergoing heparinization for deep venous thrombosis is being stressed. Chandrasekar R, Nort DM, et al. Upper limb venous gangrene, a lethal condition. Eur Vasc Surg 1993;7(4):475–477. Treatment should be directed primarily at the underlying illness but there may be a case for early amputation if permitted by the general condition of the patient. Ferrante G, Bracale GC, et al. Ischemic phlebitis and venous gangrene. Flebiti Ischemizzanti e Gangrene Venous. Minerva Chir 1977;32(7):409–414 (published in Italian). At present early venous disobstruction with a Fogarty catheter, coupled with prolonged anticoagulant management, is the best course. Lau CP, Leung WH, et al. Venous gangrene complicating heart failure from severe mitral stenosis: a case study. Angiology 1991;42(8):654–658. Venous gangrene can complicate severe mitral stenosis and must be distinguished from arterial embolization, in which urgent surgical treatment is imperative. Perhoniemi V, Kaaja R, Carpen O. Venous gangrene of the limb: pathophysiological and therapeutic considerations. Ann Chir Gynaecol 1991;80(1):68–70. This situation is the lethal form of the entity and responds poorly to established therapy. Smith BM, Shield GW, et al. Venous gangrene of the upper extremity. Ann Surg 1985;201(4):511–519. Early aggressive restoration of adequate cardiac output and thrombectomy and/or thrombolytic therapy may provide the best chance for tissue salvage and survival in this group of patients.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 96 Diagnosis and Management of Lymphedema Mark D. Iafrati and Thomas F. O’Donnell, Jr.

Lymphedema, the accumulation of excess water and protein within the subcutaneous tissue and skin, is caused by lack of lymphatic function. The classification of primary lymphedema was initially based clinically on the age of onset and subsequently by diagnostic lymphography or lymphoscintigraphy. Congenital lymphedema, present at birth, represents about 15% of cases. Aplasia, marked by absence of lymphatic trunks, or hypoplasia, associated with reduced number or caliber of lymphatic channels, are the dominant lymphographic findings. Lymphedema praecox presents during late adolescence or puberty, represents approximately 75% of cases, and is typified by a hypoplastic lymphographic pattern. Lymphedema tarda is defined by presentation following the age of 35 and represents 10% of cases. Lymphography may demonstrate either a hypoplastic or hyperplastic pattern. Hyperplasia is characterized by an increased number of dilated and tortuous trunks associated with primary lymphatic valvular incompetence. Lymphedema has been divided into two broad classifications based on the cause of the lymphatic dysfunction. Primary lymphedema results from in utero vascular dysplasia, which is associated most commonly with an insufficient number of lymphatic vessels and nodes, whereas secondary lymphedema occurs after destruction or extirpation of the lymphatic vessels or nodes or both (1).

Normal Lymphatics The lymphatic system, comprising a network of superficial and deep vessels as well as lymph nodes, is responsible for clearing interstitial fluid. The superficial lymphatic

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system begins with initial lymphatics, which are a single endothelial cell thick. The endothelial cells overlap with loose connections. These intercellular gaps allow easy transit of interstital fluids. The initial lymphatics combine to form larger vessels called precollectors and collectors, which in turn lead to lymph nodes. The collector system contains smooth muscle cells and valves to regulate flow. The regional lymph nodes drain fluid from the ipsilateral limb and torso. Lymph returns to the blood circulation at the junctions of the subclavian and internal jugular veins (2,3).

Etiology Primary Lymphedema There are several theories for the cause of primary lymphedema. Although the majority of experts agree that it is due to an in utero vascular dysplasia, two groups have favored an acquired cause of primary lymphedema. Calnan argued that the female predominance of lymphedema and predilection for involvement of the left leg favored an acquired cause (4). Calnan and Kountz theorized that the location of the right iliac artery predisposed the underlying left lymphatic vessels and left iliac vein to compression (5). Phlebography of the iliac venous system frequently shows compression of the left iliac vein by the overlying iliac artery. As Negus et al. (6) had observed normal femoral venous pressures in a group of 12 patients with primary

Chapter 96 Diagnosis and Management of Lymphedema

lymphedema who had undergone previous lymphography, they challenged the concept that iliac artery compression caused primary lymphedema. In addition, they performed postmortem studies by injecting acrylic to form casts of the left iliac vein, as well as carrying out a series of left femoral phlebograms to assess whether the iliac vein was compressed. These two studies revealed partial compression of the left iliac vein, but this narrowing was insufficient to cause significant hemodynamic obstruction. The fundamental weakness of the acquired theory for primary lymphedema is the observation that hypoplasia is the most common lymphographic pattern observed in patients with primary lymphedema. The lymphographic pattern of a decreased number of lymphatic vessels would be difficult to rationalize on the basis of obstruction. Furthermore, despite the clinical presentation of unilateral extremity involvement, a lymphangiographic pattern of structural abnormalities may be found bilaterally (7). A second proposed etiology for acquired primary lymphedema is based on the inflammatory changes that have been observed in lymphatic vessels or lymph nodes. Olszewski and colleagues biopsied lymphatic vessels in a series of patients with primary lymphedema and observed a normal number of lymphatics. However, these lymphatic vessels were hyperplastic with thickened intima and obstructed lumen (8). Olszewski postulated that recurrent infection led to histologic changes, ultimately obliterating the lymphatic vessels. A decade later, Fyfe et al. observed fibrotic changes in the afferent portion of the lymph nodes, rather than in the lymphatic vessels, and believed that such changes were due to recurrent inflammation (9). Like Olszewski, Fyfe theorized that lymph flow would be obstructed as a result of lymphatic vessel fibrosis. That in utero vascular dysplasia is the cause of primary lymphedema is consistent with the etiology of other vascular anomalies. Indeed, O’Donnell et al. observed that lymphatic anomalies were often found in the same limb with arterial and venous dysplasia (10). Browse has integrated the acquired and in utero dysplastic causes of primary lymphedema into a management-oriented classification (11). Primary lymphedema is divided by etiology into obliterative, obstructive, and lymphatic valvular incompetence. The obliterative form is found in conditions of progressive peripheral lymphatic destruction. The ob-

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structive form is due to either afferent obstruction of lymph nodes or developmental abnormalities in the abdominal or thoracic lymphatic vessels. Lymphatic valvular incompetence is secondary to maldevelopment of the valvular mechanism within lymphatic vessels, with consequent failure to coapt. Lymphatic dilatation and hyperplasia subsequently develop. The Browse classification relates causes of primary lymphedema to possible therapeutic options. Primary lymphedema has been associated with a number of genetic polymorphisms. The majority of primary lymphedema shows an autosomal dominant pattern of inheritance with reduced penetrance, variable expression, and variable age of onset (12). The gene for Milroy disease has been mapped on chromosome 5q (13). Lymphedema-distichiasis presents as a late onset form of lower extremity edema and is commonly associated with fine hairs arising inappropriately from the meibomian glands. This syndrome is linked to a defect on 16q24.3 which codes for a forkhead transcription factor. Further delineation of the predisposing genetic factors may provide avenues for better pharmacologic interventions.

Secondary Lymphedema Parasitic infections although rare in the United States are a major public health problem worldwide. Lymphatic filariasis, caused by the mosquito-borne filarial nematode Wuchereria bancrofti, affects over 100 million people in more than 70 tropical and subtropical countries (14). In countries where lymphatic filariasis is well established, the prevalence of infection continues to increase, primarily because the growth of cities and water resources creates numerous breeding sites for the disease-transmitting mosquitoes (15). Certainly the most common cause of secondary lymphedema in the United States is neoplasia and its treatment. Radiation to both lymph nodes and lymphatic vessels, surgical extirpation for the treatment of cancer, inadvertent surgical injury to the lymphatic vessels or nodes, and recurrent infections may disrupt lymphatic function and cause secondary lymphedema (Table 96.1). The removal of lymph nodes or accompanying lymphatic vessels may be followed by significant limb swelling in up to 30% of patients. In a series of postmastectomy patients, Kreel and George performed lymphography and demon-

TABLE 96.1 Secondary Iymphedema Cause

Pathophysiology

Lymphographic Pattern

Malignant disease Radiation

Obstruction of node by tumor Obstruction of lymphatic trunks by extrinsic fibrosis at lymph node level Obstruction at lymphatic vessel level Obstruction at lymph node level Obliteration of lymphatic trunks

Obstruction with collateral circulation Obstruction

Surgery or trauma Filariasis Pyogenic infection

Obstruction with collateral circulation Obstruction; widened varicose lymphatics with reflux Hypoplasia

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strated that collateral lymphatic flow was established across the mastectomy site by 1 to 2 months postoperatively (16). In several instances the collateral network traversed to the opposite axilla. This work corroborated the previous pioneering study of Kinmonth and Taylor, who showed the importance of collateral lymphatic pathways after mastectomy (17). When the critical collateral networks such as those to the parasternal and supraclavicular nodes or those crossing the mastectomy site are destroyed by postirradiation fibrosis or infection, lymphedema may ensue. Recurrent pyogenic infections may cause secondary lymphedema. Although b-streptococcus is the most frequently isolated bacterium in these infections, Staphylococcus aureus and Gram-negative aerobes have also been implicated. The infectious process causes an obliteration of the lymphatic vessels and fibrosis of the afferent lymph nodes. Obliteration of lymphatics due to repeated bouts of cellulitis may exacerbate the chronic edema observed in the post-thrombotic limb and precipitate a combined disorder. An obstructive pattern is more typical of uncomplicated thrombosis.

Diagnosis The differential diagnosis of lymphedema encompasses a broad spectrum of disorders (17) (Table 96.2). The diagnosis of lymphedema can usually be made on clinical grounds. The patient’s history and the appearance of the lymphedematous limb are quite characteristic. Although the symptoms and physical findings are similar in primary and secondary lymphedema, the history usually differs. TABLE 96.2 Differential diagnosis of Iymphedema (reproduced by permission from reference 93) Systemic disorders Cardiac failure Renal failure Hepatic cirrhosis Hypoproteinemia Allergic disorders Hereditary angioedema Idiopathic cyclic edema Venous disorders Postphlebitic syndrome (reflux) Iliac venous disease (obstructive) Extrinsic pressure (e.g., by tumor, pregnancy, retroperitoneal fibrosis) Klippel–Trenaunay syndrome Miscellaneous disorders Arteriovenous malformation Lipedema Erythrocyanosis frigida Disuse and factitious edema Gigantism Insect bite Infection Trauma

History The typical patient with primary lymphedema is a female who first notes the onset of mild to moderate foot and ankle edema, usually beginning at menarche. The left limb is more frequently involved than the right. Depending on the duration of lymphedema, the patient usually observes an insidious progression centripetally to involve the calf and lower thigh. In contrast, the typical patient with secondary lymphedema has usually undergone a surgical procedure 4 to 5 years previously and may have received adjuvant radiation. In these patients, the onset of edema may be associated with a minor infection. It is important to establish the extent of the previous surgical procedure and the amount and sites of irradiation. Subsequent evaluation of this patient should rule out recurrence of a neoplasm.

Symptoms The cosmetic deformity produced by limb swelling is usually the reason for seeking medical care and is the first symptom noted by the patient (Table 96.3). The edema usually involves the distal portion of the extremity initially and is worse at the end of the day after prolonged standing or use of the limb. The edema may resolve with elevation of the limb at night. As the process becomes more severe, the level of the edema advances to involve the more proximal portions of the extremity and may not diminish at night with simple elevation. The leg may be dragged during walking or, in the patient with upper extremity involvement, the patient may avoid use of the arm in the performance of daily tasks. A mild, aching discomfort or early fatigue of the limb is common in patients with lymphedema, but intense or severe pain is unusual. Such pain occurs only in those rare instances in which there is a rapid increase in the degree of edema or persistent, massive swelling. The pain associated with fluid accumulation is usually characterized as heaviness or occasionally as a bursting sensation. The pain is dull and is not well localized. By contrast, lymphangitis, which is a frequent complication of lymphedema, may produce a painful limb, but the pain is described as prickly or burning and is localized to the skin.

TABLE 96.3 Clinical presentation of lymphedema Symptoms

Physical Findings

Limb swelling Heaviness Recurrent lymphangitis Skin changes Fungal infections

Limb edema Dorsal buffalo hump Elephantine distribution Pink flushed skin color Lichenification Peau d’orange Subcutaneous tissue lacking resilience

Chapter 96 Diagnosis and Management of Lymphedema

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Physical Findings The diagnosis of lymphedema can be made by observation because of the pathognomonic shape of the limb due to the distribution of edema (Table 96.3). Mild lymphedema generally presents predominantly in the forefoot or hand, involving the toes or fingers. The edema may extend to the ankle or wrist joint. The distribution of the edema over the forefoot gives this portion of the extremity a characteristic “buffalo hump” profile (Fig. 96.1). The anterior margin of the ankle joint is spared by comparison with the degree of edema over the hindfoot. Another pathognomonic physical finding in lymphedema is Stemmer’s sign— tense accumulation of lymph in the digits, making it impossible to tent the skin over the dorsum of the toes. The fluid distribution in the lymphedematous limb differs from that in chronic venous insufficiency or those limbs with systemic cause of edema. In the latter instances, fluid accumulation is greatest in the ankle area and is least over the toes. It has traditionally been taught that lymphedematous limbs will not pit; however, the degree of pitting is more related to the extent of subcutaneous fibrosis than to the cause of the edema. In mild lymphedema associated with limited subcutaneous scarring, the skin and subcutaneous tissue will pit. In contrast, patients with longstanding edema of any etiology, in which subcutaneous fibrosis has occurred, will have nonpitting edema. The range of skin changes associated with lymphedema helps to classify its severity. With mild or early lymphedema the skin retains its normal texture but may appear flushed or pink because of cutaneous vasodilatation and associated increased cutaneous blood flow. In moderate lymphedema there is thickening of the skin due to chronic edema and peau d’orange is observed. In the more advanced stages of lymphedema, skin changes are characterized by thickening and coarseness. Lichenification of the toes is present, and occasionally active bacterial infection gains entry, usually at the site of a skin fissure, minor trauma, or breakdown induced by interdigital fungal infection. Because primary lymphedema is a congenital vascular defect, other associated abnormalities are frequently observed in these patients. Cardiac lesions such as pulmonic stenosis, atrial septal defect, and patent ductus arteriosus have been associated with primary lymphedema and warrant careful auscultation of the heart and consideration for noninvasive cardiac screening. Turner syndrome (gonadal dysgenesis) has been observed in 7% of patients with primary lymphedema due to hypoplastic lymphatics. Finally, pes cavus and long-bone abnormalities, particularly in the leg, have been described in association with primary lymphedema. Unfortunately, the term Milroy’s disease has been an all-inclusive eponym for lymphedema. Milroy described a hereditary lymphedema that is present at birth and accounts for only about 2% of cases of primary lymphedema (18). There is an autosomal dominant mode of transmission with an equivalent

A

B

FIGURE 96.1 (A) Lateral view of a foot from a patient with primary lymphedema. The distribution of edema over the ankle but relative sparing of the more distal portion of the foot gives the lower limb a characteristic “buffalo hump” appearance. Edema is present over the dorsum of the toes. Because of widening of the skin pores the supramalleolar skin has a “peau d’orange” appearance. (B) Posterior view of a limb with marked primary lymphedema. The limb from the lower thigh down has marked edema, giving this limb a cylindrical or “tree trunk-like” shape. Edema is most marked over the malleoli.

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male:female ratio. The degree of lymphedema is progressive and usually involves the entire limb.

Diagnostic Methods of Evaluation In the patient with suspected lymphedema, there are three goals of diagnostic studies: 1. 2. 3.

to establish the diagnosis; to assess lymphatic function; and to document objectively the degree or severity of lymphedema.

In the majority of cases, the diagnosis of lymphedema can be made by clinical examination alone. However, lymphedema may occur in the presence of lipedema (lipolymphedema) or venous edema (phlebolymphedema), or both. In patients with mild or early-onset lymphedema or in patients with mixed etiology of edema, correlative studies may be useful. Approaches to the evaluation of the edematous extremity are presented in Table 96.4.

an overflow that facilitates volumetric limb measurement in another container. The volume displacement method does not identify the particular segment of the limb that has increased or decreased in dimension. Tissue tonometry measurement, which uses devices similar to those used in assessing glaucoma, is useful for determining the degree of subcutaneous tissue fibrosis. This method is particularly important in assessing the effects of pharmacologic treatment of subcutaneous fibrosis.

Venous Imaging Our practice is to obtain noninvasive venous studies to rule out chronic venous insufficiency as an etiology of limb edema. Air plethysmography or duplex imaging is performed to rule out venous obstruction. Duplex measurement of valve closure times and air plethysmographyderived venous filling index are then obtained to evaluate valvular insufficiency (19). Normal studies argue against a venous etiology for edema.

Lymphatic Imaging Degree of Lymphedema The two standard methods for assessing the degree of lymphedema are measurement of limb circumference at specific anatomic sites and measurement of limb volume by water displacement. The degree of lymphedema is represented by a ratio of the abnormal to the normal limb caliber [(abnormal – normal)/normal]. As there are no tables of normal values applicable to a wide range of limb dimensions, most clinicians use the contralateral limb as the control, or normal, value. For those physicians who see patients with lymphedema frequently, limb-volume measurement by water displacement provides objective estimates of total limb edema. The limb is immersed in a large cylinder fitted with

TABLE 96.4 Diagnostic evaluation of the edematous extremity Degree of lymphedema Measurement of limb circumference Limb volume displacement Venous imaging Air plethysmography Duplex imaging (and valve closure times) Lymphatic imaging Lymphography Lymphoscintigraphy Computed tomography Magnetic resonance imaging Duplex imaging Lymphatic functional evaluation Lymphoscintigraphy Radioactive albumin disappearance curves Contrast or isotope transit time

Lymphography had been the most definitive method available for objectively documenting the presence of lymphedema, until supplanted by radioisotope lymphoscintigraphy. Our understanding of lymphedema owes much to the pioneering studies of Kinmonth of St Thomas Hospital (20–22). Kinmonth classified primary lymphedema based on the anatomic pattern defined by lymphography. Patients were classified into those with aplasia (absence of any lymphatic vessels) (Fig. 96.2), hypoplasia (decreased number and size of lymphatic vessels and nodes) (Fig. 96.3), and hyperplasia (increased number and size of vessels and nodes) (Fig. 96.4). Fully 90% of patients are hypoplastic or aplastic, while a smaller proportion are hyperplastic (Table 96.5). This observation is consistent with a dysplastic cause of primary lymphedema. In a combined review with Kinmonth, we evaluated 20 lymphangiograms of patients with lymphedema associated with mixed vascular deformities either of the veins alone or in combination with arteries (10). Those patients with lymphatic hypoplasia had an average of 2.1 vessels at the upper thigh–inguinal area, with an average width of 0.6 ± 0.2 mm. At this level, the normal lymphangiogram shows up to 12 lymphatic vessels, and the width of individual vessels is usually in excess of 1 mm. Patients with hyperplastic lymphatics have increased number, averaging 18.5 ± 3.5 vessels, with a width of nearly 2 mm at this level. The technique of lymphoscintigraphy has gained general acceptance for lymphatic imaging due to several marked advantages over contrast lymphography (Fig. 96.5). Lymphography is a cumbersome technique that requires microsurgical cannulation and injection of an oil contrast medium into an interdigital lymphatic trunk. This procedure may be complicated by local tissue necro-

Chapter 96 Diagnosis and Management of Lymphedema

FIGURE 96.2 Lymphatic aplasia. Because no lymphatic trunks were accessible on the dorsum of the foot, a lymph node was exposed in the groin. Infusion of contrast directly into the lymph node reveals no lymphatic vessels except for a thread-like lymphatic collateral at the level of the trochanter.

FIGURE 96.3 Lymphangiogram of patient with primary lymphedema and hypoplasia. The number of lymphatic trunks at this level is markedly reduced from the normal 10–15 vessels.

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FIGURE 96.4 Lymphangiogram of patient with primary lymphedema and hyperplasia. Multiple trunks and lymph nodes are noted.

sis, lymphangitis, exacerbation of lymphedema, and incissipation of contrast material, which can disrupt functioning lymphatics. In a comparison of contrast lymphography and lymphoscintigraphy, Stewart et al. (23) demonstrated that the findings of each technique were closely correlated (Figs. 96.6A and B and 96.7). Recent series have commonly used technetium-99m labeling of antimony trisulfide colloid as opposed to labeled human serum albumin. Lymphoscintigraphy reliably differentiates between lymphedema and edema due to other etiologies and can guide patient selection and follow-up after lymphatic surgery (24). We employ lymphoscintigraphy selectively in patients in whom the diagnosis of lymphedema is unclear. The edema that frequently occurs after arterial reconstruction, particularly after infrainguinal bypass, is due to interruption of the lymphatic vessels. Earlier it was theorized that fluid accumulation in the limb postoperatively was due to leakage of water and protein from the capillaries under the influence of improved perfusion pressure. Schmidt and associates disproved this theory in their study of 37 patients who underwent lymphography after femoropopliteal bypass (25). Lymphangiograms were performed on the third and ninth postoperative day and revealed intact vessels at the knee and groin if edema was minimal. Mild lymphedema was present when at least three lymph vessels were preserved, whereas moderate to severe lymphedema was noted when all lymph vessels had been divided and no intact lymphatic vessel was visualized. The use of computed tomography (CT) scanning has supplanted routine lymphoscintigraphy in our practice. It

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TABLE 96.5 Results of lymphography in primary lymphedema Series

No. of Cases

Hypoplasia/Aplasia

Hyperplasia

Buonocore & Young 1965 (7) Thompson 1970 (33) Kinmonth 1972 (30) Olszewski et al. 1975 (8) Saijo et al. 1975 (86) Kinmonth 1982 (22)

20 50 100 120 12 562

20 47 (17 prox*) 92 (5 aplasia) 111(24 prox*) 7 506 (0 aplasia)

— 3 8 9 5 56

Total

864

783 (91%)

81 (9%)

*Proximal hypoplasia with an obstruction.

FIGURE 96.5 (A) Normal lymphoscintigram. Column of isotope demarcates several major lymphatic trunks with concentration in femoral (A), iliac (B), periaortic lymph nodes (C), and the liver. (B) Primary lymphedema. Hyperplastic pattern of multiple varicose lymphatic trunks in the left lower extremity.

A

B

is used to assess the number of pelvic lymph nodes and their size, and may allow noninvasive, objective classification of primary lymphedema patients. A majority of patients (90%) have a decreased number of lymph nodes and are categorized into the hypoplastic group. Patients with an increased number of lymph nodes are classified into the hyperplastic group (10%). For patients with secondary lymphedema CT is the initial diagnostic method of choice to identify pelvic outflow obstruction as the cause for lymphedema. In addition to defining the status of the lymph nodes, CT shows the relative distribution of edema fluid within the extremity. A characteristic honeycomb appearance to the edema fluid within the subcutaneous tissue is diagnostic of lymphedema. Magnetic resonance imaging (MRI) has been com-

pared with lymphoscintigraphy in a study of 32 patients with lymphedema (26). MRI can identify fine details of dermal, subcutaneous, and fascial compartment anatomy and sources of lymphatic outflow obstruction. This modality is particularly useful in differentiating venous, lymphatic, and lipemic components of the edematous extremities. MRI is useful in the interpretation of primary, secondary, and mixed forms of lymphedema. Astrom et al. have proposed a transaxial fat-suppressed T2weighted spectral presaturation with inversion recovery (SPIR) sequence in conjunction with a coronal T1 spin echo as a standard format, with supplemental data on fibrosis derived from axial TSE images. The use of GdDTPA (diethylenetriamine pentaacetic acid) does not improve the images (27).

Chapter 96 Diagnosis and Management of Lymphedema

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FIGURE 96.6 (A) Lymphangiogram in patient with previous surgery to the left lower extremity and secondary lymphedema. Markedly hyperplastic “steel wool” pattern of lymphatic vessels is observed. (B) Lymphoscintigram in patient with previous surgery to right lower extremity and secondary lymphedema. Delayed transit of technetium-99m and prominent dermal backflow into superficial lymphatic collateral network is observed.

Duplex images of lymphedematous limbs are characterized by subcutaneous tissue with well-circumscribed, echo-free areas having an “ant farm” appearance (28). As a noninvasive modality, duplex imaging may be useful to support the diagnosis of lymphedema. The primary limitation appears to be the lack of sufficient flow, even upon distal limb compression, to confirm the identity of dilated channels as lymphatic trunks. Duplex imaging is the preliminary diagnostic tool in the evaluation of the lymphedematous extremity to establish the presence of venous insufficiency or thrombosis. The role of this modality in the diagnosis and management of lymphedema is currently limited.

Lymphatic Functional Evaluation Quantitative lymphoscintigraphy has been developed through a standardized isotope injection technique and

intraprocedural muscular exercise yielding a functional assessment of lymphatic isotope clearance. This technique is complementary to qualitative lymphoscintigraphy, which allows characterization of lymphatic morphology. The Weissleders studied 457 extremities and developed a scintigraphic grading system, based on quantitative isotope uptake measurements (29). This approach represents an objective and reproducible classification of lymphedema, particularly in the detection of mild or incipient cases. Lymphoscintigraphic transit time and radioactive albumen disappearance curves may be useful in the functional evaluation of lymphedema. Although measurement of the time taken by the radioactive tracer to reach a specific site or rate of its disappearance from the limb is subject to many variables, this standardized lymphoscintigraphic technique does afford the opportunity to quantitate lymphatic function. Lymphatic stasis due to

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decreased vessel caliber (hypoplasia) or varicosed channels (hyperplasia) may slow the transit time. An altered transit time may be the only evidence of lymphatic malfunction in some patients with mild edema and normal lymphatic anatomy by lymphography (30). A major function of the lymphatic tree is to clear protein from the extravascular space. The rate that labeled albumin is cleared assesses lymphatic function. Indeed, 131I-labeled albumin disappearance curves are prolonged in the lymphedematous limb (31). This delayed clearance may be related to trapping of albumin within the interstitial space and its subsequent pooling, or to reversal of the ratio of normal subcutaneous tissue pressure to muscle compartment pressure. In lymphedema, interstitial fluid

FIGURE 96.7 Secondary lymphedema. Postmastectomy lymphoscintigram in patient with lymphedema. Normal forearm image on right contrasts with marked disruption of lymphatic anatomy on left with evidence of severe dermal backflow.

protein concentration is elevated, and subcutaneous pressure is higher than muscle compartment pressure. Despite this attractive physiologic rationale, however, measurements of disappearance curves have little value in the initial assessment of lymphedema (32). Tissue clearance of injected 131I-labeled albumin is useful to determine the effects of surgical treatment of lymphedema (33).

