Vascular and Endovascular Surgery: A Comprehensive Review, Textbook with CD-ROM

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Vascular and Endovascular Surgery

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SEVENTH EDITION

Vascular and Endovascular Surgery: A Comprehensive Review Wesley S. Moore, MD Professor and Chief Emeritus David Geffen School of Medicine University of California, Los Angeles Vascular Surgeon University of California, Los Angeles, Center for the Health Sciences Los Angeles, California

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VASCULAR AND ENDOVASCULAR SURGERY: A COMPREHENSIVE REVIEW Copyright  2006, 2002, 1998, 1993, 1991, 1986, 1983 by Elsevier Inc.

ISBN 13: 978-1-4160-0183-6 ISBN 10: 1-4160-0183-2

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the Publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to checck the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relaying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Authors assume any liability for any injury and/or damage to persons or porperty arising out or related to any use of the material contained in this book. The Publisher

Library of Congress Cataloging-in-Publication Data Vascular and endovascular surgery: a comprehensive review / [edited by] Wesley S. Moore.–7th ed. p. ; cm. Rev. ed. of: Vascular surgery. 6th ed. c2002. Includes bibliographical references and index. ISBN 1-4160-0183-2 1. Blood-vessels–Surgery. I. Moore, Wesley S. II. Vascular surgery. [DNLM: 1. Vascular Surgical Procedures. 2. Vascular Diseases–surgery. WG 170 V3283 2006] RD598.5.V374 2006 617.4′13–dc22

Acquisitions Editor: Judith Fletcher Developmental Editor: Denise LeMelledo Publishing Services Manager: Tina Rebane Senior Project Manager: Amy Norwitz Interior Design Direction: Steven Stave Cover Designer: Steven Stave

Printed in the United States of America Last digit is the print number:

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The seventh edition of this book is dedicated to the next generation of vascular surgeons. The effort that has gone into this book by the editor and chapter contributors is directed primarily to the education of our trainees. The future of our specialty will be in their capable hands.

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Contributors William A. Abbott, MD Professor of Surgery Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Vascular Grafts: Characteristics and Rational Selection Samuel S. Ahn, MD Professor of Surgery and Director of Endovascular Surgery David Geffen School of Medicine University of California, Los Angeles Attending Surgeon University of California, Los Angeles, Medical Center Los Angeles, California Thoracic Outlet Syndrome and Vascular Disease of the Upper Extremity George Andros, MD Assistant Clinical Professor of Vascular Surgery University of Southern California Los Angeles, California Director, Vascular Laboratory Providence St. Joseph Medical Center Burbank, California Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters Niren Angle, MD, RVT Assistant Professor of Surgery In Residence University of California, San Diego, School of Medicine Attending Vascular Surgeon University of California, San Diego, Medical Center San Diego, California Thrombolytic Therapy for Vascular Disease Acute Arterial and Graft Occlusion Prosthetic Graft Infections J. Dennis Baker, MD Division of Vascular Surgery David Geffen School of Medicine University of California, Los Angeles Gonda (Goldschmied) Vascular Center Los Angeles, California The Noninvasive Vascular Laboratory

Jeffrey L. Ballard, MD Clinical Professor of Surgery University of California, Irvine School of Medicine Staff Vascular Surgeon St. Joseph Hospital Orange, California Anatomy and Surgical Exposure of the Vascular System Wiley F. Barker, MD Professor Emeritus (Surgery/Vascular Surgery) University of California, Los Angeles Los Angeles, California A History of Vascular Surgery Michael Belkin, MD Division of Vascular Surgery Brigham & Women’s Hospital Boston, Massachusetts Aortoiliac Occlusive Disease Robert S. Bennion, MD Professor of Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California Attending Surgeon Los Angeles County Olive View Medical Center Sylmar, California Hemodialysis and Vascular Access John Bergan, MD Professor of Surgery University of California, San Diego, School of Medicine San Diego, California Staff Surgeon Scripps Memorial Hospital La Jolla, California Varicose Veins: Chronic Venous Insufficiency Ramon Berguer, MD, PhD Professor and Chief Frankel Professor of Vascular Surgery University of Michigan Medical Center Ann Arbor, Michigan Surgical Reconstruction of the Supra-aortic Trunks and Vertebral Arteries vii

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Contributors

Frederic S. Bongard, MD Chief, Division of Trauma and Critical Care University of California, Los Angeles, Harbor View Medical Center Torrance, California Vascular Trauma Ruth L. Bush, MD Assistant Professor Division of Vascular Surgery and Endovascular Therapy Michael E. DeBakey Department of Surgery Baylor College of Medicine Assistant Professor Department of Vascular Surgery Michael E. DeBakey Veterans Affairs Medical Center Houston, Texas Angioplasty and Stenting for Aortoiliac Disease: Technique and Results Michael T. Caps, MD, MPH Division of Vascular Therapy Hawaii Permanente Medical Group Honolulu, Hawaii Angioplasty and Stenting for Infrainguinal Disease: Technique and Results Deborah R. Caswell, RN, ANP Director, Gonda Wound Care Center David Geffen School of Medicine University of California, Los Angeles Los Angeles, California The Wound Care Center and Limb Salvage Alexander W. Clowes, MD Professor of Surgery University of Washington School of Medicine Seattle, Washington Anatomy, Physiology, and Pharmacology of the Vascular Wall Sheila M. Coogan, MD Assistant Professor of Surgery Stanford University School of Medicine Chief, Vascular and Endovascular Surgery Palo Alto VA Hospital Palo Alto, California Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters Richard H. Dean, MD Professor of Surgery Wake Forest University School of Medicine President and CEO Wake Forest University Health Sciences Winston-Salem, North Carolina Management of Renovascular Disease

Ralph G. DePalma, MD Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland Consultant in Surgery National Director of Surgery Department of Veterans Affairs District of Columbia Veterans Affairs Medical Center Washington, DC Atherosclerosis: Pathology, Pathogenesis, and Medical Management Vasculogenic Erectile Dysfunction Magruder C. Donaldson, MD Associate Professor of Surgery Harvard Medical School Staff, Brigham and Women’s Hospital Boston, Massachusetts Aortoiliac Occlusive Disease James M. Edwards, MD Associate Professor of Surgery Division of Vascular Surgery Oregon Health and Science University Chief of Surgery Portland Veterans Administration Medical Center Portland, Oregon Nonatherosclerotic Vascular Disease Cindy L. Felty, RN, MSN, CNP, FCCWS Assistant Professor of Medicine Mayo Clinic College of Medicine Director, Vascular Ulcer/Wound Healing Clinic Vascular Center Mayo Clinic Rochester, Minnesota Lymphedema D. Preston Flanigan, MD Clinical Professor of Surgery University of California, Irvine School of Medicine Medical Director St. Joseph’s Hospital Vascular Institute Orange, California Aneurysms of the Peripheral Arteries Julie A. Freischlag, MD William Stewart Halsted Professor and Chairman of Surgery Johns Hopkins School of Medicine Surgeon-in-Chief The Johns Hopkins Hospital Baltimore, Maryland Prosthetic Graft Infections Brian Funaki, MD Associate Professor of Radiology Section Chief, Angiography and Interventional Radiology University of Chicago Pritzker School of Medicine Chicago, Illinois Visceral Ischemic Syndromes

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Contributors

Hugh A. Gelabert, MD Professor of Surgery David Geffen School of Medicine University of California, Los Angeles Attending Staff University of California, Los Angeles, Medical Center Los Angeles, California Primary Arterial Infections and Antibiotic Prophylaxis Portal Hypertension Bruce L. Gewertz, MD Dallas B. Phemister Professor and Chairman, Department of Surgery University of Chicago Pritzker School of Medicine Chief, Section of Vascular Surgery University of Chicago Medical Center Chicago, Illinois Visceral Ischemic Syndromes Peter Gloviczki, MD Professor of Surgery Mayo Clinic College of Medicine Chair, Division of Vascular Surgery Director, Gonda Vascular Center Mayo Clinic Rochester, Minnesota Vascular Malformations Thoracic and Lumbar Sympathectomy: Indications, Technique, and Results Jerry Goldstone, MD Professor of Surgery Case School of Medicine Case Western Reserve University Chief, Division of Vascular Surgery University Hospitals of Cleveland Cleveland, Ohio Aneurysms of the Aorta and Iliac Arteries Antoinette S. Gomes, MD Professor of Radiological Sciences and Medicine Department of Radiological Sciences David Geffen School of Medicine University of California, Los Angeles Los Angeles, California Principles of Imaging in Vascular Disease Carlos Gracia, MD Associate Professor of Surgery Chief of Minimally Invasive Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California Laparoscopic Aortic Surgery for Aneurysms and Occlusive Disease: Technique and Results Lazar J. Greenfield, MD Professor of Surgery Chair, Emeritus University of Michigan Medical School Ann Arbor, Michigan Venous Thromboembolic Disease

ix

Kimberley J. Hansen, MD Professor of Surgery Head, Section on Vascular Surgery Wake Forest University School of Medicine Winston-Salem, North Carolina Management of Renovascular Disease Paul B. Haser, MD Clinical Assistant Professor of Surgery University of Medicine and Dentistry of New Jersey Medical School Newark, New Jersey Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters Kim J. Hodgson, MD Professor and Chairman, Division of Vascular Surgery Southern Illinois University School of Medicine Springfield, Illinois Endovascular Treatment of Renovascular Disease Larry H. Hollier, MD Professor of Surgery and Dean Louisiana State University School of Medicine New Orleans, Louisiana Thoracoabdominal Aortic Aneurysms Douglas B. Hood, MD Assistant Professor of Surgery and Radiology Keck School of Medicine University of Southern California Los Angeles, California Endovascular Treatment of Renovascular Disease Glenn C. Hunter, MD Professor of Surgery Chief of Vascular Surgery University of Texas Medical Branch Galveston, Texas Noninfectious Complications in Vascular Surgery Ted R. Kohler, MD, MSc Professor of Surgery University of Washington School of Medicine Chief, Peripheral Vascular Surgery Puget Sound Healthcare System Seattle, Washington Anatomy, Physiology, and Pharmacology of the Vascular Wall Myointimal Hyperplasia Toshifumi Kudo, MD, PhD Endovascular Research Fellow Division of Vascular Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California Thoracic Outlet Syndrome and Vascular Disease of the Upper Extremity

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Contributors

Gregory J. Landry, MD Associate Professor of Surgery Division of Vascular Surgery Dotter Interventional Institute Oregon Health and Science University Portland, Oregon Nonatherosclerotic Vascular Disease Natural History and Nonoperative Treatment of Chronic Lower Extremity Ischemia Peter F. Lawrence, MD Bergman Professor and Chief of Vascular Surgery David Geffen School of Medicine University of California, Los Angeles Director, Gonda (Goldschmied) Vascular Center Los Angeles, California The Wound Care Center and Limb Salvage Timothy K. Liem, MD Associate Professor of Surgery Oregon Health and Science University Attending Surgeon Oregon Health Science University Legacy Emanuel Hospital Portland, Oregon Hemostasis and Thrombosis Peter H. Lin, MD Assistant Professor Division of Vascular Surgery and Endovascular Therapy Michael E. DeBakey Department of Surgery Baylor College of Medicine Assistant Professor Department of Vascular Surgery Michael E. DeBakey Veterans Affairs Medical Center Houston, Texas Angioplasty and Stenting for Aortoiliac Disease: Technique and Results Evan C. Lipsitz, MD Associate Professor of Surgery Albert Einstein College of Medicine of Yeshiva University Attending Physician Montefiore Medical Center Bronx, New York Femoral, Popliteal, and Tibial Occlusive Disease G. Matthew Longo, MD Assistant Professor of Vascular Surgery University of Nebraska Medical Center Omaha, Nebraska Endovascular Repair of Abdominal Aortic Aneurysms: Technique and Results Alan B. Lumsden, MD Professor and Division Chief Division of Vascular and Endovascular Therapy Michael E. DeBakey Department of Surgery Baylor College of Medicine Professor and Chief of Division of Vascular Surgery Department of Vascular Surgery Michael E. DeBakey Veterans Affairs Medical Center Houston, Texas Angioplasty and Stenting for Aortoiliac Disease: Technique and Results

James M. Malone, MD Clinical Professor of Surgery University of Arizona College of Medicine Tucson, Arizona Chief of Vascular Services Scottsdale Healthcare-Shea Scottsdale, Arizona Lower Extremity Amputation John A. Mannick, MD Professor of Surgery Harvard Medical School Staff, Brigham and Women’s Hospital Boston, Massachusetts Aortoiliac Occlusive Disease Jon S. Matsumura, MD Associate Professor of Surgery Feinberg School of Medicine Northwestern University Attending, Northwestern Memorial Hospital Chicago, Illinois Endovascular Repair of Abdominal Aortic Aneurysms: Technique and Results David S. Maxwell*, MD Formerly, Professor of Anatomy and Cell Biology David Geffen School of Medicine University of California, Los Angeles Formerly, Professor of Surgery and Anatomy Charles Drew Medical School Los Angeles, California Embryology of the Vascular System James F. McKinsey, MD Associate Professor of Clinical Surgery Columbia University College of Physicians and Surgeons Adjunct Associate Professor Weill Medical College of Cornell University Site Chief, Division of Vascular Surgery Columbia University Medical Center Assistant Attending Surgeon New York-Presbyterian Hospital New York, New York Visceral Ischemic Syndromes Louis M. Messina, MD Professor of Surgery and Chief Division of Vascular Surgery University of California, San Francisco Moffitt Hospital San Francisco, California Splanchnic and Renal Artery Aneurysms Erica L. Mitchell, MD University of Colorado Health Sciences Center Division of Vascular and Interventional Radiology Denver, Colorado Hemostasis and Thrombosis Natural History and Nonoperative Treatment of Chronic Lower Extremity Ischemia *Deceased

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Contributors

Gregory L. Moneta, MD Professor of Surgery and Chief of Vascular Surgery Oregon Health Sciences University Portland, Oregon Natural History and Nonoperative Treatment of Chronic Lower Extremity Ischemia

Charles M. Peterson, MD, MBA Director, Division of Blood Diseases and Resources National Heart, Lung, and Blood Institute National Institutes of Health Bethesda, Maryland Influence of Diabetes Mellitus on Vascular Disease and Its Complications

Wesley S. Moore, MD Professor and Chief Emeritus David Geffen School of Medicine University of California, Los Angeles Vascular Surgeon University of California, Los Angeles, Center for the Health Sciences Los Angeles, California Extracranial Cerebrovascular Disease: The Carotid Artery Myointimal Hyperplasia

K. Todd Piercy, MD Vascular Fellow Wake Forest University School of Medicine Winston-Salem, North Carolina Management of Renovascular Disease

Matthew M. Nalbandian, MD Assistant Professor of Surgery New York University School of Medicine Chief, Vascular and Endovascular Surgery Bellevue Hospital Center New York, New York Spine Exposure: Operative Techniques for the Vascular Surgeon Mark R. Nehler, MD Vascular Surgery Section Denver, Colorado Natural History and Nonoperative Treatment of Chronic Lower Extremity Ischemia Takao Ohki, MD, PhD Associate Professor of Surgery Albert Einstein College of Medicine of Yeshiva University Chief, Division of Vascular and Endovascular Surgery Montefiore Medical Center Bronx, New York Technique of Carotid Angioplasty and Stenting Luigi Pascarella, MD Postdoctorate Researcher Department of Bioengineering Clinical Instructor Department of Surgery University of California, San Diego San Diego, California Varicose Veins: Chronic Venous Insufficiency Malcolm O. Perry, MD Professor Emeritus, Vascular Surgery University of Texas Southwestern Medical School Chairman, Department of Surgery St. Paul Medical Center Dallas, Texas Vascular Trauma

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William J. Quiñones-Baldrich, MD Professor of Surgery David Geffen School of Medicine University of California, Los Angeles Attending Vascular Surgeon University of California, Los Angeles, Center for Health Sciences Los Angeles, California Thrombolytic Therapy for Vascular Disease Acute Arterial and Graft Occlusion Todd D. Reil, MD Assistant Professor of Surgery Division of Vascular Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California Pharmacology of Drugs Used in the Management of Vascular Disease David A. Rigberg, MD Assistant Professor of Surgery David Geffen School of Medicine University of California, Los Angeles Gonda (Goldschmied) Vascular Center Los Angeles, California Portal Hypertension Thom W. Rooke, MD Krehbiel Professor of Vascular Medicine Mayo Clinic College of Medicine Head, Section of Vascular Medicine Mayo Clinic Rochester, Minnesota Lymphedema Stephanie S. Saltzberg, MD Assistant Professor of Surgery New York University School of Medicine New York, New York Spine Exposure: Operative Techniques for the Vascular Surgeon Peter A. Schneider, MD Hawaii Permanente Medical Group Honolulu, Hawaii Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters Angioplasty and Stenting for Infrainguinal Disease: Technique and Results

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Contributors

Lewis B. Schwartz, MD Lecturer University of Chicago Pritzker School of Medicine Chicago, Illinois Divisional Vice President Drug Fluting Stent Program Abbott Laboratories Abbott Park, Illinois Visceral Ischemic Syndromes

Frank J. Veith, MD Professor of Surgery Albert Einstein College of Medicine of Yeshiva University William von Lebig Chair Attending Physician Vice Chairman, Department of Surgery Montefiore Medical Center Bronx, New York Femoral, Popliteal, and Tibial Occlusive Disease

Roger F. J. Shepherd, MB, BCh Assistant Professor of Medicine Mayo Clinic College of Medicine Rochester, Minnesota Lymphedema

Alex Westerband, MD Surgeon St. Mary’s Hospital Tucson, Arizona Noninfectious Complications in Vascular Surgery

Michael B. Silva, Jr., MD Texas Tech University Health Sciences Center Lubbock, Texas Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters James C. Stanley, MD Professor of Surgery Section of Vascular Surgery University of Michigan Director of Vascular Surgery Cardiovascular Center University of Michigan Hospital Ann Arbor, Michigan Splanchnic and Renal Artery Aneurysms Michael C. Stoner, MD Brody School of Medicine at East Carolina University Division of Vascular Surgery Greenville, North Carolina Vascular Grafts: Characteristics and Rational Selection D. Eugene Strandness, Jr., MD* Formerly, Professor of Surgery University of Washington School of Medicine Seattle, Washington Hemodynamics for the Vascular Surgeon Carlos H. Timaran, MD Assistant Professor of Surgery University of Texas, Southwestern Medical Center Dallas, Texas Technique of Carotid Angioplasty and Stenting

*Deceased

Anthony D. Whittemore, MD Professor of Surgery Harvard Medical School Chief of Vascular Surgery Brigham and Women’s Hospital Boston, Massachusetts Aortoiliac Occlusive Disease Samuel E. Wilson, MD Professor of Surgery University of California, Irvine Irvine, California Attending Surgeon University of California, Irvine, Medical Center Orange, California Hemodialysis and Vascular Access Jay Yadav, MD Director, Vascular Intervention The Cleveland Clinic Foundation Cleveland, Ohio Technique of Carotid Angioplasty and Stenting Gerald B. Zelenock, MD Director, Surgical Services William Beaumont Hospital Royal Oak, Michigan Splanchnic and Renal Artery Aneurysms R. Eugene Zierler, MD Professor of Surgery University of Washington School of Medicine Medical Director, Vascular Diagnostic Service University of Washington Medical Center Seattle, Washington Hemodynamics for the Vascular Surgeon

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Preface to the Seventh Edition The seventh edition has been completely revised, beginning with its title. In recognition of the increasing role of endovascular surgery in our specialty, the title has been revised to VASCULAR AND ENDOVASCULAR SURGERY: A COMPREHENSIVE REVIEW. The signature chapters remain, and the authors fully updated their material. The increasing use of drugs in the management of our patients is recognized by a chapter entitled “Pharmacology of Drugs Used in the Management of Vascular Disease.” New material covering endovascular surgery includes a chapter on arterial access, guidewires, catheters, sheaths, angioplasty catheters, and stents. Specific anatomic regions with attention to the technical considerations and results of endovascular techniques are included in chapters addressing aortoiliac disease, mesenteric and renal disease, infrainguinal disease, and cerebrovascular disease. A new chapter on stent grafting

for aneurysms of the abdominal aorta brings us up to date on the various devices currently available as well as comparative techniques and results. We have added a new chapter that addresses the emerging field of laparoscopic aortic surgery. A new chapter has been included on wound care, with specific emphasis on limb salvage. Additionally, a new chapter has been included addressing the vascular surgeon’s role in spine exposure. Finally, with this new edition comes a DVD-ROM containing video clips of key procedures, case studies and questions and answers (also found in the book) for review and assessment, and references linked to PubMed abstracts. In summary, we now have a completely revised and up-todate volume directed to the comprehensive management of patients with vascular disorders. Wesley S. Moore, MD

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Preface to the First Edition During the past 20 years of rapid growth and development in vascular surgery, many graduates of general surgery programs found that their training in vascular surgery represented a valuable new resource for their hospital and practice communities. That training in vascular surgery often provided an important edge in establishing a new practice and led to the widespread use of the term general and vascular surgery on the community announcements and business cards of new surgeons. Yet in 1969, a survey conducted by a committee composed of James A. DeWeese, F. William Blaisdell, and John H. Foster discovered that among the 83 residents graduating from the 22 general surgery training programs surveyed, only 19 had performed more than 40 arterial reconstructive procedures during the course of their training, and more than half of the graduating residents had performed fewer than 20 arterial reconstructive procedures. The DeWeese committee, which had been established in 1969 to develop a document on optimal resources in vascular surgery, thus concluded that there was considerable suboptimal vascular surgery being performed in the United States, owing to a combination of both inadequate training and continued deficiencies in vascular surgery experience following training. A survey of the frequency of vascular operations in 1143 hospitals across the United States had revealed that in over 75% of these hospitals, fewer than 10 aneurysm resections and 10 femoropopliteal arterial reconstruction were conducted annually. This discovery led to the unfortunate conclusion that many surgeons were performing only occasional vascular operations, often leading to poor results. The substance of the DeWeese report was reviewed by the two national vascular societies and their responsible leadership. This paved the way for, among other things, the definition of adequate training in vascular surgery and the recommendation that physicians who wish to practice vascular surgery spend an additional year of training to guarantee adequate experience in the speciality. To ensure prospective candidates that a given fellowship program in vascular surgery would provide a broad and responsible experience, the vascular societies established a committee for program evaluation and endorsements from which program directors could request review. Programs reviewed and found

to meet the criteria of appropriate education as established by the committee would be announced annually. Program evaluation by the joint council of the two national vascular societies was taken on as a temporary responsibility because the role would ultimately become the purview of the Residency Review Committee and the Liaison Committee for Graduate Medical Education. It was recognized that once adequate training programs were developed, the certification of candidates successfully completing training rested with the American Board of Surgery. After approximately 10 years of experience, debate, and review, the American Board of Medical Specialties approved an application by the American Board of Surgery to grant “Certification of Special Competence in General Vascular Surgery.” The first examination for certification was given to qualified members of the American Board of Surgery and Thoracic Surgery in June 1982. The second written examination was held in November 1983 in several centers across the United States. The intent of this textbook is to provide a comprehensive review of vascular surgery, together with the related medical and basic science disciplines. This edition of the text has been developed to accompany a postgraduate course designed to help candidates prepare for the examination leading to certification in general vascular surgery. Accordingly, a list of questions designed to aid the reader in self-examination completes each chapter. All question sets simply represent the authors’ opinion, a fair and adequate survey of the material covered, as none of the chapter authors is a member of the American Board of Surgery (this would be a conflict of interest). Although chapter outlines were suggested by an editorial committee, the final chapter test represents, in the opinion of its authors, core material in each subject. Particular effort to identify and separate generally accepted concepts from new or controversial material was made. Although this book was designed as a comprehensive review to prepare for an examination, it is also in view of its organization and content, a comprehensive text of vascular surgery. Wesley S. Moore, MD

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Contents

1

A History of Vascular Surgery, 1

14

Wiley F. Barker

2

Embryology of the Vascular System, 21

J. Dennis Baker

15

David S. Maxwell*

3

Natural History and Nonoperative Treatment of Chronic Lower Extremity Ischemia, 263 Gregory L. Moneta • Erica L. Mitchell • Gregory J. Landry

Anatomy, Physiology, and Pharmacology of the Vascular Wall, 36 Alexander W. Clowes • Ted R. Kohler

The Noninvasive Vascular Laboratory, 247

16

Principles of Imaging in Vascular Disease, 280 Antoinette S. Gomes

4

Anatomy and Surgical Exposure of the Vascular System, 46 Jeffrey L. Ballard

5

17

Hemostasis and Thrombosis, 69

George Andros • Michael B. Silva, Jr. • Paul B. Haser Sheila M. Coogan • Peter A. Schneider

Erica L. Mitchell • Timothy K. Liem

6

Atherosclerosis: Pathology, Pathogenesis, and Medical Management, 91

18

Ralph G. DePalma

7

Nonatherosclerotic Vascular Disease, 107

Arterial Access; Guidewires, Catheters, and Sheaths; and Balloon Angioplasty Catheters, 303

Angioplasty and Stenting for Aortoiliac Disease: Technique and Results, 325 Ruth L. Bush • Peter H. Lin • Alan B. Lumsden

19

Gregory J. Landry • James M. Edwards

Endovascular Treatment of Renovascular Disease, 334 Douglas B. Hood • Kim J. Hodgson

8

Influence of Diabetes Mellitus on Vascular Disease and Its Complications, 141

20

Charles M. Peterson

Angioplasty and Stenting for Infrainguinal Disease: Technique and Results, 343 Michael T. Caps • Peter A. Schneider

9

Pharmacology of Drugs Used in the Management of Vascular Disease, 166

21

Todd D. Reil

Technique of Carotid Angioplasty and Stenting, 355 Takao Ohki • Carlos H. Timaran • Jay Yadav

10

Primary Arterial Infections and Antibiotic Prophylaxis, 177 Hugh A. Gelabert

11

22

Vascular Malformations, 198

Endovascular Repair of Abdominal Aortic Aneurysms: Technique and Results, 383 G. Matthew Longo • Jon S. Matsumura

Peter Gloviczki

12

Vasculogenic Erectile Dysfunction, 214

23

Ralph G. DePalma

Laparoscopic Aortic Surgery for Aneurysms and Occlusive Disease: Technique and Results, 396 Carlos R. Gracia

13

Hemodynamics for the Vascular Surgeon, 225 R. Eugene Zierler • D. Eugene Strandness, Jr.*

*Deceased

24

Thrombolytic Therapy for Vascular Disease, 414 Niren Angle • William J. Quiñones-Baldrich

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Contents

Thoracic and Lumbar Sympathectomy: Indications, Technique, and Results, 443

38

Hemodialysis and Vascular Access, 694 Robert S. Bennion • Samuel E. Wilson

Peter Gloviczki

39 26

Vascular Grafts: Characteristics and Rational Selection, 452 Michael C. Stoner • William A. Abbott

Vascular Trauma, 713 Malcolm O. Perry • Frederic S. Bongard

40

Acute Arterial and Graft Occlusion, 732 Niren Angle • William J. Quiñones-Baldrich

27

Thoracoabdominal Aortic Aneurysms, 469 Larry H. Hollier

41

Myointimal Hyperplasia, 755 Ted R. Kohler • Wesley S. Moore

28

Aneurysms of the Aorta and Iliac Arteries, 488 Jerry Goldstone

42

Prosthetic Graft Infections, 772 Niren Angle • Julie A. Freischlag

29

Aneurysms of the Peripheral Arteries, 512 D. Preston Flanigan

30

43

Splanchnic and Renal Artery Aneurysms, 523

Noninfectious Complications in Vascular Surgery, 783 Glenn C. Hunter • Alex Westerband

James C. Stanley • Louis M. Messina • Gerald B. Zelenock

44 31

Aortoiliac Occlusive Disease, 537 Michael Belkin • Anthony D. Whittemore Magruder C. Donaldson • John A. Mannick

Portal Hypertension, 817 David A. Rigberg • Hugh A. Gelabert

45

Venous Thromboembolic Disease, 845 Lazar J. Greenfield

32

Femoral, Popliteal, and Tibial Occlusive Disease, 551 Evan C. Lipsitz • Frank J. Veith

46

Varicose Veins: Chronic Venous Insufficiency, 857 John Bergan • Luigi Pascarella

33

Management of Renovascular Disease, 575 Kimberley J. Hansen • K. Todd Piercy • Richard H. Dean

47

Lymphedema, 869 Thom W. Rooke • Roger F. J. Shepherd • Cindy L. Felty

34

Visceral Ischemic Syndromes, 603 Lewis B. Schwartz • James F. McKinsey • Brian Funaki Bruce L. Gewertz

35

Extracranial Cerebrovascular Disease: The Carotid Artery, 617 Wesley S. Moore

48

The Wound Care Center and Limb Salvage, 876 Peter F. Lawrence • Deborah R. Caswell

49

Lower Extremity Amputation, 890 James M. Malone

36

Surgical Reconstruction of the Supra-aortic Trunks and Vertebral Arteries, 659 Ramon Berguer

50

Spine Exposure: Operative Techniques for the Vascular Surgeon, 929 Stephanie S. Saltzberg • Matthew M. Nalbandian

37

Thoracic Outlet Syndrome and Vascular Disease of the Upper Extremity, 675 Samuel S. Ahn • Toshifumi Kudo

Index, 935

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1

Wiley F. Barker

A History of Vascular Surgery History is not a precise record, for it is only that which has been remembered or written down. Inevitably, there is much personal interpretation of that original material. In addition, interpreting events from the past is often difficult, and “history” sometimes changes as new information becomes available. It is often hard for an observer to see recent events in proper perspective, especially when the observer is close to or even involved with those events. In the last few years, there have been immense developments in molecular biology and in the techniques of minimally invasive surgery and interventional endovascular procedures. The value of these developments remains difficult to assess, despite their incalculable promise for the future. As Mao Zedong reportedly replied when asked about the effect of the French Revolution on the revolution in China, “It is much too soon to tell.” This chapter is presented in sections that may be thought of as a series of scenes and acts. As with many modern stage plays, different actors appear in different scenes in different roles, and many scenes take place concurrently and must be observed from different points of view, depending on the subject at hand. Ultimately, the whole fits together.

Prologue Although some might argue that Guy de Chauliac or Ambroise Paré should properly be called the sire of surgery, to me, John Hunter above all others is the prototype of the modern vascular surgeon. He was an unbelievably productive and tireless worker, cut from the same Scottish mold as his brother William, who was 10 years older. John was largely unlettered, whereas William had become sophisticated through his education at Glasgow, yet they shared a frenetic capacity for work and an incurable curiosity. To place the Hunters in a clear perspective with regard to nonmedical history, one should note that they were contemporaries of George Washington and Benjamin Franklin. William Hunter was born in Scotland in 1718, his brother John 10 years later; William died in 1783, John in 1793.1,2 John was even made a member of the American Philosophical Society, although he never attended a meeting. William Hunter preceded John to London, where he soon established a busy medical practice and interested himself in

many subjects, including aneurysms. In fact, William proposed the concept that a lancet used carelessly during bloodletting might enter both artery and vein, and after healing, the two channels might be connected. He thus imagined an arteriovenous fistula. He soon found just such a patient and described the clinical manifestations with great accuracy.3 William’s primary activity, however, was focused on obstetrics and on the teaching of anatomy. In this latter project John became his assistant. John Hunter is remembered for many things, but especially for his studies of the dynamics and efficiency of collateral arterial circulation. This he described in the vessels feeding the antlers of a stag after he had interrupted the major arteries in its neck. More renown came from his ligation of the femoral artery in its subsartorial course at a distance above a popliteal aneurysm—in Hunter’s canal.1,2 To be sure, others had preceded him in performing proximal ligation of arteries to treat aneurysms. In the third century, a Roman surgeon, Antyllus, had described proximal and distal ligation of the artery, followed by incision of the aneurysm and removal of its contents—a formidable operation without either anesthesia or asepsis.4 In 1680, Purmann, faced with a large aneurysm in the antecubital space, carried out ligation of the vessels and excision of the aneurysmal mass.5 In 1714, Anel described an operation in which he placed one ligature on the artery at the proximal extent of the aneurysm. Hunter, however, had found that the ligature would sometimes cut through the artery when it was placed too close to the popliteal aneurysm, so he chose a site that was more remote, but one that was easily reached by the surgeon and would preserve collaterals. Most of Anel’s patients suffered from false aneurysms caused by bloodletting in otherwise healthy arteries. The femoropopliteal aneurysms treated by Hunter were due to degenerative processes, probably a mixture of syphilis and trauma.1,6 Many other surgeons were ligating aneurysms in various anatomic sites at this time. Cooper, one of John Hunter’s students, was soon established as one of the early vascular surgeons when he ligated the carotid artery for an aneurysm in 1805,7 as well as the aorta for an iliac artery aneurysm.8 Only these few important events occurred before the latter part of the 19th century. At the time, ligation was virtually the only procedure available to surgeons for the management of arterial problems, 1

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and those problems were limited to the control of hemorrhage and the treatment of aneurysms. Hallowell in Newcastle-onTyne carried out one arterial repair of an artery torn during bloodletting. The laceration was a short one, and at the suggestion of Lambert, he placed a short (1/4-inch) steel pin through the edges of the wound and looped a ligature around it in a figure-of-eight pattern, approximating the edges of the wound with apparent success. Hallowell wrote to William Hunter concerning this operation in 1761, foreseeing that if this were a successful technique, “we might be able to cure wounds of some arteries that would otherwise require amputation, or be altogether incurable.”9 That Hallowell wrote to William instead of John is probably due to William’s published work on arteriovenous fistulas secondary to inept bloodletting. Twelve years later (1773), Asman reviewed the Newcastle repair, attempted some experiments of his own that were disastrous, and concluded that such a procedure could not work and that Lambert and Hallowell’s efforts had probably failed as well.10 After Asman’s criticism, the matter of arterial repair rested quietly for nearly another hundred years. John Hunter’s less widely known contributions are scattered throughout the immense museum he left to the Royal College of Surgeons of England, and they hint at an understanding of arterial pathology that would not be general knowledge for half a century. They include dissections of several atherosclerotic aortic bifurcations (specimens P.1177 and P.1178), showing the atheromatous lesion at the aortic bifurcation that Leriche would describe 150 years later; a carotid bifurcation with an ulcerated atheroma from a patient who died of a ruptured syphilitic thoracic aneurysm (specimen P.1171); and an extracranial internal carotid aneurysm (specimen P.282) in a patient whose neatly described symptoms are almost typical of what today are recognized as classic transient ischemic episodes.11 Regrettably, most of Hunter’s notes did not survive to give us more than this fragmentary view of his understanding of vascular disease. To cap it all, in a postmortem specimen, Hunter had dissected the atheromatous layers (although the term atheroma had not yet come into use) from the remaining intact wall of an atherosclerotic terminal aorta (specimen P.1176), foreshadowing dos Santos by a century and a half. Both Hunter and Cooper seemed to hold with the teleologic belief of the times that when senile or spontaneous gangrene occurred in older persons, thrombosis of the major vessels supervened so that the patient would not bleed to death when the gangrenous part separated.12 It was Cruveilhier who first clearly stated that the phrase “gangrene due to obstruction of the arteries” by thickening and by thrombosis should replace the terms spontaneous and senile gangrene,13 but he attributed the concept to Dupuytren. The recognition that arterial obstruction causes functional disability that limits the use of the affected part may have arisen in the veterinary world. Bouley described the clinical picture in a horse in 1831.14 Four years later (1835), a nearly anonymous physician on the ward of a Professor Louis provided the first clear description of human claudication. Barth’s patient was a 51-year-old woman who died of heart failure due to mitral valvular disease. His report described her incidental history of claudication in terms that we would recognize today.15 In the postmortem report he noted thrombosis of the terminal aorta and included a sketch that suggests that the lesion was a thrombosed

hypoplastic terminal aorta, a contracted atherosclerotic lesion, or a combination of both. Barth also repeated Hunter’s observation that the obstructing material could easily be separated from the residual intact arterial wall. Barth was never identified further, not even by an initial. Charcot is often erroneously given credit for recognizing the syndrome of intermittent claudication due to arterial insufficiency in humans.16 Charcot described, just as Bouley had done, the vanishing pulses, the cold extremity, and what we now recognize as the loss of sympathetic tone in a horse in the throes of a spasm of severe claudication; he reported a human case as well. Homans liked to joke that Charcot observed the former because he spent so much time at the horse races. As a neurologist, Charcot was familiar with intermittent claudication in humans caused by various neurologic processes. The patient Charcot described, however, suffered claudication in one leg secondary to an old gunshot wound that resulted in occlusion of the iliac artery as well as an aneurysm proximal to the occlusion. The aneurysm, which was adherent to and in communication with the jejunum, gave rise to a series of small gastrointestinal hemorrhages before the final fatal episode. Charcot thus deserves credit for identifying the herald hemorrhages that often presage major bleeding from an aortoenteric fistula. (Charcot credited both Bouley and Barth with their prior observations regarding claudication.)

Successful Arterial Suture Such information was of little utility to surgeons, however, until arterial repair became a reality. Consistent with the observations of Asman, several German masters had ex cathedra deemed arterial repair (as opposed to ligation) to be impossible. Langenbeck stated in 1825 that because the primary requirement for healing is perfect rest, as long as the pulsatile movements of the arterial wall continued, an arterial incision could never heal.17 Heinecke was certain that the patient would bleed to death through the suture holes and the apposed edges of the arterial wall.18 Repair of small injuries to veins, however, was becoming an established procedure. The lateral ligature, in which a clamp is placed on the defect in the venous wall and a ligature is tied around the puckered wall, had been performed in 1816 (Travers, cited by Jassinowsky).19 The first lateral suture of a venous defect (an erosion of the common jugular vein from an infected neck wound) was undertaken by Czerny in 1881, but the patient died of sepsis and hemorrhage.20 Jassinowsky19 credits Schede21 with the first successful repair of a large venous injury (to the common femoral vein) by lateral sutures. Going beyond the stage of venous repair, Eck reported the experimental creation of a portocaval fistula in dogs.22 The original description hints that he had little to confirm his success. Among a series of eight dogs, one died within 24 hours, six lived 2 to 6 days, and the one survivor “tired of life in the laboratory and ran away after two months.” The doctoral dissertation of Jassinowsky, written in 1889 and based purely on library research, reviewed the published information on arterial suture and concluded that it could not be successful at that time, but there might be hope in the future.19 Only 2 years later, however, Jassinowsky himself succeeded. In 1891, he reported his successful animal experiments involving arterial suture.23 The suture he described was passed carefully only two thirds of the way through the media; he tried to

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avoid penetrating the intima, except in very thin-walled vessels. This effort should be recognized for its intrinsic difficulty using even the finest milliner’s needles, for without sutures swaged onto needles, two pieces of suture have to be dragged through the arterial wall. Dörfler modified Jassinowsky’s method and passed the suture through all thicknesses of the arterial wall.24 He also recognized that the arterial suture exposed in the lumen of the vessel did no harm if uninfected. He observed that it soon became covered with a glistening membrane. Shortly thereafter, in 1896, Jaboulay and Briau described successful end-to-end carotid arterial anastomoses in animals using an everting U-shaped suture.25 Jaboulay was one of the surgeons at Lyon under whom Carrel studied. When Sadi Carnot, the president of the Republic of France, was wounded by an assassin and died because no one dared to try to repair his portal vein, Carrel was highly critical, for he believed that blood vessels could be sutured as well as any other tissue.26 He soon undertook experimental arterial anastomoses. Some of the earliest of these were arteriovenous communications in which the high-flow system ensured patency. Carrel’s contributions to technical arterial surgery included methods that vascular surgeons routinely use today.27,28 He devised the triangulation suture to facilitate end-to-end anastomosis, described the patch technique to anastomose a small vessel to the side of a larger one (as in replantation of an inferior mesenteric artery), and pioneered the use of vessel grafts and organ transplantation. His work, however, was not fully accepted in the United States for many years. In part, this stemmed from disputes that arose between him and Guthrie, who was his coworker for a year.29 In contrast, European surgeons not only accepted Carrel’s work but also began to follow his lead. In 1906, Goyanes of Madrid resected a popliteal aneurysm, then restored arterial continuity with an in situ venous graft using the popliteal vein, probably the first successful clinical vascular replacement.30 Surgeons in America were beginning to perform vascular surgery in their own way. In New Orleans in 1888, Matas described a landmark operation.31 He stumbled onto the surgical procedure for which he is commonly remembered, endoaneurysmorrhaphy, when an aneurysm for which he had ligated only the proximal brachial artery, with apparent initial success, began to pulsate again 10 days later. Reportedly, it was a medical student who called this to the professor’s attention. He chose to reoperate and to ligate the brachial artery distally. Even after this distal ligation, the aneurysm continued to pulsate, and he was forced to open the aneurysm, clean out the sac (the operation performed by Antyllus), and oversew the other arteries feeding the aneurysm from inside the sac. This foreshadowed the problems with endoleaks that harass vascular surgeons who place endovascular aortic prostheses today. Matas’s operation differed from that of Antyllus, in that he used a suture within the aneurysmal sac to obliterate the feeding vessels instead of ligating them outside the sac. The extensive dissection that would have been required outside might have damaged the collateral circulation and other adherent anatomic structures. It was many years before Matas performed another endoaneurysmorrhaphy, for most patients were treated successfully by simple proximal ligation.32 Matas ultimately expanded the descriptions of his technique to include “restorative” and “reconstructive” modifications, and he reported an approach to the arteriovenous fistula through the venous component,33 as had been proposed by Bickham.34

3

Murphy, of Chicago, performed a series of experiments on animals in which he successfully restored continuity by invagination of the proximal into the distal vessel. In 1897, he presented a successful human case.35 Edwards briefly revived this anastomotic technique of invagination when he recommended the use of the first braided nylon grafts.36 Murphy’s invagination techniques were reflected in other nonsuture methods of anastomosis: Nitze37 and Payr38 used small metal or ivory rings through which the vessel was drawn, everted, and tied in place; this unit was then inserted into the mouth of the distal vessel, and another ligature secured it there. This is substantially the Blakemore tube,39 used, albeit without signal success, in World War II.40 During his tenure at Johns Hopkins Hospital, W. S. Halsted had an abundance of traumatic and syphilitic aneurysms commanding his attention. In the early 1900s, Carrel visited Halsted and described his own technical experiments, including his early arteriovenous anastomoses. As a result, Halsted almost made history in 1907 when he faced the dilemma of a patient whose popliteal artery and vein had been sacrificed during an en bloc dissection of a sarcoma of the popliteal space.41 Halsted went to the other leg, took the saphenous vein, reversed it, and anastomosed the distal saphenous vein to the proximal femoral artery. For his distal anastomosis, however, he chose the popliteal vein. Although the graft pulsated for 40 minutes, it soon thrombosed. It is possible that Halsted was pursuing the chimera of reversal of arterial flow through the venous bed. One can only imagine what a dramatic leap forward vascular surgery would have made if Halsted, with his superb supporting cast of talented surgeons, had chosen the popliteal artery for the distal anastomosis and had achieved a truly successful arterial reconstruction in the pattern of the modern vascular surgeon. There is a considerable literature on attempts to revascularize ischemic extremities via arteriovenous anastomoses. San Martín42 and A. E. Halsted43 attempted to improve the distal circulation using arteriovenous anastomoses. Meanwhile, German surgeons such as Höpfner,44 Lexer,45,46 and Jeger47 had become familiar with the use of short (80-fold) by the presence of fibrin.22 Factor XIIIa covalently cross-links adjacent fibrin monomers, forming a stable clot that is more resistant to lysis by plasmin.

IX XII

XIIa

Thrombomodulin TM is a proteoglycan expressed on the surface of most endothelial cells, except within the central nervous system.2 TM readily binds to thrombin, causing a conformational change in the substrate binding site. The thrombin molecule is rendered incapable of binding active coagulation factors but is able to bind and activate circulating protein C. TM also accelerates the inactivation of thrombin by AT III.26,27 A procoagulant function for TM also has been found: TM

IXa

IX

Ca2+ • VIIIa • PL Xa

X

X

Ca2+ • Va • PL IIa

II

Antithrombin • Heparin

A Heparin • TFPI IX XII

XIIa

XI

VIIa Ca2+ • TF • Xa XIa

IXa

IX

Ca2+ • VIIIa • PL

Several mechanisms have evolved to control the rate of thrombin and fibrin formation (Fig. 5-2). Antithrombin III is a serine protease inhibitor that is synthesized in the liver and endothelial cells. AT III inhibits numerous coagulation factors, including thrombin (IIa), TF-VIIa, and factors IXa, Xa, XIa, and XIIa, but its most important targets are factors IIa and Xa. AT III activity is enhanced at least 1000-fold whenever it binds to circulating heparin or endothelial-bound heparin-like molecules. After the AT III–heparin complex binds to an activated coagulation factor, the heparin dissociates and continues to act as a catalyst for the formation of other AT III–serine enzyme complexes. TFPI is a Kunitz-type enzyme inhibitor that is synthesized by the endothelium and megakaryocytes.23,24 It binds to the TF-VIIa-Xa complex and inhibits the further conversion of factors X to Xa and IX to IXa.25 TFPI is constitutively expressed on the endothelium, and it circulates bound to plasma lipoproteins (hence the former name lipoproteinassociated coagulation inhibitor). TFPI activity and antigen levels increase severalfold after the administration of heparin.

XIa

XI

Coagulation Inhibition

Tissue Factor Pathway Inhibitor

VIIa Ca2+ • TF • Xa

X

Xa Ca2+ • Va • PL IIa PS

X

II PS

IIa PC

APC Thrombomodulin

B FIGURE 5–2 • Sites of activity for natural anticoagulants. Dotted lines indicated inhibitory activity. APC, activated protein C; AT, antithrombin; PS, protein S; TF, tissue factor; TFPI, tissue factor pathway inhibitor.

accelerates the activation of thrombin-activatable fibrinolysis inhibitor compared with free thrombin alone.28 Protein C and Protein S Both protein C and protein S are synthesized by the liver, but protein S has also been found in endothelium and platelets.29,30 Both proteins undergo several post-translational modifications, including the γ-carboxylation of glutamine residues via a vitamin K–dependent reaction. Protein S (a nonenzymatic cofactor for protein C) circulates either free or bound to the C4b binding protein. Activated protein C binds to protein S on the endothelial or platelet surface and cleaves several peptide bonds in factors Va and VIIIa, resulting in decreased formation of the prothrombinase and tenase complexes.

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Heparin Cofactor II

PREOPERATIVE EVALUATION

Heparin cofactor II is another specific thrombin inhibitor that forms a stable 1:1 complex with thrombin. Heparin, heparan-like molecules, and dermatan sulfate accelerate the activity of heparin cofactor II. Unlike AT III, heparin cofactor II cannot inhibit other coagulation factors. The plasma concentration of heparin cofactor II (70 µg/L) is much lower than that of AT III (150 mg/L), and it is unlikely that heparin cofactor II plays a major role in the regulation of hemostasis.

A good history and thorough physical examination detect the majority of bleeding disorders preoperatively. Laboratory testing is warranted if a bleeding disorder is present or suspected. Careful questioning should distinguish a congenital bleeding disorder from an acquired one. Determining the pattern of inheritance may further aid in identifying a congenital deficiency. A history of bleeding problems beginning in childhood or at the beginning of menses implies an inherited bleeding disorder. A history of postoperative or spontaneous bleeding in a family member is important, because many patients with inherited disorders do not experience serious bleeding until challenged by an operative procedure or trauma. All patients should be asked about bleeding after tooth extraction, minor trauma, circumcision, and other surgical procedures. An acquired hemostatic disorder should be suspected in adults who bleed during or after surgery or trauma but who have no previous history of bleeding disorders. However, some patients with congenital disorders, such as von Willebrand’s disease, may not demonstrate a bleeding diathesis until challenged. Patients with liver disease are at increased risk for developing a coagulopathy during surgery, after trauma, and after massive transfusion. Patients resuscitated with more than 20 mL/kg of hetastarch in 24 hours are at risk for bleeding from decreased platelet adhesiveness and deficiencies in coagulation proteins. Patients receiving more than 1.5 mg/kg of dextran in 24 hours are also at increased risk for bleeding as a result of impaired platelet function and reduced plasma concentration of vWF. A detailed history of drug use is also important, because many drugs alter platelet function and predispose patients to bleeding complications. Physical examination should include a thorough inspection for ecchymoses, petechiae, purpura, hemangiomas, jaundice, hematomas, and hemarthroses. Petechiae, ecchymoses, and mucocutaneous bleeding (epistaxis, gastrointestinal or genitourinary bleeding, menorrhagia) are more commonly associated with defects in primary hemostasis. Bleeding into deep tissues (hemarthroses, muscle and retroperitoneal hematomas) tends to occur with defects in coagulation. Splenomegaly may be associated with thrombocytopenia. Signs of hepatic insufficiency should be noted, because these patients may have decreased production of coagulation proteins. Patients suffering from myeloproliferative disorders, some malignant neoplasms, collagen disorders, or renal insufficiency are at increased risk for bleeding complications. Screening laboratory tests include platelet count and examination of peripheral blood smear; bleeding time; and prothrombin time (PT), activated partial thromboplastin time (aPTT), and thrombin time. The bleeding time, a very sensitive test for hemostasis, is prolonged with qualitative platelet deficiencies, as well as with decreased levels of fibrinogen, factor V, and vWF. The PT assesses the extrinsic pathway and is prolonged by deficiencies of prothrombin, fibrinogen, and factors V, VII, and X. The aPTT is prolonged by deficiencies of factors in the intrinsic pathway, including VIII, IX, XI, and XII. To a lesser extent, aPTT detects factor deficiencies in the common pathway: V, X, prothrombin, and fibrinogen. The aPTT is also prolonged by heparin. The lupus anticoagulant prolongs phospholipid-dependent coagulation reactions in vitro: PT, aPTT, and dilute Russell’s viper

Fibrinolysis Plasminogen, an inactive precursor that is synthesized in the liver, can be converted to plasmin by several plasminogen activators. Circulating t-PA (synthesized in the endothelium) does not activate plasminogen efficiently. However, both t-PA and plasminogen have high affinity for fibrin, which acts as a template for accelerated plasminogen activation (>1000-fold).31,32 Thus, the primary role for t-PA–activated plasmin is the formation of fibrin degradation products. However, exogenously administered t-PA also may activate plasminogen, which is bound to one of the fibrin degradation by-products (the DD[E] complex), resulting in the release of free plasmin.33,34 This may lead to the limited breakdown of fibrinogen, factor V, and factor VIII and to a systemic fibrinolytic state. Three types of urokinase plasminogen activator (u-PA) have been studied. The precursor, pro-urokinase (singlechain u-PA), has a low level of enzymatic activity and no affinity for fibrin, but it does demonstrate specificity against fibrin-bound plasminogen. This may be caused by a conformational change in the plasminogen, exposing the critical peptide bond and making it more susceptible to activation by single-chain u-PA.35 Single-chain u-PA is readily converted by plasmin or kallikrein to the more active two-chain u-PA, which has a high-molecular-weight and a low-molecularweight form. Commercially produced urokinase is composed primarily of the low-molecular-weight variant. Two-chain u-PA activates circulating plasminogen and fibrin-bound plasminogen equally well, resulting in a more pronounced systemic fibrinolysis.36 Plasmin activated by u-PA also performs numerous other functions related to cell migration and remodeling, including the activation of matrix metalloproteinases.37 Monocytes and endothelial cells express the u-PA receptor, which binds to u-PA and localizes plasmin to the cell surface. Each step within the plasminogen activation system has a known inhibitor. PAI-1 is released by endothelial cells, platelets, and hepatocytes. This inhibitor efficiently inactivates t-PA and two-chain u-PA and performs other functions, including the inhibition of thrombin and smooth muscle cell migration. PAI-2 is a less potent inhibitor of t-PA and twochain u-PA, but its role in physiologic hemostasis remains uncertain. PAI-2 is released into the circulation during pregnancy, indicating a greater role for hemostasis during pregnancy and delivery. Neither PAI-1 nor PAI-2 inhibits pro-urokinase (single-chain u-PA). α2-Antiplasmin inactivates circulating plasmin more readily than it does fibrin-bound plasmin, thus decreasing overall systemic fibrinolysis. Other less specific proteases that inhibit fibrinolysis are α1-protease inhibitor and α2-macroglobulin.

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venom time. However, it does not cause clinical bleeding. The thrombin time is prolonged by hypofibrinogenemia, fibrin abnormalities, and heparin. PLATELET DISORDERS Hemorrhagic complications may occur because of quantitative or qualitative platelet disorders that are acquired or congenital in origin. Thrombocytopenia and qualitative platelet defects are among the most common causes of bleeding in surgical patients. Spontaneous bleeding may occur when platelet counts fall below 20,000/mm3. Platelet counts between 30,000 and 50,000/mm3 are adequate to ensure hemostasis, provided that there are no associated functional platelet or coagulation disorders. Platelet counts of 50,000 to 100,000/mm3 are required to restore hemostasis during bleeding. Thrombocytopenia Thrombocytopenia may occur from increased platelet destruction, abnormal production, dilution, or temporary sequestration (usually in the spleen). Increased destruction may occur via nonimmune or immune mechanisms. Nonimmunemediated thrombocytopenia occurs in hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation (DIC), and some vasculitides. In these syndromes, platelets are stimulated to aggregate within the microcirculation, often affecting the brain, kidneys, heart, lungs, and adrenal glands.38 Early plasmapheresis and plasma transfusion (platelet-poor fresh frozen plasma, cryoprecipitate-poor plasma), along with high-dose glucocorticoid administration, can reverse most cases of thrombotic thrombocytopenic purpura.39,40 Platelet transfusions should be used only for intracerebral or other life-threatening hemorrhagic complications. The treatment for hemolytic-uremic syndrome varies considerably but may include hemodialysis, heparin therapy, and plasma exchange, depending on the duration and severity of the illness. GP IIb-IIIa inhibitors may become a useful adjunct in hemolytic-uremic syndrome.41 Immune-mediated platelet destruction may occur with certain collagen vascular diseases (lupus erythematosus), immune thrombocytopenic purpura, and lymphoproliferative disorders (chronic lymphocytic leukemia, non-Hodgkin’s lymphoma), or it may be drug induced. Acute immune thrombocytopenic purpura is a postinfectious thrombocytopenia that occurs predominantly in children and is usually self-limited. Chronic immune thrombocytopenic purpura is idiopathic and results when autoimmune antibodies are generated against the platelet membrane. Initial therapy for the chronic form consists of corticosteroids (prednisone, methylprednisolone), followed by splenectomy in nonresponders. Severely thrombocytopenic patients with major hemorrhagic complications and patients requiring urgent surgery can be treated with platelet transfusions, intravenous (IV) gamma globulin, and plasmapheresis. Some drugs (quinidine, quinine, sulfonamides, penicillins, valproic acid, heparin) may induce thrombocytopenia via the formation of antigen-antibody complexes on the platelet surface, increasing platelet destruction. In general, discontinuation of the drug reverses the thrombocytopenia within 2 to 5 days. Adjuvant therapy for active bleeding may include corticosteroids, platelet transfusions, and, in some cases,

IV gamma globulin. Heparin-induced thrombocytopenia is a prothrombotic condition that is discussed later in the section on thrombosis. Impaired platelet production may be caused by aplastic anemia, megakaryocytic aplasia, radiation, myelosuppressive drugs, viral infections, vitamin B12 and folate deficiencies, and several other drugs (ethanol, estrogens, interferon, thiazides). Thrombocytopenia also has been described in association with numerous congenital disorders (Fanconi’s aplastic anemia, sex-linked recessive thrombocytopenia, Alport’s syndrome). Thrombocytopenia commonly occurs after massive transfusions of banked blood. Only 10% of platelets remain viable in blood held in cold storage for longer than 24 hours. In general, the replacement of one blood volume decreases the platelet count by one third to one half.42 Nevertheless, abnormal bleeding is uncommon, and the routine administration of platelets following massive transfusion is not warranted unless hemorrhage is ongoing.43 Hypothermia (temperature lower than 32°C) also may cause thrombocytopenia, but the mechanism remains unclear. However, sequestration of platelets during hypothermia is well documented. Platelets appear to activate, release α-granule products, aggregate, and sequester in the portal circulation. Rewarming may cause a significant portion to return to the circulation. Cold-induced coagulopathy is best prevented by transfusing warmed blood products and maintaining the core body temperature above 32°C. The centrifugation of one unit of whole blood yields 8 to 10 × 1010 platelets. Approximately 4 to 8 units of whole blood are required to yield enough platelets for administration in the average adult. Current apheresis techniques can yield 2.5 to 10 × 1011 platelets from a single donor (over 1 to 2 hours). One unit of single-donor platelets usually increases the platelet count by 10,000/mm3 per square meter of body surface area. Qualitative Disorders of Platelet Function Qualitative platelet disorders should be suspected when bleeding occurs in patients with normal coagulation studies and platelet counts. Qualitative disorders may be congenital or acquired; acquired disorders are much more common. Disturbances of platelet adherence and aggregation rarely cause bleeding spontaneously but certainly exacerbate bleeding secondary to surgery and trauma. Congenital qualitative disorders of platelet function include von Willebrand’s disease, Bernard-Soulier syndrome, Glanzmann’s thrombasthenia, storage pool diseases, and diseases of platelet activation. Von Willebrand’s disease is the most common inherited bleeding disorder, characterized by a deficiency or defect in vWF. It has been classified into six subtypes (1, 2A, 2B, 2M, 2N, 3), with type 1 being the most common (70%).44 Type 1 von Willebrand’s disease is usually transmitted as an autosomal dominant trait with incomplete penetrance. In general, patients manifest epistaxis, ecchymoses, menorrhagia, and post-traumatic or postsurgical bleeding. Decreased platelet adherence causes prolongation of the bleeding time. The aPTT also may be elevated, because most patients with this disease have concomitant decreases in factor VIII coagulation activity (VIII:C). Ristocetin agglutination of platelets is impaired but can be corrected with the addition of vWF-rich cryoprecipitate.

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Treatment of von Willebrand’s disease may consist of replacement (cryoprecipitate, purified factor VIII concentrates, platelet transfusions) or nonreplacement (vasopressin, antifibrinolytic agents) therapy. Approximately 80% of patients with type 1 disease respond to desmopressin acetate (DDAVP) with increased vWF:Ag and VIII:C (within 60 minutes), which may last for 4 to 6 hours. Unfortunately, response to therapy cannot be predicted without trial administration. Repeated administration of DDAVP (every 12 hours) may be required in patients with type 1 disease who undergo surgical procedures. Most type 2 and type 3 patients do not respond to DDAVP. Antifibrinolytic agents (ε-aminocaproic acid, tranexamic acid) have been used for the treatment of mucocutaneous bleeding and for prophylaxis during oral surgical procedures.45 Patients who are unresponsive to DDAVP may require replacement therapy during the perioperative period. Until recently, cryoprecipitate (rich in vWF, factors VIII and XIII, and fibronectin) was the treatment of choice. More recently, some purified factor VIII concentrates (which contain large quantities of multimeric vWF) and a newly formulated vWF concentrate have been used successfully.46 There are no clear guidelines regarding the amount and frequency of administration; replacement therapy is largely empirical. The bleeding time and factor VIII levels are used to monitor response to replacement therapy. Bernard-Soulier syndrome is transmitted as an autosomal recessive trait and is characterized by a deficiency in the GP Ib-IX-V complex (primary binding site for vWF). These patients have prolonged bleeding times (>20 minutes), mild to moderate thrombocytopenia, and absent ristocetininduced platelet agglutination. Heterozygous patients have half the normal amount of GP Ib-IX-V but demonstrate normal platelet responses. Platelet transfusions are the mainstay of therapy, but they are limited by the development of antibodies to human leukocyte antigens (HLAs) (alloimmunization) and to the GP Ib-IX-V complex. The use of HLA crossmatched and leukocyte-depleted platelets should minimize alloimmunization. Other unproved therapies include DDAVP and corticosteroids. Glanzmann’s thrombasthenia is a rare autosomal recessive trait in which platelet membranes lack GP IIb-IIIa receptors, leading to failure of platelet aggregation regardless of the initial stimulus. These patients have normal platelet counts, markedly prolonged bleeding times, deficient clot retraction, and normal ristocetin-induced agglutination. Patients who are heterozygous exhibit normal platelet aggregation responses. As with Bernard-Soulier syndrome, platelet transfusions are the primary form of therapy. Again, the use of HLA crossmatched and leukocyte-depleted platelets is optimal. Storage pool diseases are a group of rare hereditary disorders characterized by deficiencies in platelet granules, their contents, or both. These include deficiencies in α-granule contents (gray platelet syndrome), δ-granule storage diseases (Wiskott-Aldrich syndrome, Hermansky-Pudlak syndrome, Chédiak-Higashi syndrome), and αδ-granule storage diseases.47 Cryoprecipitate and platelet transfusions may be used in the perioperative period. DDAVP also has been used to decrease the requirement for transfusions. Acquired qualitative platelet abnormalities may be caused by certain drugs, uremia, cirrhosis, myeloproliferative disorders, and dysproteinemias. Aspirin irreversibly acetylates

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platelet cyclooxygenase-1, inhibiting thromboxane- and endoperoxide-mediated platelet activation for the life of the platelet. The effect of aspirin on the bleeding time is variable and may depend largely on the technique used to perform the test.48,49 Nonsteroidal anti-inflammatory drugs (indomethacin, phenylbutazone, ibuprofen) reversibly inhibit cyclooxygenase. Numerous antibiotics, including some beta-lactams, cephalosporins, and nitrofurantoin, impair platelet aggregation and prolong the bleeding time. Mechanisms may include inhibition of agonist binding to the membrane receptor and inhibition of intracellular signal transduction. Platelet GP IIb-IIIa inhibitors (abciximab, eptifibatide, tirofiban) block the binding of fibrinogen to the GP IIb-IIIa receptor and effectively prevent platelet aggregation in a dose-dependent fashion. Correction of bleeding may be accomplished with platelet transfusions. Uremia causes defective platelet adherence and aggregation, resulting in a prolonged bleeding time. Clinical manifestations may include petechiae, ecchymoses, and mucocutaneous bleeding. The pathophysiology remains unclear but may involve impaired thromboxane and calcium metabolism or defective platelet-subendothelial adhesion (via vWF). DDAVP has been shown to shorten bleeding times preoperatively in uremic patients.50 IV DDAVP, 0.3 to 0.4 µg/kg over 15 to 30 minutes, shortens the bleeding time in most patients within 1 hour. Hemodialysis, peritoneal dialysis, and infusions of cryoprecipitate and conjugated estrogens have been used with some success.51 Coagulation factor deficiencies, DIC, dysfibrinogenemias, impaired thrombopoiesis, platelet sequestration, and impaired platelet aggregation all contribute to the hemostatic defects associated with liver failure. Therapy is nonspecific but may include DDAVP and platelet transfusions for severe thrombocytopenia. COAGULATION DISORDERS Congenital Disorders Congenital disorders of coagulation usually involve a single factor. Preoperative transfusion of the appropriate factor is necessary and may be required during surgery and postoperatively as well. Deficiencies of factor XII, HMWK, and prekallikrein cause prolongation of the aPTT but do not cause significant bleeding diatheses. Deficiencies of the remaining factors may result in serious bleeding after surgery or trauma. Hemophilia A (factor VIII deficiency) is the most common of the inherited coagulation defects, with a prevalence of 1 in 10,000 males. Hemophilia B (Christmas disease, factor IX deficiency) has a prevalence of approximately 1 in 50,000 males. Both are X-linked recessive disorders that are clinically indistinguishable. The severity of these disorders depends on the levels of factor VIII or IX that are present. Severely affected individuals (factor levels 5%) may develop hemorrhagic complications only after surgery or trauma. Patients with hemophilia A who require major surgery should receive factor VIII replacement to achieve 100% of normal activity just before the procedure. For each unit per

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kilogram of body weight infused, the factor VIII level is increased by approximately 0.02 U/mL (normal activity is 1 U/mL).52 Levels should be monitored postoperatively, and replacement therapy should be repeated every 12 hours to maintain at least 50% of normal activity until all wounds are healed.53 Factor VIII levels may be restored using donordirected cryoprecipitate, virus-inactivated factor VIII concentrate, or recombinant factor VIII. DDAVP (which increases factor VIII levels) and ε-aminocaproic acid may be used as adjunctive therapies in patients with mild hemophilia to reduce or avoid the need for replacement therapy during oral or minor surgical procedures. Patients with hemophilia B should have at least 50% of normal activity before major surgery and for the first 7 to 10 days postoperatively. Factor IX may be replaced with prothrombin complex concentrates (containing factors II, VII, IX, and X), purified factor IX, or recombinant factor IX. Replacement therapy may be limited by several factors. Prothrombin complexes are associated with the development of arterial or venous thromboses in some patients. In addition, therapy with recombinant factor IX may not achieve as much activity as purified factor IX. This may be due to the need for post-translational modifications (γ-carboxylation) that are not present in recombinant factor IX. In addition, replacement therapy for hemophilia A and B is complicated by the development of inhibitors to factors VIII and IX in approximately 15% of patients. Alternative strategies include the use of high-dose factor VIII or recombinant factor VIIa and attempts to induce immune tolerance. Rare coagulation factor deficiencies of factors II, V, VII, and X occur with a prevalence of 1:500,000 to 1:1,000,000. They are usually transmitted with an autosomal recessive pattern. The most severe complications occur with deficiencies of factors II and X.54 In general, only low levels of factor activity (10% to 20% of normal) are required for normal hemostasis. Replacement therapy for factors II and X may be accomplished with fresh frozen plasma or factor concentrates. Factor IX concentrates contain significant amounts of factors II and X and may be used for their replacement. The short halflife of factor VII requires a more frequent replacement schedule using factor VII concentrates. Recombinant factor VIIa also may be used for factor VII deficiencies. Factor V deficiencies can be treated with fresh frozen plasma because factor V concentrates are not yet commercially available. Abnormalities of fibrinogen and fibrinolysis are also heritable. Afibrinogenemia is a rare disorder transmitted as an autosomal recessive trait; hypofibrinogenemia may occur in heterozygous individuals. Clinical manifestations include gastrointestinal and mucous membrane bleeding, hemarthroses, intracranial hemorrhage, and recurrent fetal loss. The PT and aPTT, which are markedly prolonged, usually correct when mixed with normal plasma. Replacement therapy with cryoprecipitate is usually reserved for active bleeding, the perioperative period, and prophylaxis during pregnancy. The level of fibrinogen necessary for hemostasis ranges between 50 and 100 mg/dL. Each unit of cryoprecipitate usually increases the fibrinogen level by approximately 10 mg/dL.55 Dysfibrinogenemias are a heterogeneous group of disorders that may cause defective fibrin formation, polymerization, cross-linkage, or impaired fibrinolysis. Patients may manifest mild to moderate bleeding diatheses (30%) or recurrent thromboses (20%).56 The PT and aPTT usually are prolonged.

Functional assays for fibrinogen are abnormal, whereas antigenic assays are normal. Cryoprecipitate is indicated for hemorrhage but contraindicated for acute thrombotic episodes. Congenital hyperfibrinolytic states may result in delayed bleeding. The congenital hyperfibrinolytic states include heterozygous and homozygous α2-antiplasmin deficiencies and functionally abnormal or deficient PAI-1.57 The whole blood clot lysis time and the euglobulin clot lysis time are characteristically shortened. Antifibrinolytic agents (ε-aminocaproic acid or tranexamic acid) are recommended for the management of active bleeding.58 Acquired Disorders Patients develop coagulation disorders because of deficiencies of coagulation proteins, synthesis of nonfunctioning factors, and consumption or inadequate replacement of coagulation proteins. Hepatic insufficiency may cause decreased plasma levels of several coagulation factors (including factors II, V, VII, IX, X, XIII, and fibrinogen) because of a decreased synthetic capacity, defective post-translational modification (γ-carboxylation), and increased breakdown of activated factors (because of subclinical DIC). Thrombocytopenia also may occur because of increased splenic sequestration. However, levels of factor VIII and vWF may be elevated because they are synthesized in extrahepatic locations. Correction of the coagulation factor deficits and the thrombocytopenia is accomplished with fresh frozen plasma and platelet transfusions, respectively. Vitamin K administration alone does not completely reverse the coagulopathy. Vitamin K deficiency may cause a bleeding diathesis as a result of the synthesis of nonfunctional forms of the vitamin K–dependent coagulation factors II, VII, IX, and X. Normal sources of vitamin K include dietary intake (leafy green vegetables, soybean oil) and vitamin K synthesis by normal intestinal flora. Vitamin K deficiency may be caused by poor dietary intake, decreased intestinal absorption of vitamin K, decreased production by the gut flora, and liver failure. This situation more commonly arises in patients receiving antibiotic bowel preparations or long-term parenteral nutrition (without vitamin K supplementation). Vitamin K deficiency also occurs in patients who have a prolonged recovery after intestinal surgery and in those with intrinsic bowel diseases (Crohn’s disease, celiac sprue, ulcerative colitis), as well as in patients with obstructive jaundice. Vitamin K should be administered preoperatively to patients with hepatic insufficiency, obstructive jaundice, malabsorption states, or malnutrition. Patients with an intact enterohepatic circulation can receive vitamin K orally (2.5 to 5 mg), with normalization of the PT within 24 to 48 hours. Slow IV administration should be used in patients with biliary obstruction or malabsorption. Patients who require urgent correction of the PT should receive slow IV vitamin K and replacement therapy (fresh frozen plasma or prothrombin concentrates). DIC is characterized by the systemic generation of fibrin, often resulting in the thrombosis of small and medium-size blood vessels. The consumption of clotting factors and platelets also results in impaired coagulation and hemorrhagic complications. DIC is mediated by several cytokines (including tumor necrosis factor-α and interleukin-6), which result

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in the systemic generation of TF, thrombin, and fibrin.59 Fibrinolytic activity, which is initially increased via the release of t-PA, becomes depressed in response to elevated PAI-1.59,60 DIC may develop in association with bacterial infections (gram-positive and gram-negative infections), trauma, malignancy, obstetric complications, hemolytic transfusion reactions, giant hemangiomas (Kasabach-Merritt syndrome), and aortic aneurysms. A compensated DIC (present in more than 80% of patients who undergo major surgery), in which coagulation factors and platelets are replaced as they are consumed, may be asymptomatic or may appear with ecchymoses and petechiae. Surgery, trauma, hypotension, or transfusion reactions may exacerbate the coagulopathy and hypofibrinolysis, leading to excessive bleeding and intravascular thrombosis. A combination of laboratory tests may help confirm the clinical diagnosis of DIC. These include detection of thrombocytopenia or a rapidly decreasing platelet count, prolongation of the PT and aPTT, and the presence of fibrin degradation products (D-dimer assay, latex agglutination for fibrous degradation products). Extrinsic pathway coagulation proteins (factors II, V, VII, and X) and physiologic coagulation inhibitors (AT III, protein C) usually are depressed, whereas vWF and factor VIII levels may be increased.61 The fibrinogen level is variably affected by DIC. The first goal of management is elimination of the cause of DIC. When this is possible, the intravascular coagulation ceases with the return of normal hemostasis. In severe DIC, with ongoing blood loss, patients are best managed by replacement of deficient blood elements using fresh frozen plasma (up to 6 units per 24 hours) and platelets while the precipitating cause of DIC is eliminated.59 Administration of AT III and protein C concentrates may retard the consumption of coagulation factors, although this remains to be proved. Some trials have demonstrated a benefit with the administration of heparin or low-molecular-weight heparin (LMWH).62,63 Given that patients with DIC already have a coagulopathy, heparin should be used cautiously (lower IV dosages of 300 to 500 units/hour), with careful clinical observation and laboratory monitoring. Direct thrombin inhibitors (hirudin, recombinant TM), activated protein C, and extrinsic pathway inhibitors (recombinant TFPI) are under investigation as well.

Thrombosis In 1856, Virchow suggested that thrombus formation was the result of an interaction among an injured surface, stasis, and the hypercoagulability of blood. One or more components of Virchow’s triad can be invoked when determining the cause of an in vivo thrombosis. Hypofibrinolysis is the only major process not recognized by Virchow that contributes to intravascular thrombosis. Most of the inherited thrombophilic conditions, with the exception of congenital hyperhomocysteinemia, are more closely associated with venous than with arterial thromboembolism. Acquired conditions such as the presence of antiphospholipid antibodies and heparin-associated antibodies have a well-recognized association with both arterial and venous thromboses. The more common inherited and acquired hypercoagulable states are discussed later, as are the indications for testing and the optimal timing for the performance of these assays. The more commonly used antithrombotic

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agents, as well as alternative agents, are discussed with regard to the management of established thromboses and prophylaxis against thromboembolism. PROTHROMBOTIC CONDITIONS Inherited Prothrombotic Conditions Activated protein C (APC) resistance is most commonly caused by a mutation in the factor V gene, during which Arg506 is replaced with Gln (factor V Leiden), making activated factor V resistant to degradation by APC.64 It is the most common inherited hypercoagulable condition, occurring in approximately 12% to 33% of patients with venous thromboembolism.65-68 In contrast, it has a prevalence of 3% to 6% in control populations.66-68 The white population is affected more commonly than black, Asian, or Native American populations. Individuals who are heterozygous for the factor V mutation have a 2.7- to 7-fold increased risk for venous thromboembolism, whereas homozygous patients may have an 80-fold increased risk.67,68 A small percentage of patients with APC resistance do not have the Leiden mutation. Other factor V mutations (factor V Cambridge, factor V HR2 haplotype) also may cause APC resistance.69,70 Functional APC resistance can be detected by performing the aPTT in the presence and absence of purified APC. In general, an aPTT ratio (aPTT with APC/aPTT without APC) of less than 2.0 is considered a positive study (normal is 2.4 to 4.0). Numerous factors may affect the accuracy of the aPTT ratio, including protein C deficiency, the presence of anticoagulants, and antiphospholipid antibodies. Modifications to this functional assay have improved its sensitivity and specificity.71 DNA testing using the polymerase chain reaction to amplify the factor V Leiden mutation has already become standardized. The optimal management of patients with APC resistance remains to be defined. APCresistant individuals in high-risk situations (e.g., pregnancy, surgery) should receive thrombosis prophylaxis. Those patients with prior thrombotic episodes may benefit from long-term warfarin therapy. This is especially true for patients with multiple prior episodes, thromboses in unusual locations, and multiple inherited thrombophilic mutations. Prothrombin 20210A is a mutation (G to A substitution) in the prothrombin gene at nucleotide 20210, resulting in increased levels of plasma prothrombin.72 The prothrombin 20210A mutation is present in 18% of selected patients with strong family histories of venous thromboembolism, 6.2% of unselected patients with a first episode of thrombosis, and 2.3% of healthy controls. The prevalence is even higher in southern European whites.73 A significant number of patients have more than one congenital thrombophilic condition, further increasing their risk for venous thromboembolism.72,74 AT III deficiency was the first reported congenital thrombophilic condition.75 It is transmitted with an autosomal dominant pattern and has a prevalence of 1:5000 in the population.76 AT III deficiency has been detected in approximately 1% of patients with venous thromboses, conferring a risk that may be as high as 50-fold greater than normal.77,78 The lifetime risk for developing a thrombotic episode ranges between 17% and 50%.79 Although thromboembolism may occur spontaneously, it is usually associated with a precipitating event such as surgery, trauma, or pregnancy.

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Arterial thromboses, although less common than venous thromboses, also occur. AT III levels may be reduced to less than 80% of normal in other conditions, including hepatic insufficiency, DIC, acute venous thrombosis, sepsis, and nephrotic syndrome, and in patients receiving heparin or estrogen supplementation. The mainstay of therapy in AT III–deficient patients with venous thromboembolism is still heparin anticoagulation, although supranormal dosages may be required.80 AT III concentrates may be appropriate in patients who do not achieve adequate anticoagulation with heparin alone. The minimum level of AT III necessary to prevent thrombosis is unknown; however, it is suggested that levels be adjusted to greater than 80% of normal activity. Antithrombin may be replaced with AT III concentrate (1 U/kg increases the AT III activity by 1% to 2%) or fresh frozen plasma. Asymptomatic patients should receive thrombosis prophylaxis during high-risk situations such as prolonged immobilization, surgery, or pregnancy. However, long-term warfarin therapy is usually reserved for AT III–deficient patients who have experienced thrombotic events. Protein C and protein S deficiencies account for a number of disorders. Congenital protein C deficiency may be transmitted as an autosomal dominant or recessive trait and has a prevalence of 1:200 to 1:500.81,82 The incidence of thrombosis varies, depending on the population in question. Studies identifying protein C deficiency in healthy blood donors demonstrate a low prevalence of venous thrombosis, whereas studies that screen patients with venous thromboembolism find a higher prevalence of protein C deficiency compared with controls.77,81-83 Overall, inherited protein C deficiency is associated with approximately a sevenfold increased risk for developing a first venous thromboembolic event.83 Common sites for venous thromboses include the lower extremities, mesenteric veins, and cerebral venous sinuses. Functional and immunologic assays are available to establish the diagnosis of protein C deficiency. Normal adults have protein C antigen levels ranging from 70% to 140% of normal. Patients with antigen levels less than 55% are likely to have heterozygous protein C deficiency. Approximately 60% of the total protein S circulates bound to C4b complement-binding protein.84 Deficiency states may occur with decreased total protein S, decreased free protein S, and decreased functional protein S activity (with total and free protein S concentrations in the normal range). Histories of patients with congenital protein S deficiencies are very similar to those of patients with protein C deficiency, although arterial thromboses also have been described in patients with protein S deficiency. Protein S may be measured with functional assays, assessing the ability to catalyze the inhibition of factor Va by APC, or immunologic assays. Both protein C and protein S are vitamin K–dependent proteins synthesized in the liver. Consequently, plasma levels may be decreased in patients with hepatic insufficiency. Acquired protein C and protein S deficiencies also may occur with warfarin administration, vitamin K deficiency (malabsorption, biliary obstruction), sepsis, DIC, and acute thromboses and in patients receiving some chemotherapeutic medications. Because C4b is also an acute-phase reactant, inflammatory conditions may increase C4b levels, causing a decrease in free protein S and an increased tendency toward thrombosis.85

Heparin is the first line of therapy in the management of acute thromboembolic episodes in patients with known protein C and S deficiencies. Because warfarin-induced skin necrosis is more likely to occur in patients with protein C deficiency, heparin therapy should overlap with the first 4 or 5 days of warfarin therapy, and large loading dosages of warfarin should be avoided. Longer-term treatment with warfarin is effective in the prevention of recurrent venous thromboembolic episodes in patients with protein C and protein S deficiencies. Fresh frozen plasma occasionally may be required to restore functional levels of protein C and protein S. Abnormalities of fibrinogen and fibrinolysis include dysfibrinogenemias, which may impair any of the steps involved in the generation and cross-linkage of fibrin. They have been reported in association with bleeding diatheses (30%) and venous thromboembolism (20%). Therapeutic alternatives have been described earlier. Elevated factor XI is a mild risk factor for the development of venous thrombosis.86 Factor XI levels in the 90th percentile or greater confer a 2.2-fold relative risk for the development of venous thrombosis. Even lower factor XI levels demonstrate a linear dose-response relationship with thrombotic risk. The underlying cause for elevated factor XI levels remains to be determined. Acquired Prothrombotic Conditions Many clinical disorders predispose to thrombosis by activating the coagulation system or causing platelet aggregation. Soft tissue trauma, thermal injuries, and operative dissection all predispose to thrombosis through the release of tissue factor and activation of the extrinsic coagulation pathway. Sepsis predisposes to thrombosis via multiple mechanisms. Gram-positive bacteria may directly cause platelet aggregation and subsequent thrombosis. Gram-negative bacterial endotoxin may stimulate platelet aggregation but may also, through interaction with leukocytes and endothelial cells, cause TF-like activation of the coagulation system. Endotoxin is known to be a major stimulus for the development of DIC. As many as 11% of patients with malignancies have venous thromboembolic complications.87 Pancreatic, prostate, gastrointestinal, and lung cancers have a particularly strong association with thrombosis. Conversely, patients with idiopathic venous thromboembolism are more likely to be diagnosed with cancer (up to 7.6%).88 Aggressive screening for occult malignancies in patients with venous thromboembolism has not yet been shown to be cost-effective or to result in improved long-term survival. Pregnancy is associated with a fourfold increased risk for venous thromboembolism.78,89 The risk may be three to five times greater in the immediate postpartum period. Oral contraceptives also are associated with an approximately threefold increased risk, which is conferred immediately and is reversible.90 Newer preparations with lower dosages of ethinylestradiol may lower the risk. Although the exact mechanism is unclear, these women demonstrate increased levels of thrombin and fibrinogen, with decreased levels of protein S and plasminogen activators. Antiphospholipid antibodies, including lupus anticoagulants and anticardiolipin antibodies, are IgG, IgM, or IgA immunoglobulins, which are directed against phospholipidbinding proteins (prothrombin and β2-GP I). These antibodies

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interfere with in vitro phospholipid-dependent clotting assays, such as aPTT, kaolin clotting time, and the dilute Russell’s viper venom time. In vivo, antiphospholipid antibodies may promote thrombosis by interfering with the activation of protein C.91 The presence of antiphospholipid antibodies is associated with a ninefold increased risk for venous thrombosis. Clinical manifestations of the antiphospholipid syndrome may include venous and arterial thromboses (coronary, cerebral) and recurrent fetal loss. Lupus anticoagulants are also associated with arterial thrombosis. As many as 50% of patients who are positive for lupus anticoagulants and undergo vascular surgical procedures develop thrombotic complications.92 Patients with thrombotic episodes should receive heparin and warfarin anticoagulation. Longterm warfarin therapy (at higher intensity, international normalized ratio > 3) has been shown to reduce the recurrence of thrombosis.93 Warfarin may be discontinued when the IgM or IgG immunoglobulins are no longer detectable. Heparin-associated antibodies (HAAbs) and heparininduced thrombocytopenia (HIT) are important considerations for patients receiving anticoagulation therapy. HAAbs IgG and IgM target the heparin–platelet factor 4 complex. These immune complexes bind to the Fcγ-RII platelet receptor, causing pathophysiologic platelet activation, aggregation, and thrombocytopenia. The incidence of HAAb formation varies widely, depending on the indications for heparin, the type of heparin used, and the tests used to detect HAAbs. LMWHs are associated with a significantly decreased incidence of HAAb formation and HIT.94 Up to 20% of patients who undergo vascular surgical procedures develop HAAbs, which are associated with a greater than twofold increased risk for thrombotic complications.95 The incidence of HIT ranges between 2% and 9%, depending on the type of heparin used, the route of administration, and the definition of thrombocytopenia used.96,97 Most authors use a platelet count of less than 100,000/mm3 to define HIT-associated thrombocytopenia. However, thrombocytopenia is not a prerequisite for the development of thrombotic complications. The diagnosis of HIT may be made according to the following criteria: 1. The development of thrombocytopenia or a significantly decreased platelet count while receiving heparin. 2. Resolution of thrombocytopenia after cessation of heparin. 3. Exclusion of other causes for thrombocytopenia. 4. A positive HAAb assay (two-point platelet aggregation assay, serotonin release assay, enzyme-linked immunosorbent assay). Patients who develop HIT or thrombosis in the setting of a positive HAAb assay should discontinue heparin immediately. Most patients require continued anticoagulation with alternative agents such as recombinant hirudin and danaparoid. Longterm antithrombotic therapy with warfarin remains effective. Hyperhomocysteinemia may be caused by inborn errors of metabolism (cystathionine β-synthase deficiency, methylene tetrahydrofolate reductase variant) or, more commonly, by acquired deficiencies in vitamin B6, vitamin B12, and folic acid. Elevated homocysteine is an independent risk factor for myocardial infarction, stroke, and peripheral arterial atherothrombosis.98 It is also an independent risk factor for venous thrombosis, with an odds ratio of approximately 2 to 2.5.99-101 The risk may be much higher in patients with

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combined hyperhomocysteinemia and other thrombophilic conditions.102,103 Homocysteinemia may be detected using fasting plasma levels or after methionine loading (100 mg/kg). Elevated homocysteine levels may be effectively reduced with folate, vitamin B6, and vitamin B12 supplementation.104 Whether vitamin supplementation and correction of hyperhomocysteinemia are protective against venous thromboses remains to be determined. Surgery and trauma are very strong risk factors for the development of venous thrombosis. Venous thromboembolism occurs in up to 25% of patients undergoing general surgical procedures without thrombosis prophylaxis. Orthopedic procedures (hip and knee replacement, hip fracture repair) are associated with an even greater risk for venous thromboembolism (45% to 61%). The incidence of venous thromboembolism in trauma patients depends on the severity of injury. Multisystem trauma is associated with a greater than 50% incidence.105 Myeloproliferative diseases (polycythemia vera, chronic myelogenous leukemia, myeloid metaplasia, essential thrombocytosis), hypergammaglobulinemia, and hyperfibrinogenemia may predispose to thrombosis by causing a hyperviscous state. At clinical presentation, patients manifest cerebral (arterial and venous), coronary, pulmonary, and peripheral arterial and venous thromboemboli. Hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura cause microvascular thromboses and thrombocytopenia. Indications and Timing for Thrombophilia Screening Before 1993, inherited prothrombotic conditions were detected in less than 10% to 15% of patients with venous thromboembolism. Since the discovery of factor V Leiden and the prothrombin 20210A mutation, the number of patients with detectable thrombophilia has increased significantly. Patients who develop venous thromboembolism at a young age, patients with recurrent thrombosis, and those with a positive family history or thromboses in unusual locations are candidates for screening. Patients who develop warfarininduced skin necrosis also have a significant chance of having protein C deficiency. Patients with suspected thrombophilia should be screened for APC resistance, prothrombin 20210A mutation, antiphospholipid antibodies, hyperhomocysteinemia, HAAbs, and deficiencies of AT III, protein C, and protein S. Patients with arterial thrombosis who require screening for thrombophilia should be tested for antiphospholipid antibodies (including lupus anticoagulants and anticardiolipin antibodies), HAAbs, and hyperhomocysteinemia. Because acute thrombosis may be associated with transient depletion of AT III, protein C, and protein S, screening should not be performed during this period. Heparin and warfarin therapy also interfere with screening tests for APC resistance, whereas warfarin decreases functional and antigenic levels of protein C and protein S. Accurate screening is most easily accomplished approximately 2 to 3 weeks after the patient has discontinued warfarin therapy. If the risk of recurrent thromboembolism is deemed too great to discontinue warfarin, the patient may be converted to subcutaneous heparin or LMWH during this 2- to 3-week period. Protein C and S levels should not be affected by heparin administration. Testing for the presence of HAAbs

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should be performed after heparin has been discontinued, because false-negative results may be obtained for up to 72 hours. MANAGEMENT OF ESTABLISHED THROMBOSIS Unfractionated heparin, warfarin, and aspirin are the most commonly used antithrombotic agents. Several newer drugs have been made available by the Food and Drug Administration for limited indications. These include danaparoid, recombinant hirudin, ticlopidine, clopidogrel, and several GP IIb-IIIa receptor antagonists. Although numerous other agents are in development or in clinical trials (recombinant TFPI, GP Ib inhibitors, other factor IIA and Xa inhibitors), they are not discussed in this chapter. Unfractionated and Low-Molecular-Weight Heparins Unfractionated bovine lung and porcine intestinal heparin have been the mainstay of therapy for episodes of acute arterial (coronary, cerebral, peripheral arterial) and venous (deep venous) thromboses for the past several decades. Unfractionated heparins are glycosaminoglycans composed of repetitive disaccharide units (uronic acid and glucosamine) with molecular weights ranging from 4000 to 40,000 Da. LMWHs are derived from the enzymatic or alkaline degradation of unfractionated heparin purified from porcine intestinal mucosa. The average molecular weight of the various preparations ranges from 3000 to 6000 Da.106 Unfractionated heparin and LMWH bind to AT III via a specific pentasaccharide sequence that is present in only 30% of molecules. This exposes an active site for the neutralization of numerous activated coagulation factors. Factor Xa is inactivated via this mechanism. In contrast, factor IIa (thrombin) inactivation requires the formation of a ternary complex in which thrombin and AT III bind to heparin molecules with at least 18 to 20 saccharide units. Only 25% to 50% of LMWH molecules contain this critical length, thus reducing their anti-IIa activity while maintaining anti-Xa activity. Unfractionated heparin and LMWH also cause a two- to sixfold increase in TFPI, via release from the endothelial surface. TFPI forms a complex with factors VIIa, Xa, and TF, inhibiting the conversion of factor IX to IXa and factor X to Xa. Unfractionated heparin binds to numerous plasma proteins (platelet factor 4, vitronectin, fibronectin), platelet glycoprotein receptors, and vascular endothelium. This may be responsible for the variable bioavailability and anticoagulant response. Heparin is cleared via the reticuloendothelial cells (saturable) and kidneys (nonsaturable), resulting in a dose-dependent half-life that ranges from 45 to 150 minutes. LMWHs demonstrate less binding to plasma proteins and endothelium, resulting in a greater bioavailability and a more predictable therapeutic response. As a result, weight-adjusted dosages may be administered without therapeutic monitoring. LMWHs are cleared primarily via the kidneys, with plasma half-lives that are twofold to fourfold longer than that of unfractionated heparin. Unfractionated heparin may be administered as an IV bolus of 80 to 100 U/kg, followed by an infusion of 15 to 18 U/kg per hour. The aPTT is monitored every 6 hours

until the dosage and therapeutic response have stabilized. The therapeutic range of 1.5 to 2.5 times control varies from one laboratory to another and should be standardized by protamine titration. Alternatively, direct heparin assays may be used for therapeutic monitoring of patients receiving parenteral unfractionated heparin infusions. Platelet counts should be monitored on a regular basis to allow the early detection of HIT. LMWHs are rapidly absorbed after subcutaneous injection. The dosage varies according to the commercial preparation used. Some preparations with longer half-lives require only once-daily dosing. LMWH is at least as effective as and is perhaps safer than unfractionated heparin for some treatment indications (e.g., venous thromboembolism).107 The primary advantage of LMWH is the convenience of infrequent subcutaneous dosing without the need for therapeutic monitoring assays, which may allow outpatient treatment in some cases. The lower incidence of HIT is another advantage of LMWH. Disadvantages of LMWH include expense and the need for monitoring in certain patients, including those with advanced renal failure, morbid obesity, and pregnant patients. Heparinoids Danaparoid (Organon Inc., West Orange, N.J.) is the most widely tested heparinoid. It is composed of heparan sulfate (83%), dermatan sulfate (12%), and chondroitin sulfate (5%). Like LMWH, danaparoid is derived from animal intestinal mucosa. It has a mean molecular weight of 6000 Da. The heparan sulfate component of danaparoid binds to AT III via the specific pentasaccharide sequence, with preferential inactivation of factor Xa. The dermatan sulfate component of danaparoid also has slight anti-IXa activity through a mechanism involving heparin cofactor II. Rapid anticoagulation may be achieved with an IV bolus of 2250 to 2500 U (adjustment for weight may be required), followed by a continuous infusion with a stepwise decreasing rate (400 U/hour for 2 to 4 hours, then 300 U/hour for 2 to 4 hours, then 150 to 200 U/hour).108 Danaparoid has been used successfully as an alternative antithrombotic agent in patients with HIT. However, danaparoid carries a 10% to 20% rate of cross-reactivity with antiheparin antibodies.108,109 Before using danaparoid in HIT-positive patients, cross-reactivity testing should be performed. Direct thrombin inhibitors have largely supplanted danaparoid in HIT. Direct Thrombin Inhibitors Indirect thrombin inhibitors (unfractionated heparin and LMWH) have a limited ability to neutralize fibrin-bound thrombin and are dependent on adequate levels of AT III. In contrast, direct thrombin inhibitors are capable of inhibiting thrombin on established thrombi and do not require the presence of antithrombin in order to exert anticoagulant effects.110 Direct thombin inhibitors are based on the naturally occurring anticoagulant produced in the salivary gland of the medicinal leech (Hirudo medicinalis). Hirudin derivatives (lepirudin and desirudin) and bivalirudin (a hirudin analog) are bivalent direct thrombin inhibitors. Univalent direct thrombin inhibitors include argatroban and ximelagatran.