Treatment Nonsurgical Treatment More than 90% of patients with lymphedema can be managed by nonsurgical means. Wolfe and Kinmonth demonstrated that the extent of the disease could be assessed accurately within the first year of diagnosis by the response to therapy (34). The goals of therapy are to reduce limb size, preserve and improve the quality of the skin and subcutaneous tissue, and prevent infection (Table 96.6). Initial treatment of mild lymphedema may require only exercise, elevation of the limb at night, and the use of compression stockings during the day to maintain a reduced limb girth. The rationale behind the use of exercise in the lymphedema patient is predicated on the observation that muscle contraction promotes lymph flow and increases protein absorption (35). This muscle pump function results from changes in tissue pressure which opens the gaps in the lymphatic endothelium, allowing influx of lymph. The use of nonfatiguing exercises represents the ideal since this will not promote additional fluid production (3). Elevation of the extremity can be accomplished by placing blocks under the foot of the bed or by suspending the arm in a sling. Measurement of the extremity for compression stockings is carried out in the reduced state before reaccumulation of edema fluid because the elastic compression effect is related to the initial unstretched circumference. We use a 40 to 50 mmHg gradient stocking for most patients. The length of the stocking should be matched to the extent of the disease. Below-

TABLE 96.6 Treatment of lymphedema Nonsurgical

Surgical

Reduction in limb size Elevation Elastic compression Full-thickness skin bridge Massage External pneumatic compression Heat

Physiologic procedures Buried dermal flap (Thompson) Lymphovenous shunt Omental transposition Subcutaneous tunnels Lysis of fibrotic venous obstruction Enteromesenteric bridge Other bridging procedures

Improvement in skin quality Treatment of fungal and bacterial infections Skin lotion Benzopyrones

Excisional procedures Skin and subcutaneous tissue excision with split-thickness skin graft coverage Staged excision of subcutaneous tissue with vascularized local flaps (Homans)

Chapter 96 Diagnosis and Management of Lymphedema

knee stockings are more comfortable because they do not bind behind the knee and are easier to don and remove. This length is appropriate for patients with foot, ankle, and calf swelling. Thigh-length stockings or pantyhose are preferable for patients with significant thigh edema. Our younger patients have had success with the use of double stockings to increase compressive pressure (36). Two full-length 30 to 40 mmHg elastic stockings are used initially. At 2 months the outer stocking is changed to 40 to 50 mmHg, and at 4 months the inner stocking is increased to 40 to 50 mmHg. At 6 months the outer stocking is increased to 50 to 60 mmHg. In our studies, digital plethysmography showed no adverse hemodynamic effect on distal arterial flow. Our trial included eight patients with limb girths measured sequentially at 10 constant points for the 10-month treatment period. No patient discontinued therapy, and all demonstrated a decrease in limb girth. Some patients experienced an initial increase in thigh girth, but this decreased after 4 months of therapy. Similar to the findings of Zeissler et al. (37) in more than 100 of our patients followed for 5 years, the conscientious use of elastic stockings maintained limb girth in a reduced state. Our initial experience with pneumatic compression involved a low-pressure unicell boot or sleeve inflated to 60 mmHg for 12.5 seconds of compression followed by a 35-s rest period. A group of 17 patients were included in our initial prospective study reported by Raines et al. (38); 9 patients with upper extremity lymphedema showed a 50% reduction in hand girth, but forearm and upper arm reduction was less than 20%. The patients with lower extremity lymphedema had a similar response pattern with less reduction of the ankle and calf circumference than of the foot. Patients with a greater degree of subcutaneous fibrosis responded less well to pneumatic compression therapy than did patients with softer subcutaneous tissues. We now use a high-pressure sequential pneumatic compression device, the Lympha-Press, developed by Zelikovski et al. (39). The compression garment is constructed of multiple circumferential chambers that are pressurized to 110 to 150 mmHg in a sequential centripetal fashion to milk the edema fluid in the extremity centrally. Because only a few chambers are fully pressurized at any one time, the higher pressures are better tolerated by the patient than with the unicell design compression device, and the limb reduction is achieved more rapidly. In a more recent study, Pappas and O’Donnell reported long-term follow-up (mean 25 months) of 49 patients managed with the Lympha-Press garment (40). Among 43 patients with lymphedema of the lower extremities, 26 maintained a full response, defined by maintenance of limb girth reductions at more than three of nine measured levels. Ten patients maintained a partial response, or reduction at no more than three levels. At the late follow-up, calf and ankle girths were reduced by an absolute value of 5.37 and 4.63 cm in the full response

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group and 5.43 and 3.98 cm, respectively, in the partial response group, over pretreatment measurements. In this study, lymphedema type (primary or secondary), gender, extremity involved, or pretreatment burden of lymphedematous tissue were not predictive of the best long-term results. Optimal results have been dependent on patient compliance and the condition of the subcutaneous tissue. Short-term results have been reported for the Wright Linear Pump (41) and compression therapy using hydrostatic pressure of mercury (42) in the management of lymphedema. Initial findings have been similar to those with the Lympha-Press garment. Long-term follow-up will be necessary before meaningful comparisons can be made. Heating of lymphedematous extremities in combination with compressive bandaging is a therapeutic modality developed primarily in China. Experience with large numbers of patients using electrical appliances (43) and more recently microwave heating (44) has documented the long-term durability of this technique. The physiologic contribution of heating beyond that of compressive bandaging is unclear. Manual massage techniques are frequently used in conjunction with compression therapy. Lymphatic massage, also known as manual lymphatic drainage (MLD) or decongestive lymphatic therapy (DLT), has become a mainstay of treatment. Gentle pressure is applied in order to stimulate and stretch the lymphatic collectors. Proximal areas are cleared prior to distal and attention is paid to watershed areas. Intensive regimens have been shown to be effective in reducing lymphedema; however, results are variable and no consensus exists as to the best protocol (45–47). Improvement and preservation of skin quality is the second goal of nonoperative therapy. Maintaining the skin in good condition is imperative to prevent serious sequelae and progression of the lymphedema process. The skin should be cleansed daily, and a water-based lotion such as polysorb hydrate should be applied twice daily. Minor trauma to the skin should be avoided. Pruritic skin should be treated with a steroid cream. Fungal infections are common and should be eradicated with antifungal agents. Bacterial infections should be treated aggressively, often requiring intravenous therapy initially for at least 7 days, followed by a prolonged course (2 to 4 weeks) of oral antibiotics. The hardening of subcutaneous tissue in patients with advanced lymphedema is related to a fibrotic process that occurs as plasma proteins are deposited in the tissue. These proteins osmotically retain edema fluid and induce an inflammatory reaction leading to fibrosis. Experimentally produced lymphedema softens when treated with benzopyrones (48). Coumarin, a benzopyrone, experimentally enhances macrophage lysis of proteins responsible for edema and fibrosis. A prospective randomized trial reported efficacy of benzopyrones in the management of primary and secondary forms of lymphedema (49). However, a more recent trial found coumarin to be ineffective and to have a significant risk of hepatotoxicity (50).

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Part XII Venous and Lymphatic Surgery

Recurrent lymphangitis, typically due to b-hemolytic streptococci, is a common problem among 15% to 20% of patients with lymphedema. The sudden onset of infection with rapid progression, sometimes leading to the development of shock, is related to the lack of normal lymphatic immunologic barriers. Patients should be resuscitated and treated with intravenous penicillin or oxacillin, guided by culture results. Often the site of entry is created by tinea pedis infection or within hair follicles with no apparent break in the skin. Cultures can be obtained by saline aspiration of the cellulitic margin. We treat patients with an aggressive regimen of intravenous antibiotics for at least 7 days, followed by an additional 3 to 6 weeks of oral antibiotics. Local fungal infections are treated with topical creams. More invasive fungal infections require oral or intravenous treatment. In patients with two or more bacterial infections in one year, oral prophylaxis with penicillin (PEN-VEE-K, 250 mg twice daily) or erythromycin (250 mg twice daily) can reduce the number of infectious episodes. Effective intervention at the earliest possible point in the development of lymphedema would minimize the amount of irreversible lymphatic injury and provide much better outcomes than are typically obtained today. For primary lymphedema, new genetic data may provide leads to better diagnosis and treatment in the near future. Filarial-induced lymphedema has been targeted by largescale programs of mosquito control and antibiotic prophylaxis. A number of less developed nations with high prevalence of lymphedema have instituted prophylaxis with a single annual dose of diethylcarbazine. While they have documented reductions in microfilariae prevalence (51), the lack of controlled studies leaves the efficacy of this treatment in doubt (52).

Surgical Treatment The indications for surgical treatment of lymphedema have been cosmetic, to improve the size and shape of the limb; functional, to reduce limb weight and improve skin texture; and preventive, to decrease the number of infections or to prevent the occurrence of angiosarcoma, a lethal complication. A wide variety of surgical procedures have been described, all with inconsistent results. Patients with a severe functional disability due to marked skin change or with immobility secondary to massive and refractory edema are candidates for surgical treatment. Surgery should be avoided in patients with minimal edema (less than 3 cm of circumferential difference between normal and affected limb), gross obesity, and disease that is actively progressing, and in those in whom a firm diagnosis of lymphedema is not established as the cause of limb swelling. Chilvers and Kinmonth divided surgical treatment of lymphedema into two types: physiologic and excisional (53). Physiologic procedures are utilized primarily in cases of obstructive lymphedema, to promote alternative means of lymphatic drainage. Excisional procedures at-

tempt to improve symptoms by surgical reduction of limb size and have primary application in cases of obliterative lymphedema.

Physiologic Procedures The goal of physiologic procedures is to promote drainage of lymph from the abnormal superficial subcutaneous lymphatics either into the normal lymphatics of the deep system (fascial lymphatics) or proximally into the venous system (Table 96.7). The most widely performed operation for lymphedema is the Thompson procedure (54). A portion of subcutaneous tissue is excised and a posterior dermal flap is fixed to the deep fascia (Fig. 96.8). The intent of the buried flap is to encourage spontaneous anastomoses between the superficial and deep fascial lymphatics. Thompson (33) and Harvey (55) used radioactive albumin disappearance curves to assess the results and showed increased transit of albumin. Sawney (56) found similar results and reduction of limb girth in the early postoperative period, but subsequent albumin studies no longer demonstrated the improvement. Kinmonth performed lymphangiograms after the Thompson procedures but was unable to demonstrate any superficial to deep lymphaticolymphatic anastomoses. He concluded that the improvement after operation was due to the excision of the subcutaneous tissue and perhaps to a compressive massaging effect by the calf muscles on the lymphatics of the buried flap as demonstrated on cinelymphographic studies. Chilvers and Kinmonth demonstrated that overall only 30% of patients undergoing this procedure retained long-term benefit (53). Most patients had returned to their preoperative girth 2 to 4 years after the original surgery. Only those patients with massive edema appeared to benefit. The surgical morbidity associated with the procedure, particularly skin-flap necrosis in nearly 25%, resulted in prolonged hospitalization and convalescence. Table 96.7 summarizes the results of several series of the Thompson procedure. Kerstein and Licalzi described the use of direct lymph node to venous anastomosis in 1963 (57). Nielubowicz and Olszewski published the first clinical results of lymphovenous shunts (58). They reported on four patients with secondary lymphedema who had reduced limb size after a lymphovenous shunt. Three patients underwent lymphography demonstrating patent anastomoses. The fourth patient died of her primary disease, but postmortem examination showed patency in the medullary sinuses. This surgical approach suggested that a physiologic reconstruction was possible in patients with lymphedema and stimulated worldwide interest and research. Lymphovenous anastomosis can be performed in several ways. The lymph node can be sectioned sagittally and anastomosed to a vein. A direct microsurgical anastomosis can be performed between a vein and lymphatic vessel. A specially constructed tube can be used to create the anastomosis (59). Longstanding obstructive lymphedema

2

1

3

1 2 2 2 2 3

1 2 1 1 1

Type*

28(88%)

6 (75%)

10 (46%)

147 (50%)

8 15 25 72 22 5

74 (38%)

29 14 0 2 29

Good

4 (13%)

0

4 (18%)

95 (32%)

6 28 46 15 0 0

90 (46%)

17 8 0 4 61

Fair

†Author’s interpretation of varied criteria for each series.

0

0

0

11 (4%)

0 0 0 0 6 5

5 (3%)

0 0 5 0 0

Unchanged

Results†

*1, Primary lymphedema; 2, secondary lymphedema; 3, missed, primary, and secondary lymphedema.

32

8

Enteromesenteric bridge Hurst et al. 1985 (68)

Venous interposition Campisi 1991 (70)

22

296

Total

Omental transposition Goldsmith 1974 (65)

16 50 73 91 52 14

196

Total

Lymphovenous anastomosis Politowski et al. 1969 (89) Milanov et al. 1982 (90) Krylov et al. 1982 (91) Gong-Kang et al. 1985 (60) O’Brien et al. 1990 (62) Gloviczki et al. 1988 (64)

50 23 5 10 108

No. of Patients

Buried dermal flap Thompson 1970 (33) Thompson 1969 (87) Sawney 1974 (56) Bunchman & Lewis 1974 (88) Kinmonth et al. 1975 (67)

Series

TABLE 96.7 Physiologic operations for lymphedema

0

2 (25%)

8 (36%)

43 (15%)

2 7 2 4 24 4

27 (14%)

4 1 0 4 18

Poor

Circumference, surgeon’s evaluation

Circumference, contrast lymphography, isotope lymphography

Size, function, frequency of cellulitis attacks

Circumference, volume displacement Circumference, volume displacement, frequency of cellulitis attacks

Circumference, clearance studies Circumference, clearance studies Circumference, clearance studies Circumference, volume displacement Circumference, patient’s and surgeon’s evaluation

Criteria

1–5 years

2.5–7 years

1–7 years

3–24 months 3–4.3 years 5–57 months

1–10 years 1–9 years 1 year 1 year 1 year

Length of Follow-up

1163

1164

Part XII Venous and Lymphatic Surgery

results in destruction of lymphatics and renders the patients unacceptable as candidates for microlymphaticovenous anastomosis (60). O’Brien and Das showed that three or more anastomoses were needed to reduce limb size (61). However, in a later series, O’Brien et al. reported on 134 patients with obstructive lymphedema who underwent microlymphaticovenous anastomosis alone or in addition to reductive or ablative surgery and found that the number of anastomoses and duration of edema did not influence results (62). O’Brien and Das (61) and Clodius et al. (63) have emphasized the need for technical experience in microvascular surgery as a prerequisite for good results. Fibrotic changes in the subcutaneous tissue associated with lymphedema result in a change in the lymphatic system that may prevent reconstruction in patients with

A

primary lymphedema. Gloviczki et al. reported on 14 patients with either primary or secondary lymphedema managed with lymphaticovenous anastomosis and found that those with primary lymphedema had disappointing results (64). Thus lymphaticovenous anastomosis appears to be better suited to the treatment of obstructive forms of secondary lymphedema. Soft tissue grafts have been attempted to bypass lymphatic obstruction. Goldsmith attempted to bridge an area of lymphatic insufficiency by omental transposition (65). Long-term results were disappointing and included one patient who died secondary to an incarcerated hernia along the tract of the omentum to the groin. Hurst et al. experimented with a mesenteric pedicle graft of mucosally stripped ileum as an interposition between obstructed lymphatics and sectioned lymph nodes distal to the obstruction (66). They reported the first clinical result in 1978 (67) and the long-term follow-up in 1985 (68). In all, eight patients with iliac lymph node and vessel obstruction were treated. Follow-up was 2.5 to 7 years, and sustained clinical improvement was noted in six patients. The two patients who failed to improve initially subsequently required a reducing operation. Other techniques of bridging lymphatic obstruction have been proposed that employ adipose venolymphatic transfer (69), autologous interposition vein grafting (70), rotation of myocutaneous flaps (1,72), or direct lymphaticolymphatic anastomosis (73). The design of these procedures is limited only by the ingenuity of the surgeon. Medgyesi cited criteria for lymphatic bridges to function including requirement for competent lymphatic trunks and properly oriented valves to ensure lymphatic bypass (74).

B

B

FIGURE 96.8 Thompson procedure. In this procedure subcutaneous tissue is debulked, but a segment of the skin covering the calf is de-epithelialized and attached to the deep fascia. This “buried flap” encourages spontaneous anastomoses of the subcutaneous to the deep lymphatics and may also compress the underlying lymphatics in a massaging fashion when the patient walks.

A

C

FIGURE 96.9 Charles procedure. The skin and the subcutaneous tissue, including the fascia, are removed in most instances to debulk the limb. Split-thickness skin grafts are then placed on the underlying muscle. This procedure is usually reserved for patients with extensive skin changes.

1165

Chapter 96 Diagnosis and Management of Lymphedema TABLE 96.8 Excisional operations for lymphedema Results No. of Patients

Lymphedema Type*

Good

Fair

1

6

0

14

1

14

12

1

Staged subcutaneous excision Staged subcutaneous excision Staged subcutaneous excision

14 21 5

Staged excisions (pediatric age group)

3

Series

Types of Procedures

Fonkalsrud 1979 (80)

Subcutaneous lymphangiectomy

6

Bunchman & Lewis 1974 (88) Dellon & Hoopes 1977 (92) Miller 1975 (78) Miller 1977 (79) Bunchman & Lewis 1974 (88) Feins et al. 1977 (81)

Charles (complete excision of subcutaneous tissue and skin) Charles

Criteria

Length of Follow-up (years) ≥1

0

Cosmetic, functional —

5

12

0

Circumference

10.5

Mixed Not specified 1

0 0 5

14 21 0

Circumference Circumference —

0.5–6 1–4 1

1

0

39

Patient interview

—

*1, Primary lymphedema; mixed, primary and secondary lymphedema.

Excisional Procedures Charles worked in an area endemic for tropical elephantiasis and developed an operation that consisted of removing both skin and subcutaneous tissue (75). Figure 96.9 illustrates the details of the Charles procedure. Splitthickness skin grafts were used to cover the exposed fascia. At present, the Charles procedure is restricted to those patients with severe skin changes that prevent the use of vascularized skin flaps or subcutaneous lipectomy. Hyperkeratotic skin, recurrent sepsis, graft failure, and condylomata development are late complications. Dellon and Hoopes reported long-term results in 10 patients observed for as long as 20 years after a Charles procedure (75). No recurrence of lymphedema and excellent functional results were noted. Miller, however, found less satisfactory results in five patients treated this way (76). Three of his patients eventually underwent amputation for severe skin changes or chronic cellulitis (Table 96.8). Homans described a procedure in which subcutaneous tissue was excised in stages through the development of well-vascularized flaps (77). Large volumes of subcutaneous tissue can be excised, and complications such as flap necrosis and sinus formation appear to occur less frequently than with the buried dermal flap. Miller has reported his results for staged subcutaneous excision and believes that the procedure is associated with a consistent reduction in size and an improvement in function (78,79). Fonkalsrud (80) and Feins et al. (81) have reported results for pediatric patients with moderate to severe lymphedema and noted good results with minimal morbidity. Evaluation of follow-up data is difficult because of the lack of uniform objective measurements or criteria for assessing the degree of lymphedema preoperatively and the postoperative results. The follow-up period for many of the studies is short, which further frustrates critical assessment.

The recent evolution of cosmetic liposuction has led to applications in lymphedematous extremities. The technique has been used by Sando and Nahai in cases of primary and secondary lymphedema and as a secondary procedure after failed bridging or debulking procedures (82). Although their experience was restricted to a small sample population and limited follow-up, this technique may limit the considerable morbidity that can accompany other excisional procedures.

Venous Obstruction Several authors have argued that relief of venous obstruction should be the primary target for intervention in cases of secondary lymphedema. Hughes and Patel lysed the fibrotic encasement around the axillary vein in patients with postmastectomy lymphedema (83). They noted “good results” in 15 of 19 patients, as did Larsen and Crampton (84) in four of eight patients undergoing a similar procedure. A component of lymphedema may coexist in patients with congenital mixed vascular disorders. Treatment should be directed to the more prominent clinical problem in these patients. Elastic stocking support is commonly the appropriate initial therapy in these settings (85).

References 1. Allen E, Barker N, Hines F. Peripheral vascular diseases. Philadelphia: WB Saunders, 1946. 2. Szuba A, Rockson S. Lymphedema: anatomy, physiology, and pathogenesis. Vasc Med 1997; 2:321–326. 3. Cohen S, Payne D, Tunkel R. Lymphedema. Cancer 2001; 92:980–987. 4. Calnan L. Lymphoedema: the case for doubt. Br J Plast Surg 1968; 21:32. 5. Calnan J, Kountz S. Effect of venous obstruction on lymphatics. Br J Surg 1965; 52:800.

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6. Negus D, Edwards J, Kinmouth J. The iliac veins in relation to lymphedema. Br J Surg 1969; 56:481. 7. Buonocore F, Young J. Lymphangiographic evaluation of lymphedema and lymphatic flow. Am J Roentgenol 1965; 95:751. 8. Olszewski M, Machowski Z, et al. Clinical studies in primary lymphedema. Pol Med 1972; 11:1560. 9. Fyfe N, Rutt D, et al. Intralymphatic steroid therapy for lymphedema: preliminary studies. Lymphology 1982; 15:23. 10. O’Donnell T, Edwards J, Kinmonth J. Lymphography in the mixed vascular deformities of the lower extremities. J Cardiovasc Surg (Torino) 1976; 17:453. 11. Browse N. Primary lymphedema. In: Ernst C, Stanely J, eds. Current therapy in vascular surgery. Philadelphia: BC Becker, 1987. 12. Greenlee R, Hoyme H, et al. Developmental disorders of the lymphatic system. Lymphology 1993; 26:156–168. 13. Evans AL, Brice G, et al. Mapping of primary congential lymphedema to the 5q35.3 region. Am J Hum Genetic 1999; 64:547–555. 14. Ottesen EA, Ramachandran C. Lymphatic filariasis infection and disease: control strategies. Parasitol Today 1995; 11:129–131. 15. Service M. Problems of vector borne disease and irrigation projects. Insect Sci Appl 1984; 5:227–231. 16. Kreel L, George P. Post-mastectomy lymphangiography: detection of metastases and edema. Ann Surg 1966; 163:470. 17. Kinmonth J, Taylor G. The lymphatic circulation in lymphedema. Ann Surg 1954; 139:129. 18. Milroy W. An undescribed variety of hereditary oedema. NY State J Med 1982; 56:505. 19. Shepard A, Mackey W, et al. Light reflection rheography (LRR): a new non-invasive test of venous function. Bruit 1984; 8:266. 20. Eustace P, Kinmonth J. The normal lymphatic vessels of the inguinal and iliac areas with special emphasis on the efferent inguinal vessels. Lymphology 1976; 5:23. 21. Kinmonth J. Primary lymphedemas: classification and other studies based on oleolymphography and clinical features. J Cardiovasc Surg (Torino) 1969; Suppl. 22. Kinmonth J. The lymphatics: surgery, lymphography and diseases of the chyle and lymph systems. London: Edward Arnold, 1982. 23. Stewart C, Gaunt J, et al. Isotope lymphography: a new method of investigating the role of the lymphatics in chronic limb oedema. Br J Surg 1985; 72:906–909. 24. Gloviczki F, Calcagno D, et al. Noninvasive evaluation of the swollen extremity: experiences with 190 lymphoscintigraphic examinations. J Vasc Surg 1989; 9:683–690. 25. Schmidt K, Weltei H, et al. Lymphangiographische Untersuchungen zum Extremitatenodem nach rekonstruktiven Gefaseingriffen in Femoropoplitealbereich. Rofo: Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin 1978; 128:194–202. 26. Case T, Witte C, et al. Magnetic resonance imaging in human lymphedema: comparison with lymphangioscintigraphy. Magn Reson Imaging 1992; 10:549–558. 27. Astrom K, Abdsaleh S, et al. MR imaging of primary, secondary, and mixed forms of lymphedema. Acta Radiologica 2001; 42:409–416.

28. Drinan K, Wolfson P, et al. Duplex imaging in lymphedema. J Vasc Tech 1993; 17:23–26. 29. Weissleder H, Weissleder R. Lymphedema: evaluation of qualitative and quantitative lymphoscintigraphy in 238 patients. Radiology 1988; 167:729–735. 30. Kinmonth J. The lymphatics: diseases, lymphography and surgery. Baltimore: Williams & Wilkins, 1972. 31. Taylor G, Kinmonth J, et al. Lymphatic circulation studied with radioactive plasma protein. Br Med J 1957; 5011:133. 32. Emmett A, Barton J, Veall N. The use of I-131 albumin tissue clearance measurements and other physiological tests for clinical assessment of patients with lymphoedema. Br J Plast Surg 1967; 20:1. 33. Thompson N. Buried dermal flap operation for chronic lymphedema of the extremities: ten year survey of results in 79 cases. Plast Reconstr Surg 1970; 45:451. 34. Wolfe J, Kinmonth J. The prognosis of primary lymphedema of the lower limbs. Arch Surg 1981; 116: 1157. 35. Mortimer P. Managing lymphoedema. Clin Exp Dermatol 1995; 20:98–106. 36. O’Donnell T. Abnormal peripheral lymphatics. In: Clouse M, Wallace S, eds. Lymphatic imaging, lymphography, computed tomography and scintigraphy. Baltimore: Williams & Wilkins, 1985:142. 37. Zeissler R, Rose G, Nelson P. Postmastectomy lymphedema: late results of treatment in 3855 patients. Arch Phys Med Rehabil 1972; 53:159. 38. Raines J, O’Donnell TF Jr, et al. Selection of patients with lymphedema for compression therapy. Am J Surg 1977; 133:430. 39. Zelikoski A, Manoach M, et al. Lympha-Press, a new pneumatic device for the treatment of lymphedema of the limbs. Lymphology 1980; 13:68. 40. Pappas C, O’Donnell T. Long-term results of compression treatment for lymphedema. J Vasc Surg 1992; 16:555–564. 41. Klein M, Alexander M, et al. Treatment of adult lower extremity lymphedema with the Wright linear pump: statistical analysis of a clinical trial. Arch Phys Med Rehabil 1988; 69:202–206. 42. Palmer A, Macchiaverna J, et al. Compression therapy of limb edema using hydrostatic pressure of mercury. Angiology 1991; 42:533–542. 43. Chang T, Wang W, Huan L. Heating and bandage treatment for chronic lymphoedema of the extremities. Chin Med J 1984; 97:567–577. 44. Chang T, Han L, et al. Microwave: an alternative to electric heating in the treatment of peripheral lymphedema. Lymphology 1989; 22:20–24. 45. Boris M, Weindorf S, Lasinski B. Persistence of lymphedema reduction after noninvasive complex lymphedema therapy. Oncology 1997; 11:99–114. 46. Ko D, Lerner R, Klose G, et al. Effective treatment of lymphedema of the extremities. Arch Surg 1998; 133:452–458. 47. Johansson K, Albertson M, Ingvar C. Effects of compression bandaging with or without manual lymph drainage treatment in patients with postoperative arm lymphedema. Lymphology 1999; 32:103–110. 48. Casley-Smith J, Foldi-Borcsok F, Fold M. A fine structural study of the removal of the effectiveness of ben-

Chapter 96 Diagnosis and Management of Lymphedema

49.

50.

51.

52. 53.

54.

55.

56.

57. 58.

59.

60.

61.

62.

63.

64.

65. 66.

67.

zopyrone treatment of lymphedema by the destruction of the macrophages by silica. Br J Exp Pathol 1978; 59:116. Casley-Smith J, Morgan R, Piller N. Treatment of lymphedema of the arms and legs with 5,6-benzo-[d]pyrone. N Engl J Med 1993; 329:1158–1163. Loprinzi C, Kugler J, et al. Lack of effect of coumarin in women with lymphedema after treatment for breast cancer. N Engl J Med 1999; 340:346–350. Mataika J, Kimura E, et al. Efficacy of five annual single doses of diethylcarbamazine for treatment of lymphatic filariasis in Fiji. Bull World Health Organ 1998; 76. Ravindran B. Filariasis control: ethics, economics, and good science. Lancet 2001; 358:246. Chilvers A, Kinmonth J. Operation for lymphedema of the lower limbs: a study of the results in 108 operations using vascularized dermal flaps. J Cardiovasc Surg 1975; 16:115. Thompson N. The surgical treatment of chronic lymphoedema of the extremities. Surg Clin North Am 1967; 47:445. Harvey R. The use of I-131 labeled human serum albumin in the assessment of improved lymph flow following buried dermis flap operations in cases of postmastectomy lymphedema of the arm. Br J Radiol 1969; 42:260. Sawney C. Evaluation of Thompson’s buried dermal flap operation for lymphedema of the limbs: a clinical and radioisotopic study. Br J Plast Surg 1974; 27:2–8. Kertein M, Licalzi L. Microvascular procedures in the management of lymphedema. Vasc Surg 1977; 11:188. Nielubowicz I, Olszewski W. Surgical lymphaticovenous shunts in patients with secondary lymphedema. Br J Surg 1968; 9:262. Degni M. New techniques of lymphatic-venous anastomosis for the treatment of lymphedema. J Cardiovasc Surg 1978; 19:577. Gong-Kang H, Ru-Qi H, et al. Microlymphaticovenous anastomosis in the treatment of lower limb obstructive lymphedema: analysis of 91 cases. Plast Reconstr Surg 1985; 76:671. O’Brien B, Das S. Microlymphatic surgery in management of lymphoedema of the upper limb. Ann Acad Med Singapore 1979; 8:474. O’Brien B, Mellow C, et al. Long term results after microlymphaticovenous anastomoses for the treatment of obstructive lymphedema. Plast Reconstr Surg 1990; 85:562–572. Clodius L, Piller N, Casley-Smith J. The problems of lymphatic microsurgery for lymphedema. Lymphology 1981; 14:69. Gloviczki P, Fisher J, et al. Microsurgical lymphovenous anastomosis for treatment of lymphedema: a critical review. J Vasc Surg 1988; 7:647–652. Goldsmith H. Long term results of omental transposition for chronic lymphoedema. Ann Surg 1974; 180:84. Hurst P, Kinmonth J, Rutt D. A mesenteric pedicle graft for bridging lymphatic obstruction. Br J Surg 1978; 65:358. Kinmonth J, Hurst P, et al. Relief of lymph obstruction by use of a bridge of mesentery and ileum. Br J Surg 1975; 5:829.