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Hirudin is a 65–amino acid polypeptide derived from the salivary gland of the medicinal leech. It forms a stoichiometric complex with thrombin, blocking the catalytic site, substrate groove, and anion binding site, preventing the formation of fibrin and factors Va, VIIIa, and XIIIa.111 Hirudin also inhibits thrombin-induced platelet activation and aggregation. Hirudin therapy is initiated with an IV bolus of 0.4 mg/kg, followed by a continuous infusion of 0.15 mg/kg per hour. Therapy may be monitored using the aPTT (therapeutic range, 1.5 to 2.5 times reference) or a more recently developed assay, the ecarin clotting time.112 After an initial distribution phase, hirudin follows first-order elimination kinetics. It is excreted via the kidneys and has a half-life ranging from 1 to 2 hours. Patients with renal insufficiency or failure and patients weighing more than 110 kg require significant dosage adjustments. Hirudin may also be administered subcutaneously. Hirudin is currently approved for the management of HIT complicated by thrombosis.113 However, the rate of adverse events still remains significant (up to 30%), probably reflecting the severity of illness in HIT patients. Numerous clinical trials have compared hirudin with heparin in the treatment of patients undergoing coronary angioplasty and coronary thrombolysis and patients with unstable angina. Hirudin was associated with a decreased risk for ischemic events compared with heparin therapy. Some trials also demonstrated an increased incidence of major hemorrhage, although this complication usually occurred when hirudin was given in conjunction with thrombolytic agents.114 As with heparin, hirudin has the potential to cause an immunologic reaction with resulting anaphylaxis. Approximately 40% of patients develop detectable antihirudin antibodies. Unlike heparin antibodies, however, these are not associated with the development of any resistance to therapy or with thromboembolic or bleeding complications.115 Bivalirudin is a synthetic 20–amino acid polypeptide analog of hirudin that reversibly binds to thrombin. When compared with hirudin, it has several advantages, including the ability to administer the medication intravenously or subcutaneously. Bivalirudin also has a shorter half-life, a nonrenal route of metabolism, and decreased immunogenicity. Currently it is approved in the United States as an anticoagulant in patients with unstable angina who undergo angioplasty.116 Argatroban is a synthetic univalent direct thrombin inhibitor that reversibly binds to thrombin.110 It is approved for use as an anticoagulant for prophylaxis or treatment of thrombosis in patients with HIT. It is also approved as an anticoagulant in patients undergoing percutaneous coronary intervention who are at risk for HIT. Argatroban has a short half-life of 39 to 51 minutes and reaches a steady state with IV infusion at 1 to 3 hours. The level of anticoagulation may be monitored with the aPTT or activated clotting time. Argatroban is metabolized primarily by the liver and is excreted in the feces via biliary secretion. Therefore, doses should be decreased in patients with hepatic impairment. Ximelagatran is a promising new oral anticoagulant that is in late-phase clinical trials.117 It is already approved for use in the European Union for the prevention of venous thromboembolism in patients undergoing hip or knee replacement. It can be administered orally without food interactions and has predictable pharmacokinetics. There is also little variability

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in bioavailability between obese and nonobese individuals. Ximelagatran is a rapidly absorbed prodrug that is converted into its active form melagatran, a reversible direct thrombin inhibitor. Melagatran is excreted renally. Therefore, dosage adjustments should be made in patients with renal insufficiency. In clinical trials, ximelagatran has been as effective as LMWH or warfarin in preventing the progression of deep venous thrombosis.118 Prolonged administration of ximelagatran is associated with elevated liver enzymes in approximately 2% to 6% of patients.119 Rare cases of fulminant hepatic failure have been reported. Warfarin Coumarin derivatives, including warfarin, block the vitamin K–dependent γ-carboxylation of glutamine residues on factors II, VII, IX, and X and proteins C and S. This results in the production of vitamin K–dependent proteins, which have a decreased number of Gla residues and decreased enzymatic activity. A reduction in the number of Gla residues from the usual 10 to 13 to 6 decreases the coagulation factor biologic activity by more than 95%. An antithrombotic state depends on the replacement of functional coagulation factors present in the circulation with the altered coagulation proteins. Factor VII and protein C have the shortest half-lives— approximately 6 hours each. Factor II and factor X have longer half-lives of approximately 72 and 36 hours, respectively. Although warfarin may prolong the PT within 24 hours, owing to factor VII depletion, an antithrombotic state is usually not attained for 2 to 4 days. Warfarin is rapidly absorbed and reaches a maximum plasma concentration within 2 to 12 hours. Ninety-seven percent of warfarin circulates bound to albumin, with the unbound portion responsible for the anticoagulant effect. The amount of warfarin required to cause a prolongation of the PT depends on the amount of dietary vitamin K, the age of the patient, and comorbid conditions (liver failure, obstructive jaundice, starvation). Numerous medications have been found to potentiate or interfere with the activity of warfarin (Table 5-2). Patients on long-term oral anticoagulation who begin or stop a medication that may interfere with or potentiate warfarin activity should be monitored with more frequent PT measurements. Warfarin therapy is initiated by the oral intake of 5 to 7.5 mg once a day. Reduced dosages should be given to elderly patients and patients with liver disease or vitamin K deficiency as a result of malnutrition or long-term parenteral feeding. Because factor II and factor X depletion may not be effective for 2 to 4 days, heparin or an alternative agent should be administered during the first few days of warfarin therapy for patients who require immediate anticoagulation. The PT assay is most commonly used to monitor warfarin therapy. This test is sensitive to changes in activity of factors II, VII, IX, and X. The PT assay is performed by adding thromboplastin and calcium to citrated plasma. Thromboplastins vary according to their ability to activate the external coagulation cascade and are graded by the international sensitivity index (ISI). The international normalized ratio (INR) attempts to standardize PT assays, which use different thromboplastins, according to the following equation: INR = [patient PT (sec)/population PT (sec)]ISI

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TABLE 5–2

Common Drug Interactions with Oral Anticoagulants

Potentiate

Antagonize

Acetaminophen Anabolic steroids Cephalosporins Chloral hydrate Cimetidine Ciprofloxacin Clofibrate Cotrimoxazole Disulfiram Erythromycin Fluconazole Isoniazid Itraconazole Metronidazole Omeprazole Phenylbutazone Phenytoin Piroxicam Propafenone Propoxyphene Propranolol Quinidine Sulfinpyrazone Tamoxifen Tetracycline

Barbiturates Carbamazepine Chlordiazepoxide Cholestyramine Dicloxacillin Griseofulvin Nafcillin Rifampin Sucralfate Vitamin K

From Hirsh J, Dalen JE, Anderson DR, et al: Oral anticoagulants: Mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 114(Suppl):445S-469S, 1998; and Wells PS, Holbrook AM, Crowther NR, et al: The interaction of warfarin with drugs and food: A critical review of the literature. Ann Intern Med 121:676-683, 1994.

PT should be monitored on a daily basis for the first 4 to 5 days of warfarin therapy. The INR usually achieves the desired range during this period. A longer period of daily monitoring is required in patients resistant to warfarin. Once the therapeutic range is attained, the PT can be monitored two to three times a week and then, when stable, every 4 to 6 weeks. Many patients are receiving heparin at the time that warfarin is initiated. Concomitant administration of heparin prolongs the PT, owing to the inactivation of factors IIa, IXa, and Xa by AT III. It should be expected that the PT will decrease when heparin is discontinued. The effect of heparin on the PT can be reduced by removing the heparin from the test plasma or by stopping the heparin infusion 4 to 6 hours before obtaining blood for the PT. The primary complication of warfarin therapy is hemorrhage, which occurs in 3% to 12% of patients.120 Less common complications include alopecia, urticaria, dermatitis, fever, nausea, diarrhea, abdominal cramping, and hypersensitivity reactions. Dermal gangrene is a rare complication (0.01% to 0.1% of patients receiving warfarin) caused by the rapid depletion of protein C before depletion of factors II, IX, and X.121 This risk increases to approximately 3% in patients with protein C deficiency.122 Concomitant administration of unfractionated heparin or LMWH should decrease the risk of this complication.

THROMBOEMBOLISM PROPHYLAXIS Venous Thromboembolism Prophylaxis The annual incidence of deep venous thombosis (DVT) is between 69 and 139 cases per 100,000 people in the general population.123 The prevalence of venous thomboembolism (VTE) in hospitalized patients is approximately 350 cases per 100,000 admissions and is a cause of death in approximately 250,000 people per year.124,125 Pulmonary embolism contributes to or causes up to 12% of all deaths in hospitalized patients.126 DVT poses an immediate threat to life because of the potential for pulmonary embolism and may also lead to long-term impairment due to resultant venous insufficiency. The 20-year cumulative incidence rate is 26.8% and 3.7% for the development of venous stasis changes and venous ulcers, respectively, after an episode of DVT.127 General risk factors for VTE include blood flow stasis, endothelial damage, and hypercoagulability. Relative hypercoagulability appears to be most important in the majority of cases of spontaneous DVT, whereas stasis and endothelial damage are more important in DVT following surgery or trauma. Specific risk factors include prior history of VTE, age, surgery, malignancy, obesity, trauma, varicosities, cardiac disease, hormones, immobilization or paralysis, pregnancy, venous catheterization, and hypercoagulable states.88,89,126,128-135 In one population-based study, more than 90% of patients hospitalized for VTE had more than one risk factor.126 In surgical patients, the risk of VTE is dependent on the type of operation and the presence of one or more risk factors.136 Without prophylaxis, patients undergoing surgery for intraabdominal malignancy have a 25% incidence of DVT; orthopedic patients undergoing hip fracture surgery have a 40% to 50% incidence of DVT in the postoperative period. Those at highest risk are elderly patients undergoing major surgery or those with previous VTE, malignancy, or paralysis. The incidence of venous thrombosis and pulmonary embolism may be reduced by limiting venous stasis, administering drugs to inhibit coagulation, or a combination of these approaches. Stasis is reduced by ambulation and pneumatic compression of the lower extremities. Intermittent pneumatic compression (IPC) devices reduce lower extremity venous stasis, enhance fibrinolytic activity, and increase plasma levels of TFPI.137 Elastic stockings also decrease stasis and increase venous flow velocities. Both devices appear to decrease the incidence of DVT in patients who undergo general, urologic, and gynecologic surgical procedures. The incidence of DVT in control patients ranges from 20% to 27%, whereas the use of IPC is associated with a DVT incidence of 10% to 18%.129,138 IPC devices also decrease the incidence of DVT in patients undergoing hip or knee replacement. However, mechanical prophylaxis alone is probably not sufficient in patients undergoing total hip replacement and should be supplemented with either LMWH or adjusted-dose unfractionated heparin or warfarin.105 IPC provides effective thrombosis prophylaxis in patients who undergo neurosurgical procedures (6% incidence with IPC, 23% in controls).139 The effectiveness of IPC devices is limited by a lack of compliance among patients and nursing staff. Intermittent pneumatic foot compression devices may improve patient acceptance. However, these newer devices are less effective than other forms of DVT prophylaxis, especially in patients undergoing orthopedic procedures.140

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Subcutaneous heparin is used to decrease the incidence of VTE. Unfractionated heparin (5000 U SC 2 hours preoperatively, followed by 5000 U every 8 to 12 hours postoperatively) decreases the overall incidence of venous thrombosis to approximately 8%.105 The incidence of pulmonary embolism is reduced as well. This regimen is probably adequate in moderate- and high-risk general surgical patients. Two large meta-analyses have demonstrated that LMWH confers no additional protection in this population and may be associated with an increased risk of hemorrhagic complications.141,142 However, fixed low-dose unfractionated heparin prophylaxis is not as effective in patients with hip fractures or in those undergoing total hip or knee replacement. Orthopedic and very high-risk general surgical patients (those with additional risk factors) should receive more effective DVT prophylaxis (LMWH, adjusted-dose warfarin, adjusted-dose unfractionated heparin, or combination prophylaxis with IPC). The aPTT does not require monitoring in patients receiving fixed-dose unfractionated heparin or LMWH prophylaxis. Platelet counts should be monitored for the detection of HIT. LMWH produces fewer thromboembolic complications than unfractionated heparin does. In a large randomized, double-blinded study comparing low-dose heparin (5000 U SC twice a day) and LMWH (enoxaparin 30 mg SC twice a day) in trauma patients without intracranial hemorrhage, there was a 30% risk reduction (P = 0.01) of DVT in patients given LMWH.143 The overall major bleeding complication rate was 2%, with no statistical difference between the two groups. Early use of LMWH for VTE prophylaxis is contraindicated in patients with intracranial bleeding, spinal hematoma, ongoing and uncontrolled hemorrhage, or uncorrected coagulopathy. Patients who undergo major orthopedic procedures without DVT prophylaxis are at high risk for thromboembolic complications (45% to 61%). Depending on the preparation, LMWH decreases the incidence significantly (15% to 31%) compared with fixed-dose unfractionated heparin (27% to 42%).105,144 Preoperative initiation of LMWH (vs. beginning postoperatively) may decrease the overall incidence of DVT in patients undergoing hip replacement (10% preoperative vs. 15.3% postoperative) without increasing the incidence of hemorrhage.145 There is also evidence that longer durations of prophylaxis are more effective. Several randomized trials have found a significantly lower rate of thrombosis with 21 to 35 days of LMWH administration.146-148 The additional use of IPC devices may decrease the incidence even further. Numerous randomized trials have compared various LMWH preparations (enoxaparin, certoparin, dalteparin, nadroparin, parnaparin, reviparin, tinzaparin) against unfractionated heparin as DVT prophylaxis in general surgical patients. Only 4 of 29 trials identified a significant improvement with LMWH.149 Although the dosage regimens varied widely among trials, there was a tendency toward superior prophylaxis with LMWH when higher dosages were used. Very high-risk patients who undergo general surgical procedures (multiple risk factors, malignancy, thrombophilia) may benefit most from LMWH prophylaxis. The optimal timing for the first prophylactic dose of LMWH remains in question. General surgical patients who receive the first dose before surgery do not appear to experience any additional hemorrhagic complications.149

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Fondaparinux is a chemically synthesized agent that binds and activates antithrombin, which then selectively inhibits factor Xa. It does not act against thrombin (factor IIa). Because it is chemically synthesized, fondaparinux does not contain any animal products. It is specific to antithrombin and does not bind to platelets, therefore minimizing the risk of HIT. The results of a randomized, double-blinded trial comparing fondaparinux and LMWH for the prevention of VTE after elective hip replacement surgery were recently published.150 There was no statistical difference between the two groups in the incidence of VTE. The incidence of VTE was 6% in the fondaparinux group and 8% in the enoxaparin group. There was also no difference in the incidence of major bleeding complications, with 20 events in the fondaparinux group and 11 events in the LMWH group. Fondaparinux is commercially available but has not been evaluated as prophylactic therapy for VTE in patients other than those undergoing surgery of the hip and knee. Warfarin has been established in several studies as efficacious prophylaxis against VTE. Sevitt and Gallagher found that the incidence of clinical venous thrombosis in patients with hip fractures decreased from 28.7% in the control group to 2.7% in the group treated with oral anticoagulation. At autopsy, the incidence of thrombosis in the two groups was 83% and 14%, respectively.151 In other studies, oral anticoagulants with an INR range of 2.0 to 3.0 were effective in preventing venous thrombosis in patients undergoing orthopedic and gynecologic surgery.152,153 Very high-risk patients, such as those undergoing major orthopedic procedures, should receive either LMWH or adjusted-dose warfarin. LMWH may be more effective than warfarin, but the difference is probably small. If warfarin is selected, it should be started preoperatively or immediately after surgery. The dosage should be adjusted to achieve a target INR between 2.0 and 3.0.105 With warfarin, the duration of prophylaxis can easily be extended in patients who continue to have risk factors for VTE (immobility, malignancy, a history of previous venous thrombosis). Current recommendations for VTE prophylaxis in surgical patients vary according to the type of surgical procedure planned and underlying risk factors in a given patient. Table 5-3 summarizes current recommendations from the American College of Chest Physicians’ 2004 consensus statement on prophylaxis for surgical patients.154 Arterial Thromboembolism Prophylaxis Arterial thrombosis occurs in regions with disturbed flow or disrupted endothelial coverage (as with plaque rupture or endarterectomy). Subendothelial collagen and vWF initiate platelet adhesion and activation, whereas TF activates the coagulation cascade, leading to the generation of thrombin and fibrin. Arterial thrombi contain relatively higher concentrations of platelets. As a result, most long-term arterial antithrombotic regimens focus on the inhibition of platelet function. Aspirin acetylates platelet cyclooxygenase-1 (prostaglandin H synthase-1), blocking the conversion of arachidonic acid to the prostaglandin endoperoxides PGH2 and PGG2. This effectively inhibits the synthesis of TXA2 for the life span of the platelet. Aspirin also inhibits prostacyclin

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TABLE 5–3

Recommendation for Venous Thromboembolism Prophylaxis in Surgical Patients

Indication

Prophylaxis Method

Low-risk general surgery (minor surgery, age < 40 yr, no risk factors) Moderate-risk general surgery (minor surgery with risk factors; major surgery, age > 40 yr, no risk factors) High-risk general surgery (minor surgery with risk factors, age > 60 yr; major surgery, age > 40 yr or additional risk factors) Very high risk general surgery (multiple risk factors) Elective hip replacement Elective knee replacement Hip fracture surgery Major trauma Acute spinal cord injury

Early ambulation LDH, LMWH, ES, or IPC LDH, LMWH, or IPC LMWH, fondaparinux, warfarin (INR 2-3), or IPC/ES + LDH/LMWH

ES, elastic compression stockings; INR, international normalized ratio; IPC, intermittent pneumatic compression; LDH, low-dose heparin; LMWH, low-molecular-weight heparin.

synthesis by endothelial cells. However, endothelial cells have nuclei and can synthesize new prostacyclin synthetase, reversing the effects of aspirin. Noncoated aspirin is rapidly disintegrated and absorbed in the stomach. Enteric-coated aspirin dissolves in the more neutral to alkaline pH within the duodenum. Enteric coating does not significantly delay the bioavailability compared with noncoated aspirin. Aspirin is the most widely employed antithrombotic agent, and there is considerable evidence supporting its efficacy in reducing the relative risk of serious vascular events (nonfatal myocardial infarction, nonfatal stroke, vascular death) in patients at high risk of these complications. The Antithrombotic Trialists’ Collaboration (ATTC) reviewed 287 studies encompassing more than 135,000 patients and noted absolute reductions in serious vascular events in patients with recent or remote myocardial infarction, stroke or transient ischemic attack, stable angina, peripheral arterial disease, and atrial fibrillation.155 Nonfatal myocardial infarction risk was reduced by 33%, nonfatal stroke was reduced by 25%, and vascular death was reduced by 16%. Aspirin is also efficacious in the primary prevention of stroke and myocardial infarction in patients with known risk factors for these conditions; however, the risk of hemorrhagic complications outweighs the benefits of aspirin therapy in patients at low risk for cardiovascular events.107,114,156 In general, lower doses of aspirin (75 to 150 mg/day) are effective. The ATTC trialists concluded that aspirin 75 to 150 mg/day is recommended routinely for all patients without contraindications who are at high or intermediate risk of vascular events (>2% per year risk), whether or not they have had a prior vascular event. Aspirin is also efficacious in maintaining vascular graft patency in patients following lower extremity revascularization. The Seventh Antithrombotic Consensus Conference, the American Heart Association, and the American College of Cardiology recommend aspirin 80 to 325 mg/day for prosthetic or saphenous vein peripheral bypass grafts and after carotid endarterectomy.154,157 Ticlopidine and clopidogrel are thienopyridine derivatives that irreversibly inhibit ADP-mediated platelet activation. Intact ticlopidine and clopidogrel have no effect on platelets in vitro, suggesting that their metabolites may be the more potent platelet inhibitors. Both are rapidly absorbed after oral

administration and are highly bound to plasma proteins (albumin and lipoproteins). Ticlopidine may alter platelet function within 24 to 48 hours, but maximum inhibition is not achieved for 8 to 11 days. Clopidogrel induces a dosedependent inhibition of platelet aggregation that is more rapid (within 2 hours). Ticlopidine significantly improves the patency of femoropopliteal and femorotibial saphenous vein grafts (66% vs. 51% at 2 years) compared with placebo.158 Compared with aspirin, ticlopidine also is associated with a decreased risk of stroke (10% vs. 13%).159 Other studies have demonstrated a decreased risk of myocardial infarction in patients with unstable angina and improved walking distance in patients with claudication.160,161 However, no studies have demonstrated that ticlopidine is superior to aspirin in improving lower extremity vascular graft patency. In addition, widespread use of ticlopidine is limited by the potentially severe side effects of pancytopenia and neutropenia.162 Clopidogrel has been advocated as an antiplatelet agent with an efficacy superior to that of aspirin. The Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) study evaluated more than 19,000 patients with a history of recent ischemic stroke, recent myocardial infarction, or symptomatic atherosclerotic peripheral vascular disease.163 Clopidogrel was associated with a relative risk reduction of 8.7% for future ischemic events, representing an absolute reduction of only 0.5% (5.32% with clopidogrel, 5.83% with aspirin). However, subgroup analyses demonstrated that patients with peripheral vascular disease received the greatest degree of risk reduction. Clopidogrel may be more beneficial as a combination therapy agent, because aspirin and clopidogrel inhibit platelet function via different signal transduction pathways (TXA2 and ADP inhibition). Some evidence for this comes from the more recent Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial, involving more than 12,500 patients.164 Patients receiving clopidogrel and aspirin had a decreased incidence of cardiovascular death, myocardial infarction, or stroke when compared with those receiving aspirin alone (9.3% vs. 11.4%, representing a 20% relative risk reduction). The incidence of neutropenia and pancytopenia with clopidogrel is similar to the incidence with aspirin or placebo.

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Glycoprotein IIb-IIIa inhibitors have been evaluated for stroke prevention in clinical trials. Fibrinogen binds to the platelet GP IIb-IIIa receptor via the amino acid sequence ArgGly-Asp (RGD), representing the final common pathway for platelet aggregation regardless of the platelet agonist. The first GP IIb-IIIa inhibitor to be developed was c7E3 (abciximab), the antigen-binding fragment (Fab) of a monoclonal anti-GP IIb-IIIa antibody. Subsequently, naturally occurring RGD peptides (trigramin, bitistatin) have been isolated from the venom of several species of vipers. Synthetic RGD peptides (eptifibatide, tirofiban, lamifiban), as well as more potent KGD analogs, have been manufactured and undergone clinical trials.17 Most trials involved patients who had coronary angioplasty and those with unstable angina or myocardial infarction.165-167 The primary indication for the use of GP IIbIIIa receptor antagonists is for acute coronary syndromes. GP IIb-IIIa inhibitors have no role in the long-term prevention of stroke or complications related to peripheral vascular disease. The major risk of using GP IIb-IIIa receptor antagonists is bleeding. Abciximab has a very short half-life (10 to 30 minutes) caused by rapid binding to the platelet GP IIb-IIIa receptor. Significant platelet function inhibition continues for up to 48 hours after infusions are discontinued.166 Synthetic RGD peptides (eptifibatide, tirofiban) demonstrate more reversible platelet inhibition. The half-lives of these agents range from 2 to 2.5 hours, with most of the elimination occurring via the kidneys. Platelet function generally returns to near normal within 4 to 8 hours. Warfarin has an established role in the prevention of thromboembolism in selected patients with atrial fibrillation and prosthetic heart valves. Other possible indications for long-term warfarin therapy include the prevention of myocardial ischemia and the prevention of systemic embolism after acute myocardial infarction.168 Several studies also indicate that warfarin may improve the patency of lower extremity bypass grafts. In a randomized trial involving 130 patients who underwent femoropopliteal vein bypass surgery, Kretschmer and coworkers found improved patency, limb salvage, and overall survival in patients receiving phenprocoumon (a coumarin derivative).169,170 Flinn and colleagues also found that warfarin improved patency in patients with infrageniculate prosthetic grafts.171 More recent studies involving patients at high risk for failure (suboptimal vein, poor outflow, redo procedures) have confirmed an improved patency with warfarin plus aspirin compared with aspirin alone.172 Long-term warfarin therapy is a reasonable option for most patients with prosthetic infrainguinal or axillofemoral bypass grafts, suboptimal venous conduit, or poor outflow tracts (e.g., isolated popliteal arteries). Patients who are treated with warfarin should receive overlapping unfractionated heparin, LMWH, or IV heparin until the therapeutic INR is achieved (target INR, 2.0 to 3.0). KEY REFERENCES Almeida JI, Coats R, Liem TK, Silver D: Reduced morbidity and mortality of the heparin-induced thrombocytopenia syndrome. J Vasc Surg 27: 309-314, 1998. Antiplatelet Trialists’ Collaboration: Collaborative overview of randomised trials of antiplatelet therapy. I. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 308:81-106, 1994.

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147. Dahl OE, Andreassen G, Aspelin T, et al: Prolonged thromboprophylaxis following hip replacement surgery—results of a double-blind, prospective, randomised, placebo-controlled study with dalteparin (Fragmin). Thromb Haemost 77:26-31, 1997. 148. Lassen MR, Borris LC, Anderson BS, et al: Efficacy and safety of prolonged thromboprophylaxis with a low molecular weight heparin (dalteparin) after total hip arthroplasty—the Danish Prolonged Prophylaxis (DaPP) Study. Thromb Res 89:281-287, 1998. 149. Breddin HK: Low molecular weight heparins in the prevention of deep-vein thrombosis in general surgery. Semin Thromb Hemost 25 Suppl 3:83-89, 1999. 150. Turpie AG, Bauer KA, Eriksson BI, et al: Postoperative fondaparinux versus postoperative enoxaparin for prevention of venous thromboembolism after elective hip-replacement surgery: A randomised double-blind trial. Lancet 359:1721-1726, 2002. 151. Sevitt S, Gallagher NG: Prevention of venous thrombosis and pulmonary embolism in injured patients: A trial of anticoagulant prophylaxis with phenindione in middle-aged and elderly patients with fractured necks of femur. Lancet 2:981-989, 1959. 152. Powers PJ, Gent M, Jay RM, et al: A randomized trial of less intense postoperative warfarin or aspirin therapy in the prevention of venous thromboembolism after surgery for fractured hip. Arch Intern Med 149:771-774, 1989. 153. Poller L, McKernan A, Thomson JM, et al: Fixed minidose warfarin: A new approach to prophylaxis against venous thrombosis after major surgery. BMJ (Clin Res Ed) 295:1309-1312, 1987. 154. Geerts WH, Pineo GF, Heit JA, et al: Prevention of venous thromboembolism. The seventh ACCP Conference on antithrombotic and thrombolytic therapy. Chest 126:3385-4005, 2004. 155. Antithrombotic Trialists’ Collaboration: Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 324:71-86, 2002. 156. Spinal Cord Injury Thromboprophylaxis Investigators: Prevention of venous thromboembolism in the rehabilitation phase after spinal cord injury: Prophylaxis with low-dose heparin or enoxaparin. J Trauma 54:1111-1115, 2003. 157. Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA guideline update for the management of patients with unstable angina and nonST-segment elevation myocardial infarction—2002. Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients with Unstable Angina). Circulation 106:1893-1900, 2002. 158. Becquemin JP: Effect of ticlopidine on the long-term patency of saphenous-vein bypass grafts in the legs: Etude de la Ticlopidine apres Pontage Femoro-Poplite and the Association Universitaire de Recherche en Chirurgie. N Engl J Med 337:1726-1731, 1997. 159. Hass WK, Easton JD, Adams HP Jr, et al: A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients: Ticlopidine Aspirin Stroke Study Group. N Engl J Med 321:501-507, 1989. 160. Balsano F, Rizzon P, Violi F, et al: Antiplatelet treatment with ticlopidine in unstable angina: A controlled multicenter clinical trial. The Studio della Ticlopidina nell’Angina Instabile Group. Circulation 82:17-26, 1990. 161. Arcan JC, Blanchard J, Boissel JP, et al: Multicenter double-blind study of ticlopidine in the treatment of intermittent claudication and the prevention of its complications. Angiology 39:802-811, 1988. 162. Yusuf S, Mehta SR, Zhao F, et al: Early and late effects of clopidogrel in patients with acute coronary syndromes. Circulation 107:966-972, 2003. 163. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet 348:1329-1339, 1996. 164. Yusuf S, Zhao F, Mehta SR, et al: Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 345:494-502, 2001. 165. Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty: The EPIC Investigation. N Engl J Med 330:956-961, 1994. 166. Simoons ML, de Boer MJ, van den Brand MJ, et al: Randomized trial of a GPIIb/IIIa platelet receptor blocker in refractory unstable angina: European Cooperative Study Group. Circulation 89:596-603, 1994.

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167. Kleiman NS, Ohman EM, Califf RM, et al: Profound inhibition of platelet aggregation with monoclonal antibody 7E3 Fab after thrombolytic therapy: Results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) 8 Pilot Study. J Am Coll Cardiol 22:381-389, 1993. 168. Hirsh J, Dalen JE, Anderson DR, et al: Oral anticoagulants: Mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 114:445S-469S, 1998. 169. Kretschmer G, Wenzl E, Piza F, et al: The influence of anticoagulant treatment on the probability of function in femoropopliteal vein bypass surgery: Analysis of a clinical series (1970 to 1985) and interim evaluation of a controlled clinical trial. Surgery 102:453-459, 1987. 170. Kretschmer G, Herbst F, Prager M, et al: A decade of oral anticoagulant treatment to maintain autologous vein grafts for femoropopliteal atherosclerosis. Arch Surg 127:1112-1115, 1992. 171. Flinn WR, Rohrer MJ, Yao JS, et al: Improved long-term patency of infragenicular polytetrafluoroethylene grafts. J Vasc Surg 7:685-690, 1988. 172. Sarac TP, Huber TS, Back MR, et al: Warfarin improves the outcome of infrainguinal vein bypass grafting at high risk for failure. J Vasc Surg 28:446-457, 1998.

Questions 1. Which of the following statements regarding antiplatelet therapy is true? (a) Lower dosages of aspirin (75 to 150 mg/day) are not as effective as higher dosages (325 mg/day) for the prevention of cerebrovascular ischemic events (b) Ticlopidine is associated with a small but significant incidence of neutropenia (c) When compared with aspirin, clopidogrel is associated with a significantly greater incidence of neutropenia (d) For the prevention of ischemic events, combination therapy with clopidogrel and aspirin is no better than aspirin alone 2. Regarding the management of heparin-induced thrombocytopenia (HIT), which of the following is true? (a) Unfractionated heparin and low-molecular-weight heparin have a similar incidence of heparinassociated antibody formation (b) Low-molecular-weight heparin may be safely administered in patients with established HIT (c) The platelet count must be 1

Various

Relative Risk Reduction (%)

CVD mortality and morbidity CVD mortality and morbidity

29 20 42 45 26 62 69 51 –12 38 30 11

ABCD, Appropriate Blood Pressure Control in Diabetes; CVD, cardiovascular disease; HOT, Hypertension Optimal Treatment; MI, myocardial infarction; SHEP, Systolic Hypertension in the Elderly; Syst-Eur, Systolic Hypertension in Europe Trial; UKPDS, United Kingdom Prospective Diabetes Study.

There has been less enthusiasm for calcium channel blockers in persons with diabetes.60 Nevertheless, there is evidence that they can be effective as well, as shown in Table 8-3.

Evidence for the Influence of Glucose on the Pathophysiology of Vascular Disease Hyperglycemia is associated with vascular disease, as documented earlier. The reasons for this association remain speculative. Table 8-4 documents some of the hypothesized means by which glucose might influence pathologic vascular changes. These factors are discussed here in some detail. GLYCATION AND ADVANCED GLYCATION END PRODUCTS, OR EARLY AND LATE MAILLARD REACTIONS In 1976, it became clear that a minor hemoglobin component, Hb A1c, resulted from a post-translational modification of hemoglobin A by glucose and that there was a clinical relationship between Hb A1c and fasting plasma glucose, the peak on the glucose tolerance test, the area under the curve on the glucose tolerance test, and mean glucose levels over the preceding weeks.61-64 It soon became apparent that an improvement in ambient blood glucose levels resulted in correction of Hb A1c levels50-54 and that these nonenzymatic glycosylation reactions might provide a hypothesis that could explain a number of the pathologic sequelae of diabetes mellitus via toxicity arising from glucose adduct formation with proteins or nucleic acids.64 As early as 1912, Maillard suggested that the chemical reactions that now bear his name might play a role in the pathologic changes associated with diabetes mellitus.65

The ability of reducing sugars to react with the amino groups of proteins is now widely recognized, as is the natural occurrence of many nonenzymatically glycosylated proteins. Important details about the nature of such reactions are still unclear, however. The initial step (or early Maillard reaction) involves the condensation of an amino moiety with the aldehyde form of a particular sugar. Only a very small fraction of most common sugars is normally present in the aldehyde form.66,67 A number of transformations are possible following the addition of an amine to a sugar carbonyl group. Considerable evidence now exists that supports the involvement of an Amadori-type rearrangement for the adduct of glucose with the N-terminal

TABLE 8–4

Glucose Toxicity Hypothesis: Hyperglycemia Initiates or Propagates Vascular Disease by Multiple Mechanisms

Glycation of proteins and genetic material leading to dysfunctional or toxic products Interference with the fluid, vascular, and platelet phases of coagulation Perturbations in oxidation-reduction pathways Production of abnormal lipid metabolism Vascular volume shifts associated with changes in glycemia, or intracellular osmotic shifts associated with alternative metabolic pathways invoked when glucose is elevated, are toxic to the vascular tree Abnormal insulin or proinsulin levels in response to hyperglycemia contribute to vascular disease Perturbations in the immune system, including lymphokine production and polymorphonuclear leukocyte function, contribute to vascular disease

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of the β chain of hemoglobin. The labile Schiff base aldimine adduct is transformed into a relatively stable ketoamine adduct via the Amadori rearrangement. Because hemoglobin circulates in its red blood cell for approximately 120 days, there is little opportunity in this cell for late Maillard reactions, or nonenzymatic browning, to occur. In these late Maillard reactions, the Amadori product is degraded into deoxyglucosones that react again with free amino groups to form chromophores, fluorophores, and protein cross-links.68,69 In tissues that are longer lived, these reactions may be important mediators of diabetic changes as well as the aging process. Although the structure of a large number of nonenzymatic browning products has been elucidated, few have been obtained under physiologic conditions, thus making detection in vivo difficult and their pathologic role uncertain.70 Table 8-5 summarizes some of the

TABLE 8–5

Hypotheses Regarding the Potential Role of Nonenzymatic Glycation and Browning in the Pathologic Changes Associated with Diabetes Mellitus

I. Structural proteins A. Collagen: decreased turnover, flexibility, solubility, strength; increased aggregating potential for platelets; binding of immunoglobulins; cross-linking; and immunogenicity B. Lens crystallina and membrane: opacification, increased vulnerability to oxidative stress C. Basement membrane: increased permeability, decreased turnover, increased thickness D. Extracellular matrix: changes in binding to other proteins E. Hemoglobin: change in oxygen binding F. Fibrin: decreased enzymatic degradation G. Red blood cell membrane: increased rigidity H. Tubulin: cell structure and transport I. Myelin: altered structure and immunologic recognition II. Carrier proteins A. Lipoproteins: alternative degradative pathways and metabolism by macrophages and endothelial cells, increased immunogenicity B. Albumin: alteration in binding properties for drugs and in handling by the kidney C. IgG: altered binding III. Enzyme systems A. Copper-zinc superoxide dismutase: altered redox defense B. Fibrinogen: altered coagulation C. Antithrombin III: hypercoagulable state D. Purine nucleoside phosphorylase: aging of erythrocytes E. Alcohol dehydrogenase: substrate metabolism F. Ribonuclease A: loss of activity G. Cathepsin B: loss of activity H. N-acetyl-D-glucosaminidase: loss of activity I. Calmodulin: decreased calcium binding IV. Nucleic acids A. Age-related changes, congenital malformations V. Potentiation of other diseases of postsynthetic protein modification A. Carbamoylation-associated disorders in uremia B. Steroid cataract formation C. Acetaldehyde-induced changes in alcoholism

observations and hypotheses whereby glycation might promote pathologic changes in persons with elevated blood glucose. The Maillard reaction is ubiquitous in nature. The accumulation of advanced glycation end products (AGEs) in tissues in the human body has been implicated in the complications of diabetes, aging, and renal failure.71 The links between these reactions and the pathogenesis of nephropathy, macro- and microangiopathy, and cataracts in diabetic subjects are increasingly strong.72 AGEs accumulate in vivo on long-lived proteins in the vascular wall collagen and basement membranes as a function of age and levels of glycemia.73 They are capable of producing cross-linking of proteins and have been shown to display diverse biologic activities, including increased endothelial cell permeability,74 binding to receptors on macrophages and endothelial mesangial cells,75-77 activation of macrophages with secretion of cytokines after AGE ligand-receptor interaction,78 quenching of nitric oxide with the consequent inhibition of vascular dilatation,79 enhancement of oxidative stress,80 and oxidation of lowdensity lipoprotein.81 Thus, there is a growing body of evidence supporting a connection between circulating and tissue-accumulated AGEs and diabetic complications. COAGULATION FACTORS The coagulation cascade has been implicated in diabetesrelated complications through disorders of the platelet, fluid phase, and vascular components of clotting. The following sections briefly review the abnormalities in glucose metabolism and their relationship to these factors. Platelet The platelet, when obtained from patients with diabetes mellitus, has long been recognized as showing abnormal behavior in in vitro50 and in vivo studies.54 In general, the correction of hyperglycemia is associated with an improvement in platelet behavior and release. The potential role of the platelet in vascular disease in general is discussed elsewhere in this book. The lesion of the platelet associated with hyperglycemia appears to be related to a hypersensitivity to stimuli. Thus, platelet aggregation in vitro may occur spontaneously by stirring in plasma obtained from persons with Hb A1c greater than 10%, with concomitant release of vasoactive substances including serotonin, adenosine diphosphate, prostaglandins, and so on. The increased functional properties of diabetic platelets result in part from the primary release of larger platelets with enhanced thromboxane formation capacity and increased numbers of the functional glycoprotein (GP) receptors GP Ib and GP IIb/IIIa, which are synthesized in megakaryocytes.82 Insulin exerts an antiaggregating effect, but that effect is diminished in the obese and in subjects with NIDDM.83 Increased platelet aggregation to arachidonic acid has also been linked to reduced antioxidant properties seen in persons with diabetes.84 Platelet-rich or fibrin clots are less amenable to lysis in patients with diabetes than in controls.85 Further, the release of platelet plasminogen activator inhibitor-1 (PAI-1) in whole blood has been found to be increased in NIDDM subjects.86 PAI-1 levels have been noted to decrease with the lowering of blood glucose in NIDDM.87 Therefore, the platelet contributes not only to a prethrombotic state in persons with

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diabetes but also to problems of clot lysis in hyperglycemic subjects. The Evaluation of Platelet IIb/IIIa Inhibitor for Stenting Trial substudy is the most extensive evaluation of stenting and platelet IIb/IIIa blockade in persons with diabetes and provides additional evidence for the platelet’s role in the morbidity and mortality of heart disease and the associated processes in diabetes.88 The trial involved 491 diabetic patients who were divided into three groups: the first group received both a stent and abciximab, the second group underwent balloon angioplasty and also received the drug, and the third group had a stent implanted but received only a placebo. The reblockage rate was cut in half in the patients who received both the stent and the drug. Those patients had an 8.1% reblockage rate in the 6 months after the procedure, which was about half that of the other two groups. Ongoing trials of eptifibatide and tirofiban should help determine whether platelet IIb/IIIa receptor blockers should be used routinely to reduce restenosis after stenting in diabetic subjects, as well as the role of activated platelets and endothelium in pathologic conditions.88 These agents will become more attractive, in part because of the report of thrombotic thrombocytopenic purpura associated with ticlopidine in the setting of coronary artery stents.89 Fluid Phase of Coagulation Fibrinogen is increasingly recognized as a potential cardiovascular risk factor.90-92 Fibrinogen levels generally have been found to be elevated in diabetes. Fibrinogen synthesis is increased in part because of increased turnover and feedback to the liver with fragment D and because insulin increases fibrinogen synthesis.93 Early studies of fibrinogen kinetics in diabetic subjects documented a reversible disorder associated with hyperglycemia that was corrected with normal glucose levels or heparin administration, consistent with a lesion of antithrombin III activity in hyperglycemic subjects.94,95 These findings were confirmed by the PLAT Group study.96 Oxidative stress, which is accentuated in diabetic subjects, has been linked to thrombin activation, and a correlation between markers of oxidative stress and fibrinogen has been reported in diabetic subjects. Thus, oxidative stress, which is mediated by hyperglycemia and compounded by glycation, may represent an additional link between diabetes and hyperfibrinogenemia.97-99 Glycated fibrin is also less susceptible to plasmin degradation.100 Endothelial Phase of Coagulation Studies indicate that elevated glucose levels can be toxic to vascular endothelial cells through multiple mechanisms.101 Having observed that glucose levels mimicking diabetic hyperglycemia induce in vitro endothelial cell overexpression of extracellular matrix molecules, decreased replication, and increased levels of transforming growth factor-β (TGF-β) messenger RNA (mRNA), Cagliero and colleagues examined whether the effects of high glucose are mediated by autocrine TGF-β.101 Whereas the inhibitory effect of high glucose levels on endothelial cell replication was reversible, that of TGF-β was not. Both perturbations induced upregulation of fibronectin expression, but the effects were additive.

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Thus, there are growth-inhibitory effects of high glucose levels that are independent of TGF-β, and high glucose levels and TGF-β exert their effects through distinct pathways and at different loci. Pieper and coworkers attempted to evaluate the relative roles of hyperglycemia and insulin lack on endothelial cell dysfunction in diabetes.102 Rats were continuously infused with glucose or saline for 72 hours to achieve peak plasma glucose concentrations of approximately 25 mM. Plasma insulin rose by 12-fold in glucose-infused rats. Blood pressure was not altered by this intervention. Aortic rings taken from control rats relaxed to the administration of the endothelium-dependent vasodilators acetylcholine and A-23187 and the endothelium-independent vasodilator nitroglycerin. Relaxation to acetylcholine but not to A-23187 or nitroglycerin was impaired in glucose-infused rat aortic rings. Incubation in vitro with either indomethacin or superoxide dismutase did not restore the impaired relaxation to acetylcholine in rings taken from glucose-infused rats. Thus, hyperglycemia with hyperinsulinemia selectively impairs receptor-dependent, endothelium-dependent relaxation. These studies are consistent with the idea that elevated glucose may be a common pathway leading to endothelial dysfunction in IDDM and NIDDM. Baumgartner-Parzer and associates showed that adhesion molecule gene expression can be modulated by ambient glucose levels as well.103 These authors found an increase in intercellular adhesion molecule-1 (ICAM-1) but not platelet endothelial cell adhesion molecule expression in response to a high glucose level in human umbilical vein endothelial cells. These findings are also consistent with the specific abnormalities in endothelial dysfunction occurring in diabetes. In vivo–generated nitric oxide circulates in plasma mainly as an adduct of serum albumin. Compared with free nitric oxide, this nitric oxide adduct is relatively long-lived and exhibits vasodilating and platelet inhibitory properties. Farkas and Menzel documented that proteins lose their nitric oxide– stabilizing function after advanced glycosylation, thus providing another mechanism by which AGE-modified proteins can promote vascular disease.104 LIPIDS Hyperlipidemia is a normal concomitant of hyperglycemia. Both triglyceride and cholesterol levels tend to improve with normalization of blood glucose levels, as documented by ambient glucose levels and glycated hemoglobin levels.51 Further, glycation of low-density lipoproteins and modification by AGEs leads to a more atherogenic pattern of lipid metabolism.81 The presence of renal failure accelerates the pathologic changes associated with the presence of AGEs.105,106 Thus, improvement in glycemia corrects at least some of the perturbations of lipid metabolism unique to the individual with diabetes. Oxidation-Reduction Pathways Both the metabolism of excess glucose and the Amadori rearrangement product resulting from excess glycation can promote pro-oxidant activity.107,108 Lipid peroxides are thought to be formed by free radicals and may play an important role in the development of atheromatous vascular disease.

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Velazquez and colleagues investigated the relationship among lipids, lipoproteins, coagulation factors, and lipid peroxides (measured as thiobarbituric acid reacting species [TBARS]) in NIDDM patients with macrovascular disease.109 Eighteen diabetic and 20 nondiabetic subjects with clinical evidence of ischemic heart disease or peripheral vascular disease were investigated, together with 28 healthy subjects without evidence of vascular disease. TBARS concentration, as a measure of oxidation status, did not differ significantly in nondiabetic (mean, 5.0 mmol/L [95% CI, 4.5 to 5.7]) and diabetic (5.6 [range, 5.1 to 6.0] mmol/L) groups with macrovascular disease, although values were higher in both groups of patients with vascular disease compared with control subjects (2.7 [range, 2.4 to 3.1] mmol/L; P < 0.001). Significant univariate correlations between TBARS concentration and measures of blood glucose control (fructosamine, blood glucose, and Hb A1c) were found for all 66 subjects (P < 0.001 to 0.01). Thus, diabetes confers a pro-oxidant internal environment consistent with the promotion of vascular disease. VASCULAR VOLUME SHIFTS In studies of fibrinogen turnover, it became apparent that it was important to correct for vascular volume shifts induced by changes in glucose. When blood glucose was elevated from 100 mg/dL to 300 mg/dL, a rise in vascular volume of 8% was documented by double-labeling techniques.95 The implications for these types of recurrent volume shifts and the resultant stresses on the vascular tree have not been studied. INSULIN LEVELS In NIDDM there is thought to be an increased atherogenic potential related to the presence of insulin resistance, hyperinsulinemia, central obesity, and dyslipidemia. This syndrome, now known as syndrome X,110 was previously called CHAOS (coronary artery disease, hypertension, NIDDM, obesity, stroke) or the “deadly quartet” of upper body obesity, glucose intolerance, hypertriglyceridemia, and hypertension. All were associated with the early development of coronary artery disease. Because of these syndromes, insulin resistance with hyperinsulinemia has been studied as a risk factor for CVD. There have been several epidemiologic studies showing a correlation of hyperinsulinemia with CVD.110-112 Angiographically documented coronary artery disease has been linked with impaired glucose and insulin metabolism.110 The proposed pathophysiology of hyperinsulinemia and atherosclerotic disease is complicated. Hyperinsulinemia is associated with increased triglycerides, increased verylow-density lipoproteins, decreased high-density lipoproteins, central obesity, vascular intimal hyperplasia, and possibly hypertension, each of which may accelerate the development of atheroma. However, some studies implicate proinsulin as the culprit, rather than insulin itself, and suggest that exogenous insulin does not increase the risk of CVD.113,114 Intervention studies of the effect of glucose control on the initiation and progression of large vessel disease in persons with diabetes mellitus are sorely needed. These interactions have been modified to include a role for insulin and glucose in regulating central sympathetic activity.115 Thus, the links among obesity, diet, insulin resistance, hyperinsulinemia,

sympathetic activity, and lipid disorders are becoming better defined. IMMUNOLOGIC MECHANISMS There are multiple potential interactions of the immune system in the genesis of vascular disease. A number of the cytokine-lymphokine perturbations induced by glycation were discussed earlier. Immune perturbations specific to diabetes and the development of vascular disease have not yet been identified. Because diabetes is heterogeneous and exhibits similar vascular changes despite the cause or the phenotype, it is unlikely that a particular genetic lesion of the immune system will be linked to the accelerated vascular disease seen in diabetes. The one lesion in the immune system of importance to the surgeon is that of the polymorphonuclear leukocyte. The polymorphonuclear leukocyte functions abnormally in a person with hyperglycemia, with decreased adherence, migration, chemotaxis, and killing.50,116 The lesion of the polymorphonuclear leukocyte reverses within a marrow transit time of 14 days.50 Therefore, the optimal surgical candidate is one who has had normoglycemia for 2 weeks before surgery. INFLAMMATORY PROCESSES The Atherosclerosis Risk in Communities study found a role for inflammation and endothelial dysfunction in the pathogenesis of type 2 diabetes.117 It also appears that circulating inflammatory factors such as tumor necrosis factor-α and interleukin-6 may cause insulin resistance and obesity.118,119 SMOKING The Speedwell study emphasized the critical role of smoking in the genesis of vascular disease, especially in persons with diabetes.120 Systolic blood pressure, fasting plasma glucose, triglycerides, and white blood cell count were all independently associated with the development of intermittent claudication, angina, and death, but the most striking association was with smoking.

Other Risk Factors for Diabetesor Hyperglycemia-Associated Vascular Disease IMPAIRED GLUCOSE TOLERANCE Approximately 16% of American adults aged 40 to 74 years have impaired glucose tolerance (IGT), and approximately 6.6% have diabetes.121 Because 1% to 5% of those with IGT and 5% to 10% of those at high risk for NIDDM become diabetic each year, IGT is an important risk factor for diabetes.122-130 In addition, macrovascular disease is present, and mortality rates are higher in individuals with IGT.123,127,130 It appears that individuals with IGT have diabetic risk factor values (defined later) that fall between the values for normoglycemic individuals and those for diabetic individuals. Harris suggested “that IGT and NIDDM may have similar natural histories and may reflect a continuum of declining glucose tolerance from IGT to overt diabetes.”128

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PHYSICAL INACTIVITY AND OBESITY Over the last few decades, the importance of physical activity for disease prevention and health maintenance has been increasingly recognized. The benefits of exercise and increased physical activity include enhanced insulin sensitivity and glucose effectiveness, decreased risk for hypertension, improved plasma lipids and lipoproteins, decreased obesity and improved body fat distribution, enhanced immunologic function, decreased anxiety and depression, improved sleep, improved psychological characteristics in both normal and psychiatric patients, and disease prevention.131 Obesity and an unfavorable body fat distribution, with increased abdominal fat, are well-established risk factors for diabetes, confounded by ethnicity and family history.132-134 For obese individuals, the rates of diabetes are higher in Hispanics than in African Americans, and the rates in African Americans are higher than those in whites. Up to 50% of obese Native Americans develop diabetes.122 Data from the Second National Health and Nutrition Examination Survey revealed that 24.2% of men and 27.1% of women aged 20 to 74 years were overweight (BMI = 27.8 kg/m2 for men and BMI = 27.3 kg/m2 for women).135 It is estimated that in the United States there are 34 million overweight adults, 12.5 million of whom are “severely overweight.”136 In a study of 8715 men (mean age, 42 years) followed for an average of 8.2 years, the age-adjusted death rate increased with higher levels of fasting glucose, and fit men had a lower age-adjusted all-cause death rate compared with unfit men regardless of glycemic status.137 Fit men with a fasting blood glucose (FBG) less than 6.4 mM had the lowest age-adjusted death rate (21.4 per 10,000 person-years). Within each class of glycemic status (FBG < 6.4 mM, FBG 6.4 to 7.8 mM, FBG ≥ 7.8 mM, or diagnosed NIDDM), those who were fit had lower mortality rates than those who were unfit. Men who were fit but in the highest glycemic status group had an age-adjusted all-cause mortality rate (45.9 per 10,000 person-years) similar to that of men who were unfit but in the lowest glycemic status group. The data suggest that the risk of death for fit men with an FBG of 7.8 mM or with NIDDM is similar to that of men who are unfit with a normal FBG. The authors suggested that because cardiorespiratory fitness can be improved by regular physical activity, using exercise to improve fitness could be a “cornerstone to the effective management of patients with abnormal blood glucose profiles or NIDDM.”137 No primary prevention projects for NIDDM have used increased physical activity or exercise as the sole intervention for the prevention or deferment of disease.137-139 Nevertheless, there is evidence of an association between exercise and diabetes from societies that have abandoned a traditional active lifestyle for a more sedentary “modern” lifestyle. There is a dramatic increase in NIDDM in people who become more sedentary.140,141 Conversely, physically active societies have lower rates of NIDDM than do more sedentary societies.142-147 ETHNICITY Ethnic minority populations in the United States have high rates of IGT and are at higher risk for NIDDM.147 Minorities are especially afflicted with obesity, especially minority women. The age-adjusted percentages of overweight and severely overweight individuals are 24.6% and 9.6%, respectively, for white women, 45.1% and 19.7% for African American

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women, and 41.5% and 16.7% for Mexican American women. It is acknowledged that although some races tend to be “heavier” than others, without adverse health effects, and that perhaps the norms and standards need to be adjusted for different races, maintaining a normal weight according to the overall population norm was associated with a 23% lower risk of mortality compared with being persistently overweight. Results from the National Health and Nutrition Examination Survey Epidemiologic Follow-up Study suggest that the higher rate of lower extremity amputations in black compared with white Americans with diabetes is not attributable to biologic causes but rather to a combination of social and environmental factors, including obesity.148 The findings included an analysis of more than 14,000 people who participated, 2240 of whom had diabetes at baseline or developed it during the study. The authors found that during 20 years of follow-up, the age-adjusted rate of all lower extremity amputations was 2.8 times higher in black than in white subjects. Diabetes and its duration were strong predictors of risk, as were hypertension, smoking, low educational level, and low socioeconomic status.148 POSITIVE FAMILY HISTORY Mitchell and colleagues compared the prevalence of NIDDM and IGT in 4914 subjects of white, African American, and Hispanic origin.149 Men with a parental history of diabetes (in one or both parents, regardless of which one) had a higher prevalence of diabetes and IGT than did men without a parental history. In women, only a maternal history of diabetes (or both maternal and paternal, but not paternal alone) was associated with a higher prevalence of NIDDM and IGT. GESTATIONAL DIABETES A history of gestational diabetes mellitus, defined as glucose intolerance of variable severity with an onset or first recognition during pregnancy,150 represents an independent risk factor for the development of subsequent diabetes.151-163 (Gestational diabetes is generally viewed by obstetricians as a potential risk factor for adverse pregnancy outcome.) The original criteria put forth by O’Sullivan and Mahan for the diagnosis of gestational diabetes were developed and validated for their predictive value for subsequent diabetes.164 Because of the different means used to diagnose diabetes during pregnancy and to define diabetes outside of pregnancy, the prevalence of subsequent diabetes after gestational diabetes has been reported to be 19% to 87% for combined glucose intolerance and diabetes and 6% to 62% for diabetes alone. When only the O’Sullivan and Mahan criteria were used for the diagnosis of gestational diabetes,164 the prevalence of subsequent diabetes using the National Diabetes Data Group criteria21 varied from 2.7% to 20.9%, depending on the length of follow-up.

Protocols to Improve Glucose Control Before, During, and After Surgery The rationale for maintaining near-normal glucose levels was established earlier. Another consideration for a patient with diabetes who faces surgery is the possibility of hemodynamic

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instability during anesthesia due to dehydration and osmotic shifts. In addition, as noted earlier and in a 1999 review,165 a diabetic patient is more prone to infection,13,166 has slower wound healing,167 and may have increased free fatty acids, the metabolism of which requires greater myocardial oxygen consumption.121 This section provides guidelines for various situations encountered preoperatively, perioperatively, and postoperatively. PREPARATION FOR ELECTIVE SURGERY Ideally, all patients with diabetes should have attained good glucose control before elective surgery. Good glucose control is defined as the glycemic level that provides the optimal setting for elective surgery, minimizes the risk of infection, facilitates healing, and prevents thrombogenesis. The ideal targets for glucose control are 80 to 100 mg/dL before meals and no higher than 180 mg/dL 1 hour after meals. Maintenance of these glucose targets achieves an Hb A1c level that is associated with the lowest risk of diabetic complications ( 64 µg/mL is considered resistant. Values are approximate and may vary among institutions. †Many strains are resistant. ALP, alkaline phosphatase; R, resistant. Data from Mandell RGD (ed): Principles and Practice of Infectious Diseases, 3rd ed. New York, Churchill Livingstone, 1989.

predominant organisms responsible for graft infection at their particular institutions. Cefamandole,75 cefuroxime,104 and cefotaxime98 have all been used effectively as prophylactic agents in prospective trials. However, cefamandole has fallen out of favor for routine use owing to an association with hypoprothrombinemia and bleeding, particularly in elderly patients and those with renal insufficiency. Cefuroxime has been shown to have antistaphylococcal potency and pharmacokinetic properties inferior to those of cefazolin.100 The third-generation agents such as cefotaxime have broad anti– gram-negative activity but are generally less active against staphylococci. Moreover, the later-generation cephalosporins are, in most instances, significantly more expensive than the first-generation agents. Cefazolin, therefore, remains the antibiotic of choice, except in specific instances when in vitro testing has revealed that another agent more adequately covers the principal pathogens of graft infection. A potential disadvantage of cefazolin prophylaxis is the inconsistent activity of this agent against the organism that is currently responsible for the greatest number of graft infections, S. epidermidis. It has been shown that during hospitalization, patients acquire multiply resistant strains of this bacterium.105,106 Up to 75% of S. epidermidis isolates at some institutions are now cefazolin resistant. Vancomycin is highly active against both S. epidermidis and S. aureus; resistance in these organisms is rarely encountered. Vancomycin, however, provides no gram-negative coverage. It is the drug of choice for prophylaxis in patients with a history of anaphylaxis to beta-lactam antibiotics, often in combination with an aminoglycoside in procedures in which there is significant risk of gram-negative infection, such as aortic reconstruction. Vancomycin is also considered the antibiotic of choice for the prophylaxis of prosthetic hemodialysis access grafts and for patients known to be colonized with methicillin-resistant S. aureus. It is excreted primarily by glomerular filtration and therefore persists in high serum concentrations in patients with end-stage renal disease.

The broad antibacterial spectrum, excellent tissue penetration, and low toxicity of the fluoroquinolones make them potentially ideal agents for the prophylaxis of surgical infections. Limited data are available concerning the use of fluoroquinolones for this indication, but there are reports of efficacy equal or superior to that of cephalosporin antibiotics in the prophylaxis of colorectal,107,108 biliary,107,109 and urologic surgery.110-112 Auger and coauthors reported a randomized study of pefloxacin, a nalidixic acid analog, and cefazolin in patients undergoing cardiac surgery.113 Of 111 patients, 14 receiving pefloxacin developed bacterial colonization at culture sites, compared with 11 in the cefazolin group. One patient who received cefazolin developed mediastinitis from a cefazolinresistant strain of S. epidermidis. As yet, there are no published clinical trials of a fluoroquinolone versus a cephalosporin in the prophylaxis of peripheral vascular surgery procedures. Antibiotic Administration Prophylactic antibiotics are administered just before surgery and redosed intraoperatively during long procedures. Pharmacokinetic studies suggest that prophylactic antibiotics should be administered more frequently and in higher doses during surgery than is recommended for routine therapeutic indications (e.g., cefazolin 1.5 g every 4 hours).65,100,114 Prophylaxis is usually continued postoperatively for up to 24 hours and possibly longer when there is a theoretical risk of postoperative bacteremia from indwelling venous catheters, arterial lines, bladder catheters, and endotracheal tubes. The advantage of continuing coverage beyond the operating room, however, has not been clearly demonstrated. In the absence of these risk factors, there is clearly no advantage in extending antibiotic prophylaxis for longer than 24 hours. Regimens of prophylaxis should be tailored to the type of vascular reconstruction undertaken. Cefazolin prophylaxis is recommended in all procedures involving the placement of prosthetic materials. It is probably not necessary in “clean”

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vascular procedures of the neck and upper extremities that do not involve the use of synthetic grafts. In contrast, the marked colonization and favorable bacterial environment of the lower abdomen and groin necessitate the use of antibiotic prophylaxis in all aortofemoropopliteal vascular procedures. The risk of gram-negative infection in aortic reconstruction may necessitate the addition of an aminoglycoside, particularly in institutions with a high degree of cefazolin resistance among gram-negative isolates. Alternatively, a second- or third-generation cephalosporin with broader anti–gramnegative activity may be substituted, as this obviates the risk of aminoglycoside-associated nephrotoxicity. Cephalosporins should be avoided in patients with a history of anaphylaxis to beta-lactam antibiotics. Patients with a history of minor allergic reactions to penicillin antibiotics may be given a cephalosporin test dose to determine whether cross-reactivity is present. Reduced dosing of cefazolin and most other cephalosporins is recommended in renal insufficiency, based on the calculated creatinine clearance. There is evidence that remote bacteremia may be implicated in vascular graft infection. Accordingly, oral prophylaxis for procedures that are highly associated with bacteremia, such as tooth extraction, cystoscopy, and colonoscopy, is recommended. Wooster and colleagues demonstrated in 200 vascular surgery patients undergoing cystoscopy that the incidence of bacteremia was 64% among inpatients and 8% among outpatients.68 For procedures such as tooth extraction and colonoscopy, prophylaxis must be tailored to the most common normal flora of the traumatized site. Penicillins are appropriate choices for major dental procedures, whereas broader gram-negative and anaerobic coverage may be warranted in colonoscopy. It should be emphasized, however, that the true risk of graft infection after procedures associated with bacteremia is unclear, and there is currently no consensus on the role of antibiotic prophylaxis in this setting. REFERENCES 1. Rokitansky K: Handbuch der pathologischen Anatomie, 2nd ed. 1844, p 55. 2. Koch L: Über Aneurysma der Arteriae mesenterichae superioris [dissertation]. Erlangen, Germany, 1851. 3. Osler W: The Gulstonian lectures on malignant endocarditis. BMJ 1:467, 1885. 4. Crane A: Primary multilocular mycotic aneurysm of the aorta. Arch Pathol 24:634, 1937. 5. Ponfick E: Über embolische Aneurysmen, nebst Bemerkungen über das acute Herzaneurysma (Herzgeschwur). Virchows Arch 58:528, 1873. 6. Eppinger H: Pathogenese (Histogeneses und Aetiologie) der Aneurysmen einschliesslich des Aneurysma equiverminosum. Arch Klin Chir 35:404, 1887. 7. Weisel J: Die Erkrankungen arterieller Gefässe im Verlaufe akuter Infektionen. Z Heilkd 27:269, 1916. 8. Lewis D, Schrager V: Embolomycotic aneurysms. JAMA 53:1808, 1909. 9. Cathcart R: False aneurysms of the femoral artery following typhoid fever. South Med J 2:593, 1909. 10. Revell S: Primary mycotic aneurysms. Ann Intern Med 22:431, 1943. 11. Hawkins J, Yeager G: Primary mycotic aneurysm. Surgery 40:747, 1956. 12. Yellin A: Ruptured mycotic aneurysm, a complication of parenteral drug abuse. Arch Surg 112:981, 1977. 13. Lande A, Beckman Y: Aortitis—pathologic, clinical and arteriographic review. Radiol Clin North Am 14:219, 1976. 14. Hirst AJ, Affeldt J: Abdominal aortic aneurysm with rupture into the duodenum: A report of eight cases. Gastroenterology 10:504, 1951. 15. Reddy DJ, Ernst CB: Infected aneurysms: Recognition and management. Semin Vasc Surg 1:541, 1984. 16. Brown SL, Busuttil RW, Baker JD, et al: Bacteriologic and surgical determinants of survival in patients with mycotic aneurysms. J Vasc Surg 1:541, 1984.

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17. Stengal A, Wolferth C: Mycotic (bacterial) aneurysms of intravascular origin. Arch Intern Med 31:527, 1923. 18. Magilligan D, Quinn E: Active infective endocarditis. In Magilligan DJ, Quinn E (eds): Endocarditis: Medical and Surgical Management. New York, Marcel Dekker, 1986, p 207. 19. Wilson S, Van Wagenen P, Passaro EJ: Arterial infection. Curr Probl Surg 15:5, 1978. 20. Bennett D, Cherry J: Bacterial infection of aortic aneurysms: A clinicopathological study. Am J Surg 113:321, 1967. 21. Jarrett F, Darling R, Mundth E, et al: Experience with infected aneurysms of the abdominal aorta. Arch Surg 10:1281, 1975. 22. Ernst C, Campbell H, Daugherty M, et al: Incidence and significance of intra-operative bacterial cultures during abdominal aortic aneurysmectomy. Ann Surg 185:626, 1977. 23. Reddy D, Smith R, Elliot JJ, et al: Infected femoral artery false aneurysms in drug addicts: Evolution of selective vascular reconstruction. J Vasc Surg 3:718, 1986. 24. Wakefield T, Pierson C, Schoberg D, et al: Artery, periarterial adipose tissue, and blood microbiology during vascular reconstructive surgery: Perioperative and postoperative observations. J Vasc Surg 11:624, 1990. 25. Chan F, Crawford E, Coselli J, et al: In situ prosthetic graft replacement for mycotic aneurysm of the aorta. Ann Thorac Surg 47:193, 1989. 26. Crawford E, Crawford J: Diseases of the Aorta Including an Atlas of Angiographic Pathology and Surgical Techniques. Baltimore, Williams & Wilkins, 1984. 27. Mundth E, Darling R, Alvarado RH, et al: Surgical management of mycotic aneurysms and the complications of infections in vascular reconstructive surgery. Am J Surg 110:460, 1969. 28. Kaufman J, Smith R, Capel G, et al: Antibiotic therapy for arterial infection: Lessons from the successful treatment of a mycotic femoral artery aneurysm without surgical reconstruction. Ann Vasc Surg 4:592, 1990. 29. Ewart J, Burke M, Bunt T: Spontaneous abdominal aortic infections: Essentials of diagnosis and management. Am Surg 49:37, 1983. 30. Lemos D, Raffetto J, Moore T, Menzoian J: Primary aortoduodenal fistula: A case report and review of the literature. J Vasc Surg 37:686, 2003. 31. Daugherty M, Shearer GR, Ernst CB: Primary aortoduodenal fistula: Extra-anatomic vascular reconstruction not required for successful management. Surgery 86:399, 1979. 32. Bandyk DF, Novotney ML, Johnson BL, et al: Use of rifampin-soaked gelatin-sealed polyester grafts for in situ treatment of primary aortic and vascular prosthetic infections. J Surg Res 95:44, 2001. 33. Batt M, Magne J, Alric P, et al: In situ revascularization with silvercoated polyester grafts to treat aortic infection: Early and midterm results. J Vasc Surg 38:983, 2003. 34. Schulman ML, Badhey MR, Yatco R, Pillari G: An 11-year experience with deep leg veins as femoropopliteal bypass grafts. Arch Surg 121:1010, 1986. 35. Clagett GP, Valentine RJ, Hagino RT: Autogenous aortoiliac/femoral reconstruction from superficial femoral-popliteal veins: Feasibility and durability. J Vasc Surg 25:255, 1997. 36. Kieffer E, Bahnini A, Koskas F, et al: In situ allograft replacement of infected infrarenal aortic prosthetic grafts: Results in forty-three patients. J Vasc Surg 17:349, 1993. 37. Leseche G, Castier Y, Petit MD, et al: Long-term results of cryopreserved arterial allograft reconstruction in infected prosthetic grafts and mycotic aneurysms of the abdominal aorta. J Vasc Surg 34:616, 2001. 38. Berchtold C, Eibl C, Seelig MH, et al: Endovascular treatment and complete regression of an infected abdominal aortic aneurysm. J Endovasc Ther 9:543, 2002. 39. Koeppel TA, Gahlen J, Diehl S, et al: Mycotic aneurysm of the abdominal aorta with retroperitoneal abscess: Successful endovascular repair. J Vasc Surg 40:164, 2004. 40. Johnson J, Ledgerwood A, Lucas C: Mycotic aneurysms: New concepts in therapy. Arch Surg 118:577, 1983. 41. Patel K, Semel L, Clauss R: Routine revascularization with resection of infected femoral pseudoaneurysm from substance abuse. J Vasc Surg 8:322, 1988. 42. Wright D, Shepard A: Infected femoral artery aneurysm associated with drug abuse. In Stanley J, Ernst C (eds): Current Therapy in Vascular Surgery. Philadelphia, BC Decker, 1990, p 350. 43. Hoffert P, Gensler S, Haimovichi H: Infection complicating arterial grafts. Arch Surg 90:427, 1965. 44. Fry WJ, Lindenauer SM: Infection complicating the use of plastic arterial implants. Arch Surg 94:600, 1967.

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45. Szilagyi DE, Smith RF, Elliott JP, Vrandecic MP: Infection in arterial reconstruction with synthetic grafts. Ann Surg 106:321, 1972. 46. Lorentzen JE, Nielsen OM, Arendrup H: Vascular graft infection: An analysis of sixty-two graft infections in 2411 consecutively implanted synthetic vascular grafts. Surgery 98:81, 1985. 47. Goldstone J, Moore WS: Infection in vascular prostheses: Clinical manifestations and surgical management. Am J Surg 128:225, 1974. 48. Bandyk D, Berni G, Thiele B, Towne J: Aortofemoral graft infection due to Staphylococcus epidermidis. Arch Surg 119:102, 1984. 49. Jamieson G, DeWeese J, Rob C: Infected arterial grafts. Ann Surg 181:850, 1975. 50. Liekweg WG, Greenfield LJ: Vascular prosthetic infections: Collected experience and results of treatment. Surgery 81:335, 1977. 51. Lindenauer S, Fry W, Schaub G, Wild D: The use of antibiotics in the prevention of vascular graft infections. Surgery 62:487, 1967. 52. Yashar J, Weyman A, Burnard R, Yashar J: Survival and limb salvage in patients with infected arterial prostheses. Am J Surg 135:499, 1978. 53. Buchbinder D, Pasch AR, Rollins DL, et al: Results of arterial reconstruction of the foot. Arch Surg 121:673, 1986. 54. Edwards MJ, Richardson D, Klamer TW: Management of aortic prosthetic infections. Am J Surg 155:327, 1988. 55. O’Hara PJ, Hertzer NR, Beven EG, Krajewski LP: Surgical management of infected abdominal aortic grafts: Review of a 25-year experience. J Vasc Surg 3:725, 1986. 56. Reilly L, Stoney R, Goldstone J, Ehrenfeld W: Improved management of aortic graft infection: The influence of operation sequence and staging. J Vasc Surg 5:421, 1987. 57. Reilly LM, Altman H, Lusby RJ, et al: Late results following surgical management of vascular graft infection. J Vasc Surg 1:36, 1984. 58. Yeager R, McConnell D, Sasaki T, Vetto R: Aortic and peripheral prosthetic graft infection: Differential management and causes of mortality. Am J Surg 150:36, 1985. 59. Samson RH, Veith FJ, Janko GS, et al: A modified classification and approach to the management of infections involving peripheral arterial prosthetic grafts. J Vasc Surg 8:147, 1988. 60. Conn J, Hardy J, Chavez C, et al: Infected arterial grafts. Ann Surg 101:704, 1970. 61. Elek S, Conen P: The virulence of Staphylococcus pyogenes for man: A study of the problems of wound infection. Br J Exp Pathol 38:573, 1957. 62. Smith R, Lowry K, Perdue G: Management of the infected arterial prosthesis in the lower extremity. Am Surg 33:711, 1967. 63. Edwards W, Martin R, Jenkins J, et al: Primary graft infections. J Vasc Surg 6:235, 1987. 64. Quiñones-Baldrich WJ, Hernandez JJ, Moore WS: Long-term results following surgical management of aortic graft infection. Arch Surg 126:507, 1991. 65. Kaiser A, Clayson K, Mulherin J: Antibiotic prophylaxis in vascular surgery. Ann Surg 188:283, 1978. 66. Close A, Stengel B, Love H: Preoperative skin preparation with povidone-iodine. Am J Surg 108:398, 1964. 67. Cruse P: A five-year prospective study of 23,649 surgical wounds. Arch Surg 107:206, 1973. 68. Wooster D, Louch R, Kradjen S: Intraoperative bacterial contamination of vascular grafts: A prospective study. Can J Surg 28:407, 1985. 69. Bouhoutsos J, Chavatsas D, Martin P, Morris T: Infected synthetic arterial grafts. Br J Surg 61:108, 1974. 70. Scobie K, McPhail N, Barber G, Elder R: Bacteriologic monitoring in abdominal aortic surgery. Can J Surg 22:368, 1979. 71. DeBakey M, Ochsner J, Cooley D: Associated intraabdominal lesions encountered during resection of aortic aneurysms: Surgical considerations. Dis Colon Rectum 3:485, 1960. 72. Stoll W: Surgery for intraabdominal lesions associated with resection of aortic aneurysms. WMJ 65:89, 1966. 73. Hardy J, Tompkins W, Chavez C, Conn J: Combining intra-abdominal arterial grafting with gastrointestinal or biliary tract procedure. Am J Surg 126:598, 1973. 74. Becker R, Blundell P: Infected aortic bifurcation grafts: Experience with 14 patients. Surgery 80:544, 1976. 75. Lalka S, Malone J, Fisher D, et al: Efficacy of prophylactic antibiotics in vascular surgery: An arterial wall microbiologic and pharmacokinetic perspective. J Vasc Surg 10:501, 1989. 76. Buckels J, Fielding J, Black J, et al: Significance of positive bacterial cultures from aortic aneurysm contents. Br J Surg 72:440, 1985. 77. Macbeth G, Rubin J, McIntyre KJG, Malone J: The relevance of arterial wall microbiology to the treatment of prosthetic graft infections: Graft infection vs arterial infection. J Vasc Surg 1:750, 1984.

78. Durham J, Malone J, Bernhard V: The impact of multiple operations on the importance of arterial wall cultures. J Vasc Surg 5:160, 1987. 79. Moore WS, Chvapil M, Sieffert G, Keown K: Development of an infection resistant vascular prosthesis. Arch Surg 116:1403, 1981. 80. White J, Benvenisty A, Reemtsma K, et al: Simple methods for direct antibiotic protection of synthetic vascular grafts. J Vasc Surg 1:372, 1984. 81. Chervu A, Moore WS, Gelabert HA, et al: Prevention of graft infection by use of prostheses bonded with a rifampin/collagen release system. J Vasc Surg 14:521, 1991. 82. Bunt TJ, Mohr J: Incidence of positive inguinal lymph node cultures during peripheral revascularization. Am J Surg 50:522, 1984. 83. Johnson JA, Cogbill TH, Strutt PJ, Gundersen AL: Wound complications after infrainguinal bypass: Classification, predisposing factors, and management. Arch Surg 123:859, 1988. 84. Kwaan J, Dahl R, Connolly J: Immunocompetence in patients with prosthetic graft infection. J Vasc Surg 1:45, 1984. 85. Pulaski E, Schaeffer J: The background of antibiotic therapy in surgical infections. Surg Gynecol Obstet 93:1, 1951. 86. Pulaski E: Discriminate antibiotic prophylaxis in elective surgery. Surg Gynecol Obstet 108:385, 1959. 87. Linton R: The appropriate use of antibiotics in clean surgery. Surg Gynecol Obstet 112:218, 1961. 88. Altemeier W, Culbertson W, Vetto M: Prophylactic antibiotic therapy. Arch Surg 71:2, 1955. 89. Altemeier W, Culbertson W, Sherman R, et al: Critical re-evaluation of antibiotic therapy in surgery. JAMA 157:305, 1955. 90. Alexander J, McGloin J, Altemeier W: Penicillin prophylaxis in experimental wound infections. Surg Forum 11:299, 1960. 91. Alexander J, Altemeier W: Penicillin prophylaxis of experimental staphylococcal wound infection. Surg Gynecol Obstet 120:243, 1965. 92. Moore W, Rosson C, Hall A: Effect of prophylactic antibiotics in preventing bacteremic infection in vascular prostheses. Surgery 69:825, 1971. 93. Perdue G: Antibiotics as an aid in the prevention of infections after peripheral arterial surgery. Am Surg 41:296, 1975. 94. Pitt H, Postier R, MacGowan W, et al: Prophylactic antibiotics in vascular surgery. Ann Surg 192:356, 1980. 95. Salzmann G: Perioperative infection prophylaxis in vascular surgery: A randomized prospective study. Thorac Cardiovasc Surg 31:239, 1983. 96. Hasselgren P, Ivarsson L, Risberg B, Seeman T: Effects of prophylactic antibiotics in vascular surgery. Ann Surg 200:86, 1984. 97. Bennion R, Hiatt J, Williams R, et al: A randomized prospective study of perioperative microbial prophylaxis for vascular surgery. J Cardiovasc Surg 26:270, 1985. 98. Robbs J, Reddy E, Ray R: Antibiotic prophylaxis in aortic and peripheral arterial surgery in the presence of infected extremity lesions. Drugs 35(Suppl 2):141, 1988. 99. Mutch D, Richards G, Brown R, et al: Bioactive antibiotic levels in the human aorta. Surgery 92:1068, 1982. 100. Edwards W, Kaiser A, Kernodle D, et al: Cefuroxime versus cefazolin as prophylaxis in vascular surgery. J Vasc Surg 15:35, 1992. 101. Kernodle D, Classen D, Burke J, et al: Failure of cephalosporins to prevent surgical wound infections. JAMA 263:961, 1990. 102. Slama T, Sklar S, Misinski J, et al: Randomized comparison of cefamandole, cefazolin, and cefuroxime in open-heart surgery. Antimicrob Agents Chemother 29:744, 1986. 103. Mandell G, Sande M: Penicillins, cephalosporins and other betalactam antibiotics. In Gilman A, Rall T, Nies A, Taylor P (eds): Goodman and Gilman’s The Pharmacologic Basis of Therapeutics, 8th ed. Elmsford, NY, Pergamon Press, 1990, p 1065. 104. Herbst A, Kamme C, Norgren L, et al: Infections and antibiotic prophylaxis in reconstructive vascular surgery. Br J Vasc Surg 3:303, 1989. 105. Levy M, Schmitt D, Edmiston C, et al: Sequential analysis of staphylococcal colonization of body surfaces of patients undergoing vascular surgery. J Clin Microbiol 28:664, 1990. 106. Archer G, Tenenbaum M: Antibiotic-resistant Staphylococcus epidermidis in patients undergoing cardiac surgery. Antimicrob Agents Chemother 10:269, 1980. 107. Cooreman F, Ghyselen J, Penninckx F: Pefloxacin vs cefuroxime for prophylaxis of infections after elective colorectal surgery. Rev Infect Dis 11(Suppl 5):S1301, 1989. 108. Offer C, Weuta H, Bodner E: Efficacy of perioperative prophylaxis with ciprofloxacin or cefazolin in colorectal surgery. Infection 16(Suppl 1): S46, 1988. 109. Kujath P: Brief report: Antibiotic prophylaxis in biliary tract surgery: Ciprofloxacin vs ceftriaxone. Am J Med 87(Suppl 5A):255S, 1989.

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110. Gombert M, DuBouchet L, Aulicino T, et al: Brief report: Intravenous ciprofloxacin versus cefotaxime prophylaxis during transurethral surgery. Am J Med 87(Suppl 5A):250S, 1989. 111. Cox C: Comparison of intravenous ciprofloxacin and intravenous cefotaxime for antimicrobial prophylaxis in transurethral surgery. Am J Med 87(Suppl 5A):252S, 1989. 112. Christensen M, Nielsen K, Knes J, et al: Brief report: Single-dose preoperative prophylaxis in transurethral surgery: Ciprofloxacin versus cefotaxime. Am J Med 87(Suppl 5A):258S, 1989. 113. Auger P, Leclerc Y, Pelletier L, et al: Efficacy and safety of pefloxacin vs cefazolin as prophylaxis in elective cardiovascular surgery. Rev Infect Dis 11(Suppl 5):S1302, 1989. 114. Guglielmo B, Salazar T, Rodondi L, et al: Altered pharmacokinetics of antibiotics during vascular surgery. Am J Surg 157:410, 1989. 115. Casali R, Tucker W, Thompson B, Read R: Infected prosthetic grafts. Arch Surg 115:577, 1980. 116. McAuley C, Steed D, Webster M: Bacterial presence in aortic thrombus at elective aneurysm resection: Is it clinically significant? Am J Surg 147:322, 1984. 117. Schwartz J, Powell T, Burnham S, Johnson G Jr: Culture of abdominal aortic aneurysm contents, an additional series. Arch Surg 122:777, 1987. 118. Ilgenfritz F, Jordan F: Microbiological monitoring of aortic aneurysm wall and contents during aneurysmectomy. Arch Surg 123:506, 1988. 119. Brandimarte C, Santini C, Venditti M, et al: Clinical significance of intraoperative cultures of aneurysm walls and contents in elective abdominal aortic aneurysmectomy. Eur J Epidemiol 5:521, 1989.

Questions 1. True or false: Arterial trauma is involved in the pathogenesis of most primary arterial infections. 2. When should prosthetic grafts be used to replace excised mycotic aneurysms? (a) If the surgical field is laved with antibiotics (b) In the upper extremities (c) Only in carefully selected instances (d) In fungal arterial infections (e) Never 3. Since 1965, what organism is most commonly associated with microbial aortitis? (a) Salmonella species (b) Fungi (c) Mycobacteria (d) Pseudomonas species (e) Staphylococcus aureus 4. In the management of a mycotic mesenteric aneurysm located in the distal arterial arcade (adjacent to the intestine), what is the recommended management? (a) Reconstruction with a Dacron graft (b) Reconstruction with a PTFE graft (c) Reconstruction with an umbilical vein graft (d) Reconstruction with a vein graft (e) Ligation and excision without reconstruction

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5. True or false: The recommended management of an infrarenal mycotic aneurysm involves the use of antibiotics, débridement of infected tissues, and reconstruction through a remote (extra-anatomic) uninfected field. 6. What is the average reported incidence of prosthetic graft infection? (a) 1% to 6% (b) 6% to 10% (c) 10% to 15% (d) Greater than 15% (e) 0% to 1% 7. True or false: The study by Pitt and colleagues revealed that intravenous antibiotics were much more effective than antibiotic irrigation. 8. Risk factors for prosthetic graft infection include which of the following? (a) Multiple reoperations (b) Inguinal incisions (c) Open, infected wounds on the extremities (d) Prior graft infections (e) Positive arterial wall cultures (f) All of the above 9. Avenues of infection include which of the following? (a) Skin (b) Arterial wall (c) Open wounds on the distal limb (d) Intestinal transudate accumulated during aortic bypass (e) Foley catheter (f) All of the above 10. What are the most common organisms found in prosthetic graft infections? (a) Proteus species (b) Escherichia coli (c) Staphylococcus aureus (d) Streptococcus viridans (e) Staphylococcus epidermidis

Answers 1. true 6. a

2. c 7. false

3. a 8. f

4. e 9. f

5. true 10. e

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11

Peter Gloviczki

Vascular Malformations Vascular malformations (VMs) are developmental abnormalities of the vascular system. They should be differentiated from vascular tumors or hemangiomas, because they have different causes, growth patterns, treatments, and outcomes. Malformations may involve any segment of the vascular tree: arteries, capillaries, veins, or lymphatics. High-flow arteriovenous malformations are associated with shunting of large amounts of arterial blood into the venous system; these lesions can have alarming hemodynamic manifestations, such as venous engorgement, distal limb ischemia, and high-output cardiac failure. Predominantly venous malformations are the most common type seen at vascular clinics; most have a benign clinical course and require no special treatment. In one series, the ratio of venous to arteriovenous malformations was 4:1.1 Most VMs are mixed, and some complex malformations such as Klippel-Trénaunay syndrome or Parkes Weber syndrome are associated with developmental abnormalities of other tissues, including bone and soft tissue overgrowth or digital abnormalities.2-4

Historical Notes Birthmarks and congenital deformities have been described by historians and depicted by painters for centuries. One of the first detailed medical descriptions of an arteriovenous malformation with pulsating varices of the head, caused by a so-called cirsoid aneurysm, dates back to the 16th century.5 Slowing of the heart rate after compression of a high-shunt congenital arteriovenous malformation was first described by Nicoladoni in 1875.6 This so-called bradycardia sign of arteriovenous fistulas was observed later by Branham in a patient with acquired arteriovenous fistula.7 Excellent early descriptions of arteriovenous malformations can be found in the works of Reid,8 Holman,9 de Takats,10 and Coursley and associates.11 Malan and Puglionisi presented a detailed classification of vascular malformations (angiodysplasia),12 although the first practical guidelines for clinical classification and treatment were given by Szilagyi and coworkers.13,14 In excellent reviews, Rutherford and colleagues15 and Rosen and Riles16 summarized the state of the art of VMs. Of the multiple classifications published, the Hamburg classification is the one used most frequently today.1,17,18 Although surgical excision may be 198

recommended for local lesions, selective catheterization, embolotherapy, and percutaneous sclerotherapy (usually with absolute alcohol) have changed the management of VMs in the last 2 decades.19-22

Definitions Vascular malformations are localized errors of angiogenic development, whereas hemangiomas are vascular tumors. Mulliken and colleagues defined the endothelial characteristics and cell biology of VMs and vascular tumors.23-25 The term hemangioma should be reserved for vascular tumors alone. During the proliferative phase they undergo growth, and then they resolve. The proliferative phase occurs during the first year, and spontaneous involution of hemangiomas is observed in 95% of cases by age 7 years. The female-male ratio is 5:1. Thirty percent of hemangiomas are present at birth, and the rest develop within the first 3 months of life. Endothelial hyperplasia is evident on biopsies obtained from hemangiomas; these cells grow in tissue culture, and in the proliferative phase they incorporate 3H-thymidine and have an increased mast cell count.25 Most patients with hemangiomas require no treatment at all. In contrast, VMs are developmental, congenital abnormalities. There is increasing evidence that aberrant signaling at the molecular level results in dysfunction of normal proliferation, differentiation, maturation, and apoptosis of the vascular cells.26 Localized, superficial, mostly venous or capillary VMs—“birthmarks” of the skin and mucosa—are most common, but VMs also occur in the skeletal muscles, the pelvis or chest, visceral organs such as the lungs, the gastrointestinal system, and the brain.15,16,26 The abnormal vascular channels are lined by a continuous endothelium and surrounded by an abnormal complement of mural cells. Ninety percent of them are present at birth, and the male-female ratio is 1:1. VMs show no endothelial proliferation, and no cell growth is observed in tissue culture; the cells do not incorporate 3H-thymidine, and no mast cells have been observed in biopsy specimen.23-25 Clinically, no proliferation or spontaneous involution has been observed in VMs. The growth of the malformation is usually commensurate with the growth of the child, although hemodynamic factors (arteriovenous shunting, venous stasis)

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can accelerate growth and morbidity. Most low-flow VMs have a benign course, although complications such as bleeding, thrombophlebitis, skin changes, or infection may need treatment. High-flow arteriovenous malformations usually have a more ominous course and a worse prognosis. Treatment of these lesions is frequently needed.