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68. Hurst P, Stewart G, et al. Long term results of the enteromesenteric bridge operation in the treatment of primary lymphoedema. Br J Surg 1985; 72:272. 69. Pho R, Bayon P, Tan L. Adipose veno-lymphatic transfer for management of post-radiation lymphedema. J Reconstr Microsurg 1989; 5:45–52. 70. Campisi C. Use of autologous interposition vein graft in management of lymphedema: preliminary experimental and clinical observations. Lymphology 1991; 24:74–76. 71. Chitale V. Role of tensor fascia lata musculocutaneous flap in lymphedema of the lower extremity and external genitalia. Ann Plast Surg 1990; 23:297–306. 72. Kambayashi I, Ohshiro T, Mori I. Appraisal of myocutaneous flapping for treatment of postmastectomy lymphedema. Acta Chir Scand 1990; 156:175–177. 73. Baumeister R, Siuda S. Treatment of lymphedemas bv microsurgical lymphatic grafting: what is proved? Plast Reconstr Surg 1990; 85:64–74. 74. Medgyesi S. Successful operation for lymphedema using a myocutaneous flap as a “wick.” Br J Plast Surg 1983; 36:64. 75. Charles R. A system of treatment. In: Latham A, English T, eds. Vol. 3. London: J & A Churchill Ltd, 1912:504. 76. Miller T. Charles procedure for lymphedema: a warning. Am J Surg 1980; 139:290. 77. Homans J. Treatment of elephantiasis of legs. N Engl J Med 1936; 215:1099. 78. Miller T. Surgical management of lymphedema of the extremity. Plast Reconstr Surg 1975; 56:633. 79. Miller T. A surgical approach to lymphedema. Am J Surg 1977; 134:191. 80. Fonkalsrud E. Surgical management of congenital lymphedema in infants and children. Arch Surg 1979; 114:1133. 81. Feins N, Rubin R, et al. Surgical management of 39 children with lymphedema. J Pediatr Surg 1977; 12:471. 82. Sando W, Nahai F. Suction lipectomy, in the management of limb lymphedema. Clin Plast Surg 1989; 16: 369–373. 83. Hughes J, Patel A. Swelling of the arm following radical mastectomy. Br J Surg 1955; 53. 84. Larsen N, Crampton A. A surgical procedure for postmastectomy edema. Arch Surg 1973; 106:475. 85. O’Donnell TF. Congenital mixed vascular deformities of the lower limb: the relevance of lymphatic abnormalities to their diagnosis and treatment. Ann Surg 1977; 185:162–168. 86. Saijo M, Monroe I, Mancer K. Lymphedema: a clinical review and follow-up study. Plast Reconstr Surg 1975; 56:513. 87. Thompson N. The surgical treatment of advanced postmastectomy lymphedema of the upper limb: with the later results of treatment by buried dermis flap operation. Scand J Plast Reconstr Surg 1969; 3:54. 88. Bunchman M, Lewis S. The treatment of lymphedema. Plast Reconstr Surg 1974; 54:64. 89. Politowski M, Bartowski S, Dynowski J. Treatment of lymphedema of the limbs by lymphatico-venous fistula. Surgery 1969; 66:639. 90. Milanov N, Abalmasov K, Lein A. Correction of lymph flow disturbances following radical mastectomy. Vestn Khir 1982; 128:63.

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91. Krylov V, Rabkin I, et al. Rol’limfografi pri opredelenii pokazanii k nalozheniiu priamogo limfovenoznogo anastomoza. Khirurgiia (Mosk) 1979; 9:3. 92. Dellon A, Hoopes J. The Charles procedure for primary lymphedema: long-term clinical results. Plast Reconstr Surg 1977; 60:589.

93. Wolfe JHN. Diagnosis and classification of lymphedema. In: Rutherford 14, ed. Vascular surgery, 3rd edn. WB Saunders, 1989.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

PART XIII Amputations and Rehabilitations

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 97 Amputation of the Lower Extremity: General Considerations Henry Haimovici

It is generally recognized that the incidence of lower extremity amputations is the highest of the total number of amputations in the United States. Glattly, of the National Research Council, estimated in 1966 that 25,500 of 30,000 (85%) cases in 1 year were for the lower extremity (1). Of these, 80% were for severe ischemic lesions of the lower extremity. What distinguishes the importance of these numbers is the associated morbidity and mortality with major amputations. Collin and Collin reported a 45% 2-year survival and a 75% mortality after amputation in dysvascular patients. Additionally, only 26% of these patients have been found to walk outside 2 years after their amputation (2,3). The advances in reconstructive treatment for arterial disease by bypass procedures of the femoropopliteal as well as of more distal vessels (tibioperoneal and smaller foot vessels) are being applied frequently, when indicated. However, the incidence of lower leg amputations appears largely unchanged. Indeed, despite the current era of increased arterial reconstructive procedures, a relatively large number of patients, especially those with associated diabetes mellitus, still fall in the group with unsalvageable lesions of the lower extremity. This situation is seen in geriatric patients in particular. In 1975, Kay and Newman reported on 6000 new amputations and showed that 93% were performed in patients over 60 years old (4). Stern mentions in his report on this problem that the national data indicate no decline in the number and rates of amputations from 1981 to 1985.

However in hospitals with busy vascular services amputation statistics may differ, depending on a number of factors leading not rarely to substantial salvage of limbs.

General Principles As a result of accumulating experience since the mid1960s, new concepts in amputee management have emerged. The main reasons for the recent progress are the availability of multidisciplinary services and a few basic guiding principles: 1.

2.

3.

Amputation, as an operative act, should be considered in the context of preoperative and postoperative care. This can be achieved by the services of skilled teams, including vascular surgeons, rehabilitation personnel, prosthetists, and psychosocial guidance personnel. Gentle, atraumatic handling of the tissues is essential to avoid failures, usually because of the critical wound healing of the ischemic tissues. Amputation should not be looked on merely as a synonym for cutting off a limb. It must be considered a plastic and reconstructive operation requiring great respect for tissues and careful wound management, with a view to early patient rehabilitation. Unfortunately, amputations in general are regarded as devoid of any challenge and are often relegated to the junior

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Part XIII Amputations and Rehabilitations

member of the staff, who is usually lacking in knowledge and experience. Selection of a site for amputation is often a critical decision that requires proper evaluation of the degree of blood supply at this level. It should be based not on the preconceived “safest” site for healing but on vascular assessment of tissue viability. Although it is obvious that the first amputation must be the last, this principle should in no way substitute a safe judgment for a properly evaluated level of amputation. This attitude has much too often led the surgeon with little experience to do an above-the-knee amputation, the acknowledged safest site for early healing, when a more distal one should have been indicated.

tibacterial solution such as povidone iodine has been added, the skin should be dried and a fungicidal powder applied. Analgesics are required for severe rest pain, which usually prevents sleep. One may have to try the entire gamut of these medications, ranging from aspirin to opiates, before relieving this ischemic pain. Smoking is to be avoided completely. It aggravates all arterial diseases. Vasodilating drugs have been recommended in the management of chronic arterial diseases, but they are of little or no value in the presence of advanced ischemic lesions.

Principles of Preoperative Management The detailed criteria for levels of amputation will be described below. Suffice it to state at this point that healing not only at the below-the-knee but also at the foot level may occur more often if the basic principles of evaluating arterial insufficiency and careful technique are observed rigorously.

Principles of Conservative Management (Nonsurgical) In the presence of severe ischemia of the extremities characterized by rest pain and impending or frank gangrene, the scope of conservative nonsurgical management is necessarily limited. Its basic principles include: 1. 2. 3.

protection of the involved extremity; meticulous treatment of the lesions; and use of antibiotics, analgesics, and vasodilators.

Protective measures, such as bed rest and avoidance of any pressure or trauma to the affected extremity, are essential. Thus a cradle should be placed over the feet, and the patient’s limb should rest on a pillow to prevent pressure on the toes and heel, the two areas most vulnerable to any degree of trauma. Meticulous foot care is one of the prerequisites for successful conservative management. Soap-and-water footbaths should be followed by the application of local dressings consisting of antibiotic ointment or plain petrolatum gauze on the lesion. Special attention should be paid to the interdigital spaces, where ulcers or draining sinuses may be overlooked. The dressing should cover the entire involved area. Local debridement of lesions should be done only if there is evidence of their separation from the adjacent tissues and should not be carried beyond their demarcation line. Antibiotics are essential, especially for the lesions associated with lymphangitis or cellulitis. In diabetic patients, fungal infection, mostly in the interdigital spaces, is prevalent. After the footbath, to which an an-

The first step in the care of the patient with an ischemic foot and gangrene is bed rest. The major objectives in the preoperative phase are: 1. 2. 3. 4.

avoidance of trauma; control of infection control of pain; and preservation of muscular strength and joint motion (rehabilitation).

Avoidance of Trauma The patient should be in Fowler’s position, with the limb slightly dependent, the leg and thigh being supported by a pillow to avoid any possible pressure on the heel. A lambskin mat placed under it may help to prevent decubitus pressure. A heel protector consisting of a 1- to 1.5-inchthick foam pad secured to the heel may be more helpful. Overhead handles should be provided so the patient can turn over in bed without pushing with the feet and elbows. A cradle should be placed over the foot to avoid the weight of blankets on the toes. Control of Infection Foot care is an integral part of the preoperative treatment and should consist of: 1. 2. 3. 4.

5.

daily gentle washings of the foot and leg with lukewarm water and soap; removal of all scabs; debridement of calluses or corns, under which an abscess is often present; application of antibiotic ointment in the open ulcerations or in the necrotic lesions with denuded edges; and systemic antibiotics.

Control of Pain Control of pain is an important facet of the management, especially in patients who have dependency edema as a result of prolonged sitting during the day and often during the night because of rest pain. Use of analgesics is particu-

Chapter 97 Amputation of the Lower Extremity: General Considerations

larly necessary to enable the patient to sleep with the legs horizontal and thus to reduce edema so as to render the tissues more suitable for local surgery. Rehabilitation Before Amputation The patient’s rehabilitation should be started before amputation, to prevent deterioration of function in the muscles and joints. An integrated program with the rehabilitation department is an important part of the preoperative and postoperative management of the amputee.

General Principles for Selection of Level of Amputation Selection of the level of amputation depends on local and systemic factors. Among the local factors are the type of onset of the ischemia, which may be acute, progressive, or chronic, the extent of gangrene or ulceration, the degree of infection, the condition of adjacent areas, the degree of arterial impairment, and of severity of pain. Gangrene Acute ischemia is usually due to arterial embolism, thrombosis, or vascular injuries. The clinical features and treatment differ from those of the other two types of ischemia, especially the chronic. As described previously, in the presence of acute ischemia, with pregangrenous or frank gangrenous lesions not suitable for salvage procedures, the level of amputation in the majority of patients is above the knee. The timing of the amputation will depend on the degree of pain, systemic toxicity, presence of myoglobinuria due to myonecrosis, and renal toxicity (oliguria or anuria). These factors are characteristic of acute rhabdomyolosis and are not seen in progressive or chronic arterial occlusions. Chronic ischemia is most commonly due to arteriosclerosis. The extent of gangrene and the presence or absence of a demarcation line are important factors. Absence of a line of demarcation usually indicates a spreading process, which precludes a local conservative procedure. The presence of a demarcation line, on the other hand, implies that the gangrene has become localized and that vascularity proximal to this point is adequate. Unless the general condition of the patient contraindicates delay, it is always an advantage to wait for the development of a sharp line of demarcation. Infection Local infection associated with gangrene is often present in varying degree, especially in diabetic patients. Infection may become a major problem if spreading lymphangitis or cellulitis that cannot be checked is present. In such cases, and in the presence of suppuration, surgery cannot be delayed. Exclusive use of antibiotics may not be helpful and ultimately may prove disastrous in uncontrollable sepsis.

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Condition of Adjacent Areas Evaluation of the tissues proximal to the gangrenous area is essential when local surgery is contemplated. Color changes, trophic lesions of the skin, edema, and bone involvement are important criteria. Thus cyanosis of the skin proximal to the gangrenous area that is not reversible on elevation of the limb usually indicates advanced ischemia of the tissues and contraindicates local surgery. Thin, shiny skin with marked loss of subcutaneous tissue suggests poor vascularity. Edema in the absence of venous obstruction or cardiorenal disease is generally due to dependency and can be eliminated by keeping the limb horizontal. Degree of Arterial Impairment For evaluating the degree of arterial insufficiency, noninvasive modalities, arteriography, and clinical criteria may provide most of the desired information. The acute or chronic mode of onset often determines not only the extent of the gangrene but also the level of amputation. The patency of major arteries is determined by palpation and should be checked with Doppler ultrasound, a pulse-volume recorder (PVR), and an ankle–arm pulse index. Although the presence of a popliteal or pedal pulse appears to ensure prompter healing of a toe or transmetatarsal amputation wound, absence of these pulses is not a contraindication to surgery at this level. This also holds true for the below-the-knee level. Use of xenon-133 for blood flow measurement has been advocated as another index. In the absence of functioning major arteries, it is axiomatic that vascularization of the tissues depends on the degree of collateral circulation. Elevationdependency tests and skin temperatures at different levels determined under basal conditions are helpful guides in assessing the collateral arterial supply. Rapid blanching of the toes and foot on elevation and marked rubor on dependency suggest poor collateral circulation. A sharp difference in skin temperature between the proximal and distal areas of the extremity indicates recent arterial occlusion. Under these circumstances, the level of amputation must be well above the cold area. Whenever possible, surgery is delayed in the hope that collateral circulation may develop and thereby permit a more distal amputation. Pain Pain is commonly associated with ischemic tissues and is more severe when gangrene is spreading. When pain radiates from the involved toes toward the ankle or leg and remains unrelieved by heavy sedation, it should be regarded as a contraindication to a toe or transmetatarsal procedure. A higher level for amputation is then indicated. Systemic Factors The general condition of the patient should always be evaluated as to age, severity of diabetes, toxicity, cardiac

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status, presence of hypertension, cerebrovascular accidents, renal function, and water–electrolyte balance. An attempt is made to grade each patient according to these factors. Although the local signs are the chief criteria determining the level of amputation, in some patients the poor or precarious general condition is important in guiding the choice of the surgical procedure. Finally, in assessing both local and systemic factors, it is important to consider the duration of the lesions, the initiating cause, the effectiveness of previous treatments, and the condition of the other leg.

Levels of Amputation There are six possible levels of amputation for ischemic gangrene: 1) toes, 2) transmetatarsal, 3) ankle (Syme amputation), 4) supramalleolar, 5) midleg (below the knee), 6) supracondylar (above the knee), and 7) thigh (above the knee) (Fig. 97.1).

References 1. Glattlly HW. Aging and amputations. Artif Limbs 1966; 10:1. 2. Geertzen JHB, Martina JD, Rietman HS. Lower limb amputation Part 2: Rehabiliation: a 10 year literature review. Prosthet Orthot Int 2001; 25:14. 3. Collin C, Collin J. Mobility after lower-limb amputation. Br J Surg 1995; 82:1010. 4. Kay HW, Newman JD. Relative incidence of new amputations: statistical comparisons of 6000 new amputations. Orthot Prosthet 1975; 29:3.

FIGURE 97.1 Levels of amputation for ischemic gangrene.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 98 Above-the-knee Amputations Henry Haimovici

Indications Indications for primary thigh amputation are restricted to those cases in which a below-the-knee procedure does not meet the criteria for a successful outcome. Although since the mid-1950s the percentage of below-the-knee amputations has steadily increased, the ratio of below-the-knee to above-the-knee still ranges from 1:2 to 1:4. In our experience, indications for above-the-knee amputations are essentially: 1. 2. 3.

extensive gangrene and infection of the foot extending above the ankle; associated painful flexion contracture of the knee joint; and recent acute occlusion of the femoral or iliac artery (Figs.98.1 and 98.2).

Anatomic Review A brief review of the anatomic structures may be helpful in undertaking the different types of amputations through the thigh (Fig. 98.3). There are three groups of muscles in the thigh. The anterolateral group consists of the sartorius and quadriceps femoris. The quadriceps is formed by the rectus femoris and the three vasti, which combine to form the patellar tendon. The vasti surround the shaft of the femur on its lateral, anterior, and medial surfaces. The medial group consists of the gracilis and the three adductors. The adductor magnus, by far the largest

of the group, extends down as far as the adductor tubercle. The posterior group (hamstrings) comprises the biceps and the semitendinosus and semimembranosus. The biceps muscle is inserted into the head of the fibula. The other two muscles both pass to the medial side of the upper end of the tibia. The vessels of the thigh include the femoral and the popliteal. The femoral artery lies along the upper twothirds of a line drawn from the midinguinal point to the adductor tubercle when the thigh is slightly flexed. In the upper third of the thigh, the artery is medial to the sartorius. In the subsartorial canal, which is the middle third, it is posterolateral. At the junction of the middle and lower third, it passes through the opening of the adductor magnus to become the popliteal artery, which is closely applied to the femur. The femoral vein in its lower part is posteromedial to its artery. The profunda vessels lie deep on the anterior surface of the adductor magnus. The long saphenous vein ascends in the superficial fascia on the medial side. The femoral nerve breaks up into branches immediately below the inguinal ligament. The only branch of the latter to be recognized in an amputation of the thigh is the saphenous nerve, which accompanies the femoral artery as far as the opening of the adductor magnus. The sciatic nerve, the largest nerve of the body, divides at a varying level in the thigh into medial and lateral popliteal nerves, the former still being called the posterior tibial and the latter called the peroneal nerve. They lie on the posterior surface of the adductor magnus, the peroneal nerve passing under cover of the biceps.

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FIGURE 98.1 Gangrene involving distal portion of the foot, caused by acute thrombosis of popliteal and tibial arteries. Both foot and leg were cold. An abovethe-knee amputation was carried out.

FIGURE 98.2 Massive gangrene involving foot and half of leg, caused by acute thrombosis of femoral artery and necessitating a midthigh amputation.

FIGURE 98.3 (A) Levels of skin incision and bone division for supracondylar and midthigh amputations. (B) Cross-section of midthigh.

Surgical Techniques The literature on thigh amputation includes discussions of a great variety of techniques. These techniques are classified into two groups: 1) the end-bearing and 2) the ischialbearing. The level of division of the extremity between the knee joint and the supracondylar region is an end-bearing amputation, whereas the one carried out above the junction of the middle and lower thirds of the femur is ischialbearing. Both the end-bearing and the ischial-bearing amputations are satisfactory, provided the technical performance of the procedure and the application of the prosthesis are carried out properly. With few exceptions, vascular surgeons employ either the supracondylar or the

mid thigh amputation. Indications for these two levels differ to some extent according to the type of vascular abnormality. The end-bearing amputations are usually classified into three groups: 1) disarticulation of the knee, 2) osteoplastic, and 3) tendinoplastic.

Disarticulation of Knee The knee joint disarticulation may be used either as a preliminary guillotine amputation or as a definitive procedure. It is used very rarely in the United States and is applied primarily by orthopedic surgeons to nonischemic

Chapter 98 Above-the-knee Amputations

A

B

A

1177

B

FIGURE 98.4 Gritti–Stokes amputation. (A) Levels of skin incision and bone section. (B) Closed stump showing suture line.

FIGURE 98.5 Tendinoplastic amputation. (A) Level of skin incision. (B) Closed stump showing suture line.

conditions. The advantage of a knee disarticulation is twofold: it helps prevent progressive hip contracture, and offers a better prospect for rehabilitation than transfemoral amputations. The disarticulation, however, is also known for its cosmetic difficulties.

Because of the length of the stump, there are some difficulties in fitting the best type of mechanical knee joint. Such amputations are used mostly by orthopedic surgeons and find little favor with the majority of vascular surgeons. Ischial-bearing amputations are performed through the lower or middle third of the thigh. These two levels of amputation are most widely used for vascular conditions.

Osteoplastic Procedure The Gritti-Stokes amputation is an osteoplastic procedure. It appears to have the favor of vascular surgeons in Great Britain and Canada because of its good end-bearing features. Martin and Wickham believe that in advanced arterial occlusive disease with gangrene of the foot, this procedure results in a stump that is functional at an early date (1). In this technique (Fig. 98.4), the femur is divided at the supracondylar level, and the posterior surface of the patella is sawed away and fixed to the end of the femur. These authors reported that, of the 75 patients of a group of 80 who survived the operation, the stumps healed by first intention in 58 and there was delayed healing in 17. The average time of healing was 14 days for patients with arteriosclerosis, whereas in those with diabetes the average time was 32 days.

Tendinoplastic Amputation Several techniques have been described for tendinoplastic amputations (Fig. 98.5): the aperiosteal supracondylar tendinoplastic amputation of Kirk, the rounded epicondylar tendinoplastic amputation of Slocum, and the Callander amputation. The first two techniques are used primarily for nonvascular conditions, whereas the third is designed to be used in the presence of vascular disease. It is a supracondylar amputation with long anterior and posterior flaps, the section of the muscles being performed through the tendinous insertions. These three techniques of amputation provide a stump that is sufficiently broad for end-bearing. Thus the weight is borne in a more normal fashion through the hip joint instead of being transmitted to the ischial tuberosity.

Myodesis and Osseointegration Increasing success has been achieved with myodesis. This technique was improved in 1999 by Gottschalk by concentrating on the adductors. This technique aims to prevent contraction and create musclular balance. It has been found most effective in distal amputations (2,3). An additional development is the use of osseointegration to fix titanium to the end of the femur. With the fears of implant loosening and ascending infections, this is a technique predominantly used by orthopedic rather than vascular surgeons. To avoid these problems, some have advocated a two-stage approach over a 6-month span (2,4).

Amputations Through Lower Third of Thigh The operation is performed with the patient in a supine position. Although a circular incision may be used, our preference is for anterior and posterior flaps, the anterior being slightly longer (Fig. 98.6). The distal anterior incision is just above the proximal border of the patella. The posterior flap is slightly shorter. The quadriceps tendon is divided at the level of the anterior incision and is raised in the flap. After the skin incision has been completed, the posterior group of muscles is divided as indicated in Figure 98.6. The femoral vessels are identified as they pass through the adductor magnus foramen. The popliteal ves-

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FIGURE 98.6 Amputation through lower third of thigh, indicating level of skin incision (A) and level of bone section (B).

sels that are present at this lower-third level are divided individually near the junction with the femoral and are doubly ligated with absorbable sutures. The sciatic nerve, found on the back of the adductor magnus, is mobilized and injected with 10 ml of 1% lidocaine before being transected with a sharp knife. A ligature applied gently without too much tension is placed around the nerve. Before its division, the nerve is pulled downward. Then, after its transection, it retracts under the posterior group of muscles. The femur is then sawed transversely at the junction between the middle and lower thirds. The stump is irrigated with an antibiotic solution of kanamycin and bacitracin. The quadriceps tendon is turned over the bone stump, and the fascia is sutured with interrupted absorbable suture material. Drainage for 48 hours may be advisable as a precautionary measure, but it is not mandatory unless oozing cannot be controlled. The skin is closed with simple sutures. A layer or two of petrolatum gauze is applied on the suture line, a gauze dressing is placed over the end of the stump and held in place with gauze bandages, and a stockinette covering the entire area is secured around the root of the extremity. Postoperatively, the patient is encouraged to extend the stump, which demonstrates the ability to hyperextend the hip joint spontaneously. It is not necessary to place the stump on a pillow, as this may have a tendency to produce some degree of flexion contracture. The patient is out of bed the next day. The immediate postoperative use of a prosthesis, when indicated, is described in Chapter 99.

FIGURE 98.7 Amputation through middle third of thigh, indicating level of skin incision (A) and level of bone section (B).

Amputations Through Middle Third of Thigh Indications for the midthigh amputation are the presence of acute occlusion of the femoral or iliac artery and poor collateral circulation owing to involvement of the profunda femoris. In such cases, it is inadvisable to perform a more distal amputation because of the inadequate vascularity at that level, which would often result in breakdown of the stump. Furthermore, for patients who are debilitated and whose prospects for rehabilitation with a prosthesis are remote, it is safer to divide the femur at its middle third. The technique used is depicted in Figure 98.7. The femoral and profunda arteries are dealt with in the same fashion as in the previously described technique. The sciatic nerve is usually represented by an undivided trunk at this level. The flaps are approximated in a fashion similar to that in the previous method. Drainage may be used more frequently in this case because of the larger area of cut muscle, from which considerable oozing may occur. In our experience with the above-the-knee amputation in the elderly patient with advanced ischemic changes, primary healing occurred in 95% of the cases. Breakdown of the suture line has been minimal in the majority of cases and has necessitated only a minor delay in the discharge of the patient from the hospital. The disadvantages of thigh amputation versus belowthe-knee amputation have already been mentioned. The postoperative mortality rate is much higher in this group of cases, according to most statistical studies, including

Chapter 98 Above-the-knee Amputations

our own. Rehabilitation of above-the-knee amputees is less effective than that of the below-the-knee group. Recent developments in the immediate postoperative stump fitting, however, have improved the outlook even of the above-the-knee amputee.

Failed Grafts and Level of Amputation The fate of an extremity after graft failure is not always predictable, and a variety of factors, singly or in combination, may account for this uncertainty. Thus, whereas late graft failure (i.e., beyond 1 year) does not necessarily lead to recurrence of the pregraft level of ischemia, early graft thrombosis (within days or 4 to 6 weeks) may seriously compromise the viability of the extremity. For example, early implantation failure of a graft may result in gangrene and major amputation. The incidence of this complication is variously reported, but at issue is the controversy that revolves around the level of amputation and the rate of revision procedures after graft failures. In an attempt to determine the incidence of the effects of graft failures, a few series of primary amputations without prior revascularization procedures were compared (5); the published statistics differed widely. Although a few centers reported that only a few limbs were worse after occlusion of femoral popliteal or infrapopliteal grafts (5–7), others found that in 60% to 70% of the patients, amputations had been carried out higher than would have been the case otherwise (9–12). To gain some insight into the underlying reasons for the wide range of results, one may find it desirable to compare series of limb amputations after graft failures with series of primary amputations without prior revascularization procedures. Although it is well recognized that no two series of patients are entirely comparable, analysis of the overall results of the two groups may nevertheless shed some light on the incidence of the respective procedures and their relative significance in the postgraft failures. Thus, Warren and Record, in a series of 802 cases collected from the literature, found healing occurred in 86% of below-the-knee amputations, of which 73% healed by primary and 27% by secondary intention (13). In a series of 400 cases of below-the-knee amputations collected from the Montefiore Vascular Service (more than 50% were my patients), healing occurred in 96.7% of cases, of which 76.5% healed by primary and 20.2% by secondary intention. Healing of amputation to the above-the-knee level occurred in 13 (3.3%) cases. Of these patients, 75% had a nonpalpable popliteal artery as disclosed by oscillometry and in many instances by arteriography. In addition, 80% of these patients had arteriosclerosis and diabetes. The overall hospital mortality rate was 4.5%. Burgess and Marsden reported on 140 patients with primary amputation in whom healing at the below-the-

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knee level occurred in 113 patients, or 80% of the cases (5). Admittedly, it is sometimes difficult to predict which of the patients who finally had higher amputations would have had a more distal one if it had been a primary procedure. Nevertheless, there is little doubt that the effects of sudden and early graft closure may affect negatively the already compromised circulatory status of the grafted limb. The notion that, if the graft fails, rarely, if ever, is anything lost may be self-deluding. As Warren (14) stated in commenting editorially on the article by Burgess and Marsden (6), “Few vascular surgeons fail to remember at least one patient whose limb became more ischemic after closure of a graft.” Unfortunately, both the surgeon and the patient must be aware of such a possibility, even though it may be rare. These facts should eliminate the optimistic interpretation that if a graft fails, no more of the limb will be lost than would otherwise have been lost. Nevertheless, reconstructive arterial procedures in the presence of threatening ischemia of the limb are of immense value.

Pitfalls Pitfalls of amputation include a variety of factors, most important of which are: 1. 2. 3. 4. 5.

wrong level of amputation; technical errors; delayed or inadequate prophylaxis against infection; unrecognized venous thrombosis; and failure to immobilize the stump postoperatively.

The wrong level of amputation may result from inadequate assessment of the optimum area of possible healing. Indeed, if a toe or a transmetatarsal amputation is carried out through borderline or poorly vascularized tissues, with failure of the stump to heal, higher amputation becomes unavoidable. If, on the other hand, the amputation is carried out above the knee because it is the so-called safest site for healing, adequate rehabilitation without the knee joint may be hampered, especially in an elderly individual. It cannot be too strongly emphasized that selection of the level of amputation should be carried out with great care. Technical errors may encompass excessive length of bones, redundancy of the soft tissues, inadequacy of hemostasis, and poor approximation of the skin edges. Excessive length of bones will cause tension of the soft tissues and will inevitably lead to their breakdown. Therefore, before one attempts to close, it is important to approximate the flaps, and if there is the slightest tension, shortening of the bones should be carried out at this time. Redundancy of the soft tissues, on the other hand, can result in an unsightly stump that may cause pain and be difficult to fit with a prosthesis. If noted at the time of closure, tailoring of the flaps should be done to match the length of bones with that of the musculocutaneous tissues.

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Inadequacy of hemostasis may result in a hematoma, which in turn will produce pressure from inside, leading to ischemic changes of the skin. If oozing is present, a drain must be inserted in the subfascial space and left in place for 24 to 48 hours. Closure of the skin edges should be done with extreme care to avoid puckering or scalloping. Poor matching of the edges leads to delayed healing of the scar. Skin approximation should be accomplished by single-loop monofilament interrupted sutures just tight enough to hold the edges together. Mattress sutures, unless applied without tension, should be avoided, because they have a tendency to strangulate the tissues. Delayed or inadequate prophylaxis against infection, especially in diabetic patients, may lead to sepsis of the wound. Antibiotics should be used routinely for 7 to 10 days postoperatively. Before the stump is closed, irrigation of the tissues with an antibiotic solution should be done routinely. Venous thrombosis in an extremity with a gangrenous foot of several weeks’ duration is not an unusual finding. The popliteal, tibial, peroneal, or sural veins may contain fresh or organized thrombi, the potential source of pulmonary emboli. The surgeon is then faced with a dilemma of whether to ligate the femoral or just institute anticoagulation. Although it is difficult to formulate a definitive policy in the presence of these findings, ligation of the superficial femoral at this time may be seriously considered. As an alternative, anticoagulants should be instituted within 12 hours postoperatively, and the patient should be carefully monitored for possible chest pain. If such a condition develops, the proximal venous ligation should be carried out without delay. Failure to immobilize a below-the-knee amputation may result in serious complications. The natural tendency of the patient to bend the knee and press the end of the stump against the bed mattress may injure the stump and result in severe pain. Immobilization of the stump is essential, whether an immediate postoperative prosthesis or a posterior splint is used. The knee should remain straight for 2 to 3 weeks to allow healing without flexion contracture, pain, and breakdown. Ischemic muscles may be encountered at the level of amputation, especially in the soleus and in the anterior tibial compartment. If focal necrosis or discoloration is found, the muscle should be excised until normalappearing tissue is obtained.

Complications Postoperative complications may be divided into early and late. The early complications include infection, delayed wound healing, painful stump, phantom sensations, and pressure sores related to the cast or splint application. Late complications include phantom pain, flexion contracture, and gangrene of the stump.

Early Complications Infection Before the advent of the antibiotic era, one of the dreadful aspects of gangrene was the vulnerability of the patient, especially the diabetic, to bacterial invasion of the tissue from the necrotic area. Since then, the incidence of morbidity and death due to infection has decreased markedly. In patients with infected gangrene of the toes or foot, antibiotics should be used before and after surgery. In patients with dry gangrene who are undergoing elective amputation, antibiotics should be administered for a period of 7 to 10 days postoperatively. The decision as to the type of drug to be used should be based on bacterial cultures of tissue specimens and the susceptibility of bacteria to antibiotics. Although these tests may facilitate a logical choice of drug, it is not always advisable to wait for the laboratory results. A broad-spectrum antibiotic is then used routinely. Adherence to this policy should result in very little postoperative infection of the stump. However, if an abscess develops in the stump, early and adequate drainage is mandatory. Fever and leukocytosis are indicative of possible local infection, and the stump should be examined for this possibility. If a superficial extrafascial infection is present, removal of a few sutures and the use of wet dressings, changed twice daily and closely supervised, may suffice to control this sepsis. However, should there be a subfascial infection, the stump must be opened, preferably in the operating room, and the wound irrigated, drains placed in the stump, and a proper antibiotic solution used topically. Prompt recognition of this complication may prevent further damage and obviate the need for high revision of the amputation site. However, in diabetic patients, in spite of all the measures, the infectious process may spread subfascially, and additional counterincisions may be necessary for control of the sepsis. This complication will prolong morbidity and delay rehabilitation of the patient. Delayed Stump Healing Delayed stump healing is seen mostly in transmetatarsal and below-the-knee amputations, although it is not unusual in an above-the-knee amputation. As a rule, the delay in wound healing is due to marginal necrosis of the skin edges and less frequently to involvement of the subfascial tissues. Treatment of the necrotic lesions must be carried out with extreme care. One should not attempt to excise the necrotic edge of the skin until there is evidence of separation of the lesions. Daily dressings with wet saline applications or use of an enzymatic debriding agent may be helpful. If the necrotic lesions are superficial, revision of the stump may not be necessary. However, if necrosis is extensive, revision of the stump, either at the same level or above the proximal joint, may be indicated. Indeed, in the latter event, early reamputation at a higher level must be

Chapter 98 Above-the-knee Amputations

considered to prevent prolonged illness and bedrest. In the absence of infection, primary closure of the wound is usually desirable and feasible. Painful Stump; Phantom Sensations The early postoperative pain is located in the stump or consists of phantom sensations and is most common in below-the-knee and above-the-knee amputations. The stump pain, when unrelated to infection or marginal necrosis, represents a normal course of events in the healing process. Should the pain be unusually severe and persistent, a different explanation for the painful syndrome should be sought. The phantom sensations, consisting of the patient’s perception of the missing distal portion of the limb, usually without actual pain, occur in the early postamputation period. This is a self-limiting phenomenon, and the patient should be reassured about it. The pressure sores caused by a tight cast or splint application may result in severe pain. The cast or the splint should be removed without delay to prevent any further damage to the skin, either at the end of the stump or around the patella. If the lesions resulting from the pressure due to the cast or splint are superficial, reapplication is permissible, provided the lesions are reviewed periodically. Should there be a deep pressure sore, it is preferable to delay reapplication of the splint or cast, and treatment of the lesions should be undertaken vigorously. Unfortunately, especially in a debilitated individual or in a diabetic patient with marked diabetic neuropathy, the necrosis of the skin is sometimes unaccompanied by any clinical signs, and the lesions are discovered only at the routine removal of the cast. Local treatment of the necrotic area must be carried out without delay, and obviously the cast should not be reapplied.

Late Complications Phantom Limb Pain Unlike the phantom sensations, phantom limb pain occurs 2 to 3 months after the amputation or even later. Phantom pain is more frequently noted and is more severe in above-the-knee amputations. The cause of the persistent excruciating pain is not well understood, and it has been described to occur in anywhere from 0.5 to 100% of amputations. No significant difference has been found in the incidence of phantom pain for vascular and traumatic causes. The only condition which has been clearly demonstrated to increase the risk is preamputation pain (15,16). Neuroma of the cut end of the nerve has often been incriminated as a cause of phantom pain. What is known about phantom pain is that it causes serious problems with rehabilitation efforts (17,18). In the past, prefrontal lobotomy was used for control of this type of pain. Alternatives to this radical procedure are section of the sciatic nerve proximal to the stump,

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lumbar sympathectomy, and cordotomy. They have not always been successful in relieving this dreadful complication, although sciatic nerve section, in our experience, has produced gratifying results. It has been suggested that a better psychologic adjustment of the patient to the loss of the extremity, with a greater effort in rehabilitating the patient, may be helpful in preventing this phantom pain. Flexion Contracture Flexion contracture of the knee joint or of the hip joint may occur often as a result of stump or phantom pain or as a result of persistent ischemia of the stump or a combination of the two. It is likely that, in some cases, the level of amputation was too distal. Gangrene of the Stump In some patients, after a period of a few weeks or months, the arterial disease of the affected limb may progress to the point of inducing superimposed ischemia, leading to necrosis of the stump. Under those circumstances, a higher amputation is unavoidable. In connection with the progression of the arteriosclerotic process in the amputated limb, it is well to point out that, in diabetic patients, the remaining limb may also progress to gangrene and necessitate, within a period of 3 years, amputation of this limb in about 30% to 40% of the cases. It is therefore important to evaluate the arterial tree of the remaining limb in the hope that a bypass graft or a lumbar sympathectomy may be possible as a prophylactic measure.

References 1. Martin P, Wickham JE. Gritti-Stokes amputation for atherosclerotic gangrene. Lancet 1962;2:16. 2. Persson B. Lower limb amputation Part 1: Amputation methods — a 10 year literature review. Prosth Orth Int 2001;25:7. 3. Gottschalk F. Trans-femoral amputation, biomechanics and surgery. Clin Orthop 1999;261:15. 4. Branemark PI, Rydevik B, Skalak R. Osseointegration in skeletal reconstruction. Chicago; Quintessence, 1997. 5. Haimovici H. Failed grafts and level of amputation [editorial]. J Vasc Surg 1985;2(3):371. 6. Burgess EM, Marsden FW. Major lower extremity amputations following arterial reconstruction. Arch Surg 1976;108:655. 7. Sumner DS, Strandness DE Jr. Hemodynamic studies before and after bypass grafts to the tibial and peroneal arteries. Surgery 1979;86:442. 8. Samson RH, Gupta SK, et al. Level of amputation after failure of limb salvage procedures. Surg Gynecol Obstet 1982;154:56. 9. Stoney RJ. Ultimate salvage for the patient with limbs threatening ischemia. Am J Surg 1978;136:228.

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10. Szilagyi DE, Hagemann JH, et al. Autogenous vein grafting in femoropopliteal atherosclerosis. Surgery 1979;86:836. 11. Ramsburgh SR, Lindenauer SM, et al. Femoropopliteal bypass for limb salvage surgery. Surgery 1977;81:453. 12. Kagmers M, Satiami B, Evans WE. Amputation level following successful distal limb salvage operations. Surgery 1980;87:683. 13. Warren R, Record EE. Lower extremity amputations for arterial insufficiency. Boston: Little, Brown, 1967. 14. Warren R. Editorial comment on paper by Burgess and Marsden [Ref. 6]. Arch Surg 1974;108:660.

15. Geertzen JHB, Martina JD, Rietman HS. Lower limb amputation Part 2: Rehabiliation — a 10 year literature review. Prosth Orth Int 2001;25:14. 16. Houghton AD, Nicholls G, et al. Phantom pain: natural history and association with rehabilitation. Ann R Coll Surg Eng 1994;76:22. 17. Nikolaisen L, Ilkiaer S, et al. The influence of preamputation pain on postamputation stump and phantom pain. Pain 1997;72:393. 18. Smith DG, Ehde DM. Phantom limb, residual limb, and back pain after lower extremity amputations. Clin Orth 1999;361:29.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 99 Postoperative and Preprosthetic Management for Lower Extremity Amputations Yeongchi Wu

When amputation of the lower extremities becomes inevitable because of severe ischemia, trauma, or disease, proper reconstructive procedures and postoperative care of the residual limbs will affect the eventual functional outcome. Edema and pain following amputation are common problems. In addition, immobilization of the surgical wound and prevention of further trauma are important during the healing process. To minimize postoperative complications and discomfort, many methods have been used, mainly soft dressings (1), elastic bandages (2,3), elastic shrinkers (2), pneumatic shrinkers (4), and rigid dressings (1,5–13). At the Rehabilitation Institute of Chicago, elastic stockinettes (13) and removable rigid dressings (9–11,13) are routinely used for various levels of lower limb amputations. Therefore, in this chapter, I intend to describe only these two techniques, which are proven clinical procedures, simple to learn and apply by the staff and patients, and cost-effective compared with other techniques. Elastic bandaging, providing compression over the sterile dressing of a surgical wound, requires frequent reapplication and often causes edema from proximal constriction or ulceration over the bony prominences from excessive pressure. Although it has not been considered reliable, elastic bandaging is still used by many surgeons who demand frequent inspection of the surgical wound. Elastic shrinkers, commercially ready-made and indi-

vidually packaged, have been used for preprosthetic care of the residual limbs with some success. Their use is limited by the cost and the need to stock different sizes of shrinkers in the office or surgical suite. Many commercial compression shrinkers with limited sizes and lengths are not suitable for obese patients with short residual limbs or for children with amputated limbs. The ready-made shrinker sometimes is either too tight to put on or too loose to have enough compression on the stump. On the other hand, elastic stockinette, commercially available in rolls and in various sizes, can be used to replace the conventional elastic bandage and stump shrinkers for control of edema and shaping of the residual limbs (13). The elastic stockinette is much less expensive. It can be stretched easily onto the residual limbs or edematous limbs of patients with venous insufficiency (14). One can achieve a desirable gradient pressure by applying as many layers as needed with careful monitoring of distal circulation and pressure over bony prominences (Fig. 99.1). In the 1960s, the experience of immediate postsurgical fitting (IPSF) by Berlement et al. in France (5) and Weiss in Poland (6), and by Burgess in the United States (6–8) led to major advances in the rehabilitation of amputees. However, the need for frequent removal and reapplication of the IPSF by trained clinicians limited its acceptance. Furthermore, the immediate postoperative prosthetic fitting and weight bearing was noted to inter-

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A

C FIGURE 99.1 Elastic stockinettes of various length and sizes can be easily applied on an edematous limb or residual limb to achieve desirable gradient pressure and reduction of swelling.

fere with wound healing (1). A modified approach, using rigid dressing alone following transtibial amputation and bearing weight only after the surgical wound is healed, has been adapted as early postsurgical fitting (EPSF). In order to begin prosthetic fitting, the surgical wound must be healed and able to tolerate weight bearing. In general, proper management of the residual limb after the amputation and before prosthetic fitting includes prevention of wound infection, immobilization of soft tissue to facilitate healing, and provision of constant compression to control edema and shrinkage. It should prevent accidental trauma to the residual limb and be easy for reapplication by the staff or patient.

D

B

FIGURE 99.2 Application of elastic stockinette in hip disarticulation or hemipelvectomy. First, pull the elastic stockinette, 10 to 12 in. wide (25 to 30 cm) for most adult patients, over to the waistline (A), then twist the distal end (B), and finally fold it back over to the waist (C). Another, shorter elastic stockinette can be added for more distal compression (D).

stockinette] around the waist. This allows the elastic stockinette to be held toward the waistline so that the soft tissue on the medial thigh is always covered. Once the proximal end of the elastic stockinette is secured in place, the distal end is cut to proper length, twisted, and rolled back up to the thigh proximally. If more distal pressure is needed, additional layers of shorter elastic stockinette can be applied (Fig. 99.3).

Hip Disarticulation The surgical wound following hip disarticulation or hemipelvectomy is traditionally wrapped with elastic bandage around the stump and the waist. Use of an elastic stockinette 10 or 12 in. (25 or 30 cm) wide makes the procedure very easy and reliable. With this technique, a gradient pressure over the operated area is far more effective than that of the elastic bandaging (Fig. 99.2). From my clinical experience, support of the soft tissue by the elastic stockinette reduces downward pulling and thus minimizes the intensity of stump pain.

Through-the-knee Amputation The residual limb following knee disarticulation can be managed initially with a nonremovable plaster cast and followed either by a removable rigid dressing as used in transtibial amputations or by elastic stockinette (see Fig. 99.11). Rigid dressing, nonremovable or removable, is preferred for stump protection.

Transtibial Amputation Transfemoral Amputation Stump wrapping with elastic bandage, used for many decades and still described in recent books (2,3), is a complicated technique and requires reapplication at regular intervals. It is not possible for many geriatric patients to apply properly as they often lack fine motor control and have difficulty learning new skills. A simple method using elastic stockinette can be easily applied after transfemoral amputation. An 8-in.-wide (20-cm) elastic stockinette with a 6-in. (15-cm) longitudinal cut medially is pulled to waist height and the longitudinal cut is made to the groin medially. Several holes are made on the elastic stockinette for it to be held by the belt [3-in.-wide (7.5-cm) regular casting

In most hospitals, after removal of thigh-high rigid dressings in EPSF, elastic bandaging has been used to achieve further shrinkage of the transtibial residual limb. Inconsistent residual limb wrapping technique, by the staff or the patient, frequently caused either pretibial sores or distal edema. In order to remedy this problem, removable rigid dressing (RRD) was developed. It is an expansion of the IPSF or EPSF concept with modification of its casting and suspension methods. The principles that made the RRD an effective procedure are: 1. 2. 3.

use of a nonexpandable plaster cast to prevent edema; use of supracondylar suspension to make the cast removable; ability to inspect the condition of the wound;

Chapter 99 Postoperative and Preprosthetic Management for Lower Extremity Amputations

A

B

C

D

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E

FIGURE 99.3 For the adult patient with transfemoral amputation, pull an 8-in. wide (20 cm) elastic stockinette, with a medial longitudinal cut (A), toward the waistline to cover the soft tissue of the inner thigh (B). Apply a narrow regular casting stockinette around the waist as a suspension belt after passing through the holes on the elastic stockinette (A,B). Once the proximal end is secured in place, the distal end is cut to the proper length, twisted about half of a turn (C), then folded back up to the thigh (D). If more distal pressure is needed, another shorter elastic stockinette can be added (E).

4. 5. 6. 7.

8.

ability to add prosthetic socks to facilitate shrinkage; immobilization of soft tissue to secure wound healing and control residual limb pain; prevention of further trauma; use of cotton spacer in casting procedure to avoid excessive pressure over bony areas and skin breakdown; and possibility of graded weight bearing.

Because of complete elimination of skin breakdown, fast stump shrinkage, and easy reapplication, rehabilitation of the transtibial amputee has been improved since the development of RRD in 1977 (9–13). There are four components in the RRD: 1) tube socks or prosthetic soft socks, 2) below-the-knee plaster cast, 3) suspension stockinette, and 4) supracondylar cuff (Fig. 99.4).

FIGURE 99.4 Components of the removable rigid dressing (RRD) (from left to right): athletic tube sock or prosthetic sock, transtibial plaster cast, suspension stockinette, and supracondular suspension cuff.

Tube Socks or Prosthetic Socks Either athletic tube socks with the top rubber band removed or prosthetic soft socks are used under the cast to maintain a comfortable snug fit and constant pressure. Short tube socks are used to provide localized distal compression without building up the thickness proximally (Fig. 99.5). When “dog ear” is present, layers of pancakelike cotton padding can be applied right over the bulbous area before the last sock and the cast are worn (Fig. 99.5). Pressure marks on the skin from stump socks provide excellent indication of pressure distribution over the residual limb and are very useful during weightbearing exercise or prosthetic socket adjustment.

Plaster Cast The casting technique of the RRD differs slightly from that of the IPSF. Casting cotton padding is used as

“spacer” in the RRD, while felt is used to bridge the bony areas in IPSF to prevent pressure sores. In RRD, tapered cotton padding, six layers at the center and one layer along the margins, is used as “spacer” over the bony prominences of the tibial tubercle, tibial crest, fibular head, and any pressure-sensitive areas. Excessive padding over the end of the tibia is acceptable as there has been no distal edema experienced from too much pressure relief. The “cotton spacers” are discarded after the cast is set. The cotton spacer provides controlled pressure relief between the cast and the skin and has completely prevented the skin breakdown that is commonly seen in elastic bandaging (Fig. 99.6). The trim line of the plaster cast is made lower posteriorly to allow knee flexion. The cast should be wide enough proximally for easier reapplication. This is especially true

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FIGURE 99.5 Short tube socks (left) or pancake-like cotton padding (right) provide localized compression on distal portion of a bulbous residual limb under the plaster cast.

FIGURE 99.7 Sufficient padding in the concave section (shaded area) ensures a wider opening of plaster cast for easier reapplication (left). A narrow opening of the cast makes reapplication impossible and calls for recasting (right).

to replace the prosthetic socket if the patient is fitted prematurely.

Suspension Stockinette The suspension stockinette, made of 4-in. (10-cm) casting stockinette with one end tied, secures the cast to the suspension cuff (see Fig. 99.4).

Supracondylar Suspension Cuff

FIGURE 99.6 Casting cotton padding is used as “spacer” (shaded area) in the transtibial removable rigid dressing for pressure relief. The cotton padding is discarded after the cast is made.

The suspension cuff is made of thermoplastic material with a Velcro closure to keep the cuff in place and a strip of Velcro hook along the upper edge for the suspension stockinette to be anchored (Fig. 99.8). For the obese patient with very limited purchase over the femoral condyles, a fork strap and waist belt can be used for suspension of the rigid dressing. Application of the removable rigid dressing is very simple and only takes a few steps: 1.

for bulbous residual limbs (Fig. 99.7). If the cast is made too narrow proximally, it is necessary to recast the residual limb with more proximal padding. At times, when it is too tight to reapply the cast, a plastic film can be used to reduce the friction between the tube socks and the plaster cast. As the residual limb shrinks and too many tube socks are used, it is easy to make a new cast. Often two or three casts are needed for a bulbous residual limb before the patient is ready for a preparatory prosthesis. Economically, it is more cost-effective to replace the cast and achieve maximal stump shrinkage before prosthetic fitting than

2. 3. 4. 5.

Over the wound dressing, apply proper layers of tube socks; then apply the plaster cast; pull the suspension stockinette upward covering the plaster cast; place the supracondylar cuff and fasten the Velcro closure; finally, pull the suspension stockinette tight and fold it downward and anchor on the suspension cuff (Fig. 99.9).

To make the application easier for geriatric patients to remember, a semicircular mark is made on the plaster cast and another on the supracondylar cuff so that the patient

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FIGURE 99.8 Supracondylar suspension cuff made of thermoplastic with Velcro closure to keep the cuff in place and to anchor the suspension stockinette.

can match both marks over the patella. Drawing a smiling face on the front surface of the cast makes it easier for the patient not to apply the cast backward. Finally, the patient is instructed to practice removal and reapplication of the RRD. If it is too hard to reapply the cast, use a layer of thin plastic film over the socks to reduce the friction. If more distal pressure is needed, use short tube socks or pancakelike cotton padding over the edematous area. When excessive pressure with localized redness is noted, the cast can be softened or hammered from outside and then pushed from inside to reduce the compression. At the Northwestern Medical Center, a thigh-high plaster cast is routinely applied at the completion of a transtibial amputation. This thigh-high cast is removed for wound inspection or when the cast is too loose. This cast is then replaced with RRD. The RRD can be used by any recent or previous amputees for shrinkage. It is worn continuously to prevent swelling and trauma of the residual limb. It is removed for periodic wound inspection and hygiene, monitoring of skin condition before and after weightbearing exercise, or when the prosthesis is being used. Mild pressure on the residual limb with RRD against the wheelchair strap tied to the armrests without causing discomfort can be done in 7 to 10 days after surgery, depending on the wound condition (Fig. 99.10). Weightbearing exercise, by standing on a padded car jack (Fig. 99.10), can be initiated once the wound is healed adequately, usually 14 days after surgery. Stitches or staples are kept in place until 4 or 5 weeks after surgery. For bilateral amputees, the tilt table is used for weight bearing. The degree of weight stress is controlled by the inclination of the tilt table and the duration of standing. Being removable, tube socks can be conveniently added in the RRD for progressive stump shrinkage. It also allows frequent inspection of wound condition and monitoring of the skin’s

FIGURE 99.9 Steps of application of removable rigid dressing. Over the wound dressing apply layers of tube socks followed by the plaster cast. Roll and pull the suspension stockinette up to the thigh. Secure the supracondylar suspension cuff. Then pull and fold the suspension stockinette downward and over the supracondylar cuff. Finally, press to secure the suspension stockinette on to the Velcro hook of the supracondylar cuff.

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FIGURE 99.10 Padded car jack (left) and wheelchair strap (right) for weightbearing exercise with removable rigid dressing.

response to weightbearing exercise. Either undesirable skin breakdown from early weightbearing exercise or unnecessary delay for weight bearing can be reduced. Commercial residual limb shrinker is effective for residual limb shrinkage, but lacks protection of the residual limb from trauma such as accidental falls or weightbearing exercise. In certain cases, when the residual limb is very bulbous, combined use of elastic stockinette and RRD can be very effective. Delayed wound healing is not a contraindication for using RRD. On the other hand, it is a useful means to facilitate wound healing. Because the system reduces edema and tissue tension, the edges of the wound can be brought closer. When elastic stockinette is used for very bulbous conditions, one can begin with a layer of thigh-high elastic stockinette and then two or three layers of elastic stockinettes only over the distal portion of the residual limb (Fig. 99.11). This way, elastic stockinettes are not too tight to apply, and desirable pressure is obtained by adding more layers of elastic stockinettes. The sizes and layers of elastic stockinettes are determined by the degree of edema and the circumference of the residual limb to be treated.

Syme’s Amputation Syme’s amputation, either the one-stage procedure as initially used for traumatic foot injury or the two-stage procedure recommended by Wagner (15), must have the entire surgical area protected in a non-weightbearing plaster cast for 6 weeks to permit the blood supply to become established. In the modified technique, using the same principles as RRD for transtibial amputation, an RRD for Syme’s amputation can be used about 3 to 4 weeks after surgery. Proper casting technique is applied to

A

C B

E

D

FIGURE 99.11 Elastic stockinettes for bulbous residual limb. Stretch and pull the elastic stockinette over the residual limb (A), twist the distal end of the stockinette about one-third of a turn (B), and stretch it over to the residual limb (C). Other shorter elastic stockinettes can be added the same way (C, D, E) to increase the compression on the distal portion of the residual limb. Make sure not to cause excessive pressure over the bony prominences.

make sure a moderate weight is borne at the proximal portion of the residual limb, similar to that of a walking cast. The procedure of making such a Syme’s RRD involves the following (Fig. 99.12). 1.

2. 3.

Measure the maximal circumference of the heel and determine the level where the calf has a similar circumference. Pad the concave portion between the calf and heel with cotton padding (used as a spacer for casting). Use cotton padding as a spacer for casting over the bony prominences, including tibial crest, tibial tuber-

Chapter 99 Postoperative and Preprosthetic Management for Lower Extremity Amputations

C

A

B

D

FIGURE 99.12 Removable rigid dressing for Syme’s amputation. A stovepipe-like walking cast (A) made with cotton padding around the concave section (B) and bony prominences (C) permits removal and reapplication of the rigid dressing for wound inspection. Being removable, tube or prosthetic socks can be added for progressive stump shrinkage. A rubber heel (D) can be attached for progressive proximal and distal weight bearing after the wound is adequately healed.

4.

5. 6.

cle, and fibular head, for pressure relief between the cast and the residual limb. Make a total contact cast, as for a fracture walking cast, and attach a rubber heel for weight bearing as needed. Remove the cast when it is set and discard the cotton spacer. Tape the suspension stockinette on the proximal portion of the cast.

Application of the RRD for Syme’s amputation is similar to that of the transtibial RRD system: after wearing proper layers of prosthetic socks or tube socks, apply the cast, suspension stockinette, and supracondylar cuff and secure the suspension stockinette to the cuff. Some degree of edema above the ankle can be controlled by a short elastic stockinette. Progressive shrinkage of the residual limb is achieved by adding stump socks before the patient is fitted with a prosthesis.

References 1. Mooney V, Harvey IP Jr et al. Comparison of postoperative stump management: plaster vs. soft dressings. J Bone Joint Surg 1971;53A:241–249.

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2. Wilson BW Jr. Limb prosthetics. New York: Demo Publications, 1989:33–34. 3. Galley RS Jr, Clark CR. Management of adult lower-limb amputees. In: Bowker JH, Michael JW eds. Atlas of limb prosthetics: surgical, prosthetic, and rehabilitation principles, 2nd edn. St Louis: The Mosby Year Book, 1993:569–597. 4. Haimovici H. Immediate postoperative pneumotic temporary prosthesis for below knee amputees. In: Haimovici H, ed. Vascular surgery: principles and techniques. Norwalk, CT: Appleton-Century-Crofts, 1976:1139–1142. 5. Berlement M, Weber R, Willet JP. Ten years of experience with immediate application of prosthetic devices to amputees of the lower extremities on the operating table. Prosthet Orthot Int 1969;3(8):. 6. Burgess EM. Postoperative management. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby, 1981:19–23. 7. Burgess EM, Romano RL. The management of lower extremity amputees using immediate post-surgical prostheses. Clin Orthop 1968;57:137–146. 8. Burgess EM, Romano RL, Zettl JH. The management of lower extremity amputations. Technical Report TR1O6. Washington, DC: Prosthetic and Sensory Aids Service, Departments of Medicine and Surgery, Veterans Administration, 1969. 9. Wu Y, Flanigan DP. Rehabilitation of the lower-extremity amputee with emphasis on a removable below-knee rigid dressing. In: Bergan JJ, Yao ST, eds. Gangrene and severe ischemia of the lower extremities. New York: Grune & Stratton, 1978:435–453. 10. Wu Y, Keagy RD, et al. An innovative removable rigid dressing technique for below-the-knee amputation. J Bone Joint Surg 1979;61A:724–729. 11. Wu Y,Krick HJ. Removable rigid dressing for below-knee amputees. Clin Prosthet Orthot 1987;11:33–44. 12. Mueller MJ. Comparison of removable rigid dressing and elastic bandages in pre-prosthetic management of patients with below-knee amputations. Phys Ther 1982;62:1438–1441. 13. Wu Y. Post-surgical and early management of lower limb amputations. In: Proceedings of 7th World Congress of the International Society for Prosthetics and Orthotics, 1992:454. 14. Wu Y. Clinical advances in assistive devices, orthotics, and prosthetics. In: Kottke FJ, Amate EA, eds. Clinical advances in physical medicine and rehabilitation. Scientific Publication No. 533, Pan American Health Organization. Geneva: World Health Organization, 1991:306–333. 15. Wagner FW Jr. Syme’s amputation for ischemia of the toes and forefoot. In: Bergan JJ, Yao ST, eds. Gangrene and severe ischemia of the lower extremities. New York: Grune & Stratton, 1978:419–434.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

CHAPTER 100 Prosthetics for Lower Limb Amputees Jan J. Stokosa

Amputation is palliative. The amputation stump is a new limb that must serve the same function as the removed foot but with an anatomy not intended for such a purpose. It must be prepared for this new responsibility, to ultimately potentiate medical and prosthetic rehabilitation. As technology advances, the capabilities of prostheses, amputation surgery must reciprocate, and vice versa. The goal of the prosthetist is to aid the amputee in reentering and regaining his or her place in society: working, playing, and engaging in a full range of human relationships. Progress in this endeavor will be marked by the amputee’s placing a diminishing emphasis on the amputation and prosthesis. Ideally, amputation and prosthesis will move outside the inner circle of the patient’s life concerns. The prosthetist’s role in this process, in the broadest terms, is to enhance the amputee’s mobility and appearance, with maximum comfort. The ultimate achievement of the prosthetist’s goal is dependent on five factors: 1. 2. 3. 4. 5.

general physical and mental condition of the patient; the patient’s understanding of the rehabilitation process; level of amputation; quality of surgery and resultant physiology; and the degree of mobility, comfort, and cosmesis afforded by the prosthetist.