Development of the Vascular System Because the classification, clinical presentation, and prognosis of VMs depend to a great extent on the point at which there is an arrest or abnormality in the development of the vascular system, it is worthwhile to review briefly the normal development of the vascular tree of the limbs. Primitive vascular channels first appear in the third week of gestation. During its development, the vascular system undergoes differentiation through multiple stages, first described by Woollard in 1922.27 Stage 1 is the undifferentiated stage, with only a capillary network being present. Stage 2 is the retiform stage, when large plexiform structures can be seen. In stage 3, by the third week of gestation, the maturation stage includes the development of large channels, arteries, and veins. Vascular endothelial growth factor (VEGF), secreted by keratinocytes, has been found to be responsible for inducing the penetration of capillary vessels into the avascular epidermis.28,29 This invasion and the subsequent arterial differentiation are also guided by VEGF originating from sensory nerves.30 A defective migratory response of endothelial cells to VEGF is the consequence of abnormal signaling of VEGF receptors. Malformations develop if the differentiation is abnormal and there is an arrest in the development of normal vascular tissue. It is the persistence of the normal embryonic vascular system and any additional abnormal development that result in VMs.

Capillary malformation

Microfistulous AV malformation

Microfistulous AV malformation

FIGURE 11–1 • Capillary malformation, microfistulous arteriovenous (AV) malformation, and macrofistulous arteriovenous malformation.

malformations are low-shunt lesions. Between these two extremes, a whole spectrum of malformations exists. The most recent and now widely used classification is the 1988 Hamburg classification, with modifications by Rutherford and Lee (Table 11-1).1,17,18 A malformation is first

Classification Because of the complex presentation and frequently mixed nature of VMs, classification has been difficult. Malan and Puglionisi attempted to separate them based on anatomic appearance and the presence or absence of arteriovenous shunting.12 The classification of Szilagyi and colleagues13,14 was based primarily on Woollard’s stages of embryologic development. Capillary malformations develop when there is an arrest in stage 1 (Fig. 11-1). Although Szilagyi named these malformations hemangiomas, they are not tumors but capillary or cavernous VMs. Microfistulous or macrofistulous arteriovenous malformations develop if there is an arrest in stage 2 (see Fig. 11-1). Persistence of large embryonic veins that develop in stage 3 is seen in patients with persistent sciatic vein (Fig. 11-2) or in those with large lateral veins of the leg (Fig. 11-3). There are many mixed VMs owing to involvement of several segments of the vascular system (capillaries, veins, lymphatics). Forbes and associates distinguished VMs based on hemodynamics and contrast angiographic appearance.20 Depending on the amount of blood supplying the malformation, highflow and low-flow lesions are distinguished. These are called high-shunt and low-shunt lesions; the size of the shunt is determined by the volume of blood that enters the feeding vessels. High-shunt lesions correspond with macrofistulous arteriovenous malformations, whereas microfistulous arteriovenous

FIGURE 11–2 • Persistent sciatic vein (arrow) in a 12-year-old girl. Surgical resection of the painful vein through a posterior approach resulted in an excellent clinical result at 7 years’ followup. The dilated vein contained no valves. (From Cherry KJ, Gloviczki P, Stanson AW: Persistent sciatic vein: Diagnosis and treatment of a rare condition J Vasc Surg 23:490-497, 1996.)

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TABLE 11–1 The Hamburg Classification of Vascular Malformations (Revised) Affected Segment of the Vascular System Arterial malformations

Venous malformations

Arteriovenous (AV) malformations (with shunting)

Lymphatic malformations FIGURE 11–3 • Persistent lateral embryonic veins in a 19-year-old man with Klippel-Trénaunay syndrome. (From Noel AA, Gloviczki P, Cherry KJ Jr, et al: Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg 32:840-847, 2000.)

FIGURE 11– 4 • Abdominal aortic coarctation associated with renal and mesenteric artery stenosis in a 9-year-old boy with renovascular hypertension. The arrow indicates right renal artery stenosis; the arrow in the inset shows superior mesenteric artery stenosis. (From West CA, Delis KT, Service G, et al: Middle aortic syndrome: Surgical treatment in a child with neurofibromatosis, renovascular hypertension, superior mesenteric artery stenosis and intermittent claudication. J Vasc Surg [in press].)

Combined vascular malformations

Anatomic Forms Truncular forms Aplasia or obstruction Dilatation Extratruncular forms Infiltrating Limited Truncular forms Aplasia or obstruction Dilatation Extratruncular forms Infiltrating Limited Truncular forms Deep AV fistula Superficial AV fistula Extratruncular forms Infiltrating Limited Truncular forms Aplasia or obstruction Dilatation Extratruncular forms Infiltrating Limited Truncular forms Arterial and venous Hemolymphatic Extratruncular forms Infiltrating hemolymphatic Limited hemolymphatic

classified by the predominant vascular defect (arterial, venous, arteriovenous, lymphatic, or combined); it is further classified into truncular or extratruncular form, depending on the involvement of major axial vessels or branches of major arteries or veins. The truncular forms of predominantly arterial VMs include aplasia or obstruction, stenosis, coarctation, dilatation, and aneurysm. These include malformations such as the persistent sciatic artery or an aberrant left subclavian artery that runs behind the esophagus and causes the typical syndrome of dysphagia lusoria.31 Thoracic or abdominal aortic coarctation (Fig. 11-4),32 anomalies of the aortic arch, and persistence of embryonic mesenteric vessels are other examples of these malformations. The extratruncular forms can be diffuse or localized. Predominantly venous malformations may also be truncular; these include aplasia or obstruction, stenosis or hypoplasia, dilatation, and aneurysm. Many patients with KlippelTrénaunay syndrome have persistence of large embryonic veins or hypoplasia, dilatation, or aneurysmal dilatation of the deep veins of the limb (Fig. 11-5).33-36 The estimated prevalence of deep venous anomalies in patients with predominantly venous malformations was 47% in one study.35 Phlebectasia was the most common (36%), followed by

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causing congenital lymphedema40-43 or dilatation leading to valvular incompetence and rupture of lymphatics, causing chylous effusions or chylocutaneous fistulas due to reflux of chyle.44 Most lymphatic cysts and “lymphangiomas” are lymphatic malformations, and many venous malformations contain lymphatic tissue. More than 70% of VMs are mixed, and these complex abnormalities may include arterial, capillary, venous, or lymphatic elements as well. Although the Hamburg classification discourages the use of eponyms, some of them were named after the physicians who first described the conditions, and these names have become widely accepted and used. The list of clinical syndromes of VM includes Parkes Weber, KlippelTrénaunay, Servelle-Martorell (Fig. 11-10; see color plate), Sturge-Weber, Rendu-Osler-Weber, von Hippel-Lindau, Kasabach-Merritt, Proteus (Fig. 11-11; see color plate), and Mafucci’s syndromes, among others (Table 11-2).15,16,38,39,45-47

Genetics

FIGURE 11–5 • Aneurysmal dilatation of the popliteal vein with bandlike narrowing associated with atypical lateral varicosity in a 19-year-old man with Klippel-Trénaunay syndrome. (From Noel AA, Gloviczki P, Cherry KJ Jr, et al: Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg 32:840847, 2000.)

aplasia or hypoplasia of the deep venous trunks (8%) and venous aneurysms (8%). Extratruncular venous VMs are the most frequent malformations, and they can be diffuse (Fig. 11-6; see color plate) or localized. Most venous malformations are localized defects of vascular morphogenesis that present as single or multiple bluish purple lesions, mainly in the skin and the mucosa.26 Specimens obtained at biopsy show enlarged, endotheliallined veinlike channels with abnormal smooth muscle cells. Predominantly arteriovenous malformations are divided into truncular and extratruncular lesions; both can be either localized or diffuse. Lesions with clinical or angiographic evidence of arteriovenous communication in the limbs (Parkes Weber–type malformations) or pelvis are the type most frequently seen by vascular surgeons. Low-shunt (Fig. 11-7) and high-shunt (Fig. 11-8) malformations are distinguished. The hereditary arteriovenous VMs in the lung and sometimes in the brain and gut are part of hereditary hemorrhagic telangiectasia syndrome.37 Arteriovenous malformations are perhaps most frequent in the central nervous system, and vascular surgeons performing carotid arteriography and stenting should recognize and be familiar with arteriovenous VMs and high-flow arteriovenous fistulas of the brain. Capillary malformations, or port-wine stains, are frequent. These cutaneous lesions appear as a red macular stain that darkens over years (Fig. 11-9). Capillary malformations are typical in patients with Sturge-Weber syndrome, KlippelTrénaunay syndrome, and Parkes Weber syndrome.38,39 Lymphatic malformations are also frequent findings in some series. Truncular forms include obstruction or hypoplasia

Genetic information on VMs has greatly increased in recent years. Most VMs are sporadic, but autosomal dominant inheritance has also been described. Genetic studies of families have resulted in the identification of mutated genes,26,39,48-54 which play an important role in angiogenesis. These mutated genes in some patients encode tyrosine kinase receptors and intracellular signaling molecules.26 Vikkula and coworkers identified the endothelial-specific angiopoietin receptor TIE2/ TEK, located on chromosome 9p21, as the cause of familial mucocutaneous VMs.26,52 Glomuvenous malformations (venous malformations with glomus cells, or glomangiomas) are similar to VMs; most of these lesions are inherited, and Boon and colleagues identified the gene glomulin, a novel locus on the short arm of chromosome 1.53 Port-wine stains have also been observed in families, and a genetic susceptibility for capillary malformations was suggested. Eerola and associates identified a large locus, CMC1, on chromosome 5q.39 These authors used genetic fine mapping to identify a positional candidate gene, RASA1; heterozygous inactivating RASA1 mutations were detected in families manifesting capillary malformations. Of interest, arteriovenous malformation, arteriovenous fistula, or Parkes Weber syndrome was also documented in all the families with this mutation. Arteriovenous malformations in the lungs, brain, or gut may be part of hereditary hemorrhagic telangiectasia (HHT).37 Two genes encoding proteins associated with transforming growth factor-β receptor have been identified, causing HHT1 and HHT2, respectively. Primary congenital lymphedema can be hereditary (Milroy disease), and late-onset primary lymphedema has been observed in multiple members of the same families (Meige disease).40-43 Congenital lymphedema has been linked to chromosome 5q35.3, where the VEGFR3 gene is located. It is likely that congenital lymphedema is caused by lack of sufficient signaling via the VEGFR3 receptor.26

Incidence Vascular malformations occur in 1.5% of the population.35 Published series of VMs seen at referral centers suggest that predominantly venous malformations are the most common

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A

B

FIGURE 11–7 • A, Low-shunt arteriovenous malformation supplied mainly by branches of the lateral circumflex femoral artery. B, Selective catheterization of the feeding vessel was performed, and the lesion was treated with absolute ethanol injection. C, Completion arteriography shows no filling of the lesion. (Courtesy of Michael A. McKusick, MD, Mayo Foundation.)

C

vascular anomalies.35 They are estimated to occur in 1 in 5000 to 10,000 childbirths.26 Venous malformations are certainly the most frequent type that requires medical attention. Still, it is likely that capillary malformations or port-wine stains of the skin and mucosa are the most frequent VMs, occurring in 0.3% of childbirths.39 Among 797 patients with VMs reported by Lee and colleagues, 40% had predominantly lymphatic malformations.1 Arteriovenous shunts occurred in 9.5% of the cases in their series.

Clinical Presentation Patients with VMs are frequently asymptomatic, and a birthmark of the skin or mucosa is often only a cosmetic deformity. However, those patients who seek consultation with a vascular surgeon may have a complex presentation, and the limbs or pelvis may be extensively involved. Clinical presentations include varicose veins (see Fig. 11-3), limb edema or overgrowth (Fig. 11-12; see color plate), port-wine stain, and

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A

C

203

B

D

FIGURE 11–8 • A, High-shunt, high-flow arteriovenous malformation involving the left arm and hand of a 26-year-old woman. B, Left arm arteriogram reveals an 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 numerous 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, MD, Mayo Foundation.)

digital anomalies (Figs. 11-13 and 11-14; see color plate). The affected limb or pelvis may harbor a mass that is pulsatile; there may be a systolic-diastolic bruit and a palpable thrill. The varicose veins are usually atypical, lateral or suprapubic, although varicosity occasionally involves the great saphenous

vein and its tributaries. Bleeding or leakage of lymph fluid from VMs is not infrequent. Thrombophlebitis, cellulitis and lymphangitis, skin lesions, induration, pigmentation, and ulcerations can be signs of chronic venous insufficiency. Many patients with mixed lesions have associated lymphedema.

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consequences of an arteriovenous shunt (Fig. 11-16), such as a low-resistance waveform in the arteries and pulsatile flow in the veins. Duplex scans can also establish the patency of the superficial and deep veins, as well as other abnormalities such as aneurysm or dilatation, hypoplasia, or valvular incompetence. To document arteriovenous shunting, labeled microspheres are useful. Technetium 99m–labeled human albumin microspheres are injected into the artery proximal to an arteriovenous shunt. Less than 3% of the microspheres should pass through a normal capillary bed. The percentage of the shunted material is calculated based on radioactivity in the lungs, measured after a separate injection of the colloid in a vein of the body.15 Contrast echocardiography is also useful to establish arteriovenous shunting. It can detect the appearance of indocyanine green on the venous side, after intra-arterial injection; the test was used by Pritchard and coworkers to determine residual shunts after surgical excision.56,57

Imaging Studies

FIGURE 11–9 • Port-wine stain (capillary malformation) on the affected extremity of a patient with Klippel-Trénaunay syndrome. Note also the large lateral embryonic vein of the thigh. (From Noel AA, Gloviczki P, Cherry KJ Jr, et al: Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg 32:840-847, 2000.)

Patients with pelvic involvement may present with hematuria and rectal bleeding. Any patient with varicose veins or portwine stains with a longer or shorter limb must be suspected of having an underlying VM. Patients with primary or secondary lymphedema have limbs of identical length. In a Mayo Clinic study of 185 patients with arteriovenous malformations of the extremities and pelvis, the most frequent clinical sign was skin discoloration (43%), and the most frequent symptom was pain (37%).55 Thirty-five percent had a palpable mass, and 34% had limb hypertrophy. A bruit was present in 26%, and 20% of patients had some skin necrosis or ulceration. Increased skin temperature at the level of the lesion, decreased distal pulses, pulsatile veins, and edema of the extremity were additional clues to the diagnosis.

Evaluation Diagnostic tests should focus on evaluating the type and extent of the malformation; the presence or absence of any arteriovenous shunting must also be established. Physical examination of limb and pelvic lesions should be complemented by segmental systolic limb pressure measurement and establishment of the ankle-brachial index. Pulse volume recording is helpful in patients with arteriovenous shunting (Fig. 11-15). Placement of a tourniquet on a limb with a high-flow, high-shunt arteriovenous malformation and occlusion of the fistula will increase systolic blood pressure, followed by a slowing of the heart rate due to a vagal response in the baroreceptors in the aorta and carotid arteries (bradycardia sign). Duplex scans can confirm other hemodynamic

Scanograms are performed to document any length discrepancy between the limbs. Scanograms are long bone radiographic films that provide the most accurate measurement of the length of the different long bones of the upper and lower limbs (Fig. 11-17). Computed tomography (CT) scans and three-dimensional CT-angiography have progressed rapidly in recent years, and they provide excellent pictures of the malformations; highquality angiography is also possible with the advent of new CT technology (Fig. 11-18; see color plate). CT can show the extent of involvement, but arteriovenous malformations may not always be distinguishable from venous malformations. Because intravenous contrast is required, appropriate timing of the imaging is necessary, depending on the amount of blood shunted in the VM. Magnetic resonance imaging and magnetic resonance angiography have multiple advantages. They can differentiate muscle, bone, fat, and vascular tissue without the need for radiation or intravenous contrast, which may be harmful to the kidneys. Axial, coronal, and sagittal images can be generated (Fig. 11-19), and gadolinium enhancement provides high-quality angiography. High-flow and low-flow fistulas can be distinguished. Contrast arteriography is reserved for patients who are potential candidates for arterial embolization (Figs. 11-20 and 11-21). Arteriovenous shunting is confirmed by contrast arteriography, which also delineates the feeding arteries and excludes the presence of any vascular tumor (see Fig. 11-8). The size of the feeding arteries can be measured, and the size of the arteriovenous shunts (2 mm in large shunts, 100 to 200 µm in small shunts) can be estimated based on the appearance of contrast in the vein. The flow volume is determined by the size and rate of opacification of the feeding arteries, whereas the shunt volume can be estimated with acceptable accuracy by the time and appearance of contrast medium in the veins. Contrast venography is reserved for patients who are potential candidates for venous intervention (see Fig. 11-5). Contrast venography is frequently done through multiple injections in the limb, with the use of a tourniquet or Esmarch bandage to visualize the deep system, and with direct injection into the malformation before or after ethanol sclerotherapy.

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TABLE 11–2

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Clinical Syndromes Associated with Vascular Malformations

Syndrome

Inheritance

Type

Location

Parkes Weber

Somatic AVM (intraosseous Extremities mutations or close to Pelvis epiphyseal plate) Port-wine stain

Soft tissue and bone hypertrophy Varicosity (atypical) Capillary and high-flow, high-shunt AVM

Klippel-Trénaunay

Somatic No- or low-shunt Extremities mutations AVM Pelvis Venous or lymphatic Trunk Port-wine stains

Soft tissue and bone hypertrophy Varicosities (lateral lumbar to foot pattern) Capillary or venous vascular malformation, lymphatic malformation Epistaxis Transfusions Good if bleeding Hematemesis, melena Embolization vs. can be Hematuria laser treatment controlled Hepatomegaly ± excision and no CNS Neurologic symptoms manifestations

Rendu-Osler-Weber Autosomal (hereditary dominant hemorrhagic telangiectasia)

Punctate angioma Telangiectasia GI tract AVM

Sturge-Weber (encephalotrigeminal angiomatosis)

No

Port-wine stains

von Hippel-Lindau (oculocerebellar hemangioblastomatosis) Blue rubber bleb nevus

Autosomal dominant

Hemangioma

Retina Cerebellum

Autosomal dominant

Cavernous venous malformation

Kasabach-Merritt

Autosomal dominant

Large cavernous venous malformation

Skin GI tract Spleen Liver CNS Trunk Extremities

Maffucci’s (dyschondroplasia with vascular hamartoma)

Probably AVM autosomal Cavernous dominant lymphangioma

Characteristic Features Treatment

Skin Mucous membranes Liver Lungs Kidneys Brain Spinal cord Trigeminal area Leptomeninges Choroid Oral mucosa

Fingers Toes Extremities Viscera

Prognosis

Observation Deep, diffuse Elastic support lesions have Embolization ± poor prognosis excision (localized lesions only) Elastic support Usually good Seldom: epiphyseal stapling or selective excision or ablation of varicose veins

Convulsions Hemiplegia Ocular deformities Mental retardation Glaucoma Intracerebral calcification Cysts in cerebellum, pancreas, liver, adrenals, kidneys

Anticonvulsants Neurosurgical procedure

Guarded Depends on intracranial lesion

Excision of cysts

Depends on intracranial lesion

Bluish, compressible rubbery lesions GI bleeding, anemia

Transfusions Depends on Electrocoagulation CNS and GI Excision involvement

Thrombocytopenia Hemorrhage Anemia Ecchymosis Purpura Enchondromas Spontaneous fractures Deformed, shorter extremity Vitiligo

Compression Death from Transfusion of hemorrhage or blood, platelets infection

Orthopedic management

Chance of malignancy 20%

AVM, arteriovenous malformation; CNS, central nervous system; GI, gastrointestinal. Adapted from Gloviczki AA, Noel AA, Hollier LH: Arteriovenous fistulas and vascular malformations. In Ascher E (ed): Haimovici’s Vascular Surgery, 5th ed. Malden, Mass, Blackwell, 2004, pp 991-1014.

Treatment INDICATIONS There are absolute and relative indications for the treatment of VMs. The absolute indications include hemorrhage, ischemia, refractory ulcers, and congestive heart failure. Bleeding from malformations may occur through defects in

the skin or mucosa, or the patient may have intramuscular or retroperitoneal hematoma, hematuria, rectal bleeding, hematemesis, hemoptysis, or intracerebral or intraspinal bleeding. Relative indications for treatment include pain, claudication, functional impairment, limb asymmetry, and cosmetic reasons. A multidisciplinary approach in the evaluation and treatment of VMs provides the best result for

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RIGHT ARM Systolic pressure

LEFT ARM

Pulse volume recording

Pulse volume recording Upper arm/ brachial artery

105 mm Hg

Forearm/ radial artery 110 mm Hg

Index finger

140 mm Hg

Systolic pressure

130 mm Hg

130 mm Hg

50 mm Hg

the patient. The team may include a pediatrician; pediatric, orthopedic, plastic, and vascular surgeons; an interventional radiologist; a cardiologist or vascular internist; and a physical therapy physician. Conservative treatment is used for most patients. Laser therapy has been used effectively for capillary malformations (port-wine stains). Effective minimally invasive percutaneous techniques include transcatheter embolization and percutaneous or transcatheter sclerotherapy. Surgical excision is reserved for the minority of patients with localized superficial lesions or for those who have symptomatic juvenile varicose veins or localized venous malformations.

FIGURE 11–15 • Systolic limb pressures and pulse volume recording in a 13-year-old girl with an arteriovenous malformation of the left hand. Increased brachial systolic pressure proximal to the fistula and decreased pressure of the index finger distal to the fistula were recorded. The pulse volume recording shows sharp, high systolic peaks and slightly decreased anacrotic notches proximal to the fistula. (From Rutherford RB, Anderson BO, Durham JD: Congenital vascular malformations of the extremities. In Moore WS [ed]: Vascular Surgery: A Comprehensive Review, 5th ed. Philadelphia, WB Saunders, 1998, pp 191-202.)

CONSERVATIVE TREATMENT Treatment of VMs is usually conservative. An elastic garment or bandage, local wound care, compression dressings, special orthopedic footwear, and lifestyle modification may be required to manage daily life and improve limb function. Lymphedema is frequently managed using elastic garments, intermittent compression treatment, or lymphatic massage treatment by a physical therapist. The psychological problems caused by a visible deformity should not be underestimated. Long-term antibiotic therapy may be needed for recurrent cellulitis, and patients with recurrent deep vein thrombosis are treated with lifelong anticoagulants. EMBOLIZATION

Increased arterial and venous flow Increased venous collaterals

Increased venous pressure

Decreased mean and diastolic pressure Increased arterial collaterals

Fistula resistance Decreased systolic pressure

FIGURE 11–16 • Hemodynamic consequences of an arteriovenous fistula. (Courtesy of the Mayo Foundation.)

Embolization with selective catheterization has emerged as the primary therapy of arteriovenous malformations. Materials for embolization include polyvinyl alcohol particles (100 to 500 µm in size), absolute ethanol, stainless steel coils (usually with tufted Dacron), absorbable gelatin pledgets, powder coils, and cyanoacrylate adhesives. Each of these agents acts at different levels in the arterial system. Coils are equivalent to surgical ligation, although the tufted Dacron and the addition of thrombin generate more extensive arterial thrombosis than that achieved with ligation alone. Coils occlude medium to small arteries; liquid agents and the smaller-diameter particles occlude at the arteriolar level or the capillary bed.56 Forbes and associates reported on 31 therapeutic embolizations of 23 patients with extra-axial VMs of the head.20 Of the nine patients with arteriovenous malformations, embolization produced excellent results in seven; the degree of obstruction was 80% or more. Two patients with high-shunt flow needed combined radiological-surgical treatment.

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FIGURE 11–20 • Magnetic resonance image of a predominantly venous malformation involving the superficial and deep compartments of the distal calf.

FIGURE 11–17 • Long bone film (scanogram) confirms leg length discrepancy in bilateral Klippel-Trénaunay syndrome.

Rosen and Riles reported that 25% of 215 patients were cured 3 years after treatment of arteriovenous malformations with embolization.16 Overall, improvement was noted in 76%. Four percent of the patients were worse, with complications including temporary hemiparesis or massive hematuria. Highflow, high-shunt arteriovenous malformations are difficult to treat, and major complications, including tissue necrosis, pulmonary embolization, and limb amputations, have also been reported by others.15,16,55 Jacobowitz and colleagues reported on transcatheter embolization of pelvic arteriovenous malformations in 35 patients.58 A mean of 2.4 embolization procedures (range, 1 to 11 procedures) were needed 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 53% of the patients. Adjunctive surgical excision was done in only five patients (15%). Eighty-three percent of patients were asymptomatic or significantly improved at a mean follow-up of 84 months (range, 1 to 204 months). SCLEROTHERAPY

FIGURE 11–19 • Sagittal magnetic resonance image of an arteriovenous malformation involving the head of the right femur.

Absolute ethanol induces denaturation of tissue protein, precipitating protoplasm, and destroys the endothelial cells. It is delivered through selective arterial catheterization for arteriovenous malformations and through direct percutaneous injections into the lesions for predominantly venous malformations (see Figs. 11-7 and 11-21). Unfortunately, alcohol sclerotherapy causes significant pain; therefore, general anesthesia and pain control are required. Absolute ethanol can also cause significant side effects; treatment should be performed selectively, and it must be done by a physician with

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A

B

C

D

FIGURE 11–21 • A, Large arteriovenous malformation surrounding the right hip, with partial destruction of the hip joint. Previous embolization of the feeding vessels with coils was performed. B, Repeat embolization with Ivalon particles and with absolute alcohol was performed through selective catheterization of the lateral circumflex femoral artery. C and D, Additional ethanol sclerotherapy with direct percutaneous injections of absolute alcohol into the lesion. (Courtesy of Michael A. McKusick, MD, Mayo Foundation.)

expertise and knowledge of the dose and toxicity-related complications. For large arteriovenous malformations, pulmonary artery catheter and arterial pressure line monitoring is suggested by Coldwell59 and Yakes60 and their respective coauthors, who also recommend giving dexamethasone sodium phosphate, 3 to 10 mg, intravenously before the procedure. The maximum dose should not exceed 1.0 mL/kg body weight.

Pulmonary hypertension should be monitored when large doses are given, and nitroglycerin can be used to treat pulmonary vasospasm. Yakes reported a complication rate that ranged from 10% to 30%, depending on the physician’s years of experience.60 Tissue necrosis, sloughing of the skin, and pulmonary hypertension are the most frequent side effects, followed by deep vein thrombosis and motor and sensory nerve injury.

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One of the largest experiences using ethanol sclerotherapy for venous malformations was compiled by Lee and coworkers and reported in multiple publications.1,21,22 In 87 patients who underwent 399 sessions of sclerotherapy for the treatment of VMs, Lee reported an initial success rate of 95%. The mean follow-up was 24 months, and 71 of the 87 patients (82%) showed no recurrence of the treated lesion. Minor to major complications, mostly skin damage, developed after 47 sessions (12%) in 24 patients (28%). There was one permanent facial nerve palsy and one peroneal nerve palsy. The authors concluded that absolute ethanol sclerotherapy can deliver excellent results to patients with diffuse venous malformation, with a 25% rate of early complications and a 3% rate of permanent complications. The low complication rate in this series was remarkable; most authors report complication rates between 10% and 30%. Complication rates in predominantly venous malformations are significantly less than in those patients who have arteriovenous shunting. The benefits and potential major complications of absolute alcohol sclerotherapy were emphasized in an editorial by Villavicencio.61 Other materials that have been used for sclerotherapy include sotradecol and polidocanol foam.61-67 The advantage of foam detergent solutions is that smaller amounts can be used to achieve thrombosis. Polidocanol is less allergenic and produces less pain and inflammatory response than do other sclerosing solutions. Tessari uses 1% polidocanol for duplexguided foam sclerotherapy: two syringes are attached by a three-way stopcock—one is filled with polidocanol, the other with air—and the foam is obtained by mixing the contents of the two syringes.62,63 Five to 10 mL of the foam is injected under duplex and venographic guidance into the venous malformation. Foam has been used with increasing frequency and with good results for both occlusion of varicose veins and venous malformations.61-67 Although longer follow-up is required, early complication rates are lower than those associated with ethanol sclerotherapy, and foam may have great promise in the treatment of venous malformations.

A

209

B

FIGURE 11–22 • A, Large macrofistulous arteriovenous malformation of the right thigh. B, Arteriogram 5 months after surgical resection, which was preceded by multiple embolizations of the lesion. (From Gloviczki AA, Noel AA, Hollier LH: Arteriovenous fistulas and vascular malformations. In Ascher E [ed]: Haimovici’s Vascular Surgery, 5th ed. Malden, Mass, Blackwell, 2004, pp 991-1014.)

Cutaneous capillary malformations (port-wine stains) were initially treated with argon lasers, with good results in many patients; however, scarring occurred in 5% to 24% of patients.68 The best results were obtained in adults with purple, wellvascularized lesions. Scarring has become less frequent with the introduction of the yellow light lasers.69,70 The best results today are achieved with the flashlamp-pumped pulsed dye laser. The 585-nm wavelength achieves deep tissue penetration while maintaining vascular specificity.70 Both pale and dark skins can be treated with minimal intraoperative discomfort and a low chance of postoperative epidermal damage or pigmentary change. As stated by Tanzi and coworkers, the pulsed dye laser has revolutionized the treatment of superficial vascular lesions, especially port-wine stains and facial telangiectasias.70

in only 10 patients. Surgical attempts at excision can result in significant blood loss, and ligation of major feeding vessels is not a good option. It prevents the later use of selective catheterization and embolotherapy. Excision of venous malformations, if they are localized, can be done with a higher rate of success. Exsanguination of the limb with an elastic (Esmarch) bandage and the use of a proximal tourniquet greatly decrease blood loss and make the operation technically easier.71 If excision is decided on, preoperative sclerotherapy or embolization should be considered to minimize bleeding (Fig. 11-22). Use of the rapid cell saver is mandatory. In highflow, high-shunt lesions, the only operation that can be performed in some patients is amputation. Trout and colleagues attempted surgical treatment of large lower extremity arteriovenous malformations, but two of the four patients required amputation.72 Schwartz and associates reported on 82 patients treated at the Mayo Clinic for arteriovenous malformations; 18 patients required amputation at various levels of the extremity.55 Still, for many patients, amputation means cure, and a prosthesis offers the possibility of functional recovery.

SURGICAL EXCISION

Complex Malformations

Surgical excision of arteriovenous malformation is rarely curative. In the classic series of Szilagyi,13,14 18 of 82 patients underwent surgical treatment, and improvement was documented

For vascular surgeons, the management of two complex clinical syndromes involving VMs deserves a separate discussion. These are Parkes Weber syndrome and Klippel-Trénaunay syndrome.

LASER TREATMENT

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PARKES WEBER SYNDROME Congenital arteriovenous malformation of a limb associated with soft tissue and bony hypertrophy was described as “hemangiectatic hypertrophy” in 1907 and again in 1918.73,74 Parkes Weber syndrome should be differentiated from Klippel-Tréaunay syndrome, which is done by establishing the presence of arteriovenous shunting. Patients with Parkes Weber syndrome have clinically significant microfistulous or macrofistulous arteriovenous shunts, affecting usually one extremity. There is associated soft tissue and skeletal hypertrophy of the affected limb, and there are port-wine stains, usually on the lateral aspect of the limb. The patient has dilated, frequently pulsatile varicose veins and other visible signs of arteriovenous shunting. There is a palpable mass, the temperature of the skin is frequently elevated, and there is a cutaneous blush.75 The abnormality is sporadic; it is likely a somatic mutation. There is frequent intraosseous involvement. These patients may develop cardiac failure due to the longstanding arteriovenous shunting; progression of the disease, because of hemodynamic involvement, is much more frequent in Parkes Weber syndrome than in Klippel-Trénaunay syndrome. Management is initially conservative, using elastic compression. In limbs with high-flow lesions, repeated embolization may be required to treat the malformation, decrease pain, and diminish the hemodynamic effects of the high-shunt fistula. Occasionally, amputation of the limb is the only alternative. KLIPPEL-TRÉNAUNAY SYNDROME The clinical triad of Klippel-Trénaunay syndrome is capillary malformations (port-wine stains); soft tissue and bone hypertrophy; and atypical, usually lateral varicosity and venous and lymphatic malformations (see Figs. 11-3, 11-5, 11-12, and 11-13). This mixed malformation was described at the turn of the 20th century by the French physicians it is named for.76 The deep veins are frequently affected; the most common deep venous anomalies include ectasia or aneurysm, external compression, hypoplasia, aplasia, and persistent sciatic veins.2,3 KlippelTrénaunay syndrome is clearly a mixed VM that includes predominantly venous, lymphatic, and capillary elements but no arteriovenous shunting. Many patients have lymphedema, and some have cavernous lymphatic malformations. In 1998, Jacob and colleagues from the Mayo Clinic reported a retrospective review of 252 patients with KlippelTrénaunay syndrome.3 Of these, 246 (98%) had capillary malformations, 236 (94%) had soft tissue or bone hypertrophy, and 182 (72%) had varicosities or venous malformations. The lower extremities were involved in 70%, and the malformation was bilateral in 19%. The upper extremity was involved in 74 of 252 patients (29%). In this review, symptoms of KlippelTrénaunay syndrome included swelling (70%), pain (7%), and bleeding (17%). Thirty-nine patients (15%) had a history of superficial phlebitis, 4% had a history of deep vein thrombosis, and 4% had pulmonary embolism, which was fatal in one patient. Lateral varicose veins were frequent (56%). One percent had suprapubic varicosities due to iliac vein agenesis or aplasia, and 19% of the patients had medial varicosities. Management of Klippel-Trénaunay syndrome is largely conservative. Most patients who undergo surgical treatment

do so because of overgrowth of one limb; these patients are managed with epiphysiodesis, with good results.3,33,34 Vascular interventions must be preceded by careful evaluation of the patency of the deep venous system.2,34,77-80 Noel and colleagues from the Mayo Clinic reported on 20 patients who underwent surgical treatment.2 All had varicosities with a lateral distribution, although 65% had medial varicosities as well. Stripping and avulsion were performed in all patients; avulsion of varicose veins and excision of superficial venous malformations were usually accomplished with the help of a thigh tourniquet. Additional concomitant or staged procedures included release of the constricted popliteal veins, deep vein reconstruction, perforator ligation, and excision of an incompetence, persistent sciatic vein. Mean follow-up was 64 months. The results were excellent or good in 18 patients; only 2 patients showed no improvement. Twelve percent developed hematomas that required drainage, but no deep vein thrombosis, pulmonary embolism, or nerve injury was observed in this group of patients. The improvement was excellent in patients with varicosities, although some recurrence was noted in half of the patients. The clinical severity score significantly decreased in the entire group—from 4.3 to 3.1—documenting significant clinical benefits. In patients with a history of deep vein thrombosis, preoperative placement of a vena cava filter should be considered. Because of the rarity of this disorder and the presence of a mixed malformation, a multidisciplinary management approach is clearly warranted.

Conclusion Vascular malformations are caused by developmental abnormalities of the vascular system. They should be classified based on the predominant vascular structure and the presence or absence of arteriovenous shunting. Careful evaluation by a multidisciplinary team is required. Duplex scanning, CTangiography, or magnetic resonance imaging can reveal the type and extent of the lesion. Arteriovenous shunting, if detected, can be treated using transcatheter embolotherapy. Symptomatic, predominantly venous malformations can be managed by percutaneous sclerotherapy, whereas localized capillary malformations of the skin respond well to laser therapy. High-flow, high-shunt malformations may develop severe complications, in spite of combined radiological-surgical management, and amputation may be the only option for optimal treatment. In patients with Klippel-Trénaunay syndrome, conservative management is favored, but vascular interventions can be beneficial, with ablation of the symptomatic incompetent superficial veins if the deep venous system is patent. As molecular genetic information about VMs is rapidly gained, traditional treatment strategies of destroying the intravascular spaces with sclerotherapy and lasers or excising the lesions with surgery may be replaced, at least in part, by gene therapy to prevent or treat angiogenic disorders. KEY REFERENCES Lee BB, Do YS, Yakes W, et al: Management of arteriovenous malformations: A multidisciplinary approach. J Vasc Surg 39:590-600, 2004. Lee BB, Kim I, Huh S, et al: New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation. J Vasc Surg 33:764-772, 2002.

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Mulliken JB, Young AE: Vascular Birthmarks: Hemangiomas and Malformations. Philadelphia, WB Saunders, 1988. Noel AA, Gloviczki P, Cherry KJ Jr, et al: Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg 32:840-847, 2000. Rutherford RB: Classification of peripheral congenital vascular malformations. In Ernst C, Stanley J (eds): Current Therapy in Vascular Surgery. St. Louis, Mosby, 1995, pp 834-838. Vikkula M, Boon LM, Mullikan JB: Molecular genetics of vascular malformations. Matrix Biol 20:327-335, 2001.

REFERENCES 1. Lee BB, Do YS, Yakes W, et al: Management of arteriovenous malformations: A multidisciplinary approach. J Vasc Surg 39:590-600, 2004. 2. Noel AA, Gloviczki P, Cherry KJ Jr, et al: Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg 32:840-847, 2000. 3. Jacob AG, Driscoll DJ, Shaughnessy WJ, et al: Klippel-Trenaunay syndrome: Spectrum and management. Mayo Clin Proc 73:28-36, 1998. 4. McGrory BJ, Amadio PC: Klippel-Trenaunay syndrome: Orthopaedic considerations. Orthop Rev 22:41-50, 1993. 5. Virchow R: Pathologie des tumeurs: cours professé à l’Université de Berlin, vol 4. Paris, Germer-Bailliére, 1876, p 169. 6. Nicoladoni C: Phlebarteriectasie der rechten oberen Extremität. Arch Kim Chir 18:252, 1875. 7. Branham HH: Aneurismal varix of the femoral artery and vein following a gunshot wound. Int J Surg 3:250, 1890. 8. Reid MR: Studies on abnormal arteriovenous communicanons, acquired and congenital. I. Report of a series of cases. Arch Surg 10:601, 1925. 9. Holman E: Arteriovenous Aneurysm: Abnormal Communications between the Arterial and Venous Circulations. New York, Macmillan, 1937. 10. de Takats G: Vascular anomalies of the extremities: Report of five cases. Surg Gynecol Obstet 55:227, 1932. 11. Coursley G, Ivins JC, Barker NW: Congenital arteriovenous fistulas in the extremities: An analysis of sixty-nine cases. Angiology 7:201, 1956. 12. Malan E, Puglionisi A: Congenital angiodysplasias of the extremities: Generalities and classifications: Venous dysplasias. J Cardiovasc Surg 5:87-130, 1964. 13. Szilagyi DE, Elliott JP, et al: Peripheral congenital arteriovenous fistulas. Surgery 57:61, 1965. 14. Szilagyi DE, Smith RF, et al: Congenital arteriovenous anomalies of the limbs. Arch Surg 111:423-429, 1976. 15. Rutherford RB, Anderson BO, Durham JD: Congenital vascular malformations of the extremities. In Moore WS (ed): Vascular Surgery: A Comprehensive Review, 5th ed. Philadelphia, WB Saunders, 1998, pp 191-202. 16. Rosen RJ, Riles TS: Congenital vascular malformations. In Rutherford RB (ed): Vascular Surgery, 5th ed. Philadelphia, WB Saunders, 2000, pp 1451-1465. 17. Belov ST: Anatomopathological classification of congenital vascular defects. Semin Vasc Surg 6:219-224, 1993. 18. Rutherford RB: Classification of peripheral congenital vascular malformations. In Ernst C, Stanley J (eds): Current Therapy in Vascular Surgery. St. Louis, Mosby, 1995, pp 834-838. 19. Natali J, Merland JJ: Superselective arteriography and therapeutic embolisation for vascular malformations (angiodysplasias). J Cardiovasc Surg (Torino) 17:465, 1976. 20. Forbes G, Earnest FIV, et al: Therapeutic embolization angiography for extra-axial lesions in the head. Mayo Clin Proc 61:427, 1986. 21. Lee BB: Critical issues in management of congenital vascular malformation. Ann Vasc Surg 18:380-392, 2004. 22. Lee BB, Kim I, Huh S, et al: New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation. J Vasc Surg 33:764-772, 2002. 23. Mulliken JB, Zetter BR, Folkman J: In vitro characteristics of endothelium from hemangiomas and vascular malformations. Surgery 92:348, 1982. 24. Glowacki J, Mulliken JB: Mast cells in hemangiomas and vascular malformations. Pediatrics 70:48, 1982. 25. Mulliken JB, Glowacki J: Hemangiomas and vascular malformations in infants and children: A classification based on endothelial characteristics. Plast Reconstr Surg 69:412-420, 1982. 26. Vikkula M, Boon LM, Mullikan JB: Molecular genetics of vascular malformations. Matrix Biol 20:327-335, 2001.

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27. Woollard RH: The development of the principal arterial stems in the forelimb of the pig. Contrib Embryol 14:139-154, 1922. 28. Ballaun C, Weninger W, Uthman A, et al: Human keratinocytes express the three major splice forms of vascular endothelial growth factor. J Invest Dermatol 104:710, 1995. 29. Brown LF, Yeo KT, Berse B, et al: Expression of vascular permeability factor (vascular endothelial growth factor) by epidermal keratinocytes during wound healing. J Exp Med 176:1375-1379, 1992. 30. Mukouyama YS, Shin D, Britsch S, et al: Sensory nerves determine the pattern of arterial differentiation and blood vessel branching in the skin. Cell 109:693-705, 2002. 31. Nicholson CP, Gloviczki P: Embryology and development of the vascular system. In White RA, Hollier LH (eds): Vascular Surgery: Basic Science and Clinical Correlations. Philadelphia, JB Lippincott, 1994. pp 3-20. 32. West CA, Delis KT, Service G, et al: Middle aortic syndrome: Surgical treatment in a child with neurofibromatosis, renovascular hypertension, superior mesenteric artery stenosis and intermittent claudication. J Vasc Surg (in press). 33. Gloviczki P, Hollier LR, et al: Surgical implications of KlippelTrenaunay syndrome. Ann Surg 197:353, 1983. 34. Gloviczki P, Stanson AW, et al: Klippel-Trenaunay syndrome: The risks and benefits of vascular interventions. Surgery 110:469-479, 1991. 35. Eifert S, Villavicencio L, Kao TG, et al: Prevalence of deep venous anomalies in congenital vascular malformations of venous predominance. J Vasc Surg 31:462-471, 2000. 36. Servelle M: Klippel Trenaunay syndrome: 768 operated cases. Ann Surg 201:365-373, 1985. 37. Guttmacher AE, Marchuk DA, White RI: Hereditary hemorrhagic telangiectasia. N Engl J Med 33:918-924, 1995. 38. Gloviczki AA, Noel AA, Hollier LH: Arteriovenous fistulas and vascular malformations. In Ascher E (ed): Haimovici’s Vascular Surgery, 5th ed. Malden, Mass, Blackwell, 2004, pp 991-1014. 39. Eerola I, Boon LM, Mulliken JB, et al: Capillary malformationarteriovenous malformation, a new clinical and genetic disorder caused by RASA1 mutations. Am J Hum Genet 73:1240-1249, 2003. 40. Milroy WF: An undescribed variety of hereditary edema. N Y Med J 56:505, 1892. 41. Milroy WF: Chronic hereditary edema: Milroy’s disease. JAMA 91:1172, 1928. 42. Meige H: Dystrophie oedemateuse hereditaire. Presse Med 2:341, 1898. 43. Gloviczki P, Wahner HW: Clinical diagnosis and evaluation of lymphedema. In Rutherford RB (ed): Vascular Surgery, 5th ed. Philadelphia, WB Saunders, 2000, pp 2123- 2142. 44. Noel A, Gloviczki P, Bender CE, et al: Treatment of symptomatic primary chylous disorders. J Vasc Surg 34:785-791, 2001. 45. Collins PS, Han W, Williams LR, et al: Maffucci’s syndrome (hemangiomatosis osteolytica): A report of four cases J Vasc Surg 16:364-371, 1992. 46. Lublin M, Schwartzentruber DJ, Lukish J, et al: Principles for the surgical management of patients with Proteus syndrome and patients with overgrowth not meeting Proteus criteria. J Pediatr Surg 37:1013-1020, 2002. 47. Tasnadi G: Epidemiology and etiology of congenital vascular malformations. Semin Vasc Surg 6:200-203, 1993. 48. Boon LM, Mulliken JB, Vikkula M, et al: Assignment of a locus for dominantly inherited venous malformations to chromosome 9p. Hum Mol Genet 3:1583-1587, 1994. 49. Vikkula M, Boon LM, Mulliken JB, Olsen BR: Molecular basis of vascular anomalies. Trends Cardiovasc Med 8:281-292, 1998. 50. Timur AA, Sadgephour A, Graf M, et al: Identification and molecular characterization of a de novo supernumerary ring chromosome 18 in a patient with Klippel-Trenaunay syndrome. Ann Hum Genet 68:353-361, 2004. 51. Tian XL, Kadaba R, You SA, et al: Identification of an angiogenic factor that when mutated causes susceptibility to Klippel-Trenaunay syndrome. Nature 427:640-645, 2004. 52. Vikkula M, Boon LM, Carraway KLI, et al: Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE2. Cell 87:1181-1190, 1996. 53. Boon LM, Brouillard P, Irrthum A, et al: A gene for inherited cutaneous venous anomalies (“glomangiomas”) localizes to chromosome 1p21-22. Am J Hum Genet 65:125-133, 1999. 54. Boon LM, Mulliken JB, Enjolras O, Vikkula M: Glomuvenous malformation (glomangioma) and venous malformation: Distinct clinicopathologic and genetic entities. Arch Dermatol 140:971-976, 2004.

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55. Schwartz RS, Osmundson PJ, Rollier LH: Treatment and prognosis in congenital arteriovenous malformation of the extremity. Phlebology 1:171, 1986. 56. Pritchard DA, Maloney JD, et al: Surgical treatment of congenital pelvic arteriovenous malformation. Mayo Clin Proc 53:607, 1978. 57. Pritchard DA, Maloney JD, et al: Peripheral arteriovenous fistula: Detection by contrast echocardiography. Mayo Clin Proc 52:186, 1977. 58. Jacobowitz GR, Rosen RJ, Rockman CB, et al: Transcatheter embolization of complex pelvic vascular malformations: Results and long-term follow-up. J Vasc Surg 33:51-55, 2001. 59. Coldwell DM, Stokes KR, Yakes WF: Embolotherapy: Agents, clinical applications, and techniques. Radiographics 14:623-643, 1994. 60. Yakes WF, Rossi P, Odink H: How I do it: Arteriovenous malformation management. Cardiovasc Intervent Radiol 19:65-71, 1996. 61. Villavicencio JL: Primum non nocere: Is it always true? The use of absolute ethanol in the management of congenital vascular malformations J Vasc Surg 33:904-906, 2001. 62. Yamaki T, Nozaki M, Fujiwara O, Yoshida E: Duplex-guided foam sclerotherapy for the treatment of the symptomatic venous malformations of the face. Dermatol Surg 28:619-622, 2002. 63. Tessari L: Nouvelle technique d’obtention de la sclero-mousee. Phlebologie 53:129, 2000. 64. Tessari L, Cavezzi A, Frullini A: Preliminary experience with a new sclerosing foam in the treatment of varicose Monfreux A. Traitement sclérosant des troncs saphènies et leurs collatérals de gros caliber par le method MUS. Phlebologie 50:3513, 1997. 65. Henriet JP: Un an de pratique quotidienne de la sclérothérapie (veines reticulaires et télangiectasies) par mousse de polidocanol faisabilité, resultants, complications. Phlebologie 50:355-360, 1997. 66. Cavezzi A, Frullini A: The role of sclerosing foam in ultrasound guided sclerotherapy of the saphenous veins and of recurrent varicose veins: our personal experience. Aust N Z J Phlebol 3:4950, 1999. 67. Cabrera Garrido JR, Cabrera Garcia-Olmedo JR, Garcia-Olmedo Dominguez MA: Elargissement des limites de la sclérothérapie: Nouveaux produits sclérosants. Phlebologie 50:1818, 1997. 68. 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 65:130, 1980. 69. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J: Treatment of port-wine stains (capillary malformation) with the flashlamp-pumped pulsed dye laser. J Pediatr 122:71-77, 1993. 70. Tanzi EL, Lupton JR, Alster TS: Lasers in dermatology: Four decades of progress. J Am Acad Dermatol 49:1-31, 2003. 71. Villavicencio JL, Gillespie DL, Kreishman P: Controlled ischemia for complex venous surgery: The technique of choice. J Vasc Surg 34: 947-951, 2001. 72. Trout RH III, McAllister RA Jr, et al: Vascular malformations. Surgery 97:36, 1985. 73. Weber FP: Angioma-formation in connection with hypertrophy of limbs and hemi-hypertrophy. Br J Dermatol 19:231, 1907. 74. Weber FP: Haemangiectatic hypertrophy of limbs: Congenital phlebarteriectasis and so-called congenital varicose veins. Br J Child Dis 15:13, 1918. 75. Mulliken JB, Young AE: Vascular Birthmarks: Hemangiomas and Malformations. Philadelphia, WB Saunders, 1988. 76. Klippel M, Trénaunay P: Du naevus variquex osteohypertrophique. Arch Gen Med (Paris) 3:641-672, 1900. 77. Baskerville PA, Ackroyd JS, Lea TM, Browse NL: The KlippelTrenaunay syndrome: Clinical, radiological and haemodynamic features and management. Br J Surg 72:232-236, 1985. 78. Lindenauer SM: The Klippel-Trenaunay syndrome: Varicosity, hypertrophy and hemangioma with no arteriovenous fistula. Ann Surg 162:303-313, 1965. 79. Villavicencio JL: Congenital vascular malformations of venous predominance: Klippel-Trenaunay syndrome. In Raju S, Villavicencio JL (eds): Surgical Management of Venous Disease. Baltimore, Williams & Wilkins, 1997, pp 445-461. 80. Baskerville PA, Ackroyd JS, Browse NL: The etiology of the KlippelTrenaunay syndrome. Ann Surg 202:624-627, 1985.

Questions 1. Which predominant type of vascular malformation is seen most often in vascular clinics? (a) Venous (b) Arterial (c) Arteriovenous (d) Lymphatic 2. Temporary occlusion of flow to a vascular malformation with a high-flow arteriovenous fistula will result in which of the following? (a) Tachycardia (b) Venous hypertension proximal to the fistula (c) Arrhythmia (d) Bradycardia (e) Decrease of mean arterial pressure 3. Microfistulous arteriovenous malformations are caused by an inborn error at which stage of limb bud development? (a) Undifferentiated (b) Retiform (c) Syncytial (d) Maturational 4. Which of the following statements regarding hemangiomas encountered during infancy is not true? (a) They have a high endothelial turnover (b) They may exhibit high-flow characteristics (c) The female-male ratio is 5:1 (d) Their growth is commensurate with the child’s growth 5. Which of the following presentations is not typical of Klippel-Trénaunay syndrome? (a) Increased limb size (b) Increased pulsatility with a palpable thrill (c) Varicose veins (d) Capillary malformation (port-wine stain) (e) Malformation of the deep veins 6. Which noninvasive test finding is not characteristic of a high-flow arteriovenous malformation (fistula) of the thigh? (a) Increased systolic pressure proximal to the lesion (b) High end-diastolic velocity in the proximal artery (c) Elevated pulse volume recording (plethysmographic tracing) distally in the foot (d) Decreased ankle-brachial index (e) Elevated venous pressure distal to the malformation 7. In young patients with symptomatic lateral varicose veins, preoperative evaluation must establish which of the following findings? (a) Patency of the deep veins (b) Presence of port-wine stains (c) Limb length discrepancy (d) Positive family history of varicosity (e) History of hematuria or rectal bleeding

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8. Which of the following malformations is not considered hereditary? (a) Milroy disease (b) Meige disease (c) Glomuvenous malformation (d) Klippel-Trénaunay syndrome (e) HHT1 9. Which of the following is not true about catheterdirected injections of absolute alcohol into the nidus of a vascular malformation? (a) They require multiple sessions (b) They must be done under general anesthesia (c) They selectively destroy endothelium and cause thrombosis without resulting in surrounding tissue necrosis (d) They can cause permanent nerve injury in as many as 10% of cases (e) They can permanently control some vascular malformations

10. Neither excision of a localized malformation nor embolotherapy is justified for which of the following indications in patients with vascular malformations? (a) Recurrent hemorrhage from skin lesions (b) Uneven limb growth (c) Ischemic ulcer (d) Symptomatic arterial steal

Answers 1. a 6. c

2. d 7. a

3. b 8. d

4. d 9. c

5. b 10. b

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12

Ralph G. DePalma

Vasculogenic Erectile Dysfunction Impotence, or male erectile dysfunction (ED), is defined as “the persistent or repeated inability to attain and/or maintain an erection sufficient for satisfactory performance in the absence of an ejaculatory disorder.”1 ED is now better understood and more effectively treated than in the past. Comprehension of the physiology of erection and the central role of cavernous sinus smooth muscle relaxation2 resulted in the development of medical therapy for men with ED.3 Vascular surgeons require information about the prevention of ED and other sexual dysfunctions, including ejaculatory and orgasmic disorders, particularly as these conditions relate to aortoiliac interventions. They also need to be able to assess the contribution of macrovascular disease to vasculogenic ED and to treat occlusive or aneurysmal disease that contributes to ED. Aortoiliac reconstruction itself can cause ED by failing to perfuse the internal iliac arteries or by damaging autonomic genital nerves.4 Techniques of particular importance to vascular surgeons are those that minimize or completely avoid damage to the pelvic nerves while restoring or maintaining flow into the internal iliac arteries. These techniques may prevent sexual dysfunction and, in selected cases, restore potency after aortoiliac interventions.5,6 This chapter describes surgical approaches for the prevention of postoperative ED during aortoiliac interventions. Vasculogenic ED due to small vessel disease, cavernous smooth muscle dysfunction, and primary ED are complex disorders; some of the pertinent approaches to treatment are summarized here, and readers with a specific interest in the subject are referred to the comprehensive volume Male Sexual Function.7 Microvascular procedures for vasculogenic ED, which are now performed infrequently, are briefly described. Vascular surgeons should also be aware of female sexual dysfunction (FSD), which may occur after aortoiliac surgery8 and radical hysterectomy.9 Nerve-sparing and revised operative techniques may prevent or minimize these effects in gynecologic surgery.10,11

These endothelium-mediated relaxation responses are stimulated by neural mechanisms.14 The roles of nitric oxide (NO) as the chemical mediator,15 as well as the importance of blood flow and oxygenation of the cavernous smooth muscle,16 are fundamental to an understanding of erectile physiology. With increased intracavernosal flow, a greater amount of oxygen stimulates NO synthesis by cavernosal nerves and endothelium. Cavernosal oxygenation promotes penile erection, whereas hypoxemia is inhibitory. Testosterone, in addition to its central effects, has been shown in animals to stimulate NO synthase activity in corporal tissues,17 thus enhancing sensitivity to cavernosal nerve stimulation. NO, in turn, activates conversion of guanosine triphosphate to cyclic guanosine monophosphate (GMP). The latter provides the message leading to relaxation of the smooth muscle within the corpora cavernosa.18 Agents that inhibit hydrolysis of cyclic GMP increase messenger cyclic GMP and facilitate smooth muscle relaxation to promote penile erection.19 Cyclic nucleotide phosphodiesterase (PDE) isoenzymes increase hydrolysis of cyclic GMP; among these, PDE-5 and PDE-6 are specific for the substrate in human cavernosal tissue.20 Specific PDE-5 inhibitors constitute an important new class of oral agents, including sildenafil, vardenafil, and tadalafil. PDE-5 inhibitors are currently available and widely used for the treatment of ED. As corporal arterial pressure increases, draining emissary veins are compressed against the tunica albuginea, causing venous outflow occlusion. During full erection, cavernosal artery flow virtually ceases. During flaccidity, a constant venous leak balances baseline penile inflow and outflow. With insufficient arterial inflow, the corpora do not pressurize adequately, and secondary venous leakage occurs. Intracavernous pressure increases from 10 to 15 mm Hg to levels ranging from 80 to 90 mm Hg in the erect state. Intracavernous pressures higher than systemic pressure, generated by perineal muscle contraction,13 contribute to penile rigidity.

Physiology of Erection

Approaches to the Investigation of Erectile Dysfunction

Penile erection requires adequate arterial inflow and closure of cavernosal outflow, mediated by a complex interplay between neural and local factors.12,13 Erection results primarily through relaxation of the smooth muscle of the corporal bodies. 214

Table 12-1 summarizes general factors contributing to erectile dysfunction. In modern practice, more cases are now recognized as being organic in origin than were previously appreciated;

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TABLE 12–1

General Causative Factors in Erectile Dysfunction

Vasculogenic Neurogenic Endocrine Drug induced Psychogenic

however, men with organic impotence may exhibit psychogenic problems as well. Of 1023 impotent men screened for diagnosis and treatment, 461 demonstrated some type of arterial inflow problem, based on noninvasive criteria using the penile brachial index and pulse volume recordings.21,22 However, many men exhibited other contributing factors, including diabetes, neuropathy (about 20%), antihypertensive medication, and other types of cavernous dysfunction, including Peyronie’s disease. Older men with multiple factors contributing to ED are generally not candidates for vascular surgical intervention for this complaint alone. About 6% to 7% of the men who were investigated ultimately became candidates for vascular intervention. In my experience, only 15.6% of men with decreased arterial perfusion exhibited large vessel disease. Thus, imposing a selective screening sequence for surgical case selection yields a sharp funnel effect that minimizes candidacy for vascular intervention for ED.22 However, for young men with small vessel disease or men of any age with macrovascular disease, vascular intervention is a logical first step for those who fail aggressive medical therapy and for those who do not desire prosthetic implantation.23 Table 12-2 offers an updated classification of vasculogenic ED. Some type of small vessel, cavernosal, or arteriolar cause appears to be present in 43.3% of men exhibiting abnormal penile perfusion. An additional 41.1% of men with the primary complaint of impotence exhibit a combination of large and small vessel involvement, as ascertained by noninvasive and physical criteria. Most men with the primary complaint of ED are more likely to have small vessel or cavernosal disorders than macrovascular disease. Importantly, the complaint

TABLE 12–2 Arterial Large vessel Small vessel Combined Cavernosal Fibrosis Peyronie’s disease Refractory states Venous Acquired Congenital

Classification of Vasculogenic Erectile Dysfunction Aorta and branches to internal iliac artery Anterior division of internal iliac artery and penile arteries Atheroembolism from aortoiliac segment Postpriapic, drug injection, idiopathic with aging Deformity; venous leakage Hormonal, diabetic, blood pressure medication Various patterns; dorsal vein, crural, spongiotic Cavernous spongiosis leak

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of impotence has also been associated with occult aortoiliac occlusive or aneurysmal disease. In men with Leriche syndrome,24,25 impotence as a sentinel complaint sometimes precedes the onset of claudication. Men younger than 55 years are often potent before reconstruction for aneurysm or occlusive disease, and an accurate history of their sexual activity must be obtained. Despite the best surgical techniques to preserve sexual function, ED and other sexual disabilities continue to occur after reconstructions for aneurysms and occlusive disease. Therefore, before intervention, the surgeon must make careful inquiries into the patient’s sexual function and, when necessary, assess preoperative penile artery perfusion. A detailed history and noninvasive testing are particularly important when postoperative sexual function is an expressed concern of the patient.

History and Physical Examination A history of gradual erectile failure, in the absence of traumatic life events and correlated with symptoms such as claudication, suggests large vessel arteriogenic ED. In these men, both the intensity and the duration of atherosclerotic risk factors, mainly cigarette smoking, hypertension, diabetes, and hypercholesterolemia, contribute to atherosclerosis. This pattern signals patients who have involvement of the aorta or the iliac system. Abdominal aneurysms or ulcerated aortoiliac disease can cause penile vessel emboli.21 In such instances, the onset of ED is characteristically sudden. Perineal injury predisposes to thrombosis of the pudendal arteries. The immediate onset of erectile failure after urologic, vascular, or rectal operations is an important diagnostic clue suggesting neurovascular damage. Although either neural or vascular interruption can cause ED, periaortic, sympathetic, or hypogastric neural interruption can cause ejaculatory disorders. Alcohol and drug abuse contributes to progressive erectile failure, along with drugs used to treat hypertension because of their neuropathic and metabolic effects. Other hormonal disorders, such as hypogonadism, rarely seem to cause ED. Our group detected two prolactinomas during the screening of approximately 1400 men; these men exhibited dramatic responses to medical therapy. The major findings of aortoiliac disease on physical examination are decreased femoral pulses, bruits, or palpation of an abdominal aortic aneurysm in those whose waists measure less than 38 to 40 inches. Sensory testing of the extremities, perineum, or glans occasionally reveals neuropathies associated with diabetic impotence. However, these abnormalities are most reliably quantified by neurovascular testing, using pudendal evoked potentials and measurement of bulbocavernosus reflex times.26,27 Currently, neurologic screening is not routinely performed initially, because medical treatment with vasoactive agents is often effective, even in cases of neuropathy. In cases of postoperative or post-traumatic dysfunction, neurologic testing is an important factor in decision making, particularly in recommending prosthetic implantation as an option. Considerable overlap exists between vascular and neurologic ED. The prostate must be examined, and nodular abnormalities investigated. Prostate-specific antigen determinations should routinely be obtained before the prostate examination. Methodical palpation of the corpora cavernosa for Peyronie’s plaques and estimation of testicular size complete

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the examination. In most men presenting with primary ED, the physical examination is completely normal. At this point, the erectile mechanism can be tested in the clinic by intracavernous injection of 10 to 20 µg of Prostin E1.28 Rigid erection sufficient for intercourse demonstrates adequate arterial inflow and veno-occlusive mechanisms. Provided that aneurysmal disease has been ruled out (e.g., by sonography), treatment with oral, injectable, or intra-arterial vasoactive agents is the first step. Such treatment may succeed in up to 70% to 80% of cases. Multiple factors contribute to ED, which is a symptom, not a single disease. These factors, summarized in Table 12-1, help guide approaches to the diagnosis and treatment of sexual dysfunction and, in some respects, are relevant to both sexes. An important area, hitherto neglected, has been the study of female sexual dysfunction (FSD), which appears in women with diabetes29,30 or cardiovascular disease31 and in postmenopausal women as disordered sexual arousal,32 failure to achieve orgasm, and dyspareunia with failure to lubricate. Feminine arousal and vaginal lubrication are difficult to assess, whereas penile erection can be seen and quantified. Progress in understanding the cause, physiology, and treatment of FSD continues.33 Treatment modalities similar to those suggested in men have been proposed, and treatment trials have included oral PDE-5 inhibitors34,35 (which are probably not as effective as in men) and topical alprostadil.36 From the standpoint of aortic reconstruction, vascular surgeons should now recognize the potential benefits of nervesparing dissections with preserved internal iliac flow for women as well as for men. No universally accepted approach to managing ED exists; as mentioned, ED is a symptom, not a single disease. The initial approach is directed by the patient’s goals and depends on the response to simple therapy.37 When oral medication fails, more elaborate investigations might be considered.38 Should the intracavernous administration of vasoactive agents fail and vacuum constrictor devices prove ineffective, and if vascular intervention is an option, evaluation may progress to more elaborate invasive tests that delineate abnormal physiology.

Neurovascular Testing Neurovascular testing was initially used for all patients by our group22 to screen candidates for reconstructive procedures23 and to help determine the initial dosage for intracavernous injection of vasoactive agents; patients with neurologic deficits are often exquisitely sensitive to such agents, and their dosage must be reduced to avoid priapism. With the advent of giving a trial of oral medication as the first step in treatment, such testing is needed less frequently. Testing may be useful for the investigation of postoperative onset or traumatic ED or when legal issues exist. The penile brachial index (PBI) is the ratio between systolic pressure detected by a Doppler probe placed distal to the penile cuff and systemic or brachial arm pressure.39 A cuff of 2.5 cm is used for an average-size penis. The cuff is inflated, then deflated, and the reappearance of Doppler signals in the dorsal artery branch proximal to the corona signals reflow. Normally, this pressure approaches systemic pressure. A PBI above 0.75 suggests no major obstacle between the aorta and the distal measurement point. Generally, PBIs less than 0.6

relate to major vascular obstructions in the aortoiliac bed, whereas PBIs between 0.6 and 0.75 are considered abnormal. Flow can be further characterized by penile pulse volume recording, which uses a pneumoplethysmographic cuff (Buffington) with a contained transducer. This test is performed with the penis in the flaccid state. The variables recorded are the same as those used for the lower extremity. These include crest time, waveform, and the presence or absence of a dicrotic notch. This technique measures the total pulsation of all penile arteries as the cuff compresses the cavernous tissues. The measurements are taken with the cuff inflated to mean arterial pressure and are calculated as diastolic pressure plus one third of systemic pulse pressure. Waveforms on a polygraph with a chart speed of 25 mm/sec and a sensitivity setting of 1 demonstrate in normal patients that the upstroke of the waveform is completed by 0.2 second, whereas normal waveform amplitudes vary from 5 or 6 to 30 mm in height. Waveforms might be distinctly abnormal with small vessel disease or cavernosal disorders, whereas PBI is normal. These noninvasive tests are not completely sensitive and specific. I found that the combination of PBI and pulse volume recording predicts an abnormal arteriogram with a sensitivity of 85% and a specificity of 70%. In suspected cases of venogenic impotence (i.e., normal arterial noninvasive tests), 23% of men examined with normal noninvasive studies had associated arterial lesions demonstrated angiographically.40 Therefore, before small vessel interventions, which are done only for those failing medical therapy,18 both pudendal arteriography and dynamic infusion cavernosography are required for proper case selection. PBI detects inadequate arterial inflow from large arteries. Vasculogenic impotence caused by venous leak, Peyronie’s disease, or cavernosal fibrosis is not detected. In these instances, color-flow duplex scanning after an intracavernous injection to produce erection or tumescence has been used extensively by urologists, sometimes in combination with visual erotic stimulation, to measure deep cavernosal and dorsal blood flow velocity at intervals after the injection of a vasodilator.41 Based on these studies, ED can be classified as arterial, venous, or mixed vascular. Studies of local blood flow dynamics yield little information about proximal macrovascular inflow. Radionuclide phallography and pelvic magnetic resonance imaging are currently research applications. Nocturnal penile tumescence and rigidity monitoring, using noninvasive strain gauge techniques, are ideally performed in a sleep laboratory over several nights. Home monitoring devices are available. A normal rigid erection during sleep rules out organic impotence.42

Cavernosometry and Cavernosal Artery Occlusion Pressure Invasive studies provide quantitative information about arterial inflow and veno-occlusive mechanisms.43 A calibrated pump provides a flow of warm, heparinized saline via 20-gauge needles inserted into the corpora. During maximal erection, intracavernous pressure at some point equilibrates with arterial inflow pressure, and flow in the deep cavernosal artery stops. This value is called cavernosal artery occlusion pressure, and it is measured by using Doppler insonation at

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the point of full erection. Normal is considered greater than 90 mm Hg. A pressure gradient from brachial levels greater than 30 mm Hg suggests arterial inflow occlusion. Dynamic infusion cavernosography measures the flow required to maintain erection. This value is normally 40 mL or less after intracavernous injection of a standard papaverinephentolamine mixture. Nonionic dilute contrast is injected to visualize venous leaks. Spot filming in various obliquities identifies specific abnormal or leaking veins when cavernosography is positive. As mentioned previously, failure of erection is associated with an excess of venous leakage over inflow. Venous leakage can be due to arterial insufficiency, so before contemplated venous ablation, I recommend highly selective pudendal arteriography.

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A

Incision line Sutures in orifice of inferior mesenteric artery

B

Aortoiliac Reconstruction Principles Given the standard indications for large vessel aortoiliac reconstruction (i.e., aneurysm or occlusive disease), the procedure, whether endovascular44,45 or open,46,47 should be planned to provide perfusion of both internal iliac arteries whenever possible. Flushing of debris into the internal iliacs should be avoided, and endovascular repair should attempt to maintain internal iliac flow—at least to one internal iliac artery.17 The dissection in open cases must spare the neural fibers about the aorta and the iliac arteries (which are especially rich on the left side) and about the inferior mesenteric artery. In all these cases, a specific history of preoperative sexual activity must be sought. If an elderly person manifests no interest in this activity, complicated preoperative testing is unnecessary. However, when interest exists, preoperative PBI and pulse volume recordings are helpful for comparison with postoperative findings. In addition, positive findings of abnormal pudendal and somatosensory evoked potentials are helpful to demonstrate neuropathy.

Operative Techniques Operative techniques have been described previously,46 and illustrations have been reproduced from prior reviews.47 Exposure for aortoiliac reconstruction is best accomplished by dissecting the aortoiliac segment from the right and sparing the nerves and inferior mesenteric artery. In cases of aortoiliac aneurysm, perfusion of the internal iliac is ensured by an inlay technique, illustrated in Figure 12-1. Again, the aneurysmal sac is incised well to the right, avoiding interruption of a dominant left periaortic nerve plexus. The inferior mesenteric artery is sutured from within the aneurysmal sac. Figures 12-2 and 12-3 show the techniques for occlusive disease. In men with buttock claudication and impotence related to local disease in the arterial distribution of the internal iliac artery, an extraperitoneal approach with endarterectomy or bypass is not a difficult procedure, although endovascular interventions have been also used. This open approach uses a longitudinal incision along the edge of the rectus muscle, with reflection of the peritoneum medially (Fig. 12-4). In renal transplant patients, end-to-side renal artery anastomosis to the external iliac artery avoids division of an internal iliac artery. Fredberg and Mouritzen described sexual dysfunction resulting from conventional aortoiliac operations.48 In their series,

Tube graft

Aneurysm wall

C

Bifurcated graft

FIGURE 12–1 • Inlay nerve-sparing techniques for aneurysm repair. Note the incision on the right side of the aneurysm. (From DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW [ed]: Current Operative Surgery. Eastborne, East Sussex, England, Bailliere-Tindall, 1985, pp 781-788.)

55% of men (11 of 20) with aneurysms were preoperatively impotent, whereas 95% (19 of 20) were postoperatively impotent. Among those with occlusive disease, 31% (15 of 48) were preoperatively impotent, and 60% (29 of 48) were postoperatively impotent. Miles and colleagues found that about 22% of 76 patients receiving conventional aortoiliac operations reported preoperative sexual dysfunction; an additional 30% of those operated on for aneurysm or occlusive disease were rendered impotent.49 Impotence was twice as common in men reporting unspecified preoperative “minor dysfunction.” It seems unlikely that prospective trials comparing conventional aortic reconstructions with nerve-sparing, internal iliac revascularization techniques will surface, given that attention to the details of these procedures imposes little additional surgical burden or risk. Rich interconnections of the vegetative nervous system about the aortoiliac vessels and the inferior mesenteric artery include both sympathetic and parasympathetic fibers that promote normal ejaculatory function. Damage to these fibers also causes other types of sexual dysfunction: retrograde ejaculation with or without erection and orgasm, anejaculation, failure of emission, and, rarely, normal erection with failure to achieve either ejaculation or orgasm. Ejaculatory disorders are reportedly the most prevalent sexual dysfunction, occurring in nearly 40% of men.50 This condition is more likely to be encountered in urologic51 or fertility practices and has not

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A

B

FIGURE 12–2 • Techniques for aortoiliac or aortofemoral bypass: A and B, End-to-end aortic anastomosis with suprainguinal endto-side bypass in which the external iliac and common femoral arteries are spared. C and D, End-to-end aortic anastomosis with side-to-side reconstruction of the right internal iliac artery and two limbs on the left side. (From DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW [ed]: Current Operative Surgery. Eastborne, East Sussex, England, BailliereTindall, 1985, pp 781-788.)

C

been a prominent complaint in vascular practice. Ejaculatory disorders should be differentiated from ED, although the psychological consequences of ejaculatory disorders can interfere with erection. Women were once thought to be less susceptible to sexual dysfunction after aortoiliac surgery.52 In my experience, three women regained arousal, lubrication, and orgasm after aortoiliac surgery using nerve-sparing aortoiliac reconstructions that provided internal iliac flow. In this anecdotal experience, the operations were performed using the same technique as in men. The approach was chosen out of habit, with no intention of influencing sexual function; these women reported favorable effects later. Scanty data exist; few women in their sexually active years require aortoiliac reconstruction, and objective measurement of female arousal is difficult to perform. Hultgren and coworkers described sexual dysfunction, based on questionnaires, in women before and after aortoiliac operation.8 They stressed the possibility of iatrogenic nerve damage as a cause of postoperative sexual dysfunction. Several reports indicated that up to 25% of men regained erectile function after aortoiliac reconstructions using open repairs in patients of varying ages for obstructive disease or aneurysms.53-61 The prevalence and exact cause of preoperative

D

ED in various series are difficult to assess with accuracy. Erectile function depends on age; comorbid factors, including the use of drugs; and methods of subjective or objective documentation available to clinicians. Flanigan and coworkers stated that, with planning to avoid the diversion of pelvic blood flow, nerve-sparing aortoiliac dissections, and selective use of indirect methods, iatrogenic impotence can be minimized, and a significant proportion of patients can regain normal sexual function postoperatively.54 In their series of 110 patients using direct and indirect aortoiliac revascularization, 45% of patients with preoperative vasculogenic impotence regained normal sexual function postoperatively, no patients with normal preoperative sexual function were rendered impotent, and two men developed retrograde ejaculation. A series of men I operated on using techniques previously described were followed for at least 3 years (up to 1990) using direct interrogation and penile plethysmography. Of 126 men who underwent operation for aortoiliac disease, 4 became impotent as a result of emergency operations or the presence of internal iliac aneurysms. In all the instances of ED, penile plethysmography showed flat-line recordings, and PBIs were well below 0.5. Fifty-three men, average age 64.6 years, were impotent both preoperatively and postoperatively; 30 men,

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Inferior mesenteric artery

A

B

FIGURE 12–3 • Dissection of infrarenal aorta for endarterectomy. A, Aorta exposed without mobilization, and inferior mesenteric artery spared along with neural fibers. B, Internal iliacs controlled, and common or external iliacs clamped with minimal mobilization. (From DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW [ed]: Current Operative Surgery. Eastborne, East Sussex, England, Bailliere-Tindall, 1985, pp 781-788.)

average age 57 years (range, 39 to 71), were potent both preoperatively and postoperatively; 39 men, average age 58.0 years (range, 38 to 69), were impotent preoperatively and regained function postoperatively. Thus, among 126 men undergoing aortoiliac surgery, about 3% were rendered impotent, commonly in emergency settings. Overall, function was restored or maintained in 54% of men requiring aortoiliac surgery. The data from these series are necessarily retrospective and nonconcurrent. A recent randomized trial compared immediate elective repair to imaging surveillance of abdominal aortic aneurysms measuring 4.0 to 5.5 cm in men aged 50 to 79 years.62 Quality of life, impotence, and activity level were later assessed using the SF-36 health status instrument in men followed from 3.5 to 8 years (mean, 4.9 years). For most measures and times, there was no difference between the randomized groups, but overall, significantly more men became impotent after immediate repair than after surveillance (P < 0.03). There was a higher prevalence of impotence in the surgical group more than 1 year after randomization, paradoxically associated with an improved perception of health during the first 2 years. The data suggest that open intervention for small abdominal aortic aneurysms carries a finite risk of sexual dysfunction, and decreasing potency with age does not appear to be related to patient perception of health status. Possibly, the loss of erectile function was not considered important by some of these older men. Schiavi showed that age-related changes in frequency, duration, and degree of nocturnal penile tumescence correlated with desire, arousal, and coital frequency.63 Thus, the age of a patient preoperatively and normal postoperative aging contribute to diminished sexual function. This decrement in function with age does not appear to be linearly related to arterial inflow compromise.

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A retrospective questionnaire study of 90 men showed that sexual orgasmic and erectile function deteriorated after open aneurysm repair compared with endovascular repair.64 In my experience, the focus of endovascular interventions for ED has been directed toward the common or external iliac arteries.45 Others have described selective dilatation of the internal iliac arteries, with modest success.65,66 Procedures attempting endovascular intervention below this level—that is, in the pudendal arteries—have failed.67 Recently, Lin and associates reported severe pelvic ischemia and erectile dysfunction due to internal iliac embolization associated with endovascular repair.68 The severity of ischemia was related to both bilateral embolization and the presence of disease in the deep femoral arteries. Endovascular repair may require occlusion of the orifice of one or both internal iliac arteries to achieve safe and adequate landing sites. Bilateral internal iliac occlusion is associated with a finite risk of pelvic ischemia; adequate hypogastric flow, through at least one of these vessels, relates to normal sexual function. The risk of internal iliac occlusion is not absolute; femoral collaterals sometimes compensate for internal iliac occlusion, and femoral artery branches have been shown to provide significant collateral circulation to the penis in the face of hypogastric artery occlusion.69 Internal iliac collateral flow in the presence of acute hypogastric artery ligation is more dependent on the ipsilateral external iliac artery than it is on the contralateral internal iliac artery, even though abundant collateralization between the left and right internal iliac arteries is common in chronic ischemia.70,71 The variability of responses to internal iliac embolization before endovascular repair has been emphasized.72 Buttock or thigh claudication and late ischemic complications, seen in 3 of 10 patients after 6 months, led the investigators to suggest limiting bilateral internal iliac embolization before endovascular repair to only those patients considered unfit for open aortic repair. Clearly, more work is needed to make pelvic perfusion a regular facet of endovascular repair. Femorofemoral bypass combined with intraluminal dilatation of donor external or common iliac arteries is an excellent choice for certain candidates with occlusive disease (Fig. 12-5). The procedure completely avoids aortoiliac dissection, and patency remains quite durable. Objective information from pulse volume recordings before and after femorofemoral bypass correlates with improved patterns of penile plethysmography and pressures after reconstruction.73 Common iliac artery transluminal dilatation is both practical and useful. Transluminal dilatation of the external iliac arteries can also improve penile perfusion by relieving steal via the internal iliac and gluteal arteries. Although transluminal dilatation of the common iliac arteries is effective, the internal iliac arteries can be difficult to dilate. A report in the Italian literature describes three successful cases among 25 men treated with endovascular interventions for ED.66 Transluminal dilatation of the pudendal and penile arteries was plagued by restenosis.74

Microvascular Procedures Small vessel reconstructions initially used direct arterialization of the corpus cavernosum, but this approach was soon abandoned. These procedures induced priapism or thrombosis due to fibrosis at the anastomosis between the artery and the corpus cavernosum. Although interest in small vessel

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A

B

Knitted Dacron graft

C

Gruentzig dilating catheter

FIGURE 12–4 • Femorofemoral bypass with transluminal angioplasty. A, Initial lesion. B, Left iliac angioplasty. C, Femorofemoral bypass using dilated left iliac donor limb. (From DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW [ed]: Current Operative Surgery. Eastborne, East Sussex, England, Bailliere-Tindall, 1985, pp 781-788.)

Extraperitoneal incision, lateral border of rectus sheath

B A

Internal iliac artery

C

External iliac artery

FIGURE 12–5 • Isolated iliac artery endarterectomy. A, Incision for retroperitoneal exposure. B, Incision for isolated plaque of internal iliac artery. C, Linear incision when the external iliac artery is also involved. (From DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW [ed]: Current Operative Surgery. Eastborne, East Sussex, England, Bailliere-Tindall, 1985, pp 781-788.)

reconstruction persists,75 a 1996 meta-analysis by a urology guidelines panel stated that the chances of success with venous or arterial surgery did not justify its routine use.76 These procedures are applicable to men who fail to respond to medical therapy and who do not wish to have prostheses. With the availability of effective vasoactive drugs, these procedures are rarely performed. Two types of microvascular bypasses have been used: bypass into the dorsal artery, and arterialization of the deep dorsal vein. The inferior epigastric artery is a readily available inflow source, behaving much like the internal mammary artery. Some use a vein graft originating from the femoral artery. I recommend using the inferior epigastric artery and direct arterial reconstruction rather than deep dorsal vein arterialization.

Patient and Procedure Selection Candidates for microvascular correction of ED must be rigorously screened. They must have failed to respond to lifestyle alterations, maximal oral PDE-5 inhibitors, and other measures such as cavernosal or intraurethral injection therapy and vacuum erection devices. The options, risks, and benefits of prosthetic insertion should be explored with these patients. Candidates for microvascular surgery are young men with a history of trauma or localized disease.21,23 Some exhibit

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diffuse distal penile lesions of unknown origin. Candidates should be free of neural, hormonal, and medication-induced causes of impotence. All patients require selective pudendal arteriography. Communication between the dorsal penile artery and the cavernosal artery requires detailed visualization of individual penile vessels after intracavernous injection of a vasoactive agent to produce tumescence. As mentioned previously, a full erection masks inflow into the cavernosal artery and is not appropriate for evaluation of the penile microvasculature. The inferior epigastric artery, dissected in continuity, is turned down for microvascular anastomosis to the appropriate dorsal artery, anatomy permitting. DEEP DORSAL VEIN ARTERIALIZATION Candidates for deep dorsal vein arterialization are younger men with small vessel disease whose dorsal arteries are not suitable for direct bypass. The rationale of this operation was postulated to be reverse flow via emissary veins into the corpus cavernosum. However, my own arteriographic observations and those of others indicate that flow is largely by the

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circumflex veins into the spongiosum. Follow-up data at 12 to 84 months (average, 34.5 months) showed that 33% of these men attained spontaneous erections, 47% responded to intracavernous injections, and 21% remained impotent.21 A microvascular anastomosis is done between the inferior epigastric artery and the deep dorsal vein. Glans hyperperfusion is a serious, specific complication of venous arterialization. Venous hypertension, often preceded by urinary spraying due to edema, ultimately causes glans ulceration and necrosis. To minimize this complication, the anastomosis should be performed proximally under the arch of the pubis, and the dorsal vein is ligated proximally and distally, sparing the circumflex veins, which provide outflow. This complication, which can occur late, urgently requires further distal penile vein ligation or ligation of the inflow source. VENOUS INTERRUPTION Reported success rates for venous ligation vary considerably, and opinions about this procedure range from advocacy to qualified reservation to condemnation. This variability

Erectile dysfunction History, physical examination, baseline blood levels

Noninvasive neurovascular testing

Risk factor modification Oral drugs: sildenafil, apomorphine, yohimbine ICI with increasing doses of PGE and other agents Transurethral PGE and other agents VCD and other devices

Noneffective response

Effective response

Further testing

No further testing

Duplex Surgical treatment

DICC Arteriography

FIGURE 12–6 • Algorithm for erectile dysfunction. DICC, Dynamic Infusion Cavernosometry and Cavernosography; ICI, intracavernous injection; PGE, prostaglandin E1; VCD, vacuum erection constrictor device.

Arterial

Venous

Large vessel reconstruction

Interruption transcatheter occlusion

Dorsal artery bypass Dorsal vein arterialization

Prosthetic

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probably relates to patient selection and failure to evaluate all factors, including arterial supply or prior penile trauma that can cause venous leakage. At follow-up ranging from 12 to 100 months (average, 48 months), 33% of men functioned spontaneously, 44% used intracavernous injection, and the remainder were impotent.21,23 Venous ligation requires direct ligation and excision of the veins in cases selected by dynamic infusion cavernosography. I confine these procedures to excision of the dorsal vein and do not approach the crural veins directly.77 Other draining veins can be occluded using coils inserted by an invasive radiologist. At times, an introducing catheter inserted via the deep dorsal vein is useful. Yu and associates recommend routine dynamic cavernosography and cavernosometry at 3 months in all cases of venous ligation to rule out sham effect.78 At this time, embolization for recurrent leaks can be done; with these procedures, about 70% of men can regain erectile function and are able to function with supplemental intracavernous injection.

Medical Treatment Once aneurysms, large vessel disease, and uncontrolled diabetes have been ruled out, the branched logic sequence shown in Figure 12-6 can be used. Treatment begins with control of risk factors such as cigarette smoking, hyperlipidemia, and obesity. It is possible to minimize the necessity for antihypertensive treatment by weight control or exercise or to minimize the sexual effects of such treatment by changing drugs (e.g., to an angiotensin-converting enzyme inhibitor). Some men improve after one or two intracavernous injections have produced artificial erection, and they then resume spontaneous function. Specific medical therapy and risk factor modification are done synchronously with initial oral therapy using selected PDE-5 inhibitors widely available in oral form. With dosage titration, sildenafil was effective in 59% of individuals, compared with 20% in the placebo group.79 Administration of nitrates, antihypertensive agents, or alpha blockers is a specific contraindication to PDE-5 therapy. Other oral agents include apomorphine, recently formulated for sublingual administration; approval of phentolamine mesylate for ED has been delayed because of toxicologic concerns.80 Men with ED who fail oral agents can progress to intraurethral or cavernosal injections. Vacuum devices can also be prescribed.

Conclusion Vascular surgeons must recognize the basic requirements for open and endovascular aortoiliac interventions that prevent or relieve ED associated with large vessel disease. They need to collaborate with urologists and other experts in treating men with primary ED. After screening and medical treatment, few individuals are candidates for vascular surgical intervention for the sole purpose of treating a sexual disability. Those with macrovascular disease, occult aneurysms, and poorly controlled diabetes, however, need attention. Treating men and, more rarely, women with sexual disabilities requires a unique sensitivity to individual needs. Outcomes of medical treatment and surgical interventions continue to improve in concert with more accurate diagnosis, advances in technique, and meticulous patient selection.

KEY REFERENCES DePalma RG, Levine SB, Feldman S: Preservation of erectile function after aortoiliac reconstruction. Arch Surg 113:958, 1978. DeTejada IS, Goldstein I, Azadzoi K, et al: Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med 32:1025, 1989. Flanigan DP, Schuler JJ, Keifer T, et al: Elimination of iatrogenic impotence and improvement of sexual dysfunction after aortoiliac revascularization. Arch Surg 117:544, 1982. Goldstein I, Lue TF, Padma-Nathan H, et al: Oral sildenafil in the treatment of erectile dysfunction. N Engl J Med 338:1397, 1998. Harris JD, Jepson RP: Aorto-iliac stenosis: A comparison of two procedures. Aust J Surg 34:211, 1965. Leriche R, Morel A: The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg 127:193, 1948. Merchant RF Jr, DePalma RG: Effects of femorofemoral grafts on postoperative sexual function: Correlation with penile pulse volume recordings. Surgery 90:962, 1981. Rajfer J, Aronson WJ, Bush PA, et al: Nitric oxide as a mediator of the corpus cavernosum in response to nonadrenergic noncholinergic neurotransmission. N Engl J Med 326:90, 1992.