These five points can be achieved only through the cooperation of the essential participants: the patient, the surgeon, and the prosthetist. The psychiatrist, nurse, phy-

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sical therapist, rehabilitation counselor, family members, and others may also be productively involved.

Preoperative Considerations and Preparation It is generally agreed that the earliest possible explanation of why the surgery is necessary and of the entire process from preoperative preparation to prosthetic fitting and follow-up is of extreme benefit to the patient (1–4). The development and presentation of this plan involves at least the surgeon and the prosthetist; others will be involved according to individual need and available resources. A visit from a mature person, with similar amputation history and characteristics, is highly beneficial. Above all else, the entire orientation process should be realistic. Ranges of expectation, rather than high points, should be communicated. Unfortunately, even with the best of intentions and with considerable effort expended, this orientation process often fails. Patients consistently enter the prosthetic phase of their rehabilitation encumbered by misconceptions and unnecessary fears. Psychological preparation of the patient is a fertile area for research and innovation. In addition to general patient orientation, prosthetist and surgeon should collaborate on surgical objectives. The prosthetist will have a particular point of view that the surgeon should give some consideration. The pros-

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C A

D

B

E

F

FIGURE 100.1 (A–C) Xeroradiogram of ideal below-the-knee amputation stump. Space needed for prosthesis: 61/4 to 85/8 in. (16 to 22 cm). (D–F) Xeroradiogram of above-the-knee amputation stump. Space needed for prosthesis: 4 in. (10 cm).

thetist, along with the surgeon, will be concerned that the patient’s general physical condition be maintained or improved, especially in regard to strength, balance, and range of motion of the hips and knees. The prosthetist will wish the stump to be as long as possible, to be free of pain, and to retain as much of the physical and physiologic characteristics of the intact natural extremity as possible (Fig. 100.1). This will maximize the weightbearing surface and provide a long lever for more effective control of

the prosthesis. Problems, such as sharp bones, neuroma, and adherent tissue, will, of course, be of great concern as they reduce the area of support and have a negative effect on the comfort and control of the prosthesis. The position of the scar, as long as it is nonadhered, thin, and flat, is not of importance. Beyond these general considerations, surgeon and prosthetist must choose a specific postoperative management mode. There are four options:

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rigid dressing, with or without weight bearing (IPSF, immediate postsurgical fitting) (5); semirigid dressing (6,7); controlled-environment treatment (8); and soft dressing (9).

4.

continued until well after the prosthesis has been fit. When using the hypobaric compression sleeve, the sleeve is removed and reapplied several times per day. Begin physical therapy training to maintain or increase strength in the upper and lower extremities as soon as possible. Upon discharge from the hospital, a home exercise program will be monitored by a designated member of the rehabilitation team. Weekly visits to the prosthetist will be scheduled to monitor stump fluid volume changes and overall physical and emotional condition. Ambulation with or without prosthesis will begin as soon as possible — the sooner the patient is restored to maximum function, the less likely it is that psychological problems will arise.

The postoperative management mode may, of course, require modification if contraindicating information presents itself during surgery. IPSF, semirigid dressing, and controlled-environment treatment methods achieve highly positive results, both physical and psychological, but are contraindicated unless specifically trained personnel are available for around-the-clock postoperative care.

5.

Immediate Postoperative Considerations

When stump fluid volume is more stable and the patient has developed sufficient general strength and joint range of motion, prosthetic fitting can begin.

In the case of elective surgery, postoperative treatment will be a continuation of the preoperative plan. The plan is reiterated in full to the patient. In the instance of emergency surgery, the plan must be established and communicated as soon as possible within the constraints of the situation. The prosthetist will have a number of specific items to add to the surgeon’s postoperative treatment plan. Most will involve physical therapy, intended to prevent nonuse degenerative processes. Generally the plan will include the following: 1.

2.

3.

Knee and hip-flexion contractures must be avoided. The patient must lie face down three to five times each day for 30 minutes or more, with the head turned away from the amputated side and both anterosuperior iliac spines in contact with the bed or floor. Rest the foot of the other leg over the back edge of the bed or support it under its dorsal aspect. Always support the below-the-knee stump in its entire length. The amputation stump must not be allowed to assume a position of hanging down, i.e., over bed or chair. Control postoperative edema by wrapping with elastic compression bandage, hypobaric compression interlace (HCI ±), or equal. To ensure adequate suspension when employing the elastic compression bandage method, the wrap in the below-the-knee amputation must include the femoral condyles and be above the superior border of the patella; in the abovethe-knee amputee it must be wrapped around the waist at or above the iliac crests using one continuous bandage (double, triple, and sometimes quadruplelength bandages are necessary) (Fig. 100.2). As the fluids move from the amputation stump, it will become smaller. It is therefore best to unwrap and rewrap three to five times during the day, and often the wrap is left on overnight. Wrapping should be

6.

7.

A Unified Approach* In the design, fabrication, and fitting of any extremity prosthesis, comfort to the wearer must be an overriding concern. Discomfort will result in rejection or improper use of the prosthesis, thwarting other benefits. The most sophisticated component part with the most accurate biomechanical alignment is of little value if walking causes pain or skin breakdown, or both. Comfort can be accomplished only if proper fitting of the prosthetic socket (the receptacle in which the amputation stump is contained) to the amputation stump is achieved (the term fitting refers to the shaping and contouring of the inner surface of the socket, toward achieving a functional and comfortable union between prosthesis and amputation stump). Other comfortenhancing aspects of the prosthesis and its alignment are subordinate to and dependent on proper socket fit. The amputation stump, together with the socket, forms a lever to control the prosthesis during the swing and stance phases of the walking cycle. The stump also must transmit the entire weight of the body to the prosthesis. The more accurately the socket fits the stump, the greater the comfort and efficiency. The optimum-fitting socket is one that utilizes the entire skin surface of the amputation stump that will be contained within the socket. Weightbearing loads are distributed to advantage biomechanical efficiency, and to proportionate tolerable levels of underlying tissues. A loose-fitting socket reduces the overall proportionate pressures, thereby increasing stress on smaller areas. This *The prosthetic treatment of patients with other amputation levels (e.g., transmetatarsal, Syme’s, upper extremity) and with multiple amputations follows the same general course described in this section, with obvious differences in detail that are beyond the scope of this chapter.

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C

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D

FIGURE 100.2 (A) Below-the-knee compression wrapping. (B) Above-the-knee compression wrapping.

results in pain and skin abrasions. An extremely tightfitting socket causes the same problems as a loose-fitting socket and may also cause such problems as stump edema syndrome, sebaceous cyst formation, and folliculitis. In the optimum-fitting socket, most of the pressure of weight bearing will be borne by direct vertical loading: of the tibia in the below-the-knee amputee, of the femur in the above-the-knee amputee. This, of course, is more ex-

ceptional than routine. Usually the pressure of weight bearing is applied to the stump obliquely, as when a solid cone is forced into a hollow cone — an example of oblique pressure is the fitting condition brought about in a belowthe-knee amputation when the fibula has been sectioned more than 1 in. (2.5 cm) above the distal tibia and the pretibial and posterior muscle groups have atrophied, resulting in a cone-shaped stump.

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The entire design, fitting, and fabrication process consists of six basic steps: 1) impression mold, 2) cast design, 3) test socket fitting including static biomechanical analysis, dynamic biomechanical analysis, and alignment, 4) definitive prosthesis including fabrication and design theory, 5) definitive dynamic biomechanical alignment, and 6) final finishing. This process may take 8 to16 visits to the prosthetist, at approximately 1.5 hours per appointment. Another 25 to 40 hours will be necessary for laboratory fabrication and preparation procedures.

Anatomic and Physiologic Considerations The anatomy of the remaining portion of the limb after amputation is quantitatively and qualitatively different from the anatomy of an intact limb. The differences become manifest usually several months after surgery. Conventional amputation techniques render the greatest physiologic disturbance. Amputation techniques emphasizing a biological approach, such as in the Ertl technique, result in a superior physiologic and biomechanical end-organ. Ertl developed an osteoplastic flap to close the medullary cavity, thereby maintaining intermedullary pressure and concomitantly minimizing or eliminating bone hypersensitivity and improving venous return. A standard procedure in this technique is the anchoring of the antagonistic muscle groups, myoplasty, or myodesis. This provides active muscle function, which in turn reduces atrophy and fatty degeneration (10–13). Of the numerous differences between intact limb and stump, the following are of particular importance to prosthetic fitting: 1. 2.

FIGURE 100.3 Cross-sectional comparison of intact limb: Ertl amputation stump and conventional amputation stump.

3. 4.

Cross-sectional area. Increased area provides reduced per-square-inch pressure (Fig. 100.3). The capability of the bones to bear weight in the long axis (Fig. 100.4). As more weight is borne through the long axis of the bones, tangential loads are reduced. Circulatory condition. Proprioceptive ability.

FIGURE 100.4 (A) End-bearing capability of short amputation stump after osteoplastic-myoplastic (Ertl) procedure. (B) End-bearing capability of long amputation stump after osteoplastic-myoplastic (Ertl) reconstructive surgery. Patient is insulin-dependent diabetic and also has a history of neuropathy in both legs and hands.

Chapter 100 Prosthetics for Lower Limb Amputees

A

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B

FIGURE 100.5 Outlining anatomic landmarks on below-the-knee stump.

All points listed are positively influenced by osteomyoplastic procedures. Another important consideration is the poor ability of the soft tissues of the stump to accept stresses necessarily imposed with prosthesis use (14). The stump shape that provides the best function is one that is more cylindrical. The cylindrical shape provides greater area and aids in rotational control of the prosthesis (see Fig. 100.1A).

on underlying anatomy, and a molding technique is chosen. It is essential that the prosthetist’s repertoire include a number of molding approaches. In selecting the impression-molding technique, knowledge and experience are the best guides. Criteria can be delineated, but this would require a much longer work. Of the many different techniques, limited in the final analysis only by the innovativeness and expertise of the prosthetist, those explained and illustrated herein are of good general utility.

Initial Mold

Below-the-Knee Molding

The initial mold is the first of three basic procedures (initial mold, cast reduction modification, test socket fitting including static and dynamic biomechanical analysis) that will ultimately provide the model from which the socket and prosthesis will be constructed. Mindful of the patient’s general physical condition, a meticulous examination and palpation of the stump must be performed to discover conditions that will affect the fit of the prosthetic socket. Multiple-angle xeroradiographs are used to observe the condition and quality of bone, muscle, and subcutaneous tissue. The prosthetist must form a multidimensional visual perception of the optimal socket design. A topographical weightbearing map is envisioned, anticipating the effect

During the molding procedure, the patient with a belowthe-knee amputation may be in the standing or sitting position. A hypobaric compliant interface is applied. And desired anatomic landmarks are indicated using a marker (Fig. 100.5). These markings transfer automatically to the inner surface of the mold and ultimately to the cast. A five-stage technique is used, beginning with the application of elasticized plaster bandage, under appropriate tension, circumferentially encasing the stump from the tibial tubercle distally (Fig. 100.6). Then a series of rigid plaster segments is applied to specific areas of the amputation stump. Hands and fingers are used to model the plaster to enhance the underlying anatomy. Simultaneously,

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FIGURE 100.6 (A) Application of plaster splint to below-the-knee stump. (B) Deformation of plaster splint on below-the-knee stump.

the patient performs a series of stump muscle contractions to assist in forming the plaster as it hardens. After the plaster has hardened, it is removed from the stump in one piece (Fig. 100.7). This is the mold — a hollow plaster replica of the stump — with transferred anatomic landmarks (Fig. 100.8). Into this hollow mold, liquid plaster of Paris is poured (Fig. 100.9). This is the casting process. When the plaster of Paris hardens, the mold is stripped away (Fig. 100.10). A solid, three-dimensional cast of the stump as it is under slight compression and deformation remains. The indelible marks, originally applied to the outer surface of the hypobaric compliant interface, now appear on the outside of the cast (Fig. 100.11). The cast is ready for design modification. Above-the-Knee Molding With the patient in the weightbearing position, a hypobaric compliant interface is donned. Anatomic landmarks are identified and indicated using a transferable marker. Plaster splints are applied in the anteroposterior plane along the line of and to cover the perineum, the medial aspect of the ischial tuberosity, and the superior border of Scarpa’s triangle. An assistant ensures proper positioning posteriorly. Elastic plaster is then applied circumferentially to encase the entire stump, and around the

hips with considerable compression to ensure intimate contour. The wet plaster is hand-molded to conform to the anatomy and enhance desired areas for biomechanical advantage. When hardened, the mold is removed and the cast is prepared as previously described.

Cast Design Modification The cast is a three-dimensional representation of the amputation stump as it is under partial compression or stress. We are not able to achieve the ideal shape during the impression mold. The purpose of cast modification is to create a model, necessarily subjective (i.e., based on observation and judgment as well as measurement), that is representative of the stump shape and volume under full stress of static and dynamic weight bearing (the shape and volume the stump would take as it transmits the weight of the body to the socket during standing and walking). This is accomplished by sculpting the cast. The outer surface of the finished model (Fig. 100.12) will ultimately represent the inner surface of the socket. Shaving plaster from the cast will therefore increase pressure to the stump in that area; conversely, it will reduce pressure in adjacent areas. To achieve an optimum-fitting socket, a cast must be modified:

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FIGURE 100.8 The mold.

FIGURE 100.7 Removing the mold.

1. 2.

3. 4. 5.

to allow normal physiologic function; to ensure that pressure per unit area is within an acceptable pain threshold, with special care to ensure maximum axial loading of the tibia in the below-knee amputation; to provide maximum rotational control of the prosthesis; to distribute pressure over the entire surface of the stump; and to achieve a geometric shape that will generate maximum biomechanical efficiency.

It has been reported that specific areas of the stump are not able to accept pressures of weight bearing (15). These areas are the head of the fibula, the tibial tubercle, the crest of the tibia, and the distal terminal tibia in the below-the-knee amputation and the distal terminal femur in the above-the-knee amputation. It has been shown, however, that these areas are able to bear significant pressures (16,17). The total surface area available for pressure distribution may, of course, be reduced significantly by such problems as exostotic bone, adhered scar, and neuroma, as well as any other condition that causes discomfort during prosthetic use.

Diagnostic Socket Fitting: Static and Dynamic Biomechanical Analysis A sheet of transparent plastic is vacuum-formed over the completed model to produce a diagnostic socket. This socket is used to evaluate the degree of comfort, stability, and function of the model design. A stepwise refinement approach is used. This socket is initially fit under static, weightbearing conditions. The stump, with hypobaric compliant interface and sock of desired thickness in place, is slid into the socket, which is positioned and supported for standing by a Trowbridge universal foot/ankle device. Biomechanical alignment adjustments are made to provide balance and stability. The patient, standing in a comfortable posture, shifts his weight onto the stump (Fig. 100.13). The effect of pressure is observed through the plastic and empirically evaluated along with subjective information from the patient. Fitting refinements are made in one of two ways: 1) direct modification to the socket (removing material from the internal surface, heating and reshaping, or filling), or 2) rectification of the model and fabrication of another socket. The degree of refinement required will dictate the modification method. When maximum adjustment is achieved, the socket is cast to capture the improvements and another socket is prepared. This is the stepwise refinement method.

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FIGURE 100.10 Separating the mold from the cast.

FIGURE 100.9 Casting the mold.

When an acceptable fit is achieved under static weightbearing conditions, the socket is readied for dynamic analysis. The necessary components (foot, ankle, knee) are attached to the socket with adjustable alignment couplings and a metal tube (Fig. 100.14). Under close supervision, the patient dons the test prosthesis and begins walking within parallel bars. Additionally, videofluoroscopy is increasingly being utilized to demonstrate the limb–socket relationship during gait. The purpose of dynamic biomechanical analysis is to establish an efficient gait while maintaining comfort. The amputee provides valuable input beyond the prosthetist’s ability to visualize deviations. Alignment couplings allow minute and infinite adjustments to be made (Fig. 100.15). Various foot, ankle, and knee (in the above-the-knee amputation) components are tested and evaluated by the amputee. Walking imposes different and additional forces that may affect the comfort of the socket. The efficiency of alignment and the characteristics of the prosthetic foot also have a significant influence on the comfort of the socket. Fitting refinements are made as needed in the previously described way. As in the below-the-knee amputa-

tion, several iterations are usually required to optimize the fit. This is the stepwise refinement method. Common errors in the use of test sockets are: 1. 2. 3. 4.

5.

not using transparent plastic; using a plastic that is too flexible, allowing excessive plastic deformation under weightbearing loads; using more than five-ply prosthetic fitting socks; restricting the number of test sockets (the number of test sockets required varies with the complexities of each case — this writer has utilized as few as one and as many as 30); and confusing “total contact” with “total surface bearing.”

Total contact is the condition brought about when the entire surface of the stump is in total contact with the socket, not necessarily under compression. Total surface bearing is the condition brought about when the entire surface of the stump is in total contact with the socket while every unit area is under compression to its proportionate tolerable level. When optimum fit and biomechanical alignment are achieved in the test prosthesis, preparation is made for fabrication of the definitive prosthesis. The relative

FIGURE 100.11 The cast.

FIGURE 100.12 The model. FIGURE 100.13 (A) Static biomechanical analysis of below-the-knee test socket. (B) Static biomechanical analysis of above-the-knee test socket.

A

B

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Part XIII Amputations and Rehabilitations FIGURE 100.14 (A) Below-the-knee test socket ready for dynamic biomechanical analysis. (B) Above-theknee diagnostic socket ready for dynamic biomechanical analysis.

A

B

FIGURE 100.15 (A) Below-the-knee dynamic biomechanical analysis. (B) Above-the-knee dynamic biomechanical analysis.

A

B

Chapter 100 Prosthetics for Lower Limb Amputees

position of the test socket to the foot, ankle, and knee components must be precisely recorded, usually accomplished by clamping the test prosthesis within a stationary measuring device designed specifically for this purpose. A final model of the amputation stump will then be made from the final test socket.

Definitive Prosthesis: Fabrication and Design Theory The definitive prosthesis comprises a definitive socket, the required mechanical foot, ankle, and knee analog components, and structural connections with anatomic external shape. The definitive plastic socket is formed over the final model. This is accomplished by either a liquid lamination, prepregnated lamination, or vacuum-formed sheet plastic. Various liquid resins can be used. The type and amount of reinforcing material and matrices can vary infinitely. Over the past decade, there has been increasing utilization of thermoplastic methods over traditional lamination techniques. This is the result of many factors: 1) ease of construction, 2) ability to recycle resources, and 3) less risk of human error. The concern lies in the decreased durability of these products (18,19). In many below-the-knee casts, additional soft padding (of a variety of materials) is used between stump and socket to increase comfort. Prosthetic fitting socks are used to adjust the fit on a daily — sometimes hourly — basis. The socks vary in material (nylon, Orlon Lycra, cotton, or wool) and in thickness, or ply, from a sheer nylon to six-ply wool or cotton. These liners reduce the amount of shear forces and improve the “breathability” of the prosthetic (18,20). The completed definitive socket must be attached to the selected foot, ankle, and knee components. This is done by either endoskeletal design or exoskeletal design. In the endoskeletal design, foot, ankle, and knee components and socket are connected by a central tubular shin segment. The entire system is encased in a removable, soft plastic foam material that is anatomically shaped. The final step is to apply a protective synthetic skin that matches the patient’s skin pigmentation. In the exoskeletal design, components and socket are connected by wood or rigid plastic foam. The wood or plastic foam is glued directly to the socket. Limb contours will be achieved by shaping the external surface of the wood or plastic foam. Finally, a thin, rigid plastic is laminated over the wood or plastic foam for structural integrity and anatomic shape. Endoskeletal design prostheses normally have alignment adjustability. They also have maximum modularity, allowing for quick and easy exchange of components. The exoskeletal design prosthesis has no alignment adjustability and minimum modularity.

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Definitive Dynamic Biomechanical Alignment With the definitive socket attached to components, along with adjustable alignment couplings, the prosthesis is returned to the previously mentioned alignment apparatus, and the dynamic biomechanical alignment established during earlier trials is reestablished. This accomplished, the patient dons the prosthesis and begins walking. Alignment and component refinements will be necessary because of subtle differences (e.g., material, swing weight, socks) between the definitive prosthesis and the test prosthesis on which the existing biomechanical alignment was achieved. The patient is encouraged to test a full complement of activities, approximating activities of daily living. Special vocational or avocational activities are included with appropriate trials devised. When the patient and prosthetist agree that optimum alignment has been reached, the prosthesis is ready for finishing. The adjustable alignment couplings remain within the prosthesis in the endoskeletal design. This feature sustains absolute fidelity of alignment. In the exoskeletal design the adjustable couplings must be removed before proceeding to the finishing stage.

Finishing The goal of this final step in the fabrication process is to achieve the patient’s desire with respect to prosthesis weight, durability, and appearance (Figs. 100.16 and 100.17). In preparation for the actual shaping and finishing, an impression of the patient’s contralateral extremity is made. In addition, careful circumference measurements, caliper measurements, tracings, and photographs are taken of the patient’s intact limb. Soft foam plastic is shaped to match the patient’s intact limb. Similar steps are followed in anatomically shaping a prosthesis of exoskeletal design. The patient dons the prosthesis and examines his or her appearance in a full-length mirror. Family members or other persons significant to the patient are often involved in this procedure examination. After approving the appearance of the prosthesis, the patient receives instruction in its proper care and maintenance.

Postfitting Follow-up Use of a prosthesis causes physical changes in the amputation stump: subcutaneous tissue shrinkage and either myoatrophy or myohypertrophy. No diagnostic apparatus is available to accurately predict physical stump changes or to measure the amount of change, or precisely where on the stump the change has occurred. Experience suggests, however, that systemic observation could produce a useful formula to predict stump change. Variables of high saliency affecting stump change are amputation surgery technique, somatotype, body weight and body

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A

Part XIII Amputations and Rehabilitations

B

C

FIGURE 100.16 (A–C) Endoskeletal below-the-knee prosthesis.

weight fluctuation, physical activity — the type, its duration, and how consistently it is indulged in — and design of the prosthesis. Changes in the amputation stump result in changes in the relation between stump and socket. These changes may cause severe pain and skin breakdown if refitting adjustments are not made immediately. The amputee makes initial refitting adjustments by altering the thickness of fitting socks. When this no longer maintains comfort, the prosthetist may apply plastic filler or soft padding material to the inner surface of the socket to compensate for the reduction in stump size. In the case of an increase in stump size, the prosthetist may remove plastic from the inner surface of the socket by grinding or sanding. The amount of adjustment that can be made in a socket is quite limited. When maximum refitting adjustments are reached, socket replacement is necessary. Amputees will experience periodic changes in stump size for the remainder of their lives. A case in point is my experience with a World War I veteran in his 90s, who required fitting adjustments as a result of soft tissue shrinkage — even though he had been wearing a prosthesis for more than 70 years. Excess modification and failure to refabricate new sockets when needed is one of the most common prosthetist errors. This is far from a simple issue. The policies of third-party reimbursers often obstruct clinical deci-

sions. I have found, however, that taking time to inform and educate third-party reimbursers is very helpful. Repair and replacement of worn or broken foot, ankle, or knee components will also be required on an ongoing basis.

Common Stump Problems State-of-the-art amputation surgery and prosthetic care will eliminate a large share of the chronic pain and mobility problems suffered by many lower extremity amputees. Burgess (21) and McCullough et al. (22) have previously made this statement. Beyond the issue of optimum versus suboptimum care, the amputee is subject to a variety of problematic situations. The largest share of these problems concern the amputation stump. Those practitioners concerned with the amputee should be aware of several pathologic stump conditions that, if left untreated, can result in incapacitation. Unfortunately, there is a dearth of information in the prosthetic-related literature regarding stump problems and their causes. It will therefore be necessary to rely a great deal on clinical experience and judgment in this section. I refer the interested reader to a single monograph on this subject that covers 30 years of experience and re-

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A

B

1203

C

FIGURE 100.17 (A–C) Endoskeletal above-the-knee prosthesis.

search, and is the best single reference on the subject, Skin Problems of the Amputee, by S. William Levy, M.D. (23).

Neuroma Painful neuroma should not be a postoperative problem in the amputation stump if the nerve is treated properly during surgery. However, if the nerve end is positioned over bone or adhered to bone or scar tissue, it may be irritated by pressure and traction from the prosthetic socket and be a source of continual pain. Surgical intervention is the only complete solution to this problem.

Back Pain and Residual Limb Pain A special note should be made of these problems, as it was recently demonstrated that these entities lead to narcotic usage in amputees as often as does phantom limb pain. Residual limb pain is defined as pain emanating from the stump, as opposed to phantom limb pain (24).

Stump Edema Syndrome Initially in this syndrome (venous and lymphatic congestion of the distal stump), the stump appears cyanotic and edematous, and the patient may be only minimally un-

comfortable. If the condition is allowed to persist, the distal stump skin becomes darkly pigmented, increasingly edematous, ulcerated, and painful. The cause of stump edema syndrome is a prosthetic socket that is excessively tight circumferentially at its proximal border or imposes excessive pressure over vein and lymph vessels. Recontouring the socket will correct the problem. Another cause is physical, requiring surgical revision.

Skin Lesions Abrasions, blisters, sebaceous cysts, hair root infections, furuncles, and cysts are almost exclusively caused by localized pressure and friction due to an ill-fitting prosthetic socket (25). Skin lesions usually occur in areas on the stump that coincide with the proximal border of the socket where the potential for friction and localized pressure is great: inferior patellar and popliteal regions in the below-the-knee amputation; inguinal, perineal, and gluteal fold areas in the above-the-knee amputation. Limiting use of the prosthesis, allowing the skin lesion to heal, and socket correction will solve this problem. If the prosthesis is used when active lesions are present, the condition may be exacerbated to the degree that surgical intervention becomes necessary. In severe cases, the problem may not be correctable.

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Part XIII Amputations and Rehabilitations

Adherent Scar Adherent scar tissue is unable to accept weightbearing pressure. This condition therefore increases the per unit pressure over the remaining skin surface. In most instances surgical revision is necessary to correct this problem.

often will not accommodate technologic advances; 2) current education and training standards do not regularly produce prosthetists capable of applying technologic advances; 3) sufficient markets do not exist to make highly specialized technologic advances feasible to mass produce; and 4) most third-party reimbursers will not accept charges for new technology until it is in standard use (27).

Sharp Bone Sharp, distal bone terminations, as a result of poor surgical technique or having become exostotic, reduce, in the same manner as adherent scar, the total surface area of support. Recontouring the socket in some instances will afford relief for the patient. More often, surgical reconstruction is necessary.

Skin Grafts With proper prosthetic fitting, adequately fashioned and healed skin grafts do not create problems.

General Comments More sensitivity and attention to stump problems and more knowledge about them are needed on the part of both doctors and prosthetists. Unfortunately, at present, the inability of many practitioners to deal effectively with stump problems results in neglect of patients or mistaken psychiatric referrals.