REFERENCES 1. Process of Care Consensus Panel, position paper: The process of care model for evaluation and treatment of erectile dysfunction. Int J Impot Res 11:59, 1999. 2. DePalma RG: New developments in the diagnosis and treatment of impotence. West J Med 164:54, 1996. 3. DePalma RG: The best treatment for impotence. Vasc Surg 32:519, 1998. 4. May AG, DeWeese JA, Rob CG: Changes in sexual function following operations on the abdominal aorta Surgery 65:41, 1969. 5. DePalma RG, Levine SB, Feldman S: Preservation of erectile function after aortoiliac reconstruction. Arch Surg 113:958, 1978. 6. DePalma RG, Kedia K, Persky L: Surgical options in the correction of vasculogenic impotence. Vasc Surg 14:92, 1980. 7. Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001. 8. Hultgren R, Sjogren B, Soderberg M, et al: Sexual function in women suffering from aortoiliac occlusive disease. Eur J Vasc Endovasc Surg 17:306, 1999. 9. Saini J, Kuczynski E, Gretz HF 3rd, Sills ES: Supracervical hysterectomy versus total abdominal hysterectomy: perceived effects on sexual function. BMC Women’s Health 2:1, 2002. 10. Graesslin O, Martin-Morille C, Leguillier-Armour MC, et al: Local investigation concerning psychic and sexual functioning a short time after hysterectomy. Gynecol Obstet Fertil 6:474, 2002. 11. Trimbos JB, Maas CP, Deruiter MC, et al: A nerve sparing radical hysterectomy: Guidelines and feasibility in Western patients. Int J Gynecol Cancer 11:180, 2001. 12. Andersson KE, Wagner G: Physiology of penile erection. Physiol Rev 75:191, 1995. 13. DePalma RG: Anatomy and physiology of normal erections: Pathogenesis of impotence. In Sidawy AN, Sumpio BE, DePalma RG (eds): Basic Science of Vascular Disease. Armonk, NY, Futura, 1996, pp 761-773. 14. DeTejada IS, Goldstein I, Azadzoi K, et al: Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med 32:1025, 1989. 15. Rajfer J, Aronson WJ, Bush PA, et al: Nitric oxide as a mediator of the corpus cavernosum in response to nonadrenergic noncholinergic neurotransmission. N Engl J Med 326:90, 1992. 16. Azadzoi KM, Nehra A, Siroky MB: Effects of cavernosal hypoxia and oxygenation on penile erection [abstract]. Int J Impot Res 6(Suppl I): A26, 1994. 17. Brock GB, Zvara P, Sioufi R, et al: Nitric oxide synthase is testosterone dependent [abstract]. Int J Impot Res 6(Suppl I):D42, 1994. 18. Burnett AL: Role of nitric oxide in the physiology of erection. Biol Report 52:485, 1995. 19. Beavo JA: Cyclic nucleotide phosphodiesterases: Functional implication of multiple isoforms. Physiol Rev 75:725, 1995. 20. Gingell C, Ballard SA, Tang K, et al: Cyclic nucleotide phosphodiestrase and erectile function. Int J Impot Res 9(Suppl I):510, 1997.

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21. DePalma RG, Olding M, Yu GW, et al: Vascular interventions for impotence: Lessons learned. J Vasc Surg 21:576, 1995. 22. DePalma RG, Emsellem HA, Edwards CM, et al: A screening sequence for vasculogenic impotence. J Vasc Surg 5:228, 1987. 23. DePalma RG: Vascular surgery for impotence: A review. Int J Impot Res 9:61, 1997. 24. Leriche R, Morel A: The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg 127:193, 1948. 25. Leriche R: Des oblitérations artériele hautes (oblitération de la términation de l’aorte) comme cause de insufficances circulatoires des membres inférieurs [abstract]. Bull Mem Soc Chir 49:1404, 1923. 26. Fabra M, Porst H: Bulbocavernosus-reflex latencies and pudendal nerve SSEP compared to penile vascular testing in 669 patients with erectile failure and other sexual dysfunction. Int J Impot Res 11:167, 1999. 27. Emsellem HA, Bergsrud DW, DePalma RG, et al: Pudendal evoked potentials in the evaluation of impotence [abstract]. J Clin Neurophysiol 359:5, 1988. 28. Stackl W, Hasun R, Marberger M: Intracavernous injection of prostaglandin E1 in impotent men. J Urol 140:66, 1988. 29. Guay AT: Sexual dysfunction in the diabetic patient. Int J Impot Res 13(Suppl 5):S47, 2001. 30. Enzlin P, Mathieu C, Van den Bruel A, et al: Sexual dysfuntion in women with type 1 diabetes: A controlled study. Diabetes Care 25:672, 2002. 31. DeBusk R, Drory Y, Goldstein I, et al: Management of sexual dysfunction in patients with cardiovascular disease: Recommendations of the Princeton Consensus Panel. Am J Cardiol 86:62F, 2000. 32. Meston CM, Worcel M: The effects of yohimbine plus L-arginine glutamate on sexual arousal in postmenopausal women with sexual arousal disorder. Arch Sex Behav 31:323, 2002. 33. Berman JR, Berman LA, Lin H, Goldstein I: Female sexual dysfunction: Epidemiology, physiology and treatment. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 123-140. 34. Caruso S, Intelisano G, Lupo L, Agnello C: Premenopausal women affected by sexual disorder treated with sildenafil: A double blind, crossover, placebo-controlled study. BJOG 108:623, 2001. 35. Laan E, van Lunsen RH, Everaerd W, et al: The enhancement of vaginal vasocongestion by sildenafil in healthy premenstrual women. J Womens Health Gend Based Med 11:357, 2002. 36. Islam A, Mitchell J, Rosen R, et al: Topical alprostadil in the treatment of female sexual arousal disorder: A pilot study. J Sex Marital Ther 27:531, 2001. 37. Lue TF: Impotence: A patient’s goal-directed approach to treatment. World J Urol 8:67, 1990. 38. DePalma RG: What constitutes an adequate impotence workup? World J Urol 10:157, 1992. 39. DePalma RG, Michal V: Point of view: Déjà vu-again: Advantages and limitations of methods for assessing penile arterial flow. Urology 36:199, 1990. 40. DePalma RG, Dalton CM, Gomez CA, et al: Predictive value of a screening sequence for venogenic impotence. Int J Impot Res 4:143, 1992. 41. Sanchez-Ortiz RF, Broderick GA: Vascular evaluation of erectile dysfunction. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 167-202. 42. Levine LA, Elterman L: Nocturnal penile tumescence and rigidity testing. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 151-166. 43. DePalma RG: New developments in the diagnosis and treatment of impotence. West J Med 164:54, 1996. 44. Reis JM, Alves CR, Garro MA, et al: Endovascular surgery for erectile dysfunction. Int J Impot Res 10(Suppl 3):398, 1998. 45. DePalma RG: Iliac artery occlusive disease: Impotence and colon ischemia. In Moore WS, Ahn SS (eds): Endovascular Surgery. Philadelphia, WB Saunders, 2001, pp 335-360. 46. DePalma RG, Edwards CM, Schwab FJ, Steinberg DL: Modern management of impotence associated with aortic surgery. In Bergen JJ, Yao JST (eds): Arterial Surgery: New Diagnostic and Operative Techniques. Orlando, Fla, Grune & Stratton, 1988, pp 337-348. 47. DePalma RG: Prevention of sexual dysfunction in aortoiliac surgery. In Jamieson CW (ed): Current Operative Surgery: Vascular Surgery. London, Bailliere-Tindall, 1988, pp 80-84. 48. Fredberg U, Mouritzen C: Sexual dysfunction as a symptom of arteriosclerosis and as a complication to reconstruction of the aortoiliac segment. J Cardiovasc Surg 29:149, 1988.

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49. Miles JR, Miles DG, Johnson G Jr: Aortoiliac operations and sexual dysfunction. Arch Surg 117:1177, 1982. 50. Laumann EO, Paik A, Rosen RC: The epidemiology of erectile dysfunction: Results from the National Health and Social Life Survey. Int J Impot Res 11:S60, 1999. 51. McCullough AR Jr: Ejaculatory disorders. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 351-370. 52. Queral LA, Flinn WR, Bergan JJ, et al: Pelvic hemodynamics after aortoiliac reconstruction. Surgery 86:799, 1979. 53. DePalma RG, Levine SB, Feldman S: Preservation of erectile function after aortoiliac reconstruction. Arch Surg 113:958, 1978. 54. Flanigan DP, Schuler JJ, Keifer T, et al: Elimination of iatrogenic impotence and improvement of sexual dysfunction after aortoiliac revascularization. Arch Surg 117:544, 1982. 55. Hallbrook T, Holmquist B: Sexual disturbances following dissection of the aorta and the common iliac arteries. J Cardiovasc Surg 11:255, 1970. 56. Harris JD, Jepson RP: Aorto-iliac stenosis: A comparison of two procedures. Aust J Surg 34:211, 1965. 57. Castaneda-Zuniga WR, Smith A, Kaye K, et al: Transluminal angioplasty for treatment of vasculogenic impotence. AJR Am J Roentgenol 139:371, 1982. 58. Sabri S, Cotton LT: Sexual function following aortoiliac reconstruction. Lancet 2:1218, 1971. 59. Spiro M, Cotton LT: Aorto-iliac thrombo-endarterectomy. Br J Surg 57:161, 1979. 60. Weinstein MH, Machleder HI: Sexual function after aortoiliac surgery. Ann Surg 181:787, 1975. 61. DePalma RG: Impotence as a complication in aortoiliac reconstruction. In Bernhard VM, Towne JB (eds): Complications in Vascular Surgery. New York, Grune & Stratton, 1980, pp 427-442. 62. Lederle FA, Johnson GR, Wilson SE, et al: Quality of life, impotence, and activity level in a randomized trial of immediate repair versus surveillance of small abdominal aortic aneurysm. J Vasc Surg 38:745, 2003. 63. Schiavi RC, Schreiner-Engel P, Mandeli J, et al: Healthy aging and male sexual function. Am J Psychiatry 147:766, 1990. 64. Xenos ES, Stevens SL, Freeman MB, et al: Erectile function after open or endovascular abdominal aortic aneurysm repair. Ann Vasc Surg 17:530, 2003. 65. Lee CW, Kaufman JA, Fan CM, et al: Clinical outcome of internal iliac occlusions during endovascular treatment of aortoiliac aneurysmal disease. J Vasc Interv Radiol 11:567, 2000. 66. Urigo F, Pischedda A, Maiore M, et al: The role of arteriography and percutaneous transluminal angioplasty in the treatment of arteriogenic impotence [Italian]. Radiol Med (Torino) 88:80, 1994. 67. Valji K, Bookstein JJ: Transluminal angioplasty in the treatment of arteriogenic impotence. Cardiovasc Intervent Radiol 11:245, 1988. 68. Lin PH, Bush RL, Chen C, et al: A prospective evaluation of hypogastric artery embolization in endovascular aortoiliac aneurysm repair. J Vasc Surg 36:500, 2002. 69. Kawai M: Pelvic hemodynamics before and after aortoiliac vascular reconstruction: The significance of penile blood pressure. Jpn J Surg 18:514, 1988. 70. Iliopoulos JI, Horwanitz PE, Pierce GE, et al: The critical hypogastric circulation. Am J Surg 154:671, 1987. 71. Iliopoulos JI, Hermreck AS, Thomas JH, et al: Hemodynamics of the hypogastric arterial circulation. J Vasc Surg 9:637, 1989. 72. Engelke C, Elford J, Morgan RA, Belli AM: Internal iliac artery embolization with bilateral occlusion before endovascular aortoiliac aneurysm repair: Clinical outcome of simultaneous and sequential intervention. J Vasc Interv Radiol 13:667, 2002. 73. Merchant RF Jr, DePalma RG: Effects of femorofemoral grafts on postoperative sexual function: Correlation with penile pulse volume recordings. Surgery 90:962, 1981. 74. Bookstein JJ, Valji K: The arteriolar component in impotence: A possible paradigm shift. AJR Am J Roentgenol 157:932, 1991. 75. Jarrow JP: Vascular surgery for erectile dysfunction. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 293-306. 76. Montague DK, Barada JH, Belker AM, et al: Clinical Guidelines Panel on Erectile Dysfunction: Summary report on the treatment of organic erectile dysfunction. American Urological Association. J Urol 156:2007, 1996.

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77. DePalma RG, Schwab F, Druy EM, et al: Experience in diagnosis and treatment of impotence caused by cavernosal leak syndrome. J Vasc Surg 10:117, 1989. 78. Yu GW, Schwab FJ, Melograna FS, et al: Preoperative and postoperative dynamic cavernosography and cavernosometry: Objective assessment of venous ligation for impotence. J Urol 147:618, 1992. 79. Goldstein I, Lue TF, Padma-Nathan H, et al: Oral sildenafil in the treatment of erectile dysfunction. N Engl J Med 338:1397, 1998. 80. Padma-Nathan H, Guiliano F: Oral pharmocotherapy. In Mulcahy JJ (ed): Male Sexual Function: A Guide to Clinical Management. Totowa, NJ, Humana Press, 2001, pp 203-224.

Questions 1. Which of the following occurs during full penile erection? (a) Deep cavernosal artery flow increases (b) Venous valves close (c) Cavernosal oxygen tension falls (d) Cavernosal smooth muscle relaxes (e) Arterial pressure in the dorsal arteries falls 2. Men with erectile dysfunction most often exhibit which of the following? (a) Decreased dorsal arterial flow (b) Failure to respond to PDE-5 inhibition (c) Occult aneurysms (d) Neurologic abnormalities (e) Normal physical examination 3. Which of the following statements about endovascular aortoiliac procedures is true? (a) They require bilateral internal iliac artery occlusion (b) They may result in buttock ischemia (c) They may result in more ED postoperatively (d) They spare periaortic nerves (e) They may increase the bulbocavernosus reflex time 4. When does the penile brachial index (PBI) indicate aortoiliac occlusive disease? (a) PBI between 0.6 and 0.75 (b) PBI 0.6 or less (c) PBI 0.8 or less (d) PBI 0.8, accompanied by flat pulse volume waves (e) PBI 0.75, accompanied by abnormally shaped pulse waves 5. Women with female sexual dysfunction may have which of the following? (a) Failure to lubricate (b) Dyspareunia (c) Aortoiliac occlusive disease (d) Arousal failure (e) All of the above

6. When a sexually active man expresses concern about possible erectile dysfunction before aneurysm repair, what should the physician do? (a) Reassure the patient and spouse that this is preventable (b) Refer the patient to a psychiatrist (c) Measure baseline levels of testosterone and prolactin (d) Obtain preoperative penile brachial index and pulse volume recordings (e) Perform preoperative selective pudendal arteriography 7. Useful techniques in preventing sexual dysfunction after aortic surgery include which of the following? (a) Restoration of flow to internal iliac arteries (b) Suture of inferior mesenteric artery within the aortic sac (c) Avoidance of the aortic bifurcation (d) Retrograde flushing of internal iliacs (e) All of the above 8. Age most likely affects potency by what means? (a) Decreasing arterial inflow (b) Causing nerve deterioration (c) Causing smooth muscle dysfunction (d) Causing progressive venous fibrosis (e) Decreasing cardiovascular function 9. Artificial erection is most safely obtained by which of the following? (a) Intracavernous papaverine injection (b) Intracavernous prostaglandin E1 injection (c) Intracavernous phentolamine injection (d) Roller pump cavernosal infusion of 40 mL normal saline per minute (e) All of the above 10. Screening and medical treatment for erectile dysfunction most often require which of the following? (a) PDE-5 inhibitors (b) Cavernosometry (c) Arteriography (d) Psychotherapy (e) Psychological counseling along with medical therapy

Answers 1. d 6. d

2. e 7. e

3. d 8. c

4. b 9. b

5. e 10. a

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13

R. Eugene Zierler • D. Eugene Strandness, Jr.*

Hemodynamics for the Vascular Surgeon Blood flow in human arteries and veins can be described in terms of strict hemodynamic principles. Although the elements of hemodynamics are derived from engineering, mathematics, and physiology, these principles also form the theoretical foundation for the surgical treatment of vascular disease. The major mechanisms of arterial disease are obstruction of the lumen and disruption of the vessel wall. Arterial obstruction or narrowing may result from atherosclerosis, emboli, thrombi, fibromuscular dysplasia, trauma, or external compression. The clinical significance of an obstructive lesion depends on its location, severity, and duration, as well as on the ability of the circulation to compensate by increasing cardiac output and developing collateral pathways. Surgical treatment requires the identification and correction of arterial lesions associated with significant hemodynamic disturbances. Disruption of the arterial wall is caused by ruptured aneurysm or trauma. The tendency of aneurysms to rupture is determined by arterial wall characteristics, intraluminal pressure, and size. In this situation, the role of surgery is to prevent rupture or to reestablish arterial continuity after rupture occurs. On the venous side of the circulation, the major hemodynamic mechanisms of disease are obstruction and valvular incompetence. These are generally the sequelae of thrombosis in the deep venous system, and they produce venous hypertension in the circulation distal to the involved venous segment. The clinical consequences of venous hypertension are the signs and symptoms of the post-thrombotic syndrome: pain, edema, subcutaneous fibrosis, pigmentation, stasis dermatitis, and ulceration. Treatment of this condition involves elevation, external compression, venous interruption, and, rarely, direct venous reconstruction. This chapter begins with a discussion of the hemodynamic principles and wall properties that govern arterial flow. The hemodynamic alterations produced by arterial stenoses and their effect on flow patterns in human limbs are considered next. These principles are then related to the treatment of arterial obstruction. Finally, the hemodynamics of the venous system are briefly reviewed and related to the pathophysiology and treatment of venous disease. *Deceased

Basic Principles of Arterial Hemodynamics FLUID PRESSURE The pressure in a fluid system is defined as force per unit area (given in dynes per square centimeter). Intravascular arterial pressure (P) has three components: (1) the dynamic pressure produced by contraction of the heart, (2) the hydrostatic pressure, and (3) the static filling pressure. Hydrostatic pressure is determined by the specific gravity of blood and the height of the point of measurement above a specific reference level. The reference level in the human body is considered to be the right atrium. The hydrostatic pressure is given by the following equation: P (hydrostatic) = –ρgh

[1]

where ρ is the specific gravity of blood (approximately 1.056 g/cm3), g is the acceleration due to gravity (980 cm/sec2), and h is the distance in centimeters above or below the right atrium. The magnitude of hydrostatic pressure may be quite large. In a man 5 feet 8 inches tall, this pressure at ankle level is approximately 89 mm Hg.1 The static filling pressure represents the residual pressure that exists in the absence of arterial flow. This pressure is determined by the volume of blood and the elastic properties of the vessel wall, and it is usually in the range of 5 to 10 mm Hg. FLUID ENERGY Blood flows through the arterial system in response to differences in total fluid energy. Although pressure gradients are the most obvious forces involved, other forms of energy drive the circulation.2 Total fluid energy (E) can be divided into potential energy (Ep ) and kinetic energy (Ek ). The components of potential energy are intravascular pressure (P) and gravitational potential energy. The factors contributing to intravascular pressure have already been discussed. Gravitational potential energy represents the ability of a volume of blood to do work because of 225

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its height above a specific reference level. The formula for gravitational potential energy is the same as that for hydrostatic pressure (see Equation 1) but with an opposite sign: +ρgh. Because the gravitational potential energy and hydrostatic pressure usually cancel each other out and the static filling pressure is relatively low, the predominant component of potential energy is the dynamic pressure produced by cardiac contraction. Potential energy can be expressed as follows: Ep = P + (ρgh)

[4]

FLUID ENERGY LOSSES Bernoulli’s Principle When fluid flows from one point to another, its total energy (E) along any given streamline is constant, provided that flow is steady and there are no frictional energy losses. This is in accordance with the law of conservation of energy and constitutes Bernoulli’s principle: P1 + ρgh1 + 1/2 ρν12 = P2 + ρgh2 + 1/2 ρν22

[5]

This equation expresses the relationship among pressure, gravitational potential energy, and kinetic energy in an idealized fluid system. In the horizontal diverging tube shown in Figure 13-1, steady flow between point 1 and point 2 is accompanied by an increase in cross-sectional area and a decrease in flow velocity. Although the fluid moves against a pressure gradient of 2.5 mm Hg and therefore gains potential energy, the total fluid energy remains constant because of the lower velocity and a proportional loss of kinetic energy. In other words, the widening of the tube results in the conversion of kinetic energy to potential energy in the form of pressure. In a converging tube, the opposite would occur; a pressure drop and increase in velocity would result in potential energy being converted to kinetic energy. The situation depicted in the preceding example is not observed in human arteries because the ideal flow conditions specified in the Bernoulli relationship are not present. The fluid energy lost in moving blood through the arterial circulation is dissipated mainly in the form of heat. When this source of energy loss is accounted for, Equation 5 becomes the following: P1 + ρgh1 + 1/2 ρν12 = P2 + ρgh2 + 1/2 ρν22 + heat

V1⫽80 cm/sec

V2⫽5 cm/sec

P1⫽100 mm Hg

P2⫽102.5 mm Hg

1

2

[3]

By combining Equations 2 and 3, an expression for the total fluid energy per unit volume of blood (in ergs per cubic centimeter) can be obtained: E = P + ρgh + 1/2 ρν2

A2⫽16 cm2

[2]

Kinetic energy represents the ability of blood to do work on the basis of its motion. It is proportional to the specific gravity of blood and the square of blood velocity (ν), in centimeters per second: Ek = 1/2 ρν2

A1⫽1 cm2

[6]

Viscous Energy Losses and Poiseuille’s Law Energy losses in flowing blood occur either as viscous losses resulting from friction or as inertial losses related to changes in the velocity or direction of flow. The term viscosity describes

FIGURE 13–1 • Effect of increasing cross-sectional area on pressure in a frictionless fluid system. While pressure increases, total fluid energy remains constant as a result of a decrease in velocity. (Redrawn from Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

the resistance to flow that arises because of the intermolecular attractions between fluid layers. The coefficient of viscosity (η) is defined as the ratio of shear stress (τ) to shear rate (D): τ [7] η= D Shear stress is proportional to the energy loss due to friction between adjacent fluid layers, whereas shear rate refers to the relative velocity of adjacent fluid layers. Fluids with particularly strong intermolecular attractions offer a high resistance to flow and have high coefficients of viscosity. For example, motor oil has a higher coefficient of viscosity than water.3 The unit of viscosity is the poise, which equals 1 dyne-sec/cm2. Because it is difficult to measure viscosity directly, relative viscosity is often used to relate the viscosity of a fluid to that of water. The relative viscosity of plasma is approximately 1.8, whereas for whole blood, the relative viscosity is in the range of 3 to 4. Because viscosity increases exponentially with increases in hematocrit, the concentration of red blood cells is the most important factor affecting the viscosity of whole blood. The viscosity of plasma is determined largely by the concentration of plasma proteins. These constituents of blood are also responsible for its non-Newtonian character. In a Newtonian fluid, viscosity is independent of shear rate or flow velocity. Because blood is a suspension of cells and large protein molecules, its viscosity can vary greatly with shear rate (Fig. 13-2). Blood viscosity increases rapidly at low shear rates but approaches a constant value at higher shear rates. In most of the arterial circulation, the prevailing shear rates place the blood viscosity on the asymptotic portion of the curve. Thus, for arteries with diameters greater than about 1 mm, human blood resembles a constant-viscosity, or Newtonian, fluid. Poiseuille’s law describes the viscous energy losses that occur in an idealized flow model. This law states that the pressure gradient along a tube (P1 – P2, in dynes per square centimeter) is directly proportional to the mean flow velocity

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Pressure drop (dynes⭈cm⫺2⫻103)

0.6 0

0.5

1.0

1.5

500

8.0 ␩⫽0.025 poise L⫽9.45 cm ri⫽0.28 cm

Flow (cm3/min)

Apparent viscosity (poise)

400

0.4

0.3

P⫽103.5Q 6.0

300 4.0

P⫽143.5Q⫹11.0Q2 200

Flow (cm3/sec)

0.5

2.0

100

0.2 0

0 0

0.1

1.0

10

100

1000

Shear rate (sec⫺1) FIGURE 13–2 • Viscosity of human blood as a function of shear rate. Values range between the two lines. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

– – (V, in centimeters per second) or volume flow (Q, in cubic centimeters per second), the tube length (L, in centimeters), and the fluid viscosity (η, in poises), and is inversely proportional to either the second or fourth power of the radius (r, in centimeters): P1 − P2 = V

8Lη r

2

=Q

8 Lη πr 4

1.2

1.4

diameter, and changes in the direction of flow at points of curvature and branching. The combined effects of viscous and inertial energy losses are illustrated in Figure 13-3. When the pressure drop across an arterial segment is measured at varying flow rates, the experimental data fit a line with both linear (viscous) and squared (inertial) terms. The viscous energy losses predicted by Poiseuille’s law are considerably less than the total energy loss actually observed.

[8] Vascular Resistance

When this equation is simplified to pressure = flow × resistance, it is analogous to Ohm’s law of electrical circuits. The strict application of Poiseuille’s law requires the steady, laminar flow of a Newtonian fluid in a straight, rigid, cylindrical tube. Because these conditions seldom exist in the arterial circulation, Poiseuille’s law can only estimate the minimum pressure gradient or viscous energy losses that may be expected in arterial flow. Energy losses due to inertial effects often exceed viscous energy losses, particularly in the presence of arterial disease. Inertial Energy Losses Energy losses related to inertia (∆E) are proportional to a constant (K), the specific gravity of blood, and the square of blood velocity: ∆E = K1/2 ρν2

0.4 0.6 0.8 1.0 Pressure drop (mm Hg)

FIGURE 13–3 • Pressure drop across a 9.45-cm length of canine femoral artery at varying flow rates. The experimental data line (solid) has both linear and squared terms, corresponding to viscous and inertial energy losses. The pressure-flow curve predicted by Poiseuille’s law (dashed line) depicts much lower energy losses than those actually observed. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

0 0.1

0.2

[9]

Because velocity is the only independent variable in this equation, inertial energy losses result from the acceleration and deceleration of pulsatile flow, variations in lumen

Hemodynamic resistance (R) can be defined as the ratio of the energy drop between two points along an artery (E1 – E 2) to the mean blood flow (Q): R=

E1 − E 2 P1 − P2 ≅ Q Q

[10]

If the kinetic energy term (1/2 ρν2) is considered to be a small component of the total energy, and the artery is assumed to be horizontal so that the gravitational potential energy terms (ρgh) cancel, Equation 4 can be used to express resistance as the simple ratio of pressure drop (P1 – P2) to flow. Thus, Equation 10 becomes a rearranged version of Poiseuille’s law (Equation 8), and the minimum resistance or viscous energy losses are given by the resistance term: R=

8 Lη πr 4

[11]

The hemodynamic resistance of an arterial segment increases as the flow velocity increases, provided that the lumen size

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0

Flow (cm3⭈sec⫺1) 4.0 6.0

2.0

8.0

Resistance (PRU⫻10⫺3)

R⫽143.5⫹11.0 Q 200 2.0

150 100 R⫽103.5

1.0

50 0 0

100

200 300 Flow (cm3⭈min⫺1)

Resistance (dyne⭈sec⭈cm⫺5)

250

3.0

0 500

400

FIGURE 13– 4 • Resistance derived from the pressure-flow curve in Figure 13-3. The resistance increases with increasing flow. Constant resistance predicted by Poiseuille’s law is shown by the dotted line. PRU, peripheral resistance unit. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

remains constant (Fig. 13-4). These additional energy losses are related to inertial effects and are proportional to 1/2P + ρν2. According to Equation 11, the predominant factor influencing hemodynamic resistance is the fourth power of the radius. The relationship between radius and pressure drop for various flow rates along a 10-cm vessel segment is shown in Figure 13-5. For a wide range of flow rates, the pressure drop

is negligible until the radius is reduced to about 0.3 cm; for radii less than 0.2 cm, the pressure drop increases rapidly. These observations may explain the frequent failure of femoropopliteal autogenous vein bypass grafts less than 4 mm in diameter.4 The calculation of total resistance (Rt) depends on whether the component resistances (R1 … Rn) are arranged in series or in parallel. This is also analogous to electrical circuits. Rt (series) = R1 + R2 + … Rn

[12]

1 1 1 1 = + + .... + R t (parallel) R1 R 2 Rn

[13]

The standard physical units of hemodynamic resistance are dyne-seconds per centimeter to the fifth power. A more convenient way of expressing resistance is the peripheral resistance unit (PRU), which has the dimensions of millimeters of mercury per cubic centimeter per minute. One PRU is approximately 8 × 104 dyne-sec/cm5. In the human circulation, approximately 90% of the total vascular resistance results from flow through the arteries and capillaries, whereas the remaining 10% results from venous flow. The arterioles and capillaries are responsible for more than 60% of the total resistance, whereas the large and medium-size arteries account for only about 15%.2 Thus, the arteries that are most commonly affected by atherosclerotic occlusive disease are normally vessels with very low resistance. BLOOD FLOW PATTERNS

Flow (cm3/sec)

In the steady-state conditions specified by Poiseuille’s law, the flow pattern is laminar. All motion is parallel to the walls of the tube, and the fluid is arranged in a series of concentric layers, or laminae, like those shown in Figure 13-6. While the velocity within each lamina remains constant, the velocity is lowest adjacent to the tube wall and increases toward the center of the tube. This results in a velocity profile that is parabolic in shape (Fig. 13-7). As previously discussed, the

40 50

8Lη

∆P=Q

100

Laminar Flow

10 15 20 1 30

πr1

4

1=10 cm

90

η=0.035 poise

80 ∆P (mm Hg)

70 60 50 40 30 20 10 0 0.5

0.4

0.3 0.2 Inside radius (cm)

0.1

0.0

FIGURE 13–5 • Relationship of pressure drop to inside radius of a cylindrical tube 10 cm in length at various rates of steady laminar flow. Flow rates are comparable to those in the human iliac artery. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

FIGURE 13–6 • Concentric laminae of fluid in a cylindrical tube. Flow is from left to right. The center laminae move more rapidly than those near the periphery, and the flow profile is parabolic. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

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Tube wall Parabolic profile Laminar flow

229

random velocity changes, energy losses are greater for a turbulent or disturbed flow state than for a laminar flow state. Consequently, the linear relationship between pressure and flow expressed by Poiseuille’s law cannot be applied. This deviation from Poiseuille’s law in arterial flow is shown in Figure 13-3.

Tube center

Boundary Layer Separation

Blunt profile Turbulent flow Tube wall Velocity FIGURE 13–7 • Velocity profiles of steady laminar and turbulent flow. Velocity is lowest adjacent to the tube wall and maximal in the center. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

energy expended in moving one lamina of fluid over another is proportional to viscosity. Turbulent Flow In contrast to the linear streamlines of laminar flow, turbulence is an irregular flow state in which velocity varies rapidly with respect to space and time. These random velocity changes result in the dissipation of fluid energy as heat. The point of transition between laminar and turbulent flow depends on the tube diameter (d, in centimeters), the mean velocity, the specific gravity of the fluid, and the fluid viscosity. These factors can be expressed as a dimensionless quantity called the Reynolds number (Re), which is the ratio of inertial forces to viscous forces acting on the fluid: Re =

dVρ η

In fluid flowing through a tube, the portion of fluid adjacent to the tube wall is referred to as the boundary layer. This layer is subject to both frictional interactions with the tube wall and viscous forces generated by the more rapidly moving fluid toward the center of the tube. When the tube geometry changes suddenly, such as at points of curvature, branching, or alteration in lumen diameter, small pressure gradients are created that cause the boundary layer to stop or reverse direction. This results in a complex, localized flow pattern known as an area of flow separation or separation zone.6 Areas of boundary layer separation have been observed in models of arterial anastomoses and bifurcations.7,8 In the carotid artery bifurcation shown in Figure 13-8, the central rapid flow stream of the common carotid artery is compressed along the inner wall of the carotid bulb, producing a region of high shear stress. An area of flow separation has formed along the outer wall of the carotid bulb that includes helical flow patterns and flow reversal. The region of the carotid bulb adjacent to the separation zone is subject to relatively low shear stresses. Distal to the bulb, in the internal carotid artery, flow reattachment occurs, and a more laminar flow pattern is present.

High shear region

[14]

In flowing blood at Reynolds numbers greater than 2000, inertial forces may disrupt laminar flow and produce fully developed turbulence. With values less than 2000, localized flow disturbances are damped out by viscous forces. In the normal arterial circulation, Reynolds numbers are usually less than 2000, and true turbulence is unlikely to occur; however, Reynolds numbers greater than 2000 can be found in the ascending aorta, where small areas of turbulence develop.3 Although turbulent flow is uncommon in normal arteries, the arterial flow pattern is often disturbed.5 The condition of disturbed flow is an intermediate state between stable laminar flow and fully developed turbulence. It is a transient perturbation in the laminar streamlines that disappears as the flow proceeds downstream. Arterial flow may become disturbed at points of branching and curvature. When turbulence is the result of a stenotic arterial lesion, it generally occurs immediately downstream from the stenosis and may be present only over the systolic portion of the cardiac cycle when the critical value of the Reynolds number is exceeded. Under conditions of turbulent flow, the velocity profile changes from the parabolic shape of laminar flow to a rectangular or blunt shape (see Fig. 13-7). Because of the

Low shear region Cross section of carotid sinus

FIGURE 13–8 • Carotid artery bifurcation showing an area of flow separation adjacent to the outer wall of the bulb. Rapid flow is associated with high shear stress, whereas the slower flow of the separation zone produces a region of low shear. (From Zarins CK, Giddens DP, Glagov S: Atherosclerotic plaque distribution and flow velocity profiles in the carotid bifurcation. In Bergan JJ, Yao JST [eds]: Cerebrovascular Insufficiency. New York, Grune & Stratton, 1983.)

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•A •B

3

3

2

2

Fd 1 (kHz)

1

0

0

⫺1

⫺1 Apical divider

Outside wall Opposite apical divider

FIGURE 13–9 • Flow separation in the normal carotid bulb shown by pulsed Doppler spectral analysis. The flow pattern near the apical divider (A) is forward throughout the cardiac cycle, but near the outside wall (B) the spectrum contains both forward (positive) and reverse (negative) flow components. The latter pattern indicates an area of flow separation. Fd, Doppler shift frequency, in kHz. (Courtesy of J. F. Primozich, BS, and D. J. Phillips, PhD.)

The complex flow patterns described in models of the carotid bifurcation have also been documented in human subjects by pulsed Doppler studies.9,10 As shown in Figure 13-9, the Doppler spectral waveform obtained near the inner wall of the carotid bulb is typical of the forward, quasi-steady flow pattern found in the internal carotid artery. However, sampling of flow along the outer wall of the bulb demonstrates lower velocities with periods of both forward and reverse flow. These spectral characteristics are consistent with the presence of flow separation and are considered to be a normal finding, particularly in young individuals.10 Alterations in arterial distensibility with increasing age make flow separation less prominent in older individuals.11 The clinical importance of boundary layer separation is that these localized flow disturbances may contribute to the formation of atherosclerotic plaques.12 Examination of human carotid bifurcations, both at autopsy and during surgery, indicates that intimal thickening and atherosclerosis tend to occur along the outer wall of the carotid bulb, whereas the inner wall is relatively spared.8 These findings suggest that atherosclerotic lesions form near areas of flow separation and low shear stress. Whether flow separation represents a true causative factor or simply promotes the development of previously existing lesions is not known. Pulsatile Flow In a pulsatile system, pressure and flow vary continuously with time, and the velocity profile changes throughout the cardiac cycle. The hemodynamic principles already discussed are based on steady flow, and they are not adequate for a precise description of pulsatile flow in the arterial circulation; however, as previously stated, they can be used to determine the minimal energy losses occurring in a specific flow system. The complex interactions of cardiac contraction, arterial wall characteristics, and blood flow are extremely difficult to

define rigorously. For example, estimation of the inertial energy losses in pulsatile flow requires a value for the velocity term (Equation 9); however, in pulsatile flow, velocity varies with both time and position across the flow profile. Further, skewing of the velocity profile may occur as a result of curvature or branching. The resistance term of Poiseuille’s law (Equation 11) estimates viscous energy losses in steady flow, but it does not account for the inertial effects, arterial wall elasticity, and wave reflections that influence pulsatile flow. The term vascular impedance is used to describe the resistance or opposition offered by a peripheral vascular bed to pulsatile blood flow.3 Pulsatile flow appears to be important for optimal organ function. For example, when a kidney is perfused by steady flow instead of pulsatile flow, a reduction in urine volume and sodium excretion occurs.13 The critical effect of pulsatile flow is probably exerted on the microcirculation. Although the exact mechanism is unknown, transcapillary exchange, arteriolar tone, and lymphatic flow are all influenced by the pulsatile nature of blood flow. Bifurcations and Branches The branches of the arterial system produce sudden changes in the flow pattern that are potential sources of energy loss. However, the effect of branching on the total pressure drop in normal arterial flow is relatively small. Arterial branches commonly take the form of bifurcations. Flow patterns in a bifurcation are determined mainly by the area ratio and the branch angle. The area ratio is defined as the combined area of the secondary branches divided by the area of the primary artery. Bifurcation flow can be analyzed in terms of pressure gradient, velocity, and transmission of pulsatile energy. According to Poiseuille’s law, an area ratio of 1.41 would allow the pressure gradient to remain constant along a bifurcation. If the combined area of the branches equals the area of the primary artery, the area ratio is 1.0, and there is no change in the velocity of flow.14 For efficient transmission of pulsatile energy across a bifurcation, the vascular impedance of the primary artery should equal that of the branches, a situation that occurs with an area ratio of 1.15 for larger arteries and 1.35 for smaller arteries.15 Human infants have a favorable area ratio of 1.11 at the aortic bifurcation, but there is a gradual decrease in the ratio with age. In the teenage years, the average area ratio is less than 1.0; in the 20s, it is less than 0.9; and by the 40s, it drops below 0.8.16 This decline in the area ratio of the aortic bifurcation leads to an increase in both the velocity of flow in the secondary branches and the amount of reflected pulsatile energy. For example, with an area ratio of 0.8, approximately 22% of the incident pulsatile energy is reflected in the infrarenal aorta. This mechanism may play a role in the localization of atherosclerosis and aneurysms in this arterial segment.17 The curvature and angulation of an arterial bifurcation can also contribute to the development of flow disturbances. As blood flows around a curve, the high-velocity portion of the stream is subjected to the greatest centrifugal force; rapidly moving fluid in the center of the vessel tends to flow outward and be replaced by the slower fluid originally located near the arterial wall. This can result in complex helical flow patterns, such as those observed in the carotid bifurcation.9

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As the angle between the secondary branches of a bifurcation is increased, the tendency to develop turbulent or disturbed flow also increases. The average angle between the human iliac arteries is 54 degrees; however, with diseased or tortuous iliac arteries, this angle can approach 180 degrees.3 In the latter situation, flow disturbances are particularly likely to develop. PHYSICAL PROPERTIES OF THE ARTERIAL WALL Composition Blood vessels are viscoelastic tubes. In this context, viscosity refers to the resistance of a material to shear, and elasticity describes the tendency of a material to return to its original shape after being subjected to a deforming force. As blood proceeds from the large arteries of the thorax and abdomen to the medium-size arteries of the extremities, the relative amount of elastic tissue in the vessel wall decreases as the amount of collagen and smooth muscle increases. At the level of the arteriole, the wall consists almost entirely of smooth muscle. Thus, the viscoelastic properties of an artery depend primarily on the elastin-collagen ratio. Elastin is the predominant component of the thoracic aorta that allows energy to be stored during cardiac systole and returned to the system in diastole. Because collagen is much less extensible than elastin, the more distal arteries, such as the brachial and femoral, do not store much of the pulsatile energy but serve mainly as conduits for blood. The function of the muscular arterioles is to control blood pressure and flow by actively altering the lumen diameter. As the structure of the arterial wall changes, each successive branching also increases the total cross-sectional area of the arterial tree. The cross-sectional area at the arteriolar level is approximately 125 times that of the aorta; at the capillary level, it has increased approximately 800 times.3 The reduced elastin-collagen ratio and increased stiffness of the peripheral arteries result in a more rapid pulse wave velocity and a high vascular impedance. Although the impedance of the thoracic aorta must be low to minimize cardiac work, the impedance of peripheral arteries should match the high arteriolar impedance to decrease the reflected components of the pulse wave. Tangential Stress and Tension The tangential stress (τ) within the wall of a fluid-filled cylindrical tube can be expressed as follows: r [15] τ=P δ where P is the pressure exerted by the fluid (in dynes per square centimeter), r is the internal radius (in centimeters), and δ is the thickness of the tube wall (in centimeters). Stress (τ) has the dimensions of force per unit area of tube wall (dynes per square centimeter). Thus, tangential stress is directly proportional to pressure and radius but inversely proportional to wall thickness. Equation 15 is similar to Laplace’s law, which defines tangential tension (T) as the product of pressure and radius: T = Pr

[16]

Tension is given in units of force per tube length (dynes per centimeter). The terms stress and tension have different

231

dimensions and describe the forces acting on the tube wall in different ways. Laplace’s law can be used to characterize thin-walled structures such as soap bubbles; however, it is not suitable for describing the stresses in arterial walls. Arterial Wall Properties in Specific Conditions AGING AND ATHEROSCLEROSIS. Arterial walls become less distensible with age. This increase in stiffness cannot be explained on the basis of atherosclerosis alone.3 Alterations in the elastin fibers and elastic lamellae, together with an increase in wall thickness, probably account for this increase in arterial stiffness. Changes associated with aging include fragmentation of elastic lamellae and deposition of collagen between the elastin layers. This tends to maintain the elastin fibers in the extended state. Calcium is also deposited near the elastin fibers and contributes to the increased thickness of the arterial wall. The effects of atherosclerosis on the mechanical properties of the arterial wall are complex and difficult to distinguish from those due to aging. In the early stages, arterial distensibility may actually increase as elastin fibers are disrupted; however, as the disease progresses, fibrosis and calcification tend to make the arterial wall less distensible. ENDARTERECTOMY. During an endarterectomy the atherosclerotic plaque is removed, along with the intima and a portion of the media, leaving behind a tube consisting of the outer media and adventitia. This reduces the wall thickness to approximately one third of its original value and should result in an increase in tangential stress, according to Equation 15. As would be expected, endarterectomy decreases the stiffness of an artery to circumferential expansion.18 Still, the endarterectomized artery remains stiffer and less distensible than a normal artery. This indicates that the components responsible for strength and stiffness are concentrated in the outer layers of the arterial wall. It is because of this anatomic arrangement that endarterectomy is possible. ANEURYSMS. When the structural components of the arterial wall are weakened, aneurysms may form. Rupture occurs when the tangential stress within the arterial wall becomes greater than the tensile strength. Figure 13-10 shows a tube with an outside diameter of 2.0 cm and a wall thickness of 0.2 cm, dimensions similar to those of atherosclerotic aortas.1 If the internal pressure is 150 mm Hg, the tangential wall stress is 8.0 × 105 dynes/cm2. Expansion of the tube to form an aneurysm with a diameter of 6.0 cm results in a decrease in wall thickness to 0.06 cm. The increased radius and decreased wall thickness increase the wall stress to 98.0 × 105 dynes/cm2, assuming that the pressure remains constant. In this example, the diameter has been enlarged by a factor of 3, and the wall stress has increased by a factor of 12. Although the tensile strength of collagen is extremely high, it constitutes only about 15% of the aneurysm wall.19 Further, the collagen fibers in an aneurysm are sparsely distributed and subject to fragmentation. The tendency of larger aneurysms to rupture is readily explained by the effect of increased radius on tangential stress (Equation 15) and the degenerative changes in the arterial wall. The relationship between tangential stress and blood pressure accounts for the contribution of hypertension to the risk of rupture. The diverging and converging geometry of aneurysms can result in complex flow patterns that include areas of

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75 Pressure (mm Hg)

dynes⭈cm⫺2 3

Radius (cm)

2

␶⫽8.0⫻105 dynes⭈cm⫺2

1 0

150 mm Hg

150 mm Hg

10 Heat

8

50

25

ergs⭈cm⫺5 ⫻ 104

␶⫽98.0⫻105

Contraction Viscous

6

Potential energy (Pressure)

4

Kinetic energy (1/2pV2)

Expansion

2

0

0

1 0.5 cm 2 3

ro⫽1.0 cm ri⫽0.8 cm ␦⫽0.2 cm

0 ro⫽3.0 cm

ri⫽2.94 cm

␦⫽0.06 cm

FIGURE 13–10 • End-on view of a cylinder, 2 cm in diameter, that is expanded to 6 cm in diameter while the wall area remains constant. δ, wall thickness, ri, inside radius, ro , outside radius; t, wall stress. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

reversal.20

boundary layer separation and flow These patterns explain the frequent accumulation of clot in aneurysms, which confines the flow stream to an area not much larger than the native artery. Because this clot increases the effective thickness of the vessel wall, it may reduce tangential stress and provide some protection against rupture. However, the tensile strength of clot and arterial wall is not the same, and the contribution of clot to the integrity of an aneurysm is impossible to predict.3 Further, the clot within an aneurysm is often not circumferential. In this situation, Equation 15 can be applied to the wall segment without clot, and the tangential stress at that site depends on the maximum internal radius. Another factor to consider is that in about 55% of ruptured abdominal aortic aneurysms, the site of rupture is in the posterolateral aspect of the aneurysm wall.21 The posterior wall of the aorta is relatively fixed against the spine, and repeated flexion of the wall in that area could result in structural fatigue. This would produce a localized area of weakness that might predispose to rupture.

Hemodynamics of Arterial Stenosis ENERGY LOSSES According to Poiseuille’s law (Equation 8), the radius of a stenotic segment has a much greater effect on viscous energy losses than does its length. Inertial energy losses, which occur at the entrance (contraction effects) and exit (expansion effects) of a stenosis, are proportional to the square of blood velocity (Equation 9). Energy losses are also influenced by the geometry of a stenosis; a gradual tapering results in less energy loss than an irregular or abrupt change in lumen size. A converging vessel geometry tends to stabilize laminar flow and flatten the velocity profile, whereas a diverging vessel produces an elongated velocity profile and a less stable flow pattern. The energy lost at the exit of a stenosis may be

1

2

3

Length (cm) FIGURE 13–11 • Energy losses resulting when blood flows steadily through a 1-cm-long stenosis. Inertial losses (contraction and expansion) are more significant than viscous losses. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

quite significant because of the sudden expansion of the flow stream and dissipation of kinetic energy in a zone of turbulence. The energy lost in expansion (∆P) can be expressed in terms of the flow velocity distal to the stenosis (v) and the radii of the stenotic lumen (rs) and the normal distal lumen (r):   2  r ρ ∆P = k ϑ 2   − 1 2  rs    

2

[17]

Figure 13-11 illustrates the energy losses related to a 1-cmlong stenosis. The viscous losses are relatively small and occur within the stenotic segment. Inertial losses due to contraction and expansion are much greater. Because most of the energy loss in this example results from inertial effects, the length of the stenosis is relatively unimportant.1 BRUITS AND POSTSTENOTIC DILATATION The presence of an audible sound or bruit over an artery is usually regarded as a clinical sign of arterial disease. Stenoses or irregularities of the vessel lumen produce turbulent flow patterns that set up vibrations in the arterial wall. These vibrations generate displacement waves that radiate through the surrounding tissues and can be detected as audible sounds. Such vibrations are probably the main source of sound in the arterial system.3 Generally, a soft, midsystolic bruit is associated with a relatively minor lesion that does not significantly reduce flow or pressure. A bruit with a loud diastolic component suggests a stenosis severe enough to reduce flow and produce a pressure drop. Thus, the intensity and duration of a bruit serve as a rough guide to the severity of an arterial stenosis. A bruit may be absent when an artery is nearly occluded or when the flow rate is extremely low. A dilated area distal to a stenosis is a common clinical finding. Poststenotic dilatation has been observed in the thoracic aorta below coarctations, distal to arterial stenoses at

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the thoracic outlet, and distal to atherosclerotic lesions. The most likely explanation for this phenomenon is that arterial wall vibrations result in structural fatigue of elastin fibers. In a series of animal model studies, poststenotic dilatations did not develop unless a bruit was present distal to the stenosis.22 It appears that vibrations in the audible range may weaken elastin fibers and break down links between collagen fibers. When this occurs, the arterial wall distal to the stenosis becomes more distensible and subject to localized dilatation.

% Stenosis 90 95 0 10 20 30 40 50 60 70 80

90

r1⫽0.5 cm

r2⫽x

80 I I⫽1.0 cm ␩⫽0.035 poise P⫽1.056 g/cm3

⌬P (mm Hg)

70

CRITICAL ARTERIAL STENOSIS The degree of arterial narrowing required to produce a significant reduction in blood pressure or flow is called a critical stenosis. Because the energy losses associated with a stenosis are inversely proportional to the fourth power of the radius at that site (Equations 8 and 17), there is an exponential relationship between energy loss (pressure drop) and reduction in lumen size. When this relationship is illustrated graphically, the curves have a single sharp bend (Fig. 13-12; also see Fig. 13-5). These observations provide theoretical support for the concept of critical stenosis.23,24 As previously noted, blood flow velocity is a major determinant of fluid energy losses (Equations 8, 9, and 17). Thus, the pressure drop across a stenosis varies with the flow rate. Because flow velocity depends on the distal hemodynamic resistance, the critical stenosis value also varies with the resistance of the runoff bed. In Figure 13-12, a system with a high flow velocity (low resistance) shows a reduction in pressure with less narrowing than a system with low flow velocity (high resistance). The higher flow velocities produce curves that are less sharply bent, making the point of critical stenosis less distinct.

100

100

60 50 40 30

Velocity (cm/sec) 50 40 30 20 15 10 5

20

1

10 0 0.5

0.4 0.3 0.2 0.1 Inside radius of stenosis (cm)

0.0

FIGURE 13–12 • Relationship of pressure drop across a stenosis to the radius of the stenotic segment and the flow velocity. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

Another observation related to critical stenosis is that the decrease in flow is linearly related to the increase in pressure gradient, as long as the peripheral resistance remains constant24 (Fig. 13-13). In this situation, the curves for pressure drop and flow reduction are mirror images of each other,

1.0-cm-long stenosis in 10-cm-long artery with radius of 0.5 cm (flow⫽5.0 cm3/sec) Percent stenosis 0 10 20 30 40 50 60 70 80 90

95

100

Flow cm3/sec 100 5.0

⌬P mm Hg 28.6

Percent of maximum flow Percent of maximum pressure drop

90

FIGURE 13–13 • Effect of increasing stenosis on blood flow and pressure drop across the stenotic segment. Collateral and peripheral resistances are considered to be fixed. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

⌬P

80

4.0

25.0

Flow 70

20.0 3.0

60

15.0

50 2.0

40

10.0

30 1.0

20

5.0

10 0.0

0 0.5

0.4

0.3 0.2 0.1 Inside radius of stenosis (cm)

0.0

0.0

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and the critical stenosis value is the same for both. Many vascular beds are able to maintain a constant level of blood flow over a wide range of perfusion pressures by the mechanism of autoregulation. This is achieved by constriction of resistance vessels in response to an increase in blood pressure and dilatation of resistance vessels when blood pressure decreases. For example, autoregulation permits the brain to maintain normal flow rates down to perfusion pressures in the range of 50 to 60 mm Hg.25 Significant changes in pressure and flow begin to occur when the arterial lumen has been reduced by about 50% of its diameter or 75% of its cross-sectional area; however, the concept of critical stenosis is strictly valid only when the flow conditions are specified. Consequently, a stenosis that is not significant at resting flow rates may become critical when flow rates are increased by reactive hyperemia or exercise. For example, iliac stenoses that do not appear severe by arteriography may be associated with significant pressure gradients during exercise.26 Because of the complex geometry of atherosclerotic lesions and the wide variation in arterial flow rates, it is often difficult to predict the hemodynamic significance of a lesion based on the apparent reduction in lumen size. Therefore, physiologic testing by blood pressure measurement must be used to document the clinical severity of arterial lesions.27,28 EFFECT OF STENOSIS LENGTH AND MULTIPLE STENOSES Poiseuille’s law predicts that the radius of a stenosis will have a much greater effect on viscous energy losses than will its length (Equation 8). If the length of a stenosis is doubled, the viscous energy losses are also doubled; however, reducing the radius by one half increases energy losses by a factor of 16. Further, inertial energy losses are independent of stenosis length and are especially prominent at the exit of a stenosis (see Fig. 13-11 and Equation 17). Because energy losses are primarily due to entrance and exit effects, separate short stenoses tend to be more significant than a single longer stenosis. It has been shown experimentally that when stenoses that are not significant individually are arranged in series, large reductions in pressure and flow can occur.29 Thus, multiple subcritical stenoses may have the same effect as a single critical stenosis. Based on the preceding discussion, several points can be made about stenoses in series. When two stenoses are of similar diameter, removal of one provides only a modest increase in blood flow. If the stenoses have different diameters, removal of the least severe has little effect, whereas removal of the most severe improves blood flow significantly. These principles apply only to unbranched arterial segments such as the internal carotid. In the presence of a severe stenosis in the carotid siphon, removal of a less severe lesion at the carotid bifurcation is not likely to result in significant hemodynamic improvement. In contrast, when the proximal lesion involves an artery that supplies a collateral bed that parallels a distal lesion, removal of the proximal lesion can be beneficial. For example, when there is an iliac stenosis and superficial femoral occlusion, removal of the iliac lesion usually improves perfusion of the lower leg by increasing flow through the profunda-geniculate collateral system.

Arterial Flow Patterns in Human Limbs COLLATERAL CIRCULATION When arterial obstruction occurs, blood must pass through a network of collateral vessels to bypass the diseased segment. The functional capacity of the collateral circulation varies according to the level and extent of occlusive lesions. As mentioned in the preceding example, the profunda-geniculate system can compensate to a large degree for an isolated superficial femoral artery occlusion; however, the addition of an iliac lesion severely limits collateral flow. A typical hemodynamic circuit includes the diseased major artery, a parallel system of collateral vessels, and the peripheral runoff bed (Fig. 13-14). The collateral system consists of stem arteries, which are large distributing branches; a midzone of smaller intramuscular channels; and reentry vessels that join the major artery distal to the point of obstruction.30 These vessels are preexisting pathways that enlarge when flow through the parallel major artery is reduced. The main stimuli for collateral development are an abnormal pressure gradient across the collateral system and increased velocity of flow through the midzone vessels.31 This mechanism is consistent with the gradual improvement in collateral circulation that results from a regular exercise program in patients with lower extremity arterial occlusive disease.32 Collateral vessels are smaller, longer, and more numerous than the major arteries they replace. Although considerable enlargement may occur in the midzone vessels, collateral

QT

Stem arteries

Midzone collateral

Re-entry arteries Peripheral vascular bed (runoff)

PI QC

QS

Stenosis RC

RS

P2

QT RP

Venules and veins FIGURE 13–14 • Major components of a hemodynamic circuit containing a stenotic artery. The analogous electrical circuit is shown on the right, with the heart represented as a battery and the central veins as a ground. Flows are represented by QT (total), QC (collateral), and QS (stenosis). Resistances are represented by RC (collateral), RS (stenosis), and RP (peripheral runoff); RC and RS are fixed, and RP is variable. (From Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB [ed]: Vascular Surgery. Philadelphia, WB Saunders, 1977.)

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DISTRIBUTION OF VASCULAR RESISTANCE AND BLOOD FLOW Unlike collateral resistance, the resistance of a peripheral runoff bed is quite variable. The muscular arterioles are primarily responsible for regulating peripheral resistance and controlling the distribution of blood flow to various capillary beds. Arteriolar tone is mainly determined by the sympathetic nervous system, but it is also subject to the influence of locally produced metabolites. When discussing blood flow in the lower limb, it is useful to separate vascular resistance into segmental and peripheral components. Segmental resistance consists of the relatively fixed parallel resistances of the major normal or diseased artery and the bypassing collateral vessels, such as the superficial femoral artery and the profunda-geniculate system. Peripheral resistance includes the highly variable resistances of the distal calf muscle arterioles and cutaneous circulation. The total vascular resistance of the limb can be estimated by adding the segmental and peripheral resistances (Equations 12 and 13). Normally, the resting segmental resistance is very low and the peripheral resistance is relatively high; therefore, the pressure drop across the femoropopliteal segment is minimal. With exercise, the peripheral resistance falls, and flow through the segmental arteries increases by a factor of up to 10, with little or no pressure drop. With moderate arterial disease, such as an isolated superficial femoral artery occlusion, the segmental resistance is increased as a result of collateral flow, and an abnormal pressure drop is present across the thigh. Because of a compensatory decrease in peripheral resistance, the total resistance of the limb and the resting blood flow often remain in the normal range.34 During exercise, the segmental resistance remains high and fixed, whereas the peripheral resistance decreases further. However, the capacity of the peripheral circulation to compensate for a high segmental resistance is limited, and exercise flow is less than normal. In this situation, exercise is associated with a still larger pressure drop across the diseased arterial segment. The clinical result is calf muscle ischemia or claudication. When arterial disease becomes severe, as in combined iliofemoral and tibioperoneal occlusive disease, the compensatory decrease in peripheral resistance may be unable to provide normal blood flow at rest. In this case, there is a marked pressure drop across the involved arterial segments and little or no increase in blood flow with exercise. Claudication is severe, and ischemic rest pain or ulceration may develop. These changes in the distribution of vascular resistance in the lower limb explain the alterations in blood pressure and flow observed in patients with arterial occlusive disease.

a progressive decrease in arterial compliance and reflections originating from the relatively high peripheral resistance. Consequently, the systolic pressure at the ankle is higher than that in the upper arm, and the ankle-arm pressure ratio is greater than 1. However, the diastolic and mean pressures gradually decrease as the blood moves distally. When blood flows through an arterial stenosis or a highresistance collateral bed, the distal pulse pressure is reduced to a greater extent than the mean pressure.35 This indicates that the systolic pressure beyond a lesion is a more sensitive indicator of hemodynamic significance than is the mean pressure. It is well known that palpable pedal pulses in patients with superficial femoral artery stenosis can disappear after leg exercise. This occurs when increased flow through high-resistance vessels causes a reduction in pulse pressure. The contour of the pressure pulse also reflects the presence of proximal arterial disease. These changes can be demonstrated plethysmographically and include a delayed upslope, rounded peak, and bowing of the downslope away from the baseline.36 Changes in the flow pulse are also useful to characterize the state of the arterial system. As the peak pressure increases, the peak of the flow pulse decreases as the periphery is approached.3 The flow pattern in the major arteries of the leg is normally triphasic (Fig. 13-15). An initial large forwardvelocity phase resulting from cardiac systole is followed by a brief phase of flow reversal in early diastole and a third smaller phase of forward flow in late diastole. This triphasic pattern is modified by a variety of factors, including proximal arterial disease and changes in peripheral resistance. For example, body heating, which causes vasodilatation and decreased resistance, abolishes the second phase of flow reversal; on exposure to cold, resistance increases and the reverse-flow phase becomes more prominent. Because a stenotic lesion is

20

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resistance is always greater than that of the original unobstructed artery. In addition, the acute changes in collateral resistance during exercise are minimal.33 Therefore, the resistance of a collateral system is, for practical purposes, fixed.

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ARTERIAL PULSES AND WAVEFORMS The heart generates a complex pressure pulse that is modified by arterial wall properties and changes in vascular resistance as it progresses distally. Normally, the peak systolic pressure is amplified as it passes down the lower limb.3 This is due to

FIGURE 13–15 • Velocity flow waveforms obtained with a directional Doppler velocity detector from the femoral artery of a normal subject, a patient with external iliac stenosis, and a patient with common iliac occlusion. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

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PRESSURE AND FLOW IN LIMBS WITH ARTERIAL OBSTRUCTION If an arterial lesion is hemodynamically significant at rest, there is a measurable reduction in distal blood pressure. Generally, limbs with a lesion at one anatomic level have an anklebrachial index between 0.9 and 0.5, whereas limbs with occlusions at multiple anatomic levels have an index less than 0.5.28 The ankle-brachial index also correlates with the clinical severity of disease: in limbs with intermittent claudication, the index has a mean value of 0.59 ± 0.15; in limbs with ischemic rest pain, 0.26 ± 0.13; and in limbs with impending gangrene, 0.05 ± 0.08.37 Because of the increased segmental vascular resistance in limbs with arterial occlusive disease, the ankle systolic blood pressure falls dramatically during leg exercise. As indicated in Figures 13-16 to 13-18, the extent and duration of the pressure drop are proportional to the severity of the arterial lesions. Recovery of pressure to resting levels may require up to 30 minutes.28 Resting leg or calf blood flow in patients with intermittent claudication is not significantly different from values obtained in normal individuals. However, the capacity to increase limb blood flow during exercise is quite limited, and pain occurs in the muscles that have been rendered ischemic. The pain of claudication is presumably due to the accumulation of metabolic products that are removed under normal flow conditions. As the occlusive process becomes more severe,

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As the pressure pulse moves distally, the systolic pressure rises, the diastolic pressure falls, and the pulse pressure becomes wider. The fall in mean arterial pressure between the heart and ankle is normally less than 10 mm Hg. In normal individuals at rest, the ratio of ankle systolic pressure to brachial systolic pressure (ankle-brachial index) has a mean value of 1.11 ± 0.10.37 Moderate exercise in normal extremities produces little or no drop in ankle systolic pressure. Strenuous effort may be associated with a drop of several millimeters of mercury; however, pressures return rapidly to resting levels after cessation of exercise. The average blood flow in the normal human leg is in the range of 300 to 500 mL/minute under resting conditions.3 Blood flow to the muscles of the lower leg is approximately 2.0 mL/100 g per minute. With moderate exercise, total leg blood flow increases by a factor of 5 to 10, and muscle blood flow rises to around 30 mL/100 g per minute. During strenuous exercise, muscle blood flow may reach 70 mL/100 g per minute. After cessation of exercise, blood flow decreases rapidly and returns to resting values within 1 to 5 minutes.

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FIGURE 13–16 • Pre-exercise and postexercise ankle blood pressure and calf blood flow in a patient with severe stenosis of the superficial femoral artery. (From Sumner DS, Strandness DE: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65:763-771, 1969.)

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accompanied by a compensatory decrease in peripheral resistance, one of the earliest changes noted distal to a stenosis is the disappearance of the reverse-flow phase (see Fig. 13-15). As a stenosis becomes more severe, the distal flow pattern becomes monophasic, with a slow rise, a rounded peak, and a gradual decline toward the baseline in diastole. The character of the flow pulse proximal to an arterial obstruction is variable and depends on the capacity of the collateral circulation. These flow patterns can be studied noninvasively using a Doppler velocity detector and strip-chart recorder.

Calf blood flow (mL/100 mL/min) Ankle blood pressure (mm Hg)

Hemodynamics for the Vascular Surgeon

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FIGURE 13–17 • Pre-exercise and postexercise ankle blood pressure and calf blood flow in a patient with iliac stenosis and superficial femoral artery occlusion. (From Sumner DS, Strandness DE: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65:763-771, 1969.)

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Between the fixed resistances of these two arterial lesions is the profunda orifice, which supplies the variable resistance of the thigh. The resistance of the distal calf runoff bed is also variable. Under resting conditions, normal leg blood flow can be maintained by a nearly maximal decrease in calf resistance and a moderate decrease in thigh resistance. This is apparent clinically as an abnormally low ankle systolic pressure. With the increased metabolic demands of exercise, the thigh resistance can decrease further, but the calf resistance has already reached its lower limit. This results in a further pressure drop across the proximal iliac lesion, which reduces the pressure perfusing the calf. Blood flow to the calf is decreased until the thigh resistance rises and thigh blood flow begins to fall. In this situation, the effect of exercise is to increase thigh blood flow, decrease calf blood flow, and decrease distal blood pressure. The thigh steals blood from the calf because the proximal iliac lesion restricts inflow to both runoff beds.

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Hemodynamics for the Vascular Surgeon

Subclavian Steal Syndrome 0

the decrease in peripheral vascular resistance can no longer compensate, and resting flow may be less than normal. When this occurs, ischemic rest pain or ulceration may appear. As shown in Figures 13-16 to 13-18, the capacity to increase calf blood flow with exercise depends on the severity of arterial disease. With increasing degrees of disease, the hyperemia that follows exercise becomes more prolonged, and the peak calf blood flow is both decreased and delayed. In some cases, flow may fall below resting levels.28 The ankle blood pressure returns to normal after peak flows have started to decline. The changes in blood pressure and flow in lower limbs with arterial occlusive disease provide the basis for noninvasive diagnostic tests. By monitoring the ankle systolic pressure before and after treadmill exercise or reactive hyperemia, two components of the physiologic response can be evaluated: (1) the magnitude of the immediate pressure drop, and (2) the time for recovery to resting pressure. The changes in both of these parameters are proportional to the severity of arterial disease.38

In the subclavian steal syndrome, reversal of flow in the vertebral artery is associated with subclavian artery occlusion and symptoms of brainstem ischemia.39 When occlusion is present in the proximal subclavian artery on the left or the innominate artery on the right, the pressure at the origin of the ipsilateral vertebral artery is reduced. This can result in reversal of flow in the vertebral artery, which then serves as a source of collateral circulation to the arm. The increased demands of arm exercise tend to augment the reversed flow, and the patient may experience ischemia of the brainstem. The hemodynamic effect is more severe with innominate artery occlusion than with isolated subclavian occlusion. With innominate occlusion, the origin of the right common carotid is also subject to reduced pressure, and the patterns of collateral circulation to the arm and brain become quite complicated. Blood passing down the vertebral artery on the side of the occlusion may be recovered, in part, by the right common carotid artery; however, during arm exercise, flow in the right common carotid may be reduced. It is important to distinguish between symptomatic and asymptomatic subclavian steal. The presence of reversed vertebral artery flow, as demonstrated by arteriography, may be a normal variant without clinical significance.40 In true subclavian steal syndrome, there is often a definite relationship between arm exercise and symptoms of brainstem ischemia. There will also be objective evidence of decreased blood flow to the involved arm, such as a diminished radial pulse and lowered brachial blood pressure relative to the contralateral arm.41

VASCULAR STEAL

Extra-anatomic Bypass Grafts

Hemodynamic arrangements in which one vascular bed draws blood away or “steals” from another can occur in a variety of situations. A vascular steal may arise when two runoff beds with different resistances must be supplied by a limited source of inflow.

When an extra-anatomic bypass is performed, a single donor artery must supply several vascular beds. In the case of a femorofemoral crossover graft, one iliac is the donor artery, the leg ipsilateral to the donor artery is the donor limb, and the contralateral leg is the recipient limb. Studies of crossover grafts in animal models have shown that the immediate effect of the graft is to double the flow in the donor artery.42,43 When an arteriovenous fistula is created in the recipient limb, graft flows may increase by a factor of 10 without any evidence of a steal from the donor limb.

Pre-exercise 2

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10 14 18 22 Minutes after exercise

26

30

FIGURE 13–18 • Pre-exercise and postexercise ankle blood pressure and calf blood flow in a patient with occlusion of the iliac, common femoral, and superficial femoral arteries. This patient had moderate rest pain and severe claudication. (From Sumner DS, Strandness DE: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65:763-771, 1969.)

Multiple-Level Occlusive Disease One example of the steal phenomenon involves a limb with lesions in both the iliac and superficial femoral arteries.1

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These experimental observations are consistent with hemodynamic data from patients with femorofemoral grafts.44 Improvement in the ankle-brachial index on the recipient side can be achieved, even in the presence of significant occlusive disease in both the donor and recipient limbs. Although the ankle-brachial index may decrease slightly on the donor side, a symptomatic steal is extremely uncommon. The most important factor contributing to vascular steal with a femorofemoral graft is stenosis of the donor iliac artery. With iliac stenosis, a steal is most likely to occur during exercise, when flow rates are increased. A mildly stenotic iliac can be used as a donor artery when high flow rates are not needed, such as in the treatment of ischemic rest pain. However, when increased flow rates are required to improve the walking distance of a patient with claudication, stenosis of the donor iliac may result in a steal from the donor limb. Occlusive disease in the arteries of the donor limb distal to the origin of the graft does not result in a steal, provided that the donor iliac artery is normal. These principles also apply to other types of extra-anatomic bypass grafts, including axillary-axillary, carotid-subclavian, and axillofemoral grafts.42,45

Hemodynamic Principles and the Treatment of Arterial Disease It should be apparent from the preceding discussion that the high fixed segmental resistance of the diseased major arteries and collaterals is responsible for decreased peripheral blood flow. Therefore, to be most effective in improving peripheral blood flow and relieving ischemic symptoms, therapy must be directed toward lowering this abnormally high segmental resistance. Because the peripheral resistance has already been lowered to compensate for the increased segmental resistance, attempts to further reduce the peripheral resistance are seldom beneficial.46 Although exercise therapy has been shown to improve collateral function, the degree of clinical improvement is usually modest.32 In general, exercise therapy is best suited for patients with mild, stable claudication who are not candidates for direct intervention. Another method for improving peripheral blood flow in limbs with arterial disease is medically induced hypertension.46 The administration of mineralocorticoid and sodium chloride raises systemic blood pressure and increases the head of pressure perfusing the diseased arterial segment. Although this technique has not been widely applied, it has been used successfully in patients with severe distal ischemia and ulceration. DIRECT ARTERIAL INTERVENTION The most satisfactory approach to reducing the fixed segmental resistance is direct intervention by surgical or radiological techniques. Depending on the nature of the lesions, endarterectomy, embolectomy, replacement grafting, or bypass grafting may be indicated. Percutaneous transluminal angioplasty may also be appropriate in selected cases.47 In patients with occlusive disease involving a single anatomic level, a successful procedure should return all hemodynamic parameters to normal or near normal. This should be evident as an increase in the ankle-brachial index and an improvement

in the ankle pressure response to leg exercise.48 However, because it is seldom possible to perform a perfect arterial reconstruction, it is common to detect a minor degree of residual hemodynamic impairment. When occlusions involve multiple levels, the treatment of one level should result in significant improvement, and the persisting hemodynamic abnormality should then reflect the remaining untreated disease. In such cases, the improvement is usually sufficient to increase claudication distance or relieve ischemic rest pain. The relative severity of lesions at different levels is often difficult to determine clinically; however, the basic principle is to initially treat the most proximal level of hemodynamically significant occlusive disease. The factors required for optimal function of arterial bypass grafts can be analyzed in terms of basic hemodynamic principles. As previously noted, vessel diameter is the main determinant of hemodynamic resistance, so the diameter of a graft is considerably more important than its length. All prosthetic grafts develop a pseudointimal layer of variable thickness that further reduces the effective diameter.3 Therefore, whenever the situation permits, a graft with a relatively large diameter should be used. Graft diameter is often limited by arterial size. To minimize energy losses associated with entrance and exit effects, the diameter of a graft should approximate that of the adjacent artery. When arteries of unequal size must be joined, a gradual transition is preferable. Thus, the graft should be slightly smaller than the proximal artery and slightly larger than the distal artery. Theoretically, end-to-end anastomoses are preferable to those done end to side, because the end-to-end configuration eliminates energy losses due to curvature and angulation. However, these losses appear to be minimal under physiologic conditions, and in most clinical situations the anastomotic angle is determined by technical factors. For example, reversed angulation has been used successfully in the construction of aortorenal and femorofemoral bypass grafts. Nevertheless, as a general rule, the smallest anastomotic angle that is technically feasible should be used. The width of an end-to-side anastomosis should be approximately equal to the diameter of the graft; the length of an anastomosis is less important but does serve as the main determinant of anastomotic angle. A carefully everted suture line also helps minimize energy losses at anastomoses. Bifurcation grafts, such as those used for aortofemoral bypass, are subject to the same general hemodynamic considerations as arterial bifurcations and branches. Most commercially available grafts have secondary limbs with diameters that are one half that of the primary tube, resulting in an area ratio of 0.5. In this configuration, each of the secondary limbs has 16 times the resistance of the primary tube, and in parallel they offer 8 times the primary tube resistance. The flow velocity in the secondary limbs is doubled, and almost 50% of the incident pulsatile energy is reflected at the graft bifurcation.3 As previously discussed, the area ratio determines the hemodynamic characteristics of a bifurcation with respect to pressure gradient, flow velocity, and transmission of pulsatile energy. However, the optimal area ratio for grafts has not been established, and the geometry of bifurcation grafts has received relatively little attention. Instead, the development of prosthetic grafts has emphasized features such as graft material, porosity, and surface characteristics. Despite their theoretical disadvantages, commercially available

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grafts have functioned extremely well in a variety of clinical applications. VASODILATORS The rationale for the use of vasodilators is that they lower peripheral vascular resistance and improve limb blood flow. Although this may occur in normal limbs, it is unlikely to be beneficial in limbs in which peripheral resistance is already decreased as a result of arterial disease. There is even a theoretical possibility that dilating vessels in relatively normal areas could divert blood away from the areas of ischemia. Most clinical studies of vasodilator therapy have failed to show a significant effect.49,50 There is no conclusive evidence that vasodilators can increase flow in either collateral vessels or severely ischemic tissues. Consequently, there is no theoretical or clinical support for vasodilator therapy. SYMPATHECTOMY Because the purpose of sympathectomy is to reduce peripheral resistance by release of vasomotor tone, it is subject to the same general criticisms as vasodilator therapy. Because sympathectomy has little, if any, influence on collateral resistance, there is no rational basis for its use in the treatment of intermittent claudication.51 Further, exercise-induced muscle ischemia alone is a potent stimulus for peripheral vasodilatation. The use of sympathectomy for cutaneous ischemia has some physiologic basis, because the predominant effect is dilatation of cutaneous arterioles. However, clinical improvement can occur only if the ischemic tissues are capable of further vasodilatation, as demonstrated by reactive hyperemia testing.36 Beneficial results have been obtained in patients with mild rest pain and superficial ischemic ulcers; patients with severe rest pain and extensive tissue loss are not likely to respond.51 Although sympathectomy has been recommended as an adjunct to arterial operations, there is little objective evidence that it improves either the early or the late results of arterial reconstructive surgery.52 RHEOLOGIC AGENTS According to Poiseuille’s law, hemodynamic resistance is directly proportional to blood viscosity (Equations 8 and 11). If the pressure remains constant and viscosity is reduced, flow increases in proportion to the fall in viscosity. Procedures for lowering blood viscosity are most often used in the immediate postoperative period to increase flow through a reconstructed arterial segment. Low-molecular-weight dextran (molecular weight 40,000) is the most commonly used agent for reducing blood viscosity. The increased peripheral blood flow observed after intravenous administration of low-molecular-weight dextran is the result of both peripheral vasodilatation secondary to blood volume expansion and changes in viscosity due to hemodilution.3 Dextran solutions also influence red blood cell aggregation and platelet function.53 An orally administered rheologic agent, pentoxifylline, has been evaluated in a multicenter clinical trial for the treatment of patients with intermittent claudication.54 Pentoxifylline reduces blood viscosity by improving the membrane flexibility of red blood cells. The drug also has an inhibitory effect on

239

platelet aggregation. During the clinical trial, the distance walked before the onset of claudication increased in both the pentoxifylline and the placebo groups; however, the degree of improvement was significantly greater in those receiving pentoxifylline. It was concluded that pentoxifylline is a safe and effective drug for use in patients with intermittent claudication. Although this agent may provide a modest degree of functional improvement in some patients, its effect on the progression of arterial disease is unknown.

Hemodynamics of the Venous System The structure of the vein wall is considerably different from that of the companion arteries. Some of these major differences are as follows: (1) the vein wall is much thinner, being anywhere from one third to one tenth as thick as that of the systemic arteries; (2) there is very little elastic tissue in the wall of the vein; (3) the venous media is almost exclusively a muscular layer; (4) venules have no media and no smooth muscle; and (5) a major part of the walls of the larger veins is composed of adventitia. An important characteristic of the veins is the presence of valves, which are essential for proper function. The distribution and number of valves correspond quite well to those regions in which the effects of gravity are greatest. They have a bicuspid structure with a fine connective tissue skeleton covered by endothelium on both surfaces. Their major function is to ensure antegrade flow and prevent reflux from the deep to the superficial veins. From a clinical standpoint, the area of greatest interest is below the knee. This is the most common site for the development of venous thrombosis, and it is also the region of the leg where the complications of post-thrombotic syndrome are evident. The veins of the soleus muscle are often termed the “soleal sinuses” because of their capacious size and lack of venous valves. These sinuses are the most common site for the development of venous thrombosis. The perforating veins that normally carry blood from the superficial to the deep veins are key elements in venous function. These short channels have the following features: they penetrate the deep fascia; they contain valves; they are found predominantly below the knee; the majority are small and inconstant in location; and they vary in number from 90 to 200.55 Although not commonly thought of as such, the greater and lesser saphenous veins have all the characteristics of perforating veins. One relatively constant large perforator can be found on the medial aspect of the distal thigh, and this is one of the few that establishes a direct communication between the greater saphenous vein and the deep venous system. A common misconception is that the perforating veins along the medial aspect of the lower leg communicate directly with the greater saphenous vein. In fact, they communicate most commonly with its major tributary, the posterior arch vein. Normally, there are four relatively constant perforators that join the posterior arch vein, and when these are diseased, they contribute to the pathogenesis of postthrombotic syndrome. The region in the vicinity of the lowest two perforating veins is often referred to as the gaiter area.55 As discussed later in this chapter, the function of the venous wall and its associated valves becomes evident when the effects of gravity and the calf muscle pump are considered.

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NORMAL PRESSURE AND FLOW RELATIONSHIPS A major factor in venous physiology that explains the capacitance function of these vessels is that they can undergo large changes in volume with very little change in transmural pressure. This is due not to the elastic properties of the walls but rather to the fact that they tend to collapse under the influence of a low transmural pressure. Veins are actually stiffer than arteries when compared at the same distending pressure. This results from the paucity of elastic tissue and the very prominent adventitia, which consists largely of collagen. One of the remarkable features of the venous system is the wide range of flow rates that can be found—from high flows to nearly complete stasis. Flow rates depend on a host of complex interactive factors such as body position, level of activity, vascular fluid volume, and ambient temperature. Because it is virtually impossible to measure instantaneous venous flow in either the superficial or the deep veins, it is necessary to look at measurements of venous pressure and relate these to specific conditions or disease states. Resting Venous Pressure The pressures that exist in the absence of pulsatile flow are shown in Figure 13-19, which is the hydrostatic model of a 6-foot-tall “dead man.” If the case of an open rigid tube is considered, pressure at the top would be zero (atmospheric). In the body, the arteries and veins can be represented as a series of parallel tubes, with the veins being collapsible and the arteries rigid. When the system is filled with fluid, but not enough to entirely distend the collapsible tube (venous), the pressure in the collapsed portion of the tube is atmospheric. Pressures in the rigid tube (arterial) must be equal to those in the collapsible tube up to the zero point. Above the zero pressure point, the pressures in the rigid tube are negative, because the collapsed tube representing the veins prevents free communication between the two segments. When we examine the pressure relationships in a living man, supine and erect, some important facts can be noted56 (Fig. 13-20). There is a point just below the diaphragm where the pressures in the arteries and veins remain constant regardless of position. This has been termed the hydrostatic indifferent point (HIP). This point changes only when the subject is placed head down, and then it is located at the level of the

Arterial pressure (mm Hg)

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FIGURE 13–19 • Hydrostatic pressures measured in the upright “dead man.” The pressures in the open tube are those expected in a rigid tube of equal height. The pressures in the closed tubes are those expected in a system of closed, connected parallel tubes. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

right atrium. The zero pressure level is in the region of the right atrium, usually at the level of the fourth intercostal space. The effect of gravity is the same throughout the vascular system in a supine subject. Raising an arm above the head in the erect position produces some dramatic changes. The arteriovenous pressure gradient in the foot remains the same (83 mm Hg), but in the hand it falls to a level of 31 mm Hg.57 Although there is no difference in the pressure gradient across the capillaries in the feet between the supine and the standing positions, some important changes do occur. On assuming the standing position, there is a translocation of blood into the veins of the legs, about 500 mL.58 There is also a marked increase in the transmural venous pressure at the foot as a result of the effect of gravity. With this increase in pressure, fluid is forced out of the capillaries into the tissues. Although some of this fluid may be picked up by the lymphatics, other factors must come into play if edema is to be prevented. The single most important element in preventing the continued accumulation of interstitial fluid is the calf muscle pump. This can dramatically lower the pressure in the veins and capillaries, thus promoting the return of interstitial fluid to the circulation.

Venous pressure (mm Hg) 0

Height (cm) ⫹80 ⫹60

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FIGURE 13–20 • Intravascular pressures present in the normal supine and erect human. The hydrostatic indifferent point (HIP) is located just below the diaphragm. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

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1.0% volume change

Hemodynamics for the Vascular Surgeon

Features that distinguish normal subjects from patients with venous disease are best understood by examining the pressure changes that occur with leg exercise. Although patients with chronic arterial disease can usually be distinguished from normal subjects under resting conditions by measurement of distal arterial blood pressure, this is not the case with venous disease. For patients with venous problems, it is only when the muscle pump is activated that the abnormality is apparent. The calf muscle pump produces important changes in venous volume, flow rate, and flow direction. The muscle pump fulfills three useful functions: it lowers the venous pressure in the dependent limb; it reduces venous volume in the exercising limb; and it increases venous return. With quiet standing, the venous pressure at the level of the foot remains constant, but this is dramatically altered with even a single step (Fig. 13-21). As noted in Figure 13-21, at the completion of a single step, the venous pressure is very low and requires several seconds to return to the prestep level.59 When a normal subject walks, the venous pressure remains at a low and steady level throughout the period of exercise. Calf volume initially falls but gradually increases during exercise as the arterial inflow rises (Fig. 13-22). It is essential to understand that the observed pressure changes at the level of the foot are entirely dependent on intact and functioning venous valves in the distal limb. The calf muscle pump essentially empties the local venous system during contraction. With relaxation, the veins are nearly empty, and the venous pressure is very low. These changes are vital to maintaining normal venous return and protecting the limb. As shown later in the chapter, destruction of the valves dramatically alters these changes.

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Calf volume

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Venous pressure dorsum of foot Exercise

FIGURE 13–22 • Normal calf volume and venous pressure response to calf muscle exercise. Pressure changes were measured in a dorsal foot vein. Venous pressure falls rapidly, remains low throughout the period of exercise, and returns slowly to the baseline after calf muscle contraction ceases. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

Venous Flow Patterns Flow on the venous side of the circulation is influenced by a variety of factors, including respiration, the filling pressure of the right heart, body position, the activity of the calf muscle pump, and the amount of arterial inflow. The patterns of blood flow in the femoral artery and vein are shown in Figure 13-23. Flow velocity in the normal femoral vein is lowest at peak inspiration, when the intra-abdominal pressure resulting from descent of the diaphragm is at its maximum. In theory, the changes in velocity of venous flow in the subclavian vein should be opposite to those in the femoral vein—that is, highest at peak inspiration, when intrathoracic pressure is at its minimum. As noted earlier, the presence of competent valves prevents reflux of blood and an increase in venous pressure. This can be shown when the pressure is suddenly increased above a competent iliofemoral valve (Fig. 13-24). A cough and a Valsalva maneuver result in a sharp increase in pressure above the valve but not below it. There is no reflux of blood flow through the valve during either of these maneuvers.

80

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60 66.6% of control value 50 Heel starts to ground Control

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012345

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FIGURE 13–21 • Changes in the mean saphenous vein pressure measured at the level of the ankle that occur with a single step. (Redrawn from Pollack AA, Wood EH: Human venous pressure in the saphenous vein at the ankle in during exercise and changes in posture. J Appl Physiol 1:649-662, 1949.)

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0

0

500

5

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FIGURE 13–23 • Comparison of the flow velocity patterns in the common femoral artery (top) and vein (bottom) in the supine position with normal respiration. The venous velocity patterns are dominated by the pressure changes that occur with respiration. F, Doppler shift frequency, which is proportional to velocity. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

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Foot b

R Supine

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0 C

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Venous pressure (mm Hg)

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0 c

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b

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40 Walking in place

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The most common manifestations of abnormal venous function are primary varicose veins and the post-thrombotic syndrome. Current evidence suggests that primary varicose veins are often familial. The initial abnormality in this condition appears to be incompetence of the terminal valves of the greater and lesser saphenous veins, which permits reflux of blood. With the passage of time, progressive incompetence of the other valves occurs. Dodd and Cockett also include patients with idiopathic perforator vein incompetence in the primary varicose vein group.60 Although this may be valid, it is likely that many of these incompetent perforators occur secondary to episodes of calf vein thrombosis that result in destruction of the valves. The flow abnormality produced by loss of valvular competence at any level of the venous system is easily demonstrated with a Doppler ultrasonic velocity detector. The flow patterns shown in Figure 13-25 are from the greater saphenous vein of a patient with primary varicose veins. In the supine position, flow with calf contraction is antegrade, with a slight and transient period of reflux during relaxation; however, with standing, the opposite is noted, with flow being toward the foot. Walking in place clearly illustrates the rapid changes in direction that occur with each step as a result of loss of valvular competence. When the pressure in the veins on the dorsum of the foot is measured during exercise in a patient with primary varicose veins, the deviations from normal are evident (Fig. 13-26). The pressure does not fall to normally low levels, and it returns to the pre-exercise level much faster when walking is stopped. If a tourniquet is placed around the upper calf, this

seconds

Head

10

pattern is normalized as long as the valves in the deep system are competent. With the development of acute deep vein thrombosis, two major factors determine the long-term outcome: the location and extent of the residual venous obstruction, and the condition of the valves below the knee in the area of the calf

1.0% volume change

ABNORMAL PRESSURE AND FLOW RELATIONSHIPS

0

C

FIGURE 13–25 • Venous velocity changes recorded from an incompetent greater saphenous vein in a patient with primary varicose veins. The effects of muscular contraction (C) and relaxation (R) are indicated for the supine and standing positions. The bidirectional flow that occurs with walking is also shown. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

Venous pressure (mm Hg)

FIGURE 13–24 • Effect of a cough (c) and a Valsalva maneuver (b) on the venous pressure in a patient with a competent valve at the iliofemoral level. Upper panel, Pressure changes above the valve. Lower panel, Pressure changes below the valve. (From Ludbrook J, Beale G: Femoral venous valves in relation to varicose veins. Lancet 1:79-81, 1962.)

C

Calf volume

150 100 50

Venous pressure dorsum of foot

0

Exercise FIGURE 13–26 • Calf volume and venous pressure changes recorded from a dorsal foot vein of a patient with primary varicose veins. The pressure does not fall to the low levels seen in normal subjects, and it returns to the baseline much faster. (From Strandness DE, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975.)

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C

Venous pressure (mm Hg) 1 2 3 4 5 6 7 8 9 10 11 1213 Time (sec)

A

Venous pressure (mm Hg)

FIGURE 13–27 • Pressure changes in the greater saphenous vein at the ankle during four steps. In each panel, the normal response is noted by the solid line. A, Primary varicose veins and no leg ulcers. B, Varicose veins, incompetent ankle perforators, normal deep veins, no leg ulcers. C, Varicose veins, incompetent ankle perforators, normal deep veins, leg ulcers present. D, Varicose veins, incompetent ankle perforators, abnormal deep veins, leg ulcers present. (From Arnoldi CC, Linderholm H: On the pathogenesis of the venous leg ulcer. Acta Chir Scand 134:427-440, 1968.)

100 80 60 40 20 0 ⫺20 ⫺40 ⫺60

100 80 60 40 20 0 ⫺20 ⫺40 ⫺60 1 2 3 4 5 6 7 8 9 10 11 1213 Time (sec)

muscle pump.61-64 Because these vary greatly from one patient to another, it is not surprising that the pressure responses also show a wide variation. Four examples of the types of patterns that can be observed are shown in Figure 13-27. It is clear that even with primary varicose veins, the pressure changes at the level of the foot are abnormal with exercise (see Figs. 13-26 and 13-27). However, patients with this very common condition generally complain of minimal edema and rarely develop ulceration. The factors that appear to be responsible for the development of post-thrombotic syndrome relate primarily to the status of the deep veins below the knee and the perforating veins. The most abnormal venous pressures and flows occur in the area where ulceration develops and are due to valvular incompetence in both the distal deep veins and their connections with the superficial venous system. With this combination, the very high pressures that can be generated by activation of the calf muscle pump result in ambulatory venous hypertension in the lower leg. Browse and Burnand, in 1978, offered a reassessment of the factors responsible for the development of post-thrombotic syndrome.65 They recognized that the clinical condition could occur only with damage to the deep venous system and postulated that the abnormally high venous pressures would lead to the development of multiple new capillaries in the dermis, with large pores in the venular side. As a result, there would be extravasation of large molecules such as fibrinogen and coagulation factors. These, in conjunction with tissue factors, would lead to the conversion of fibrinogen to fibrin. If this were combined with inadequate fibrinolysis, fibrin would accumulate in the tissues and produce a barrier to the diffusion of both oxygen and nutrients. The end result would be tissue anoxia and death of the skin in the affected region.

D

243

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Hemodynamics for the Vascular Surgeon

100 80 60 40 20 0 ⫺20 ⫺40 ⫺60 1 2 3 4 5 6 7 8 9 10 11 1213 Time (sec)

Hemodynamic Principles and the Treatment of Venous Disease In contrast to the arterial side of the circulation, there are very few direct therapeutic approaches that can correct the underlying hemodynamic abnormalities of venous disease. Although obstruction of inflow to a limb is the most commonly treated arterial abnormality, mechanical interference with venous outflow is a rare cause of chronic venous insufficiency. One exception to this observation is the patient with venous claudication. This entity is uncommon and may not be recognized. It occurs in the specific clinical setting of chronic iliofemoral venous occlusion. In most cases, the major deep veins distal to the groin are patent and competent. With vigorous exercise, the patient is unable to adequately decompress the deep venous system, and the thigh becomes tense and very painful. After the patient stops exercising, it often requires 15 to 30 minutes for the pain and tightness to disappear. It is important to recognize that this syndrome rarely occurs with ordinary exercise and thus tends to be seen in relatively young patients who indulge in vigorous activities such as jogging, skiing, or tennis. The underlying mechanism of venous claudication involves the collateral veins that bypass the obstructed segment and have a relatively high, fixed resistance.66 This high outflow resistance results in a marked increase in venous volume during exercise. In some circumstances, it may be feasible to provide therapeutic relief with a crossover saphenous vein graft using the proximal saphenous vein from the opposite limb. This is rarely done, however, because the symptoms in most patients produce only minimal disability.

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Other surgical procedures designed to treat chronic venous insufficiency do so by either removing the offending vein or interrupting it at some point in its course. This is done to eliminate sites of reflux and restore the pressure-flow relationship to normal. The value of this particular approach is limited because the most common site of the disease responsible for chronic venous insufficiency is the distal deep veins, an area that is not amenable to direct surgical intervention. There has been a good deal of interest in promoting valvular competence in the proximal superficial femoral vein. This has been done by a direct surgical approach through a longitudinal venotomy or by transposition of a competent venous valve.67,68 The validity of these techniques is questionable, however, because there is no evidence to support the concept of the so-called critical valve; the alterations of pressure and flow are nearly always secondary to deep venous abnormalities in the distal limb, and proof of the effectiveness of such an approach is currently lacking. The most common form of therapy for chronic venous insufficiency is the use of support stockings that provide external compression and thus minimize the amount of edema that occurs during ambulation.69 The exact mechanism of compression therapy remains poorly understood.70 In theory, the stocking should reduce the transmural venous pressure gradient in a graduated fashion, with the highest compression pressures in the ankle area and diminishing pressures proximally up the limb. The amount of pressure exerted by a stocking depends on the elastic tension in the garment and the radius of the limb. Compression pressure should be in the range of 80 to 90 mm Hg while standing, 50 to 60 mm Hg while sitting, and 0 mm Hg in the recumbent position. This is obviously not possible with any single stocking, so a compromise must be accepted. Elevation of the legs above the level of the heart is also a standard method for relieving the symptoms of chronic venous insufficiency. The physiologic basis for the use of elevation depends on three major effects: it reduces venous pressure by decreasing the hydrostatic component related to gravity; it promotes the reabsorption of edema fluid; and it prevents ambulatory venous hypertension. Periodic elevation and external compression therapy are essential for the treatment of chronic venous insufficiency. When strictly adhered to, a regimen of elevation and compression minimizes edema, improves skin nutrition, and avoids ulceration in the majority of patients.

Conclusion The fundamental principles of hemodynamics often seem remote from the everyday clinical problems faced by vascular surgeons. The purpose of this chapter has been to show how these mathematical and physical concepts provide the basis for a rational approach to the pathophysiology, diagnosis, and treatment of vascular disease. These principles are also important for understanding the noninvasive diagnostic techniques that are discussed elsewhere in this book. The use of objective hemodynamic data is an essential step in the clinical evaluation of patients. This increased reliance on physiologic testing should encourage vascular surgeons to consider patients with vascular disease in terms of basic hemodynamic principles.

KEY REFERENCES Berguer R, Hwang NHC: Critical arterial stenosis—a theoretical and experimental solution. Ann Surg 180:39-50, 1974. Carter SA: Response of ankle systolic pressure to leg exercise in mild or questionable arterial disease. N Engl J Med 287:578-582, 1972. Flanigan DP, Tullis JP, Streeter VL, et al: Multiple subcritical arterial stenosis: Effect on poststenotic pressure and flow. Ann Surg 186:663-668, 1977. Johnson BF, Manzo RA, Bergelin RO, 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 oneto six-year follow-up. J Vasc Surg 21:307-313, 1995. Killewich LA, Martin R, Cramer M, et al: Pathophysiology of venous claudication. J Vasc Surg 1:507-511, 1984. Ku DN, Giddens DP, Phillips DJ, et al: Hemodynamics of the normal human carotid bifurcation—in vitro and in vivo studies. Ultrasound Med Biol 1:13-26, 1985. May AG, Van de Berg L, DeWeese JA, Rob CG: Critical arterial stenosis. Surgery 54:250-259, 1963. Phillips DJ, Greene FM Jr, Langlois Y, et al: Flow velocity patterns in the carotid bifurcations of young, presumed normal subjects. Ultrasound Med Biol 1:39-49, 1983. Sumner DS, Strandness DE Jr: The hemodynamics of the femorofemoral shunt. Surg Gynecol Obstet 134:629-636, 1972. Sumner DS, Strandness DE Jr: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65:763-771, 1969.

REFERENCES 1. Sumner DS: The hemodynamics and pathophysiology of arterial disease. In Rutherford RB (ed): Vascular Surgery. Philadelphia, WB Saunders, 1977, pp 25-46. 2. Burton AC: Physiology and Biophysics of the Circulation, 2nd ed. St. Louis, Mosby-Year Book, 1972, pp 86-94. 3. Strandness DE Jr, Sumner DS: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975. 4. Barnes RW: Hemodynamics for the vascular surgeon. Arch Surg 115:216-223, 1980. 5. Attinger EO: Flow patterns in vascular geometry. In Attinger EO (ed): Pulsatile Blood Flow. New York, McGraw-Hill, 1964, pp 179-200. 6. Gutstein WH, Schneck DJ, Marks JO: In vitro studies of local blood flow disturbance in a region of separation. J Atheroscler Res 8:381-388, 1968. 7. Logerfo FW, Soncrant T, Teel T, Dewey F: Boundary layer separation in models of side-to-end arterial anastomoses. Arch Surg 114:1364-1373, 1979. 8. Zarins CK, Giddens DP, Glagov S: Atherosclerotic plaque distribution and flow velocity profiles in the carotid bifurcation. In Bergan JJ, Yao JST (eds): Cerebrovascular Insufficiency. New York, Grune & Stratton, 1983, pp 19-30. 9. Ku DN, Giddens DP, Phillips DJ, et al: Hemodynamics of the normal human carotid bifurcation—in vitro and in vivo studies. Ultrasound Med Biol 1:13-26, 1985. 10. Phillips DJ, Greene FM Jr, Langlois Y, et al: Flow velocity patterns in the carotid bifurcations of young, presumed normal subjects. Ultrasound Med Biol 1:39-49, 1983. 11. Reneman RS, van Merode T, Hick P, et al: Flow velocity patterns in and distensibility of the carotid artery bulb in subjects of various ages. Circulation 71:500-509, 1985. 12. Fox JA, Hugh AE: Localization of atheroma: A theory based on boundary layer separation. Br Heart J 28:388-394, 1966. 13. Milnor WR: Pulsatile blood flow. N Engl J Med 287:27-34, 1972. 14. Malan E, Noseda G, Longo T: Approach to fluid dynamic problems in reconstructive vascular surgery. Surgery 66:994-1003, 1969. 15. McDonald DA: Blood Flow in Arteries, 2nd ed. London, Edward Arnold, 1974. 16. Goaling RG, Newman DL, Bowden NLR, et al: The area ratio of normal aortic junctions—aortic configuration and pulse wave reflection. Br J Radiol 44:850-853, 1971. 17. Lalleman RC, Gosling RG, Newman DL: Role of the bifurcation in atheromatosis of the abdominal aorta. Surg Gynecol Obstet 137:987-990, 1973. 18. Sumner DS, Hokanson DE, Strandness DE Jr: Arterial walls before and after endarterectomy, stress-strain characteristics and collagen-elastin content. Arch Surg 99:606-611, 1969.

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19. Sumner DS, Hokanson DE, Strandness DE Jr: Stress-strain characteristics and collagen-elastin content of abdominal aortic aneurysms. Surg Gynecol Obstet 130:459-466, 1970. 20. Scherer PW: Flow in axisymmetrical glass model aneurysms. J Biomech 6:695-700, 1973. 21. Darling RC: Ruptured arteriosclerotic abdominal aortic aneurysms—a pathologic and clinical study. Am J Surg 119:397-401, 1970. 22. Roach MR: Changes in arterial distensibility as a cause of poststenotic dilatation. Am J Cardiol 12:802-815, 1963. 23. Berguer R, Hwang NHC: Critical arterial stenosis—a theoretical and experimental solution. Ann Surg 180:39-50, 1974. 24. May AG, Van de Berg L, DeWeese JA, Rob CG: Critical arterial stenosis. Surgery 54:250-259, 1963. 25. James IM, Millar RA, Purves MY: Observations on the intrinsic neural control of cerebral blood flow in the baboon. Circ Res 25:77-93, 1969. 26. Moore WS, Hall AD: Unrecognized aortoiliac stenosis—a physiologic approach to the diagnosis. Arch Surg 103:633-638, 1971. 27. Carter SA: Response of ankle systolic pressure to leg exercise in mild or questionable arterial disease. N Engl J Med 287:578-582, 1972. 28. Sumner DS, Strandness DE Jr: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65:763-771, 1969. 29. Flanigan DP, Tullis JP, Streeter VL, et al: Multiple subcritical arterial stenosis: Effect on poststenotic pressure and flow. Ann Surg 186:663-668, 1977. 30. Longland CJ: The collateral circulation of the limb. Ann R Coll Surg Engl 13:161-176, 1953. 31. John HT, Warren R: The stimulus to collateral circulation. Surgery 49:14-25, 1961. 32. Skinner JS, Strandness DE Jr: Exercise and intermittent claudication. II. Effect of physical training. Circulation 36:23-29, 1967. 33. Ludbrook J: Collateral artery resistance in the human lower limb. J Surg Res 6:423-434, 1966. 34. Sumner DS, Strandness DE Jr: The effect of exercise on resistance to blood flow in limbs with an occluded superficial femoral artery. Vasc Surg 4:229-237, 1970. 35. Keitzer WF, Fry WT, Kraft RO, et al: Hemodynamic mechanism for pulse changes seen in occlusive vascular disease. Surgery 57:163-174, 1965. 36. Strandness DE Jr, Bell JW: Peripheral vascular disease: Diagnosis and objective evaluation using a mercury strain gauge. Ann Surg 161(Suppl):1-35, 1965. 37. Yao JST: Hemodynamic studies in peripheral arterial disease. Br J Surg 57:761-766, 1970. 38. Zierler RE, Strandness DE Jr: Doppler techniques of lower extremity arterial diagnosis. In Zwiebel WJ (ed): Introduction to Vascular Ultrasonography, 2nd ed. New York, Grune & Stratton, 1986, pp 305-331. 39. Reivich MH, Holling HE, Roberts B, Toole JF: Reversal of blood flow through the vertebral artery and its effect on the cerebral circulation. N Engl J Med 265:878-885, 1961. 40. Gonzales L, Weintraub RA, Wiot JF, Lewis C: Retrograde vertebral artery blood flow: A normal phenomenon. Radiology 82:211-216, 1964. 41. Kelly WA, Strandness DE Jr: The subclavian steal syndrome. In Strandness DE Jr (ed): Collateral Circulation in Clinical Surgery. Philadelphia, WB Saunders, 1969, pp 570-582. 42. Ehrenfeld WK, Harris JD, Wylie EJ: Vascular “steal” phenomenon—an experimental study. Am J Surg 116:192-197, 1968. 43. Shin CS, Chaudhry AG: The hemodynamics of extraanatomic bypass grafts. Surg Gynecol Obstet 148:567-570, 1979. 44. Sumner DS, Strandness DE Jr: The hemodynamics of the femorofemoral shunt. Surg Gynecol Obstet 134:629-636, 1972. 45. Mozersky DJ, Sumner DS, Barnes RW, et al: The hemodynamics of the axillary-axillary bypass. Surg Gynecol Obstet 135:925-929, 1972. 46. Larsen DA, Lassen NA: Medical treatment of occlusive arterial disease of the legs—walking exercise and medically induced hypertension. Angiologica 6:288-301, 1969. 47. Freiman DB, Ring EJ, Oleaga JA: Transluminal angioplasty of the iliac, femoral, and popliteal arteries. Radiology 132:285-288, 1979. 48. Strandness DE Jr, Bell JW: Ankle pressure responses after reconstructive arterial surgery. Surgery 59:514-516, 1966. 49. Coffman JD, Mannick JA: Failure of vasodilator drugs in arteriosclerosis obliterans. Ann Intern Med 76:35-39, 1972. 50. Strandness DE Jr: Ineffectiveness of isoxsuprine on intermittent claudication. JAMA 213:86-88, 1970. 51. Strandness DE Jr: Role of sympathectomy in the treatment of arteriosclerosis obliterans and thromboangiitis obliterans. In Strandness DE Jr (ed): Collateral Circulation in Clinical Surgery. Philadelphia, WB Saunders, 1969, pp 450-459.

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52. Barnes RW, Baker WH, Shanik G: Value of concomitant sympathectomy in aortoiliac reconstruction. Arch Surg 112:1325-1330, 1977. 53. Gruber UF: Dextran and the prevention of postoperative thromboembolic complications. Surg Clin North Am 55:679-696, 1975. 54. Porter JM, Cutler BS, Lee BY, et al: Pentoxifylline efficacy in the treatment of intermittent claudication: Multicenter controlled double-blind trial with objective assessment of chronic occlusive disease patients. Am Heart J 104:66-72, 1982. 55. Strandness DE Jr, Thiele BL: Anatomy of the venous system of the lower limb. In Selected Topics in Venous Disorders. New York, Futura, 1981, pp 1-26. 56. Gauer OH, Thron HL: Postural changes in the circulation. In Hamilton WF, Dow P (eds): Handbook of Physiology. Section 2: Circulation, vol 3. Washington, DC, American Physiological Society, 1965, pp 2409-2439. 57. Holling HE, Verel D: Circulation of the elevated forearm. Clin Sci 16:197-213, 1957. 58. Henry JP, Slaughter OL, Greiner T: A medical massage suit for continuous wear. Angiology 6:482-494, 1955. 59. Pollack AA, Wood EH: Venous pressure in the saphenous vein at the ankle in man during exercise and changes in posture. J Appl Physiol 1:649-662, 1949. 60. Dodd H, Cockett FB: The Pathology and Surgery of the Veins of the Lower Limbs. Edinburgh, Churchill Livingstone, 1976. 61. Strandness DE Jr, Langlois YE, Cramer M, et al: Long-term sequelae of acute venous thrombosis. JAMA 250:1289-1292, 1983. 62. van Bemmelen PS, Bedford G, Beach K, et al: Status of the valves in the superficial and deep venous system in chronic venous disease. Surgery 109:730-734, 1990. 63. Markel A, Manzo RA, Bergelin RO, et al: Valvular reflux after deep vein thrombosis: Incidence and time of occurrence. J Vasc Surg 15:377-384, 1992. 64. Johnson BF, Manzo RA, Bergelin RO, 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 21:307-313, 1995. 65. Browse NL, Burnand KG: The postphlebitic syndrome—a new look. In Bergan JJ, Yao JST (eds): Venous Problems. St Louis, Mosby-Year Book, 1978, pp 395-404. 66. Killewich LA, Martin R, Cramer M, et al: Pathophysiology of venous claudication. J Vasc Surg 1:507-511, 1984. 67. Kistner RL: Transvenous repair of the incompetent femoral vein valve. In Bergan JJ, Yao JST (eds): Venous Problems. St Louis, Mosby-Year Book, 1975, pp 493-509. 68. Queral LA, Whitehouse WM, Flinn WR, et al: Surgical correction of chronic deep venous insufficiency by valvular transposition. Surgery 87:688-695, 1980. 69. Husni EA, Ximenes JOC, Goyette EM: Elastic support of the lower limbs in hospital patients—a critical study. JAMA 214:1456-1462, 1970. 70. Mayberry JC, Moneta GL, DeFrang RD, et al: The influence of elastic compression stockings on deep venous hemodynamics. J Vasc Surg 13:91-100, 1991.

Questions 1. Viscous energy losses in flowing blood result from which of the following? (a) Changes in the velocity and direction of flow (b) Friction between adjacent layers of moving blood (c) Turbulent flow in areas of stenosis (d) Disturbed flow at points of branching (e) Areas of boundary layer separation 2. Poiseuille’s law states that pressure gradients in an idealized flow model are inversely proportional to which of the following? (a) Mean flow velocity (b) Tube or stenosis length (c) Blood viscosity (d) Tube or stenosis radius (e) Volume flow rate

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3. Inertial energy losses in blood flow are related primarily to which of the following? (a) Changes in the velocity and direction of flow (b) Blood viscosity (c) Specific gravity of blood (d) Friction between adjacent layers of moving blood (e) Mean blood pressure 4. The critical stenosis value for a particular artery depends on which of the following? (a) Length of the arterial segment (b) Tangential wall stress (c) Blood viscosity (d) Compliance of the arterial wall (e) Flow rate and peripheral vascular resistance 5. Which of the following statements about the collateral circulation is false? (a) Collateral vessels are preexisting pathways that enlarge when the parallel major artery is occluded (b) The vascular resistance of the collateral bed is relatively fixed (c) Collateral artery resistance is usually less than that of the original unobstructed parallel artery (d) An abnormal pressure gradient across the collateral bed may stimulate the further development of collateral pathways (e) The midzone of the collateral bed consists of small, intramuscular vessels 6. Which of the following is not related to tangential stress and rupture of arterial aneurysms? (a) Volume flow rate through the aneurysm (b) Arterial blood pressure (c) Internal radius of the aneurysm (d) Tensile strength of collagen (e) Thickness of the aneurysm wall 7. With an extra-anatomic bypass, such as a femorofemoral crossover graft, a vascular steal from the “donor” limb is most likely to occur in which of the following circumstances? (a) There is occlusive disease in both the donor and the recipient limbs (b) There is an occlusive lesion in the donor artery (c) Severe occlusive disease is present in the donor limb (d) The recipient limb has only mild occlusive disease (e) The donor limb is hemodynamically normal

8. Venous claudication is characterized by all of the following except (a) Chronic iliofemoral venous occlusion (b) Thigh pain with vigorous exercise (c) High-resistance venous collaterals (d) Minimal disability with ordinary activities (e) Valvular incompetence in the tibial veins 9. Which of the following is not a function of the calf muscle pump? (a) It lowers venous pressure in the dependent limb (b) It reduces venous volume in the exercising limb (c) It improves arterial blood flow to the exercising muscle (d) It increases venous return to the right heart (e) It minimizes the accumulation of interstitial fluid in the distal limb 10. All of the following contribute to the pathogenesis of the post-thrombotic syndrome except (a) Deep vein thrombosis with chronic obstruction of the deep veins (b) Extravasation of blood components into the subcutaneous tissues (c) Incompetence of the venous valves in the deep veins below the knee (d) The presence of primary varicose veins (e) Ambulatory venous hypertension

Answers 1. b 6. a

2. d 7. b

3. a 8. e

4. e 9. c

5. c 10. d

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14

J. Dennis Baker

The Noninvasive Vascular Laboratory In the early days of vascular surgery, patient assessment was based on a careful history and physical examination. Although a few clinicians used the Collins oscillometer to estimate the pulse pressure in an extremity, there was little help available in terms of quantitative assessment of arterial or venous disease. Angiography provided the only objective determination of pathologic changes. Early experience with arteriography and phlebography highlighted some of the limitations of these techniques, especially the problem of underestimating the severity of stenotic lesions on singleplane studies. In addition, the cost, patient discomfort, and risk of complications associated with contrast studies precluded their routine use for screening evaluations and follow-up. The growing interest in more accurate differential diagnosis, localization of disease, determination of its severity, and documentation of progression stimulated the development of objective measurement techniques. In the 1960s, investigators started working with different plethysmographic techniques to quantitate arterial occlusive disease in the leg. Modification of ultrasound equipment to measure blood flow by the Doppler shift principle represented an important step forward in instrumentation and led to the rapid development of noninvasive studies. Additional techniques were designed to evaluate carotid artery disease as well as deep venous occlusion and insufficiency. This chapter describes the main diagnostic techniques used in the noninvasive laboratory and discusses their clinical application for patients with vascular disease. With an understanding of the merits and limitations of each method, clinicians can make the best use of these tests.

Instrumentation DOPPLER VELOCITY MEASUREMENT TECHNIQUES High-frequency sound waves (2 to 10 MHz) penetrate soft tissues and are reflected by the different interfaces encountered. Reflection from a moving interface results in the reflected frequency being increased if the motion is toward the point of observation and decreased if the motion is away

from it. The magnitude of the shift is determined by the following equation: fs =

2Vf0 cos φ C

where fs is the frequency shift, V the velocity, f0 the transmitted frequency, φ the angle between the ultrasound beam and the velocity vector, and C the speed of sound in tissue (1540 m/sec). For a given velocity, a greater frequency shift is obtained with a higher transmitting frequency. In contrast, tissue penetration varies inversely with probe frequency, so the selection of a frequency for a given application is a balance between depth and velocity requirements. Continuous-wave detectors are the simplest systems. The probe has two separate crystals, one transmitting and one receiving continuously. This system detects all velocities within the intersecting paths of the sound beams. If this zone includes more than one vessel (e.g., an artery and a vein), the resulting signal represents a combination of both velocities. Pulsed Doppler systems use a single crystal that repeatedly transmits a short burst of sound followed by a waiting period, during which the crystal functions in a receiving mode. By selecting the time and duration of the listening phase, one can define a sample volume, or the portion of the vessel from which velocity is to be measured. Modern duplex scanners use complex scan probes made up of many elements in an array, but the principle of selective sampling is the same. The shifted frequency obtained from a vessel is within the audible range, so the data can be presented to the examiner as an audio signal. Although qualitative interpretation is helpful in some patient examinations, quantitative measurements provide more objective testing. Spectral analyzers are used to determine the main frequency components obtained from a given vessel. This information is usually displayed on a sonogram, which shows the frequency content in time (Fig. 14-1). In some applications, it is more useful to have a measure of velocity rather than the raw frequency data. If the probe angle can be measured, the velocity is estimated using the Doppler equation. The accuracy of the estimate depends greatly on the accuracy of the angle measurement. Errors are greatest when the probe is at a right angle to flow and 247

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FIGURE 14–1 • Comparison of sonograms from continuous-wave (CW) and pulsed Doppler systems. Sonograms display the different frequency contents detected at each point in time. The CW system detects all velocities across the vessel, whereas the pulsed system detects only those velocity vectors within the sample volume, indicated by the marks on the ultrasound beam. A, Normal arterial signals. CW has more low-frequency content, because it detects flow near the walls as well as in the center stream. B, Within stenosis, there is increased peak frequency, and the frequency distributions of both types of Doppler systems are similar, because the sample volume encompasses the entire flow stream. C, Beyond stenosis, peak frequency is elevated, with increased frequency distribution resulting from turbulent flow. Spectral width is greater with CW systems.

Spectral width

CW

Pulsed

A

B

least when it is at a low angle. Whenever possible, velocities should be measured with an angle less than 60 degrees. DUPLEX SCAN During the 1960s, B-mode ultrasound imaging was used for visualization of soft tissue structures. Although early devices had only crude resolution, equipment has improved to the point that clear, detailed images of vessels can be produced in real time (Fig. 14-2). In general, experience shows that when high-quality imaging is obtained, the diagnostic accuracy is very high; however, in patients with advanced atherosclerosis, it is difficult to obtain optimal studies, and diagnostic accuracy is lower. A common problem is incomplete imaging of the vessel wall as a result of calcification, which is present in varying degrees in up to half of patients studied. The extent of interference may be limited, but in some vessels there is no visualization of substantial portions of the artery. Although calcified plaques stand out sharply in the ultrasound image, some atheromas are visualized poorly or not at all. A major source of error is that recent thrombus may have the same echo density as flowing blood, so that an occluded vessel may look normal on the ultrasound image. To overcome the limitations of ultrasound imaging, the research team at the University of Washington developed the duplex scanner, combining a real-time B-mode ultrasound image system with a pulsed Doppler detector.1 The ultrasound image shows not only the vessel under study but also the location of the sample volume of the Doppler beam so that the examiner can position it to study velocity patterns at specific locations in the vessel. The device can study calcified vessels by analyzing the Doppler velocity signal distal to the areas of calcification. The evaluation of the Doppler signal from the common carotid artery and its branches is carried out using spectral analysis (Fig. 14-3). Based on the peak systolic velocity, end-diastolic velocity, velocity ratios, and

C

degree of spectral broadening, a category of stenosis is assigned to the vessel segment. In the past 20 years, there has been extensive improvement of duplex scanners in terms of both image resolution and Doppler signal processing. The early devices were limited to the study of superficial vessels; however, the availability of low-frequency probes (2.0 to 3.5 MHz) permits the evaluation of abdominal vessels, including the aorta, vena cava, and main visceral branches. Study of intracranial artery branches is also possible. The most recent development is the color-coded Doppler system. A linear array transducer composed of many separate elements is used to produce a grid of sample volumes encompassing the area covered by the B-mode image (Fig. 14-4). A portion of the grid is selected for color coding of velocity information. Each of the sample volumes within the area is examined. If the returning ultrasound signal has no change in phase or frequency, the amplitude information is used to create the gray-scale image at that point in the matrix. If there is a change in phase or frequency, the information is analyzed in terms of velocity. A color is assigned to represent the mean velocity occurring at that point in the field. Red and blue show flow toward and away from the transducer, respectively. The magnitude of the velocity is represented by the hue of the color: a dark shade indicates slow flow, and a lighter shade or white indicates high flow. The aggregate of the color representation from the sample volumes detecting motion produces a real-time representation of the flow patterns within the vessels superimposed on the gray-scale image of the stationary tissue. Figure 14-5 (see color plate) illustrates examples of the advantages of color duplex scans. A more recent development is color coding of the Doppler power (as opposed to velocity) detected. Power is proportional to the square of the velocity, so this measurement provides more sensitive detection of very slow flow or flow in small vessels. A good example of the benefit of power imaging is the detection of

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A B

FIGURE 14 –2 • B-mode images from carotid duplex scan. A, Normal bifurcation. B, Moderate heterogeneous plaque with varying echogenicity. C, Calcified lesion with high echogenicity and shadowing below the plaque. CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

C

an internal carotid string sign. Squaring the velocity eliminates the positive or negative value, so that power values have no directional representation. Power is represented in a single color, usually orange.

Carotid Artery Studies The internal carotid artery (ICA) poses a unique challenge to physical examination, because it is impossible to palpate a distal pulse. It is not uncommon to find a patient whose carotid pulse in the neck is normal to palpation but who has occlusion of the internal carotid branch. This limitation stimulated the development of physiologic tests to assess the status of the ICA. Most of the early tests provided indirect measurement by detecting distal changes in blood flow characteristics produced by advanced stenosis. Common features of the indirect methods are that they detect only lesions that are sufficiently advanced to reduce mean blood flow, and they cannot separate a tight stenosis from an occlusion because the physiologic changes in the distal bed may be indistinguishable. These methods achieved a variable degree of clinical use in the 1970s and 1980s but were ultimately replaced by duplex scanning. DUPLEX SCAN The routine examination covers as much of the common carotid artery (CCA) and its branches as can be visualized with the configuration of the transducer used. In some patients,

the origins of the CCAs can be visualized. Figures 14-2A and 14-5A (see color plate) show normal carotid bifurcations. The color image demonstrates the reverse velocity detected in the carotid bulb as a result of the complex flow pattern at the bifurcation. Many older patients have tortuosity that precludes the CCA, the bulb, and the branches from being visualized in a single plane; in such cases, careful scanning is required to obtain satisfactory imaging. Figure 14-5B (see color plate) shows an example of tortuosity in an elderly patient. Although such arteries can be studied with a conventional scanner, the color-coded unit simplifies the examination. The scan usually identifies the pathologic regions, but with advanced atherosclerosis, it is often difficult to get an adequate image to accurately estimate the degree of stenosis. Much of the classification of stenosis is based on interpretation of the Doppler signal. The two branches are distinguished by the image and the velocity signals. The ICA has a low peripheral resistance at all times, resulting in forward flow throughout diastole, whereas the high resistance in the external carotid artery results in a diastolic flow of zero. Stenoses produce an increased velocity at the site of the lesion and turbulence beyond it (see Fig. 14-1). The turbulence is identified as spectral broadening on the sonogram (see Fig. 14-3). Mild stenoses may not produce a significant increase in peak systolic velocity but are identified by a moderate degree of spectral broadening. Based on the peak systolic velocity and the degree of spectral broadening, the ICA is placed into one of six diagnostic categories. There are two sets of criteria that have been

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A A

B

FIGURE 14–4 • Color-coded duplex system. A linear array transducer is used to create a matrix of sample volumes. A grayscale image is created within area A. Most examinations are carried out with color coding of velocities limited to a portion of the image (area B). Within this portion of the matrix, ultrasound signals from sample volumes with a change in phase or frequency are interpreted as velocity data. Otherwise, the data are coded as part of the gray-scale image.

B

C FIGURE 14–3 • Doppler sonograms from carotid duplex scans. A, Normal study with normal spectral width. B, Moderate stenosis with spectral broadening but no increase in peak frequency. (Note that frequency scales are different in the three records.) C, Severe stenosis with high peak velocity and extensive spectral broadening.

used for many years, and although some laboratories have made modifications or adjustments, the basic principles continue to be applied. The criteria developed at the University of Washington use primarily ICA velocity parameters (Table 14-1).2 Further improvements in accuracy may be obtained using ratios of ICA velocities to CCA velocities in normal portions of the artery (Table 14-2).3 The diagnosis of ICA occlusion must be based on image as well as Doppler information, because the very low flow found with some

“string signs” is below the velocity detection threshold of many scanners. Newer color duplex devices have improved our ability to find small residual flow channels, especially using power flow mapping. Both the stippled appearance of chronic thrombus and a small diameter of the ICA point to occlusion. Overall, low-grade stenoses are best assessed with the image, whereas advanced lesions are best evaluated with the Doppler information. There has been a rapid growth in the use of duplex scanning for carotid diagnosis. Different investigators have demonstrated that the technique can be highly accurate. Studies have shown rates of 92% to 96% accuracy in the identification of severe stenosis.4-6 When these studies are analyzed in terms of correct category of stenosis, exact agreement is found in 77% to 87%, with poor agreement in only 1% to 2%. Of particular importance is the fact that experienced laboratories make very few errors in separating severe stenosis from occlusion. Mansour and coauthors reported a 98% positive predictive value and 99% negative predictive value in the correct determination of ICA occlusion.7

TABLE 14–1 Categories of Internal Carotid Artery (ICA) Stenosis: University of Washington Criteria ICA Stenosis

ICA Velocity

Spectrum

Normal vessel 1-19% 20-59% 60-79% 80-99%

Peak systolic velocity < 125 cm/sec Peak systolic velocity < 125 cm/sec Peak systolic velocity < 125 cm/sec Peak systolic velocity < 125 cm/sec; end-diastolic velocity < 125 cm/sec End-diastolic velocity < 125 cm/sec (severe stenosis may have very low velocity) No ICA Doppler signal; flow to zero in common carotid artery

No broadening Limited broadening in late systole Broadening throughout systole Broadening throughout systole Broadening throughout systole

Occlusion

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TABLE 14–2

251

Categories of Internal Carotid Artery (ICA) Stenosis: Bluth Criteria

ICA Stenosis

Peak Systolic Velocity

Diastolic Velocity

ICA/CCA Velocity

Normal vessel 1-39% 40-59% 60-79% 80-99% Occlusion

100 cm/sec No ICA Doppler signal

65 >65 55-75 55-75 >55 >55

16.0 13.0 11.7 11.9 24.6 9.1 13.9 11.4 11.0 8.6 16.9 20.5

Risk Factors SMOKING The specific mechanisms by which tobacco exerts its adverse effects on arteries remain poorly understood; however, a direct relationship between tobacco smoking and peripheral vascular disease has been well established.22 All epidemiologic studies of lower extremity arterial disease have confirmed cigarette smoking as a strong risk factor for the development of such disease, with relative risk ratios ranging from 1.7 to 7.5.1,10,12,23-27 A case-control study revealed a sevenfold higher risk of developing PAD in ex-smokers compared with those who had never smoked, and the risk increased to 16-fold in current smokers compared with those who had never smoked.28 The diagnosis of lower extremity arterial disease is made up to a decade earlier in smokers compared with nonsmokers. More than 90% of all patients referred to vascular clinics for PAD have a history of smoking.29 In addition to the chronic effects of smoking on the development of atherosclerosis, smoking has acute effects on lower extremity function. Smoking two cigarettes within a 10-minute period resulted in an acute lowering of the ABI in chronic smokers from 0.64 ± 0.14 to 0.55 ± 0.11 (P = 0.008).30 In addition to having adverse influences on atherosclerosis, the carbon monoxide in tobacco smoke may directly contribute to claudication. Smoking is associated with acute drops in treadmill walking distances, presumably owing to carbon monoxide.31 An immediate and significant decrease in the time or distance that patients can walk on the treadmill before they get claudication symptoms has been demonstrated when air containing carbon monoxide is breathed.31,32 Smokers have an increased risk of peripheral vascular disease progression,33 myocardial infarction, stroke, and death.34 Smokers also have an increased risk of major amputation.35,36 DIABETES MELLITUS A strong association exists between diabetes mellitus and PAD. Two types of vascular disease are seen in patients with diabetes: microcirculatory dysfunction involving the capillaries and arterioles of the kidneys, retina, and peripheral nerves,

and a macroangiopathy involving the peripheral and coronary arterial circulation.37 The Framingham Study was one of the first major epidemiologic studies to demonstrate the association between diabetes and PAD. Diabetes increased the risk of claudication by a factor of 3.5 in men and 8.6 in women.38 Numerous subsequent studies have associated impaired glucose tolerance with a two- to fourfold increase in the risk of developing intermittent claudication.39-44 In an elderly white population, 20.9% of patients with diabetes mellitus and 15.1% of patients with an abnormal glucose tolerance test had an ABI less than 0.9.45 In a Swedish study, 21% of patients with diabetes had signs of PAD.46 The duration and severity of diabetes mellitus correlate strongly with the incidence and severity of PAD. Patients with diabetes mellitus often develop symptomatic forms of PAD and have poorer lower extremity function than do those with PAD alone.47 The prevalence of diabetes in patients undergoing lower extremity revascularization ranges from 25% to 50%, compared with a prevalence of 6% in the general population.48 The rate of lower extremity amputation is 7- to 10-fold higher in diabetic patients than in those without diabetes,23,49-51 and in fact, diabetes leads to most nontraumatic lower extremity amputations in the United States. In addition to diabetes, insulin resistance and hyperinsulinemia are risk factors for PAD.26,52 GENDER Early epidemiologic studies focused on the prevalence of PAD in men. The popular notion based on the Framingham Study was that symptomatic PAD in women lagged behind men by 10 years53 and that women were generally not affected by PAD until after menopause. However, more recent epidemiologic studies indicate that PAD prevalence and incidence in men and women are similar. Several studies have demonstrated that the age-adjusted incidence of intermittent claudication is equal in both genders,20,54 with the frequency of PAD among diabetic women markedly higher than that among diabetic men.20 Among subjects with a low ABI, coronary artery disease was less prevalent among women. Women also had a lower frequency of cerebrovascular disease.54 In another study, the prevalence of PAD was almost identical in

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men and women; however, other cardiovascular disease was twice as prevalent in men.7 Progression of PAD in men and women is the same, with correction for other risk factors.55 Epidemiologic studies have shown that women may be more susceptible to aortoiliac arterial occlusive disease than men are.56 Autopsy findings also provide important information about gender differences in the occurrence of atherosclerotic changes in various arterial beds. Compared with men, women have a greater extent of fatty streaks in the abdominal aorta, but not in the coronary arteries.57 It is possible that PAD is underdiagnosed in women to a greater degree than in men. Studies have shown that women are less likely than men to be diagnosed with PAD on the basis of symptoms, even if clinically significant PAD is present on noninvasive examinations.58,59 Also, it has been shown that infrainguinal arterial reconstructions performed on women tend to be for more advanced disease compared with men, and the women tend to be older.60,61 The reasons for the more advanced presentation in women are unclear. It has been speculated that because women more frequently assume a caretaker role, they are more likely to ignore their own medical care; or perhaps women are more likely to ignore mild to moderate pain, attributing it to a consequence of “old age.”62 It is clear that the previous dictum of PAD being primarily a disease of men is changing as more data about its effect on women emerge.

A number of prospective and retrospective studies have suggested an association between elevated levels of plasma homocysteine and premature vascular disease in the coronary, cerebrovascular, and peripheral circulation.68-71 Early studies suggesting this association, however, were based on small numbers of patients. Darius and colleagues evaluated plasma homocysteine levels as an independent risk factor for PAD in 6880 primary care patients older than 65 years.72 Although PAD (defined as an ABI 24 hr and < 4 wk) Unstable angina (CCS class III or IV) Severe pulmonary disease Contralateral carotid occlusion Contralateral laryngeal nerve palsy Radiation therapy to neck Previous CEA with recurrent stenosis High cervical ICA lesions or CCA lesions below the clavicle Severe tandem lesions Age older than 80 yr *Based on the SAPPHIRE trial. At least one factor is required. CCA, common carotid artery; CCS, Canadian Cardiac Society; CEA, carotid endarterectomy; ICA, internal carotid artery.

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TABLE 21–2

357

Cumulative Incidence of Adverse Events at 30 Days Intention-to-Treat Analysis: No. of Patients (%) Stent (n = 167)

Event Death Stroke Major ipsilateral Major nonipsilateral Minor ipsilateral Minor nonipsilateral Myocardial infarction Q wave Non-Q wave Death, stroke, or myocardial infarction Major vascular complications

2 6 1 1 4 1 4 0 4 8

(1.2) (3.6) (0.6) (0.6) (2.4) (0.6) (2.4)

Endarterectomy (n = 167)

Actual Treatment Analysis: No. of Patients (%) P Value

Stent (n = 159)

Endarterectomy (n = 151)

P Value

(2.4) (4.8)

4 (2.5) 5 (3.1) 2 (1.2) 1 (0.6) 1 (0.6) 1 (0.6) 10 (6.1) 2 (1.2) 8 (4.9) 16 (9.8)

0.39 0.77 0.55 1.00 0.18 1.00 0.10 0.15 0.23 0.09

1 (0.6) 5 (3.1) 0 1 (0.6) 4 (2.5) 1 (0.6) 3 (1.9) 0 3 (1.9) 7 (4.4)

3 (2.0) 5 (3.3) 2 (1.3) 1 (0.7) 1 (0.7) 1 (0.7) 10 (6.6) 2 (1.3) 8 (5.3) 15 (9.9)

0.29 0.94 0.15 0.97 0.20 0.97 0.04 0.15 0.11 0.06

2 (1.2)

1 (0.6)

0.57

2 (1.3)

1 (0.7)

0.60

From Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 351: 1493-1501, 2004.

Freedom from Major Adverse Events (%)

high-risk patients. This trial was performed in stages as the CAS technique evolved and was refined. ARCHeR 1 used just the stent, ARCHeR 2 included the stent under embolic protection, and ARCHeR 3 used rapid-exchange systems for delivering the stent and the CPD. The major stroke or death rate in the first 30 days was low in all trials: 3.8%, 2.5%, and 2.8% for ARCHeR 1, 2, and 3, respectively (Fig. 21-2). At 1 year, the major adverse event rate was 8.3% and 10.2% for ARCHeR 1 and 2, respectively. Another high-risk registry, the Study to Evaluate the NeuroShield Bare Wire Cerebral Protection System and Xact Stent in Patients at High Risk for

100 Stent

90 80

Endarterectomy

70 60 50 0 0

30

60

90 120 150 180 210 240 270 300 330 360 Days after procedure

FIGURE 21–1 • Freedom from major adverse events at 1 year. The rate of event-free survival at 1 year was 88.0% among patients who received a stent, compared with 79.9% among those who underwent endarterectomy (P = 0.048). I-bars represent 1.5 times the standard error. (From Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in highrisk patients. N Engl J Med 351: 1493-1501, 2004.).

Carotid Endarterectomy (SECURITY), enrolled 305 patients and assessed the outcome of CAS with the MedNova NeuroShield bare wire filter and the Xact self-expanding carotid stent system (Abbott Laboratories, Abbott Park, Ill.).23 The composite rate of death, any stroke, and myocardial infarction at 30 days was 7.2%, whereas the expected rate in these patients (based on historical controls of CEA) would be 11% to 15%. The Boston Scientific/EPI: A Carotid Stenting Trial for High Risk Surgical Patients (BEACH) is another single-arm, prospective, nonrandomized trial that completed the enrollment of 480 patients in the pivotal phase of the trial. Early results were presented but have not been published yet.24 Figure 21-2 summarizes the reported outcomes of various trials. Because the majority of patients with carotid stenosis are either asymptomatic or not considered high risk for CEA, efforts have focused on defining the role of CAS in “realworld” patients with carotid disease. The multicenter, prospective, nonrandomized Carotid Revascularization Using Endarterectomy or Stenting Systems (CARESS) clinical trial was designed as an equivalence cohort study to determine whether the stroke and death rates following CAS with CPD were comparable to those for CEA in treating all patients with symptomatic (≥50%) and asymptomatic (≥75%) carotid stenosis.25 At 14 centers, 397 patients with carotid disease were treated—254 with CEA, and 143 with CAS. Both the 30-day and 1-year results of this phase I trial have been reported, with equivalent stroke and death rates following CAS with cerebral protection and CEA in a broad risk population of patients with carotid stenosis. The 30-day combined all-cause mortality and stroke rate for CEA and CAS was the same (2%), whereas the 30-day all-cause mortality, stroke, and myocardial infarction rates were 2% for CAS and 3% for CEA. The 1-year combined all-cause mortality and stroke rate was 13.6% for CEA and 10.0% for CAS, whereas the 1-year combined all-cause mortality, stroke, and acute myocardial infarction rate was 14.3% for CEA and 10.9% for CAS.

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TABLE 21–3

Carotid Stenting Trials

Trial Name

Type

Patient Population

Sponsor

Stent

CPD

SAPPHIRE CREST ARCHeR SECURITY MAVERIC BEACH CABERNET ArteriA CARESS

Randomized and registry Randomized Registry Registry Registry Registry Registry Registry Registry

High risk Low risk High risk High risk High risk High risk High risk High and low risk High and low risk

Cordis, JNJ NINDS, Guidant Guidant MedNova, Abbott Medtronic BSC BSC ArteriA ISES

Precise AccuLink AccuLink Xact Exponent Wallstent Nexstent Wallstent Wallstent

AngioGuard AccuNet AccuNet NeuroShield GuardWire EPI FilterWire EPI FilterWire PAEC GuardWire

BSC, Boston Scientific Corporation; CPD, cerebral protection device; ISES, International Society for Endovascular Specialists; JNJ, Johnson and Johnson; NINDS, National Institute for Neurological Disorders; PAEC, Parodi Anti-Embolization Catheter.

The Carotid Revascularization Endarterectomy versus Stent Trial (CREST) is the first randomized, multicenter clinical trial funded by the National Institutes of Health to assess the safety and efficacy of CAS in symptomatic patients eligible for CEA (see Table 21-3). In fact, the inclusion and exclusion criteria of CREST are very similar to those of the North American Symptomatic Carotid Endarterectomy Trial (NASCET); therefore, CREST will enroll only patients with standard surgical risks for CEA. To compare CAS and CEA, approximately 2500 patients with symptomatic severe carotid stenosis (i.e., those with ≥70% stenosis by duplex criteria or ≥50% by NASCET angiographic criteria) will be enrolled. A preliminary result was recently presented, showing that CAS was associated with a 13% stroke and death rate in patients older than 80 years.26 This was statistically higher than the rate in patients younger than 80 years. As a result, the trial has stopped enrolling octogenarians. Until the results of this clinical trial are available, CAS should be reserved for patients for whom CEA would be considered a high-risk procedure.

Patient Selection for Carotid Angioplasty and Stenting As mentioned earlier, CEA remains the gold standard therapy for carotid stenosis. Although ongoing trials comparing the

efficacy and safety of CEA and CAS may prove that CAS is also indicated for good-risk patients, CAS is currently indicated only in select high-risk cases. Patients considered high-risk surgical candidates for CEA can be grouped into two main categories according to anatomic and physiologic conditions.3,4 Anatomic characteristics associated with a high risk for CEA include (1) restenosis after previous CEA, particularly because of the risk of cranial nerve injury; (2) high or low lesions, defined as those above C-2 or below the clavicle, respectively; (3) “hostile” neck, related primarily to previous radical neck dissection, radiation therapy, presence of a permanent tracheostomy, or a frozen neck; or (4) other carotid lesions, including tandem lesions within the same carotid artery or contralateral ICA occlusion. Physiologic characteristics are associated with the presence of significant comorbid conditions, which include (1) class III or IV angina or congestive heart failure; (2) severe chronic obstructive pulmonary disease (forced expiratory volume ≤ 1 or the need for home oxygen); or (3) cardiac disease necessitating open heart surgery within 4 weeks. Although CAS has also been performed in patients not considered at high risk for CEA as part of several clinical trials, definite results and clinical evidence from these trials are not available; therefore, CAS should be reserved for high-risk surgical patients (see Table 21-1). In addition, because the Center for Medicare and Medicaid Services’ national noncoverage

14 12

Patients (%)

10 8

5.8% 6 4

4.9% 3.1%

6.2%

4.2% 3.3%

2

3.2% 1%

0 SAPPHIRE Rand

Non–Rand

BEACH ARCHeR SECuRITY Maveric Cabernet ArteriA 2 2

FIGURE 21–2 • Thirty-day risk of stroke in highrisk carotid stenting registries.

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policy will still be in effect for good-risk patients after CAS is approved for high-risk patients, there will be no reimbursement if CAS is performed on the former. Because the learning curve for CAS is prolonged, patient selection is critical when experience with the procedure is limited.10,11 Medical and anatomic risk factors may affect the safety of both CEA and CAS, but anatomic factors may influence CAS to a greater extent.5,27 Details of factors that make CAS difficult and dangerous are discussed in the angiography section.

Antiplatelet and Anticoagulant Therapy Patients should receive aspirin 325 mg and clopidogrel 75 mg daily for at least 3 days before the procedure.28 Patients not treated preoperatively with clopidogrel should be loaded with 300 mg at least 4 hours before the procedure; if this is not possible, the procedure should be rescheduled. The improved results of modern CAS series owe a lot to the use of dual antiplatelet treatment. For example, the Schneider Wallstent trial was terminated prematurely owing to a high complication rate following CAS, which is thought to be due in part to the fact that clopidogrel was not used.16 Dual antiplatelet therapy should be continued for at least 30 days after the procedure. In certain situations, particularly if there is a need for major surgery, antiplatelet therapy can be stopped after 2 weeks, but it should be restarted immediately postoperatively. Heparin should be administered to maintain the activated clotting time (ACT) at longer than 250 seconds. If one is using a CPD, especially a filter type, it is advisable to maintain the ACT at longer than 275 seconds, because these devices carry the risk of thrombosis and thrombus formation if the patient is inadequately anticoagulated. Because there is significant patient variability in the response to heparin, it is important to monitor ACT intraprocedurally in all patients. Recently, direct thrombin inhibitors such as bivalirudin (Angiomax) have been shown to reduce complications associated with heparin, such as groin hematomas, but there is a lack of firm data relative to the use of these agents for CAS. Some investigators have used glycoprotein (GP) IIb/IIIa inhibitors during CAS to reduce the microcirculatory impact of distal embolization.29 However, because CPDs are now widely available and higher rates of major bleeding complications have been reported with these agents, the use of GP IIb/IIIa inhibitors has largely been abandoned during uncomplicated CAS. GP IIb/IIIa inhibitors may be beneficial for treating embolic complications. As is the case with CEA, postprocedure blood pressure control is also important to avoid hyperperfusion syndrome and intracranial hemorrhage.

Diagnostic Aortic Arch, Cervical Carotid, and Cerebral Angiography There are four purposes in obtaining a carotid and cerebral angiogram: stratifying risk, confirming the degree of stenosis, understanding the intracranial collateral circulation, and obtaining a baseline cerebral angiogram that can be compared with the postprocedure angiogram. Diagnostic angiography is usually performed at the time of CAS, but during

359

the learning phase, it may be advisable to perform it beforehand so that one can carefully assess the difficulty of the case and select the appropriate techniques and tools. Either way, it is essential to have a good-quality, complete diagnostic cerebral angiogram before performing CAS. Digital subtraction capabilities are critical in performing intracranial angiography. Although it may be desirable to perform CAS in an angiography suite with a fixed C-arm, it can be done equally well with a high-quality portable C-arm with high resolution, such as the GE/OEC 9800 series (OEC, Salt Lake City, Utah). The recent development of a motorized, portable C-arm has narrowed the gap between fixed and portable even further. It is also important to perform the procedure using only local anesthesia without sedation, so as not to impair the intraprocedural neurologic evaluation. AORTIC ARCH ANGIOGRAPHY The ability to safely deliver the stent to the lesion is probably the most difficult part of the procedure, and the level of difficulty can be assessed with the diagnostic aortic arch and carotid angiogram. The aortic arch angiogram is probably the most important diagnostic image because it helps determine the difficulty of CAS. It should be obtained in a 20- to 45-degree left anterior oblique orientation to open up the aortic arch adequately. A 5 French pigtail catheter with markers is inserted through a 5 French femoral sheath. Contrast material injected at a rate of 20 mL over 1.5 seconds is generally sufficient for good opacification, particularly when using digital subtraction techniques. A nonionic contrast medium is preferred. The field of view should be large enough to visualize the origin of the great vessels, as well as the carotid bifurcations. Arch anatomy has been categorized into three types, based on the relationship between the origins of the great vessels and a transverse line drawn at the level of the apex of the aortic arch (Fig. 21-3).30 In type I aortic arches, all the great vessels originate at the same level, and carotid cannulation is easy. If the origins of the innonimate or the left common carotid artery (CCA) are progressively lower than this line, the arch is classified as type II (two fingerbreadths) or type III (more than three fingerbreadths). Aortic arch angiograms are also helpful in demonstrating any anatomic anomalies such as the bovine origin of the left CCA. Delivering a stent to the target site is difficult and challenging in patients with type III arches and in those with anomalies such as a bovine takeoff of the left CCA. With type II or III arches, catheters advanced from the descending aorta tend to prolapse into the ascending aorta when cannulation of the inferiorly located great vessels is attempted. Although experience and advanced technical skills can overcome these difficult situations, one should reassess the risks and benefits of CAS, CEA, and medical treatment before proceeding. When faced with difficult anatomy, it is perfectly reasonable to abort CAS and perform CEA later or treat the patient with medical therapy. Patient selection and sound judgment are the keys in achieving a good outcome. SELECTIVE CATHETERIZATION AND CERVICAL CAROTID ANGIOGRAPHY The type of aortic arch helps determine which diagnostic catheter is preferable. Although a variety of diagnostic catheters

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B

C

D

FIGURE 21–3 • Classification of aortic arch. A, Type I aortic arch. All the great vessels originate at the same level as the apex of the aortic arch. B, Type II aortic arch. The innonimate artery orifice is one fingerbreadth below the apex of the arch. C, Type III aortic arch. D, Bovine origin of the left common carotid artery.

are available for cerebral angiography, one does not need to be familiar with every type. For example, we perform 95% of our angiograms with a Vitek catheter, a Headhunter, or an angled vertebral catheter (Cook, Inc., Indianapolis, Ind.) (Fig. 21-4). In types I and II arches, the Headhunter or the vertebral catheter can be used to rapidly access all the great vessels. For a type III arch or a bovine takeoff of the left CCA, a Vitek or Simmons catheter is more appropriate (see Figs. 21-3 and 21-4). The Simmons 1.5 catheter is usually reserved for type III arches because it requires a certain amount of manipulation within the arch to re-form its shape and is thus associated with an

FIGURE 21–4 • Commonly used selective catheters for carotid angioplasty and stenting. From top: vertebral, AL 4, Headhunter, Vitek.

increased risk of embolization. One should choose three or four catheters and become familiar with their use, indications, strengths, and weaknesses (Table 21-4; Figs. 21-5 and 21-6). With the exception of the left CCA angiogram, which can be obtained as soon as the catheter engages the vessel, a guidewire must be used to advance the catheter selectively into the right CCA or the vertebral artery. For the right common carotid angiogram, the catheter first must be placed in the innominate artery. Then an angiogram can be obtained to visualize the takeoff of the right CCA and the carotid bifurcation. Alternatively, the initial aortic arch angiogram may suffice for this purpose. Using these images as a road map, a 0.038- or 0.035-inch stiff Glidewire (Terumo Inc., Somerset, N.J.) is advanced into the right CCA. Care is taken not to advance the Glidewire into the lesion, because this can cause embolization. Because the guidewire purchase is limited, use of a stiff Glidewire is critical; it enables passage of the catheter with less purchase compared with a standard Glidewire (Fig. 21-7). It is especially important to choose stiff Glidewires when using a reversed curve catheter such as the Vitek or Simmons catheter. The same principle applies when one is obtaining a selective vertebral angiogram. After selective catheterization, anteroposterior and lateral angiograms are taken. In addition, a magnified “worst-view” angiogram of the lesion is taken; this view varies from patient to patient and may not be either the anteroposterior or the lateral. Angiographic assessment of the degree of stenosis is done using the NASCET criterion of comparing the smallest diameter at the lesion with a reference diameter of the distal ICA in a segment with parallel walls.1 Care is taken to avoid air embolization by confirming return of blood into the syringe before injecting contrast material. The target carotid artery angiogram should be obtained after obtaining the contralateral carotid and vertebral angiograms. By doing so, one can proceed directly to CAS

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TABLE 21–4

361

Characteristics of Various Selective Catheters

Indication Use in anomalous left CCA Ease of use Ease of advancement Risk of emboli

JR, Vertebral

Headhunter

Vitek

Simmons

Type I arch No Easy Easy Minimal

Type I, II arch No Easy Easy Minimal

Type I, II, III arch Yes Moderate Moderate Minimal

Type III arch Yes Difficult Difficult Moderate

CCA, common carotid artery.

after obtaining the angiogram and minimize the number of selective catheterizations. Lesions that may make CAS difficult include very tight stenoses with the string sign, acute occlusions, lesions with intraluminal thrombus, those with dense calcification, tandem lesions, and severe stenosis or tortuosity within the CCA (Table 21-5; Fig. 21-8). Tight stenosis makes passage of the CPD difficult and may require predilatation. Intraluminal thrombus increases the chance of embolization during passage of the CPD, balloon, and stent (see Fig. 21-8). Dense calcification may result in acute recoil refractory to repeat balloon dilatation, and it may cause difficulty in passing the stent. In addition, although the likelihood is very remote, the risk of vessel rupture is increased with dense calcification. Tortuous

A

B

vessels make passage of the CPD and stent challenging. The tortuosity is exaggerated distal to the stent after stent implantation because current stents tend to straighten out the vessel, extending the tortuosity distally. Tandem lesions in the CCA in addition to the ICA pose a challenge. An occluded external carotid artery (ECA) makes safe cannulation of the CCA difficult. As discussed earlier in the aortic arch section, these lesions should be avoided if alternative treatment options are feasible. Although simultaneous treatment of bilateral carotid artery stenosis is possible, it should generally be staged at least 30 days apart, as it is with CEA. The major risks of a simultaneous bilateral approach are severe bradycardia and hypotension due to overstimulation of both carotid sinuses, as well as cerebral hyperperfusion syndrome.

C

FIGURE 21–5 • Use of the Vitek catheter. A, The reversed curve Vitek catheter is a push catheter. After the catheter re-forms its shape in the descending thoracic aorta, it is slowly pushed proximally (arrow). B, Once it engages the great vessel, the tip of the Vitek catheter flips cranially (arrow). C, Then the catheter should be pulled back. This maneuver puts the catheter farther into the target vessel. A Glidewire is used to selectively cannulate the right common carotid or the vertebral artery.

Fig. 21-8

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B

C

D

E

F

FIGURE 21–6 • Technique to cannulate a bovine left common carotid artery (CCA). A, Arch angiogram shows bovine origin of the left CCA. B, The Vitek catheter is re-formed in the distal arch and then slowly pushed forward. C, As it engages the innonimate artery, the tip of the catheter “flicks” cranially. D, The catheter is pushed farther proximally. Counterclockwise rotation of the catheter may be helpful. E, A Glidewire is used to probe the left CCA. F, Once the left CCA is cannulated with the Glidewire, the Glidewire and the catheter should be pulled back as a unit to enter the CCA. If counterclockwise rotation were applied earlier, clockwise rotation should be applied as one pulls the catheter-Glidewire complex back.

CEREBRAL ANGIOGRAPHY A complete cerebral angiogram requires defining the intracranial anatomy of both carotid arteries as well as one vertebral artery, preferably the dominant one. Anteroposterior and lateral views are obtained for each injection of 7 to 10 mL of

A

B FIGURE 21–7 • The difference between 0.035- and 0.038-inch Glidewire. A, A 0.035-inch regular-stiffness Glidewire is placed inside the Vitek catheter. Note that the catheter has not completely straightened; this will make delivery of the catheter difficult because it will prolapse in the arch. B, A 0.038-inch Glidewire has been placed inside the Vitek catheter. Note that with the same amount of purchase as in A, the catheter has straightened significantly, allowing the catheter to be introduced into the target vessel.

contrast agent over 1 second. Digital subtraction angiography is very useful. A parenchyma-gram, which can be obtained by increasing the gain of the late-phase image, is useful in understanding the perfusion of the brain parenchyma (Fig. 21-9). This baseline image can be compared with the postprocedure image to quickly identify the presence or absence of emboli. In the presence of cerebral emboli, there would be an area that does not stain in either the anteroposterior or the lateral projection. It is crucial to define the collateral circulation to the brain hemisphere of interest. These collaterals include the anterior and posterior communicating arteries. The use of CPDs of the balloon occlusion type mandates a good understanding of the collateral circulation to the hemisphere to be treated. In the absence of good collateral circulation, the patient may not tolerate the procedure with the use of occlusive CPDs, which could necessitate a rapid or even aborted procedure.

Introducing the Sheath into the Common Carotid Artery Although direct cervical carotid percutaneous and open approaches, as well as a brachial approach, have been used for CAS, the transfemoral route is preferred. After the diagnostic angiogram has been obtained and the decision to proceed with CAS has been made, a sheath or a guiding catheter must be placed into the CCA so that one can safely introduce the stent and perform angiography during percutaneous transluminal angioplasty and stent deployment. Before introducing the sheath, 70 to 100 IU/kg of heparin is administered to raise the ACT to longer than 250 seconds (>270 seconds if a CPD is used). There are three different ways to introduce the sheath or guiding catheter: the sequential over-the-wire technique, the telescoping technique, and the direct coronary technique. Each has advantages and disadvantages that

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TABLE 21–5

363

Causes of Difficult Access

Iliac Artery

Aortic Arch

Great Vessels

Carotid Artery

Tortuosity Stenosis or occlusion

Type III arch Bovine arch Diseased arch

Ostial stenotic lesion Anomalous origin Tortuous CCA

Occluded ECA Tortuous ICA at and distal to lesion Heavy calcification

CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

are discussed in the following sections. The operator needs to be familiar with each technique, because the approach used is generally related to the nature of the aortic arch. In addition to choosing the access technique, one needs to decide whether to use a sheath or a guiding catheter. The pros and cons of each are described in Table 21-6. Because the current stent delivery systems are mostly 6 French and smaller, a long 6 French sheath or an 8 French guiding catheter is sufficient in most cases. We prefer to use a 90-cm 6 French Shuttle sheath (Cook, Inc., Indianapolis, Ind.) in the majority of the cases; it has a smooth transition and a flexible tip, allowing safe introduction. Guiding catheters may be helpful in placing both CPDs and the capturing sheaths needed to retrieve CPDs. In addition, guiding catheters may be repositioned when they slide out of the CCA, which is generally not possible when a sheath prolapses out of the CCA during CPD or stent delivery (Fig. 21-10). Another advantage of guiding catheters in cases of severe tortuosity and elongation of the left CCA is the possibility of using an angulated stiff

guidewire to cannulate the CCA; this allows CAS to be performed without having to advance the sheath into the carotid artery itself, thereby avoiding exaggerated kinking of the vessel. SEQUENTIAL OVER-THE-WIRE TECHNIQUE This approach is probably the safest and is definitely most useful when there is severe arch tortuosity (types II, III; see Fig. 21-3). It is, however, the most time-consuming approach, requiring more steps than the others. This approach is most appropriate if one has not decided to perform CAS at the time of the diagnostic angiogram (Table 21-7). The selective catheter that was used to engage the CCA is used to obtain an angiogram that adequately separates the ECA and ICA. The image intensifier should be positioned such that one can view the ECA-ICA bifurcation as well as the aortic arch (Fig. 21-11). By doing so, one can keep an eye on the tip of the guidewire as well as monitor the behavior of the sheath Fig. 21-11

A

B

C

D

E

F

FIGURE 21–8 • Anatomies that make carotid angioplasty and stenting difficult. A, Very tight stenosis with string sign. B, Tortuous internal carotid artery (ICA). C, Dense calcification. D, Tandem lesion in the common carotid artery (CCA) orifice and ICA. E, Tortuosity within the CCA. F, Lesion with mural thrombus.

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A

B

FIGURE 21–9 • Ιntracranial angiogram. A, Lateral view shows normal anterior and middle cerebral arteries. Note the presence of a fetal posterior communicating artery (arrow). B, Parenchyma-gram of the angiogram shown in A.

within the aortic arch as it is introduced. Posteroanterior or left anterior oblique views are usually adequate for this purpose. Use of road-mapping may be helpful in selectively cannulating the ECA. Right anterior oblique views are often better for opening up the right carotid bifurcation, but visualization of the aortic arch may be suboptimal. A stiff or a 0.038-inch angled Glidewire is advanced deep into the ECA, and the diagnostic catheter is advanced over the wire into the ECA. The Glidewire is then exchanged for a Meier (Meditech) or Amplatz superstiff guidewire (Meditech), and the diagnostic catheter is removed, along with the 5 French sheath that was initially placed in the femoral artery (Fig. 21-12). It is important to use a 260-cm-long guidewire so that one can maintain guidewire position during catheter removal. Manual pressure is applied to the femoral artery as the 5 French sheath is

TABLE 21–6

removed to prevent groin hematoma. The 6 or 7 French Shuttle sheath is then advanced over the stiff wire. With a type II or III aortic arch, the sheath may not track the guidewire and may prolapse into the ascending aorta. This is one of the critical steps in CAS. A useful maneuver is to perform the “push-and-pull” technique, whereby the guidewire is gently

Sheath versus Guiding Catheter

Sheath

Guiding Catheter

Smaller hole in femoral artery (6-7 French) Tracks better in difficult arch (type II, III)

Less likely to kink

Smooth dilator permits atraumatic insertion into CCA

Better torque control (beneficial in guiding CPD, retrieval catheters in tortuous anatomy) Allows direct access to CCA without cannulating ECA

CCA, common carotid artery; CPD, cerebral protection device; ECA, external carotid artery.

FIGURE 21–10 • Prolapse of the sheath during stent delivery.

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TABLE 21–7

Sequential Over-the-Wire Technique

Introduce 5 French groin sheath Perform arch angiography and other diagnostic studies Make the decision whether to stent Engage target CCA with diagnostic catheter Road-map in low-magnification anteroposterior or left anterior oblique projection; visualize arch and ECA-ICA Advance 0.038-inch Glidewire into ECA Advance catheter into ECA; exchange for superstiff wire, Meier or Amplatz Remove selective catheter and 5 French sheath while maintaining superstiff wire access Insert 6 French shuttle sheath over superstiff wire Advance sheath into mid-CCA over stiff wire into ECA CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

retracted as the sheath is introduced around the aortic arch (see Fig. 21-12). Because there is little guidewire purchase, the tip of the guidewire must be monitored to avoid pulling it out of the ECA. The radiopaque tip of the Meier wire, as well as its stiffness, ensures the safety of this step, making it the preferred wire. Also, it is important to advance the sheath very slowly during this step. Deep inspiration or exhalation may change the angle of the CCA and the aortic arch and may assist in the delivery of the sheath. The sheath should be introduced deep enough into the CCA so that it will not prolapse during the CPD or stent delivery phase.

365

Conversely, the sheath should not be introduced too deep into the CCA, because this can exaggerate the preexisting tortuosity of the vessel (Fig. 21-13). Also, a deeply placed sheath can interfere with stent deployment. It is important to position the sheath appropriately at this time and avoid moving it later during the procedure. This technique may not be possible if the target lesion is located in the CCA or if the ECA is occluded. In these cases, a loop can be created in the stiff wire that generally prevents the wire from advancing through the lesion (Fig. 21-14). Alternatively, the coronary technique (described later) for vascular access should be used. TELESCOPING TECHNIQUE A 6 or 7 French Shuttle sheath or a guiding catheter is introduced into the descending thoracic aorta. A 125-cm Vitek, JR4, or Multi-purpose catheter (Cordis, Johnson and Johnson, Warren, N.J.) is inserted through the Shuttle sheath or the 8 French H1 guiding catheter (Cordis). Guidewires, diagnostic catheters, CPDs, and stents are passed through a TuohyBorst valve. With the telescoping technique, it is important to use a 120- to 125-cm catheter because the long sheath or guiding catheter is at least 90 cm long. Selective cannulation of the CCA is performed with the angiographic catheter. As described in the section on the sequential technique, an angiogram is obtained that distinguishes the ECA and ICA. The image intensifier should be positioned so that one can view the ECA as well as the aortic arch. Then, a stiff or 0.038-inch angled Glidewire is passed through the diagnostic catheter and into the ECA; the diagnostic catheter is advanced into the mid-CCA over the Glidewire. The Glidewire and the diagnostic catheter are then used as a rail to advance the sheath or guiding catheter into the mid-CCA. Small rotational movements of the sheath may be necessary to advance it into position. Again, the “push-and-pull” technique may be useful. The diagnostic catheter and Glidewire are now ready to be withdrawn; this requires the application of some countertraction to the guiding catheter or sheath, which tends to jump forward as the diagnostic catheter and Glidewire are removed. Back-bleeding from the guiding catheter or sheath must be allowed to wash out any debris that may have accumulated during positioning of the catheter or sheath. The telescoping approach is contraindicated when the CCA ostium is diseased. Sliding the sheath over the diagnostic catheter may cause plaque disruption and embolization because there is a gap between the diagnostic catheter and the larger sheath. In these cases, the sequential over-the-wire technique should be used to minimize trauma and embolization. CORONARY TECHNIQUE

FIGURE 21–11 • The image intensifier is positioned so that both the arch and the carotid bifurcation can be visualized. Using the road-mapping function, one can selectively cannulate the external carotid artery with a Glidewire.

The CCA can also be cannulated directly with an H1 guiding catheter using an approach similar to that used with the coronary arteries. This coronary approach may be safe and fast, but it requires greater experience and a favorable arch configuration (i.e., type I or II). In the presence of a bovine arch, where the left CCA originates from the innominate artery, it is more convenient to use an AL 1 guide to cannulate the ostium and proximal left CCA. When a bovine takeoff is combined with severe CCA disease or occlusion of the ECA, which makes it almost impossible to advance a 0.038-inch

Fig. 21-12

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A

B

C

D

FIGURE 21–12 • Use of the external carotid artery (ECA) as the anchoring vessel for sheath insertion. A, The Glidewire is introduced into the ECA. B, The Vitek catheter is introduced into the ECA over the Glidewire. The angiogram confirms correct positioning of the catheter. A superstiff wire is then introduced deep into the ECA, and the catheter and the 5 French sheath in the groin are removed. C, As the Shuttle sheath is introduced into the common carotid artery (CCA), a gentle “push-pull” technique may be useful. It is important to position the image intensifier so that both the tip of the guidewire and the aortic arch can be visualized. D, Once the sheath is in a good position, the dilator and the superstiff wire are removed in preparation for carotid angioplasty and stenting.

wire into the left CCA, the use of an AL 1 guide may be particularly helpful. In this situation, in addition to the stent delivery wire (CPD wire), a stiff 0.018-inch wire may need to be placed in the CCA or ECA to maintain guide stability because, unlike with a sheath, sufficient purchase of the CCA is lacking. OTHER APPROACHES

FIGURE 21–13 • Exaggeration of the tortuosity of the common carotid artery caused by introduction of the sheath.

A brachial approach may be necessary in rare cases.31 The right CCA should be accessed via the left brachial artery and the left CCA via the right brachial artery (Fig. 21-15). A helpful approach in these situations involves the use of a 6 French Ansel sheath (Cordis, Warren, N.J.) and a Simmons 1, 1.5, or 2 catheter placed into the ipsilateral CCA. A stiff wire is then advanced into the ECA. At this point, the Simmons catheter can be replaced by the introducer of the Ansel sheath, which allows the sheath to be advanced into the CCA. Percutaneous or open carotid access through a cervical approach has been described, but because of the lower profile and increased trackability of current stents, this approach is seldom necessary. Complications related to a cervical carotid puncture include carotid dissection, carotid thrombosis while achieving hemostasis after sheath removal, and airway

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compromise from hematomas. The cervical approach may, however, be the last resort in patients with severe tortuosity of the CCA and an unfavorable arch anatomy (Fig. 21-16). If there is severe occlusive disease at the ostium of the innonimate or left CCA, this lesion needs to be treated before introducing the sheath, because the sheath may cause complete cessation of blood flow. Percutaneous transluminal angioplasty of the ostial lesion is performed to achieve an adequate lumen so that flow will be maintained after sheath insertion. The sheath can then be introduced into the CCA, CAS is performed, and a stent is placed in the ostial lesion (Fig. 21-17). Stenting of the ostial lesion before CAS should be avoided because the stent may be dislodged as the sheath is advanced into the CCA; also, the stent may damage the sheath. These cases are technically demanding and should be avoided during the leaning phase.

Cerebral Protection during Carotid Angioplasty and Stenting

FIGURE 21–14 • Technique of introducing the sheath into the common carotid artery (CCA) when the external carotid artery (ECA) is occluded or when there is a lesion in the CCA. A pigtail shape is created at the tip of the stiff wire, providing sufficient support without excessive purchase. A direct introduction can be performed using an appropriately shaped guiding catheter (coronary technique).

A

B

There is considerable evidence that embolization takes place during all carotid stenting procedures, with most emboli being released at the time of balloon deflation, as detected by transcranial Doppler monitoring and confirmed in ex vivo experiments (Fig. 21-18).17,32 Moreover, with the development and availability of lower profile and more sophisticated CPDs, the concept of cerebral protection has become widely accepted, and there is a consensus among specialists that protection devices should be used routinely (Table 21-8; Fig. 21-19).3 The results of the SAPPHIRE trial and others have furnished the evidence for routine use of protection devices (see Fig. 21-2).4 The use of CPDs, however, is not without complications and may in fact add risks to the procedure. Intrinsic problems associated with the use of protection devices relate to the difficulty

C

FIGURE 21–15 • Brachial access in a patient with aortoiliac occlusion. This patient had aortic occlusion, precluding femoral access. A, Arch angiogram shows bovine origin of the left common carotid artery (CCA) and occlusion of the left subclavian artery. B, Selective catheterization of the left CCA is performed with a Sos-Omni catheter. The angiogram shows severe recurrent stenosis in the left internal carotid artery (ICA). C, Carotid angioplasty and stenting are performed.

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A

B

FIGURE 21–16 • Direct common carotid artery (CCA) access in a patient with a type III arch. A, This patient’s type III arch made introduction of the sheath difficult and risky. B, The patient was not a surgical candidate owing to a hostile neck and severe congestive heart failure. Therefore, a direct CCA puncture was performed to gain access.

of introducing and deploying the device, the effectiveness of emboli capture, CPD-induced vessel injury, and the difficulty in recapturing and withdrawing the device.33 A number of papers have been published demonstrating the safety and efficacy of cerebral protection during CAS, however.34-40 CPDs are basically of two types: occlusive and nonocclusive. Occlusive devices work through proximal or distal occlusion relative to the carotid lesion. Nonocclusive devices are either filters with supportive nitinol endoskeletons or unsupported devices that resemble a windsock. These devices have intrinsic advantages and disadvantages and specific technical features. Familiarity with several devices is helpful, allowing the most appropriate device to be selected for a particular lesion and anatomy. Once the sheath is in place, an appropriate working view must be selected. This view should allow clear visualization of the carotid lesion with maximum separation of the external and internal carotid arteries. Before we used CPDs, the lateral view was used most frequently; however, in this view, the guiding catheter or sheath in the CCA is generally not visible. When CPDs are used, visualization of the sheath should be maintained at all times, because prolapse of the sheath into the aortic arch could result in withdrawal of the deployed CPD through the lesion. An anteroposterior or ipsilateral oblique view is preferred now that CPDs are used routinely (Fig. 21-20). This view allows visualization of the entire field, including the CPD and the distal portion of the sheath.41 GUARDWIRE Before an occlusive CPD is used, a complete cerebral angiogram, including the collateral circulation to both hemispheres, must be obtained because incomplete collateral circulation to the affected hemisphere may contraindicate the use of this device. The GuardWire (PercuSurge, Medtronic,

Sunnyvale, Calif.) consists of a 0.014-inch guidewire with a central lumen connected to a compliant distal occlusion balloon (Table 21-9). Nominal balloon diameters are 5 to 6 mm. After testing for integrity, the balloon is fully deflated and introduced into the Shuttle sheath. To minimize occlusion time, it is best to have the predilatation balloon loaded on the GuardWire before occluding the ICA. The predilatation angioplasty balloon (4-mm by 4-cm Aviator, Cordis, Warren, N.J.; or Soft SV, Boston Scientific Corp., Natick, Mass.) is loaded onto the GuardWire and kept just below the lesion. Then the GuardWire is advanced across the lesion, and the GuardWire balloon is inflated until vessel size is reached (Fig. 21-21). If there is severe tortuosity in the lesion or within the distal ICA that precludes insertion of the GuardWire, a separate “buddy wire” (0.014-inch Reflex or Stabilizer, Cordis) may be placed across the lesion to straighten the vessel and facilitate insertion of the GuardWire. This technique is seldom needed because the second-generation GuardWire Plus is very flexible. An angiogram is obtained to verify complete occlusion of the ICA. The predilatation balloon within the Shuttle sheath is then advanced across the lesion, and angioplasty is performed. Following stent deployment and dilatation, the PercuSurge export aspiration catheter is introduced to aspirate the blood column as well as the embolic particles. Finally, the GuardWire occlusion balloon is deflated and removed. Once the GuardWire balloon is inflated, it is not possible to obtain an angiogram in the ICA; therefore, it is important to obtain a good angiogram beforehand, with bony landmarks that can be used as a reference during predilatation and stent deployment. DISTAL FILTER PROTECTION DEVICE A filter with a diameter matching the distal cervical ICA is advanced through the lesion (Table 21-10). It is advisable to

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A

D

B

E

369

C

F

FIGURE 21–17 • Management of tandem lesions. A and B, Arch angiograms show severe stenosis at the takeoff of the left common carotid artery (CCA) (long arrow), distal CCA, and internal carotid artery (ICA) (short arrow). C, Percutaneous transluminal angioplasty (P) is performed at the orificial lesion to maintain flow after insertion of the sheath. D, Flow is maintained with the sheath inserted into the CCA. E, Carotid angioplasty and stenting are performed in the standard manner. F, A stent is placed at the orifice of the previously angioplastied site. Stenting is not performed until the end, because introduction of the sheath may dislodge the stent.

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FIGURE 21–18 • Embolic particles released during percutaneous transluminal angioplasty and stenting. (From Ohki T, Marin ML, Lyon RT, et al: Ex vivo human carotid artery bifurcation stenting: Correlation of lesion characteristics with embolic potential. J Vasc Surg 27:463-471, 1998.)

place the filter device at the level of the distal ICA immediately before the petrous portion unless prohibitive tortuosity is present. The floppy distal tip of the wire should be kept in the petrous portion (Figs. 21-22 and 21-23). The CPD can then be stabilized in this position, decreasing forward displacement. Then the outer sheath of the filter is retrieved, and the filter deployed. It is important to obtain an angiogram to confirm good flow and circumferential opposition of the filter to the vessel wall, preferably using at least two perpendicular views (Fig. 21-24). In cases in which the stenosis is extremely tight, a 2-mm coronary balloon may be used to dilate the lesion before filter insertion. In tortuous lesions, a buddy wire is often needed to straighten the vessel; filter devices are generally stiffer than the GuardWire and may not be able to negotiate tortuous vessels. An angiogram is obtained to confirm correct positioning of the filter, as well as preservation of prograde ICA flow.

TABLE 21–8

Cerebral Protection Devices

Type

Product

Manufacturer

Distal occlusion

GuardWire Kensy Nash AccuNet AngioGuard FilterWire Interceptor NeuroShield Spider Rubicon filter PAES MOMA

PercuSurge, Medtronic Tri-Activ Guidant Cordis EPI/Boston Scientific Corp. Medtronic MedNova/Abbott EV3 Rubicon ArteriA InvaTec

Distal filter

Proximal occlusion

An angiogram must always be obtained to assess flow before collapse and removal of the filter. Large amounts of emboli may have been released, and the filter surface may be saturated; this would be suggested angiographically by reduced or absent flow through the ICA. Because of the large amount of embolic debris captured by the filter, there is a stagnant column of blood in the ICA with suspended particles, which could be carried distally into the brain once the filter is collapsed. Filters full of emboli may be difficult to withdraw because of the resistance to full capture of the device. In these instances, the filter should be only partially captured, because forcefully pulling the filter completely into the capture sheath may squeeze and release emboli. Generally, the filter can be removed safely after only the proximal part has been captured. This phenomenon may occur in approximately 5% of cases when filter devices are used. Therefore, it is essential to aspirate the proximal ICA before collapsing the filter. The PercuSurge export catheter or a 125-cm-long, 5 French multipurpose catheter can be used for this purpose. Occasionally, it may be difficult to remove a CPD because the capture sheath hits the edge of the stent, hindering its advancement. Further dilatation of the proximal end of the stent or angling the guiding catheter to change the orientation of the capture sheath may be necessary. Alternatively, placing a small balloon on a buddy wire next to the catheter sheath may displace the CPD wire, allowing the capture sheath to enter the stent. When the CPD is withdrawn from the sheath or guiding catheter, the Tuohy-Borst valve should be completely opened, and some back-bleeding should be allowed in case particles have been released into the sheath or guiding catheter during CPD withdrawal. ARTERIA PARODI ANTI-EMBOLIZATION SYSTEM When using the ArteriA device (ArteriA, San Francisco) instead of the Shuttle sheath, the Parodi Anti-Embolization Catheter (PAEC) is introduced into the CCA over a superstiff wire placed into the ECA (Table 21-11; see Fig. 21-19). The Parodi External Carotid Balloon (PEB) is introduced through the main lumen of the PAEC into the ECA (Fig. 21-25). Finally, a 5 French sheath is inserted percutaneously into the contralateral femoral vein and connected to the Parodi Blood Recovery System (PBRS), which has a filter to capture the emboli. After completing these steps, a 0.014-inch standard guidewire and a predilatation balloon are inserted through the PAEC and kept just below the lesion. Both the occlusion balloon attached at the distal end of the PAEC and the PEB are inflated to occlude prograde flow of the CCA and retrograde flow from the ECA. Finally, the proximal end of the PAEC is connected to the femoral vein through the PBRS. Contrast material is injected into the ICA to confirm reversal of flow. The guidewire positioned inside the PAEC is then used to traverse the lesion, and angioplasty and stenting are performed. Both the PEB and the PAEC balloon are deflated at the completion of the stenting procedure. Proximal occlusive CPDs are particularly helpful in lesions associated with mural thrombus, which may result in distal embolization during wire passage. Also, lesions with severe stenosis or severe tortuosity, both of which make the use of distal CPDs difficult, are ideally treated with the ArteriA device because it allows the use of any guidewire (see Fig. 21-25). Moreover, this approach probably has the highest efficiency

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A

371

B

C

E

D

F

G FIGURE 21–19 • Cerebral protection devices. A, Medtronic/PercuSurge GuardWire Plus; B, ArteriA Parodi Anti-Embolization Catheter; C, Cordis AngioGuard; D, Guidant AccuLink; E, Boston Scientific FilterWire EZ; F, Abbott/MedNova NeuroShield; G, EV3 Spider.

A

B

C

D

E

FIGURE 21–20 • A, Arch angiogram shows bovine origin of the left common carotid artery (CCA) and a severe stenosis in the left internal carotid artery (ICA). B to E, Subsequent procedures are performed in the anteroposterior–left anterior oblique view in order to visualize the cerebral protection device, the lesion, and the distal end of the sheath (guiding catheter). B, Filter passage. C and D, Delivery of the stent. E, Postdilatation.

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TABLE 21–9

Carotid Stents and Deployment

Strengths and Weaknesses of Distal Occlusion Balloon

A number of stents are available for CAS or are being evaluated for this purpose. Carotid Wallstents and nitinol stents such as the Precise (Cordis, Warren, N.J.) or the AccuLink (Guidant, Melno Park, Calif.) are used most frequently (Fig. 21-26). They differ primarily in the way they are sized.42 Wallstents are always substantially oversized because of significant foreshortening and reduced radial force; a 10- by 20-mm size works well for most bifurcation lesions (Figs. 21-27 and 21-28). When using the Wallstent, it is advisable to place it with sufficient proximal and distal lesion coverage because the stent can foreshorten proximally or distally later (Fig. 21-29; see also Fig. 21-28). Conversely, nitinol stents have minimal foreshortening and higher radial force; therefore, the nitinol stent diameter should be 1 to 2 mm greater than the artery diameter, and the stent should be 5 to 10 mm longer than the lesion (Fig. 21-30; see also Fig. 21-28). Additional advantages of nitinol stents include accurate deployment, good lesion coverage, and lesion conformability. Disadvantages include low radiopacity and the presence of stent struts protruding inside the vessel. An 8- by 30-mm Precise nitinol stent is appropriate for most lesions, whereas a 7- by 20-mm Precise stent is preferred for more focal lesions in the mid-ICA (see Fig. 21-28). It should be noted that either stent should be sized to the CCA if the stent is to be deployed across the bifurcation; therefore, there will be considerable oversizing within the ICA. For this reason, a tapered stent is being developed (see Fig. 21-26).

Strengths Better chance of crossing tight, tortuous lesion compared with filters Lower crossing profile More flexible Weaknesses Somewhat cumbersome Prolonged procedure time Inability to perform angiography during protection Some patients (~10%) may not tolerate occlusion Unprotected During passage Suction shadow Potential for ECA embolization ECA, external carotid artery.

in terms of capturing emboli because protection can be initiated before touching the lesion, and emboli of any size are effectively recovered with the reversal of flow. These devices are also available in larger profiles and require occlusion of the ECA to create adequate proximal occlusion and flow reversal through the ICA.

A

B

C

D

E

F

FIGURE 21–21 • Procedural steps for stenting with distal occlusion protection. A, Preprocedure angiogram shows severe stenosis in the left internal carotid artery (ICA). A dime (D) is placed on the ipsilateral neck for calibration. B, The GuardWire (G) is passed through the stenosis with the aid of a “puff” angiogram performed through the sheath (S). C, The GuardWire (G) is inflated to occlude the distal ICA. Angiogram is obtained to confirm complete occlusion of the ICA. D, Percutaneous transluminal angioplasty and stenting are performed under protection. E, Aspiration catheter is introduced to aspirate the embolic particles trapped by the protection device. Angiogram is performed to evaluate the completeness of the aspiration. Suction shadow (U) can be seen adjacent to the GuardWire (G). F, Completion angiogram is obtained after deflation of the GuardWire.

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TABLE 21–10

Strengths and Weaknesses of Distal Filters

Strengths Intuitive Easier to use than distal balloon in straightforward cases Preserves ICA flow Weaknesses Larger profile, less flexible, less torque; may need to predilate or use buddy wire Unprotected During passage Small particles (300 seconds). Conversely, a mechanical approach can be used. A small 1.5-mm coronary balloon is advanced to the occlusion, and gentle dilatation often dislodges the plaque fragment. Soft hydrophilic wires may also be used to cross the blockage, which may be enough to restore flow. In refractory cases, a small snare such as the NeuroNet (Guidant, Indianapolis, Ind.) may be used to remove the embolus.

Postoperative Management Closure devices may be used with caution, particularly when diseased or calcified femoral arteries are used for access. In these instances, local compression is preferable. The patient is kept overnight in a telemetry unit and usually discharged the next day. Careful neurologic monitoring throughout the recovery period is essential because of the rare occurrence of embolization within a few hours after CAS. This probably occurs owing to plaque fragments that protrude through the stent struts. Continuous blood pressure monitoring is mandatory, and systolic pressure should be maintained between

100 and 140 mm Hg. Severe hypertension should be aggressively managed because it can lead to cerebral hyperperfusion syndrome and intracranial hemorrhage. A combination of intravenous beta blockers and nitroglycerin is the initial therapy to control severe hypertension. Cerebral hyperperfusion usually occurs in patients with chronic cerebral hypoperfusion who have maximal dilatation of intracranial arterioles after CAS and abnormal cerebral autoregulation, which may not be restored for several days.43 Patients with severe stenosis (>90%), contralateral occlusions, and severe hypertension are at increased risk, similar to patients undergoing CEA. In these instances, patients usually complain of a headache ipsilateral to the CAS, which may progress to a focal neurologic deficit, confusion, stupor, and death. Cerebral hyperperfusion may occur in 0.9% of patients after CAS. Beta blockers and diuretics are the mainstays of treatment. Vasodilators should be used cautiously, because dilatation of the intracranial arteries may worsen the syndrome. Because CAS typically lowers the blood pressure for a few days postoperatively, antihypertensive medications are often reduced or stopped in the hospital. Continuous blood pressure monitoring after discharge is important, and patients should restart their antihypertensive medications as their blood pressure returns to baseline. Failure to do so may result in intracranial hemorrhage when hypertension returns. Patients should be seen at 1 and 6 months after CAS and yearly thereafter. Carotid duplex scanning is performed before discharge and repeated at 1 month, 6 months, and then annually. Duplex scanning is the standard modality for postoperative surveillance. However, a pitfall of duplex surveillance is that flow velocities may be increased in the

Fig. 21-33

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A

B

C

FIGURE 21–33 • Embolic complication. A and B, Thrombolysis of the embolus (arrow) with tissue plasminogen activator was performed through a microcatheter. Note the gradual resolution of the embolus. C, Completion angiogram shows complete lysis of the embolus, with good filling of the middle cerebral artery. Full neurologic recovery was achieved.

absence of hemodynamically significant lesions. This phenomenon is thought to be due to changes in arterial wall compliance associated with stent placement that produce alterations in flow velocities.44 Specific criteria for in-stent restenosis should therefore be validated at each vascular laboratory, as these may vary and may overestimate the degree or residual and recurrent stenosis.45 KEY REFERENCES Abou-Chebl A, Yadav JS, Reginelli JP, et al: Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: Risk factors, prevention, and treatment. J Am Coll Cardiol 43:1596-1601, 2004. Alberts MJ, McCann R, Smith TP, et al: A randomized trial of carotid stenting vs endarterectomy in patients with symptomatic carotid stenosis: Study design. J Neurovasc Dis 2:228-234, 1997. Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): A randomised trial. Lancet 357:1729-1737, 2001. Naylor AR, Bolia A, Abbott RJ, et al: Randomized study of carotid angioplasty and stenting versus carotid endarterectomy: A stopped trial. J Vasc Surg 28:326-334, 1998. Ohki T, Veith FJ: Critical analysis of distal protection devices. Semin Vasc Surg 16:317-325, 2003. Ouriel K, Hertzer NR, Beven EG, et al: Preprocedural risk stratification: Identifying an appropriate population for carotid stenting. J Vasc Surg 33:728-732, 2001. Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 351:1493-1501, 2004.