High Technology The last decade has witnessed the continued improvement in computer models. The CAD/CAM (computer aided design/computer aided manufacture) of prosthetics was first introduced in the 1980s. Although the early systems were plagued by the introduction of communication errors, each successive generation has seen the improvement in this problem. The addition of a digitiser has further served to improve the accuracy. There has additionally been an increase in recent usage of microprocessor-controlled prosthetic knees. The latest example of this technology is termed the C-Leg (Otto Bock). The embedded computer chip relies on multiple sensors, and has been demonstrated to improve the responsiveness of the swing phase of gait. It has additionally been shown to lead to a 10% improvement in energy expenditure during high-velocity gait (18,26). It is of extreme importance that prosthetists and related medical personnel not be seduced by misperceptions of the present or naive speculation about the future. Only by understanding the complex relation of high technology to prosthetics can progress be effected. Several fundamental obstacles stand in the way of rapid advancement in the use of high technology in prosthetics: 1) standard interface technology in prosthetics

Vocational and Avocational Adjustment Adjustment is a word too often used by prosthetists to mean exclusively the acceptance of limitations. This is certainly a part of a mature understanding of what a person faces after amputation of a limb, but only a part. The other aspect of the word “adjustment” is adaptation — the creative overcoming of limitations. An open mind on the part of the prosthetist can lead to innovations that open new worlds, both vocational and avocational, for the amputee. Three-track snow skiing provides an excellent example of what can be done. It should be no surprise that younger patients generally fare better than older ones. In fact, age was the only demographic variable that corresponded with the ability to reintegrate into the workplace in a recent trial. This is a problem in the dysvascular patient, as 80% of the amputees are older than 60. The other two variables that affected outcome were the wearing comfort of the prosthesis and the education level of the patient (28). Amputees, unless they are fortunate enough to be able to locate and afford private rehabilitation counseling, depend primarily on the prosthetist for information, guidance, and often inspiration. Government programs are, for the most part, job-service services, offering little else. The surgeon understandably has diminishing contact with the amputee after a successful operation. It is the prosthetist, and sometimes the family doctor, who is there when it comes time for the amputee to walk and rejoin the mainstream of life. Prosthetists should, from their first contact with the amputee, provide information and counsel regarding the complex equation of genuine physical or technical limitations modified by the individual amputee’s aspirations and will. What is possible? should always be an open question. I have developed and use a mental formula in assessing what is possible for an individual amputee: Objective physical capability + Available relevant technology + Prosthetist’s ability and willingness to innovate ¥ Amputee aspirations and will = What is possible

High levels of amputee adjustment often involve increased costs. It is essential that these costs be seen in perspective — higher quality of life and reduced long-term disability expenditures versus immediate outlay. Pros-

Chapter 100 Prosthetics for Lower Limb Amputees

thetists and doctors must take the lead in educating thirdparty reimbursers, government policymakers, and the public in general about the long-term human benefits and monetary efficiencies of high-level amputee rehabilitation and adjustment.

11.

Acknowledgments

13.

It is an extreme honor to be a contributor in Haimovici’s Vascular Surgery, 4e. Thank you, Dr Haimovici, for the opportunity to participate in such a prestigious project. I am deeply grateful to my father, Walter J. Stokosa (1917–1971), who provided the foundation for my present level of knowledge; to my mother for her love and comforting support during those years; to the Honorable William G. Barr (1920–1987) for showing me the strength of spirit and perseverance. Special thanks to Noreen Roeske Stokosa, friend and wife, for her loyal and dedicated support, and skill in achieving the highest-quality manuscript. Appreciation is given to Craig Starnaman for artwork.

12.

14.

15.

16.

17. 18.

References 1. Alldredge RH, Murphy EE. The influence of new developments on amputation surgery. In: Klopsteg PA, Wilson PD, et al., eds. Human limbs and their substitutes. New York: McGraw-Hill, 1954:1112. 2. Vultee FE. Physical treatment and training of amputees. In: Edwards JW, ed. Orthopaedic appliances atlas, vol 2. Artificial limbs. Ann Arbor, MI: JW Edwards, 1960:313. 3. Friedman LW. The surgical rehabilitation of the amputee. Springfield, IL: Charles C Thomas, 1978:88. 4. Hoffman CA, Bunch WH, Kestnbaum JS. Management of psychological problems. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby 1981:483. 5. Burgess EM. Postoperative management. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby 1981:20. 6. Holliday PJ. Early postoperative care of the amputee. In: Kostuik JP, ed. Amputation surgery and rehabilitation: the Toronto experience. New York: Churchill Livingstone, 1981:219. 7. Kay HW. Wound dressings: soft, rigid, or semirigid. Selected reading: a review of orthotics and prosthetics. Washington, DC: The American Orthotic and Prosthetic Assoc, 1980:41. 8. Burgess EM. Wound healing after amputation: effect of controlled environment treatment: a preliminary study. J Bone Joint Surg 1978;60A:245. 9. Baker WH, Barnes RW, Shurr DG. The healing of belowknee amputations, a comparison of soft and plaster dressings. Am J Surg 1977;133:716. 10. Burgess EM, Romano RL, Zettl JH. The management of lower-extremity amputations. Washington, DC: Pros-

19.

20.

21.

22.

23. 24.

25.

26.

27.

28.

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thetic and Sensory Aids Service, TR 10–6, Department of Medicine and Surgery, Veterans Administration, 1969:7. Ertl J. Regeneration: Inre Anwendung in der Chirurgie. Leipzig, E Germany: Verlag Johann Ambrosius Earth, 1939. Ertl W. Ertl amputation technique. Paper presented at the American Surgery Association, Sarasota, FL, Oct 29, 1979. Loon HE. Biological and biomechanical principles in amputation surgery. In: Prosthetics International, Proceedings of the Second International Prosthetics Course. Copenhagen: Committee on Prostheses, Braces, and Technical Aids, International Society for the Welfare of Cripples, 1960:46. Murphy EF, Wilson AB Jr. Anatomical and physiological considerations in below-knee prosthetics. Selected articles from Artificial Limbs, January 1954-Spring 1966. Huntington, NY: Krieger, 1970:283. Quigley MJU. Prosthetic methods and materials. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby, 1981:53. Katz KK, Susak Z, et al. End-bearing characteristics of patellar-tendon-bearing prostheses: a preliminary report. Bull Pros Res 1979;16:2. Pritham CH. Newsletter: Prosthetics and Orthotics Clinic 1982;6(1,3). Cochrane H, Orsi K, Reilly P. Lower limb amputation Part 3: Prosthetics — a 10 year literature review. Pros Orth Int 2001;25:21. Verhoeff TT, Poetsma PA. Evaluation of use and durability of polypropylene trans-tibial prostheses. Pros Orth Int 1999;23:249. Lake C, Supa TJ. The incidence of dermatological problems in the silicone suspension sleeve user. J Pros Orth 1999;9:97. Burgess EM. Postoperative management. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby, 1981:22. McCullough NC III, Harris AR, Hampron FL. Belowknee amputation. In: Atlas of limb prosthetics: surgical and prosthetic principles. St Louis: CV Mosby, 1981:341. Levy MD, William S. Skin problems of the amputee. St Louis: Warren H. Green, 1983. Smith DG, Ehde DM. Phantom limb, residual limb, and back pain after lower extremity amputations. Clin Orth 1999;361:29. Harris WR. Common stump problems. In: Kostuik JP, ed. Amputation surgery and rehabilitation: the Toronto experience. New York: Churchill Livingstone, 1981:192. Zheng YP, Mak AFT, Leung AKL. State-of-the-art methods for geometric and biomechanical assessments of residual limbs: a review. J Rehab Res Dev 2001; 38(5):487. Whipple L, Stokosa J. The not so simple ABC’s of high technology. Washington, DC: Disabled USA, The President’s Committee on Employment of the Handicapped, July 1983. Schoppen T, Boonstra A, et al. Factors related to successful job reintegration of people with a lower limb amputation. Arch Phys Med Rehab 2001;82:1425.

Haimovici’s Vascular Surgery, 5th Edition Edited by Enrico Ascher Copyright © 2004 by Blackwell Science

INDEX

Abciximab, 1087 Abdominal angiography, 77–9 findings, 78–9 technique and risk, 78 Abdominal aorta anatomy, 334–5 atherosclerosis, 457 computed tomography, 95–6 magnetic resonance angiography, 106–8 physiopathology, 339–40 retroperitoneal exposure, 342–7 infrarenal exposure, 342–4 juxtarenal and suprarenal exposure, 345–6 pitfalls, 346 transperitoneal exposure, 334–9 Abdominal aortic aneurysm, 196–205, 703–35 aortic autoantigens and autoimmunity, 201 aortocaval fistula, 724 aortoenteric fistula, 724 arteriography, 710 associated conditions concomitant vascular disease, 722 gallstones, 721 malignant tumors, 721–2 associated venous anomalies, 725–6 and atherosclerosis, 198 changes related to normal aging, 200 and Chlamydia, 201–2 clinical presentation, 707–8 complications cholecystitis, 728 declamping hypotension, 726 gastrointestinal, 727 graft infection, 728–9 hemorrhage, 726 ischemic colitis, 727–8 lower extremity ischemia, 727 paraplegia, 728 renal failure, 727 ureteral injury, 727 computed tomography, 709 definitions, 196 diagnosis, 707–9 endovascular repair, 736–43 early clinical experience, 736–8 future developments, 742–3 Vanguard device, 738–42 enzymatic degradation, 200 epidemiology, 196–7 etiology and pathogenesis, 704–5 family history, 197 growth rate, 706–7 history, 703–4 horseshoe/ectopic kidneys, 724–5 indications for therapy, 710–11 inflammatory, 200–1, 722–3

life expectancy, 714 magnetic resonance imaging, 710 management medical, 707 small aneurysms, 711–12 surgical, 714–20 molecular genetics, 197–8 molecular mimics, 201 mortality, 196–7 mycotic, 725 natural history and risk of rupture, 706–7 nonruptured aneurysm retroperitoneal approach, 720 transabdominal approach, 717–20 transfemoral endovascular approach, 720 outcome, 729 perioperative care, 716–17 physical examination, 708 postoperative care and follow-up, 726 preoperative evaluation, 714–16 cardiac, 714–16 evaluation of pulmonary function, 716 evaluation of renal and hepatic function, 716 peripheral vascular disease, 716 prevalence, 196–7 radiography, 708 risk factors, 197 age, 705 carotid stenosis, 706 Chlamydia pneumoniae, 706 chronic obstructive pulmonary disease, 706 diabetes, 706 family history, 706 gender, 706 hernia, 706 hyperlipidemia, 706 hypertension, 706 tobacco, 705 risk of repair, 712–14 age, 712 disease, 712–13 emergency repair, 713–14 experience, 713 gender, 712 rupture, 720–1 incidence of, 707 screening for, 704 structural pathophysiology, 199–200 structural physiology, 198–9 suprarenal, 723–4 ultrasound, 708–9 and vitamin E deficiency, 202 Abdominal trauma, 429–30 aortic cross-clamping, 429

exposure, 430 laparotomy and initial control, 429 Above-knee amputation, 1175–82 anatomy, 1175–6 complications, 1180–1 delayed stump healing, 1180–1 flexion contracture, 1181 gangrene of stump, 1181 infection, 1180 phantom limb pain, 1181 failed grafts and level of amputation, 1179 indication for, 1175 pitfalls, 1179–80 surgical techniques, 1176–7 disarticulation of knee, 1176–7 myodesis and osseointegration, 1177 osteoplastic procedure, 1177 tendinoplastic amputation, 1177 through lower third of thigh, 1177–8 through middle third of thigh, 1178–9 see also Amputation Acrocyanosis, 493 Acute deep venous thrombosis bedside diagnosis, 26–7 duplex ultrasound, 26–7 see also Deep venous thrombosis Acute visceral ischemia, 863–4 embolic occlusion, 862 etiology, 862 thrombotic occlusion of visceral arteries, 862–3 Acylated streptokinase–plasminogen complex (APSAC), 191 ADAM study, 197 Age abdominal aorta changes related to, 200 as risk factor for abdominal aortic aneurysm, 705, 712 as risk factor in carotid endarterectomy, 794 Amaurosis fugax, 792 e-Aminocaproic acid, 191 Amputation, 435, 577, 1148–9 above-knee, 1175–82 anatomy, 1175–6 complications, 1180–1 failed grafts and level of amputation, 1179 indication for, 1175 pitfalls, 1179–80 surgical techniques, 1176–7 through lower third of thigh, 1177–8 through middle third of thigh, 1178–9 lower extremity, 1171–4 conservative management, 1172

1207

1208

Index

hip disarticulation, 1184 postoperative/preprosthetic management, 1183–9 preoperative management, 1172–3 prosthetics, 1190–205 selection of level, 1173–4 Syme’s amputation, 1188–9 through-the-knee amputation, 1184 transfemoral amputation, 1184 transtibial amputation, 1184–8 Anastomoses see Vascular anastomoses Anastomotic intimal hyperplasia, 169–70 effects of flow augmentation on, 170–1 Aneurysms abdominal aortic, 196–205, 703–35 aortic, 55, 56, 666–7 aortic arch, 672–3 aortoiliac, 463 autogenous arteriovenous fistula, 1020–1 common iliac artery, 764 external iliac artery, 764 extracranial, 847–8 false, 555 graft arteriovenous fistula, 1025 hand, 968 iliac, 763–6 iliofemoral, 764 internal iliac artery, 765–6 mycotic, 666, 725 renal artery, 898–9 ruptured, endovascular grafts, 744 sinus of Valsalva, 667–8 subclavian, 950–1 subclavian artery, 967–8 thoracic aortic, 663–86 thoracoabdominal aortic, 695–703 visceral artery, 902–12 Angina, mesenteric, 21 Angina pectoris, 931 Angioaccess, 1015–29 acute temporary complications, 1019 external shunt, 1017–18 large-vein catheters, 1018–19 removal of Dacron cuff catheters, 1019 autogenous arteriovenous fistula, 1019–22 complications, 1020–2 graft arteriovenous fistula, 1022–7 complications, 1023–7 technique, 1023 historical aspects, 1015–16 prerequisites for, 1016 techniques, 1016–17 Angiogenesis clinical trials, 179–81 growth factors, 177 mechanisms of drug delivery, 178–9 potential side effects, 179 therapeutic, 176–82 Angiogenic protein, 177–8 fibroblast growth factor, 178 hepatocyte growth factor, 178 vascular endothelial growth factor, 177–8

Angiogenic proteins, 178 Angiogenin, 177 Angiography, 61–86 abdominal, 77–9 adverse reactions, 66 aortic dissection, 76, 77 arteriovenous malformations, 1001–2 cardiovascular toxicity, 65 carotid arteriography, 72–3 carotid endarterectomy, 606 catheters and guidewires, 65 complications, 68–70 digital subtraction, 63, 64, 74 equipment, 62, 65 findings, 77 head and neck, 70–2 history, 61–2 interpretation, 70 low- versus high-osmolarity contrast media, 65 lower limb bypass, 606–7 magnetic resonance see Magnetic resonance angiography mesenteric revascularization, 607 nephrotoxicity, 65–6 neurotoxicity, 65 operative, 606–7 patient preparation, 66–7 peripheral, 79–82 pulmonary, 73–5 Raynaud’s disease, 920 technique, 67 thoracic, 75–7 traumatic aortic injury, 76–7 Angioplasty aortoiliac occlusive disease, 531–2 balloon see Balloon angioplasty carotid, 828–9 patch graft, 231–6 percutaneous transluminal, 56–7 Angiopoietin-1, 177 Angioscopy, 285–97 bypass surgery, 287–92 carotid endarterectomy, 295 indications for, 287 instrumentation, 285–6 interpretation, 287 percutaneous, 296 in situ vein bypass, 561 technique, 286–7 vascular access surgery, 292–5 venous surgery, 295–6 Anistreplase, 191 Ankle fasciotomy, 447–50 Anterior tibial artery bypass, 573 Anticoagulants heparin, 243–4, 1082–3 ischemic thrombosis, 1147 low-molecular-weight heparin, 1084–5 oral, 1083–4 Anticoagulation, 188–90 deep vein thrombosis, 1082 development of, 190 femoropopliteal bypass, 552 thrombin inhibition, 188–90 Antihemophiliac factors, 186 Antiplatelet therapy, 530–1

Aorta arteriography, 18 calcified, 512 duplex scanning, 18 small, 512–13 total occlusion, 511–12 traumatic injury, 76–7 see also Aortic Aortic aneurysm, 55, 56, 666–7 ascending aorta, 668–72 descending thoracic aorta, 673–5 endovascular grafts, 744–52 para-anastomotic, 775–84 diagnostic evaluation, 777 endovascular technique, 780–2 false, 776–7 incidence, 775–6 indications for repair, 777–8 interventions and results, 778 open technique, 778–80 surveillance, 782–3 true, 776 presentation, 777 ruptured, 744–52 thoracoabdominal aorta, 675–83, 695–702 transverse aortic arch, 672–3 see also Abdominal aortic aneurysm; Thoracic aortic aneurysms Aortic arch, 14 aneurysm, 672–3 magnetic resonance angiography, 106–8 trans-sternal exposure of great vessels, 315–21 Aortic bifurcation atherosclerosis, 454–5 embolectomy, 394–8 postoperative care, 398 retrograde or transfemoral, 395–7 retroperitoneal, 398 transperitoneal, 397–8 Aortic coarctation, 666–7 Aortic cross-clamping, 429 Aortic dissection ascending aorta, 671–2 descending thoracic aorta, 673–5 and thoracic angiography, 76, 77 thoracic aorta, 692 Aortic grafts endovascular, 744–52 infection, 753–62 Aortitis, 665–6 Aortocaval fistula, 724 Aortoenteric fistula, 724 Aortofemoral bypass graft, 506–9 Aortofemoral occlusive disease see Aortoiliofemoral occlusive disease Aortography, 55 Aortoiliac aneurysm, 463 Aortoiliac endarterectomy, 505–6 Aortoiliac occlusive disease see Aortoiliofemoral occlusive disease Aortoiliac stenosis, 458, 462–4, 469 collateral circulation, 459 Aortoiliofemoral occlusive disease, 499–521

Index adjunctive lumbar sympathectomy, 511 aortofemoral bypass grafting, 506–9 aortoiliac endarterectomy, 505–6 arteriography, 501–2 associated renal and visceral artery lesions, 514 calcified aorta, 512 clinical manifestations, 499–501 diagnosis, 501 hemodynamic assessment, 502–3 imaging, 502 indications for operation, 504 operative procedure, 509–11 percutaneous interventions, 522–33 access, 529–30 angioplasty and stenting, 531–2 antiplatelet medications, 530–1 endoluminal grafting, 532 equipment, 524–8 indications for, 529 patient selection, 528–9 use of thrombolysis, 530 postoperative complications, 515–17 results, 515 simultaneous distal grafting, 513–14 small aorta, 512–13 surgical treatment, 504–5 total occlusion of aorta, 511–12 unilateral iliac disease, 514 Aortorenal bypass, 894–6 Aortovisceral bypass grafting, 869–70 Argatroban, 189, 1088 Arterial embolism, 962 Arterial patch grafts, 232 Arterial sheath, 222 Arterial stenosis, 119–25 and arterial circuit, 123–5 collaterals and segmental resistance, 125 pressure and flow, 120–1 pulse wave contours, 121–2 shear rate and atherogenesis, 122–3 velocity, 121, 122 Arterial surgery, 958–73 Arterial thoracic outlet syndrome, 949–57 clinical manifestations, 951–2 clinical pathology, 950 diagnostic tests classic shoulder girdle maneuvers, 952 imaging arteriography, 952 noninvasive tests, 952 routine roentgenograms, 952 differential diagnosis, 952 early ischemic phase, 952 historical background, 949 prodromal phase, 951–2 severe ischemic phase, 952 subclavian aneurysms, 950–1 subclavian artery, 950 extrinsic compression, 950 treatment, 953–7 arterial reconstruction, 954–5 cervicothoracic sympathectomy, 955–6 removal of compressive structures, 953–4

results of, 956–7 surgical exposure for subclavian artery decompression, 953 Arterial thromboembolectomy, 412–14 Arterial thrombolysis, 273–7 clinical trials, 273 contraindications to, 274 localization of gastrointestinal bleeding, 277 technique, 275–7 thrombolytic therapy, 273–5 Arteries adaptive remodeling, 167 adaptive responses of, 165–7 clamping, 222–3 exposure and mobilization, 221–3 ligation, 223–5 wall shear stress, 165–6, 171–3 wall tensile stress, 166–7 see also individual arteries Arteriogenesis, 177 Arteriography abdominal aortic aneurysm, 710 aortoiliac segment, 538 arterial thoracic outlet syndrome, 952 arteriosclerotic occlusive disease, 501–2 atherosclerosis of lower extremity, 453–74 aortoiliac patterns, 453–9 collateral circulation, 466–73 femoropopliteal patterns, 459–64 methods, 453 tibioperoneal patterns, 464–6 axillary, 82 carotid artery, 14, 72–3 common femoral artery, 18, 81 contraindications to, 66 coronary artery, 68 duplex, 35–49 femoral artery, 537 femoropopliteal bypass, 552 femoropopliteal occlusive disease, 536–8 infrapopliteal arteries, 38–9 peripheral arterial disease, 15 peripheral vascular trauma, 434 popliteal artery, 18, 537 preoperative, 211 profunda femoris, 18, 538 superficial artery, 18 Takayasu’s arteritis, 477, 478 thromboangiitis obliterans (Buerger’s disease), 485, 486 tibial–peroneal segment, 538 upper extremity ischemia, 960–1 see also Angiography Arteriosclerotic occlusive disease aortoiliofemoral see Aortoiliofemoral occlusive disease femoropopliteal see Femoropopliteal occlusive disease Arteriotomy, 225–6 Arteriovenous fistulas, 561–2, 991–7 acquired, 993–4 after embolectomy with Fogarty balloon catheter, 997 after lumbar laminectomy, 996

1209

after nephrectomy, 996 diagnosis, 994–5 etiology, 992 historical aspects, 991–2 pathophysiology, 992–3 treatment and results, 995–6 see also Vascular malformations Arteriovenous malformations, 999–1010 clinical data, 1000–1 diagnosis, 1001–2 angiography, 1001–2 computed tomography, 1002 magnetic resonance imaging/angiography, 1002 location, 999–1000 treatment and results, 1002–7 visceral, 1007–8 Arteritis, 843 giant cell, 962–3 Takayasu’s see Takayasu’s arteritis temporal, 844 Atheroembolism, 489–90 Atherogenesis, 122–3 Atherosclerosis, 137–63, 961–2 and abdominal aortic aneurysm, 198 angiography, 69 encrustation hypothesis, 142 epidemiology, 138–9 history, 137–8 iliac artery, 455–6 initiation, 146–8, 149 intimal cell hypothesis, 141–2 IVUS, 53, 55 lipid hypothesis, 142 lower extremity, 453–74 aortoiliac patterns, 453–9 collateral circulation, 466–73 femoropopliteal patterns, 459–64 tibioperoneal patterns, 464–6 monoclonal hypothesis, 140–1 morphology and hemodynamics, 144–6 normal anatomy, 139–40, 141 plaque classification, 151, 152 plaque complications, 151, 152 plaque stability, 150–1 progression, 148–50 reaction-to-injury hypothesis, 142–3 risk factors cigarette smoking, 155, 156 diabetes mellitus, 154–5 estrogen, 155–6 homocysteinemia, 155 hyperlipidemia, 151–3 hypertension, 153–4 obesity/physical inactivity, 155 symptoms, 139 treatment, 156–7, 866 visceral ischemia, 863, 864–5 Auscultation, 1065 Autogenous arteriovenous fistula, 1019–22 complications, 1021–2 aneurysm formation, 1021 fistula thrombosis, 1020–1 hand edema, 1021 hand ischemia, 1022 infection, 1021–2

1210

Index

Autoimmunity, 201 Axillary arteriography, 82 Axillary artery anatomy, 325–6 exposure of, 325–8, 969–70 anterior approach, 326 deltopectoral approach, 327, 328 deltopectoral–subclavicular approach, 327, 328 subclavicular horizontal approach, 326 subpectoral–axillary approach, 328, 330 transpectoral approach, 327–8, 329 Axillary vein transfer, 1135–6 Axillary–axillary bypass graft, 310–11, 312 Axillobifemoral bypass, 628–30 completion angiograms, 629 management of failed axillofemoral grafts, 629–30 results, 630 two-team approach, 629 versus axillounifemoral bypass, 630 Axillofemoral bypass, 626–8 indications, 626 preoperative evaluation, 626 technique, 626–7 Axillopopliteal bypass, 632–4 preoperative evaluation, 633 results, 633–4 selection criteria, 633 techniques, 633 Axillounifemoral bypass, 627–8 versus axillobifemoral bypass, 630 Azotemic arteriopathy, 967 Balloon angioplasty, 247–56 access, 249 angioplasty, 250–1 complications, 251, 253, 254 guidewire crossing, 249–50 history, 247–8 indications, 248–9 pathophysiology, 248 preparation, 249 results, 251, 252 surveillance and follow-up, 254 Balloon embolectomy, 412–14 Balloon-expandable stents, 258–60 Gianturco–Roubin, 260 Palmaz, 258–9 Strecker, 259–60 Wiktor, 260 Balloons, 527 Basilar arteries, flow assessment, 31 Basilar circulation, 31 Behçet’s disease, 488, 845–6 Bernoulli principle, 117 Beta-blockers, preoperative, 211–12 Biceps tendinitis, 930 Bifurcation grafts, 132–3 Biplanar aortography, 866 Bird’s nest filter, 1100 Blood dyscrasias, 966 Blood flow velocity, 618 Blue rubber bleb syndrome, 998 Brachial artery anatomy, 328–9, 330

exposure of, 328–32, 970 distal artery and bifurcation, 331–2 upper half, 329, 331 Brachial plexus injury, 930 Brachiocephalic trunk artery lesions, 790 Budd–Chiari syndrome, 1040 Buerger’s disease see Thromboangiitis obliterans Bypass surgery, 125–33 anastomotic configuration, 131–2 angioscopy, 287–92 anterior tibial artery, 573 aortofemoral artery, 506–9 axillary–axillary bypass graft, 310–11, 312 bifurcation grafts, 132–3 carotid–subclavian, 309–10, 311 crossover grafts, 130–1 deep plantar artery, 584 distal peroneal artery, 573 dorsalis pedis artery, 573 extra-anatomic, 625–36 failure of, 292 femoropopliteal bypass, 42, 128, 129, 130, 539–56 flow distribution, 127 graft resistance, 126 iliofemoral bypass, 515 intraoperative duplex scanning, 614–15 lateral tarsal artery, 584 monitoring of grafts, 290–2 outflow resistance, 128–9, 130, 131 plantar artery, 582–6 posterior tibial artery, 573 pressure gradients across, 126 sequential grafts, 127–8, 129 in situ vein bypass, 559–67 small artery bypass, 568–81 subclavian–subclavian bypass, 311–12, 313, 314 thrombectomy, 292 tibioperoneal artery, 573 vein conduit preparation, 287–90 vein grafts with double lumens, 127, 128 Calcium, 186, 378–9 Calf vein thrombosis, 1085 Cannon, Walter B., 1 Captopril renal scintigraphy, 890–1 Cardiac failure, 1026 Cardiopulmonary assessment, 206–18 intraoperative cardiac management, 212–14 preoperative cardiac assessment, 206–12 preoperative pulmonary assessment, 214–15 Carotid angioplasty, 828–9 Carotid artery anatomy, 301–3 arteriography, 14, 72–3 blunt trauma, 425–6 catheterization, 73 computed tomography, 98 dissection, 848–50 Doppler ultrasound, 11 duplex scanning, 12–15, 609–11

elongation and coiling, 846–7 exposure, 301–3 extracranial aneurysm, 847–8 fibromuscular disease, 850–1 magnetic resonance angiography, 104–5 occlusion, 789–90 postoperative studies, 15 radiation injuries, 853–4 screening before intervention, 14–15 trauma, 424–5 Carotid artery disease, 795–6 Carotid artery stenosis, 13, 789 endarterectomy, 817–21 recurrent, 854–6 as risk factor for abdominal aortic aneurysm, 706 Carotid body tumors, 851–3 Carotid endarterectomy, 14, 31, 787–809 angiography, 606 angioscopy, 295 asymptomatic patients, 792–3 basivertebral symptoms, 794 carotid pathology, 788–90 bilateral carotid involvement, 789 carotid occlusion, 789–90 extracranial involvement, 790 intracranial involvement (siphon lesions), 790 stenosis and occlusion, 789 unilateral carotid involvement, 789 carotid plaque, 788 cerebral clamping ischemia, 796–8 cerebral embolization, 798–9 cerebral pathology, 796 complications, 821–5 conscious patients, 801–5 cranial nerve damage, 800 hyperperfusion, 799 indications, 787–8 late restenosis and occlusion, 800–1 local nerve injury during, 824–5 cervical plexus, 824 cranial nerves, 824–5 morbidity, 822–4 mortality, 821–2 myocardial infarction, 799–800 neurologic condition of patient, 790–4 nonneurologic factors, 794–6 operative site thrombosis, 799 postoperative blood pressure problems, 824 results, 817–21 asymptomatic carotid stenosis, 817–20 symptomatic carotid stenosis, 820–1 surgeon’s experience, 805 techniques, 796–805 see also Eversion carotid endarterectomy Carotid plaque, 788 Carotid siphon, 14, 790 Carotid stenting, 827–34 carotid angioplasty and angioplasty–stenting, 828–9 initial results, 829–31 organizational plan, 831–3

Index see also Carotid endarterectomy Carotid–subclavian bypass, 309–10, 311 Carpal tunnel syndrome, 930 Catheter injury, 966 Catheters angiography, 65 balloon ultrasound imaging, 57 IVUS, 50–2 large-vein, 1018–19 percutaneous transcatheter aspiration, 417–18, 419 Cattel–Braasch maneuver, 430 Causalgia, 986–7 CEAP classification, 1048 Celiac artery aneurysm, 908–10 Celiac artery compression syndrome, 870 Celiac axis compression, 863, 865–6 treatment, 866–7 Central venous thrombosis, 1019 Cerebral blood flow, autoregulation, 31–2 Cerebral clamping ischemia, 796–8 Cerebral edema, 799 Cerebral embolization, 798–9 Cerebral hemorrhage, 799 Cerebrovascular disease, nonatherosclerotic, 843–58 Cervical plexus injury, 824 Cervical spine disease, 930 Cervical sympathectomy, 971–2 Cervicothoracic sympathectomy, 954 Chemical mediators, 378–9 Chemotaxis, 378 Chest trauma, 426–9 blunt aortic injury, 426 diagnosis, 426–7 management options, 427–8 position and choice of incision, 426 thoracic inlet, 428–9 Chlamydia pneumoniae, as risk factor for abdominal aortic aneurysm, 201–2, 706 Chronic obstructive pulmonary disease, 706 Chronic venous disease, 27 Chronic visceral ischemia, 863–6 clinical presentation, 864–6 collateral pathways, 864 etiology, 863–4 Clamping of arteries, 222–3 Claudication, venous, 29 Claviculectomy, 953 Clopidogrel, 185 Coagulation, 185–6 Coagulation cascade, 185 Coagulation factors, 186 Coagulation pathways, 186 Collagen disease, 490–2, 965 lupus erythematosus, 492 periarteritis nodosa (polyarteritis), 490–1 scleroderma, 492 Collateral circulation, 125 aortoiliac stenosis, 459 genicular–tibial group, 466–7, 473 genicular–tibial–peroneal group, 468–9, 473 profunda femoris–genicular group,

466, 473 profunda femoris–genicular–tibial group, 468, 473 profunda femoris–iliac group, 466 Common carotid artery, exposure of, 316–19, 320, 321 Common femoral artery arteriography, 18, 81 arteriotomy, 542 duplex scanning, 16, 18 IVUS, 51 Common femoral vein, valve closure time, 28 Common iliac artery aneurysm, 764 Common ostium arteriovenous fistula, 593–4 Compartment syndrome anatomy, 441 chronic, 642–3 foot, 448 see also Fasciotomy Complementary fistulas in limb salvage, 592–9 clinical experience, 593 combined with deep vein interposition, 595–7 common ostium arteriovenous fistula, 593–4 complications, 597 experimental data, 592–3 follow-up, 597 remote arteriovenous fistula, 594 saphenous turndown arteriovenous fistula, 594–5 Composite graft, 551 Computed tomography, 87–102 abdominal aorta, 95–6 abdominal aortic aneurysm, 709 acquisition parameters, 92 angiography, 92–3 arteriovenous malformations, 1002 carotid artery, 98 data acquisition, 88 dosimetry, 94 electron beam, 89 helical and multidetector helical, 89–90 iliac arteries, 96 image display, 88–9 image reconstruction, 88 interpretation, 92–4 intravenous contrast, 91 mesenteric venous system, 98 peripheral arteries, 96–7 peripheral veins, 98 postprocessing, 92–3 spiral, 97 technical innovations, 91 thoracic aorta, 94–5 thoracic outlet, 98–9 three-dimensional, 92–3 vena cava, 98 Connective tissue disorders, 987 Contrast arteriography lower extremity revascularization, 37 renovascular hypertension, 891–2 Contrast materials adverse effects, 66 angiography, 65–6

1211

cardiovascular toxicity, 65 computed tomography, 91 low versus high osmolarity, 65 nephrotoxicity, 65–6 neurotoxicity, 65 Contrast-induced nephropathy, 46 Cordis TrapEase filter, 1102–3 Coronary artery arteriography, 68 Coronary artery disease, 794–5 Coronary steal syndrome, 249 Cragg stent, 262 Cranial nerve injury, 800, 824–5 Crescendo TIA, 791 Crossover grafts, 130–1 Cryoglobulinemia, 496 Cryopreserved cadaveric homografts, 649 Cubital tunnel syndrome, 930 D-dimer, 1081–2 Dacron prostheses, 540, 549–51 Danaparoid, 1087 Deep plantar artery bypass, 584 Deep vein interposition, 595–7 Deep venous thrombosis, 1078–90 computed tomography, 98 diagnosis, 1080–2 blood tests, 1081–2 clinical assessment, 1080–1 indirect physiologic studies, 1081 magnetic resonance venography, 1081 phlebography, 1081 venous duplex imaging, 1081 etiology, 1078–80 hypercoagulability, 1078 stasis, 1078 vein wall injury, 1078–80 lower extremity, 278–9 management, 1082–5 anticoagulation, 1082, 1083–4 heparin, 1082–3 low-molecular-weight heparin, 1084–5 treatment strategies, 1085–8 calf vein thrombosis, 1085 femoral–popliteal venous thrombosis, 1085–6 heparin-induced thrombocytopenia, 1087–8 iliofemoral venous thrombosis, 1086–7 upper extremity, 278, 1091–6 combined with lower extremity DVT, 1094–5 hypercoagulable states, 1093–4 placement of superior vena cava filters, 1092–3 Diabetes mellitus duplex arteriography in, 46 femoropopliteal reconstruction, 551–2 as risk factor for abdominal aortic aneurysm, 706 as risk factor for atherosclerosis, 154–5 Dialysis, vascular access see Angioaccess Digital subtraction angiography, 63, 64, 74

1212

Index

Dipyridamole–thallium scanning, 714–15 Distal arterial lesions azotemic arteriopathy, 967 blood dyscrasias, 966 catheter injury, 966 collagen disease, 965 drug abuse, 966 hypothenar hammer syndrome, 966–7 thromboangiitis obliterans (Buerger’s disease), 965–6 Distal peroneal artery bypass, 573 Distal popliteal artery embolism, 69 Distal splenorenal shunt, 1036–8 Distal vein patch, 603 Distal vertebral artery reconstruction, 840 Dobutamine stress echocardiography, 210–11 Doppler ultrasound, 8–12, 607–8 aliasing, 9, 11 carotid artery, 11 color, 11–12, 17 fast Fourier transform, 10 power, 11–12, 17 pressure measurements, 617–18 pulse repetition frequency, 9 sample volume, 9 superficial femoral artery, 11 transcranial, 29–31 see also Duplex scanning; Ultrasound Dorsalis pedis artery anatomy, 366–7 exposure of, 367 Dorsalis pedis artery bypass, 573 Double crush syndrome, 930 Double Pringle maneuver, 432 Drug abuse, 966 Dubos, Rene, 1 Duplex arteriography, 35–49 acute ischemia, 46–7 advantages, 44–5 contrast arteriography, 37 duplex scan examination, 35–7 intraoperative evaluation, 37 ischemia, 46–7 limitations, 43–4 machines, 46 prior studies, 42–3 renal and diabetic patients, 46 shortened protocol, 45 surgical team, 45 see also Duplex scanning Duplex scanning, 7–34, 608–15, 891 acute deep vein thrombosis, 26–7 aorta, 18 arteriovenous malformations, 1001 carotid artery, 12–15, 609–11 causes of intraoperative errors, 613–14 common femoral artery, 16, 18 deep vein thrombosis, 1081 Doppler, 8–12 external iliac artery, 16 iliac artery, 18 imaging, 7–8 intraoperative revisions, 611–13 lower extremity revascularization, 35–7

medical applications, 12–31 mesenteric arteries, 16, 21–3 peripheral arterial disease, 15–21 popliteal artery, 18 postoperative surveillance, 618–19 profunda femoris artery, 18 proximal superficial femoral artery, 16 refractive distortion, 1 renal arteries, 23–6 scan format, 7, 8 in situ bypass grafts, 614–15 superficial artery, 18 technique, 609 venous reflux, 1048–9 patterns of, 1054 validation of, 1053–4 venous thoracic outlet syndrome, 943 visceral arteries, 21–3, 615 see also Duplex arteriography DVT see Deep venous thrombosis E-selectin, 147 Echocardiography, 715–16 Ectopic kidneys, 724–5 Edema, 554 Effort thrombosis, 941 Ehlers–Danlos syndrome, 845 Eicosanoids, 378 Electrocardiography, 207–8 Electron beam computed tomography, 89 Embolectomy, 42, 388–408 anesthesia and patient monitoring, 392–3 complications, 404–7 metabolic, 405–7 venous thromboembolism, 404 fluoroscopically assisted see Fluoroscopically assisted thromboembolectomy indications for, 391–2 late, 403–4 lower extremity aortic bifurcation, 394–8 femoral, 393–4 iliac, 398 popliteal, 398–9 results, 400 percutaneous aspiration see Percutaneous aspiration thromboembolectomy preoperative evaluation, 392 technical pitfalls balloon catheters, 404–5 clamping, 404 prevention of, 405 upper limb, 400–1 indications, 402 prognosis, 401–2 Embolism arterial, 962 atheroembolism, 489–90 cardiopathy in, 389 clinical and pathologic data, 389–90 complications of, 374 differential diagnosis, 391 distal popliteal artery, 69 grading of ischemia, 392 popliteal artery, 365

problems in associated atherosclerosis of arterial tree, 402–3 late arterial embolectomy, 403–4 pulmonary, 76 small arteries, 488–9 topographic diagnosis, 390–1 visceral, 391 see also Embolectomy Encrustation hypothesis of atherosclerosis, 142 End-to-end anastomosis, 226–8, 423 End-to-side anastomosis, 228 incorrect, 546–7 Endarterectomy, 237–46 aortoiliac, 505–6 cleavage plane, 238 combined procedures, 244 endarterectomized specimen, 238, 240 femoropopliteal segment, 556–7 hemodynamic factors, 241 heparin, 243–4 open, 241, 243, 244, 245 residual arterial wall, 238, 241 semiclosed, 241, 243 terminology, 238 thromboendarterectomized specimen, 238, 242 versus percutaneous balloon catheterization, 245 Endoleaks, 741 Endoluminal grafting, 532 Endotension, 741–2 Endothelium-dependent relaxing factor, 140 Endothelium, 376–7 Endovascular repair aortic and iliac aneurysms, 744–52 advantages, 750–1 current management plan, 747 early experience, 745–7 exclusion criteria, 747 Montefiore system, 744–5 results, 750 ruptured aneurysm, 744 technique, 747–50 isolated iliac aneurysms, 767–74 anatomy, 767–8 indications for, 773 patient experience, 770–2 results, 772–3 surveillance, 773 para-anastomotic aortic aneurysm, 780–2 renovascular disease, 892–3 Endovenous obliteration, 1068 Enoxaparin, 1085 Epidermal growth factor, 177 Ergot poisoning, 963 Escherichia coli, 754 Estrogen, as risk factor for atherosclerosis, 155–6 Eversion carotid endarterectomy, 810–16 case selection, 811 limitations, 814 perioperative management, 811 results, 814–15 technique, 811–13

Index troubleshooting, 814 use of shunt, 813–14 Everting suture technique, 228–30 External carotid artery lesions, 790 External iliac artery aneurysm, 764 duplex scanning, 16 External oblique muscle, 348 External shunts, 1017–18 Extra-anatomic bypass surgery, 625–36 axillobifemoral bypass, 628–30 axillofemoral bypass, 626–8 axillopopliteal bypass, 632–4 crossover femoropopliteal bypass, 634–5 extended, 632–5 femorofemoral bypass, 630–2 False aneurysms, 555 Fasciotomy, 435, 437–46, 1148 anatomy of compartments, 441 anesthesia, 441 ankle and foot, 447–50 clinical presentation, 448 compartment pressure measurements, 448 signs and symptoms, 448 clinical and pathologic data, 437–9 four-compartment fasciotomy with fibulectomy, 443 indications, 439–41 long skin incision, 442–3 parafibular four-compartment decompression, 443 pitfalls and complications, 444 short skin incisions, 441–2 Fast Fourier transform, 10 Femoral artery anatomy, 354, 355 arteriography, 537 exposure of, 354–6, 541 combined iliac and femoral exposure, 352–3 Hunter’s canal, 355–6 Scarpa’s triangle, 354–5 Femoral artery pressure, 503 Femoral embolectomy, 393–4 Femoral–femoral graft, 131 Femoral–popliteal venous thrombosis, 1085–6 Femorofemoral bypass, 630–2 indications for, 631 inflow arteries, 631 results, 632 techniques, 631–2 Femoropopliteal arteries stenosis, 459–67 stenting, 267–8 Femoropopliteal arteriosclerotic occlusive disease, 534–58 Femoropopliteal bypass graft, 42, 128, 129, 130, 539–56 above-knee procedure, 540–3 arteriotomy of common femoral artery, 542 development of graft tunnel, 542 exposure of femoral artery, 541 exposure of proximal popliteal artery, 541

graft implantation, 542–3 handling of vein graft, 542 harvesting of saphenous vein, 541–2 incisions, 541 patient position, 540 anatomic variations of popliteal bifurcation, 544–5 anticoagulation, 552 below-knee procedure, 543–4 complications, 552–6 degenerative graft changes, 555–6 early thrombosis, 552–3 edema, 554 false aneurysms, 555 graft thrombosis, 554–5 hemorrhage, 553–4 infection, 554 lymphorrhea, 554 progression of arterial disease, 555 saphenous neuropathy, 554 crossover, 634–5 in diabetic patients, 551–2 endarterectomy of femoropopliteal segment, 556 graft materials, 539–40 improvement of graft diameter, 547 incorrect end-to-side anastomosis, 546 intraoperative arteriography, 552 limitations of venous grafts, 546 neointimal/intimal hyperplasia, 556 preoperative saphenous phlebography, 546 sequential grafting, 551 synthetic prostheses, 547–51 externally supported Dacron, 549–51 PTFE bypass graft, 548–9 use of bifid saphenous vein, 547 vein graft preparation, 546 Femoropopliteal occlusive disease, 534–58 arteriography, 536–8 clinical evaluation, 536 femoropopliteal bypass graft, 539–56 indications for reconstruction, 538–9 Femoropopliteal–tibial graft, 129, 130 Fibrin-stabilizing factor, 186 Fibrinogen, 186 Fibrinolytic system, 272 Fibrinolytics, 1147 Fibroblast growth factor, 177, 178 clinical trials, 180–1 Fibromyalgia, 930 Fibulectomy, 443–4 Fine, Jacob, 1 Fiolle, Jean, 1 Fistula thrombosis, 1020–1 Flow, 120–1 Fluoroscopically assisted thromboembolectomy, 409–16 arterial, 412–15 graft thrombectomy, 415 history, 409–10 operating room setup, 412 venous thrombectomy, 415 Follistatin, 177 Food fear, 865

1213

Foot compartment pressure measurements, 448 compartment syndrome, 448 compartments of, 448–9 fasciotomy, 449 extended, 449–50 results, 450 Forced expiratory volume, 214 Forward-looking IVUS, 53, 54 Four-compartment fasciotomy with fibulectomy, 443–4 Free flap technique, 587–91 indications, 587–9 postoperative management, 589–90 selection of, 589 Frostbite, 494 Gallstones, 721 Gangrene, 921 and amputation, 1173 of stump, 1181 venous, 1141 Gastric artery aneurysm, 910–11 Gastroduodenal aneurysm, 910 Gastroepiploic artery aneurysm, 910–11 Gastrointestinal bleeding, localization of, 277 Gender, as risk factor for abdominal aortic aneurysm, 706, 712 Giant cell arteritis, 962–3 Gianturco Z stent, 261 Gianturco–Roubin stent, 260 Graft arteriovenous fistula, 1022–7 complications, 1023–7 aneurysms, 125 cardiac failure, 1026 infection, 1024–5 ischemia, 1026–7 seroma, 1025–6 swelling, 1024 thrombosis, 1023–4 technique, 1023 Graft infections, 644–50, 728–9 aortic grafts, 753–62 cryopreserved cadaveric homografts, 649 management, 646–9 complete preservation, 648–9 partial preservation, 646–8 total graft excision, 646 microbiology, 645–6 presentation and diagnosis, 644–5 Graft-enteric erosion, 754 Grafts antibiotic-treated, 759 aortovisceral bypass, 869–70 endovascular, 744–52 materials, 539–40, 547–51 prosthetic, 759 thrombectomy, 415 thrombosis, 554–5 Granulocyte colony-stimulating factor, 177 Greater saphenous vein anatomy, 1060 exposure of, 1066–8 Greenfield vena cava filter, 1099–100 Gritti–Stokes amputation, 1177

1214

Index

Groin injuries, 434 Guidewires for angiography, 65 Hageman factor, 186 Haimovici, Henry, 1–3 Hand aneurysms, 968 Hand edema, 1021 Hand ischemia, 1022 Head, angiography, 70–2 Helical (spiral) computed tomography, 891 Helical/multidetector helical computed tomography, 89–90 Hematocrit, 118 Hematologic disorders, 495–6 cryoglobulinemia, 496 polycythemia vera, 495–6 Hemodynamic testing, 1055–6 Hemostasis, 183 Heparin, 243–4, 1082–3 necrosis and thrombosis, 1146–7 Heparin-induced thrombocytopenia, 1087–8 Hepatic artery aneurysm, 905–7 clinical presentation, 906 diagnosis, 906 etiology, 905–6 location, 906 treatment, 906–7 Hepatocyte growth factor, 177, 178 Hepatorenal artery bypass, 897–8 Hernia, as risk factor for abdominal aortic aneurysm, 706 Hip disarticulation, 1184 Hirudin, 189, 1088 Homocysteinemia, as risk factor for atherosclerosis, 155 Horseshoe kidneys, 724–5 Human umbilical cord vein graft, 540 Hunter’s canal, 355–6 Hydroureteronephrosis, 754 Hyperabduction syndrome, 931 Hypercoagulability, 1078, 1093–4 Hypercoagulable syndromes, 186–8 acquired, 187–8 congenital, 187 Hyperhidrosis, 986 Hyperhomocystinemia, 188 Hyperlipidemia as risk factor for abdominal aortic aneurysm, 706 as risk factor for atherosclerosis, 151–3 Hypersensitivity angiitis, 918 Hypertension as risk factor for abdominal aortic aneurysm, 706 as risk factor for atherosclerosis, 153–4 Hypogastric artery, 349 Hypoplastic aorta syndrome, 500 Hypothenar hammer syndrome, 966–7 Hypoxia response element, 178 Hypoxia-inducible factor, 177, 178 ICAMs, 147 in ischemia–reperfusion injury, 377 Iliac aneurysm common iliac artery, 764 external iliac artery, 764

iliofemoral aneurysm, 764 incidence, 763 internal iliac artery, 765–6 isolated, 763–6 ruptured, endovascular grafts, 744–52 surgical management, 763–6 Iliac artery, 349 anatomy, 334–5 arteriography, 18 computed tomography, 96 duplex scanning, 18 external, 349 IVUS, 55 left common, 349 magnetic resonance angiography, 107 retroperitoneal exposure, 348–53 anatomy, 348–9 combined iliac and femoral exposure, 352–3 external iliac artery, 349–50 iliac axis, 350–2 right common, 349 stenosis, 71, 455–6, 458 stenting, 265–7 transperitoneal exposure, 334–5, 340–1 trauma, 430–1 Iliac axis, extraperitoneal exposure of, 350–2 Iliac embolectomy, 398 fluoroscopically assisted, 411 Iliofemoral aneurysm, 764 Iliofemoral bypass graft, 515 Iliofemoral occlusive disease see Aortoiliofemoral occlusive disease Iliofemoral venous thrombosis, 1086–7 Imaging see specific types of imaging In situ vein bypass, 559–67 advantages and disadvantages, 560 angioscopy, 561 arteriovenous fistulas, 561–2 critique, 565 exposure of saphenous vein, 560–1 instrumentation, 563–5 method, 559–60 results, 565–7 saphenous phlebography, 560 techniques for saphenous implantation, 563–5 Infection angioaccess, 1019, 1021–2, 1024–5 aortic grafts, 753–62 graft-related, 554, 644–50, 728–9 thoracic aortic aneurysms, 666 Inferior vena cava anomalies of, 336 interruption, 1148 Inflammation, 843–4 and abdominal aortic aneurysm, 200–1 Infrapopliteal arteries, arteriography, 38–9 Innominate artery, exposure of, 316–19, 320, 321 Interleukin 8, 177 Intermittent claudication, 535 Internal iliac artery aneurysm, 765–6 Internal oblique muscle, 348

Interosseous artery, exposure of, 970 Intestinal angina, 875 Intimal cell mass hypothesis of atherosclerosis, 141–2 Intimal fibrocellular hypertrophy, 167–8 Intimal hyperplasia, 164–75, 168–9, 601 adaptive responses of arteries, 165–7 anastomotic, 169–71 hypotheses, 164–5 molecular mechanisms, 173 and restenosis, 171 in stents, 172 and subnormal wall shear stress, 171–3 Intracellular adhesion molecules see ICAMs Intracranial artery stenosis, 31 Intraluminal shunts, 423 Intraoperative cardiac management, 212–14 Intravascular ultrasound see Ultrasound Ischemia duplex arteriography, 46–7 hand, 1022 upper extremity, 958–73 clinical examination, 958–9 diagnosis, 959–61 graft arteriovenous fistula, 1026–7 symptoms, 958 treatment, 968–72 Ischemia–reperfusion injury, 373–87 chemical mediators and signaling molecules, 378–9 endothelial cell-leukocyte interactions, 377–8 etiology, 374 microvascular permeability and tissue remodeling, 382 pathophysiology, 374–6 role of endothelium in, 376–7 role of neutrophil in, 377 role of nitric oxide/nitric oxide synthase in, 379–82 signal transduction in hyperpermeability, 379–80 Ischemic venous thrombosis, 1, 1139–51 clinical manifestations phlegmasia cerulea dolens, 1140–1 venous gangrene, 1141 clinicopathologic pattern lower extremity, 1141 upper extremity, 1141–2 definitions, 1139 diagnosis, 1144 differential diagnosis, 1144–7 etiology, 1140 historical aspects, 1139–40 medical management, 1147 pathophysiology, 1142–4 prognosis, 1149–50 surgical management, 1147–9 amputations, 1148–9 distal tree clearance, 1148 fasciotomy, 1148 inferior vena cava interruption, 1148 temporary arteriovenous fistula, 1148

Index venous thrombectomy, 1147–8 see also Deep venous thrombosis IVUS see Ultrasound Jugulosubclavian vein bypass, 946–7 Kasabach–Merritt syndrome, 998 Kissing stents, 523 Klippel–Trénaunay syndrome, 998, 1008–10 Kocher maneuver, 430 Lacunar ischemia, 794 Lanoteplase, 191 Laparoscopic lumbar sympathectomy, 657–9 Large-vein catheters, 1018–19 Lateral tarsal artery bypass, 584 Leg arteries anatomy, 362 see also individual arteries Leg pain, 1063 Lepirudin, 189, 1088 Leptin, 177 Leriche, René, 1 Lesser saphenous vein, 1060 superficial thrombophlebitis, 1074 Leukotriene B4, 377 Leukotriene C4, 377 Ligation of arteries, 223–5 of damaged vessels, 423 Limb salvage, 578 complementary fistulas, 592–9 free flaps, 587–91 vein cuffs and patches, 600–5 Lipid hypothesis of atherosclerosis, 142 Livedo reticularis, 493–4 Liver transplantation, 1041 Low-molecular-weight heparin, 1084–5 Lower extremity amputation, 1171–4 postoperative/preprosthetic management, 1183–9 prosthetics, 1190–205 atherosclerosis, 453–74 deep venous thrombosis see Deep venous thrombosis embolectomy, 394–8 ischemia, 727 ischemic thrombosis, 1141 revascularization, 37 see also Foot; Leg Lumbar sympathectomy, 511 conventional, 651–6 anterior transverse exposure, 653–5 complications, 656 indications for, 651–3 operative pitfalls, 655 postoperative care, 656 laparoscopic, 657–9 neuroanatomy, 651 Lupus anticoagulant, 187 Lupus erythematosus, 492 Lymphedema, 1152–68 diagnosis, 1154–6 diagnostic evaluation, 1156–60 degree of lymphedema, 1156 lymphatic functional evaluation,

1159–60 lymphatic imaging, 1156–9 venous imaging, 1156 etiology, 1152–4 excisional procedures, 1165 history, 1154 nonsurgical treatment, 1160–2 normal lymphatics, 1152 physical findings, 1155–6 physiologic procedures, 1162–5 primary, 1152–3 secondary, 1153–4 surgical treatment, 1162 symptoms, 1154 venous obstruction, 1165 Lymphorrhea, 554 Lymphoscintigraphy, 1156–9 Maffucci syndrome, 998 Magnetic resonance angiography, 80, 103–13 aortic arch, 106–8 arteriovenous malformations, 1002 basic principles, 103–4 carotid artery, 104–5 coronary vessels, 105–6 limitations of, 111 peripheral circulation, 108–11 renal artery stenosis, 108 renovascular hypertension, 891 thoracic/abdominal aorta, 106–8 venous thoracic outlet syndrome, 943 Magnetic resonance imaging abdominal aortic aneurysm, 710 arteriovenous malformations, 1002 Magnetic resonance venography, 1081 Matrix metalloproteinases, 200 Mattox maneuver, 430 Maximal midexpiratory flow, 214 Maximal ventilatory volume, 214 Memotherm stent, 261 Mesenteric angina, 21 Mesenteric arteries duplex scanning, 16, 21–3 surgery, 867–8 trauma, 432 Mesenteric ischemia, 21, 875–86 acute diagnosis, 875–6 embolic occlusion, 876 nonocclusive, 876–7 thrombotic occlusion, 876 treatment, 877–8 chronic diagnosis, 879–80 treatment, 880–3 history, 875 Mesenteric revascularization, 607 Mesenteric venous thrombosis, 98, 279–81, 878–9 Mesocaval shunt, 1038–9 Midkine, 177 Migratory thrombophlebitis, 1074 Miller’s cuff, 602 Molecular mimics, 201 Mondor’s disease, 1074 Monoclonal hypothesis of atherosclerosis, 140–1 Montefiore endovascular grafting

1215

system, 744–5 Monteplase, 191 Mycotic aneurysm, 666, 725 Myocardial infarction, 799–800 Myointimal hyperplasia, 15 Naier, Nelicia, 1 NAIS procedure see Superficial femoropopliteal vein replacement Neck angiography, 70–2 vascular injuries, 424–6 carotid artery, 424–6 vertebral artery, 426 Neutrophils, role in ischemia–reperfusion injury, 377 Nitric oxide, 379 permeability changes in ischemiareperfusion injury, 381–2 phosphorylation in signaling, 380–1 production in hamster cheek pouch, 381 Nitric oxide synthase, 379 phosphorylation in signaling, 380–1 platelet-activating factor-induced phosphorylation, 381 Nonatherosclerotic cerebrovascular disease, 843–58 Behçet’s disease, 845–6 carotid body tumors, 851–3 carotid dissection, 848–50 elongation and coiling of carotid artery, 846–7 extracranial carotid artery aneurysm, 847–8 fibromuscular disease of carotid artery, 850–1 inflammatory process, 843–4 radiation injuries to carotid artery, 853–4 recurrent carotid stenosis, 854–6 Takayasu’s arteritis, 844–5 temporal arteritis, 844 Nonatherosclerotic small artery disease, 475–98 acute thrombosis, 488–90 Behçet’s disease, 488 collagen disease lupus erythematosus, 492 periarteritis nodosa (polyarteritis), 490–2 scleroderma, 492 hematologic disorders cryoglobulinema, 496 polycythemia vera, 495–6 occupational trauma, 495 Takayasu’s arteritis, 476–80 thromboangiitis obliterans (Buerger’s disease), 480–7 vasospastic diseases acrocyanosis, 493 frostbite, 494 livedo reticularis, 493–4 Raynaud’s disease, 493, 494–5 Normal blood flow, 117–19 inertial energy losses, 118 resistance, 118–19 Reynolds number, 119 viscous energy losses, 117–18