REFERENCES 1. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 325:445-453, 1991. 2. MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. European Carotid Surgery Trialists’ Collaborative Group. Lancet 337: 1235-1243, 1991. 3. Veith FJ, Amor M, Ohki T, et al: Current status of carotid bifurcation angioplasty and stenting based on a consensus of opinion leaders. J Vasc Surg 33(2 Suppl):S111-S116, 2001. 4. Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 351:1493-1501, 2004. 5. Yadav JS, Roubin GS, King P, et al: Angioplasty and stenting for restenosis after carotid endarterectomy: Initial experience. Stroke 27:2075-2079, 1996. 6. Yadav JS, Roubin GS, Iyer S, et al: Elective stenting of the extracranial carotid arteries. Circulation 95:376-381, 1997. 7. Diethrich EB, Ndiaye M, Reid DB: Stenting in the carotid artery: Initial experience in 110 patients. J Endovasc Surg 3:42-62, 1996. 8. Theron JG, Payelle GG, Coskun O, et al: Carotid artery stenosis: Treatment with protected balloon angioplasty and stent placement. Radiology 201:627-636, 1996. 9. Mathias K, Jager H, Sahl H, et al: [Interventional treatment of arteriosclerotic carotid stenosis.] Radiologe 39:125-134, 1999. 10. Wholey MH, Wholey M, Mathias K, et al: Global experience in cervical carotid artery stent placement. Catheter Cardiovasc Interv 50: 160-167, 2000. 11. Roubin GS, New G, Iyer SS, et al: Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic

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12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

22.

23.

24.

25. 26.

27. 28. 29. 30. 31. 32. 33. 34.

carotid artery stenosis: A 5-year prospective analysis. Circulation 103: 532-537, 2001. Ohki T, Veith FJ, Grenell S, et al: Initial experience with cerebral protection devices to prevent embolization during carotid artery stenting. J Vasc Surg 36:1175-1185, 2002. Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): A randomised trial. Lancet 357:1729-1737, 2001. Golledge J, Mitchell A, Greenhalgh RM, et al: Systematic comparison of the early outcome of angioplasty and endarterectomy for symptomatic carotid artery disease. Stroke 31:1439-1443, 2000. Naylor AR, Bolia A, Abbott RJ, et al: Randomized study of carotid angioplasty and stenting versus carotid endarterectomy: A stopped trial. J Vasc Surg 28:326-334, 1998. Alberts MJ, McCann R, Smith TP, et al: A randomized trial of carotid stenting vs endarterectomy in patients with symptomatic carotid stenosis: Study design. J Neurovasc Dis 2:228-234, 1997. Ohki T, Marin ML, Lyon RT, et al: Ex vivo human carotid artery bifurcation stenting: Correlation of lesion characteristics with embolic potential. J Vasc Surg 27:463-471, 1998. Kastrup A, Groschel K, Krapf H, et al: Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: A systematic review of the literature. Stroke 34:813-819, 2003. Ohki T, Veith FJ: Carotid artery stenting: Utility of cerebral protection devices. J Invasive Cardiol 13:47-55, 2001. Endarterectomy for asymptomatic carotid artery stenosis: Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 273:1421-1428, 1995. Biller J, Feinberg WM, Castaldo JE, et al: Guidelines for carotid endarterectomy: A statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation 97:501-509, 1998. Wholey M: The ARCHeR trial: Prospective clinical trial for carotid stenting in high surgical risk patients—preliminary 30-day results. Paper presented at the American College of Cardiology Annual Meeting, March 6–9, 2003, Chicago. Whitlow P: A registry study to evaluate the MedNova EmboShield bare-wire filter and MedNova Xact self-expanding carotid stent system in patients at high-risk for carotid endarterectomy (SECuRITY trial). Paper presented at TransCatheter Cardiovascular Therapeutics (TCT) Meeting, September 15–19, 2003, Washington, DC. Iyer SS: Boston Scientific/EPI: A carotid stenting trial for high risk surgical patients (BEACH). Paper presented at the TransCatheter Cardiovascular Therapeutics (TCT) Meeting, September 27– October 1, 2004, Washington, DC. The CARESS Steering Committee: Carotid Revascularization Using Endarterectomy or Stenting Systems (CARESS): Phase I clinical trial. J Endovasc Ther 6:1021-1030, 2003. Hobson RW II, et al: Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. Paper presented at the Vascular 2004 Annual Meeting, June 3–6, 2004, Anaheim, Calif. Ouriel K, Hertzer NR, Beven EG, et al: Preprocedural risk stratification: Identifying an appropriate population for carotid stenting. J Vasc Surg 33:728-732, 2001. Bhatt DL, Kapadia SR, Bajzer CT, et al: Dual antiplatelet therapy with clopidogrel and aspirin after carotid artery stenting. J Invasive Cardiol 13:767-771, 2001. Kapadia SR, Bajzer CT, Ziada KM, et al: Initial experience of platelet glycoprotein IIb/IIIa inhibition with abciximab during carotid stenting: A safe and effective adjunctive therapy. Stroke 32:2328-2332, 2001. Myla S: Carotid access techniques: An algorithmic approach. Carotid Interv 3:2-12, 2001. Criado E, Doblas M, Fontcuberta J, et al: Transcervical carotid artery angioplasty and stenting with carotid flow reversal: Surgical technique. Ann Vasc Surg 18:257-261, 2004. Rapp JH, Pan XM, Sharp FR, et al: Atheroemboli to the brain: Size threshold for causing acute neuronal cell death. J Vasc Surg 32:68-76, 2000. Ohki T, Veith FJ: Critical analysis of distal protection devices. Semin Vasc Surg 16:317-325, 2003. Grube E, Gerckens U, Yeung AC, et al: Prevention of distal embolization during coronary angioplasty in saphenous vein grafts and native vessels using porous filter protection. Circulation 104:2436-2441, 2001.

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35. Dietz A, Berkefeld J, Theron JG, et al: Endovascular treatment of symptomatic carotid stenosis using stent placement: Long-term follow-up of patients with a balanced surgical risk/benefit ratio. Stroke 32:1855-1859, 2001. 36. Al Mubarak N, Roubin GS, Vitek JJ, et al: Effect of the distal-balloon protection system on microembolization during carotid stenting. Circulation 104:1999-2002, 2001. 37. Tubler T, Schluter M, Dirsch O, et al: Balloon-protected carotid artery stenting: Relationship of periprocedural neurological complications with the size of particulate debris. Circulation 104:2791-2796, 2001. 38. Reimers B, Corvaja N, Moshiri S, et al: Cerebral protection with filter devices during carotid artery stenting. Circulation 104:12-15, 2001. 39. Angelini A, Reimers B, Della BM, et al: Cerebral protection during carotid artery stenting: Collection and histopathologic analysis of embolized debris. Stroke 33:456-461, 2002. 40. Al Mubarak N, Colombo A, Gaines PA, et al: Multicenter evaluation of carotid artery stenting with a filter protection system. J Am Coll Cardiol 39:841-846, 2002. 41. Topol EJ, Yadav JS: Recognition of the importance of embolization in atherosclerotic vascular disease. Circulation 101:570-580, 2000. 42. Mukherjee D, Kalahasti V, Roffi M, et al: Self-expanding stents for carotid interventions: Comparison of nitinol versus stainless-steel stents. J Invasive Cardiol 13:732-735, 2001. 43. Abou-Chebl A, Yadav JS, Reginelli JP, et al: Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: Risk factors, prevention, and treatment. J Am Coll Cardiol 43:1596-1601, 2004. 44. Timaran CH, Ohki T, Chen T, et al: Accuracy of duplex ultrasonography in evaluating in-stent restenosis after carotid angioplasty and stenting. Ann Vasc Surg (in press 2005). 45. Lal BK, Hobson RW, Goldstein J, et al: Carotid artery stenting: Is there a need to revise ultrasound velocity criteria? J Vasc Surg 39:58-66, 2004.

Questions 1. What were the 30-day stroke and death rates for CEA and CAS in the SAPPHIRE trial? (a) 7.3% versus 4.4% (b) 5.8% versus 0.3% (c) 4.4% versus 7.3% (d) 10% versus 10% (e) 0.3% versus 5.8% 2. Which of the following characteristics is not considered as a high risk for CEA? (a) Age older than 70 years (b) Recurrent stenosis following CEA (c) Unstable angina (d) Uncontrolled congestive heart failure (e) Contralateral ICA occlusion 3. Which trial is not a high-risk registry? (a) BEACH (b) CARESS (c) ARCHeR (d) SECURITY (e) CABERNET 4. Which of the following is not a rationale for performing cerebral angiogram before CAS? (a) Risk stratification for CAS (b) Rule out brain tumor (c) Confirmation of degree of stenosis (d) Understanding of intracranial collateral circulation (e) Obtaining a baseline cerebral angiogram

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5. Which catheter is not commonly used for CAS? (a) Vitek (b) Vertebral (c) Headhunter (d) Simmons (e) Cobra 6. Which lesion is ideally treated with CAS? (a) Very tight stenosis with string sign (b) Acute occlusion (c) Dense calcification (d) Severe stenosis or tortuosity within the carotid artery (e) None of the above 7. Which of the following is a disadvantage of a sheath compared with a guiding catheter? (a) Larger puncture site hole (b) Lack of torque (c) Usability in type II or III arch (d) More traumatic introduction into the common carotid artery (e) Less trackable 8. Which of the following is an advantage of a filter-type protection device compared with balloon-based protection? (a) Does not require a straight landing zone (b) Can negotiate severe stenosis (c) Can obtain angiogram during stenting (d) Captures microemboli (e) Ideal for tortuous lesions

9. Which of the following is not an advantage of nitinol stents? (a) Accurate deployment (b) Strong radial force (c) Radiopacity (d) Good lesion coverage (e) Lesion conformability 10. Which of the following medications or techniques is commonly used for carotid sinus reflex? (a) Pseudoephedrine (b) Fluid resuscitation (c) Atropine (d) Transvenous pacing (e) Norepinephrine

Answers 1. a 6. e

2. a 7. b

3. b 8. c

4. b 9. c

5. e 10. d

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22

G. Matthew Longo • Jon S. Matsumura

Endovascular Repair of Abdominal Aortic Aneurysms: Technique and Results History and General Design

Preoperative Imaging

The first endovascular aneurysm repair for an abdominal aortic aneurysm (AAA) was reported in 1986 by Volodos and colleagues.1 However, it was not until Parodi’s report in 1991 that interest in the endovascular treatment of AAA began to blossom.2 The early grafts were physicianmade devices consisting of a graft material placed over balloon-expandable or self-expanding stents. Many of the early grafts were single-unit, tubular designs. Later, the Malmo, Leicester, and Montefiore groups developed grafts that had a distal landing site in the common femoral artery.3,4 The opposite iliac artery was occluded, and a femorofemoral bypass graft was constructed to provide arterial inflow for the contralateral extremity. During this same period, the Sydney group introduced the concept of modular components, making these grafts adaptable for use with the many dimensions an aneurysm can take.5 Currently, most grafts use a modular system to account for the variability in the anatomy, length, and diameter of the patient’s aorta (Figs. 22-1 and 22-2). The graft material is either polyester (Dacron) or polytetrafluoroethylene (PTFE)—the same materials used in open repairs of AAAs. These materials are believed to be resistant to late deterioration, strong enough to prevent damage from the metallic stents, and thin enough to allow compression into small delivery catheters. Currently, other polymers are under investigation but are not yet approved by the U.S. Food and Drug Administration (FDA). The method of fixation has generated considerable interest. The current systems use columnar stiffness; radial force to provide friction; hooks, anchors, or barbs for positive fixation by embedding into the aortic wall; or a combination of these. Suprarenal fixation is another option; bare metal stents with hooks provide fixation in the suprarenal aortic neck, which may be more resistant to late neck dilatation.

When evaluating a patient with an AAA who needs treatment with an aortic endograft, an imaging study is necessary to visualize aneurysm length and diameter, characteristics of the proximal and distal necks, characteristics of the access vessels, and amount of thrombus and calcification present within the vessels. An abdominal and pelvic computed tomography (CT) scan with 1- to 1.5-mm cuts and intravenous contrast enhancement provides this information. Using digital reconstruction or CT-angiography, the necessary preoperative measurements can usually be obtained (Table 22-1). This study also allows assessment of the major branch vessels of the aorta, as well as any aberrant vessels. Certain situations involving tortuosity and kinking or a questionable luminal diameter may require an arteriogram with a calibrating catheter. This catheter has radiopaque markers at 1-cm intervals to allow precise measurement of the vessels.6

Patient Selection Certain anatomic criteria should be met, with slight variations based on the particular type of endograft (Fig. 22-3; Table 22-2). The most important area of interest is the proximal aortic neck.7-9 A cylindrical neck distal to the renal arteries with a minimum length of 1.5 cm and a diameter of 2.8 cm or less is preferred. The neck should be relatively free of thrombus, allowing adequate room for proximal fixation. A conical neck flaring more than 4 mm from its proximal to distal end is less suitable for device placement. Neck angulation—the angle between the proximal neck and suprarenal aorta—of 60 degrees or greater is challenging for endovascular repair. The second area of interest is the distal landing zone within the iliac arteries.10,11 Patients with severe circumferential calcification of the iliac arteries, greater than 90-degree angles, or a maximal distal seal zone diameter that is less than 2 mm 383

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Fixed attachment points

Variable attachment points

Limited linear variability

Wide linear variability

Fixed attachment zones

(C) Aortic cuff

(A) Stent-graft body

Unfixed attachment zones

(B) Contralateral leg

(D) Iliac cuff

(E) Bifurcated extender segment

(F) Straight extender segment FIGURE 22–1 • Stent-graft design incorporating both limited and adjustable dimensional variability for maximum versatility. The fixed attachment points on the left have limited linear variability, whereas the adjustable fixation points on the right result in increased adaptability (From Allen RC, White RA, Zarins CK, et al: What are the characteristics of the ideal endovascular graft for abdominal aortic aneurysm exclusion? J Endovasc Surg 4:195-202, 1997.)

smaller than the largest limb graft size available are suboptimal candidates. If the common iliac artery is short or the external iliac artery must be used as the landing vessel, the internal iliac artery may require embolization either before or during the procedure.11,12 Usually, one hypogastric artery can be sacrificed without causing pelvic or spinal ischemia, provided the other hypogastric artery is normal. In the presence of iliac artery ectasia, aortic or flared cuffs can be used to allow part of the enlarged iliac artery to function as a seal zone for the endograft.13 This is referred to as the bell-bottom technique. Tortuous or heavily calcified vessels cause graft kinking and prevent adequate graft-to-artery apposition.14,15 The third issue is the quality of the access vessels.16 The femoral and iliac vessel lumen diameters must allow access of the introducer sheath, or a surgical conduit may be necessary. The outer diameter and trackability of the delivery sheaths vary, depending on the device. The degree of vessel tortuosity should be carefully evaluated. Tortuosity can usually be straightened using stiff guidewires and an introducer system or a brachial-femoral wire.17 Most difficulties arise in situations of tortuosity combined with small-diameter vessels, calcification, and focal stenosis. In some situations, vessel recoil may occur as the vessel tries to resume its

FIGURE 22–2 • Modular endovascular bifurcation prosthesis including main bifurcation segment (A), contralateral leg (B), proximal aortic cuff (C), iliac cuff (D), and bifurcated (E) or straight (F) extenders. (From Allen RC, White RA, Zarins CK, et al: What are the characteristics of the ideal endovascular graft for abdominal aortic aneurysm exclusion? J Endovasc Surg 4:195-202, 1997.)

TABLE 22–1 Required Anatomic Measurements Computed Tomographic Measurements

Angiographic Measurements (CTA or DSA)

Proximal aortic neck diameter Iliac artery diameter at ipsilateral distal fixation site Iliac artery diameter at contralateral distal fixation site External iliac artery or common femoral artery diameter Maximum aortic aneurysm diameter Length of aortic neck

Length from lowest renal artery to contralateral and ipsilateral distal fixation sites Length from lowest renal artery to aortic bifurcation Degree of lateral deviation and tortuosity of aorta and iliac vessels Presence of aberrant or stenotic aortic branches

CTA, computed tomography-angiography; DSA, digital subtraction angiography.

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385

Setup

1

a

2

b

3 c

4

FIGURE 22–3 • Abdominal aortic aneurysm parameters measured with computed tomography-angiography (CTA) and digital subtraction angiography (DSA). For CTA, the maximal diameters shown are infrarenal (1), aneurysm (2), bifurcation (3), and common iliac arteries (4). Maximal lengths shown are for the proximal neck (a), aneurysm (b), and distal cuff (c). DSA shows arterial occlusive disease (visceral, renal, and iliac arteries), vascular anomalies (aberrant renal arteries), and tortuosity greater than 75 degrees in proximal iliac arteries.

Endovascular AAA repair can be performed in a variety of environments. It is used both for elective repair and for emergent repair of ruptured aneurysms.18 The procedure can be done in the operating room, radiology suite, or catheterization laboratory with general, regional, or local anesthesia. The operating room environment is advantageous if rapid conversion to a major open procedure is necessary. Also, the operating room standards of sterility are maintained while the prosthetic device is being implanted into the body. When needed, open procedures can be performed simultaneously, such as a femorofemoral bypass or a distal peripheral vascular procedure. Adequate imaging is provided by a portable C-arm unit with wide-field image intensifier, digital subtraction, roadmapping capabilities, and frame-by-frame replay. Ideally, a fixed unit system can be used because it provides many important features, including a larger field of view, better resolution, more heat capacity, and tableside controls and postprocessing. In the operating room, the patient is prepped and draped the same way as for an open aneurysm repair. The primary endovascular specialist and assistant are positioned on opposite sides of the patient. A scrub nurse is positioned at the patient’s feet, and an anesthesiologist or nurse should be present to monitor conscious sedation. It is helpful to have two monitors positioned, allowing the surgeon and the assistant an unobstructed view.

Graft Placement smaller than original shape, causing kinking, malpositioning, or limb dislocation. The patient should not have essential branch vessels that would be occluded by a stent-graft. For example, the intestinal circulation should not be dependent on the inferior mesenteric artery owing to superior mesenteric and celiac artery occlusion. Finally, any patient being considered for an aortic endograft should be able and willing to comply with the follow-up protocol. Surveillance and reintervention are commonly needed to optimize long-term clinical outcomes.

TABLE 22–2

Patient Selection Criteria for Endovascular Repair of Abdominal Aortic Aneurysm

Fusiform AAA ≥ 5.5 cm in diameter Saccular AAA Suggested aortic morphology Proximal neck length ≥ 1.5 cm Neck diameter ≤ 2.8 cm Preservation of critical side branches Iliofemoral arteries of sufficient diameter for sheath access No severe iliac artery or aortic tortuosity No hereditary connective tissue disorder Anesthesia clearance for possible conversion to open repair if necessary AAA, abdominal aortic aneurysm.

Access to the common femoral arteries is obtained either through a surgical cutdown or percutaneously if a large vessel closure device is used. Angiography is performed, identifying the levels of the renal arteries, aortic bifurcation, and iliac bifurcations. Multiple magnified views with careful selection of imaging angles help optimize placement of the endograft. The main body of the graft is inserted and positioned so that the graft material is just inferior to the lowest renal artery. A second angiogram can be performed here to confirm the position of the lowest renal artery. When positioning a modular graft, it is important to orient it so that the contralateral limb gate can be easily accessed. Deployment of the main body occurs next, with some grafts allowing for minor placement alterations at points of partial deployment. With modular systems, a directional catheter and guidewire are advanced through the contralateral femoral artery, and the contralateral gate is selectively catheterized. Anteroposterior and oblique fluoroscopic views or free rotation of a curved catheter in the proximal neck can assist in verification of device cannulation. Once the short-limb cannulation is ensured, an angiogram is obtained through the side port of the sheath to ascertain the position of the hypogastric artery. The contralateral limb size is selected to extend down to the planned distal landing zone and overlap the contralateral gate. When necessary, balloons can be used to mold the graft at the proximal and distal fixation sites. A completion arteriogram is obtained to check side branch patency; assess limbs for kinking, which may affect patency; rule out types I and III endoleaks; and monitor for accessrelated arterial injury. Each graft varies slightly in terms of its

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introduction and deployment. The specifics of each graft are covered in individual training courses and product manuals.

Perioperative Complications Several complications can occur in the immediate perioperative period. The most common are groin and wound complications. In this category are immediate postoperative bleeding, hematoma, or pseudoaneurysm formation. These are technical issues that are best avoided with diligence when initially accessing the femoral vessels and when subsequently repairing or closing the arteriotomy sites after removal of the endovascular devices. Liberal use of femoral completion arteriography and patch closure may minimize thromboembolic complications. Injuries to the access vessels, particularly diseased or tortuous vessels, can occur when passing large-bore catheters and sheaths. In situations of difficult anatomy, access through the brachial artery, with passage of a wire through the thoracic aorta and subsequent capturing of that wire with a snare catheter, allows tension to be applied at both the femoral and brachial ends. This tension can result in straightening of the iliac artery (body floss technique).17 The use of iliac conduits through a limited retroperitoneal approach also allows the operator to bypass unsuitable iliac anatomy.16 In many situations, predilatation with a dilator or balloon allows the device to pass. If arterial dissection, avulsion, or rupture occurs, stents, stent-grafts, or conversion to open repair may be necessary. Coverage of the internal iliac artery is commonly required during the endoluminal repair of extensive AAAs and internal iliac artery aneurysms. Studies have shown that the internal iliac artery can be embolized with minimal adverse consequences.12 When bilateral iliac artery occlusion is necessary, a staged approach may be helpful, in the hope of developing collateral vessel formation. Alternatively, one of the internal iliac arteries may be revascularized.11 Distal embolization can result from manipulation of the endovascular devices within either the aneurysm sac or the access vessels.19 Endovascular device manipulation within the aneurysm sac can also result in microembolization to the kidneys. Care should be taken to reduce manipulations in the aneurysm and at the renal and suprarenal levels, particularly if there is mural thrombus at this level. If distal embolization occurs, the same principles hold for endovascular repair as for open repair. Embolectomy catheters can be used to remove large pieces of distal debris, or a femoral or distal bypass can be performed to restore blood flow to the extremity, if necessary. Postimplant syndrome is characterized by fever, malaise, and sometimes back pain.20 Cultures for infection are often negative, but these symptoms can last up to 10 days. The cause may be related to cytokine release due to thrombosis within the aneurysm sac. The majority of practitioners consider this syndrome a benign event.

Late Complications One of the principle reasons for failure of endovascular aneurysm repair is the presence of endoleak.21-23 Endoleak is defined as persistent blood flow outside the graft and within the aneurysm sac. There are four general types of endoleak. Type I is persistent perigraft blood flow at the proximal or distal attachment site (or both) or blood flow around an iliac

occluder plug caused by an inadequate seal. Type II leaks occur due to retrograde flow from the inferior mesenteric artery, patent lumbar vessels, or other collateral vessels. Type III leaks are caused by disconnection of the modular graft components or by fabric tear, disruption, or disintegration. Type IV endoleaks occur when there is flow through porous graft fabric that is otherwise intact. Type IV endoleaks are observed only within the first 30 days after graft placement (Fig. 22-4; Table 22-3). Endoleaks are managed by observation, a second endovascular procedure, an endoscopic procedure, or conversion to an open repair. Observation is used by those who believe that many endoleaks will seal spontaneously. This is the strategy employed with many type II endoleaks noticed on initial implantation of an aortic graft. There is no set time limit for observation; however, if the aneurysm sac is stable or shrinking, most physicians continue observation indefinitely. Type IV endoleaks are also observed, because the porosity of the graft should subside if it becomes incorporated and the graft interstices thrombose.

Type I

Type II

Type III

Type IV

FIGURE 22– 4 • Type I endoleak (periprosthetic) occurs at the proximal or distal attachment zones, or both. Type II endoleak is caused by retrograde flow from patent lumbar or inferior mesenteric arteries. Type III endoleak arises from a defect in the graft fabric, inadequate intercomponent seal, or disconnection of modular graft components. Type IV endoleak is due to graft fabric porosity, often resulting in a generalized mild blush of contrast within the aneurysm sac.

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Endovascular Repair of Abdominal Aortic Aneurysms: Technique and Results

TABLE 22–3

387

Types of Endoleaks

Classification

Causes of Perigraft Flow

Therapeutic Options

Type I

Inadequate seal of proximal or distal end of endograft Inadequate seal of iliac occluder plug

Type II

Flow from patent lumbar, middle sacral, or inferior mesenteric artery; hypogastric, accessory renal, or other visceral vessel

Type III

Fabric disruption or tear Module disconnection Flow from fabric porosity, suture holes (24 hours) perioperative coverage with antibiotics is more effective at preventing graft infections compared with a single preoperative dose 4. The options for reconstruction of an infected aortofemoral bypass graft include all of the following except (a) Axillobifemoral bypass (b) Autogenous reconstruction with autogenous superficial femoral vein (c) Cryopreserved allograft (d) Collagen-impregnated Dacron graft

5. Which of the following statements regarding prosthetic graft infection is true? (a) Grafts involving the femoral artery have a higher rate of infection than grafts anastomosed to the iliac arteries (b) An emergency operation (e.g., for a ruptured abdominal aortic aneurysm) carries an equivalent rate of infection as an elective operation (c) The surgeon is the principal and most likely source of the organism infecting the prosthesis (d) The mortality of an operation to treat prosthetic aortic graft infection approaches 75% to 80% 6. Examples of extra-anatomic bypass include all of the following except (a) Obturator bypass (b) Axillopopliteal bypass (c) Femorofemoral bypass (d) Neoaortoiliac system involving superficial femoral vein 7. Which of the following is not a clinical presentation of graft infection? (a) Pseudoaneurysm (b) Recurrent graft thrombosis (c) Hemorrhage (d) Malaise, fever, weight loss (e) Neointimal hyperplasia at the proximal anastomosis

Answers 1. b 6. d

2. c 7. e

3. b

4. d

5. a

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43

Glenn C. Hunter • Alex Westerband

Noninfectious Complications in Vascular Surgery Complications after aortoiliac and peripheral arterial reconstruction often develop and progress rapidly to produce disastrous consequences, including loss of life or limb and major organ failure. They may be the result of technical errors, the extent of the pathologic process, or one or more frequently associated diseases. A timeworn surgical principle applies especially to vascular surgery: “A complication not anticipated is sure to be experienced.” The primary problems reviewed in this chapter are operative bleeding, thrombosis, operative embolization, iatrogenic ureteric injury, major organ failure, graft deterioration, progressing atherosclerotic disease, chylous ascites, anastomotic false aneurysm, and postoperative lower extremity edema.

the inferior vena cava include retroaortic renal vein (1.7% to 3.4%) (Fig. 43-2) and circumaortic venous rings (Fig. 43-3), in which the retroaortic segment is located in a more caudal position relative to the preaortic segment. Anomalies of the suprarenal segment of the inferior vena cava are extremely rare and are associated with either azygos or hemiazygos continuation and absence of the hepatic venous segment.3 The major veins are most vulnerable in the area of tight adherence of the right posterolateral surface of the aorta and common iliac artery to the adjacent wall of the vena cava

Aortoiliac Surgery Complications of aortoiliac arterial reconstruction are similar whether the procedure is for abdominal aortic aneurysmal or occlusive disease. OPERATIVE BLEEDING Operative bleeding is most commonly caused by venous injury resulting from venous anomalies and the close anatomic relationship of the aorta and iliac arteries to the inferior vena cava and the inferior mesenteric, left renal, left gonadal, lumbar, and iliac veins (Fig. 43-1).1 Careful operative dissection, a thorough understanding of the anatomy, and familiarity with the characteristics of major venous anomalies are essential to avoid this complication.2 Venous anomalies of the inferior vena cava can involve the subrenal, renal, or suprarenal segments. Subrenal segment anomalies include a left-sided inferior vena cava (prevalence of 0.2% to 0.5%) and a double inferior vena cava (1% to 3%). Either of these anomalies may be associated with a right or, rarely, left retrocaval ureter. When present, the proximal ureter is dorsal to the vena cava and, lower down, runs between the vena cava and the aorta. In rare instances, a double right vena cava has been observed. Anomalies of the renal segment of

FIGURE 43–1 • Sites of venous injury. (From Downs A: Problems in resection of aortoiliac and femoral aneurysms. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery. New York, Grune & Stratton, 1980, p 68.)

783

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FIGURE 43–2 • Computed tomography scan demonstrating a retroaortic left renal vein (arrow) in a patient with an abdominal aortic aneurysm.

and right iliac vein at the level of the aortic bifurcation. Complete separation of these structures by circumferential dissection is generally unnecessary, because temporary occlusion can usually be achieved by clamp control or by the use of intraluminal balloon catheters. If one of these veins is inadvertently lacerated, bleeding should be controlled by gentle finger tamponade, and the venous laceration should be closed with a few stitches of fine monofilament suture. Application of clamps is hazardous and may enlarge the rent in the vein. The left renal vein should be routinely identified early during dissection of the aorta above an aneurysm or proximal

FIGURE 43–3 • Magnetic resonance imaging reconstruction of a circumaortic renal vein (black arrow). Note the caudal position of the posterior branch (white arrow).

to the area of major aortic occlusive disease. The caudal border of the left renal vein should be clearly defined so that this structure can be easily retracted out of harm’s way. Division of its lumbar, adrenal, gonadal, or lumbar branches enhances its mobility and improves exposure. Careful consideration should be given to ligating these branches if division of the renal vein is necessary to improve exposure. Failure to find the left renal vein in its usual position suggests its aberrant location behind the aorta (see Figs. 43-2 and 43-3), where it may be readily injured during circumferential dissection of the infrarenal aorta preparatory to application of an occluding clamp.1,2,4,5 An arteriovenous (AV) fistula involving the aorta or iliac arteries is an uncommon complication of spontaneous aneurysm rupture into an adjacent vein (about 80% of cases) or of retroperitoneal injury to these major vessels (20%). The incidence of this complication is quite low; it occurs in less than 1% of all aneurysms and in only 3% to 4% of ruptured aneurysms.6-9 The presence of an AV fistula is suggested by a continuous bruit over the aneurysm associated with the sudden onset of lower extremity venous hypertension, oliguria, hematuria, and congestive heart failure. If suspected, the diagnosis of an aortocaval or iliac AV fistula can be confirmed by color Doppler imaging, computed tomography (CT) scanning, magnetic resonance imaging (MRI), or angiography. The presence of an aortocaval or ilioiliac AV fistula is unsuspected in 25% to 44% of patients at the time of surgery. Occasionally, the fistula may be unsuspected intraoperatively because it is small or obscured by the laminated thrombus within the aneurysm, becoming apparent when sudden massive venous hemorrhage occurs within the lumen of the aorta during evacuation of the laminated thrombus from the aneurysmal sac.10 In this case, direct finger pressure over the fistula, followed by proximal and distal caval compression with sponge sticks or insertion of balloon occlusion catheters, usually controls the bleeding so that the venous defect can be visualized and closed with a running suture from within the aortic sac (Fig. 43-4).11 No attempt should be made to separate the aneurysm wall from the cava at the fistula site. In all patients undergoing aortic aneurysm repair, it is wise to palpate the inferior vena cava for the presence of a thrill, indicating an aortocaval fistula, before opening the aneurysm sac to evacuate the laminated thrombus. If a fistula is suspected, the inferior vena cava should be occluded with a sponge stick or a clamp adjacent to the neck of the aneurysm before the aneurysm is occluded and opened, to prevent embolism of clot or air to the lungs.7 Intraoperative bleeding from iliac AV fistulas is often more difficult to control because of their location deep within the pelvis, the size of the defect, and the intimate relationship between the vein and artery. Elective placement of occlusion balloon catheters above and below the aneurysm via the femoral vein before entering the aneurysm may control venous bleeding and permit closure of the defect without massive blood loss. Autotransfusion is a useful adjunct in the management of aortocaval and iliac fistulas.6 Surgical treatment of aortocaval fistulas includes intraaneurysmal closure of the defect and reconstruction of the aorta with a tube or bifurcated graft. Placement of an endoluminal stent-graft may be the optimal method of treating aortocaval and iliac fistulas when they are recognized preoperatively.12,13 Prophylactic placement of a venacaval filter is

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rarely necessary. Complications following surgical repair occur in 39% of patients and include respiratory failure, stroke, myocardial infarction, paraparesis, and renal failure. The perioperative mortality rate ranges from 6% to 71%, with an average of 34%.11 Arterial bleeding usually arises from the lumbar, anomalous renal, or inferior mesenteric arteries during circumferential aortic dissection or after the aorta has been opened.14-16 Lumbar vessel injury can be avoided in aneurysm surgery by limiting the dissection to its anterior surface and by suture ligature of the lumbar orifices from within the sac after the aneurysm has been opened.9 Precaval location of the right renal artery (5%) and multiple renal arteries (30% to 40%) should be identified. A tear in a fragile aortic wall may occur from suture placement during anastomosis. Additional sutures, frequently with polytetrafluoroethylene (PTFE) pledgets, may be required to control these bleeding points.1 The aorta should be clamped briefly while additional repair sutures are being placed and tied to avoid further tears in the aortic wall. In patients with unfavorable aortic tissues, the use of biologic tissue glues may, on occasion, be helpful. These agents are no substitute for careful hemostasis, however, and their use is associated with more frequent reoperation for bleeding and the potential for infection.17,18 Bleeding in the immediate postoperative period usually comes from suture lines, inadequately ligated lumbar vessels,

A

785

or the inferior mesenteric vein. This is manifested by a continuing need for blood replacement and the development of a retroperitoneal hematoma. This can be identified by palpating the flank, usually the left, which loses its normal soft concavity and becomes distended and tense. When aortic or iliac suture line bleeding is rapid, shock is more obvious, and the patient complains of severe backache similar to the pain of a ruptured aortic aneurysm. Bleeding owing to unrecognized fibrinolysis, especially after repair of thoracoabdominal aneurysms or supraceliac clamping, is often difficult to diagnose intraoperatively. If supraceliac clamping is anticipated or repair of a thoracoabdominal aneurysm is being undertaken, consideration should be given to the infusion of antifibrinolytic agents such as aprotinin or aminocaproic acid (Amicar). It should be noted, however, that there are no prospective data available for the clinical use of these agents in vascular surgery patients.19,20 Postoperative hemorrhage is treated by immediate return to the operating room for identification and control of the bleeding site under fully monitored general anesthesia. Prevention of this complication requires thorough inspection of the intra-abdominal anastomoses and the periaortic area, with special attention to the orifices of the lumbar or anomalous renal vessels, the inferior mesenteric artery, and the ligated or oversewn stumps of the aorta or the iliac vessels. The surgeon should search for the potential bleeding site

B

FIGURE 43–4 • Aortocaval fistula. A, Abdominal aortogram showing filling of the vena cava. B, The fistula orifice is exposed through the aneurysm and controlled by simple digital occlusion of the hole into the inferior vena cava. The fistula is closed with a simple overand-over suture from within the aneurysmal sac. A clear and unencumbered field is provided by rapid aspiration and autotransfusion of blood pouring into the aneurysmal sac from the cava. (B, From Bernhard VM: Aortocaval fistulas. In Haimovici H [ed]: Vascular Emergencies. New York, Appleton-Century-Crofts, 1982, p 357.)

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when blood volume and pressure are at the patient’s normal level before closing the retroperitoneum over the aortoiliac reconstruction. Bleeding owing to unrecognized coagulopathy usually can be prevented by careful preoperative history and evaluation of the platelet count, bleeding time, prothrombin time, and partial thromboplastin time.21 These preliminary screening studies reliably identify the need to search for precise factor deficiencies and direct their replacement before and during surgery. Intraoperative monitoring of the activated clotting time before and after heparin administration is the most effective means of identifying variations in the individual response to intraoperatively administered unfractionated heparin and to determine the adequacy of its reversal before closing the incision.21 Transfusion reaction and disseminated intravascular coagulopathy are rare causes of operative or early postoperative bleeding; however, consumption coagulopathy secondary to massive blood loss and replacement is more common and requires the judicious use of fresh frozen plasma cryoprecipitate and platelets. Proper management of bleeding due to congenital or acquired deficiencies requires repeated monitoring of pertinent coagulation parameters during and immediately after the operative procedure. The rising number of percutaneous and endovascular interventions being performed has resulted in antiplatelet agents’ being administered to increasing numbers of patients. It is not uncommon for patients undergoing coronary or peripheral vessel angioplasty or stenting to receive a combination of drugs, including aspirin, clopidogrel, heparin, and glycoprotein (GP) IIb/IIIa inhibitors such as abciximab, eptifibatide, and tirofibane. Emergency surgical procedures to control bleeding from retroperitoneal hematomas or expanding groin hematomas from cannulation sites can be associated with significant perioperative blood loss into the thigh or retroperitoneum.22-25 Although thromboelastography may be a useful adjuvant to therapy, it is not universally available. Discontinuation of the agent and delay of surgery when feasible is sometimes the preferred option. However, should emergency intervention be required, careful replacement of blood coagulation factors and platelet transfusions may be necessary to control hemorrhage. Recommendations for the discontinuation of antiplatelet agents preoperatively or preprocedurally, although empirical, have to be balanced with the risk of thrombotic occlusion of recently placed stents or stent-grafts. Neilipovitz and colleagues, using decision analysis, showed that the continued use of aspirin reduces perioperative mortality, despite a 2.5% increase in hemorrhagic complications, in vascular surgery patients.25 The antiplatelet effects of clopidogrel persist for 7 to 10 days, so this drug should be discontinued 1 week before surgery. These recommendations are based on observations from case studies of patients undergoing coronary artery bypass grafting who received aspirin and clopidogrel or aspirin and placebo.26 Patients receiving both drugs had a higher rate of major postoperative bleeding (9.6% vs. 6.3%), reoperation (9.8% vs. 1.6%), and blood transfusion (3.0 units vs. 1.6 units) compared with patients receiving aspirin and placebo. The effects of GP IIb/IIIa inhibitors on platelets are quite variable. The antiplatelet effects of eptifibatide are usually abated within 8 hours of cessation of therapy in patients with

normal renal function. Abciximab has a biologic half-life of 8 hours, but its effects on the surface of circulating platelets can be detected for up to 2 weeks after discontinuing the drug.22 THROMBOSIS Graft thrombosis in the early postoperative period is almost invariably due to technical problems (Fig. 43-5) that usually occur at the distal anastomoses.27-29 These include an elevated intimal flap, narrowing of the artery at the anastomotic suture line, failure to remove clot adherent to the inner wall of the graft before completion of the anastomosis, twisting or kinking in the retroperitoneal tunnel, compression of the femoral limb of the graft by the inguinal ligament, unrecognized inflow disease, or inadequate runoff secondary to unappreciated iliac, deep femoral, superficial femoral, or infrapopliteal disease. Rarely, thrombosis after aortofemoral bypass or aneurysm replacement is due to hypercoagulability from antithrombin III deficiency, protein C or S deficiency, a mutation in factor V Leiden or prothrombin genes, homocystinemia, anticardiolipin antibodies, heparin-induced platelet aggregation, or stasis due to reduced cardiac output.30-33 The adequacy of pulsatile blood flow through the graft or endarterectomy should be evaluated in the operating room before the wounds are closed, not only by palpation of the graft itself and the arteries immediately distal to anastomoses but also by palpation of distal pulses and direct inspection of the pedal circulation beneath the drapes. If necessary, noninvasive measurements such as Doppler flow, ankle pressure, or pulse-volume recording tracings can be obtained intraoperatively.27,28,34-36 Intraoperative completion angiograms or color-flow Doppler imaging should be obtained in all patients who have had extensive reconstructive procedures of the common femoral, superficial femoral, or deep femoral arteries to ensure the adequacy of the repair. Noninvasive studies should be performed routinely in the recovery room when pulses cannot be felt distal to the repair or when the anticipated improvement in circulation has not occurred. Objective information obtained from these easily performed studies is particularly valuable in the immediate postoperative period, when patients are frequently hypothermic and peripherally vasoconstricted. Detection of unsatisfactory graft function mandates immediate direct evaluation of the involved anastomoses before wound closure or prompt return to the operating room if graft flow deteriorates subsequently. Treatment of immediate postreconstructive thrombosis consists of thorough inspection of the intraluminal aspect of the involved anastomosis. This is best accomplished through an incision in the distal end of the graft or by takedown of the anastomosis to directly view the intima and the runoff vessels adjacent to the arteriotomy. Effective revision may require stabilization of an elevated plaque, extension of an iliac limb to the common femoral artery, or patch angioplasty of a deep or proximal superficial femoral stenosis. Infrequently, complementary bypass from the femoral to the popliteal or infrapopliteal vessels may be required when adequate runoff cannot be achieved through the deep femoral artery.37,38 The lie of the graft should always be inspected throughout its length to ensure that there is no kinking, twisting, or external compression within the retroperitoneal tunnel. Prevention of early graft thrombosis depends on an accurate evaluation of the distal runoff bed by preoperative noninvasive

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787

1

3 2

5

4

6

A

B

C

FIGURE 43–5 • A, Aortic mechanical factors that may cause early thrombosis of aortofemoral graft: (1) aortic anastomosis distal to obstructing atherosclerosis at the subrenal level; (2) kinking of the graft limb due to placement of the proximal anastomosis low on the aorta, with an overly long aortic graft segment; (3) compression by the inguinal ligament; (4) inadequate runoff due to occlusion of the superficial femoral artery and severe stenosis of the deep femoral artery; (5) elevation of the distal intima; (6) peripheral embolization or thrombosis. B, Operative picture demonstrating a twist in the right limb (arrow) of an aortobifemoral graft. C, Fibrointimal ingrowth resulting in occlusion of the limb of a bifurcation graft. (A, From Bernhard VM: The failed arterial graft: Lost pulses and gangrene. In Condon RE, DeCosse JJ [eds]: Surgical Care. Philadelphia, Lea & Febiger, 1980, p 155.)

hemodynamic testing, magnetic resonance angiography or arteriography, and direct palpation of the iliac artery throughout its length before the selection of this vessel, rather than the femoral, as the site for distal anastomosis. The orifices of the runoff vessels should be inspected and calibrated with dilators. Special attention should be given to the deep femoral orifice, which often requires angioplasty when the distal anastomosis is performed at the common femoral level. Finally, technical perfection in the performance of anastomoses is mandatory to avoid narrowing of the runoff vessels. Tacking sutures may be required to prevent distal intimal dissection. The widespread use of unfractionated and low-molecularweight heparin has resulted in an increased frequency of heparin-induced thrombosis, reported to occur in 5% of patients receiving unfractionated heparin and in 0.5% receiving low-molecular-weight heparin with thrombocytopenia. The combination of heparin and platelet factor 4 stimulates an immunologic response manifested by antibodies to platelets, a decreasing platelet count, and a tendency to thrombosis. Heparin-induced thrombocytopenia should be suspected when the platelet count decreases by more than 50% from baseline or drops to 150,000 or less in patients receiving heparin therapy. Thromboembolic complications can involve the deep veins of the lower extremity, the pulmonary arteries, and major cerebral veins. Arterial thrombolic complications may involve the lower extremities and the coronary, mesenteric, renal, or cerebral arteries. When heparin-induced

thrombocytopenia is encountered intraoperatively, the surgeon has to act without confirmatory tests. If it is suspected owing to the presence of “white clots” or unexplained intraoperative thrombosis, a specimen of the thrombus should be sent to the laboratory for a touch prep to confirm the predominance of platelets in the clot. The administration of all unfractionated heparin should be discontinued.39-41 Laboratory confirmation using the heparin-induced platelet aggregation or C serotonin assay is an integral part of accurate diagnosis. Therapy with direct thrombin inhibitors such as lepirudin, argatroban, or bivalirudin should be initiated. The use of platelet GP IIb/IIIa inhibitors may also play a role. Alternative anticoagulation with aspirin or warfarin should be administered after the use of direct thrombin inhibitors has been discontinued. Thrombosis is the most frequent late complication of aortoiliac and aortofemoral procedures42,43 and usually appears as unilateral limb ischemia.44-50 Impaired outflow through the external iliac artery or the major branches of the common femoral is the most common cause and is due to progressive downstream atherosclerosis or anastomotic fibrointimal hyperplasia (Fig. 43-6). Anastomotic fibrointimal hyperplasia causes stenosis, usually at distal anastomoses, by the circumferential development of fibrous tissue at the distal graft-artery interface; occlusion occurs when flow diminishes sufficiently to result in stasis thrombosis.49 The majority of patients initially managed with aortofemoral bypass have occlusion of the superficial femoral artery at the time of the primary procedure.

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Noninfectious Complications in Vascular Surgery

FIGURE 43–6 • Progres-sive inflow and outflow obstruction. A, Aortogram demonstrating progressive atherosclerosis proximal to an incorrectly placed bifurcation graft (arrow). B, Obstruction due to intimal thickening at the distal limb of an aortobifemoral graft (arrow).

A

B

Therefore, an adequate lumen at the origin of the deep femoral artery is the most significant factor in ensuring long-term patency of these grafts.35,43,45,48,50 Underestimating the severity of outflow disease at the time of primary reconstruction is an important cofactor in progressive atherosclerosis that increases susceptibility to late graft limb occlusion.51 Despite an adequate primary procedure, progression of femoral or infrapopliteal atherosclerotic disease is more likely to occur in patients with continued exposure to atherogenic risk factors, particularly those who continue to smoke.44,51 Impaired inflow is the second most common cause of late postrevascularization thrombosis. Although it is four to nine times less frequent than impaired outflow,51 it is the most common cause of simultaneous bilateral postreconstructive lower limb ischemia after aortoiliac or femoral surgery.43,46 The most common mechanism is obstruction from progressive infrarenal aortic atherosclerosis proximal to the site of previous repair (Fig. 43-5A). This is usually the consequence of placing the proximal anastomosis too low on the aorta (i.e., at or below the inferior mesenteric artery; Fig. 43-6A). The area between this site and the renal arteries is an active site of progressive atherosclerosis.35 Likewise, following aortoiliac endarterectomy, late occlusion is more likely if the proximal infrarenal aorta is not included in the endarterectomy.52 The use of an end-to-end rather than an end-to-side aortic anastomosis may be associated with fewer thrombotic failures, although this has not been clearly defined. Superior hemodynamic flow characteristics, the absence of competitive flow, less chance of embolization from the host aorta, and less angulation of the limbs as they arise from the body graft35,52 have been cited as the advantages of the end-to-end aortic anastomosis. Angulation of the graft limb at the bifurcation may produce kinking due to failure to pull the graft limb out to full length before the distal anastomoses are performed or excessive length of the graft body, resulting in too wide a bifurcation angle (Fig. 43-5B). Inadequate retroperitoneal tunneling of the graft

limbs may promote thrombosis as a consequence of extrinsic compression from the mesentery of the sigmoid colon or the recurrent portion of the inguinal ligament (Fig. 43-5C).51 Less frequent causes of late thrombosis of aortoiliac and femoral reconstructions include accumulation of mural thrombus and false aneurysm. Mural thrombus develops when the graft diameter is significantly larger than the outflow artery. The flow pattern of the larger graft adjusts itself to the smaller outflow artery, leaving a peripheral layer of slowly moving blood that clots to form the mural thrombus. The normal, smooth, firmly adherent fibrous neointima becomes lined with a thick, gelatinous, loosely adherent mural thrombus that reduces the functioning lumen to the diameter of the outflow vessel. Fragmentation with distal embolization or progressive narrowing of the graft lumen with secondary acute thrombotic occlusion may then occur.49 Anastomotic false aneurysms, although relatively rare causes of late limb ischemia, may also produce peripheral embolization or thrombosis of the aneurysm and the adjacent vessel lumen.51 Finally, an aortoiliac reconstruction can progress suddenly to thrombosis in the presence of cardiac embolization or decreased cardiac output secondary to myocardial infarction or congestive heart failure. Rarely, no apparent cause for late thrombosis can be identified, implicating thrombogenicity of the graft surface or degeneration and disruption of the neointima. The diagnosis of late thrombosis is suggested by the sudden or progressive recurrence of symptoms, a decrease or loss of previously present distal pulses, and a concomitant reduction in ankle pressure, Doppler flow, or pulse-volume recording waveform. The degree of ischemia after thrombosis of a reconstruction is usually more severe than before the primary revascularization procedure.43,46 The frequency of late thrombosis increases from 5% to 10% in the first 5 years to 20% to 30% at 10 years.35,50,53-55 Therefore, routine and longterm follow-up of these patients at regular intervals is required to monitor the adequacy of graft function. If significant stenosis can be demonstrated before complete thrombosis, surgical

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correction is simplified. When either abrupt or gradual change is apparent, prompt aortography should be performed to determine the status of the graft, the anastomoses, the inflow, and the runoff bed.34,56 The severity of recurrent ischemia may range from minimal to severe claudication to rest pain to pregangrene, depending on the extent of compensating collaterals and the vigor of the patient’s normal activity. Arteriography is required to determine whether further surgery is feasible and to guide the surgeon in the selection of the most appropriate reoperative or interventional procedure, considering the patient’s age, state of health, and general level of activity.44,51 Correction of late thrombosis requires preoperative delineation of the underlying mechanical problem, followed by appropriate corrective maneuvers.51,57 The occlusion of one limb of an aortoiliac bifurcation graft is usually due to overlooked or progressing disease in the external iliac and femoral arteries. Thrombolytic therapy may be useful in delineating the artery involved by the progression of atherosclerosis. Balloon catheter angioplasty with stenting is not usually indicated because of the extent of the disease or location beneath the inguinal ligament. One reliable solution consists of retroperitoneal exposure of the occluded limb, balloon catheter thrombectomy, and graft extension to the femoral level. Femorofemoral bypass is an alternative if the donor iliofemoral inflow is satisfactory, especially in a high-risk patient. Axillofemoral bypass may be required if neither of the preceding methods is feasible.2,37 The most commonly encountered situation is a thrombosed aortofemoral graft limb with impaired outflow. Inflow can usually be restored by the use of thrombolytic therapy or graft thrombectomy using a balloon thromboembolectomy catheter (Fig. 43-7).57 A thromboendarterectomy stripper or adherent clot catheter is often required to complete the

789

extraction of adherent clot and old pseudointima. The Fogarty occlusion catheter is passed through the ring of the stripper into the patent aortic portion of the graft, and its balloon is fully inflated and pulled down to occlude the proximal end of the limb to control bleeding and prevent crossover embolization. The stripper is passed back and forth around the catheter within the occluded graft limb up to the distended balloon to scrape thrombus from the graft wall. Thereafter, the balloon is deflated just enough to permit its tight withdrawal through the graft limb along with the stripper and detached thrombus (see Fig. 43-7). Use of the Fogarty adherent clot catheter obviates the need for the thromboendarterectomy stripper and may be more effective in removing adherent thrombus. The patient is systemically heparinized (100 to 125 units/kg) during all these maneuvers. Thrombectomy is usually combined with a profundaplasty of varying extent to provide outflow. However, femoropopliteal or femorodistal bypass may be required, depending on the extent and location of outflow disease.37,38,57,58 If an occluded graft limb cannot be reopened by thrombectomy, a femorofemoral graft can be inserted. Replacement of the graft limb is another alternative but is technically more difficult. Endovascular options include thrombus removal by catheter aspiration, AngioJet, or some of the newer mechanical devices. These therapeutic modalities are often combined with the use of thrombolytic agents.59 If an entire bifurcation graft is thrombosed, a problem at the proximal anastomosis, such as low placement of the graft with progression or unrecognized proximal disease, kinking, or anastomotic aneurysm, is a likely cause. A CT scan is required to identify the last entity. If no proximal problem can be demonstrated, thrombectomy with either a balloon or an adherent clot catheter can be attempted but is usually not successful. The alternatives are to replace the original

Adherent clot catheter

Balloon tension

Vascular stripper

A

Balloon and stripper withdrawn together

Graft reanastomosis to patch repair of common and deep femoral arteries

B

FIGURE 43–7 • A, A ring endarterectomy stripper is used in conjunction with a balloon catheter or adherent clot catheter to remove thrombus and pseudointima adherent to the wall of an occluded limb of an aortofemoral graft. The cleared graft limb is then sutured to the common or deep femoral outflow after patch angioplasty. B, Intraoperative arteriogram demonstrating residual thrombus (arrow) in the proximal right limb of an aortobifemoral graft after attempted thrombectomy. (A, From Bernhard VM: Late vascular graft thrombosis. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery, 2nd ed. Orlando, Fla, Grune & Stratton, 1985, p 193.)

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prosthesis or insert an axillobifemoral bypass. The latter procedure is less technically demanding and less hazardous and is the reoperation of choice in a physiologically compromised patient.57 When groin scarring is especially intense, bypass to the mid-deep femoral artery simplifies the outflow repair of the reoperative procedure by avoiding a tedious and hazardous dissection in the area of a previous femoral anastomosis.60 An aggressive attitude toward reoperation after thrombotic failure of aortoiliac reconstruction is warranted, especially if the patient will derive sustained benefit from long-term patency and improved limb function.57 Operative morbidity and mortality rates are low. Reoperative mortality rates of 3% and cumulative 3-year patency rates of 68% to 75% have been reported.43,57 Judicious use of extra-abdominal approaches has contributed significantly to reduced reoperative morbidity and mortality.51 Lytic Therapy for Graft Thrombosis Whereas thrombectomy has been the treatment of choice in the management of occluded aortofemoral and femoropopliteal bypass grafts, incomplete removal of thrombotic material and the difficulties associated with reoperation have led to the evaluation of direct intra-arterial infusion of thrombolytic agents, either preoperatively or intraoperatively, for the management of this problem.61 The potential benefits of lytic therapy include delineation of the cause of the graft thrombosis (most commonly distal occlusion due to neointimal fibrous hyperplasia or progression of disease) and, as a consequence, a shorter operation, reduced blood loss, ease of extracting any residual thrombus, and reduced wound complication rate. Potential disadvantages and complications of thrombolytic therapy include the need for monitoring in an intensive care unit, delay in surgical intervention, and risk of bleeding or renal impairment from the contrast load required for frequent arteriographic evaluation. Further, mechanical thrombectomy for aortofemoral graft limb occlusion is at least as effective as clot lysis and adds little to the operative procedure required to restore outflow. Successful lysis, which does not appear to be affected by the duration and cause of the graft thrombosis, can be achieved in 50% to 90% of occluded prosthetic graft limbs, 50% to 77% of saphenous veins, and 38% to 71% of prosthetic grafts.62-67 Thrombolytic agents enzymatically break down cross-linked fibrin strands within the thrombus by converting plasminogen to plasmin. Streptokinase, the first agent to beome available, is seldom used to treat arterial or graft thrombosis. Urokinase was, for years, the agent of choice until it was withdrawn from the market. Alteplase or reteplase and, more recently, tenecteplase are currently being evaluated. Infusion of the thrombolytic agents is usually accomplished by a multi-side-hole catheter or an infusion wire placed so that it covers the extent of the thrombus. There are multiple dosage regimens advocated for the use of these agents. Urokinase is usually given in a dose of 80,000 to 100,000 units/hour, reteplase at 0.25 to 1 unit/hour, alteplase at 0.25 to 10 mg/hour, and tenecteplase at 0.25 to 0.5 mg/hour. Heparin in a dose of 300 to 500 units/hour is usually administered through the access sheath to prevent pericatheter thrombosis.68-72 Patients are carefully monitored in the intensive care unit for evidence of bleeding. Blood is drawn for hemoglobin,

hematocrit, fibrinogen, prothrombin time, and partial thromboplastin time every 4 to 6 hours. Following successful lysis, the underlying lesion is treated with either catheter-based techniques or surgery. Long-term anticoagulation with warfarin is usually indicated. Bleeding, the major complication of lytic therapy, occurs after 7% to 48% of infusions.65,73 The most common sources of bleeding are arteriography or venous puncture sites, the interstices of prosthetic grafts, and systemic bleeding from remote sites. Central nervous system bleeding is rare with urokinase. Bleeding from a groin arterial puncture site may also result in femoral pseudoaneurysm or retroperitoneal hematoma, which may compress the femoral nerve within the iliac fascia or in the thigh. The resulting femoral neuralgia, reported to occur in up to 30% of patients, may persist for as long as 1 year.74,75 Rarely, patients develop a femoral nerve palsy; this may be debilitating, especially in patients with claudication or amputation of the contralateral limb. The most important determinant of long-term success in the study by Gardiner and coworkers was the presence of a lesion correctable by surgical revision or balloon catheter dilatation.76 Such lesions responsible for the occlusion can be identified in approximately 50% of patients. Gardiner and coworkers reported an 84% 1-year patency rate in 25 grafts with underlying stenotic lesions, compared with 37% of a similar number of grafts without detectable lesions. Three prospective studies compared the efficacy of intraarterial thrombolysis and surgery in patients with lower limb ischemia.77-79 In their initial study, Ouriel and colleagues randomized 114 patients with acute lower limb ischemia of less than 7 days’ duration to receive either thrombolytic therapy or surgery.77 The authors achieved clot dissolution in 70% of their patients and observed no difference in limb salvage rates (82%) at 1 year. However, they did observe improved patient survival (82% vs. 58%) in the patients receiving thrombolytic therapy, which they attributed to the more frequent occurrence of cardiopulmonary complications in the patients undergoing surgery. In a subsequent study, Ouriel and associates randomized 213 patients with acute limb ischemia of less than 14 days’ duration to either recombinant urokinase or surgery.78 Clot lysis was achieved in a similar number of patients (71%). The authors found no differences in either mortality rates (14% vs. 16%) or amputation-free survival rates (75% vs. 65%) between the two groups at 1 year. In the Surgery versus Thrombolysis for Ischemia of the Lower Extremity (STILE) trial,79 the efficacy of recombinant tissue plasminogen activator (rt-PA) and urokinase was compared with that of surgery in 393 patients with limb ischemia of less than 6 months’ duration. Failure of catheter placement occurred in 28% of patients. Patients with ischemia of less than 14 days’ duration receiving lytic therapy had lower amputation rates than did surgical patients, whereas patients with ischemic symptoms of more than 14 days’ duration fared better with surgery. The results of these studies suggest that in selected patients, thrombolytic therapy may be a useful adjunct or alternative to surgical therapy. However, long-term patency rates of 28% to 37% of thrombolysed grafts are clearly inferior to those obtained with surgery.76,80 Thrombolytic therapy may be extremely valuable in patients with limbthreatening ischemia secondary to thrombosed popliteal aneurysm. Thrombolysis may improve the chances of achieving long-term patency and limb salvage.81

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Although there have been no large trials evaluating alteplase in the treatment of peripheral arterial occlusion, anecdotal reports suggest an increased incidence of local and remote bleeding, predominantly intracranial hemorrhage, with its use. Recently, the use of limited doses of alteplase was shown to be equivalent to urokinase in terms of the incidence of bleeding and mortality. Shortell and colleagues, in a comparison of limited-dose t-PA and urokinase, demonstrated improved clot lysis (76% vs. 50%) with t-PA at a dose of 2 mg/hour, for a total of 100 mg.69 The agents were equivalent in unmasking stenoses (85% vs. 84%), but t-PA was superior to urokinase in unmasking runoff vessels (81% vs. 39%). Reteplase, a nonglycosylated deletion mutant of t-PA, is an attractive alternative to urokinase. Reteplase catalyzes the cleavage of endogenous plasminogen to generate plasmin, which degrades the fibrin matrix of the thrombus, resulting in its dissolution. The half-life of reteplase is 13 to 16 minutes, and catheter-directed infusion doses vary between 0.25 and 1.0 unit/hour for a duration of 5 to 24 hours. Lacing or infiltrating the thrombus with a 2- to 5-unit bolus dose may be beneficial in some patients.82 In approximately half of patients, low-dose heparin is infused concomitantly. Reteplase differs from alteplase both in its structure and biochemical composition and in its lower affinity for thrombin. McNamara reported a 34% incidence of bleeding in a series of 40 patients treated with alteplase, compared with 3% among those receiving reteplase at doses of 2 to 8 mg/hour.83 Even reducing the dosage of alteplase to 0.5 to 1 mg/hour was still associated with a 25% incidence of bleeding requiring transfusion. The indications for and contraindications to the use of these two agents are similar to those of urokinase. Allie and colleagues reported a 95.8% procedural success rate, with a mean infusion time of 7.5 hours and a lower complication rate, using a combination of tenecteplase and postprocedural tirofiban.68 In all cases, the risks and benefits of the use of lytic therapy in the treatment of patients with graft limb occlusions must be carefullly evaluated. The relatively low incidence of complications, improved technique of administration, and efficacy of thrombolytic agents have reduced the need for urgent thrombectomy in patients with noncritical limb ischemia. Successful lytic therapy readily identifies the cause of the graft limb occlusion and may allow a less extensive repair. In addition, lytic therapy may reduce the risk of wound and graft complications and reduce the incidence of reperfusion edema associated with extensive redo procedures. Mechanical Thrombectomy Mechanical thrombectomy devices that theoretically permit rapid revascularization of an ischemic extremity using minimally invasive techniques are gaining in popularity. The use of mechanical energy to cause fragmentation, dissolution, and aspiration of thrombus is appealing. These devices can be broadly classified into (1) aspiration thrombectomy catheters that remove thrombus by steady manual suction through a large-lumen aspiration catheter; (2) pull-back thrombectomy catheters that withdraw thrombus with a balloon catheter or basket into a trapping device, allowing the clot to be removed; (3) recirculation thrombectomy devices that ablate thrombus by hydrodynamic vortices, which pulverize the thrombus into

791

microscopic fragments; (4) nonrecirculation thrombectomy devices, which macerate the thrombus mechanically into fragments that are larger than those produced by recirculation catheters; and (5) energy-assisted devices, which use either ultrasound, laser, or radiofrequency to lyse thrombus or enhance the effects of pharmacologic agents.84 Most of these devices presently have U.S. Food and Drug Administration approval only for use in occluded hemodialysis grafts. A number of these devices are currently being evaluated clinically, with complete angiographic success reported in approximately 50% of patients and partial success in an additional 27%.85 Concomitant lytic therapy or balloon angioplasty is often a necessary adjunct. The most extensively studied device is the AngioJet rheolytic thrombectomy system, which is approved for peripheral arterial and coronary applications.86 Adjunctive low-dose thrombolysis is necessary in 18% to 58% of patients. Chief disadvantages of the current device include the possibility of renal overload and hemolysis. The major treatment limitation of these devices is their lack of efficacy against organized thrombotic or embolic material.59 The recent report by Sarac and colleagues suggests that the combination of a lytic agent and a mechanical device may be as effective as thrombolytic dissolution of the thrombus.86a OPERATIVE EMBOLIZATION Atherothrombotic debris is present to some degree in most atherosclerotic arteries and especially in the distal aorta. Protruding atheromas of the aortic arch and descending aorta have assumed increasing importance as potential sites for embolization during cardiac catheterization or bypass surgery.87 Readily detectable by transesophageal echocardiography, lesions larger than 0.5 cm are most likely to be associated with embolic events.88,89 Variable amounts of this material may be dislodged and carried into the downstream arterial territory as a consequence of manipulation during arterial dissection.34,89,90 Embolization may also occur on reestablishment of circulation owing to the accumulation of fresh thrombus in the temporarily static blood column above or below the clamps if it is not carefully evacuated before circulation is restored. Larger emboli lodging in major vessels can usually be retrieved with a balloon thrombectomy catheter. Smaller embolic particles that cannot be retrieved will be flushed into end arteries of the feet or toes, leading to the “trash foot” syndrome.1,34,89,90 The end result is the appearance of patchy areas of painful skin gangrene at these sites (Fig. 43-8). This may be a minor and self-limited problem, or it may produce extensive gangrene of all the digits and the forefoot, leg, buttocks, and, rarely, abdominal wall. Prevention is key, because it is frequently difficult or impossible to treat this complication. A variety of technical maneuvers have been employed to prevent operative embolization.1 Unnecessary and overly vigorous handling of vessels before the application of clamps should be avoided. Effective preclamping heparinization, preferably monitored by intraoperative measurement of the activated clotting time, reduces stasis thrombus formation above the proximal clamp and in the sluggish circulation distally. In patients with suspected or demonstrable atheromatous debris within the aorta on CT scans, the distal clamps should be applied to the common femoral or iliac arteries before proximal occlusion to avoid downstream displacement of debris when the aortic

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FIGURE 43–8 • Atheroembolic ischemic lesions of the toes. (From Eastcott HHG: Complication of aortoiliac reconstruction for occlusive disease. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery. New York, Grune & Stratton, 1980, p 59.)

clamp is placed. The proximal clamp may need to be placed at the level of the diaphragm if the pararenal segment of the aorta appears to be involved. The lumen of the aortic prosthesis should be thoroughly aspirated to remove blood and debris after testing the proximal suture line, and efforts should be made to prevent the accumulation of blood within the prosthesis while distal iliac or femoral anastomoses are being performed. Vigorous prograde flushing of the proximal vessel and retrograde flushing from the distal arteries as the last few stitches are being placed in an anastomosis, before the restoration of circulation, is the most reliable maneuver to ensure that retained debris and clot are effectively removed.90 Treatment depends on the severity of embolization. Minor patchy areas of cyanosis or necrosis can be observed, with spontaneous recovery anticipated. More extensive involvement with threatened viability of the distal foot requires attempted removal of embolic material with small Fogarty catheters passed into the distal vessels through the patent popliteal artery, accompanied by distal intra-arterial infusion of urokinase or rt-PA. Occasionally, when there is severe ischemia of a single or multiple digits, lumbar sympathectomy or amputation may be necessary. In patients with a patent superficial femoral artery and severe forefoot ischemia, intra-arterial lytic therapy may reduce the level of amputation. DECLAMPING HYPOTENSION A sudden decrease in blood pressure should be anticipated after removal of the aortic clamp to restore flow to one or both extremities after aortoiliac reconstruction.91-94 The cause is hypovolemia due to incompletely replaced blood loss and

fluid sequestration during surgery, compounded by a variable degree of preoperative dehydration that is usually present.15 Contributing factors are peripheral vasodilatation secondary to limb ischemia during the period of aortic occlusion and a decrease in cardiac output caused by a sudden return of acidic blood and other vasoactive metabolites to the central circulation on restoration of limb perfusion. The major consequences are significant reduction in coronary perfusion, which may promote myocardial injury, especially in patients with significant coronary artery disease, and temporary renal ischemia, which may contribute to renal failure. Prevention is preferable to treatment after a hypotensive insult has already occurred and depends on adequate hydration and effective restoration of intravascular volume during the procedure, and especially before clamp release.93-95 Effective volume replacement requires careful monitoring of blood loss and accurate estimation of the extracellular fluid shifts due to sequestration and loss from evaporation. The extent of intravascular depletion is directly related to the duration of intraperitoneal and retroperitoneal exposure during surgery. The most reliable guide to ensuring adequate volume replacement without circulatory overload is the use of a Swan-Ganz catheter to monitor left heart filling pressures and myocardial performance.95 Cooperation between the surgeon and the anesthesiologist is essential during the critical moments before clamp release. Left atrial filling pressures should be optimized before release of the clamps. The arterial pressure must be continuously observed while blood flow is slowly restored to the extremities by gradual release of the clamp until full flow can be tolerated without hypotension. Finally, when a bifurcation graft is inserted, it is best to complete the anastomosis to one limb and restore its circulation immediately so that lower body perfusion can be resumed with the least amount of delay; this avoids washout acidosis and reduces declamping hypotension. RENAL FAILURE Acute renal failure (ARF) accompanying aortic surgery has a major impact on operative mortality. The reported incidence of ARF following elective aortic aneurysmectomy is 1% to 8%, with a mortality rate of 40%. However, if the aneurysmectomy is emergent, the reported incidence of ARF is 8% to 46%, with a mortality of 57% to 95%.96,97 The major cause is reduced renal perfusion due to decreased cardiac output, decreased blood volume, and dehydration. A contributing factor is renal cortical vasospasm produced by infrarenal application of the aortic clamp, which stimulates the reninangiotensin mechanism.98,99 Other promoting factors include suprarenal aortic cross-clamping, which totally eliminates renal perfusion; ligation of the left renal vein; and intraoperative renal arterial embolization.100 The last may originate from debris and clot accumulating proximal to the aortic clamp or from manipulation of the juxtarenal aorta.97,101 Renal artery obstruction may be produced by displacement of large atherosclerotic plaques at the orifices of the renal arteries when an aortic clamp is applied. Preoperative angiography or CT may produce a mild to moderate degree of renal dysfunction, which can be compounded by hypotension and dehydration during the operative procedure.97 Myoglobinemia can occur after restoration of circulation to limbs that have been severely ischemic for an extended period.

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Finally, nephrotoxic antibiotics and contrast agents employed perioperatively must be considered. Although the consequences of ischemic injury to the kidney are complex, injury to the tubules is central to the development of oliguria. Obstruction of the tubular lumen by cellular debris and casts results in reduction of the ultrafiltration pressure and sequestration of tubular fluid within obstructed tubules, in addition to back-leak of fluid into the interstitium.102 The critical issue is prevention, which is related primarily to the maintenance of an effective circulating blood volume and adequate hydration in the immediate perioperative period.97,103 It is essential that the patient be well hydrated and have a good urinary output at the commencement of surgery. Any significant extracellular fluid volume deficits should be restored the evening before surgery, especially if angiography, CT, or a mechanical bowel preparation has been performed recently. The creatinine level should be measured after procedures requiring contrast administration, and if a decrease in renal function is identified, surgery should be delayed, if possible. Central filling pressures should be monitored perioperatively to ensure that volume replacement is optimal in relation to cardiac output and myocardial performance.95 It is appropriate to give mannitol and commence an infusion of renal-dose dopamine just before cross-clamping the aorta to promote an osmotic diuresis and reduce the effects of renal cortical vasospasm.98 Bicarbonate is given to alkalinize the urine if there is any question of significant myoglobin washout from renewed perfusion of limbs that have undergone prolonged ischemia. Renal insufficiency is a significant complication of surgical procedures requiring cross-clamping of the suprarenal aorta. Currently, a number of therapeutic maneuvers, including fluid loading, calcium channel blockers,104 atrial natriuretic peptide, insulin-like growth factor,105 urodilatin,106,107 endothelin antagonists,108 and fenoldopam,109 are being evaluated to determine their efficacy in reducing the incidence of ARF. During dissection required to gain proximal control of large infrarenal or juxtarenal aneurysms, the left renal vein is vulnerable to injury. Access to this portion of the aorta is facilitated by division of the left renal vein.110 In the past, this maneuver was viewed as one of little long-term consequence. However, Huber and coworkers111 and Abu Rahma and associates112 demonstrated increased serum creatinine concentrations in patients who had renal vein ligation. Whether the renal dysfunction following renal vein ligation is solely a consequence of the resultant increased venous pressure or develops from a combination of venous hypertension and transient ischemia from intraoperative suprarenal clamp placement (which is required more frequently in these patients) is not yet clear. Nonetheless, it is prudent to repair the renal vein if there is congestion of the left kidney and reanastomosis can be accomplished without undue tension.110,113,114 Renal arteries should be dissected free and temporarily clamped in patients with total aortic occlusion and thrombus that extends up to the renal orifices. The quality of the renal pulses must be evaluated and the blood flow assessed by Doppler color-flow imaging after restoration of circulation through the aorta in any patient who has had significant juxtarenal aortic manipulation or if urine output suddenly diminishes. Immediate renal repair is required if renal artery occlusion is identified.

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Postoperatively, the continued retroperitoneal and intraperitoneal sequestration of extracellular fluid requires replacement with Ringer’s lactate solution, within the limits imposed by left heart filling pressures, to ensure adequate renal output.15 Volume replacement should be reduced after the second postoperative day to prevent fluid overload from the mobilization of large volumes of sequestered extravascular fluid. The urinary output is monitored continuously and should be maintained at or above 0.5 mL/kg per hour. The specific gravity is determined frequently, and the blood urea nitrogen and creatinine are measured daily for 2 or 3 days to determine the quality of renal function. Diuretics should not be given until intravascular volume has been fully restored. If ARF is diagnosed, fluid replacement should be restricted to maintain central filling pressure in the normal range. Dialysis is used aggressively to control excess volume and relieve azotemia and hyperkalemia.97,115 Intravenous hyperalimentation or parenteral nutrition should be instituted early in the clinical course of patients with ARF to minimize protein catabolism.116 Renal artery stenosis or impaired renal function is frequently present in patients undergoing aortic reconstruction for occlusive and aneurysmal disease. The liberal use of CT, magnetic resonance angiography, or aortography before surgery is recommended to identify renal anomalies, renal artery stenoses, or suprarenal extension of an aneurysm so that appropriate alterations in operative management can be planned. Often, renal revascularization can be accomplished by balloon angioplasty and stenting along with operative or endovascular correction of the aortic disease. In this setting, patients often have impaired renal function, and the considerable volume of contrast agents used for imaging studies or intervention may result in additional nephrotoxicity. The preoperative administration of acetylcysteine has been shown to reduce contrast-related ARF from 12% to 2% to 4%.117,118 Additional maneuvers to reduce the risk of renal ischemia include the use of temporary renal perfusion with cold lactated Ringer’s solution containing heparin, mannitol, and methylprednisolone.97 Postoperatively, a renal scan or aortography should be performed immediately if total renal shutdown appears, because this suggests a renal artery occlusion. This requires immediate reoperation to restore kidney circulation. INTESTINAL ISCHEMIA Intestinal ischemia may complicate aortic bypass or endarterectomy for occlusive disease, but the majority of cases follow aneurysmectomy.119,120 Almost all reported instances of intestinal ischemia following aortic surgery are a result of arterial obstruction; venous ischemia is extremely rare.121 Small bowel ischemia occurs in 0.15% of cases.119 The clinical presentation of ischemic colitis occurs in 0.2% to 10% of aortic procedures and most commonly involves the rectosigmoid area.122 However, if routine colonoscopy is performed, a much higher incidence of intestinal ischemia is noted because of the identification of subclinical ischemic colitis. Hagihara and associates found a 6% incidence of ischemic colitis in patients undergoing elective or urgent reconstruction of the abdominal aorta for aneurysmal or occlusive disease, whereas the incidence was 60% following repair of ruptured aneurysms.123 The overall mortality rate for patients with colon ischemia is approximately 50% and approaches 90% for transmural colon involvement.

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The cause of bowel ischemia is operative atheroembolization or interruption of the primary or collateral arteries to the bowel wall.119,120 Two sets of vessels are critical to colon perfusion: (1) the superior rectal branch of the inferior mesenteric artery, which connects with the middle and inferior rectal branches of the hypogastric vessels, thus connecting the visceral and systemic circulations; and (2) the inferior mesenteric artery and its left colic branch, which connect with the superior mesenteric artery through the arch of Riolan and, to a lesser extent, the marginal artery of Drummond.122 The former connection is referred to as the “meandering mesenteric artery,” especially when it becomes enlarged as a collateral to compensate for superior or inferior mesenteric artery obstruction.124 This vessel is present in about two thirds of normal people and can be seen on angiography in 27% to 35% of patients who have aneurysmal or occlusive disease.125 Areas of deficiency in this normal anatomic relationship are at Griffith’s point at the splenic flexure and in the collateral vessels of the rectosigmoid (Fig. 43-9). Obstruction of the primary arteries supplying the viscera makes viability of the bowel dependent on this collateral circulation. Occlusion of the orifice of the inferior mesenteric artery is frequently associated with aneurysmal disease and obstructive aortic atherosclerosis, thus placing the burden of bowel circulation on collaterals from the superior mesenteric artery and the hypogastric vessels. Severe obstruction or

Griffith’s point

IMA

Hypogastric artery

FIGURE 43–9 • Lack of marginal artery continuity at the splenic flexure (Griffith’s point), with inferior mesenteric artery (IMA) and hypogastric artery occlusions predisposing to left colon ischemia. (From Ernst CB: Colon ischemia following abdominal aortic reconstruction. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery. New York, Grune & Stratton, 1980, p 383.)

occlusion of the superior mesenteric artery is compensated for by branches from the celiac artery and retrograde flow from the inferior mesenteric artery through the left colic and middle colic arteries. Hypogastric obstruction requires collateral flow from branches of the inferior mesenteric artery. When this source is also impaired, colon circulation must depend on more tenuous connections between the arch of Riolan and the marginal artery and the distal branches of the hypogastric, which in turn derive their blood supply from the parietal circulation. A critical loss of blood flow to an intestinal tract that is dependent on this extensive collateral network may occur if a patent inferior mesenteric artery is ligated during aortic surgery. Collateral flow may be further compromised by ligating the inferior mesenteric artery peripherally rather than flush with the aortic wall, because this may occlude the connection between the left colic and superior rectal arteries. Failure to ensure perfusion through at least one hypogastric may promote colon ischemia if this is the primary supply in the absence of the inferior mesenteric artery or effective collateral flow from the meandering artery. Loss of the inferior mesenteric artery or the meandering artery produces right colon and small bowel ischemia when these viscera depend on retrograde flow because of superior mesenteric arterial occlusion (Fig. 43-10). The large hematoma associated with a ruptured aneurysm may compress significant collateral vessels, which may explain the high incidence of colon ischemia in this circumstance.119 Further, angiography is almost never available before repair of a ruptured aneurysm, and the surgeon has no precise information regarding intestinal circulation to allow the design of an operative procedure that will conserve or augment colon perfusion. A relatively unrecognized cause of mesenteric ischemia is cardiopulmonary bypass. Although acute ischemia occurs in only 0.49% of patients, visceral ischemia is a significant contributing factor in 11% of deaths after coronary revascularization. Preexisting visceral occlusive disease, cardiac or aortic arch embolization, use of an intra-aortic balloon, postoperative renal failure, duration of cardiopulmonary bypass, and cross-clamp times are important contributing factors.126 Depending on the severity of ischemia and the thickness of the bowel wall involved, three forms of ischemic colitis are recognized. Type I is mucosal ischemia, which is transient and mild. Type II, with mucosal and muscularis involvement, reflects more severe ischemia that may result in healing with fibrosis, scarring, and stricture. Type III is transmural ischemia, which produces irreparable damage with gangrene and bowel perforation.127 The clinical manifestations of intestinal ischemia immediately after aortic surgery are often masked by incisional discomfort and other problems that may explain abdominal pain, tenderness, fever, an elevated white blood cell count, and fluid sequestration. Findings that suggest the presence of intestinal ischemia and progressing infarction of the colon include progressive distention, sepsis, increasing peritoneal signs, and unexplained metabolic acidosis. The most common clinical presentation is diarrhea, either brown liquid or bloody, which occurs in 65% to 76% of patients with intestinal ischemia.122,128 Although the onset may occur as long as 14 days after operation, diarrhea usually appears within 24 to 48 hours after surgery.122 Bloody diarrhea has been reported to be a more ominous prognostic sign than nonbloody diarrhea129; however, some investigators have noted no correlation between extent of ischemic injury and presence of bloody diarrhea.129

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FIGURE 43–10 • A, When the superior mesenteric artery (SMA) is occluded, meandering mesenteric blood flow is from the inferior mesenteric artery (IMA) to the SMA. Meandering mesenteric sacrifice under these conditions predisposes to small bowel as well as colon ischemia. B, Selective visceral angiogram demonstrating a meandering mesenteric artery. (A, From Ernst CB: Colon ischemia following abdominal aortic reconstruction. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery. New York, Grune & Stratton, 1980, p 385.)

795

Meandering mesenteric

Occluded SMA IMA

A Postoperative Clostridium difficile colitis may mimic ischemic colitis. Therefore, in critically ill patients who develop fever, abdominal distention, diarrhea, and leukocytosis after emergency aortic procedures, stool specimens for culture and for C. difficile toxin should be obtained and endoscopic evaluation of the colon performed. Appropriate antibiotic therapy (metronidazole or vancomycin) should be instituted if the diagnosis of C. difficile is confirmed.130,131 Because of the high mortality rate associated with transmural colonic ischemia (80% to 100%), early diagnosis is the key to effective management. The diagnosis depends on a high index of suspicion and the prompt performance of endoscopy with the flexible sigmoidoscope or colonoscope.132 Sigmoid colon pH monitoring begun before surgery and continued postoperatively has been used with some success by Björck and Hedberg to identify patients at risk for ischemic colitis.133 They found that a sigmoid colon pH below 6.86 for 9 to 12 hours had a sensitivity of 100% and a specificity of 97% for predicting ischemic colitis. When sigmoid colon acidosis below 7.10 was reversed within 2 hours, no major complications developed, but when it was prolonged, 8 of 10 patients developed major complications. Further evaluation of sigmoid colon pH monitoring appears warranted before its widespread application. The occurrence of ischemic colitis without left colon involvement is rare enough that endoscopy to 40 cm is usually sufficient to establish the diagnosis.119 Once ischemic colitis is detected, endoscopy should be terminated to avoid perforation. Mild changes of ischemic colitis consist of submucosal hemorrhage and edema that is usually circumferential. Pseudomembranes, erosions, and ulcers indicate more advanced ischemia. A yellowish-green, necrotic, noncontractile surface indicates gangrene.122 Repeated endoscopy, every other day by the same individual, is required to document resolution or progression of the process. In a recent report, Acosta and colleagues demonstrated elevated D-dimer concentrations in patients with acute mesenteric ischemia.134 This elevation was especially helpful in female patients with atrial fibrillation. Wider application of this test to other causes of acute mesenteric ischemia awaits validation. Patients under observation for intestinal ischemia are managed by frequent re-examination; serial endoscopy; sigmoid colon and gastric intramucosal pH monitoring; monitoring of

B blood gases, D-dimer testing, urine output, and fluid requirements; institution of broad-spectrum antibiotic coverage; and bowel rest with nasogastric suction. If the colon appears distended, either clinically or radiographically, it should be decompressed by the gentle insertion of a rectal tube, because increased intraluminal pressure may further compromise colon blood flow.122,133 Improvement of the patient, as evidenced by diminishing diarrhea, improvement in vital signs, clinical examination, laboratory values, and resolution of the ischemia documented by endoscopy, permits continuation of nonoperative management.119 Reversible ischemic lesions should improve within 7 to 10 days.127,135 Continuing clinical evidence of ischemia beyond 2 weeks requires operative intervention, because this usually reflects a walled-off perforation with local peritonitis.122 Finally, progression of intestinal ischemia during the period of observation, identified by deteriorating clinical signs and symptoms, requires prompt celiotomy. Surgery for transmural ischemic colitis requires resection of nonviable bowel, endcolostomy, and formation of a Hartmann’s pouch or resection of the rectum, if involved.136 Prevention of intestinal ischemia depends on an appreciation of the potential for this complication and the institution of appropriate steps to either avoid injury to the collateral circulation of the colon or augment circulation to the bowel as part of the aortic reconstructive procedure.137 Spiral CT or magnetic resonance angiography is being used with increasing frequency to evaluate the abdominal aorta and its visceral branches. This technique permits multiple views of complex aortic lesions, reflects the true diameter of aortic aneurysms, and may alleviate the need for angiography.138,139 Identification of a patent inferior mesenteric artery with retrograde flow through a large meandering artery that is functioning as a collateral pathway for an obstructed superior mesenteric artery requires preservation of flow through the inferior mesenteric; this orifice is spared by constructing an end-to-side aortic anastomosis or by reimplanting the inferior mesenteric onto the side of an aortic graft using a variation of the Carrel patch technique.119 In a prospective study of 100 patients undergoing aortic reconstructive procedures, Zelenock and associates observed a 3% incidence of endoscopic colonic ischemia.140

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Adjunctive procedures were used in 12% of these patients, compared with 4% in earlier studies from their institution. Bypass to the superior mesenteric artery should also be considered.137 A large meandering artery with flow from the superior mesenteric toward the sigmoid and rectum in the presence of inferior mesenteric artery occlusion is strong evidence of adequate collateral supply to the bowel.124 Ischemic colitis is unlikely under these circumstances if this collateral is not impaired by surgery. The status of the hypogastric vessels should be identified on the aortogram or other imaging study so that arterial reconstruction can be designed to maintain flow through at least one of these arteries by direct revascularization or by retrograde perfusion from a femoral anastomosis, especially if a patent inferior mesenteric artery must be ligated.135 Measurement of the inferior mesenteric artery back-pressure during aortic reconstruction may be a useful guide to the need for restoration of flow to the inferior mesenteric artery.135 A mean pressure greater than 40 mm Hg and an inferior mesenteric artery–systemic pressure ratio greater than 0.4 indicate satisfactory collateral circulation without the need for mesenteric arterial repair. Intraoperative duplex ultrasonography in patients undergoing visceral artery repair allows prompt correction of underlying technical defects.141 Thorough mechanical preparation of the bowel before aortic surgery reduces the fecal burden to which the potentially ischemic bowel is exposed.119 During aortic surgery, every effort

should be made to prevent injury to the mesenteric vessels. Undue traction on the left colon mesentery should be avoided. When inferior mesenteric ligation is required, this should be carried out by suture ligature within the aortic lumen or immediately adjacent to the aortic wall to avoid injury to its ascending and descending branches.119 Finally, the presence of Doppler flow signals over the base of the bowel mesentery and the serosal surface of the colon suggests that adequate collateral circulation is present.128 Absence of a flow signal after reconstruction suggests the need to restore perfusion through the inferior mesenteric artery or through some other major collateral vessel. The association of severe visceral and aortic occlusive disease in younger female patients is accompanied by high mortality and morbidity rates. The severe weight loss resulting from celiac and superior mesenteric artery occlusive lesions makes complete revascularization a hazardous undertaking. In these individuals, a combination of endovascular treatment of the visceral occlusive disease before aortic revascularization may decrease the early morbidity and mortality rates, as well as improve long-term survival (Fig. 43-11).142 SPINAL CORD ISCHEMIA Spinal cord ischemia occurs most frequently during repair of thoracic and thoracoabdominal aneurysms but is occasionally encountered during resection of an abdominal aortic aneurysm and, rarely, following aortoiliac bypass for ischemia.100,143,144 The overall incidence of this complication of abdominal aortic

FIGURE 43–11 • A, Ninety percent stenosis of the celiac artery (arrow) in a patient with mesenteric ischemia treated with balloon angioplasty and stent placement (arrow) (B).

A

B

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surgery has been reported to be 0.23% and is 10 times higher after the repair of ruptured abdominal aortic aneurysms than following elective aneurysm resection.144,145 The incidence of spinal cord ischemia after thoracic aortic reconstruction is in the range of 1% to 10%, depending on the extent of the lesion repaired. The upper level of the neurologic deficit was found to be T-10 to L-2 in 39 of 44 patients (88.6%) reviewed at the Henry Ford Hospital.145 Postoperative mortality was directly related to the severity of paraplegia. When the neurologic deficit was complete initially, involving both sensory and motor function, 76% of the patients died; there were only two complete neurologic recoveries and one partial recovery. By contrast, when the initial loss was only partial motor or sensory loss, 24% died and some degree of recovery was noted in all but one patient.144,146,147 The major cause of spinal cord ischemia is interruption of flow through the great radicular artery of Adamkiewicz, which is the major source of supply to the anterior spinal artery at the lower end of the cord.143,148 The great radicular artery is a major branch of the posterior division of one of the intercostal vessels arising between T-8 and L-1. On occasion, it may originate from a lumbar branch of the infrarenal aorta. The anterior spinal artery itself is long and has rather poor collateral contributions from the posterior spinal arteries or from the radicular arteries derived from more proximal intercostal vessels. Because the spinal cord is only tenuously supplied in its lower portion by vessels other than the great radicular artery, embolization or injury to this vessel during aortic reconstruction may lead to some degree of cord infarction. The effectiveness of collateral pathways may be further compromised by hypotension, especially in patients with ruptured aneurysms. The placement of a high aortic clamp for temporary control of a ruptured aneurysm, however, does not clearly correlate with the incidence or severity of cord ischemia.144 Williams and colleagues149 and Kieffer and coworkers150 reported successful angiographic visualization of the origin of the artery of Adamkiewicz in 49% and 69% of patients with thoracoabdominal aneurysms, respectively. The very low incidence of spinal cord ischemia after operations on the infrarenal aorta and the risks associated with preoperative or operative angiographic demonstration of the major blood supply to the lower spinal cord render visualization impractical and potentially dangerous.112,148-150 Moreover, the occurrence of this complication has been unpredictable and may not be preventable in association with infrarenal aortic reconstruction. Monitoring of somatosensory evoked potentials during thoracic surgery has been shown to correlate with cord ischemia.151 These abnormal findings have been reversed by temporary shunting and implantation of intercostal vessels into the thoracic aortic graft. Practical application of this technique to abdominal aortic surgery is undergoing continued investigation.151-154 Although there are no data to identify specific preventive measures, it is prudent to avoid high aortic clamping unless absolutely necessary, to maintain cord perfusion pressure by avoiding systemic hypotension, and to prevent stasis thrombosis in collateral vessels by effective heparinization. Suturing a patch of posterior aortic wall with its intercostal vessel orifices into a window cut out of the graft has been recommended for thoracoabdominal aneurysms.100 Finally, it is important to

797

ensure pelvic perfusion through one or both hypogastric arteries to maximize collateral contribution to the spinal cord.155 When ischemic injury to the spinal cord occurs, treatment is palliative and supportive.144 URETERAL INJURY AND OBSTRUCTION The ureters are immediately adjacent to the operative field and may be easily injured during dissection and arterial repair.156 This is especially important in patients with large iliac and hypogastric aneurysms or when there is increased adherence to vascular structures in the presence of an “inflammatory” aneurysm or retroperitoneal fibrosis.157 Nachbur and associates, in a study of 220 patients with asymptomatic aneurysms evaluated with CT scanning, observed 20 cases of ureteral obstruction.158 In 8 patients, ureteral obstruction was associated with inflammatory aneurysms; in the remaining 12, it was associated with abdominal aortic, common iliac, and hypogastric atherosclerotic aneurysms. A thorough knowledge of the anatomic relationships of the ureters at the level of the iliac bifurcation is essential. Occasionally, multiple ureters may be present, or they may be in an aberrant position owing to congenital anomalies. These variations may be defined by a preoperative intravenous pyelogram or a pyelographic film during the preoperative aortogram or CT scan. A preoperative intravenous pyelogram or contrast-enhanced CT scan is especially indicated in reoperative aortoiliac surgery to identify postoperative changes in the ureteral anatomy or demonstrate possible injury incurred during the initial surgery. Direct injury to the ureter can best be avoided by keeping the dissection close to the iliac artery at the point where the ureter normally crosses the common iliac bifurcation in transit to the bladder. This is especially important during the blind development of the retroperitoneal tunnel for aortofemoral bypass. The ureter should be elevated away from the iliac vessels so that the graft will lie dorsal to it. Inadvertent passage of the graft ventral to the ureter may cause it to be compressed between the graft limb and the underlying iliac artery, producing hydronephrosis. The incidence of ureteral obstruction after aortic grafting in one prospective study was 2%.159 However, the ureter may be entrapped in perigraft scar even if it is placed in its proper position ventral to the prosthesis.156 Both ureters should be demonstrated before closing the retroperitoneum. The right ureter must be carefully protected during retroperitoneal closure, because this structure can easily be caught up in the suture line. Iatrogenic ureteral injuries sustained during placement or revision of a vascular graft should be repaired primarily. Although renal salvage is possible when the diagnosis is delayed, nephrectomy is often necessary if there has been extensive contamination of the graft.160 Occasionally, an intraoperative ureteral injury is overlooked, and the diagnosis is delayed for days or weeks. Once recognized, placement of a percutaneous nephrostomy tube may be associated with a shorter hospital stay and lower infection rate than with open repair.161,162 Retroperitoneal fibrosis secondary to the surgical procedure is the most common cause of ureteral obstruction after aortic surgery. Postoperative hydronephrosis can be categorized as early (occurring within 6 months) or late (after 6 months). Temporary asymptomatic hydronephrosis can be detected on CT scans in 12% to 30% of patients, and mild to moderate

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permanent ureteral dilatation is seen in 2% to 14% of patients undergoing aortic surgery. The fibrosis is usually secondary to bleeding; excessive dissection, ligation, or devascularization of the ureter; or pseudoaneurysm formation. Ureteral obstruction is believed to be more common when the limb of the graft is tunneled anterior to the ureter. However, hydronephrosis secondary to anterior graft placement occurs in only 30% of cases. The majority of patients have a clinical presentation within 1 year of the procedure, but delayed presentation up to 14 years has been reported. Approximately 30% of patients manifest with symptoms, including pain, recurrent bouts of urinary tract infection, azotemia, or hematuria.163-165 Wright and associates reported a 35-year experience with 58 ureteral complications in 50 patients undergoing aortoiliac reconstructions.166 Two of the six patients who had ureteral obstruction treated before, or in conjunction with, repair of the aneurysm developed graft complications (one graft limb thrombosis and one graft infection). The remaining 44 patients had 46 complications, including hydronephrosis (42), ureteral leaks (3), and ureteral necrosis (1). Twenty-four patients had 36 graft complications, including anastomotic aneurysm (19), graft limb thrombosis (8), graft infection (6), and aortoenteric fistula (3). Twenty-nine of the 44 patients underwent graft or ureteral operations, or both, with a mortality rate of 21%. Patients in whom hydronephrosis is recognized preoperatively may benefit from ureteral stent placement to decompress the obstruction and facilitate ureteral identification during repair. Postoperative hydronephrosis detected by ultrasonography, CT, or intravenous pyelography can initially be followed expectantly, because it often resolves. Only 12 of the 58 patients reported by Wright and coworkers required surgical intervention for progressive hydronephrosis.166

A

B

The selective use of stents and antibiotics in conjunction with operative repair is essential if the high incidence of graft complications is to be reduced (Fig. 43-12). IMPOTENCE The loss of ability to achieve or maintain an erection adequate for satisfactory coitus may be due to vasculogenic, psychogenic, neurogenic, endocrinologic, or medication-related factors.167-171 Eighty percent of patients who have aortoiliac occlusive disease have significant erectile dysfunction.167 Nearly 25% of patients undergoing direct aortic reconstruction will suffer iatrogenic erectile dysfunction if appropriate technical modifications are not employed. Therefore, careful evaluation of penile erectile function by history, noninvasive techniques, and angiography should be included in the preoperative evaluation before elective aortic surgery.171,172 This will determine whether there is normal sexual function that should be preserved or whether there is already an established pattern of impotence that might be relieved by altering pelvic blood flow. This information provides valuable insights into the possible psychogenic and cultural factors contributing to an existing problem and gives the surgeon an estimate of the importance of sexual function to the patient. Such preoperative information may alter the type of aortic operation planned. Preoperative evaluation of erectile function includes nocturnal tumescence studies. The absence of tumescence during an adequate sleep study is strong evidence of organic impotence. Documentation of normal erections during rapid eye movement sleep establishes the psychogenic basis of the patient’s erectile dysfunction. Unfortunately, the failure of erection is often qualitative rather than complete, making

C

FIGURE 43–12 • A, A stricture is present in the distal ureter as it crosses over the limb of an aortofemoral graft (arrow). B, After dilatation of the stricture, a stent was placed. C, Erosion of the ureter by the stent resulted in a 3-cm defect in the ureter and exposure of the limb of the graft.

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tumescence studies less discriminating between organic and psychogenic impotence.167,172 If organic impotence is suspected, the next step is noninvasive vascular testing. At present, the most reliable measurement is the penile systolic pressure and the penile-brachial index (PBI).167 Kempczinski and Birinyi found that age had a deleterious effect on the PBI that was independent of sexual potency.167 Patients younger than 40 years had a mean PBI of 0.99, compared with a PBI of 0.74 for equally potent men older than 40. This difference was statistically significant. By contrast, impotent men older than 40 had a mean PBI of 0.58, also a statistically significant difference. Despite the significant differences in PBI measurements in these three groups, there is poor correlation between PBI and the degree of erectile dysfunction.172,173 Although a low PBI is not sufficient to establish the diagnosis of vasculogenic impotence, the finding of a PBI greater than 0.8 confirms the adequacy of penile blood flow and suggests that a vasculogenic cause is extremely unlikely.167 Neurogenic impotence is commonly a result of neuropathy secondary to diabetes mellitus, or it may follow autonomic nerve injury from genitourinary or abdominopelvic surgery. This diagnosis is often one of exclusion, but abnormal pudendal nerve velocity studies (sacral latency testing) and abnormal cystometrography (the anatomic pathways in micturition and erection being similar) can implicate this cause.167,174 The diagnosis of endocrinologic impotence requires measurement of thyroid function and serum levels of testosterone and other associated hormones. Finally, a thorough medication history is required.174 Preoperative angiography is useful in identifying the patency of the hypogastric vessels and their contribution to pelvic perfusion. Unfortunately, angiographic findings correlate poorly with the patient’s erectile function.167 Selective injections to identify the flow through the pudendal vessels into the penis may be required to more accurately assess patients with primarily vasculogenic impotence.167 Although the findings on preoperative angiograms correlate poorly with erectile function, preservation of adequate perfusion into at least one hypogastric artery appears to be a vital component in minimizing iatrogenic impotence.167 When possible, direct antegrade perfusion of the internal iliac artery should be ensured. This may require thromboendarterectomy of the hypogastric orifice. Occasionally, angioplasty, stenting, or operative endarterectomy of the orifices of one or both hypogastric arteries will improve erectile function. If both external iliac arteries are occluded or stenotic and bypass into the common femoral arteries is anticipated, precluding retrograde iliac flow, the proximal aortic anastomosis should be constructed end to side, when feasible, to preserve pelvic blood flow. When proximal aortic disease is extensive (requiring an end-to-end proximal anastomosis) and impaired penile perfusion has been diagnosed by preoperative noninvasive testing, it may be necessary to reimplant the hypogastric artery into one limb of an aortobifemoral graft or add a jump graft to one hypogastric artery to improve pelvic inflow.167,174 Finally, careful flushing of the graft in both directions before completion of the final suture line is important to prevent embolization of small particles into the pelvic arteries. DePalma and colleagues reported spontaneous erectile function in 58% of patients with impotence undergoing aortoiliac reconstruction, compared with 27% after microvascular procedures.175

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RETROGRADE EJACULATION Ejaculatory dysfunction is not uncommon after aortic surgery. Earlier series reported an incidence of 30% to 75%, but in more contemporary series, the incidence was only 3%.176 This lower incidence is clearly the result of an increased awareness of the anatomy controlling ejaculation and improved surgical technique. Emission and closure of the bladder neck to ensure antegrade ejaculation are dependent on innervation by postganglionic fibers of the lumbar sympathetic nerves arising from T-11 to L-3. The loss of one or both functions as a result of dissection in the region of the aortic bifurcation results in dry ejaculation.177,178 Careful preservation of the sympathetic-parasympathetic plexus overlying the aorta and its bifurcation and maintenance of blood flow through the hypogastric and pudendal arteries are the important factors in preventing impotence in men undergoing elective aortic surgery.169,171,179 Dissection should be carried down to the aortic wall on its right anterolateral surface and the para-aortic structures gently retracted to the left to avoid trauma to the nerves contained within these tissues (Fig. 43-13). During aneurysm resection, the inferior mesenteric artery should not be dissected free but should be controlled by suture ligature from inside the aorta after the aneurysm has been opened to avoid disruption of

Incision line

Sutures in orifice of inferior mesenteric artery

Bifurcated graft FIGURE 43–13 • Approaches to abdominal aortic and aortoiliac aneurysm. The sac is left intact and sutured over an inlay graft. (From DePalma RG: Impotence as a complication of aortic reconstruction. In Bernhard VM, Towne JB [eds]: Complications in Vascular Surgery. New York, Grune & Stratton, 1980, p 437.)

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nerve fibers at the junction of the inferior mesenteric artery with the aorta (see Fig. 43-13). There should be minimal division of the longitudinal periaortic tissues to the left of the infrarenal aorta, and the nerve plexuses that cross the left common iliac artery should be spared.167,179 The limbs of bifurcated grafts should be placed within the lumens of the common iliac arteries in patients undergoing aneurysm resection to avoid external dissection and minimize injury to perivascular nerve fibers. ANASTOMOTIC FALSE ANEURYSM False aneurysms can develop at any anastomotic site. They are almost invariably associated with prosthetic rather than autogenous tissue suture lines.180-186 The most common sites of occurrence are femoral anastomoses following placement of aortofemoral bypass grafts.181,183,186 Pathologically, there is a partial separation of the graft from the arterial wall.180,183,185 The perianastomotic fibrous tissue prevents immediate hemorrhage and forms a capsule around the hematoma that gradually expands, owing to the pressure transmitted from the arterial lumen. The fibrous capsule may rupture, with rapid, painful enlargement of the mass, or it may erode the overlying skin to produce infection and external hemorrhage. In the abdomen, false aneurysms are prone to erode into adjacent bowel, forming aortoenteric fistulas.186-188 Because blood flow within the pseudoaneurysm is static, its lumen becomes partially filled with thrombus, which may embolize.180,186 The luminal distortion produced by the pseudoaneurysm and its thrombus may also cause occlusion of a graft.186 In the immediate postoperative period, the integrity of all vascular anastomoses are entirely dependent on suture material alone. With time, a prosthesis-artery junction is maintained by the integrity of the suture material and also by external fibrous bonding caused by scarring.189 The important factors involved in the development of an anastomotic false aneurysm include arterial wall weakness,185 endarterectomy at the anastomotic site,190 compliance mismatch between the graft and host artery,191,192 dilatation of the graft material,188,193 prosthetic deterioration or an actual flaw in the graft material,194 increased tension at the anastomotic site due to insufficient length of the prosthesis,194 deterioration of suture material,195 and uneven tension on the anastomosis as a result of beveling of the end of the graft.189 Pseudoaneurysm is occasionally due to underlying infection, although this is seldom identified.183,186 When infection is the causative factor, a purulent perigraft exudate is usually, but not always, present. Therefore, during repair of any pseudoaneurysm, its wall and contents should be routinely cultured by aerobic and anaerobic techniques. The incidence of false aneurysm formation ranges between 1.4% and 4%.184 Recognition is usually quite simple at groin anastomoses, where a large, pulsatile, and sometimes tender mass becomes apparent to both the patient and the examining physician. False aneurysms developing in the retroperitoneum at an aortic or iliac anastomosis rarely become palpable and go unnoticed until rupture produces pain and shock or erosion occurs in an adjacent loop of bowel, with gastrointestinal hemorrhage.196 Occasionally, false aneurysms are identified during routine CT scanning or arteriography for some other vascular or unrelated problem. Ultrasonography, CT, and MRI are reliable methods for

evaluating grafts and anastomoses for dilatation and pseudoaneurysm formation.197 Diagnosis of a pseudoaneurysm is usually confirmed by arteriography, which demonstrates widening at the anastomosis and an extraluminal accumulation of contrast at the point of anastomotic disruption. Because the false aneurysm is partially filled with thrombus, the extent of extraluminal contrast accumulation only partially delineates the process. A more accurate measure of the true size of the defect can be obtained by CT scanning or MRI.196 Retroperitoneal false aneurysms should be repaired as soon as they are identified to avoid rupture or bowel erosion.184,187,196 Unfortunately, these complications are frequently the first indication that a false aneurysm is present. When there is no evidence of infection, the suture line defect can be dissected free and repaired either directly or by the interposition of fresh graft material. Endovascular treatment of thoracic, para-anastomotic aortic, iliac, and femoral pseudoaneurysms is an attractive alternative to surgery in patients with favorable anatomy.198-200 When infection or visceral erosion has taken place, the graft must be removed entirely, the aorta and iliac vessels closed, and the extremities revascularized. Management of this problem is discussed in detail elsewhere in this text. Generally, peripheral false aneurysms should be repaired as soon as they are identified. However, false aneurysms that are small, stable, and asymptomatic may be observed, especially if the patient is at increased risk for reoperation.183,185,186 If surgery is delayed, re-examination at frequent intervals is mandatory so that repair can be carried out when expansion is evident but before complications develop. Surgical repair of a false aneurysm is usually carried out through the site of the original incision. Dissection is carried down to the graft wall proximally so that it can be controlled with a circumferential tape. Further dissection is then carried distally along the graft to define the anastomosis, the aneurysmal bulge, and the branches of the common femoral artery. It is usually difficult and tedious to dissect out the major branches of the artery at the anastomotic site. When extensive scarring is encountered, further dissection may be abandoned, and the patient is given intravenous heparin. The graft is then clamped and disconnected from the aneurysm, and branch control is achieved by the insertion of balloon occlusion catheters into the lumens of the major branches.184 The anastomotic site is carefully surveyed to identify the cause of the pseudoaneurysm. The distal frayed end of the graft at the anastomosis is resected, and the edges of the artery are trimmed back to healthy tissue. To avoid tension at the new anastomosis, a short piece of new graft material is usually required to connect the proximal end of the old prosthesis with the freshened arterial orifice. The diameter of the interposed graft segment generally should not exceed 8 mm to more closely approximate the size of the outflow tract rather than the larger inflow prosthetic limb.193 Unless retrograde flow up the external iliac artery must be preserved, it is best to convert the femoral anastomosis from end to side to end to end.184 Before repairing the anastomosis, the orifices of the superficial and deep femoral arteries should be inspected so that significant stenoses can be repaired by endarterectomy or patch angioplasty to ensure adequate runoff. In a 1985 review, overall mortality for repair of anastomotic femoral false aneurysms was 3.5%, and the amputation rate

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was 2.8%.189 Results are distinctly better if this lesion is repaired electively rather than emergently.185,186 The recurrence rate of anastomotic femoral false aneurysms after initial repair has been reported to be 5.7%; these are amenable to secondary repair.189,193 RECURRENT ANASTOMOTIC ANEURYSM Femoral anastomotic aneurysms (FAAs) develop in approximately 3% of all femoral anastomoses and in 6% of patients undergoing aortofemoral bypass. Repair of FAAs remains durable in approximately 80% of patients; however, a small percentage of patients develop recurrent FAAs. In a series of 43 FAAs, Ernst and colleagues reported a 19% incidence of this complication.201 Factors predisposing to recurrent FAA include graft dilatation, local wound complications, and previous repair of an FAA in a woman.193,201 Although there appears to be an inverse relationship between atherosclerotic heart disease and recurrent FAA, the significance of this observation is difficult to explain. Furthermore, factors that have been implicated in the development of FAAs (e.g., hypertension, smoking, diabetes, suture material, type of graft, performance of an endarterectomy) have not been related to the development of recurrent FAAs. Recurrent FAAs are subject to the same complications as primary FAAs, including rupture, thrombus, and peripheral embolization. Repair is indicated in good-risk patients with recurrent FAAs larger than 2 cm. For those smaller than 2 cm, management includes careful follow-up, especially if coexisting medical problems make surgical intervention risky. The principles of repair are similar to those for primary FAAs and include careful dissection of the distal outflow vessels, use of graft material approximately the size of the outflow vessel, and conversion from end-to-side to end-to-end anastomosis.193,201 CHYLOUS ASCITES Chylous ascites, issuing from a damaged cisterna chyli and its tributaries at the root of the mesentery, is a rare complication of aortic reconstruction and performance of a Warren shunt.202 In a review of the literature, Pabst and coauthors found that approximately 75% of cases occurred following abdominal aortic aneurysm resection, 19% after aortic reconstruction for occlusive disease, and the remaining 7% after resection of infected aortic grafts.203 Interruption of the lymphatics and chylous ascites are not invariably related, because the lymphatics are often interrupted during aortic operations without apparent sequelae.202,204 Patients with chylous ascites typically present within 2 or 3 weeks of aortic repair with anorexia and progressive abdominal distention. Ascites is usually evident on physical examination and can be confirmed by abdominal radiography, ultrasonography, or CT scanning. The fluid obtained by abdominal paracentesis is milky, with a high lymphocyte count and lipid content, and is bacteriologically sterile. An additional complication is leakage of ascites to the outside through a defect in the incision; this increases the fluid and protein loss and heightens the risk of infection. Such a leak should be repaired under sterile conditions and prophylactic

801

antibiotic coverage. Methods used to identify the site of the leak include lymphoscintigraphy, lymphangiography, direct opacification of the thoracic duct with oral fat emulsion observed by CT, and injection of Evans blue dye. The reliability of these tests in identifying the location of the leak or fistula remains unestablished.205 The management of chylous ascites includes abdominal paracentesis, a low-fat diet rich in medium-chain triglycerides, and total parenteral nutrition. However, repeated paracentesis may result in the loss of large amounts of protein and lipid that cannot readily be replaced. An additional risk is that of line-related sepsis. In patients who do not respond to repeated paracentesis, a peritoneal venous shunt, in addition to diet control or total parenteral nutrition, may relieve the ascites. Whether the use of octreotide or fibrin glue accelerates the resolution of ascites remains unclear.206,207 Operative ligation may be necessary in resistant cases.202,203 ABDOMINAL WALL HERNIAS Midline, paramedian, oblique, and transverse incisions are commonly used to expose the abdominal aorta.208-212 Although transverse incisions are associated with the lowest complication rate, their use is often limited to patients with pulmonary insufficiency. Despite the reported benefits of oblique incisions, a significant number of complications, including longlasting wound pain and bulging in 11% to 23% of patients and incisional hernias in 7%, have been reported.211,213 Presumably, the diffuse bulging is due to muscle atrophy caused by a combination of factors, including division of the intercostal nerves, incision-related muscular injury, and reduced blood supply. Gardner and colleagues were able to decrease the incidence of bulging from 11% to 0.03% by preserving the 11th intercostal nerve.214 The incidence of midline ventral hernias ranges from 10% to 37%.213,215 Two distinct types of defects can be identified. Focal periumbilical defects are almost invariably the result of poor technique. The diffuse defects associated with lateral retraction of the recti are by far more commonly observed in patients with incisional hernias after undergoing aortic aneurysmal resection. A number of studies have found no differences in the incidence of the usual risk factors—age, chronic obstructive pulmonary disease, diabetes, smoking, wound infection, length of intensive care unit stay, and amount of blood transfused—between patients who developed incisional hernias and those who did not. Mass suturing of the musculoaponeurotic layers of the abdominal wall using monofilament or braided suture is the most frequently used technique to close midline incisions. A recent meta-analysis concluded that the ideal suture for abdominal fascia closure is running nonabsorbable monofilament suture. Also, a suture length–to–wound length ratio greater than 4 reduces the incidence of incision lesions.216,217 It cannot be overemphasized that careful suture technique with placement of bites 2 cm from the edge and 1 cm apart is essential if this complication is to be prevented. Primary repair using monofilament nonabsorbable suture is appropriate for closure of small periumbilical defects. Prosthetic mesh is usually necessary to repair large defects in the upper abdomen. Recently, laparoscopic repair of these lesions has gained popularity, with low rates of early recurrence.218,219

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is required to control the source of bleeding and to evacuate the hematoma, which may interfere with healing and promote infection. Long-term graft patency has been shown to be significantly reduced in patients who develop wound hemorrhage in the immediate postoperative period.220 Wound hemorrhage that occurs after 48 to 72 hours is frequently due to infection involving the graft at an anastomosis and is less likely to be caused by mechanical factors.220 However, hemorrhage may occur later in the immediate postoperative period in patients who have been maintained on anticoagulants or in whom fibrinolytic agents have been infused for graft thrombosis within 10 days to 2 weeks of surgery.221

Infrainguinal Arterial Reconstruction Femoropopliteal and femoroinfrapopliteal bypasses are the most commonly performed procedures for revascularization of the lower extremity below the inguinal ligament. Specific problems related to endarterectomy of the superficial femoral, popliteal, or deep femoral arteries are reviewed in the discussion of these procedures. The basic principles of infrainguinal bypass are similar to those for aortoiliac reconstruction, with the following significant differences: the vessels involved are smaller, and the length of the bypass conduit is greater, with a consequent increase in the incidence of early and late thrombosis; vein grafts rather than prostheses are used for the majority of procedures; and there is a tendency for less severe systemic complications owing to the more peripheral and less traumatic nature of the operative procedure.

THROMBOSIS The most common significant complication of infrainguinal bypass or endarterectomy is thrombosis of the reconstruction. In the early postoperative period (3.0 3.5 1.0-2.0 Absent Normal 1-4

2 2.8-3.5 2.0-3.0 Slight 1 or 2 4-6

3 3.0 Significant 3 or 4 >6

*5 or 6 points for class A encephalopathy. 7 to 9 points for class B encephalopathy. 10 to 15 points for class C encephalopathy.

a particularly important cause of anemia in these patients. Although splenomegaly is present in virtually all portal hypertensive patients, hypersplenism may not develop until later in the course of the disease. The size of the spleen does not correlate directly with either the degree of portal hypertension or the severity of hypersplenism, but an enlarged spleen is found in virtually all patients with portal hypertension and hypersplenism.18 Hypersplenism is defined principally in terms of splenic sequestration and destruction of platelets and WBCs. This leads to significant depressions in the platelet and WBC counts. Platelet counts below 50,000/mm3 and WBC counts below 2000/mm3 support this diagnosis. UPPER GASTROINTESTINAL ENDOSCOPY Endoscopy plays a pivotal role in the management of portal hypertensive patients. For both diagnostic and therapeutic reasons, endoscopy should be one of the first tests performed. Endoscopy identifies not only the presence of varices but also the source of bleeding in patients with hemorrhage. The diagnosis of portal hypertension may be established by noting the presence of varices. The size, appearance, and location of the varices may significantly affect the patient’s management. Endoscopy also notes the presence of other sources of bleeding in portal hypertensive patients, such as hypertensive gastropathy, gastritis, gastric ulceration, duodenal ulceration, gastric mucosal lacerations (Mallory-Weiss tears), or esophageal ulcerations. Because of the variety of possible bleeding lesions and the significant differences in the management of these lesions, patients admitted for hemorrhage must undergo upper gastrointestinal endoscopy on each admission. As many as 40% to 60% of patients with documented varices have associated gastritis or peptic ulcer disease.19 In patients with esophageal and gastric varices, the

gastric varices have been documented as the site of bleeding in up to 18%.20 LIVER BIOPSY The role of liver biopsy in the preoperative evaluation of portal hypertensive patients has been a focus of controversy. The goal of liver biopsy in this setting is to identify those patients who have active hepatitis. In alcoholic patients, this is most commonly denoted by the presence of Mallory bodies, which signifies acute hyaline necrosis. Mallory bodies may also be seen in patients with Wilson’s disease, cholestasis, and primary biliary cirrhosis. The reason for identifying patients with acute hepatic necrosis is that these patients are thought to be at increased risk of dying during shunt surgery. Mikkelsen and others noted an operative mortality of 69% in elective shunt cases and 83% in emergent cases in the presence of acute hyaline necrosis.20,21 Other authors have contested whether acute alcoholic hepatitis alters survival.14,22 Finally, it should be noted that Mallory bodies disappear when patients abstain from alcohol and the liver recovers from the insult.23 The current recommendation is that patients suspected of having acute hepatitis and who are candidates for elective shunt surgery should undergo percutaneous liver biopsy. If Mallory bodies are identified, consideration should be given to postponing the elective operation to give the liver time to recover. This must be carefully balanced against the risk of recurrent hemorrhage and the likelihood of the patient’s compliance. DUPLEX SCANNING Duplex scanning is finding greater application in the evaluation of portal hypertensive patients. In patients who are being

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821

considered for portacaval shunting or hepatic transplantation, the duplex scan is frequently sufficient to document portal vein patency. Duplex scanning determines both the patency of the portal vein and the direction of portal venous blood flow. This is the minimal anatomic information required to proceed with these operations. The combination of color-flow imaging and duplex scanning has improved the accuracy and extended the diagnostic abilities of duplex scanners.11 ANGIOGRAPHY Preoperative anatomic definition is essential for optimal surgical management, particularly when peripheral shunts are being considered. If possible, angiography should be performed on all patients who are to undergo elective shunting procedures. Techniques that are of primarily historical interest include splenoportography24 (introduction of radiopaque material into the spleen), umbilical vein catheterization, and transhepatic percutaneous portal venography.21-30 Currently, the vast majority of portal angiography is performed by selective cannulation of the celiac and superior mesenteric arteries, as well as observation of the venous phase of these angiograms. Additional studies that should be obtained include an injection of the renal veins and a hepatic wedge angiogram and pressure recording. The combination of these studies is commonly referred to as a “liver package.” The goal of these studies is to delineate the major portal tributaries—the splenic vein, the superior mesenteric vein (SMV), and the portal vein itself—and their relation to the renal vein. An additional goal of the liver package is to measure the hepatic wedge pressure and visualize the hepatic sinusoidal circulation. These last two elements are helpful in confirming the presence of portal hypertension, estimating the severity of the hypertension, and determining the cause of the elevated pressure. Low hepatic wedge pressure ( 6 mg/dL, hyaline necrosis, severe muscle wasting), a portosystemic shunt is almost sure to result in death. Because of this, numerous nonshunting surgical procedures have been developed. SPLENECTOMY Based on Banti’s theory that the diseased spleen caused portal hypertension and ascites, splenectomy was one of the first operations proposed for the treatment of Banti’s syndrome (splenomegaly, hypersplenism, and ascites, often accompanied by esophageal varices). The use of splenectomy in this setting was largely due to its advocacy by Osler, a great admirer of Banti’s work. It was not until 1936, when Rousselot reviewed the experience at Columbia University in New York, that the failings of this operation were noted: a significant incidence of recurrent hemorrhage after splenectomy and the consequent loss of the splenic and portal veins, which would preclude possible shunt surgery.143 In 1940, Thompson was able to demonstrate statistically that splenectomy was of value only to those patients with isolated splenic vein thrombosis.144 Finally, in 1945, Pemberton and Kiernan reported a 54% incidence of recurrent variceal hemorrhage with splenectomy alone.145 COLLATERALIZATION Development of collateral pathways between the portal circulation and the systemic circulation was the goal of several procedures. Omentopexy, introduced by Talma in 1898, produces collateral pathways by suturing the omentum to the peritoneum.146 It was thought to be particularly beneficial in the resolution of ascites. It was sometimes used in conjunction with splenectomy for the relief of ascites associated with splenomegaly and decreased WBC counts. Another collateral-promoting operation was the transposition of the spleen into the thorax.147,148 Like omentopexy, its goal was to allow the development of large venous collateral pathways between the portal venous system and the systemic venous circulation. Unfortunately, these collateral

pathways were never able to adequately decompress esophageal varices. Thus, the patients were doomed to repeated hemorrhage. ABLATION Ablative procedures to remove the source of bleeding were first advocated in 1947 by Phemister and Humphreys,20 who recommended total gastrectomy. Peters and Womack later encouraged splenectomy with obliteration of both the intraluminal and extraluminal vasculature of the distal varices–bearing esophagus and proximal stomach.149 Keagy and colleagues reviewed the long-term results of the so-called Womack procedure and found the risk to be prohibitively high—a 54% incidence of rebleeding and a 35% operative mortality.150 They concluded that this procedure should be used only in highly selected patients who do not have suitable anatomy for a shunt. A variation of the Womack procedure was the transthoracic ligation of esophageal varices without splenectomy. This operation was introduced in 1949 by Boerema151 and in 1950 by Crile.152 Wirthlin and associates reported on 55 patients who underwent transesophageal ligation of varices, with a 29% operative mortality and a 33% incidence of recurrent hemorrhage resulting in an additional 23% mortality.153 Despite these results, the procedure was not abandoned. Technologic innovation in the form of the EEA (end-to-end anastomosis) stapler allowed transection and reanastomosis of the distal esophagus with greater facility. The innovation resulted in reduced operative mortality and decreased postoperative hemorrhage. Wexler reported that of six Child class C patients undergoing this procedure, none had recurrent bleeding.154 Cooperman and associates reported five patients with severe hepatic dysfunction and massive variceal bleeding who underwent transabdominal EEA variceal stapling, none of whom developed recurrent bleeding up to 2 years postoperatively.155 In a logical extension of these devascularization procedures, other surgeons proposed more extensive operations. Delaney promulgated a devascularization procedure performed through a left thoracotomy; it involves devascularization of the upper half of the stomach and proximally to the level of the left inferior pulmonary vein, as well as splenectomy, staple interruption of intramural gastroesophageal collateral vessels, truncal vagotomy with pyloroplasty, and fundoplication.156 The major disadvantage of this procedure is that the splenectomy precludes the performance of selective shunts at a later time. Delaney reported, however, that none of his four patients had recurrent variceal bleeding. Perhaps the most successful devascularization procedure was that developed by Suguira in Japan.146,157,158 Because of the significant risk of encephalopathy, shunt procedures were abandoned in favor of an extensive periesophagogastric devascularization accompanied by esophageal transection. The procedure is performed via separate thoracic and abdominal incisions; in poor-risk patients, a two-stage procedure is indicated. The esophagus is devascularized from the gastroesophageal junction to the left inferior pulmonary vein. The vagus nerve is carefully preserved. At the level of the diaphragm, the esophagus is partially transected, leaving only the posterior muscular layer intact. Esophageal varices are

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occluded, not ligated, by oversewing each with interrupted sutures. The esophageal muscle is closed, but the mucosa is not sutured. The abdominal operation is performed through a separate midline incision and includes splenectomy, devascularization of the abdominal esophagus and proximal stomach, and pyloroplasty and fundoplication. The early results of this operation, as reported by Suguira and Futagawa, were excellent.146 The authors reported an overall operative mortality of 4.6%. Their emergency operative mortality was 20%. Varices were eradicated in 97% of patients, and recurrent bleeding occurred in only 2.5%. Their long-term survival was 84%. A follow-up report by the authors on 276 patients indicated equally good survival rates, with excellent control of variceal bleeding and no encephalopathy.157 In a later report, they analyzed their results according to the patients’ Child classification. They found that in class C patients, both operative mortality and long-term survival were discouraging. For classes A and B patients, the results were very good, with combined (A, B, and C) 15-year survival as high as 72%.159 Reports by Suguira’s group have been confirmed by others in Japan, as well as by selected investigators in the United States.160,161 A number of other reports have suggested the use of esophageal transection procedures in the management of selected patients with poor hepatic reserves (Child class C patients). The EEA stapler has made this a relatively simple procedure, but the possibility of esophageal perforation and leakage still makes the procedure a considerably risky one.162 Overall, these studies demonstrate that esophageal transection should be considered a reasonable option in the management of acute hemorrhage in a debilitated patient with both gastric and esophageal varices.163-165

Postoperative Care The most common problem in the postoperative period is the development of significant ascites. Fluid management is the key to minimizing this problem. Postoperative fluids should be restricted to free water and salt-poor albumin or fresh frozen plasma. These should be given to maintain adequate intravascular volume yet avoid overexpansion of the patient’s intravascular space. A diuretic should be started as soon as the patient is begun on oral fluids. Spironolactone is frequently used because of its potassium-sparing characteristics. Caution is advised in its use because of the potential complication of metabolic alkalosis. Sodium intake should be restricted to less than 90 mg/day. Prophylactic antibiotics, which should be started 12 hours before surgery, are continued for only 1 to 2 days. Chylous ascites may develop in the immediate postoperative period as a result of interruption of retroperitoneal lymphatics, and a fat-restricted diet (30 g/day) should be maintained for 4 weeks to minimize the risk of this problem.137 If variceal hemorrhage occurs within the immediate postoperative period, angiography should be performed immediately to accurately define the anatomy and patency of the shunt. If a patent collateral such as the coronary vein is identified, one should consider percutaneous transhepatic embolization. If other collateral pathways are present, re-exploration may be indicated to ligate them. If the shunt is occluded and the patient is bleeding, re-exploration should be undertaken to repair the shunt or to perform another shunt.

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Transjugular Intrahepatic Portosystemic Shunt The TIPS has become a commonly used technique for controlling variceal hemorrhage. This has had a dramatic effect on the performance of operative shunting procedures, despite the fact that TIPS has been used clinically only since 1988. Over the last few years, the indications for TIPS have expanded, although these applications have not always been backed by randomized trials. Recent developments in TIPS research, most notably the use of covered stents, have improved the patency of TIPS and will most likely lead to even more widespread use of this procedure. Rosch demonstrated 30 years ago that intrahepatic portacaval shunts could be created in a minimally invasive fashion.166 Palmaz applied his stent to this type of procedure, leading to prolonged patency of these shunts in animal models.167 After its initial application in human subjects, there was a rapid expansion in its application, so that a large number of interventionalists became skilled in this technique. Most major medical centers now perform TIPS. TIPS can be performed with conscious sedation and is frequently carried out in interventional suites. Ultrasonography should be done before the procedure to document the patency of the portal vein and assess the need for a peritoneal tap. Most interventionalists minimize the amount of ascites before performing TIPS so that the liver is not “floating” in the abdomen. Access is ideally attained via the right internal jugular vein, which provides the most direct route for cannulation of right hepatic vein branches. Wedged venogram and portal pressures are obtained, and a portal vein branch is then punctured. There are a number of commercially available devices for advancing through the liver parenchyma to the portal vein; the Rosch-Uchida transjugular liver access set (Cook Surgical, Bloomington, Ind.) in used at my institution. These devices combine a cutting needle with an aspiration port and are usually designed to fit a 10 French sheath. Portal access is confirmed by aspirating blood during needle advancement. A guidewire is advanced so that the hepatic and portal circuits are in continuity. Finally, the track is balloon-dilated and stented. At the end of the procedure, pressure measurements can be repeated to confirm that the portal-systemic gradient is less than 12 mm Hg. A completion venogram must also be obtained to assess stent placement and to ensure that varices are no longer filling. TIPS for acute variceal bleeding stops the hemorrhage in more than 90% of patients.168 This compares favorably with endoscopic sclerotherapy in many series, including at least eight prospective, randomized trials.169,170 However, most studies have shown a decreased rate of rebleeding with TIPS versus sclerotherapy. Rosch and Keller reported a 5.6% rebleeding rate at 3 months’ follow-up, compared with the 20% to 30% usually seen following endoscopic therapy.171 As with rebleeding following other therapies, a significant number of patients (25% to 30%) will have a different, nonvariceal lesion as the hemorrhage source. Confirmation of the source is thus extremely important. When the bleed is from varices, it is almost invariably associated with improper function of the shunt. As with other vascular conduits, short-term problems are usually technical in nature, whereas those developing later are related to neointima formation. Although TIPS can be revised to

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control the bleeding, one of the chief criticisms of these shunts is the need for repeated interventions.172 In fact, the primary patency of TIPS is roughly 40% at 1 year, but secondary patency approaches 90%.173 Despite the benefit in preventing rebleeding, TIPS is considered a second-line procedure after sclerotherapy owing to several factors, most notably the increased incidence of hepatic encephalopathy (roughly 50% vs. 20%). In addition, for patients whose bleeding is controlled by sclerotherapy, there is no survival benefit with TIPS. It is clear that TIPS has replaced open surgical shunt procedures for most Child classes B and C patients. This is underscored by the fact that it is not uncommon for a surgical resident to finish his or her training without performing a single shunting procedure. Interestingly, in the largest prospective trial comparing TIPS and surgical shunts (8-mm prosthetic H-grafts), TIPS was found to have higher rates of death, rebleeding, and treatment failure.174 This trial, as well as an additional 4 years of follow-up, was published by Rosemurgy and colleagues and evaluated 35 patients in each arm, pairing them based on their Child class. A comparison of the rates of post-treatment encephalopathy generally favored surgery as well. TIPS has been applied in several other clinical situations. One broad category is as a bridge to hepatic transplantation. Theoretically, the procedure leaves the porta hepatis unperturbed and allows for easier subsequent operation. Some have argued that TIPS actually accelerates liver failure in patients awaiting transplantation.175 However, several studies support the use of TIPS in this setting, particularly as a means for improving patients’ general condition, sometimes with decreased blood loss at the time of surgery.176-180 One technical note of importance is placement of the distal end of the stent well above the IVC so that it does not interfere with the transplant itself or cause damage to the portal vein. Another application of TIPS has been for the management of refractory ascites. There are numerous retrospective trials documenting the effectiveness of TIPS in this setting, but only a few randomized trials. In a randomized study by Rossle and coauthors, TIPS was shown to be more effective than paracentesis in controlling refractory ascites.181 In a study by Lebrec and coworkers, TIPS was shown to benefit Child class B patients with ascites but was of no help in class C patients, in whom it had little effect on ascites and increased mortality.182 In a more recent review of randomized trials, Saab and associates, using clinical registries, found that TIPS reduced ascites reaccumulation better than paracentesis at 3- and 12-month follow-up.183 Encephalopathy was more common in the TIPS group, but all other variables analyzed were equal. Finally, Rosemurgy and colleagues performed a randomized, prospective trial comparing TIPS and peritovenous shunts.184 They concluded that TIPS was more beneficial in patients unless they had only a very short life expectancy. Siegerstetter and colleagues reported retrospectively on the benefits of TIPS in treating refractory hydrothorax.185 TIPS has also been used with some success in the treatment of Budd-Chiari syndrome. There are several small studies investigating its use in this setting. Perello and authors managed 13 such patients with TIPS and found that 11 were doing well after a follow-up of 4 years.186 Interestingly, many of the patients’ TIPS were no longer patent but did not

require treatment owing to the absence of signs of portal hypertension. Blum and coauthors reported on 12 BuddChiari patients who underwent TIPS.187 Two of the patients had fulminant hepatic failure and died, but the remaining 10 had resolution of their ascites. In a larger series, Rossle and colleagues reported on 35 patients receiving TIPS for BuddChiari syndrome.188 The cumulative 1- and 5-year survival rates without transplantation in this group were 93% and 74%, respectively, suggesting that TIPS will continue to evolve as a treatment for this disease. One additional application of TIPS has been for hepatorenal syndrome. Brensing and colleagues reported an improvement in renal function in these patients compared with nonshunted patients.189 Other studies also support the use of TIPS in this setting.190 Recently, Wong and colleagues demonstrated prospectively that TIPS can be used in conjunction with a protocol of midodrine, octreotide, and albumin to improve renal function in type 1 hepatorenal syndrome.191 As mentioned previously, the main drawbacks of TIPS are the poor primary patency and the need for repeated interventions to maintain the shunt. It has been shown in animal studies that the use of covered stents improves the patency of TIPS, and there are now human data to support this contention. Otal and associates used PTFE-covered nitinol stents in a recent series of 20 patients and reported primary and secondary patency rates of 80% and 100% at 387 days (as opposed to 58% primary patency at 1 year for noncovered stents reported in the literature).192 Rossi and coworkers reported 1-year primary patency rates of 83.8% with these stentgrafts,193 and Maleux and associates reported only a single occlusion after 56 TIPS procedures using PTFE-covered stents at a mean follow-up of 246 days (range, 3 to 973 days).194

Orthotopic Liver Transplantation With the advent of liver transplantation as an established modality for patients with end-stage liver failure, the role of nontransplantation procedures (shunt surgery in particular) has been the subject of considerable debate. Currently, the best transplant survival rates are generally more favorable than those of Child class C patients after the best care with a combination of sclerotherapy and shunting. This issue has been the subject of two reports from Iwatsuki and colleagues at the University of Pittsburgh Liver Transplant Unit.195,196 These reports described the survival of 302 patients who had bleeding esophageal varices. According to the authors, these patients were all ranked as Child class C with regard to hepatic function. Their survival was reported in a life-table format as 79% at 1 year, 74% at 2 years, and 71% at 5 years. The authors then compared these results with shunt survival as reported in the medical literature and concluded that in Child class C patients who present with bleeding varices, liver transplantation should be considered the treatment of choice, assuming that the patients are reasonable transplant candidates. Our experience at the University of California, Los Angeles, has revealed that transplantation affords superior survival to Child class C patients (Table 44-3). In a series of 761 patients operated on between January 1986 and December 1991, 77 underwent portosystemic shunting as their initial procedure, and 684 underwent hepatic transplantation.

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TABLE 44–3 Results of Portosystemic Shunting and Liver Transplantation from January 1986 to December 1991*

Portosystemic shunt Liver transplantation

No. of Patients

Child Class C (%)

77 684

16 86

5-Year Survival 64 73

*University of California, Los Angeles, experience. Distal splenorenal shunts constituted 50% of shunt operations; 15% of shunt patients eventually underwent liver transplantation because of deterioration of hepatic function.

Of the the patients receiving transplants, 86% were Child class C, whereas only 16% of the shunt patients were class C. Despite this, 15% of shunt patients eventually required liver transplantation for progressive hepatic deterioration. Furthermore, the 5-year survival for the shunt group was 64%, in contrast to 73% for the transplant patients. Similar 5-year survival data in excess of 75% were recently published by Roberts and associates, reflecting patients studies through 1999.197 These data support the impression that portosystemic shunting is an appropriate therapy for Child classes A and B patients, but that class C patients who are reasonable candidates are best managed by liver transplantation. Further complicating the issue is the effect of a prior shunt operation on a subsequent transplant operation. It has been reported that patients who must receive a liver transplant after having a portacaval shunt have considerably greater blood loss, longer operative procedures, increased morbidity, and higher mortality.198 The portacaval shunt is a particularly troublesome procedure to overcome, because the performance of a successful liver transplantation requires dissection through the scarred tissues about the portal structures, disconnection of the shunt, and reconstitution of the normal caval anatomy; only then can the liver transplant operation begin. This is in contrast to peripheral shunt operations, such as the mesocaval shunt or the DSRS. Although these shunts have an impact on the transplantation procedure, they are not as difficult to manage as the central shunts are. In the case of a mesocaval shunt, the shunt must be disconnected or occluded before the transplant operation is completed, or the new liver may be deprived of portal nutrient blood flow. A similar problem may arise with the DSRS, although because of the nature of this shunt, the siphon effect (drainage of portal blood through peripancreatic collaterals into the shunt) is usually relatively minor, and the shunt frequently does not require dismantling. In any consideration of the role of shunting versus liver transplantation, the essential factors are the underlying cause of the hepatic disease, the current stage of hepatic dysfunction, and the expected progression (the natural and treated history) of the hepatic disease. Assuming that the patient is a reasonable transplant candidate and that the liver disease is approaching the end stage (Child class C), transplantation should be strongly considered. If the patient requires an emergent procedure to control bleeding before undergoing transplantation, all efforts should be made to provide a peripheral shunt. If the patient is not a transplant candidate, treatment should consist of the best therapy available:

835

sclerotherapy supported by either esophageal transection with devascularization or shunting.

Variceal Sclerotherapy Esophageal variceal sclerotherapy was introduced by Crafoord and Frenckner in 1939.199 These authors reported a single patient who underwent rigid endoscopic sclerotherapy to prevent further variceal bleeding. With the upsurge in the variety of surgical procedures for variceal hemorrhage in the 1940s, however, sclerotherapy was soon forgotten. Once it was recognized that therapeutic portacaval shunts, with their inherent operative mortality and risk of encephalopathy, were not the ultimate surgical procedure, attention was redirected toward less invasive, more direct methods of treatment, and there was renewed interest in sclerotherapy after the results of several controlled trials. The first major review of sclerotherapy was by Johnston and Rodgers in 1973.200 In 117 patients, bleeding was initially controlled in 92%, and the hospital mortality per admission was 18%. The average time to recurrence of variceal hemorrhage was 10 months. This group, however, made no attempt to perform sequential variceal sclerotherapy and recommended a shunt for long-term variceal control. Similar mortality and variceal hemorrhage control rates were reported by Terblanche from South Africa.201-204 Endoscopy is necessary to confirm the presence of varices and differentiate those that are actively bleeding from those that have ceased to bleed. The use of sclerotherapy to stop acute bleeding at the time of initial endoscopy has been advocated as the treatment of choice.201,202 Urgent or emergent sclerotherapy is used in many institutions after stabilization with balloon tamponade or after failure of conservative supportive therapy and somatostatin. Several controlled trials have compared sclerotherapy with medical management with the Sengstaken-Blakemore tube in the acute setting.205-209 Three studies demonstrated a significantly lower early rebleeding rate,205-207 and all the studies supported the use of sclerotherapy for acute bleeding. Only Paquet and Feussner demonstrated significantly improved overall survival with sclerotherapy.205 The ability of sclerotherapy to prevent recurrent variceal hemorrhage and improve long-term survival with extended treatment has been examined in numerous controlled trials (Table 44-4).208-212 When sclerotherapy was performed to eradicate all varices and compared with conservative medical management, sclerotherapy patients had fewer recurrent bleeds208,210 and improved long-term survival.209 Terblanche and colleagues were able to demonstrate complete eradication of varices in 95% of sclerotherapy patients; however, they could not demonstrate a significant difference in survival, and varices recurred in more than 60% of the sclerotherapy patients.210 Only since 1984 has sclerotherapy been systematically compared with portosystemic shunts in the management of variceal hemorrhage. Cello and associates compared the portacaval shunt to sclerotherapy in Child class C patients, showing greater rebleeding, increased rehospitalization, and higher blood transfusion requirements in the sclerotherapy group, with 40% of sclerotherapy patients ultimately requiring surgical therapy.213,214 However, they were unable to demonstrate any significant difference in survival (Table 44-5).

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TABLE 44–4

Sclerotherapy versus Medical Management (Control) Sclerotherapy

Study Terblanche et al210 Paquet and Feussner205 Westaby et al209 Korula et al212 Soderlund and Ihre211

Follow-up (mo)

No. of Patients

60 9-52 3-60 3-35 12-48

37 93 56 63 57

Rebleed (%) 43* 48 55* 44* †

Control Percentage Surviving (yr) 45 36 60 60 49

No. of Patients

(5) (2) (4) (2) (2)

38 97 60 57 50

Rebleed (%)

Percentage Surviving (yr)

73 54 80 70

45 25 31 56 34

†

(5) (2) (4) (2) (2)

*There was a significant decrease in transfusion requirements in the sclerotherapy group, as well as fewer rebleeding episodes per patientmonth if followed up. †Overall recurrent hemorrhage was 3.6 times more frequent in the control group.

The authors concluded that in high-risk patients, sclerotherapy and portacaval shunting are equal in the acute setting, but one must consider shunt surgery if varices are not totally obliterated. The DSRS has been compared with endoscopic sclerotherapy for the long-term management of variceal bleeding in three controlled trials (Table 44-6). Warren and coworkers showed that although early mortality was the same, there was a higher rebleeding rate with sclerotherapy, and one third of the patients failed treatment and required surgery.215 Treatment with sclerotherapy resulted in significant improvement in liver function when successful, with less encephalopathy and improved survival when backed up by surgical therapy for patients with uncontrolled bleeding. Therefore, the improved survival in the sclerotherapy group actually represents a combination of sclerotherapy and surgical therapy. Teres and colleagues found no difference in early and long-term mortality,216 nor did Rikkers and coworkers.217 However, the rebleeding rate was greater in those patients who had sclerotherapy, and encephalopathy rates were higher in shunt patients in the study of Teres and colleagues.216 In 1989, Burroughs and associates concluded a prospective, randomized study comparing staple transection with sclerotherapy for emergency control of variceal bleeding.218 They found no difference in overall mortality and improved control of bleeding with esophageal transection compared with a single injection, but there was a similar incidence of hemorrhage after three injection treatments. Teres and colleagues randomized cirrhotic patients with uncontrolled bleeding to

TABLE 44–5

portacaval shunt or staple transection in low-risk patients and staple transection or sclerotherapy in high-risk patients.219 Survival was similar in the two groups. In the low-risk patients, portacaval shunt had a greater hemostatic effect but a greater incidence of encephalopathy. In high-risk patients, sclerotherapy and staple transection had similar rebleeding rates and survival, but fewer complications were observed in the sclerotherapy group. The authors therefore recommended staple transection for low-risk patients and sclerotherapy for the initial management of high-risk patients. Although a consensus has not yet been reached, sclerotherapy may represent an appropriate alternative ablative procedure in selected patients with hepatic dysfunction.164,205,219-227 A number of complications with varying degrees of severity result from esophageal variceal sclerotherapy. Frequently, patients complain of odynophagia lasting from hours to days. This may also be associated with retrosternal chest pain lasting for several days. Not infrequently, as a result of pyrogens within the sclerosing solution, a fever greater than 101°F develops and then abates within 2 to 3 days; it is not associated with a leukocytosis. Bacteremias have been documented in as many as 50% of procedures.228 Pleural effusion sometimes occurs but does not necessarily indicate esophageal perforation.229 Variceal ulceration of varying degrees, depending on the amount of sclerosant injected, is not uncommon and usually resolves spontaneously.230 Rare serious complications, including esophageal perforation, spinal cord paralysis, and bradyarrhythmias, have also been described.25,27,28,30,204,224,227

Sclerotherapy versus Portacaval Shunt in Management of Variceal Hemorrhage Sclerotherapy (n = 32)

Rebleed rate (%) Encephalopathy (%) Surgery not required Long-term cost 18-month survival (%)

50 13 7 (22%) $23,000 28

Shunt (n = 32)

P Value

19 13

< 0.009 NS

$28,000 13

NS NS

NS, not significant. Data from Cello J, Grendell J, Crass R, et al: Endoscopic sclerotherapy versus portacaval shunt in patients with severe cirrhosis and variceal hemorrhage. N Engl J Med 311:1589-1594, 1984.

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TABLE 44–6 Sclerotherapy versus Distal Splenorenal Shunt (DSRS) in LongTerm Management of Variceal Hemorrhage* Sclerotherapy Warren et al215 No. of patients Rebleed rate (%) Portal perfusion (%) Patients requiring surgery 2-yr survival (%) Rikkers et al217 No. of patients Rebleed rate (%) Encephalopathy (%) 2-yr survival (%) Teres et al216 No. of patients Rebleed rate (%) Encephalopathy (%) 2-yr survival (%)

DSRS

P Value

36 53 95 10 (28%) 84

35 3 53

20 mV Photoelectric skin pressure 20-100 mm Hg Transcutaneous PO2 > 10 mm Hg or > 10 mm Hg increase on 100% O2 > 35 mm Hg > 20 mm Hg > 0 to < 40 mm Hg 0 mm Hg Index > 0.59 Index > 0.20 Xenon skin clearance = 3.1 mL blood flow/100 g tissue/min > 2.6 mL blood flow/100 g tissue/min Epicutaneous > 0.9 mL/100 g tissue/min Total

49

27/27 (100)

46 52

32/32 (100) 36/36 (100)

44 72 70 86 78 76, 87

38/46 (83) 12/12 (100) 24/30 (80) 24/26 (92) 25/26 (96) 60/71 (85)

62, 80 60, 64, 67 65 60 60 64 77

76/80 (95) 51/51 (100) 16/16 (100) 17/19 (89) 0/3 (0)* 17/17 (100) 33/34 (97)

*Excluded from total. DFI, dye fluorescence index; PVR, pulse-volume recording.

54 57 53, 56

No. of Healing Patients (%)

23/26 (88) 35/36 (97) 14/15 (93) 560/603 (93)

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18 below-knee amputations healed if the PO2 was greater than 35 mm Hg, while 10 of 15 failed if the PO2 was less than 35 mm Hg.67 Kram and associates noted success in 33 of 34 (97%) below-knee amputations with multisensor transcutaneous oxygen mapping when the critical PO2 index was greater than 0.20.77 In addition, all six patients with an index less than 0.20 failed to heal. All investigators have reported some amputations that healed in patients with low PO2 values. A partial explanation for this observation might be the nonlinear relationship between PO2 and cutaneous blood flow. In a careful study, Matsen and coworkers reported that PO2 measurements are most dependent on arteriovenous gradients and cutaneous vascular resistance.66 Techniques to improve the accuracy of transcutaneous PO2 probes include local heating (to 44°C, which minimizes local vascular resistance and makes PO2 more linear with respect to cutaneous blood flow), measurements before and after oxygen administration, oxygen isobar extremity mapping, and transcutaneous oxygen recovery half-time.81 Oishi and associates noted—in a study comparing skin temperature, Doppler pressure, and transcutaneous oxygen—that after the inhalation of oxygen, if the PO2 increased 10 mm Hg or more, the PO2 predicted amputation healing with a sensitivity of 98%.82 In another study, the authors prospectively compared the following tests for their accuracy in amputation level selection: transcutaneous oxygen, transcutaneous carbon dioxide, ratio of transcutaneous oxygen to transcutaneous carbon dioxide, foot-to-chest transcutaneous oxygen, intradermal 133Xe, ankle-brachial index, and absolute popliteal artery pressure.65 All metabolic parameters had a high degree of statistical accuracy in predicting amputation healing, whereas none of the other tests had statistical reliability. All amputations—transmetatarsal, below-knee, and above-knee—healed primarily if the transcutaneous PO2 level was greater than 20 mm Hg, and there was a 0% incidence of false-positive and false-negative studies. Most authors of transcutaneous oxygen testing studies suggest using a cutoff point of 35 to 40 mm Hg. I have used 20 mm Hg with excellent results. Recent data reconfirm the accuracy of a threshold of 20 mm Hg, especially in distal limb amputations.68 Also of importance is the observation that amputation site healing is not affected by the presence of diabetes mellitus, nor are the test results for any of the metabolic parameters. Similar data have been reported by Bacharach and colleagues, who stated that 51 of 52 limbs (98%) healed (primary and delayed) with a PO2 greater than or equal to 40 mm Hg, whereas a PO2 of less than 20 mm Hg was associated with universal failure.83 In that study, PO2 measurements during limb elevation improved the predictability of outcome for patients with supine PO2 values greater than 20 mm Hg but less than 40 mm Hg. Theoretically, laser-Doppler velocimetry should be an ideal tool for skin blood flow determination; it is noninvasive and “measures” capillary blood flow (good correlation between laser-Doppler blood flow measurements using microspheres, electromagnetic flow probes, and 133Xe clearance).84 However, data by Holloway and Burgess,54 Holloway and Watkins,55 Holloway,84 and Matsen (personal communication, 1978) suggest that although there is a linear relationship among techniques, there is a fair amount of variance. These groups noted that the use of local skin heating may enhance the accuracy of the laser-Doppler and make it a more valuable adjunct for amputation level selection.84

897

Holloway and Burgess reported their experience with laserDoppler velocimetry in 20 lower extremity amputations at the foot, forefoot, below-knee, and above-knee levels, and the accuracy rates were as follows: foot and forefoot, two of six (33%); below-knee, eight of eight (100%); and aboveknee, six of six (100%).73 Malone and coworkers’57 and Moore’s58 greatest postsurgical experience was with the use of 133Xe skin clearance for amputation level selection. These techniques have been well described by Moore,58 Daly and Henry,85 and Malone and associates.57 One of the major difficulties with the application of 133Xe skin clearance for amputation level selection is its reproducibility by other investigators. In an earlier publication, Holloway and Burgess were unable to document a clear-cut end point above which all amputations healed.54 In contrast, Silberstein and colleagues reported that 38 of 39 patients (11 above-knee amputations, 18 below-knee or transmetatarsal amputations, and 9 no amputation) healed when 133Xe skin blood flow was greater than 2.4 mL/100 g tissue per minute; when flow was less than 2.4 mL/100 g tissue per minute, only four of seven patients healed.59 One significant advantage of 133Xe clearance techniques that may offset both of these problems, if its ultimate reliability is demonstrated in other centers, is its potential ability to predict healing at all levels of lower extremity amputation.57 A final problem with the intradermal use of 133Xe for skin blood flow measurements is that the manufacturer no longer supplies 133Xe. The product must be made by nuclear medicine departments. This limitation may further preclude widespread use of the intradermal 133Xe technique. Finally, despite past publications and excellent results,57,58,85 I no longer use 133Xe skin clearance for amputation level selection. In part, this change was made because of the enumerated difficulties; however, the major reason for this change was a study wherein 133Xe was not found to be statistically reliable as a selection method for amputation level.65 (As noted previously, transcutaneous oxygen is very reliable.) Using the disappearance of intradermal technetium 99m pertechnetate, 131I-sodium, 131I-antipyrine, or 133Xe in the presence of external pressure, Holstein74 and Holstein and Lassen86 reported amputation level selection data comparable to data reported by Moore, Daly, Henry, Malone, and others. Because 133Xe is trapped in subcutaneous fat, there are solid theoretical reasons to use an isotope other than 133Xe. Holstein and associates found no significant difference among 131I-sodium, 131I-antipyrine, and 99mTc-pertechnetate for the measurement of skin perfusion pressure.75 Stockel and coworkers76 and Ovesen and Stockel87 reported preliminary data on the use of a photodetector and plethysmography (Medimatic, Copenhagen) for amputation level selection; these findings correlate well with the 133Xe skin perfusion pressure techniques of Holstein and colleagues.74,75 This technique uses a blood pressure cuff placed over a photoelectric detector, which is connected to a plethysmograph, to measure the minimal external pressure required to prevent skin reddening after blanching. To date, 66 of 71 (93%) below-knee amputations healed with skin pressures between 20 and 100 mm Hg. In 1992, Dwars and associates reported that skin perfusion pressure measurements were of excellent predictive value for the healing of lower extremity amputations (positive predictive value, 89%; negative predictive value, 99%).39

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In summary, it is my opinion that elective lower extremity amputation should not be performed in the absence of objective testing to determine the most distal amputation that will heal primarily, yet allow the removal of infected, painful, or ischemic tissue. A variety of techniques are available, and the technique chosen depends on the available equipment, the amputation level under consideration, and the current accuracy rates for the reported techniques. However, in my opinion, the most reliable, easiest to use, and best overall technique for prospective amputation level selection is transcutaneous oxygen testing.

Lower Extremity Amputation Levels This section discusses only those amputation levels that are relevant to patients with peripheral vascular disease or diabetes mellitus. Amputation levels that are less desirable from the standpoint of healing or rehabilitation or those that present specific prosthetic fitting problems are omitted. In my experience and that of others, Chopart’s, Lisfranc’s, and Boyd’s forefoot amputations have been fraught with controversy because of healing problems, prosthetic fitting problems, and equinus deformities.88 Because these amputation levels are occasionally used by vascular surgeons, they are reviewed here only briefly.

Indications Gangrene, infection, neuropathic ulceration, or osteomyelitis should be confined to the midphalanx or distal phalanx. There must be no dependent rubor, and venous filling time should be less than 20 to 25 seconds. Sizer and Wheelock demonstrated that the presence of pedal pulses, even in patients with diabetes, is associated with a very high rate of healing after toe amputation (98%).89 Contraindications Cellulitis proximal to the area of proposed toe excision, the presence of dependent rubor, forefoot infection, and involvement of the metatarsophalangeal joint or (distal) metatarsal head all represent specific contraindications to toe amputation. Surgical Technique

Toe amputation is the most frequently performed peripheral amputation. It is especially common in patients with diabetes mellitus, who are prone to lesions (ulceration, osteomyelitis, gangrene) that necessitate amputation. Patients who present with dry gangrene allow the surgeon a choice between direct surgical intervention and autoamputation. In the absence of supervening infection or pain, expectant management permits epithelialization to take place under the dry gangrenous eschar. As soon as epithelialization is complete, the toe will drop off, leaving a cleanly healed stump. Autoamputation is preferable to direct surgical intervention because it obviates the need for healing after amputation and probably results in a more distal site of healing than would be achieved with surgical intervention. However, this process often requires months before it is complete.

A single toe should never be amputated by disarticulation but should be transected through the proximal phalanx, leaving a small button of bone to protect the metatarsal head. Skin flaps can be of any design, as long as they obey basic surgical principles and have an adequate base for the length of flap. The flaps can be fish-mouth, plantar base, dorsal base, side to side, or any variation or combination; however, they must be long enough to close without tension. The most commonly used incision is circular (Fig. 49-2). Amputation through the metatarsophalangeal joint or an interphalangeal joint should be avoided because of the avascular nature of cartilage and the likelihood of supervening infection or failure to heal. Careful atraumatic edge-to-edge skin closure without the use of forceps maximizes the chances of primary healing. Suture material that produces minimal reaction when left in place for long periods should be used, such as monofilament wire or plastic. A soft postoperative dressing that provides gentle wound compression should be applied. Chronic osteomyelitis of the great toe without gangrene in a diabetic patient presents a difficult surgical problem. Because complete healing is not common, and total resection of the great toe results in some imbalance in walking (which can be accommodated with proper shoe orthotics), débridement and resection of the infected phalanges through a medial or lateral incision, leaving a soft tissue toe remnant in place, are probably best from a functional standpoint.

A

C

TOE AMPUTATION

B

FIGURE 49–2 • Single-toe amputation using a circular incision and transverse wound closure.

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Surgical Technique

The primary advantage of toe amputation is the lack of requirement for prosthetic rehabilitation and the fact that minimal tissue is excised. Except for the risk of nonhealing or secondary infection and stump breakdown, requiring a higher level of amputation, there are no disadvantages to this level of amputation.

The incision begins vertically on the dorsum of the foot, bifurcates laterally and medially to encircle the toe, meets on the plantar aspect of the foot, and extends for a variable distance on the plantar aspect of the foot. The plantar incision is extended proximally as needed to allow removal of the toe and distal metatarsal head. Care should be taken not to injure the digital arteries or nerves adjacent to the metatarsal bone and not to enter into the deep tension or joint spaces of the medial and lateral toes. The distal metatarsal shaft is divided at its neck, and soft tissues are removed by sharp dissection. The surgical specimen consists of the toe, metatarsophalangeal joint, and distal portion of the metatarsal shaft and head. If possible, the surgical specimen should be removed in continuity. The metatarsal shaft must be transected in an area of normal bone. “Soft bone” suggests osteomyelitis, especially in diabetic patients, and mandates higher (i.e., more proximal) bone division. I recommend that the surgical wound be generously irrigated with an antibiotic solution (the content of which is based on preoperative cultures, if available). Once again, attention is paid to meticulous hemostasis and atraumatic deep tissue and skin closure. Interrupted monofilament sutures that achieve edge-to-edge skin coaptation (without the use of forceps) should be placed (Fig. 49-3). The postoperative dressing can be either a soft dressing with an outer elastic wrap (which allows compression of the forefoot and removes tension from the suture line) or a combination of a soft dressing with foot and lower leg plaster cast (which provides maximum skin and wound protection). In the event that adequate hemostasis cannot be obtained, the use of a drain is suggested. In the presence of infection in either the metatarsophalangeal joint or skin flaps, consideration should be given to leaving the wound open and doing a delayed primary closure or allowing secondary healing.

Rehabilitation Potential Rehabilitation potential is 100%. However, the performance of a toe amputation in a patient with peripheral vascular disease, especially with concomitant diabetes, is an ominous sign with regard to long-term prognosis. Little and coworkers found that by 3.5 years after toe amputation, almost three fourths of their patients required a more proximal major amputation.90 RAY AMPUTATION Indications If the gangrenous skin or infectious process approaches the metatarsophalanged crease or includes the (distal) metatarsal head, this precludes a toe amputation. A conservative partial distal forefoot amputation can still be performed by extending the toe amputation to include the distal metatarsal shaft and head. Contraindications Gangrene, infection, cellulitis, and dependent rubor involving skin proximal to the metatarsophalangeal crease are contraindications to ray amputation. In addition, involvement of multiple toes is a relative contraindication, because a transmetatarsal amputation would be a more suitable surgical procedure. Ray amputation for gangrene or infection of the great toe also is a relative contraindication, because removal of the first metatarsal head leads to unstable weight bearing and difficulties with ambulation; however, with proper shoe orthotics, ray amputation of the first or great toe results in excellent foot salvage and provides patients with a stable gait pattern.

FIGURE 49–3 • Single-digit ray amputation of the foot. The dorsal and plantar incisions are closed in their original direction; the toe incision can be closed either vertically or transversely.

A

Advantages and Disadvantages This relatively conservative amputation results in minimal cosmetic deformity and maximum (100%) rehabilitation potential. There are no prosthetics required; however, ray resection of the first metatarsal head causes some walking

B

C

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imbalance, and the foot should be fitted with a specially constructed shoe to minimize foot trauma and improve ambulatory balance. There are no disadvantages, except for the risk of hematoma formation, nonhealing, secondary infection, or chronic osteomyelitis of the remaining metatarsal shaft. TRANSMETATARSAL AMPUTATION Indications The indication for transmetatarsal amputation is gangrene or infection involving several toes or the great toe (on the same foot). This amputation may also be used if the gangrenous or infectious process extends a small distance on the dorsal skin past the metatarsophalangeal crease (but not up to the distal third or midthird junction of the forefoot), provided that the plantar skin is uncompromised.

used to control bleeding from the metatarsal shafts; the use of electrocautery to achieve hemostasis is preferable. A well-padded short leg plaster cast is the best postoperative dressing because it controls edema and prevents stump trauma. I do not advise early ambulation after transmetatarsal amputation because of problems with flap necrosis and stump healing. If wound healing is satisfactory at the first cast change (7 to 10 days after surgery), a rubber heel may be incorporated into the second cast for ambulation. Subsequent casts are changed when they become loose, generally every 7 to 14 days, and a rigid dressing is used until the transmetatarsal flap is well healed, usually 3 to 4 weeks after surgery.

Contraindications Deep forefoot infection, cellulitis, lymphangitis, or dependent rubor involving the dorsal forefoot proximal to the metatarsophalangeal crease all represent contraindications to amputation at this level. In addition, gangrenous changes on the plantar skin of the foot, even those extending only a small distance past the metatarsophalangeal crease, is a specific contraindication to amputation at this level. Foot pulses are not necessary for healing, and venous refill should probably be less than 25 seconds. Surgical Technique An excellent description of the technique for transmetatarsal amputation was presented by McKittrick and associates in 1949.91 A skin incision is designed that uses a total plantar flap. A slightly curved dorsal incision is carried from side to side of the foot at the level of the midmetatarsal shafts. The incision extends to the base of the toes medially and laterally in the midplane axis of the foot and then across the plantar surface at the metatarsophalangeal crease. It is important to place the dorsal skin incision slightly distal to the anticipated line of bone division. The dorsal skin incision is carried down to the metatarsal bones, and each metatarsal shaft is transected with an air-driven oscillating saw approximately 4 mm to 1 cm proximal to the skin incision (Fig. 49-4). The plantar tissues in the distal forefoot are separated from the metatarsal shafts with a scalpel. The tissues of the plantar flap are thinned sharply, excising exposed tendons and leaving the underlying musculature attached to the skin flap. The plantar flap is then rotated dorsally for closure. Further tailoring or thinning of the plantar flap may be necessary to achieve good skin coaptation. The importance of attention to absolute hemostasis cannot be overemphasized. A simple closure is performed, consisting of a deep layer of absorbable interrupted sutures and skin closure with a monofilament suture using a vertical mattress technique. Once again, careful approximation of skin edges is important, and I recommend not using forceps on the skin. If adequate hemostasis cannot be readily achieved, use of a closed drainage system is suggested. Bone wax should not be

A

B FIGURE 49– 4 • A, Planned transmetatarsal plantar-based skin flap and appearance of the completed closure. B, Healed right transmetatarsal amputation treated with immediate postsurgical prosthetic fitting, 1 month after amputation.

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Advantages and Disadvantages

Surgical Technique

Transmetatarsal amputation provides an excellent result compared with more proximal foot or lower extremity amputation. Disability is minimal, and the prosthetic requirements are relatively simple. The primary disadvantages of a transmetatarsal amputation are the risks of nonhealing, infection, and hematoma formation and the necessity for a secondary higher-level amputation.

Both Lisfranc’s (tarsometatarsal joint) and Chopart’s (midtarsal joint) amputations are well described in articles by Sanders94 and Chang and coworkers,95 to which interested readers are referred.

Prosthetic Requirements and Rehabilitation Potential To achieve maximum ambulation potential, some minor prosthetic modification should be considered. A shoe that incorporates a steel shank in the sole allows normal toe-off during ambulation. The spring steel shank reproduces the action of the longitudinal arch of the foot during ambulation. A custom-molded foam pad or lamb’s wool can be used to fill the toe portion of the shoe. An alternative approach is to use a custom-molded shoe with a roller-shaped sole to provide toe-off motion during walking. There are relatively few, if any, limitations in rehabilitation for a transmetatarsal amputation. With proper shoe modification, there should be no discernible physical disability for a transmetatarsal amputee during ambulation. It is important, however, that the shoe or other prosthetic device be properly constructed to avoid stump ulceration and breakdown. There are increased numbers of anecdotal reports combining guillotine forefoot amputation with secondary distal split-thickness skin graft to achieve successful healing at this amputation level. Although this latter technique allows the salvage of more proximal transmetatarsal amputations, I do not favor its use because of frequent problems with distal stump (skin graft) breakdown in active patients. LISFRANC’S AND CHOPART’S AMPUTATIONS Indications Some reports have called attention to foot-sparing amputations when a transmetatarsal amputation is precluded because of the extent of ischemia or infection.92-95 The Lisfranc amputation is a tarsometatarsal joint amputation, and the Chopart amputation is a midtarsal joint amputation. I agree with Chang and coworkers95 that both of these midforefoot amputations are easier to perform than a Syme’s amputation and may improve long-term ambulation.96 Contraindications Both Lisfranc’s and Chopart’s amputations result in the development of equinovarus deformity and require lengthening of the Achilles tendon to achieve maximum rehabilitation potential.93,94 In addition, Hirsch and colleagues documented force plate data showing that an abnormal pattern characterized by reduced stance duration and deficient forward propulsion on the amputated side was greater in a Chopart’s prosthesis than in a transmetatarsal prosthesis.96 That study also documented stump problems as the principal difficulty with Chopart’s amputations over time.

Prosthetic Requirements and Rehabilitation Potential I agree with a modified version of the conclusion reached by Chang and coworkers that ischemic foot necrosis extending beyond the limits of conventional transmetatarsal amputation does not necessarily require a major limb amputation.95 With improvements in patient selection and surgical technique, Lisfranc’s and Chopart’s amputations are viable options when attempting to salvage mid- to hindfoot structures. From a prosthetic standpoint, fitting of these more distal and conservative amputation levels should emphasize unloading the distal part of the stump and smoothing out the impulsive force peak on the stump in late stance to minimize pain, decrease stump breakdown, and enhance ambulation capacity.96 SYME’S AMPUTATION Syme first described this amputation in 1843.97 Then, as now, there were arguments over its merit. Harris (in Toronto) has championed Syme’s amputation and has written several excellent articles concerning its development and the surgical technique necessary for successful results.98,99 I believe that the Syme’s amputation is the most technically demanding lower extremity amputation, and attention to surgical detail is crucial for its success. Indications If the gangrenous or infectious process precludes transmetatarsal amputation, the next level to be considered is an ankle disarticulation, or Syme’s amputation. Contraindications If the gangrenous or infectious process involves the heel, if there are open lesions on the heel or about the ankle, if there is cellulitis or lymphangitis ascending up the distal leg, or if dependent rubor is present at the heel, Syme’s amputation is contraindicated. The presence of a neuropathic foot in a diabetic patient, when there is absence of heel sensation, is also a relative contraindication to Syme’s amputation. A high rate of primary healing demands the use of objective, noninvasive amputation level selection techniques before surgery and preservation of the posterior tibial artery (if patent). Surgical Technique The skin incision is placed to construct a posterior flap using the heel pad. The dorsal incision extends across the ankle from the tip of the medial malleolus to the tip of the lateral malleolus. The plantar incision begins at a 90-degree angle from the dorsal incision and progresses around the plantar

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A

B FIGURE 49–5 • A, Syme’s amputation, with a posterior heelbased skin flap, performed with the one-stage surgical technique. B, Intraoperative photograph of a Syme’s amputation showing the Achilles attachment of the calcaneus (midsuperior portion of picture), the tibial plateau, and the heel flap (lower left corner).

aspect of the foot distal to the heel pad (Fig. 49-5). The dorsal incision is deepened through subcutaneous tissues and carried down to bone without dissection in the tissue planes. The anterior tendons (tibialis anterior, extensor hallucis longus, and extensor digitorum longus) are pulled down into the wound, transected, and allowed to retract. The anterior tibial artery is identified, clamped, divided, and suture-ligated. The incision is then deepened, and the capsule of the tibial-talar joint is opened. The tibialis posterior tendon is divided, and the foot is forced into plantar flexion to provide increased visualization of the tibial-talar joint. Great care should be taken during medial dissection to preserve the posterior tibial artery. The joint is further dislocated by incising the

posterior capsule. The peroneus brevis and tertius tendons are transected. The plantar aspect of the incision is deepened through all layers of the sole of the foot down to the neck of the calcaneus. The calcaneus is then carefully and sharply dissected from the heel pad. Dissection of the calcaneus is the most difficult part of the operation, and great care is needed to maintain the dissection on the bony surface of the calcaneus to prevent damage to the soft tissues of the heel, injury to the posterior tibial artery, and buttonholing of the posterior skin as the Achilles tendon is transected. Performance of Syme’s amputation by the one-stage and two-stage techniques is identical up to this point. If the surgeon chooses the one-stage technique, the lateral and medial malleoli are transected flush with the articular surface of the tibial-talar joint with an air-driven reciprocating saw. Once again, the importance of hemostasis cannot be overemphasized. If adequate hemostasis cannot be achieved, a closed drainage system should be incorporated. Even in dry surgical wounds, the use of a drain is advocated by some authors.88,98,99 I prefer to irrigate the surgical wound with copious amounts of antibiotic solution before closure. The heel pad is rotated anteriorly and sutured to the proximal dorsal skin edge with a single layer of interrupted vertical mattress sutures. Once again, atraumatic placement of skin sutures is mandatory, and forceps should not be used on the skin edges. If the two-stage technique is selected,88 the lateral and medial malleoli are not transected. A drain is placed, and the wound is closed as previously described. Approximately 6 weeks after performance of the first stage, the patient is returned to surgery for the second stage (which can be done under local anesthesia). Medial and lateral incisions are made over the dog ears on the amputation stump, and the incisions are carried down to bone with sharp dissection. The malleoli are removed flush with the ankle joint. The tibial articular cartilage is not disturbed. The distal tibia and fibula are exposed subperiosteally approximately 6 cm above the ankle joint, and the tibial and fibular flares are removed with an osteotome and a smooth rongeur. This last procedure produces a relatively square stump that simplifies postoperative prosthetic fitting and improves cosmesis. If the heel pad is loose after removal of the malleoli, it can be secured to the tibia and fibula through drill holes in the bones. The postoperative dressing for a Syme’s amputation stump (for both one- and two-stage procedures) is extremely important; it is critical to maintain correct alignment of the heel pad over the end of the tibia and fibula during healing. Either a soft compression dressing or a rigid plaster cast can be used as a postoperative dressing; however, most authors prefer the application of a short leg plaster cast. If a cast is used, great care must be taken to avoid injury to the medial and lateral skin flaps (dog ears). Weight bearing should not occur during the early phases of healing of a Syme’s amputation because of the risks of nonhealing and flap necrosis. When the first cast is removed, usually 7 to 10 days after surgery, a second cast that incorporates a walking heel can be applied if healing is satisfactory. I prefer to keep Syme’s amputation patients nonambulatory for 3 weeks after amputation to allow good heel pad fixation and healing. After ambulation begins, the patients are kept in a short leg walking cast for an additional 3 to 4 weeks before construction of a temporary removable prosthesis.

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903

Advantages and Disadvantages The Syme’s amputation stump is extremely durable because it is end-weight bearing. It involves minimal disability from the standpoint of walking. Performance of a one-stage Syme’s amputation results in a somewhat bulbous distal stump compared with a two-stage Syme’s amputation. For cosmetic reasons, a two-stage procedure is probably preferable in female patients, although I generally do not perform Syme’s amputations in young female patients because of concerns about cosmesis. Clinical evaluation by patients, prosthetists, and surgeons has consistently shown that the Syme’s amputation is superior to amputation levels above the ankle. Oxygen uptake, gait velocity, cadence, and stride length are significantly better in patients with Syme’s amputations than in those with higher-level amputations.100 Delayed healing or healing complications due to hematoma formation or infection are not uncommon. Careful preoperative amputation level selection helps ensure primary healing of a Syme’s amputation. Failure to heal almost always results in performance of a more proximal amputation. Long-term follow-up of my diabetic patients with normal or “almost normal” sensation in whom a Syme’s level was chosen demonstrates a high incidence of revision to the below-knee level because of problems resulting from a progressive insensate Syme’s stump (i.e., progressive neuropathy). Other authors have not reported similar problems. Prosthetic Requirements and Rehabilitation Potential Ambulation in the home can be achieved without the application of a prosthetic appliance; however, ambulation outside the home requires some type of prosthetic device. The usual cosmetic prosthesis consists of a foot and a plastic shell that incorporates the lower leg. A typical prosthesis for a patient with a one-stage Syme’s amputation is shown in Figure 49-6. Ambulation in the home or for limited distances can be achieved with the application of a simple strap on a cup slipper with a built-up heel. A patient with a successful Syme’s amputation and an appropriately fitted prosthesis can expect a minimal degree of disability. Energy consumption compared with that of a nonamputee is, at most, 10% above normal. Many patients with Syme’s amputations continue to be employed, including some who perform heavy manual labor. The salvage of a Syme’s amputation, especially in patients who are likely to become bilateral amputees, may be the ultimate difference between continued ambulation and nonambulation. BELOW-KNEE AMPUTATION Indications Below-knee amputation is the most common amputation level selected for the management of lower extremity gangrene, infection, or ischemia with nonhealing lesions that preclude more distal amputations. When the blood supply is inadequate for healing at more distal levels, amputation at the below-knee level can be expected to provide adequate blood supply for healing in the majority of cases. In fact, as

FIGURE 49– 6 • Bilateral lower extremity amputee with a right below-knee amputation and a left Syme’s amputation. The Syme’s prosthesis is a standard medial window design for a one-stage Syme’s amputation. Note the bulbous distal ankle on the Syme’s prosthesis (left leg), compared with the cosmetic ankle on the below-knee prosthesis (right leg).

previously noted, 83% of all patients undergoing lower extremity amputation can expect healing of a below-knee amputation44 (see Table 49-3). With objective amputation level selection, primary healing rates in excess of 94% can be expected. Contraindications A below-knee amputation is contraindicated if the gangrenous or infectious process involves skin on the anterior portion of the lower extremity within 4 to 5 cm of the tibial tuberosity or skin that would be used to construct the posterior flap. A flexion contracture of the knee greater than 20 degrees also represents a contraindication to below-knee amputation. Great caution should be used when attempting below-knee amputation in patients with an occluded deep femoral artery (the superficial femoral is almost always occluded) in the absence of objective amputation level selection data that suggest that the amputation will heal. Finally, a patient with stroke or neurologic dysfunction on the side of proposed amputation, in whom muscle spasticity or rigidity is marked, should not have a below-knee amputation because

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spastic muscles will force the knee into flexion and ultimately result in amputation failure. Surgical Technique Two significant advances in amputation technique have contributed to better results after below-knee amputation: use of a long posterior flap, and application of a rigid dressing in the immediate postoperative period. There is considerable clinical and theoretical information available to support the use of a long posterior flap. The gastrocnemius and soleus muscles and the overlying posterior calf skin derive their major blood supply through the sural arteries, which originate proximal to the knee joint. Blood flow is maintained to this area in many patients, particularly diabetic patients, in whom flow through the popliteal artery and its major branches is restricted. Blood supply via the anterior tibial artery and geniculate collaterals to the skin and soft tissues of the anterior lower leg is so poor that even if equal anterior and posterior below-knee skin flaps are used, there is a high incidence of rehabilitation failure due to wound necrosis of the anterior skin flap. The operation can be performed under general or spinal anesthesia, with the patient in the supine position on the operating table. If there are open infected lesions on the foot, a plastic bag or plastic adherent drape can be placed over the open infected portion of the extremity to isolate it. As mentioned previously, in a patient with a septic foot, a preparatory ankle guillotine amputation followed by a delayed primary below-knee amputation results in a higher rate of healing and fewer stump infections than the performance of a one-stage primary below-knee amputation.36,37 An alternative to the two-stage approach (one-stage technique with delayed primary closure) that works well for diabetic patients, except those with Wagner grade 5 foot infection, was reported by Kernek and Rozzi.101 I prefer to use a long posterior flap and no anterior flap for reasons previously stated; however, there is at least one prospective, randomized study comparing a sagittal technique and long posterior musculocutaneous flaps that found no significant difference with respect to healing, limb fitting, ambulation, and ultimate rehabilitation.102 Another report of sagittal incisions for below-knee amputation pointed out the utility of this type of incision in patients in whom a long posterior flap may be contraindicated because of infection or skin necrosis.103 A report by Ruckley and coworkers noted that for below-knee amputations in patients with end-stage peripheral vascular disease, the skew flap is an excellent alternative to the long posterior flap.104 The techniques for construction of a long posterior flap in below-knee amputation have been well documented in many previous publications10,105-107; however, the salient features of the amputation are outlined here. For a standard below-knee amputation, I select a point of bone division approximately a handbreadth, including the thumb, below the tibial tuberosity. When there is concern that the posterior flap may impinge on distal infection or ischemia, a palmbreadth (minus the thumb) can be used for the point of division below the tibial tuberosity. The absolute minimum length for a below-knee amputation is three fingerbreadths (7 to 8 cm) below the tibial tuberosity. The skin incision should be approximately 1 cm distal to the intended

point of bone division. The transverse diameter of the midshaft calf at the level of the anterior incision, plus 1 inch, represents the approximate length of the posterior skin flap. It is usually my preference to outline the flap with a marking pencil before making a skin incision. The anterior skin incision represents the anterior half of the circumference of the extremity. The skin incision then abruptly turns distally with gentle curves and proceeds down the medial and lateral aspects of the extremity, in the midplane axis of the leg, to the point of the distal extent of the posterior skin flap. The two lateral incisions are then connected posteriorly. My preference is then to incise the flap through skin and fascia in all areas before muscle transection. Use of a proximal tourniquet for hemostatic control is optional in patients undergoing traumatic below-knee amputation but is relatively contraindicated in patients undergoing elective below-knee amputation for ischemia. Use of electrocautery is preferred for division of all muscles. The anterior tibial muscle is divided at the level of bone division, and the anterior tibial neurovascular bundle is identified, clamped, divided, and suture-ligated. Electrocautery is used to incise the tibial periosteum circumferentially, and a periosteal elevator is used to mobilize the periosteum of the tibia proximal to the point of proposed bone division. The tibia is then divided with an air-driven reciprocating saw. Using electrocautery, the fibula is isolated at the level of the transected tibia and divided approximately 0.25 inch proximal to the tibia, using the saw. Following division of the fibula and tibia, proximal traction is placed on the transected tibia (use of a bone hook is easiest), and the lower extremity is bent at 90 degrees and retracted distally. The posterior tibial artery and vein and the common peroneal artery and vein are identified, clamped, transected, and individually suture-ligated. The posterior tibial nerve is identified, pulled into the wound, ligated, transected, and allowed to retract out of the area of surgical incision. The posterior calf muscle musculature is transected, leaving the gastrocnemius muscle as part of the posterior skin flap. The surgical specimen is then divided at the same point as the posterior flap skin incision, which permits removal of the surgical specimen. Care should be taken not to thin the posterior flap so much that there is inadequate coverage for the tibia when the flap is closed. The saw is used to bevel the tibia at a 45- to 60-degree angle, and the bony edges are filed smooth. Care is also taken to ensure that the distal ends of the fibula are smooth (Fig. 49-7). The wound is copiously irrigated with an antibiotic solution. Once again, the importance of meticulous hemostasis cannot be stressed enough. Generally, drains are not necessary in below-knee amputations for peripheral vascular disease; however, drains are frequently used in below-knee amputations performed for trauma or other reasons. If a drain is required, I prefer a closed suction drain, which is brought through a separate stab wound in the lateral aspect of the lower leg. The sural nerve (posterior flap) is identified, pulled down, ligated, transected, and allowed to retract back from the edge of the flap. The flap is rotated anteriorly, and the muscle fascia of the posterior flap is approximated to the anterior fascia with interrupted absorbable sutures. The skin is carefully approximated with interrupted vertical mattress sutures using a monofilament plastic or metal suture. I avoid the use of tissue forceps and believe that closure of the below-knee stump,

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A

B FIGURE 49–7 • A, Standard posterior flap below-knee amputation. Note the beveled tibia and the proximal shortening of the fibula compared with the tibia. B, Intraoperative photograph showing a below-knee amputation. Note the skin coaptation with interrupted sutures and the minimal dog ears.

especially in patients with peripheral vascular disease, should be performed with the care of a plastic surgical procedure. Tailoring the corner of the skin flap may be required to prevent excessive dog ears. The use of a rigid plaster of Paris dressing incorporating the knee is ideal, regardless of whether an immediate postoperative prosthesis will be used. A rigid dressing controls edema, promotes healing, and protects the stump during the postoperative period. In addition, a rigid dressing prevents flexion contracture. Application of an immediate postoperative prosthesis as part of the rigid dressing is described in detail later. Advantages and Disadvantages The below-knee amputation is an extremely durable amputation. The likelihood of primary healing is very good, and the ability to rehabilitate a patient with a below-knee prosthesis is excellent. In a report by Kim and coworkers in 1976, 90% of their patients with unilateral below-knee amputations were able to ambulate.108 Roon and colleagues achieved a 100% ambulation rate with unilateral below-knee amputations and a 93% ambulation rate in patients with bilateral below-knee amputations.14 In addition, 91% of the patients reported by Roon’s group were still ambulatory an average of 44 months following amputation.14 In the absence of the ability to perform a more distal amputation, there are no specific disadvantages of a below-knee amputation.