1216

Index

Obesity, as risk factor for atherosclerosis, 155 Occupational trauma, 495 Ohm’s law, 123 Oral anticoagulation, 1083–4 Outflow resistance, 128–9, 130, 131 Palmaz stent, 258–9, 523 Pamiteplase, 191 Pancreaticoduodenal aneurysm, 910 Parafibular four-compartment decompression, 443 Parkes–Weber syndrome, 998 Patch graft angioplasty, 231–6 arterial, 232 combination procedures, 234 complications and pitfalls, 234 different arterial sites, 233–4 indications, 231 materials, 231–2 methods and technique, 233–5 prosthetic, 232–3 venous, 232 Pectoralis minor syndrome, 931 Pectoralis minor tenotomy, 953 Percutaneous angioscopy, 296 Percutaneous aspiration thromboembolectomy, 417–20 arterial, 418–19 pulmonary, 419 transcatheter aspiration, 417–18 Percutaneous balloon angioplasty, 947 Percutaneous balloon catheterization, versus endarterectomy, 245 Percutaneous stainless-steel Greenfield filter, 1102 Percutaneous transluminal angioplasty, 56–7 Perforate-invaginate stripping, 1068–9 Perforating veins, 1061–2 endoscopic subfascial ligation, 1121–2 clinical results, 1123–5 hemodynamic results, 1126–7 in post-thrombotic syndrome, 1126 role in ulcer healing, 1125–6 interruption, 1119, 1136–7 pathophysiology, 1117–19 preoperative evaluation, 1119 surgical anatomy, 1115–17 surgical techniques, open, 1119–21 Periarteritis nodosa (polyarteritis), 490–2 Peripheral angiography, 79–82 findings, 81–2 indications, 79–81 technique and risk, 81 Peripheral arterial disease arterial inflow, 20 arteriography, 15 duplex scanning, 15–21 follow-up, 19–20 screening before intervention, 18–19 vein graft, 20–1 vein mapping, 19 Peripheral arteries computed tomography, 96–7 magnetic resonance angiography, 108–11

Peripheral vascular trauma, 433–4 arteriography, 434 diagnosis, 433–4 minimal vascular injuries, 433 noninvasive imaging, 434 Peroneal artery bypass see Small artery bypass Phantom limb pain, 1181 Phelan’s sign, 929 Phlebography, 1081 Phlegmasia alba dolens, 1141 Phlegmasia cerulea dolens, 1, 27, 1140–1 Physical inactivity, as risk factor for atherosclerosis, 155 Placental growth factor, 177 Plantar arteries anatomy, 367–9 exposure of, 369 Plantar artery bypass, 582–6 Plaque classification, 151 complications, 151 stability, 150–1 Plasma expanders, 1147 Plasma thromboplastin antecedent, 186 Plasmin, 272 Platelet disorders, 184 Platelet function inhibitors, 184–5 Platelet-activating factor, 379 nitric oxide synthase phosphorylation, 381 Platelet-derived endothelial cell growth factor, 177 Platelet-derived growth factor, 140, 177 Platelets, 183–5 Pleiotrophin, 177 Poiseuille’s law, 117, 126 Polycythemia vera, 495–6 Popliteal artery anatomy, 356–7 arteriography, 18, 537 balloon angioplasty, 42 distal combined exposure, 363–6 medial approach, 359–60 duplex scanning, 18 embolism, 365 entrapment, 97 exposure of, 356–61, 541 lateral/transfibular, 365–6 medial approach, 357–60, 364–5 posterior approach, 360–1 proximal, medial approach, 357–9 trauma, 434–5 Popliteal bifurcation, 544–6 Popliteal embolectomy, 398–9 Popliteal entrapment, 637–42 diagnosis, 638–41 treatment, 641 variations of, 637 Popliteal vein, valve closure time, 28 Portal hypertension, 1030–43 anatomy and pathophysiology, 1031–2 Budd–Chiari syndrome, 1040 Child–Turcotte–Pugh classification, 1033

in children, 1040–1 complications, 1034–6 acute bleeding, 1035 recurrent bleeding, 1036 variceal bleeding, 1034–5 devascularization and esophageal transection, 1041 etiology, 1032 evaluation of patient, 1032–4 historical aspects, 1030–1 liver transplantation, 1041 MELD score, 1033 radiographic evaluation, 1033–4 surgical techniques, 1036–40 distal splenorenal shunt, 1036–8 mesocaval shunt, 1038–9 portocaval shunts, 1039–40 Portal vein trauma, 432 Portocaval shunt, 1038–40 Post-thrombotic syndrome, 29, 1126 clinical features, 1133 indications for surgery, 1134 investigation, 1133–4 pathophysiology, 1131–3 patient selection, 1134 perforator interruption, 1136–7 saphenectomy, 1136 stent placement, 1134–5 valve reconstruction, 1135–6 venous obstruction, 1134 venous reconstruction, 1131–8 Posterior tibial artery bypass, 573 exposure of, 362–3 Posterior tibial vein, valve closure time, 28 Postoperative surveillance, 617–24 blood flow velocity measurement, 618 Doppler-derived pressure measurements, 617–18 duplex scanning, 618–19 effect of intraoperative modification on long-term results, 622 graft-threatening lesions, 620–1 incidence of postoperative revisions, 621–2 long-term changes in autogenous grafts, 622–3 physical examination, 617 protocol, 620 rationale for, 619–20 Postsympathectomy neuralgia, 656 Poupart’s ligament, 348, 354 Powered phlebectomy, 1068 Preoperative cardiac assessment, 206–12 arteriography, 211 dobutamine stress echocardiography, 210–11 empiric beta blockade, 211–12 radionuclide myocardial imaging, 208–10 radionuclide ventriculography, 208 stress electrocardiography, 207–8 Preoperative pulmonary assessment, 214–15 Pressure, 120–1 Pro-urokinase, 191 Proaccelerin, 186 Proconvertin, 186

Index Profunda femoris artery arteriography, 18, 538 duplex scanning, 18 Profunda femoris vein, valve closure time, 28 Proliferin, 177 Prostacyclin, 140 Prostaglandin E2, 140 Prostaglandins, 378 Prosthetic limbs, 1190–205 anatomic and physiologic considerations, 1194–5 cast design modification, 1196–7 diagnostic socket fitting, 1197–201 dynamic biomechanical alignment, 1201 fabrication and design theory, 1201 finishing, 1201 initial mold, 1195–6 postfitting follow-up, 1201–2 postoperative considerations, 1192 preoperative preparation, 1190–2 stump problems, 1202–4 adherent scar, 1204 back pain and residual limb pain, 1203 neuroma, 1203 sharp bone, 1204 skin grafts, 1204 skin lesions, 1203 stump edema syndrome, 1203 technology, 1204 vocational and avocational adjustment, 1204–5 Prosthetic patch grafts, 232–3 Protein C deficiency, 187 Protein S deficiency, 187 Prothrombin, 186 Proximal arterial lesions atherosclerosis, 961–2 arterial emboli, 962 ergot poisoning, 963 giant cell arteritis, 962 Takayasu’s arteritis, 962 radiation injury, 964–5 thoracic outlet syndrome see Thoracic outlet syndrome Proximal superficial femoral artery, 16 Proximal vertebral artery reconstruction, 839 Pseudomonas aeruginosa, 754 PTFE grafts, 539, 548–9 Pulmonary angiography, 73–5 aortic dissection, 76, 77 findings, 75, 77 indications, 73–4 risks of, 74–5, 76 technique, 75, 76 traumatic aortic injury, 76–7 Pulmonary embolism, 1097–8 differential diagnosis, 76 percutaneous embolectomy, 419 Radial artery exposure, 332, 333, 970 Radiation injury, 853–4, 964–5 Radionuclide myocardial imaging, 208–10 Radionuclide ventriculography, 208

Raynaud’s disease, 493, 915–22 angiography, 920 associated diseases, 917–18 diagnosis, 493, 918–20 digital ulceration and gangrene, 921 epidemiology, 916 pathology, 493 pathophysiology, 916–17 post-traumatic occupational, 494–5 preexisting arterial disease, 494 surgery, 921 treatment, 920–1 vasospasm, 920–1 Raynaud’s syndrome see Raynaud’s disease Reaction-to-injury hypothesis of atherosclerosis, 142–3 Reactive-adaptive remodeling, 164 Rectus abdominis muscle, 348 Reflex sympathetic dystrophy, 986–7 Remote arteriovenous fistula, 594 Renal arteries diagnostic algorithms, 23–5 duplex scanning, 23–6 screening before intervention, 25 stenosis, 25–6, 108 Renal artery aneurysm, 898–9 Renal endarterectomy, 896–7 Renal insufficiency, duplex arteriography in, 46 Renal vascular injuries, 431–2 Rendu–Osler–Weber syndrome, 998 Renin plasma levels, 889–90 renal vein levels, 890 Renovascular hypertension, 887–901 background, 887 clinical diagnosis, 889 endovascular treatment, 892–3 laboratory and radiologic diagnosis, 889–92 captopril renal scintigraphy, 890–1 contrast arteriography, 891–2 duplex ultrasonography, 891 helical (spiral) computed tomography, 891 magnetic resonance angiography, 891 plasma renin levels, 889–90 renal vein renin levels, 890 pathology, 887–8 physiology, 888–9 surgery aortorenal bypass, 894–6 indications for, 893–4 preoperative and intraoperative assessment, 894 renal artery aneurysm repair, 898–9 renal endarterectomy, 896–7 results, 899 spleno- and hepatorenal artery bypasses, 897–8 Response to injury hypothesis, 164 Restenosis, 171 Reteplase, 191, 1087 Retrohepatic vena cava, trauma, 432–3 Retroperitoneal hematoma, 433

1217

Revisions intraoperative, 611–13 postoperative, 621–2 Reynolds number, 119, 123 Rotator cuff tendinitis, 930 St Mary’s boot, 602 Saphenectomy, 1136 Saphenous neuropathy, 554 Saphenous phlebography, 546, 560 Saphenous turndown arteriovenous fistula, 594–5 Saphenous vein bifid, 547 exposure of, 560–1 harvesting of, 541–2 Scalene muscle block, 929–30 Scalenectomy, 953 Scarpa’s fascia, 348 Scarpa’s triangle, 354–5 Scleroderma, 492 Segmental resistance, 125 Self-expanding stents, 260–1 Sequential grafts, 127–8, 129 Seroma, 1025–6 Shear rate, 122–3 Shear stress, 145 Side-to-side anastomosis, 228 Simon nitinol filter, 1101–2 Sinus of Valsalva, aneurysm, 667–8 Small artery bypass, 568–81 arterial incision, 577 arterial occlusion, 576–7 calcified arteries, 577 failed/thrombosed distal bypass, 579–80 failing graft, 579 foot debridements and minor amputations, 577 incisions and approaches, 573–4 indications and contraindications, 572–3 interface with more proximal revascularization procedures, 570–2 limb salvage and palliation, 578 morbidity, 578 mortality, 577 patency of, 578 postoperative follow-up and reintervention, 578–80 reversed vein graft preparation, 576 vascular grafts, 574–6 Small artery nonatherosclerotic disease, 475–98 Small artery thrombosis, 488–90 arterial lesions of undetermined cause, 490 arterial microemboli, 488–90 atheroembolism, 489–90 thromboembolism, 488–9 SMART stent, 261–2 Smoking, as risk factor for abdominal aortic aneurysm, 155, 156, 705 Spinal cord ischemia, 698–700 Splenic artery aneurysm, 902–5 clinical presentation, 903–4 diagnosis, 904 etiology, 902

1218

Index

portal hypertension, 903 pregnancy, 902–3 treatment, 904–5 Splenorenal artery bypass, 897–8 Staphylococcus aureus, 754 Staphylococcus epidermidis, 754 Staphylokinase, 191 Stasis, 1078 Stenosis aortoiliac, 458 carotid artery, 13 iliac artery, 71, 455–6, 458 intracranial artery, 31 renal arteries, 25–6, 108 Stent-graft repair, 688 abdominal aortic aneurysm, 738, 739 results, 692–3 Stents aortoiliac occlusive disease, 527, 528, 531–2 balloon-expandable, 258–60, 527 biologic response to placement, 262 carotid, 827–34 complications, 264–5 contraindications to placement, 263–4 Cragg, 262 femoropopliteal arteries, 267–8 Gianturco Z., 261 Gianturco–Roubin, 260 iliac artery, 265–7 indications for placement, 263 intimal hyperplasia, 173 kissing, 523 Memotherm, 261 Palmaz, 258–9, 523 peripheral arteries, 257–71 peripheral veins, 257–71, 268–9 self-expanding, 260–1, 527 SMART, 261–2 Strecker, 259–60 Symphony, 261 thermal-expanding, 261–2 venous obstruction, 1134–5 Wallstent, 260–1 Wiktor, 260 STILE trial, 273 Strecker stent, 259–60 Streptokinase, 190–1, 272–3, 530 Stress echocardiography, 715–16 Stress electrocardiography, 207–8 String sign, 849 String-of-beads sign, 888 String-of-sausage sign, 877 Stroke acute, 791 established, 793–4 evolution, 791–2 Stuart–Prower factor, 186 Sturge–Weber syndrome, 998 Subarachnoid bleeding, 31 Subclavian aneurysm, 950–1, 967–8 Subclavian artery, 950 exposure of, 322–5, 968–9 left subclavian artery, 315–16, 323–4 with resection of clavicle, 324–5 right subclavian artery, 316–19, 320, 321, 324 variant techniques, 324 extrinsic compression, 950

Subclavian steal syndrome, 31, 249, 308–14 axillary–axillary bypass graft, 310–11, 312 carotid–subclavian bypass, 309–10, 311 clinical background, 308–9 subclavian–subclavian bypass, 311–12, 313, 314 Subclavian vein, 322 obstruction see Venous thoracic outlet syndrome Subclavian–subclavian bypass, 311–12, 313, 314 Subfascial endoscopic perforator surgery, 1068 Superficial artery arteriography, 18 duplex scanning, 18 Superficial femoral artery balloon angioplasty, 42 Doppler ultrasound, 11 IVUS, 53 stenosis, 463, 464 Superficial femoral vein, valve closure time, 28 Superficial femoropopliteal vein replacement, 756–9 Superficial thrombophlebitis, 1073–7 clinical presentation, 1073 diagnosis, 1075 etiology, 1073–4 lesser saphenous, 1074 migratory, 1074 Mondor’s disease, 1074 pathology, 1074 suppurative, 1074 and trauma, 1074 treatment, 1075–7 upper extremity, 1075 with varicose veins, 1074–5 Superficial venous stripping, 1055 Superior mesenteric artery aneurysm, 907–8 Supraclavicular region, 322 Swelling graft arteriovenous fistula, 1024 varicose veins, 1063 Syme’s amputation, 1188–9 Sympathetic regeneration, 656 Symphony stent, 261 Takats, Geza de, 1 Takayasu’s arteritis, 476–80, 844–5, 962 arteriography, 477, 478 clinical course and prognosis, 479–80 clinical manifestations, 476–7 diagnosis, 478–9 Japanese experience, 477–80 pathology, 477, 478 pathophysiology, 478 treatment, 477, 480 Western experience, 476–7 Taylor’s patch, 602 Temporal arteritis, 844 Temporomandibular joint dysfunction, 931 Tendinoplastic amputation, 1177 Tenecteplase, 191

Thermal-expanding stents, 261–2 Thoracic aorta computed tomography, 94–5 magnetic resonance angiography, 106–8 trauma, 426 Thoracic aortic aneurysms, 663–86 aorta, 666–7 aortitis, 665–6 ascending aorta, 668–72 clinical evaluation, 663–5 descending thoracic aorta, 673–5 endovascular repair, 687–94 device selection, 689–90 imaging studies, 689 open surgery, 688 operative approaches and technical considerations, 690–2 patient selection and preoperative assessment, 688–9 results, 692–3 stent–graft, 688 thoracic aortic dissections, 692 infection, 666 natural history, 687–8 sinus of Valsalva, 667–8 thoracoabdominal aorta, 675–83 transverse aortic arch, 672–3 Thoracic aortography, 75–7 indications, 75–6 Thoracic inlet trauma, 428–9 Thoracic outlet syndrome, 924–39, 963–4 anatomy, 924 arterial see Arterial thoracic outlet syndrome computed tomography, 98–9 conservative treatment, 931 diagnostic tests imaging, 929 neurophysiologic tests, 929 scalene muscle block, 929–30 differential diagnosis angina pectoris, 931 brachial plexus injury, 930 carpal/cubital tunnel syndromes, 930 cervical spine disease, 930 fibromyalgia, 930 pectoralis minor syndrome, 931 rotator cuff and biceps tendinitis, 930 temporomandibular joint dysfunction, 931 etiology, 925–7 historical aspects, 924 neurogenic, arterial and venous, 924–5 pathophysiology, 938 patient history, 927 persistence, recurrence and reoperation, 937–8 physical examination, 928–9 results of treatment, 937 surgery, 931–7 anterior and middle total scalenectomy, 932–5 cervical rib excision, 935 complications, 936–7 postoperative care, 936

Index supraclavicular first-rib resection, 935 transaxillary first-rib resection, 935–6 symptoms, 927–8 venous see Venous thoracic outlet syndrome Thoracoabdominal aortic aneurysms, 675–83, 695–702 complications, 698–700 bleeding and coagulopathy, 700 cardiac morbidity, 700 pulmonary, 700 renal insufficiency, 700 spinal cord ischemia, 698–700 diagnosis, 696–7 endovascular approach, 700–1 epidemiology, 695 etiology, 695 natural history, 695–6 operative management, 698 perioperative care, 698 preoperative evaluation, 697–8 Thoracoscopic sympathectomy, 981–8 anesthetic management, 983 complications, 982–3 indications and contraindications, 982 preoperative preparation, 983 requirements for success, 982 results, 985–7 connective tissue disorders, 987 hyperhidrosis, 986 nonreconstructible peripheral vascular disease and vasospastic disorders, 987 reflex sympathetic dystrophy and causalgia, 986–7 surgical technique, 983–5 Three-dimensional computed tomography, 92–3 Three-dimensional IVUS imaging, 52–3, 56 Thrombectomy, 42 Thrombin, 377 inhibition, 188–90 Thromboangiitis obliterans (Buerger’s disease), 480–7, 918, 965–6 arteriography, 485, 486 clinical course and prognosis, 487 diagnosis, 482–3, 486–7 etiology, 485 Japanese experience, 484–7 occlusive sites, 486 pathology, 485 pathophysiology, 485–6 prognosis, 483 symptoms, 486 treatment, 483–4, 487 Western experience, 480–4 Thromboembolectomy see Embolectomy Thromboemboli, 417 Thromboendarterectomy, 238, 242, 868–9 Thrombogenesis, 183–5 hemostasis, 183 platelets, 183–5 see also Coagulation

Thrombolysis, 190–3, 530 activators, 190–1 arterial, 273–7 clinical, 192–3 hyperfibrinolysis, 191–2 inhibitors, 191 physiology, 190 venous, 277–82 Thrombolytic therapy, 272–3 arterial thrombolysis, 273–5 see also individual drugs Thrombophlebitis, 26 Thromboxane A2, 378 Through-the-knee amputation, 1184 TIA see Transient ischemic attack Tibial artery bypass see Small artery bypass trauma, 434–5 Tibioperoneal artery balloon angioplasty, 42 bypass, 573 stenosis, 464, 466, 472, 473 Ticlopidine, 185 Tinel’s sign, 929 Tinzaparin, 1085 Tissue plasminogen activator, 191, 273, 530 Tissue thromboplastin, 186 Titanium Greenfield filter, 1102 TOPAS trial, 273 Tourniquet tests, 1064–5 Transcranial Doppler ultrasound, 29–31 clinical applications, 31–2 examination method, 30 study parameters, 30–1 Transfection, 179 Transfemoral amputation, 1184 Transforming growth factors, 177 Transient ischemic attacks, 139 Transtibial amputation, 1184–8 plaster cast, 1185–6 supracondylar suspension cuff, 1186–8 suspension stockinette, 1186 tube/prosthetic socks, 1185 Transversalis fascia, 349 Transversus muscle, 348 Trendelenburg test, 1064 Triple crush syndrome, 930 Tumor necrosis factor-alpha, 177 Ulnar artery, exposure of, 332, 333, 970 Ultrasound, 50–60 abdominal aortic aneurysm, 708–9 acute deep venous thrombosis, 26–7 as adjunct to endovascular interventions, 56–8 atherosclerosis, 53, 55 carotid artery, 11 catheter design, 50–2 common femoral artery, 51 computerized three-dimensional image reconstruction, 52–3 development of applications, 58–9 disease distribution and characterization, 54–6 forward-looking, 53, 54 iliac artery, 55 superficial femoral artery, 53 techniques, 53–4

1219

three-dimensional imaging, 52–3, 56 see also Doppler ultrasound; Duplex scanning Upper extremity arterial surgery, 958–73 deep venous thrombosis, 278, 1091–6 combined with lower extremity DVT, 1094–5 hypercoagulable states, 1093–4 placement of superior vena cava filters, 1092–3 embolectomy, 400–2 ischemic thrombosis, 1141–2 superficial thrombophlebitis, 1075 vasospastic diseases, 915–23 see also Hand Upper thoracic sympathectomy, 974–80 indications for, 974 neuroanatomy, 974 operative techniques, 974–7 anterior transthoracic upper dorsal sympathectomy, 976–7 supraclavicular approach, 975–6 transaxillary approach, 977 pitfalls and complications, 977–80 postsympathectomy neuralgia, 977–8 regeneration of sympathetic activity, 978–80 return of sympathetic activity, 978 sudomotor changes, 978 postoperative care, 977 Urokinase, 191, 273, 530 Valve function, 27–9 Valve incompetence, 1054–5 Valve reconstruction, 1135–6 Valvuloplasty, 1135 Variceal bleeding, 1034–6 Varicose veins, 29, 1058–72 anatomy, 1059–61 classification, 1065 clinical presentation, 1062 imaging studies, 1065 nonsurgical treatment, 1066 pathophysiology, 1058–9 perforating veins, 1061–2 physical examination, 1063–4 and superficial thrombophlebitis, 1074–5 surgical treatment, 1066–9 endovenous obliteration, 1068 exposure of great saphenous vein, 1066–8 operative procedure, 1066 perforate-invaginate stripping, 1068–9 powered phlebectomy, 1068 results, 1069–70 subfascial endoscopic perforator surgery, 1068 symptoms cutaneous manifestations, 1063 leg pain, 1063 swelling, 1063 venous dilation, 1062–3 tourniquet tests, 1064–5

1220

Index

Vascular access surgery, 292–5 Vascular anastomoses, 226–30 end-to-end, 226–8, 423 end-to-side, 228 everting suture technique, 228–30 side-to-side, 228 Vascular disease, 117–36 arterial stenoses, 119–25 bypass grafts, 125–33 normal blood flow, 117–19 Vascular endothelial growth factor, 177–8 clinical trials, 179–80 Vascular grafts, 423–4 Vascular malformations, 997–1014 arteriovenous shunting, 999–1010 classifications, 997–9 see also Arteriovenous fistulas Vascular resistance, 118–19 Vascular trauma, 421–36 abdomen, 429–30 aortic cross-clamping, 429 exposure, 430 laparotomy and initial control, 429 chest, 426–9 blunt aortic injury, 426 diagnosis, 426–7 management options, 427–8 positioning and choice of incision, 426 thoracic inlet, 428–9 complex groin injuries, 434 damage control, 422 fasciotomy, 435 iliac vessels, 430–1 initial exposure and control, 421–2 injury assessment, 422 mesenteric and portal injuries, 432 neck, 424–6 carotid artery trauma, 424–6 vertebral artery trauma, 426 patient assessment, 422 peripheral vascular trauma, 433–4 popliteal and tibial vascular injuries, 434–5 primary amputation, 435 renal vascular injuries, 431–2 repair techniques end-to-end anastomosis, 423 lateral repair, 423 ligation, 423 temporary intraluminal shunts, 423 vascular grafts, 423–4 retrohepatic vena cava, 432–3 retroperitoneal hematoma, 433 Vasculogenesis, 176–7 Vasospasm, 920–1 Vasospastic diseases, 493–4, 987 acrocyanosis, 493 frostbite, 494 livedo reticularis, 493–4 Raynaud’s disease, 493, 915–22 upper extremity, 915–23 VCAM-1, 147 Vein cuffs and patches, 600–5 distal vein patch, 603 mechanism of action, 601 Miller’s cuff, 602

results, 604 St Mary’s boot, 602 Taylor’s patch, 602 Vein grafts, 20–1, 127, 128 Vein mapping, 19 Vein patch grafts, 232 Vein wall injury, 1078–80 Velocity, 121, 122 Vena cava, computed tomography, 98 Vena cava filters, 1092–3 bird’s nest filter, 1100 Cordis TrapEase filter, 1102–3 Greenfield, 1099–100 optional, 1103 percutaneous stainless-steel Greenfield filter, 1102 Simon nitinol filter, 1101–2 titanium Greenfield filter, 1102 Vena Tech filter, 1101 Vena Tech filter, 1101 Venography, 942 Venous claudication, 29 Venous insufficiency, 1047–57 background, 1047–8 CEAP classification, 1048 diagnostic approach, 1048 duplex assessment of venous reflux, 1048–9 duplex testing patterns of venous reflux, 1054 validation, 1053–4 hemodynamic testing, 1055–6 proximal reflux, 1055 reflux examination, 1049–53 examination protocol, 1050–3 examination stand, 1049–50 office practice, 1053 quantitative measurement of venous reflux, 1049 superficial venous stripping, 1055 valve incompetence, 1054–5 see also Varicose veins Venous interruption, 1097–105 bird’s nest filter, 1100 complications of venous thrombosis and prophylaxis, 1097–8 Cordis TrapEase filter, 1102–3 Greenfield vena cava filter, 1099–100 historical aspects, 1098–9 indications for mechanical protection, 1099 optional vena caval filters, 1103 percutaneous stainless-steel Greenfield filter, 1102 preplacement assessment, 1099 pulmonary embolism, 1097–8 Simon nitinol filter, 1101–2 titanium Greenfield filter, 1102 vena tech filter, 1101 Venous obstruction, 1165 Venous pressure, 942–3 Venous reflux duplex scanning, 1048–9 patterns of, 1054 validation of, 1053–4 examination protocol, 1050–3 examination stand, 1049–50 limb diameter, 1052 office practice, 1053

proximal, 1055 quantitative measurement, 1049 superficial venous stripping, 1055 Venous thoracic outlet syndrome, 940–8 anatomy and etiology, 941 classification, 940–1 clinical manifestations physical findings, 942 side and gender, 941 symptoms, 942 diagnosis duplex scanning, 943 magnetic resonance angiography, 943 venography, 942 venous pressure, 942–3 treatment, 943–7 acute thrombus, 944 contralateral side, 948 extrinsic pressure, 944–6 intrinsic defect, 946–7 results, 947 Venous thrombectomy, 415, 1106–14, 1147–8 contemporary results, 1108–9 historical aspects, 1107–8 operative care, 1111–13 postoperative care, 1113 preoperative care, 1109–11 Venous thrombolysis, 277–82 lower extremity DVT, 278–9 mesenteric venous thrombosis, 279–82 upper extremity DVT, 279 Venous thrombosis see Deep venous thrombosis; Ischemic venous thrombosis Vertebral artery lesions of, 790 pathology, 836–7 trauma, 426 Vertebrobasilar disease, 835–42 embolic mechanism, 835–6 hemodynamic mechanism, 835 mixed etiology, 836–42 outcome of treatment, 841–2 pathology of vertebral artery, 836–7 reconstruction of distal vertebral artery, 840 reconstruction of proximal vertebral artery, 839 suboccipital approach, 840–1 surgical management, 838–9 vertebrobasilar ischemia, 837–8 Vertebrobasilar ischemia, 837–8 Vertebrobasilar system, 304–7 anatomy, 304–5 exposure, 305–7 Virchow, Rudolf, 138 Visceral arteries duplex scanning, 21–3, 615 embolic occlusion, 862 mesenteric circulation, 21–2 thrombotic occlusion, 862–3 Visceral artery aneurysm, 902–12 celiac artery, 908–10 gastric/gastroepiploic artery, 910–11

Index gastroduodenal, 910 hepatic artery, 905–7 pancreaticoduodenal, 910 splenic artery, 902–5 superior mesenteric artery, 907–8 Visceral artery surgery, 861–74 endoluminal therapy, 871–2 history, 862–3 reconstructive techniques, 868– 70 results and complications, 870

transabdominal exposure, 866–7 transabdominal exposure of mesenteric arteries, 867–8 Visceral ischemia, 862–4 Vital capacity, 214 Vitamin E deficiency, and abdominal aortic aneurysm, 202 Volkmann contracture, 437 Von Hippel–Lindau syndrome, 998 von Willebrand factor, 186

1221

Wall shear stress, 165–6 subnormal, and intimal hyperplasia, 171–3 Wall tensile stress, 166–7 Wallstent, 260–1 Warfarin, 189 skin necrosis and venous gangrene, 1145–6 White-clot syndrome, 1087–8 Wiktor stent, 260 Winslow’s anastomotic system, 459