A below-knee prosthesis is required for ambulation at this level of amputation. A variety of prostheses are available, but all generally involve total stump contact (with or without a prosthesis liner) with weight bearing on the patellar tendon and tibialfibular condyles. Newer types of below-knee prostheses incorporate total contact and total weight-bearing designs. The prosthesis can be suspended with a variety of techniques, including a thigh lacer with external joints, Silastic sleeve suspension, standard patellar tendon-bearing (PTB) strap, supracondylar medial clip, suction, and self-suspension secondary to muscle control. These prostheses can incorporate a variety of feet, some of which have flexion and extension motion or “ankle rotation” (with weight loading) or energy storage (Seattle Foot [Model & Instrument Works, Inc., Seattle]; Flex-Foot [Össur, Scheck & Siress, Gakbrook Terrace, Ill.]). The energy requirement for a unilateral below-knee amputee is increased approximately 40% to 60% compared with normal (energy consumption with an energy-storing leg has not yet been reported). It has been my experience, as well as that of others, that any patient (regardless of age) who was ambulatory before below-knee amputation and who undergoes amputation within 30 days of hospital entrance can ambulate successfully on a below-knee prosthesis. In fact, most patients who require bilateral below-knee amputations can ambulate successfully, as shown by Roon and associates.14 The importance of aggressive rehabilitation after unilateral below-knee amputation in patients who are at high risk for bilateral lower extremity amputation was stressed in a report by Inderbitzi and coworkers.109 Delay in rehabilitation resulted in a high rate of nonambulatory patients after the second amputation. The time required for gait training for a unilateral below-knee amputee is approximately 2 to 3 weeks, and most patients develop a very good gait pattern. There are some physical limitations for geriatric below-knee amputees; however, young below-knee amputees are able to negotiate ladders, stairs, and other obstacles with minimal difficulty. KNEE DISARTICULATION Indications The indications for knee disarticulation amputation are limited, and it is performed primarily on young, active males for whom the advantages of strength and serviceability outweigh prosthetic cosmesis. Disarticulation amputation of the knee is the second most technically difficult lower extremity amputation following Syme’s amputation. Successful performance of a knee disarticulation amputation with a high degree of primary healing usually requires some type of objective technique of preoperative amputation level selection. Knee disarticulation is indicated primarily when the gangrenous process, infection, trauma, tumor, or orthopedic disability encroaches too close to the anterior and posterior (or sagittal) limits of a below-knee amputation flap or has resulted in an unsalvageable knee joint. Another potential indication for knee disarticulation is a patient who has had either acute or chronic failure of a below-knee amputation in whom skin flaps at the knee are viable enough to consider knee disarticulation. In general, British surgeons have been

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more enamored of knee disarticulation than their American colleagues. Interest in this level of amputation has arisen as a result of advances in cosmetic prosthetic components and prosthetic fitting techniques. Moreover, in a study of 169 unilateral lower extremity amputees, Houghton and coworkers found that rehabilitation results were better for through-knee amputation (62%) than for above-knee (33%) (P < 0.02) or Gritti-Stokes (44%) amputation.110 Contraindications Contraindications to knee disarticulation are inadequate blood flow to the skin in the region or ulceration, gangrene, or infection involving tissues about the knee joint or the joint space. Surgical Technique There are two excellent reviews of the surgical techniques of disarticulation of the knee111,112; therefore, they are described only briefly here. I prefer the knee disarticulation technique described by Burgess,111 owing to failure with other types of knee disarticulation amputation and success using the modified Burgess technique. Anesthetic management of knee disarticulation is best handled with either spinal or general anesthesia, with the patient in the prone position. The operation can be performed, but is more difficult, with the patient in the supine position. At the discretion of the surgeon, a gown or pack can be placed beneath the thigh to hyperextend the hip joint and provide an easier working surface on the anterior portion of the knee and lower leg. The leg is held in a flexed position. Depending on the availability of suitable skin, a classic long anterior, equal flap, or sagittal flap–type incision can be used (Fig. 49-8). A marking pencil should be used to outline the skin flaps before making the skin incision. Construction of the knee disarticulation skin flaps is crucial to avoid tension on the skin suture line when the amputation stump is closed. Dissection is first carried anteriorly down to the insertion of the patellar tendon on the tibia. The tendon is severed at its insertion and sharply dissected proximally. Deep dissection on the medial side of the knee results in exposure of the

hamstring muscles. The tendons are sectioned and allowed to retract. The deep fascia is reflected with the overlying tendon and skin flap. On the lateral side of the knee, the tendon of the biceps femoris muscle and iliotibial band are sectioned low. The knee joint is entered anteriorly, the knee is flexed, and the cruciate ligaments are transected at their tibial insertion. The posterior knee capsule structures are divided, and the individual members of the popliteal vascular sheath are clamped, transected, and suture-ligated. The tibial and peroneal nerves are identified, retracted under moderate tension, ligated, sectioned with a sharp knife, and allowed to retract into the proximal amputation stump. The patella is removed subperiosteally, and the fascial defect in the patellar tendon is closed with interrupted sutures. The femoral condyles are now transected transversely, approximately 1.5 cm above the level of the knee joint (Fig. 49-9). Sharp distal femoral margins are carefully contoured. The patellar tendon is pulled down into the intracondylar notch under moderate tension and sewn to the stump of the crus ligaments. The semitendinosus and biceps tendons are likewise pulled into the notch, tailored, and sewn to the stump of the patellar tendon and cruciate ligaments. This approximation of the tendons and ligaments allows muscle stability. The superficial skin fascia is approximated with interrupted absorbable sutures, and the skin is meticulously closed using a vertical mattress technique with monofilament metal or plastic sutures, without the use of forceps. Alternatively, skin staples may be used. The use of a through-and-through or a suction drain is optional and is left to the discretion of the surgeon. A rigid dressing, with or without the incorporation of an immediate postoperative prosthesis, should be applied. Advantages and Disadvantages The advantages of a knee disarticulation amputation include excellent durability and end–weight-bearing capacity; retention of a long, powerful, muscle-stabilized femoral lever arm; improved proprioception; and a limb-socket interface with improved prosthetic suspension and rotational control (compared with an above-knee amputation). This amputation level is almost as good as a below-knee amputation and is therefore a tremendous benefit to the patient in comparison to the next higher level, the above-knee amputation. The absence of a knee joint and increased energy expenditure make this amputation level less advantageous than a below-knee amputation. Prosthetic Requirements and Rehabilitation Potential

Classic long interior

Equal flaps

Sagittal flaps

FIGURE 49–8 • The three types of skin incisions commonly used for knee disarticulation amputation. (From Burgess EM: Disarticulation of the knee: A modified technique. Arch Surg 117:1251, 1977.)

Historically, knee disarticulation amputations were not well liked in the prosthetic community because of cosmetic and knee-thigh length problems resulting from existing prosthetic components (nonequal knee centers); however, the availability of lightweight polycentric hydraulic knee joints and endoskeletal systems has helped solve these problems. The usual knee disarticulation socket incorporates some type of medial window to allow the bulbous stump to pass through the smaller lower thigh portion of the socket. Knee disarticulation amputation is probably most useful in young, active patients without peripheral vascular disease. However, this amputation is also an excellent choice for

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Medial

Lateral

Anterior

Lateral hamstrings

Medial hamstrings Posterior

A

FIGURE 49–9 • A, The femur is transected 1.5 cm above the condylar ends, the patellar tendon is sewn to the cruciate ligaments, the hamstring tendons are sutured to the cruciate-patellar ligaments, and the wound is closed over a drain. B, Anterior flap knee disarticulation amputation at the first postoperative cast change (7 to 10 days) with the patient in the supine position (in this case, the patella was removed transcutaneously). (From Burgess EM: Disarticulation of the knee: A modified technique. Arch Surg 117:1253, 1977.)

B

geriatric patients. Patient performance is better than that with a mid- to high above-knee amputation, although not nearly as good as that with a standard below-knee amputation. There are some physical limitations resulting from the absence of a knee joint, specifically involving climbing stairs and ladders and physical tasks that require rotational or flexionextension knee motions.

ABOVE-KNEE AMPUTATION Indications The indications for an amputation at the above-knee level are inadequate blood flow for healing at a more distal level, a disabled patient who is not expected to walk again, profound life-threatening infection with questionable viability of the

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lower extremity, and extensive infection or gangrene that would preclude a knee disarticulation or below-knee amputation. Historically, above-knee amputation has been the operation of choice for many surgeons because greater than 90% primary healing can be anticipated, regardless of the vascular status of the patient. Contraindications Extension of the infectious or gangrenous process to the level of the proposed above-knee amputation is the most common contraindication. Severe necrotizing lower extremity infection is a relative contraindication unless a high above-knee amputation is performed. Surgical Technique There are three basic levels for the above-knee amputation (Fig. 49-10). In general, the longer the above-knee amputation stump, the more likely the patient is to ambulate, so the stump should be as long as possible. If an amputation is being performed to control sepsis or toxicity, a midthigh or highthigh amputation provides more assurance of healing and control of systemic toxicity, although the chances of rehabilitation are less. Either a circular or a sagittal-type incision can be used. I prefer a circular (or fish-mouth) incision appropriate for the level of anticipated bone division. A circumferential line of

incision is drawn with a marking pen 2 to 3 cm below the level of the proposed bone transection. The incision is then carried down through skin and fascia. The skin and fascia are retracted superiorly to allow more proximal muscle division. I prefer to use electrocautery for muscle division. The femoral artery and vein are identified, clamped, divided, and sutureligated in the subsartorial canal. All the muscles of the anterior, medial, and lateral thigh are transected. The muscle mass is then retracted proximally, the proposed line of bone transection is exposed, and the periosteum is cut using electrocautery. An air-driven reciprocating saw is then used to transect the femur. The posterior muscles are transected using electrocautery. The sciatic nerve is identified, pulled down into the wound, ligated, transected, and allowed to retract into the proximal amputation stump. The rough edges of the femur are filed smooth. The amputation stump should be irrigated with an antibiotic solution, especially if the amputation is being performed for infection. The soft tissues and skin are drawn distally to ensure adequate soft tissue coverage for the femur. If soft tissue coverage is adequate, the wound is closed in two layers. The fascia is closed with an interrupted absorbable suture, and the skin is closed with interrupted vertical mattress sutures of plastic or metal monofilament. Good skin coaptation is important, and the use of forceps on the skin should be avoided. If the soft tissue coverage for the bone is inadequate, the femur is shortened as required to allow adequate soft tissue coverage without tension on the skin suture line (Fig. 49-11). If the amputation is being performed for infection, especially a necrotizing infection, the wound should be left open. If a fish-mouth incision is used, the apex of the “angle of the mouth” approximates the point of bony division. Closure, although spatially different, encompasses the careful atraumatic technique described previously. A rigid dressing can be applied and is advantageous for control of stump edema, but it is much more cumbersome and less valuable than a rigid dressing used at lower amputation levels. I prefer to use a soft dressing suspended with a Silesian type of elastic bandage or a modified waist suspension belt.113 After the wound has healed satisfactorily (1 to 2 weeks after surgery), a temporary removable prosthesis can be provided if appropriate. Advantages and Disadvantages The primary advantage of an above-knee amputation is the very high likelihood of primary healing. Prosthetic rehabilitation is very difficult at this level of amputation. Whereas 80% to 90% of all patients with unilateral or bilateral belowknee amputations can be expected to ambulate, only 40% to 50% of unilateral above-knee amputees can be expected to do so. It has been my experience that less than 10% of bilateral lower extremity amputees, when one side is an aboveknee amputation, will successfully ambulate. Prosthetic Requirements and Rehabilitation Potential

FIGURE 49–10 • The three common levels of above-knee amputation.

A variety of prostheses are available for above-knee amputees. Newer prosthetic devices incorporate contoured axially aligned sockets, ultralightweight materials, endoskeletal design, hydraulic-assisted knee joints, ankle rotators and motion feet, and energy storage. There is a direct correlation between successful ambulation at this level of amputation and the weight of

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the prosthesis because of the energy expenditure required for walking. Compared with normal, the energy expenditure of an above-knee amputee is increased 80% to 120%. As noted, the rehabilitation potential for a unilateral above-knee amputee is only fair and averages 10% to 50%. HIP DISARTICULATION AMPUTATION In general, hip disarticulation amputation is not an operation that general or vascular surgeons usually perform,

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because almost all patients will heal after a high above-knee amputation. Indications The indications for hip disarticulation are inadequate blood flow (usually in patients with occlusion of both the deep and superficial femoral arteries) for healing of a more distal amputation, a life-threatening infection or extensive gangrene that precludes amputation at a lower level, trauma, tumor, and failed hip reconstruction.114 Wound complications occur frequently, and their incidence is increased for urgent or emergent operations and in patients with prior above-knee amputations.115 In addition, both limb ischemia and infection increase the mortality rate. Contraindications In my experience, infection that precludes hip disarticulation amputation is almost uniformly fatal. There are no contraindications to this level of amputation, except infection and gangrene (or tumor) that extends above the level of the proposed amputation. Surgical Technique Because this procedure is performed only occasionally by general and vascular surgeons, and because there are excellent articles describing this operation,114-118 the surgical technique is not presented here. Based on a limited experience, I favor a posterior flap technique (Fig. 49-12A).

A

B FIGURE 49–11 • A, Standard circular incision technique for above-knee amputation. Sagittal flaps can be used if appropriate. The key to closure is adequate femur shortening to avoid later bone protrusion through the distal end of the stump. B, Intraoperative photograph of an above-knee amputation stump demonstrates why skin and soft tissue length for bone coverage should be checked before closure. Proximal femur shortening was required to decrease wound tension.

A

B

FIGURE 49–12 • A, Photograph of a left hip disarticulation stump 6 months after amputation. The operation was performed with a posterior gluteal flap technique. B, Ultralightweight (4.5 pounds) left hip disarticulation prosthesis based on an Aqualite plastic endoskeletal system with cosmetic cover (US Manufacturing Co., Pasadena, Calif.) and a Scotchcast Canadiantype socket (bucket).

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Advantages and Disadvantages In the absence of healing at an above-knee level, there is a higher likelihood of primary healing. Prosthetic rehabilitation at this level of lower extremity amputation is uncommon ( 20 mm Hg). The literature is somewhat controversial on healing differences between patients with and without diabetes mellitus. However, it has been my experience, as well as that of others, that there is no significant difference in the healing rates of major lower extremity amputations between diabetic and nondiabetic patients.9,20,54,57,60,65,76,134 The rate of infectious stump complications might be slightly higher in diabetics; however, this has not been my experience. In a review of 59 consecutive lower extremity amputations in diabetics, Bailey and associates noted that the preoperative hemoglobin level was statistically significantly lower in patients whose amputations healed primarily.135 Eighteen amputations done in patients with a preoperative hemoglobin value of less than 12 g/dL healed primarily, whereas all 30 amputations in patients with a hemoglobin level greater than 13 g/dL failed to heal. It seems reasonable to consider isovolemic hemodilution in patients with marginally viable skin or borderline values as measured by amputation level selection methods. In a study of skin flap survival, Gatti and colleagues suggested that isovolemic hemodilution might be a valuable technique for the salvage of marginally ischemic tissues.136 Stump Infection The incidence of infection in an amputation stump ranges from 12% to 28%.9,18,20,57,120 As might be expected, the incidence of postoperative stump infection is directly related to the reason for performing the amputation. The incidence of this complication can be reduced by appropriate management of preexisting infections, including the use of perioperative antibiotic therapy, as well as wide débridement or drainage of infection before definitive amputation. Reviews by McIntyre and coworkers36 and Fischer and colleagues37 noted a statistically significant decrease in the rate of stump infection in patients undergoing definitive below-knee amputation for a septic foot in whom prior ankle guillotine amputation was performed to control infection. The incidence of below-knee stump infection in patients managed with a one-stage surgical procedure was 22% and 21% in these reports, respectively, whereas the incidence in patients who had undergone preparatory guillotine ankle amputation was 3% and 0%, respectively (P < 0.05). My most recent incidence of stump infection is 3% (4 of 134), and most of these infections represent aggressive closure of contaminated wounds or amputations in limbs with distal ipsilateral septic foci. I recommend the use of prophylactic antibiotics in all patients undergoing lower extremity amputation, even in the absence of established limb infection. It has been my practice to treat patients with preoperative infections with broadspectrum antibiotics that provide bactericidal aerobic and anaerobic coverage. The necessity for aerobic and anaerobic coverage is especially important in diabetic patients, in whom

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the incidence of mixed facultative and obligate anaerobic infections may be as high as 60%.22 Once an infection is established in an amputation stump, the wound must be opened widely to provide adequate drainage. In general, this means that the amputation will have to be revised to a higher level; for example, a stump infection in a below-knee amputation usually results in an above-knee amputation. The importance of this complication is emphasized by the fact that for a geriatric patient, conversion from a below-knee to an above-knee amputation is often the difference between successful ambulation and the inability to walk. Stump hematoma after lower extremity amputation is a catastrophic complication, especially when the amputation has been performed for distal extremity infection. Although the correlation between stump hematoma and stump infection is not 1:1, it is high enough to make the avoidance of stump hematoma highly desirable. The importance of meticulous hemostasis after amputation cannot be emphasized enough. If an amputation is not dry, the wound should be closed with drains (closed drainage system, not Penrose drains), although several studies have suggested that the use of drains increases the risk of infection.137 Pulmonary Embolism and Deep Venous Thrombosis The incidence of pulmonary embolism and deep venous thrombosis following major lower extremity amputation is 1% to 3%7,14 and 4% to 38%,9,14 respectively. The postoperative lower extremity amputee is at high risk for venous thromboembolic complications. Usually, these patients have had a prolonged period of hospitalization and bed rest before amputation. In addition, many have undergone prior attempts at vascular surgical reconstruction that may have injured the deep veins in the leg and prolonged preamputation immobilization. The amputation itself involves division of veins, which may result in stagnation and thrombosis in these vein segments postoperatively. When an active rehabilitation program is not begun on the first day after amputation surgery, this additional period of inactivity or immobilization may further predispose the patient to venous thromboembolic complications. The morbidity and mortality from venous thromboembolic complications may be significant, and impairment of blood oxygenation may further compromise the healing of ischemic tissues. For patients undergoing elective major lower extremity amputation in whom major risk factors for venous thromboembolic complications exist, appropriate prophylaxis for pulmonary embolism should be instituted. Because there is a slight increase in stump hematoma formation, the use of a closed suction drainage system in these patients is advisable. Probably the most important factor in preventing thromboembolic complications is to not allow patients to become bedridden either preoperatively or postoperatively. A patient being prepared for lower extremity amputation should be undergoing preoperative physical therapy for range of motion and strengthening of the contralateral leg and upper extremities. A postoperative amputee, even if an immediate postoperative prosthesis is not used, should be receiving physical therapy for similar body conditioning. Attention should be paid to the nonamputated extremity, and the use of

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thromboembolic elastic stockings is recommended during the perioperative period. A final factor that must be considered is the patient’s state of hydration, both preoperatively and postoperatively. This is especially important in patients who have undergone prior attempts at vascular reconstruction or angiography. Pulmonary Complications The incidence of pulmonary complications, including pneumonia, atelectasis, and sepsis, has been estimated at 8% in patients undergoing major lower extremity amputation.14 These complications are significantly higher in patients undergoing above-knee amputation, as noted by Huston and colleagues,7 in whom the incidence of pneumonia and sepsis ranged from 8% to 60%. The same conditions of bed rest, inactivity, dehabilitation, and dehydration that predispose to thromboembolic complications also predispose to atelectasis and pneumonia. Next to myocardial infarction, pulmonary complications are probably the biggest problem with geriatric patients undergoing lower extremity amputation. Attention to good pulmonary toilet, increased muscular activity, and active exercise (physical therapy) are all valuable adjuncts to preoperative and perioperative care. Flexion Contractures Flexion contractures of the knee or hip joint can occur quite rapidly following major lower extremity amputation, especially in geriatric patients. In my experience, the incidence of such postoperative flexion contractures has been 1% to 3%.9,14,20,57 Irreversible flexion contracture prohibits the successful fitting of a prosthesis and, subsequently, patient ambulation. Such a problem may also necessitate amputation at a higher level. The use of a rigid postoperative dressing, with or without an immediate postoperative pylon, helps decrease the incidence of this complication. In patients who are not receiving immediate postoperative prosthetic treatment, physical therapy directed toward range of motion and muscle strengthening should be instituted preoperatively if possible and as soon as possible after amputation.

amputation, and 88% of the amputees were followed for up to 18 months after surgery, with no stump revision.20 The incidence of prosthesis use in those patients was 100%. Similar information was reported by Roon and coworkers, who noted that 91% of their patients were ambulatory on their prostheses 44 months following amputation.14 I believe that the frequency of stump revision is probably related to amputation level selection method, quality of prosthesis fit, and careful postoperative follow-up. My current incidence of late stump revision is 2.3% (10 of 450). Death Approximately one third of all lower extremity amputees die within 5 years of their amputation, and two thirds of these deaths are due to cardiovascular causes.120 Roon and coworkers reported a 45% overall 5-year survival following lower extremity amputation, compared with an expected 85% 5-year survival for the age-adjusted normal population.14 More striking, however, was their analysis of the projected 5-year survival following lower extremity amputation for diabetic and nondiabetic amputees. They reported a 75% 5-year survival for nondiabetics, compared with only 39% for patients with diabetes mellitus (Fig. 49-13). Analysis of the cause of death disclosed that more than one third of deaths were due to myocardial infarction, and two thirds were due to cardiovascular causes.14 There are good multivariate data showing that in dialyzed diabetic patients, apolipoprotein A-I, fibrinogen, age, and stroke are independent predictors of both cardiac and noncardiac death.138 In addition, in type 1 diabetic patients, in spite of intensified insulin therapy, nephropathy is the strongest predictor of mortality and end-stage complications, including amputation.139 Contralateral Limb Loss Estimates of the rate of contralateral limb loss range from 15% to 33% in the 5 years following major lower extremity

100

Renal Insufficiency 80 Survival (%)

Renal insufficiency represents a low-frequency complication following major lower extremity amputation, with an incidence of 1% to 3%.9,57 This complication is, for the most part, avoidable if proper attention is paid to adequate preoperative and postoperative hydration. In addition, in patients requiring prolonged antibiotic therapy for perioperative infection, attention must be paid to antibiotic dosage to avoid renal insufficiency as a complication of antibiotic therapy.

60 Cumulative survival of a normal age-adjusted male population Cumulative survival of nondiabetic, ambulatory patients following amputation Cumulative survival of diabetic, ambulatory patients following amputation

40

20

LONG-TERM COMPLICATIONS Stump Revision There is little information available in the literature regarding the frequency of stump revision in patients who have been discharged from the hospital following lower extremity amputation. In an early report by Malone and associates, there was a 97% rate of primary healing after lower extremity

0

1

2

3

4

5

6

7

Years FIGURE 49–13 • Life-table representation of survival after lower extremity amputation for both diabetic and nondiabetic amputees compared with the age-adjusted normal population. (From Roon AJ, Moore WS, Goldstone J: Below knee amputation: A modern approach. Am J Surg 134:153-158, 1977.)

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amputation.16-18 In all probability, however, diabetic amputees are likely to die before contralateral limb loss.14,120 Because of the risk of contralateral limb loss, significant attention should be paid to examination of the contralateral limb as well as patient education in prophylactic skin and foot care. Patient instructions for diabetic foot care that are used at the Tucson VA Medical Center and Maricopa Medical Center (Phoenix, Ariz.) are shown in Figure 49-14. A randomized, prospective educational study at the Tucson VA Medical Center found that an audiovisual education program decreased the incidence of subsequent amputation significantly (at 1 year) among diabetics who presented with foot ulcers, infection, prior amputation, or high-risk lesions.16 In that study, 203 patients were randomized into two groups: education and no education. There were no significant differences in medical management or clinical risk

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factors between the two groups. There was no significant difference in the incidence of infection; however, the rate of ulceration and amputation was three times higher in the no-education subgroup (ulceration: 26 of 177 vs. 8 of 177, P = 0.005; amputation: 21 of 177 vs. 7 of 177, P = 0.025), demonstrating that a simple education program significantly reduced the incidence of ulcer and amputation in diabetic patients. Other studies have documented the importance of diabetes education, protective footwear, and preventive foot care.140-143 Lehto and associates clearly demonstrated that there is a dose-response relationship between plasma glucose or hemoglobin A1 and the risk of amputation.141 Similar data have been published by Muhlhauser and colleagues, showing that the end-stage complications of blindness, amputation, and dialysis were statistically linked to the level of glycosylated hemoglobin.139 Flores Rivera documented an increased risk for amputation in diabetic patients with cholesterol levels greater than 450 mg.140 Muhlhauser and colleagues linked serum cholesterol levels to the combined end points of blindness, amputation, or dialysis.139 Clearly, good blood glucose control should decrease the incidence of amputation in diabetics. However, the benefit, if any, of cholesterol-lowering drugs in decreasing the risk of amputation in both diabetic and nondiabetic patients is not known.

Prosthetic Considerations Following Major Lower Extremity Amputation In general, as the level of amputation moves proximally up the lower extremity and the age of the patient increases, the success rates for rehabilitation decline and the length of time required to achieve ambulation increases.17,144-150 Before discussing specific prosthetic considerations, a review of some of the problems associated with rehabilitation of geriatric amputees is worthwhile. REHABILITATION OF ELDERLY AMPUTEES

FIGURE 49–14 • Patient instruction sheet for care of the diabetic foot.

In the mid- to late 1960s, the literature was replete with reports on the problems encountered in rehabilitating geriatric amputees. Many of these reports have been forgotten, but the information they presented is still valid. Among the most important work of that period was the project of Mazet and associates involving a 10-year follow-up of 1770 geriatric patients from the VA and county hospitals in Los Angeles.17 Among their findings was the fact that 60% of patients who were given prosthetic limbs discarded them within 6 months. Thirteen years later, Jamieson and Hill, in a review of amputation for peripheral vascular disease, reported that more than half the patients fitted with artificial legs never used them effectively.151 In addition, they reported that if the rehabilitation process was delayed for 2 or more months after amputation, the likelihood of ultimate ambulation was very poor. In a more recent review of rehabilitation following lower extremity amputation, Kerstein and colleagues noted that it required an average of 27 weeks (189 days) to achieve the maximum benefits of rehabilitation, and it was approximately 6 months before a successfully rehabilitated amputee was returned to society.152 In an earlier article analyzing the influence of age on rehabilitation, Kerstein and coauthors

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TABLE 49–5

Overview of Postsurgical and Rehabilitation Outcome in Several Series* Amputations (N)

Authors Warren and Kihn Chilvers et al Robinson Bradham and Smoak Block and Whitehouse Cranley et al Lim et al Ecker and Jacobs Wray et al Nagrendran et al Berardi and Keonin Averaged totals

Primary Healing (%)

Eventual Healing (%)

Mortality Rate (%)

Rehabilitation with Prosthesis (%)

Average Time from Operation to Rehabilitation (days)

121 53 47 84 43

48.8 50.0 77.0 85.7 88.0

66.9 67.9 88.0 — 95.0

4.1 7.5 17.0 — 0.0‡

69.4 60.4 83.0 —† 53.5

180-270 — — — 120-180

101 55 69 174 174 44 965

76.0 53.0 77.0 92.0 80.5 — 74.9

86.0 83.0 85.0 — 91.4 61.4 82.0

7.0 16.0 8.7 3.5 — 4.5 6.7

73.3 51.0 52.2 70.0 — 29.5 63.8

— 70 201 49-77 — 111 133

*Series reporting results with conventional techniques of rehabilitation after below-knee amputation. Note that the overall rehabilitation rate was 64% and the average time to achieve ambulation was 133 days. †Authors commented that very few patients attained ambulation; however, no numbers were given. ‡Two patients died before discharge and were not included as postoperative deaths. From Malone JM, Moore WS, Goldstone J, Malone SJ: Therapeutic and economic impact of a modern amputation program. Ann Surg 189:801, 1979.

found that many patients older than 65 required a year to achieve maximum benefit from the rehabilitation process.146 Malone and coworkers analyzed contemporary series on below-knee amputation in patients treated with conventional rehabilitation techniques and found that the average rate of rehabilitation was 64% and the average time from operation to rehabilitation (ambulation) was 133 days9 (Table 49-5). In a later review, Malone and coworkers noted that the rehabilitation times for patients treated with conventional techniques versus accelerated rehabilitation techniques (including amputation level selection and immediate postoperative prosthesis) were 128 and 31 days, respectively20 (Table 49-6). The same review pointed out that the success rate for

TABLE 49–6

ambulation after amputation with conventional rehabilitation techniques was 70%, whereas it was 100% for amputees treated with accelerated rehabilitation techniques. In addition, it has been my experience that if a geriatric patient is nonambulatory for either a month before or a month after amputation (i.e., rehabilitation is delayed), the likelihood for rehabilitation is significantly less than if the patient remains ambulatory during the perioperative period. Part of the problem with rehabilitation of geriatric amputees is their decreased cardiorespiratory reserve and the increased energy expenditure required after lower extremity amputation, especially at more proximal amputation levels. These problems are complicated by the fact that individual

Comparison of Rehabilitation Time with Conventional and Accelerated Techniques* Group 1 (days)

Group 2 (days)

Level of Amputation

Range

Mean

Transmetatarsal Syme’s Below-knee Knee disarticulation Above-knee Hip disarticulation Overall

20-60 — 60-330 — 360 — 20-360

47.0 — 132.0 — — — 128.4

Range 10-24 15-17 18-140 15-140 27-30 35 10-140

Mean

P Value

18.4 23.0 32.5 60.7 28.5 — 30.8

NS — 0.0001 — NS — 0.0001

*Rehabilitation time following lower extremity amputation for patients treated with conventional surgical and prosthetic techniques (group 1, 128 days) and accelerated techniques incorporating immediate postoperative prostheses (group 2, 31 days) (P < 0.001). NS, not significant. From Malone SM, Moore WS, Leal JM, Childers SJ: Rehabilitation for lower extremity amputation. Arch Surg 116:97, 1981.

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surgeons probably see too few amputees to treat them with maximum efficiency, and the few patients they do see place a large burden on beds, resources, and physician time. In a review of the energy cost of walking for amputees, Waters and colleagues found that in both unilateral traumatic and vascular amputees, performance was directly related to the level of amputation.149 Walking velocity, cadence, and stride length were all decreased in amputation patients compared with control groups. In a detailed analysis of velocity of ambulation, rate of oxygen uptake, respiratory quotient, and heart rate, these authors concluded that amputees adjust their gait velocity to keep their rate of energy expenditure within normal limits. The approximate energy expenditures (compared with those of controls) after lower extremity amputation are shown in Table 49-7.149,153-155 Note that the energy expenditures for both unilateral and bilateral below-knee amputees are less than those for unilateral above-knee amputees. This clearly demonstrates the importance of the knee joint in terms of energy used for ambulation. The additional effort of walking with an aboveknee prosthesis is accomplished by the use of small muscles, which are poorly designed for locomotion.155 Decreased physical strength due to age, decreased cardiorespiratory reserve due to the ravages of cardiovascular or pulmonary disease, and increased energy expenditures for ambulation after lower extremity amputation all have an additive effect that complicates the rehabilitation of geriatric amputees. It is in this setting that the salvage of the most distal amputation that will heal may mean the difference between ambulation and independence and nonambulation and dependence for an elderly amputee. These factors also explain the higher likelihood of ambulation for a young highlevel amputee compared with an elderly high-level or bilateral amputee. In their evaluation of 113 amputations in 103 patients, most of whom underwent amputation for peripheral vascular disease, diabetes, or both (mean age, 61 years), Roon and coworkers found the following rates of successful rehabilitation: 100% for unilateral below-knee amputation, 93% for bilateral below-knee amputation, 17% for a combination of above-knee and below-knee amputation, and 0% for bilateral above-knee amputation.14

915

(CET) (which at this point is probably of historical interest only), and rigid dressings with or without a postoperative prosthesis. In addition, the surgeon may choose delayed (conventional), rapid, or immediate postoperative rehabilitation. Conventional Stump Wrap (Soft Dressing) The historical standard, and a technique that is still used in many institutions, is the application of a soft postoperative dressing. Cotton gauze or fluffs are used to pad the amputation stump, and the stump is wrapped with elastic bandages (Fig. 49-15). The advantage of this technique is that it does not require a prosthetist to be present in the operating room or at the time of dressing changes. The disadvantages are that it does not readily control stump edema, the dressings are difficult to maintain in place (especially for highlevel amputees), there is minimal stump protection from postoperative trauma, the dressing does not prevent knee flexion contracture, and ambulation may be delayed as a result of the prolonged time required for stump maturity (6 months). Except for the above-knee and hip disarticulation amputation levels, where it is technically difficult to maintain a rigid dressing in good stump contact, there are no valid reasons to continue the use of this postoperative dressing technique. Constant Environmental Treatment Unit Developed and used almost exclusively in Great Britain, the CET unit consists of a control console containing a multistage centrifugal air compressor. The air passes through pressure control valves, a pressure cycle timing device, a bacteriologic filter, and a thermostatically controlled heating element that controls heat and relative humidity. The dressing on the patient consists of a transparent flexible polyvinyl bag. The bag is not in direct contact with the residual limb, except on the resting surface. A pleated air seal is incorporated into the proximal end of the bag to maintain a pressure seal. A sterile CET bag is placed over the amputation stump in the

POSTOPERATIVE PROSTHETIC TECHNIQUES After major lower extremity amputation, the surgeon has three choices for prosthetic management: soft dressings or conventional technique, constant environmental treatment

TABLE 49–7

Energy Expenditure (Compared with Controls) after Lower Extremity Amputation*

Level of Amputation Unilateral below-knee Bilateral below-knee Unilateral above-knee Bilateral above-knee

Increase in Energy Expenditure (%) 9-25 41 25-100 280

*As measured by oxygen utilization per minute149,153,155 or indirect calorimetry.154 Energy expenditure was measured at comfortable walking speeds that averaged 22% of normal.

FIGURE 49–15 • Standard, conventional soft dressing and stump wrap being applied by a patient to his right above-knee amputation.

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FIGURE 49–16 • Clear polyvinyl controlled environment treatment bag has been placed over a left below-knee amputation. Note the air supply hose at the distal end of the bag.

operating room. The amputation stump is, in essence, “enclosed” in a sterile environment with cyclic pressure (which controls stump edema) and airflow set to the desired temperature and humidity (Fig. 49-16). The CET unit was designed for use in a setting in which a prosthetist is not immediately available or one in which the surgeon wants to be able to control stump edema yet have easy access to examine the surgical wound. The system incorporates a long flexible hose so that the patient can undergo rehabilitation training at the bedside. Indications for use of the CET unit are relatively limited; it is probably best used on patients in whom there is some risk of stump infection and in whom the ability to observe the wound without dressing changes is desirable. Because of its limited application, high cost, and poor patient acceptance due to noise, the CET unit, although successful, has seen limited use in the United States.156 Rapid and Immediate Postoperative Prostheses The application of an immediate postoperative prosthesis has received considerable attention, support, credit, and discredit in the recent past. Proponents of the technique have waxed eloquently on the benefits to the patient, while opponents of the technique have cautioned about the potential detriment to the amputation stump from the casting technique. Berlemont is generally credited with the early work that led to the establishment of the technique, based on his application of temporary prostheses in patients with delayed (secondary) amputation stump healing.3 Weiss of Poland is credited with adapting this technique for stumps undergoing primary healing (i.e., immediate postoperative prosthesis). The latter technique proved highly successful, and Weiss reported his initial results at the Sixth International Prosthetic Course in Copenhagen in July 1963. This early presentation and a subsequent publication in 1966 came to the attention of surgeons worldwide.4 The Prosthetic and Sensory Aids Service of the VA was especially interested in this technique for the management of veteran amputees and was instrumental in bringing this procedure to the U.S. surgical theater. Working with the VA, Burgess, an orthopedic surgeon in Seattle, refined and developed the immediate postoperative prosthetic technique for the U.S. surgical field.5,134,157-159 Burgess and his team performed most of the

early work in the United States, and he was instrumental in training other investigators in the use of this technique. In the late 1960s and early 1970s, there were multiple reports extolling the virtues and possible pitfalls of the immediate postoperative prosthetic (IPOP) technique (also called IPPF, immediate postoperative prosthetic fitting). Initially, there was general agreement that the IPOP technique was ideally suited for nondiabetic, nondysvascular amputees. Subsequent reports in the literature, however, have shown that, if properly used, the technique may be ideal for geriatric dysvascular amputees because of its ability to shorten hospitalization time and increase rates of rehabilitation.9,14,20 In general, proponents of the technique note that its benefits include an increased rate of healing, decreased hospitalization time, decreased rehabilitation time, decreased psychological trauma to the patient, control of stump edema, protection from stump trauma in the early postoperative period, and perhaps an increased rate of rehabilitation.9,14,20,88,160-163 The paper most commonly cited against the use of the IPOP technique is that by Cohen and colleagues.164 Using conventional surgical and prosthetic techniques, they were able to achieve 97% stump healing, whereas only two of nine (22%) amputation stumps treated with the IPOP technique healed. They noted no rehabilitation advantage to the IPOP technique and recommended caution in its application. The experience of Cohen and colleagues has not been matched by other reports in the literature. Some reports noted no change in the rate of wound healing,160 but in general, most papers found no deleterious effects from the use of a rigid postoperative dressing (with or without a prosthesis), decreased hospitalization time, and decreased rehabilitation time.9,14,20,160,162,163 Importantly, Cohen and colleagues suggested that their problems with the IPOP technique might be with the plaster technique itself or in the application of the technique. A review of their paper shows that four patients sustained what are described as second-degree blisters, which almost certainly indicate problems with plaster fabrication and application rather than problems with the IPOP technique itself. In my own experience with 600 consecutive major lower extremity amputations during the past 12 years, there has been only one stump problem related to the use of an immediate postoperative prosthesis, and that problem was caused by improper application of an immediate postoperative cast. An overview of data on the use of the IPOP technique reported from the San Francisco VA Hospital, the Tucson VA Hospital, and Maricopa Medical Center by Roon and colleagues14 and Malone and associates9,20 is given in Table 49-8. A 1992 paper by Folsum and coworkers documented the overall rate of rehabilitation at 80% and the interval from amputation to ambulation at 15.2 days and 9.3 days for below-knee and above-knee amputees, respectively.165 Information not tabulated in Table 49-8 suggests that the patient’s ambulatory status before surgery is one of the most important predeterminants of postoperative ambulation. Essentially, 100% of patients undergoing unilateral major lower extremity amputation who ambulated before surgery were successfully rehabilitated after amputation, whereas less than 15% of the patients who were nonambulatory before amputation surgery were successfully rehabilitated.9,14,20 The advantages of immediate or early postoperative prostheses can be divided into two categories: those derived from

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TABLE 49–8

Overview of Immediate Prosthesis Data: San Francisco and Tucson Veterans Administration Hospitals and Maricopa Medical Center

Stump healing Rehabilitation time Rate of rehabilitation Unilateral below-knee Bilateral below-knee Bilateral above- and below-knee or above- and above-knee Unilateral above-knee

138/153 (90%) 15-32 days 155/175 (88%) 128/129 (99%) 17/19 (89%) 6/23 (26%) 4/4 (100%)

Data from references 9, 14, 20.

the rigid dressing and those derived from early weight bearing and ambulation. The advantages of the rigid dressing include edema control, stump immobilization, perhaps improved healing, prevention of joint flexion contracture, and protection of the stump from external trauma. There may be no difference between soft and rigid dressings with respect to the time required to reach eventual stump maturity (6 months), although postoperative stump edema resolves much more quickly with a rigid dressing. The advantages of immediate or early ambulation include decreased hospital stay, less time from surgery to ambulation, increased rates of rehabilitation compared with patients managed in a more conventional manner, reduction in morbid and nonmorbid complications of amputation, and improvement in the patient’s psychological outlook after amputation.9,14,20,123 In summary, there is general agreement on both the benefits and the pitfalls of the IPOP technique. I agree with Friedmann’s conclusions: “immediate postoperative prosthetic fitting should be confined to large centers with medical and prosthetic facilities available on short notice.”80 In other circumstances, he advocated the use of conventional amputation rehabilitation techniques but specified that such management should include modern postoperative methods, including the early use of temporary prostheses for evaluation and training. The best solution to the problem of choosing a postoperative prosthetic technique would be the routine use of a rigid dressing and the application or use of a temporary prosthesis when the surgeon thinks that adequate wound healing has occurred (usually 1 to 2 weeks after amputation), thereby avoiding some of the potential hazards of immediate ambulation.166-168 Another variant of a postoperative rigid dressing that allows early ambulation is the air splint.145,169 This device may be a practical alternative for a surgeon who wants to achieve early postoperative ambulation but does not have access to a prosthetist skilled in the application of immediate postoperative prostheses or temporary removable prostheses.

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Specific technical details regarding the application of immediate postoperative prostheses can be found elsewhere and are only briefly outlined here.107 Transmetatarsal and Syme’s Amputations A rigid cast with felt padding for bony prominence relief is used as the first dressing for these distal levels of lower extremity amputation; however, ambulation is not allowed until adequate primary healing has been obtained (3 weeks). Early ambulation for transmetatarsal and Syme’s amputation patients results in a higher incidence of wound complications. With Syme’s amputation, it is extremely important that the posterior heel flap be held in good approximation and alignment by the cast and that great care be taken to pad the distal stump and dog ears, as well as the bony prominences. If a two-stage surgical approach for Syme’s amputation is used,88 it is probably best to avoid weight bearing until completion of the second stage of the surgical procedure (6 to 8 weeks). Both transmetatarsal and Syme’s amputees will ultimately ambulate well, and a short delay in the ambulation process has essentially no impact on their overall rehabilitation. Avoidance of stump trauma to ensure primary wound healing during the early postoperative period is of paramount importance, and rehabilitation efforts can be confined to range of motion and strengthening of the opposite leg and upper extremities during the early postoperative period. Below-Knee Amputation Following completion of the amputation, a thin sheet of fine mesh material (Owen’s silk) is moistened in antibiotic solution or saline and applied over the suture line, with care taken to avoid wrinkling (Fig. 49-17). Next, lamb’s wool or polyurethane foam is placed over the end of the stump to provide stump compression and padding (Fig. 49-18).

TECHNIQUES OF IMMEDIATE POSTOPERATIVE PROSTHETIC APPLICATION Immediate postoperative prosthetic use has been described for all levels of major lower extremity amputation—from the transmetatarsal through the high above-knee amputation; however, it is best suited to below-knee amputation.

FIGURE 49–17 • A single sheet of moistened Owen’s silk is placed over the suture line on the below-knee amputation stump. Care is taken to avoid wrinkling of the silk material.

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FIGURE 49–18 • Lamb’s wool, Dacron, or prefabricated polyurethane foam can be placed over Owen’s silk to provide distal stump padding. Care is taken to place padding material both above and below skin dog ears, if they exist.

A Spandex stump sock is then carefully rolled over the stump, with care taken to avoid displacement of the distal stump padding (Fig. 49-19). Relief pads made from nonporous foam are fashioned and glued to the stump sock with Dow-Corning medical adhesive. These pads can be obtained precut or can be hand-fashioned in the operating room. They are placed to pad the bony prominences, specifically including the fibular head, tibial condyles, and patella. Care is taken to leave a relief area between the medial and lateral tibial pads (Fig. 49-20). Next, elastic plaster is used to form the inner layer of the immediate postoperative prosthesis.

FIGURE 49–20 • Felt relief pads are measured, trimmed, and glued to the Spandex stump sock over the bony prominences of the knee and lower leg. Care is taken to leave a relief area between the medial and lateral tibial pads.

FIGURE 49–19 • Spandex stump sock is carefully pulled over the distal end of a below-knee stump and rolled proximally up the leg. Care is taken not to displace the distal end stump padding during application of the sock. Until the postoperative cast is dry, an assistant must maintain traction on the stump sock.

It is important that an assistant maintain traction on the stump sock during plaster application. Care is taken to maintain compression from posterior to anterior (direction of the posterior skin flap) and to grade compression from the distal end of the stump to the more proximal thigh (Fig. 49-21). The suspension assembly of the immediate postoperative pylon is then contoured to the inner cast after the cast has dried (Fig. 49-22). The pylon can be attached and static alignment achieved before incorporating the suspension assembly into the cast. The pylon is removed, and the suspension assembly is secured to the inner cast using fiberglass casting tape. The use of lightweight casting tape decreases the weight of the immediate postoperative prosthesis and significantly increases its durability.167 A completed immediate postoperative prosthesis, waist suspension belt, pylon, and foot are shown in Figure 49-23. If a drain is employed, the drain should be brought out proximally (and laterally) through a separate hole made in the cast during the fabrication process. The drain should not be secured to the skin, so that it can be pulled out through the cast when appropriate. Most surgical pain is gone within 36 to 48 hours after surgery. Significant pain more than 48 hours after surgery is an indication that the cast is too tight or that there is a wound complication. In this case, the cast should be removed, the wound inspected, and the cast reapplied if appropriate. Almost all patients comment that their postoperative stump

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FIGURE 49–23 • Intraoperative photograph of a completed immediate postoperative below-knee prosthesis with pylon, foot, and waist suspension belt. Note that a relief window has been placed over the area of the patella. FIGURE 49–21 • The inner layer of the postoperative rigid cast is made using elastic plaster, which provides good control of stump compression. Compression should be from posterior to anterior, in the direction of the posterior flap, and distal to proximal so that the compression decreases as the cast moves higher on the upper leg.

pain diminishes if the heel of the prosthesis is weight-loaded (when they are in the supine position), and this test can be used as a further check for stump swelling and prosthesis fit. One of the most important principles in the postoperative management of these patients is that if there is any question about prosthesis fit or healing of the surgical wound, the prosthesis should be removed, the wound inspected by the surgeon and the prosthetist, and the cast reapplied at the discretion of the surgeon. On the first postoperative morning, the patient is helped into a standing position at the bedside and instructed in techniques of touchdown weight bearing. At this time, the prosthetist completes the initial static alignment. On the second postoperative morning, the patient goes to the physical therapy department, where he or she is taught touchdown weight bearing using the bathroom scale technique (Fig. 49-24).

FIGURE 49–22 • The metal arms of the immediate postoperative prosthetic bucket are molded to the contours of the inner plaster shell after the cast has dried.

An alternative to the scale technique is the load cell, which is a pressure-sensing device built into the prosthetic pylon.170 During the first 7 to 10 days after surgery, the patient ambulates using parallel bars with a maximum of 10 to 15 pounds touchdown weight bearing (10% of body weight). After application of the second postoperative prosthesis, the patient increases weight bearing to approximately 50% of total body weight. At the end of 14 to 21 days, on removal of the second postoperative prosthesis, a decision is made to place the patient either in a third postoperative prosthesis (if there is a question of wound healing) or in a removable temporary prosthesis (if the wound appears to be healing satisfactorily).167,168 At this time, the patient begins full weight bearing. By approximately 30 to 35 days after amputation surgery, most patients have achieved either independent ambulation or ambulation with some type of ancillary walking aid (cane, walker). If a patient lives close to the hospital and is able to come to daily physical therapy training

FIGURE 49–24 • To control the amount of postoperative weight bearing by patients, a bathroom scale is used to teach them to distribute their body weight. During the first week after surgery, weight bearing is limited to 10 to 15 pounds. After the second cast change, weight bearing is limited to 50% of total body weight.

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as an outpatient, he or she may be discharged from the hospital shortly after receiving the second postoperative prosthesis (5 to 10 days); however, if the patient lives a great distance from the hospital, discharge is usually delayed until the surgeon, prosthetist, and therapist are happy with the rehabilitation process (4 to 5 weeks). This approach may have to be modified under the economic restraints that surround current medical care. Reasonable alternatives include transfer to a rehabilitation unit or service or early discharge with outpatient care. In either case, careful follow-up by the surgeon, prosthetist, and therapist is mandatory, especially in patients undergoing early ambulation and rehabilitation. It can be anticipated that between discharge from the hospital and construction of the first permanent prosthesis (on average, 6 months after amputation), approximately three to six changes in the socket of the temporary prosthesis will be required as a result of progressive stump shrinkage. A typical lightweight, removable, temporary below-knee prosthesis is shown in Figure 49-25. The same pylon and foot can be used throughout all intermediate (temporary) cast changes, so that the only new requirement is the socket and realignment of the prosthesis. Prosthetic fit is maintained with stump socks, and the primary indication for change of the temporary prosthesis is when the patient has reached a total of 15-ply stockings to maintain a good prosthetic fit. Obviously, great care is taken

to educate the patient about the use of the prosthesis and stump care to avoid any problems due to poor prosthetic fit. Knee Disarticulation Amputation The techniques for the application of an immediate postoperative prosthesis for knee disarticulation amputation are essentially the same as those for below-knee amputation. Because of the bulbous distal end of the knee disarticulation stump, the immediate postoperative prosthesis for this amputation level is self-suspending. Great care should be taken during cast fabrication to contour the femoral flares and to bring the proximal end of the cast to at least the upper third of the thigh to minimize distal end-weight bearing. My preference is to incorporate a polypropylene quadrilateral aboveknee brim into the knee disarticulation cast to provide ischial weight bearing. The stump should be well padded, because there is more stump weight bearing with this level of amputation than with a below-knee amputation. At the discretion of the surgeon and prosthetist, polycentric hydraulic knee units can be incorporated into the initial immediate postoperative prosthesis or at any time during postoperative follow-up. The schedule for cast changes, the rehabilitation techniques, and the use of temporary prostheses are approximately the same as those for below-knee amputation. Above-Knee Amputation IPOP techniques for above-knee amputation require more attention to detail to maintain adequate suspension and socket fit. Although techniques using a modified Silesian suspension (contralateral hip sling) or waist suspension belt are simple to implement,113 I believe that the difficulties of using immediate postoperative prostheses at the above-knee level are not offset by any significant improvement in the overall rehabilitation process. Thus, I use immediate postoperative prostheses at this amputation level only for young amputees. For dysvascular amputees, a temporary above-knee prosthesis is prescribed when primary wound healing has been achieved (2 to 3 weeks). During the postoperative period, the aboveknee amputee goes to rehabilitation daily to achieve upper extremity strengthening and balance and to practice ambulation with parallel bars or other walking aids. Once a temporary prosthesis has been constructed, the schedule for prosthesis modification and the rehabilitation techniques are similar to those for below-knee or knee disarticulation amputation. Overview of Prostheses and Prosthetic Techniques

FIGURE 49–25 • Standard removable lightweight below-knee temporary or intermediate prosthesis, prescribed after removal of the last immediate postoperative prosthesis. This particular prosthesis is constructed with 3M Scotchcast (3M, St. Paul, Minn.). Fabrication with Scotchcast allows construction of a lightweight, cool, yet durable prosthesis.

There is no one type of standard prosthetic prescription for all levels of lower extremity amputation, and knowledge of available components is crucial in determining the proper prescription for each amputee based on his or her activities and lifestyle. A more complete discussion of prosthetic components is beyond the scope of this chapter; however, interested surgeons are referred to their local prosthetists or prosthetic facilities with whom they should be working. IPOP techniques do not work in all clinical settings. The success of the technique is based on the experience and dedication of the team, and there is no question that if the immediate postoperative prosthesis is improperly applied,

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significant damage to the amputation stump can occur. In the absence of an experienced prosthetist and physical therapist, I suggest that a rigid postoperative dressing be applied; then, when primary stump healing has occurred, an appropriate temporary prosthesis can be prescribed and the rehabilitation process initiated. A delay of 1 to 2 weeks in the rehabilitation process is meaningless in the overall context of amputee rehabilitation; however, it has been my experience that if the rehabilitation process is delayed for a month or more, the ultimate success of rehabilitation, especially for geriatric high-level amputees, is severely compromised. It is therefore logical and reasonable to provide a temporary prosthesis sometime between wound healing (7 to 10 days after surgery) and 1 month after surgery. Using this “between” approach (i.e., a rigid dressing with early prosthetic application), maximum rehabilitation results can be achieved even in the absence of a formal rehabilitation team. PROSTHETIC COMPONENTS For a surgeon who performs only an occasional amputation, the number and types of prostheses and prosthetic components for lower extremity amputees can be bewildering. Therefore, a general overview of prosthetic components and specific combinations of components for certain levels of lower extremity amputation may be of value. Transmetatarsal Amputation In general, there is minimal, if any, prosthetic requirement for a transmetatarsal amputation. A steel shank placed in the sole of the shoe allows near-normal toe-off, and the void spot in the shoe can be filled with cotton, lamb’s wool, or a soft foam material. The other option is construction of a specially designed shoe molded to the patient’s foot in which toe-off is built into the shoe during construction. Syme’s Amputation Depending on whether Syme’s amputation has been performed with a one- or two-stage surgical procedure, the cosmetic quality of the prosthesis will be different (two-stage is more cosmetic). In general, this is an end–weight-bearing stump, and a prosthetic foot is attached to the leg shaft portion of the prosthesis. Because of the bulbous nature of the stump, a medial window has to be cut into the prosthesis to allow the stump to pass through the narrow midportion of the prosthesis. These prostheses are usually built with a nonmotion solid ankle-cushion heel (SACH) foot (Scheck & Siress). The presence of a particularly bulbous distal end precludes a cosmetic prosthesis, and this type of amputation may be contraindicated for cosmetic reasons alone. Below-Knee Amputation In general, the below-knee prosthesis consists of a prosthetic socket that is attached to a pylon or ankle block (endoskeletal system) and a foot. The prosthetic shell can be composed of plastic laminate, wood, or one of the newer, lightweight, rolled fiberglass materials such as 3M Scotchcast (3M, St. Paul, Minn.). The socket may use no liner (skin-socket interface) or may use a liner composed of lightweight plastic

FIGURE 49–26 • This below-knee prosthesis is an ultralightweight patellar tendon weight-bearing-type prosthesis using a Silastic sleeve for suspension, a Silastic gel insert, and a stationary attachment flexible endoskeletal (SAFE) motion-type foot. This is an ideal prosthesis for a young, active amputee.

such as P-Lite, silicone gel bonded between two sheets of soft leather, or stump socks. The prosthesis can be suspended in a variety of ways, the most common of which is a standard PTB strap, supracondylar clip, Silastic sleeve suspension, suction, or thigh lacer with external hinges (Fig. 49-26). Selfsuspending prostheses or physiologic suspension (the prosthesis is held in place by changes in muscle shape and contour with contraction) may be used in young, active amputees. In a young, highly active amputee, an ankle-rotating unit may be placed between the prosthesis and the foot. The feet currently in use include the SACH foot, which is a nonmotion foot; the stationary attachment flexible endoskeletal (SAFE) foot (Scheck & Siress); or the Geisinger 5-Way foot (Danville, Pa.). The last two feet incorporate flexion, extension, and internal and external rotation when the foot is stressed under weight. The drawback to both of these motion feet is increased weight and perhaps decreased life expectancy compared with the SACH foot. The most popular motion foot, the Seattle foot, overcomes the drawbacks of the previously mentioned motion feet and has a cosmetic design that incorporates toes. A hydraulic ankle unit has recently been developed, but the unit is quite heavy, and there are still problems with oil leakage. New energy-storing feet (energy is “stored” by deformation of carbon-plastic composites and “released” on toe-off), such as the Seattle-BoeingBurgess Foot and the Flex-Foot (Scheck & Siress), offer significant improvements in gait and activity levels (such as running), especially for young, active amputees.

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The combination of a motion foot and a lightweight prosthesis provides a very high degree of function for active amputees. Prosthetist

Knee Disarticulation Historically, knee disarticulation amputations were a prosthetic nightmare because the knee centers (thigh-knee length) could not be matched; however, the availability of polycentric knee joints has allowed construction of a cosmetic knee disarticulation prosthesis. In general, this prosthesis is similar to the Syme’s-type prosthesis, in that the distal bony end of the stump is passed through the proximal portion of the prosthesis via a window cut in the medial portion of the prosthesis. The prosthetic shell can be constructed of plastic or wood. In general, the prosthetic shell extends from the end of the stump up to the ischium to provide both distal end and ischial weight bearing. Most knee disarticulation prostheses incorporate some type of hydraulic knee unit for both cosmetic and functional reasons. The lower part of the leg can be constructed of solid wood, plastic laminate, or a metal or plastic endoskeletal system for connection to the ankle block and foot. Ankle rotators and energy-storing motion or nonmotion feet can be used at the discretion of the prosthetist and surgeon.

Engineer/ electronics

Surgeon

Thirdparty carriers

Nurses Patient

Rehab medicine

Family

Referring physician

Social services Community

FIGURE 49–27 • The rehabilitation team required for successful amputation rehabilitation. Notice that the patient is at the center, and the surgeon is only one of many coequal team members.

Above-Knee Amputation The above-knee prosthesis can be constructed of plastic or wood. Suspension techniques include an external hip joint with belt, shoulder suspension, or suction socket suspension. This is not an end–weight-bearing prosthesis, and all the weight is borne by the proximal socket quadrilateral brim design (the soft tissues of the thigh and ischium). Newer prosthetic designs for above-knee sockets include the contoured adducted trochanteric–controlled alignment method (CAT-CAM) design (which holds the stump laterally and medially, providing rigid support for the femur, in contrast to the quadrilateral socket, which holds the stump anteriorly and posteriorly, with poor femur support) and a variety of new flexible socket and strut designs (outer rigid strut attached to the knee joint with a soft flexible inner socket). These new designs significantly enhance function for aboveknee amputees. A hydraulic, passive, or manual lock knee joint can be incorporated, based on the individual patient’s needs. The lower part of the prosthesis is constructed as outlined in the section on knee disarticulation prostheses. Hip Disarticulation In general, hip disarticulation prostheses are built along the lines of the Canadian system, which incorporates a pelvic bucket, an endoskeletal upper and lower leg, simple springassisted hip and knee joints, and a nonmotion foot.

Amputation Rehabilitation Team It is exceedingly difficult to achieve consistently reliable rehabilitation results in the absence of a formal, centralized, dedicated rehabilitation team that includes active participation by a prosthetist and members of the physical medicine and therapy departments. Just as some surgical procedures are

confined to regional centers because of the cost and necessity of skilled labor, it is my belief that, ideally, amputation rehabilitation should be a centralized resource in a community or group of communities to achieve the best results. My concept of the structure of the amputation rehabilitation team is shown in Figure 49-27. Note that the center of the rehabilitation team is the patient and that other members of the team interface with the patient through or with an amputation coordinator. This coordinator can be a physical therapist, occupational therapist, nurse, or layperson. In my opinion, this person is key to maintaining coordination and especially long-term follow-up among members of the team. It has been my experience that one break in this rehabilitation circle results in at least a 50% failure rate in amputee rehabilitation. This fact (i.e., a break in the rehabilitation circle) may explain why the average rate of rehabilitation after lower extremity amputation is 60% or less. There are five primary areas of concern in successful amputee rehabilitation: (1) coordination of care, (2) education of patient and family, (3) directed access to community resources, (4) discharge planning, and (5) centralized follow-up. In essence, the coordination of health care and mobilization of resources are under the direct control of the physician; however, once surgery is completed, this task is best organized by the amputation program coordinator. Discharge planning for the patient should start, if possible, before amputation. Education of the patient and family and evaluation of the financial and social resources available to the patient should also begin before amputation or as soon as possible after amputation. Centralized follow-up is important only if the team is interested in evaluating specific treatment techniques or prosthetic components. However, long-term follow-up is mandatory if reliable information on rehabilitation and postoperative complications is to be obtained.

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The role of the physician is that of team director and provider of health care. The enthusiasm and interest of the physician will be reflected by all other members of the health care team. In the absence of an interested physician, rehabilitation failures will be common. It is my belief that the prosthetist should be seen as coequal to the physician in the amputation rehabilitation process. From a practical standpoint, most patients rely more on the prosthetist than on the physician (in the absence of medical problems) once the acute phase of rehabilitation is completed. The therapist is in the unique position of being able to make or break all the efforts of the surgeon and prosthetist. Only if the rehabilitation process runs smoothly and if attention is paid to small details during the rehabilitation process will the patient successfully regain ambulation. The greatest surgery in the world or the best limb in the world can meet defeat at the hands of an unskilled therapist. The therapist is the third coequal on the rehabilitation team, along with the physician and prosthetist. Finally, the patient is the most important member of the rehabilitation team. The team can provide the patient with tools and techniques for rehabilitation, but it cannot provide the patient with motivation. It is of the utmost importance that the patient be taught to take primary control of the rehabilitation process. Included in this education are care of the amputation stump, care of the nonamputated leg, and care of the prosthesis. Failure of the patient to take an active role in the rehabilitation process will doom it to failure.171 One of the areas in which we as physicians and rehabilitation team members fail our patients is postdischarge followup and home care. An excellent review article on this topic appeared in the February 1979 issue of the Orthopedic Nurses Association Journal. All interested rehabilitation physicians and team members are advised to review this information and pass it on to their patients.121 I am now in a solo private practice without a dedicated amputation team. Although three experienced prosthetists, all of whom are well acquainted with immediate postoperative prosthesis fitting, are nearby, the lack of trained therapists and capitated-directed patient care contracts makes accelerated rehabilitation difficult if not impossible. Objective amputation level selection (transcutaneous oxygen testing), early if not immediate postoperative prosthetic filling, utilization of rehabilitation facilities after discharge, education of therapists, and persistence usually lead to a successful outcome. However, the rehabilitation results, especially in elderly or frail patients, are not as good as those documented in this chapter using a dedicated amputation team or center of care model.

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amputation level selection is the availability of computer software and microprocessors to integrate results from several different types of noninvasive techniques, resulting, in essence, in the era of the “limb viability laboratory.” It can be anticipated that multi-instrument testing will result in greater accuracy than single-instrument evaluation. In addition, many of these instruments will find use in the evaluation of limb ischemia, especially in the perioperative period. PROSTHETICS Three current areas of prosthetic development show promise: the emergence of ultralightweight and throwaway or temporary or intermediate prostheses (Fig. 49-28); the design and development of energy-absorbing and energy-returning prosthetic components (designed to return energy on toe-off), as exemplified by the Seattle-Boeing-Burgess foot and the Flex-Foot; and new fabrication techniques such as flexible sockets (ISNY socket [New York University Medical Center, Prosthetics and Orthotics, New York]), flexible suction sockets (Iceross sockets, Össur, Reykjauk, Iceland), and nonquadrilateral or medial-lateral–contoured above-knee sockets. The use of new plastics, fiberglass casting tapes, and carbon fiber polymers is allowing the construction of ultralightweight yet

What Is New in Amputation Surgery? INSTRUMENTATION As noted earlier, many new instruments are currently undergoing evaluation for amputation level selection. In addition, many of these instruments are being evaluated for their role in arterial insufficiency. Early information is available, but the definitive role for these instruments is undecided. Perhaps more promising than any specific instruments for

FIGURE 49–28 • Patients with lower extremity amputations usually sit on a stool when taking a shower. The above-knee amputee shown here is wearing an Aqualite shower prosthesis (US Manufacturing Co., Pasadena, Calif.).

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rugged, durable prostheses. These prostheses have obvious value for geriatric amputees in terms of energy-saving characteristics, especially for high-level amputees, but they also have value for young, active amputees engaging in sports or water-related activities. Lightweight prostheses constructed with these new materials are often easier to fabricate than standard plastic laminate prostheses. Artificial limbs constructed with fiberglass casting tapes, such as 3M Scotchcast, allow a decrease in skin temperature at the socket-skin interface because of the porous nature of the casting material. Preliminary work by my group demonstrated a 5°C to 7°C drop in skin temperature with 3M Scotchcast PTB belowknee prostheses compared with standard plastic laminate PTB below-knee prostheses. The importance of decreased skin temperature is unknown with respect to stump durability, but there is no question that these prostheses result in improved patient comfort in hot, humid climates. Increasing numbers of studies are now being done with young, active amputees to improve their performance abilities in activities such as running, jumping, and other sports functions.172 Projects such as this point toward future improvements in prosthetic devices and toward future research efforts, perhaps leading to greater efficiency with which amputees conduct their physical activities. SURGERY A number of articles in the surgical literature describe arterial reconstruction with free tissue transfer to save limb length,173,174 myofasciocutaneous flaps to improve stump healing and prosthesis utilization,175 and foot salvage and avoidance of major lower limb amputations in diabetic patients.176 In 45 patients with gangrenous lesions of the foot or lower leg due to severe diabetic arterial disease resulting in extensive soft tissue defects with exposed bones or tendons, Vermassen and van Landuyt reported excellent clinical results with arterial reconstruction and combined free tissue transfer.173 The combined survival and limb salvage rate was 84% after 1 year, 77% after 2 years, and 65% after 3 years. The articles cited are only a small fraction of the published literature, and interested readers can find many more publications using PubMed and doing Internet searches on amputation and skin flaps. The combination of distal vascular reconstruction and free flap utilization, rotational flaps, and other techniques for closure of soft tissue defects of the extremities all offer exciting opportunities for extended limb salvage and avoidance of major limb amputation, especially in patients with diabetes. KEY REFERENCES Bowker JH, San Giovanni TP, Pinzur MS: North American experience with knee disarticulation with use of a posterior myofasciocutaneous flap: Healing rate and functional results in seventy-seven patients. J Bone Joint Surg Am 82:1571-1574, 2000. Burgess EM, Romano RL: The management of lower extremity amputees using immediate postsurgical prostheses. Clin Orthop 57:137-156, 1968. Chang BB, Bock DE, Jacobs RL, et al: Increased limb salvage by the use of unconventional foot amputations. J Vasc Surg 19:341-348, 1994. Early JS: Transmetatarsal and midfoot amputations. Clin Orthop 361:85-90, 1999. Flores Rivera AR: Risk factors for amputation in diabetic patients: A casecontrol study. Arch Med Res 29:179-184, 1998. Hirsch G, McBride ME, Murray DD, et al: Chopart prosthesis and semirigid orthosis in traumatic forefoot amputations: Comparative gait analysis. Am J Phys Med Rehabil 75:283-291, 1996.

Koch M, Kutkuhn B, Grabensee B, et al: Apolipoprotein A, fibrinogen, age, and history of stroke are predictors of death in dialysed diabetic patients: A prospective study in 412 subjects. Nephrol Dial Transplant 12:2603-2611, 1997. Lehto S, Ronnemaa T, Pyorala K, et al: Risk factors predicting lower extremity amputations in patients with NIDDM. Diabetes Care 19:607-612, 1996. Lutz BS, Siemers F, Shen ZL, et al: Free flap to the arteria peronea magna for lower limb salvage. Plast Reconstr Surg 105:684-687, 2000. Malone JM: Revascularization versus amputation. In Rutherford R (ed): Vascular Surgery, 5th ed. Philadelphia, WB Saunders, 2000, pp 2255-2266. Misuri A, Lucertini G, Nanni A, et al: Predictive value of transcutaneous oximetry for selection of amputation level. J Cardiovasc Surg 41:83-87, 2000. Moore JC, Jolly GP: Soft tissue considerations in partial foot amputations. Clin Podiatr Med Surg 17:631-648, 2000. Muhlhauser I, Overmann H, Bender R, et al: Predictors of mortality and end-stage diabetic complications in patients with type 1 diabetes mellitus on intensified insulin therapy. Diabet Med 17:727-734, 2000. Naylor AR, Hayes PD, Darke S: A prospective audit of complex wound and graft infections in Great Britain and Ireland: The emergence of MRSA. Eur J Vasc Surg 21:289-294, 2001. Reyzelman AM, Hadi S, Armstrong DG: Limb salvage with Chopart’s amputation and tendon balancing. J Am Podiatr Med Assoc 89:100-103, 1999. Sanders LJ: Transmetatarsal and midfoot amputations. Clin Podiatr Med Surg 14:741-762, 1997. Tepel M, van der Giet M, Schwarzfeld C, et al: Prevention of radiographiccontrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 343:210-212, 2000. Vermassen FE, van Landuyt K: Combined vascular reconstruction and free flap transfer in diabetic arterial disease. Diabetes Metab Res Rev 16(Suppl 1):S33-S36, 2000. Wrobel JS, Mayfield JA, Reiber GE: Geographic variation of lower-extremity major amputation in individuals with and without diabetes in the Medicare population. Diabetes Care 24:860-864, 2001.

REFERENCES 1. Wangensteen OH, Wangensteen SD: The Rise of Surgery from Empiric Craft to Scientific Discipline. Minneapolis, University of Minnesota Press, 1978, p 18. 2. Boedner CW: Baron Dominique Jean Larrey, Napoleon’s surgeon. ACS Bull July:18-21, 1982. 3. Berlemont M: Notre expérience de l’appareillage précoce des amputés des membres inférieurs aux establissements helio Marins de Berk. Ann Med Phys Med 5: 1961. 4. Weiss M: The prosthesis on the operating table from a neurophysical point of view: Report of a workshop panel on lower extremity prosthetic fitting. Committee on Prosthetics Research Development. Paper presented to the National Academy of Sciences, Feb 1966. 5. Burgess EM, Tramb JE, Wilson AB Jr: Immediate Postsurgical Prosthetics in the Management of Lower Extremity Amputees. TR 10-5. Washington, DC, Veterans Administration, 1967. 6. Falstie-Jensen N, Christensen KB: A model for prediction of failure in amputation of the lower limb. Dan Med Bull 37:283-286, 1990. 7. Huston CC, Bivins BA, Ernst CB, Griffen WO Jr: Morbid implications of above-knee amputations: Report of a series and review of the literature. Arch Surg 115:165-167, 1980. 8. Kerstein MD, Zimmer H, Dugdale FE, Lerner E: Associated diagnoses complicating rehabilitation after major lower extremity amputation. Angiology 25:536-547, 1974. 9. Malone JM, Moore WS, Goldstone J, Malone SJ: Therapeutic and economic impact of a modern amputation program. Ann Surg 189: 798-802, 1979. 10. Moore WS, Hall AD, Lim RC: Below the knee amputation for ischemic gangrene: Comparative results of conventional operation and immediate postoperative fitting technic. Am J Surg 124:127-134, 1972. 11. Porter JM, Baur GM, Taylor LM Jr: Lower-extremity amputation for ischemia. Arch Surg 116:89-92, 1981. 12. Towne JB, Condon RE: Lower extremity amputation for ischemic disease. Adv Surg 13:199-227, 1979. 13. Otteman MG, Stahlgren LH: Evaluation of factors which influence mortality and morbidity following major lower extremity amputation for arteriosclerosis. Surg Gynecol Obstet 120:1217-1220, 1965. 14. Roon AJ, Moore WS, Goldstone J: Below-knee amputation: A modern approach. Am J Surg 134:153-158, 1977.

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15. Wrobel JS, Mayfield JA, Reiber GE: Geographic variation of lowerextremity major amputation in individuals with and without diabetes in the Medicare population. Diabetes Care 24:860-864, 2001. 16. Malone JM, Synder M, Anderson GG, et al: Prevention of amputation by diabetic education. Am J Surg 158:520-524, 1989. 17. Mazet R Jr, Schiller FJ, Dunn OJ, Alonzo NJ: The influence of prosthesis wearing on the health of the geriatric patient. Project 431. Washington, DC, Office of Vocational Rehabilitation, Department of Health, Education, and Welfare, March 1963. 18. Whitehouse FW, Jurgensen C, Block MA: The later life of the diabetic amputee: Another look at fate of the second leg. Diabetes 17:520-521, 1968. 19. Malone JM, Moore WS, Goldstone J: Life expectancy following aortofemoral arterial grafting. Surgery 81:551-555, 1977. 20. Malone JM, Moore WS, Leal JM, Childers SJ: Rehabilitation for lower extremity amputation. Arch Surg 116:93-98, 1981. 21. Pinzur MS, Littooy F, Daniels J, et al: Multidisciplinary preoperative assessment and late function in dysvascular amputees. Clin Orthop 281:239-243, 1992. 22. Fierer J, Daniel D, Davis C: The fetid foot: Lower-extremity infections in patients with diabetes mellitus. Rev Infect Dis 1:210-217, 1979. 23. Naylor AR, Hayes PD, Darke S: A prospective audit of complex wound and graft infections in Great Britain and Ireland: The emergence of MRSA. Eur J Vasc Surg 21:289-294, 2001. 24. Malone JM: Revascularization versus amputation. In Rutherford R (ed): Vascular Surgery, 5th ed. Philadelphia, WB Saunders, 2000, pp 2255-2266. 25. Brinker MR, Timberlake GA, Goff JM, et al: Below knee physiologic cryoanesthesia in the critically ill patient. J Vasc Surg 7:433-438, 1988. 26. Johansen K, Burgess EM, Zorn R, et al: Improvement of amputation level by lower extremity revascularization. Surg Gynecol Obstet 153:707-709, 1981. 27. Kazmers M, Satiani B, Evans WE: Amputation level following unsuccessful distal limb salvage operations. Surgery 87:683-687, 1980. 28. Samson RH, Gupta SK, Scher LA, Veith FJ: Treatment of limb threatening ischemia despite a palpable popliteal pulse. J Surg Res 32:535-539, 1982. 29. Samson RH, Gupta SK, Scher LA, Veith FJ: Level of amputation after failed limb salvage procedures. Surg Gynecol Obstet 154:56-58, 1982. 30. Stoney RJ: Ultimate salvage for the patient with limb threatening ischemia: Realistic goals and surgical considerations. In Bergan JJ, Yao JST (eds): Gangrene and Severe Ischemia of the Lower Extremities. New York, Grune & Stratton, 1978, pp 383-392. 31. Stirneman P, Walpoth B, Wiursten VH, et al: Influence of failed arterial reconstruction on the outcome of major limb amputation. Surgery 111:363-368, 1992. 32. Tsang GM, Crowson MC, Hickey NC, Simms MH: Failed femorocrural reconstruction does not prejudice amputation level. Br J Surg 78: 1479-1481, 1991. 33. Evans WE, Hayes JP, Vermilion BD: Effect of a failed distal reconstruction on the level of amputation. Am J Surg 160:217-220, 1990. 34. Epstein SB, Worth MH Jr, Ferzli G: Level of amputation following failed vascular reconstruction for lower limb ischemia. Curr Probl Surg 46:185-192, 1989. 35. Bloom RJ, Stevick CA: Amputation level and distal salvage of the limb. Surg Gynecol Obstet 166:1-5, 1988. 36. McIntyre KE Jr, Bailey SA, Malone JM, Goldstone J: The nonsalvageable infected lower extremity: A new look at guillotine amputation. Am J Surg 117:58-64, 1985. 37. Fischer DF, Clagett GP, Fry RE, et al: One-stage versus two-stage amputation for wet gangrene of the lower extremity: A randomized study. J Vasc Surg 8:428-433, 1988. 38. Robbs JV, Ray R: Clinical predictors of below knee stump healing following amputation for ischemia. S Afr J Surg 20:305-310, 1982. 39. Dwars BJ, Van Den Broek TA, Ravwerda JA, Bakker FC: Criteria for reliable selection of the lowest level of amputation in peripheral vascular disease. J Vasc Surg 15:536-542, 1992. 40. Golbranson FL, Yu EC, Gelberman RH: The use of skin temperature determinations in lower extremity amputation level selection. Foot Ankle 3:170-172, 1982. 41. Spence VA, Walker WF: The relationship between temperature isotherms and skin blood flow in the ischemic limb. J Surg Res 36: 278-281, 1984. 42. Stoner HB, Taylor L, Marcuson RW: The value of skin temperature measurements in forecasting the healing of below-knee amputation for end stage ischemia of the leg in peripheral vascular disease. Eur J Vasc Surg 3:355-361, 1989.

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43. Wagner WH, Keagy BA, Kotb MN, et al: Noninvasive determination of healing of major lower extremity amputation: The continued role of clinical judgment. J Vasc Surg 8:703-710, 1988. 44. Lim RC Sr, Blaisdell FW, Hall AD, et al: Below knee amputation for ischemic gangrene. Surg Gynecol Obstet 125:493-501, 1967. 45. Baker WH, Barnes RW: Minor forefoot amputation in patients with low ankle pressure. Am J Surg 133:331-332, 1977. 46. Barnes RW, Shanik GO, Slaymaker EE: An index of healing in belowknee amputation: Leg blood pressure by Doppler ultrasound. Surgery 79:13-20, 1976. 47. Bernstein EF: The noninvasive vascular diagnostic laboratory. In Najarian JS, Oelaney JP (eds): Vascular Surgery. Miami, Symposia Specialists; New York, Stratton Intercontinental, 1978, pp 33-46. 48. Gibbons GW, Wheelock FC Jr, Siembieda C, et al: Noninvasive prediction of amputation level in diabetic patients. Arch Surg 114:1253-1257, 1979. 49. Raines JK, Darling RC, Buth J, et al: Vascular laboratory criteria for the management of peripheral vascular disease of the lower extremities. Surgery 79:21-29, 1976. 50. Schwartz JA, Schuler JJ, O’Connor RJA, Flanigan DP: Predictive value of distal perfusion pressure in the healing of amputation of the digits and the forefoot. Surg Gynecol Obstet 154:865-869, 1982. 51. Verta MJ, Gross WS, Van Bellan B, et al: Forefoot perfusion pressure and minor amputation surgery. Surgery 80:729-734, 1976. 52. Yao JST, Bergan JJ: Application of ultrasound to arterial and venous diagnosis. Surg Clin North Am 54:23-38, 1974. 53. Cheng EY: Lower extremity amputation level: Selection using noninvasive hemodynamic methods of evaluation. Arch Phys Med Rehabil 63:475-479, 1982. 54. Holloway GA Jr, Burgess EM: Cutaneous blood flow and its relation to healing of below knee amputation. Surg Gynecol Obstet 146:750-756, 1978. 55. Holloway GA Jr, Watkins BW: Laser Doppler measurement of cutaneous blood flow. J Invest Dermatol 69:300-309, 1977. 56. Kostuik JP, Wood D, Hornby R, et al: Measurement of skin blood flow in peripheral vascular disease by the epicutaneous application of xenon-133. J Bone Joint Surg Am 58:833-837, 1964. 57. Malone JM, Leal JM, Moore WS, et al: The “gold standard” for amputation level selection: Xenon-133 clearance. J Surg Res 30:449-455, 1981. 58. Moore WS: Determination of amputation level: Measurement of skin blood flow with xenon-133. Arch Surg 107:798-802, 1973. 59. Silberstein EB, Thomas S, Cline J, et al: Predictive value of intracutaneous xenon clearance for healing of amputation and cutaneous ulcer sites. Radiology 147:227-229, 1983. 60. Burgess EM, Matsen FA, Wyss CR, Simmons CW: Segmental transcutaneous measurements of PO2 in patients requiring below the knee amputation for peripheral vascular insufficiency. J Bone Joint Surg Am 64:378-382, 1982. 61. Clyne CAC, Ryan J, Webster JHH, Chant AOB: Oxygen tension on the skin of ischemic legs. Am J Surg 143:315-318, 1982. 62. Franzeck UK, Talke P, Berstein EF, et al: Transcutaneous PO2 measurement in health on peripheral arterial occlusive disease. Surgery 91: 156-163, 1982. 63. Harward TRS, Volny J, Golbranson F, et al: Oxygen-inhalation induced transcutaneous PO2 changes as a predictor of amputation level. J Vasc Surg 2:220-227, 1985. 64. Katsamouris A, Brewster DC, Megerman J, et al: Transcutaneous oxygen tension in selection of amputation level. Am J Surg 147:510-516, 1984. 65. Malone JM, Anderson GG, Halka SC, et al: Prospective comparison of noninvasive techniques for amputation level selection. Am J Surg 154:179-184, 1987. 66. Matsen FA, Wyss CR, Robertson CL, et al: The relationship of transcutaneous PO2 and laser Doppler measurements in a human model of local arterial insufficiency. Surg Gynecol Obstet 159:418-422, 1984. 67. Ratliff DA, Clune CAC, Chant ADB, Webster JHH: Prediction of amputation healing: The role of transcutaneous PO2 assessment. Br J Surg 71:219-222, 1984. 68. Misuri A, Lucertini G, Nanni A, et al: Predictive value of transcutaneous oximetry for selection of amputation level. J Cardiovasc Surg 41:83-87, 2000. 69. Graham BH, Walton RL, Elings VB, Lewis F: Surface quantification of injected fluorescein as a predictor of flap viability. Plast Reconstr Surg 71:826-833, 1983. 70. McFarland DC, Lawrence PF: Skin fluorescence: A method to predict amputation site healing. J Surg Res 32:410-415, 1982.

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71. Silverman DG, Hurford WE, Cooper HS, et al: Quantification of fluorescein distribution to strangulated reticulum. J Surg Res 34:179-186, 1983. 72. Silverman DG, Rubin JM, Reilly CA, et al: Fluorometric prediction of successful amputation levels in the ischemic limb. J Rehabil Res Dev 22:29-34, 1985. 73. Holloway GA Jr, Burgess EM: Preliminary experiences with laser Doppler velocimetry for the determination of amputation levels. Prosthet Orthot Int 7:63-66, 1983. 74. Holstein P: Level selection in leg amputation for arterial occlusive disease: A comparison of clinical evaluation and skin perfusion pressure. Acta Orthop Scand 53:821-831, 1982. 75. Holstein P, Trap-Jensen J, Bagger H, Larsen B: Skin perfusion pressure measured by isotope washout in legs with arterial occlusive disease. Clin Physiol 3:313-324, 1983. 76. Stockel M, Ovesen J, Brochner-Morstensen J, Emneus H: Standardized photoelectric technique as routine method for selection of amputation level. Acta Orthop Scand 53:875-878, 1982. 77. Kram HB, Appel PL, Shoemaker WC: Multisensor transcutaneous oximetric mapping to predict below-knee amputation wound healing: Use of critical PO2. J Vasc Surg 9:796-800, 1989. 78. Kram HB, Appel PL, Shoemaker WC: Prediction of below-knee amputation wound healing using noninvasive laser Doppler velocimetry. Am J Surg 158:29-31, 1989. 79. Burnham ST, Wagner WH, Keagy BH, Johnson G Jr: Objective measurement of limb perfusion by dermal fluorometry: A criterion for healing of below knee amputation. Arch Surg 125:104-106, 1990. 80. Friedmann LW: The prosthesis—immediate or delayed fitting? Angiology 23:513-524, 1972. 81. Durham JR, Anderson GG, Malone JM: Methods of preoperative selection of amputation level. In Flanigan P (ed): Modern Methods of Perioperative Assessment in Peripheral Vascular Surgery. New York, Marcel Dekker, 1986. 82. Oishi CS, Fronek A, Golbranson FL: The role of noninvasive vascular studies in determining levels of amputation. J Bone Joint Surg Am 70:1520-1530, 1988. 83. Bacharach JM, Rooke TW, Osmundson PJ, Gloviczki P: Predictive value of transcutaneous oxygen pressure and amputation success by use of supine and elevation measurement. J Vasc Surg 15:558-563, 1992. 84. Holloway GA Jr: Cutaneous blood flow responses to infection trauma measured by laser Doppler velocimetry. J Invest Dermatol 74:1-4, 1980. 85. Daly MJ, Henry RE: Quantitative measurement of skin perfusion with xenon-133. J Nucl Med 21:156-160, 1980. 86. Holstein P, Lassen NA: Assessment of safe level of amputation by measurement of skin blood pressure. In Rutherford R, et al (eds): Vascular Surgery. Philadelphia, WB Saunders, 1977, pp 105-111. 87. Ovesen J, Stockel M: Measurement of skin perfusion pressure by photoelectric technique: Aid to amputation level selection in arteriosclerotic disease. Prosthet Orthot Int 8:39-42, 1984. 88. Wagner FW Jr: Amputation of the foot and ankle: Current status. Clin Orthop 122:62-69, 1977. 89. Sizer JS, Wheelock FC: Digital amputations in diabetic patients. Surgery 72:980-989, 1972. 90. Little JM, Stephen MS, Zylstra PL: Amputation of the toes for vascular disease: Fate of the affected leg. Lancet 2:1318-1319, 1976. 91. McKittrick LS, McKittrick MB, Risby TS: Transmetatarsal amputation for infection of gangrene in patients with diabetes mellitus. Ann Surg 130:825-842, 1949. 92. Early JS: Transmetatarsal and midfoot amputations. Clin Orthop 361:85-90, 1999. 93. Reyzelman AM, Hadi S, Armstrong DG: Limb salvage with Chopart’s amputation and tendon balancing. J Am Podiatr Med Assoc 89: 100-103, 1999. 94. Sanders LJ: Transmetatarsal and midfoot amputations. Clin Podiatr Med Surg 14:741-762, 1997. 95. Chang BB, Bock DE, Jacobs RL, et al: Increased limb salvage by the use of unconventional foot amputations. J Vasc Surg 19:341-348, 1994. 96. Hirsch G, McBride ME, Murray DD, et al: Chopart prosthesis and semirigid orthosis in traumatic forefoot amputations: Comparative gait analysis. Am J Phys Med Rehabil 75:283-291, 1996. 97. Syme J: On amputation at the ankle joint. Lond Edinb Monthly J Med Sci 3:93, 1843. 98. Harris RI: Syme’s amputation, the technical details essential for success. J Bone Joint Surg Br 38:614-632, 1956.

99. Harris RI: The history and development of Syme’s amputations. Artif Limbs 6:4-43, 1961. 100. Warren R, Kihn RB: A survey of lower extremity amputations for ischemia. Surgery 63:107-120, 1968. 101. Kernek CB, Rozzi WB: Simplified two stage below-knee amputation for unsalvageable diabetic foot infections. Clin Orthop 261:251-256, 1990. 102. Termansen NB: Below-knee amputation for ischaemic gangrene: Prospective, randomized comparison of a transverse and a sagittal operative technique. Acta Orthop Scand 48:311-316, 1977. 103. Persson BM: Sagittal incision for below-knee amputation in ischaemic gangrene. J Bone Joint Surg Br 56:110-114, 1974. 104. Ruckley CV, Stonebridge PA, Prescott RJ: Skewflap versus long posterior flap in below-knee amputations: Multicenter trial. J Vasc Surg 13:423-427, 1991. 105. Block MA, Whitehouse FW: Below-knee amputation in patients with diabetes mellitus. Arch Surg 87:682-689, 1963. 106. Dellon AL, Morgan RF: Myodermal flap closure of below the knee amputation. Surg Gynecol Obstet 153:383-386, 1981. 107. Moore WS: Immediate postoperative prosthesis. In Rutherford R, Bernhard V, et al (eds): Vascular Surgery. Philadelphia, WB Saunders, 1977, pp 1333-1343. 108. Kim GE, Imparato AM, Chu DS, Davis SW: Lower limb amputation for occlusive vascular disease. Am Surg 42:589-601, 1976. 109. Inderbitzi R, Biuttiker M, Pfluger D, Nachbur B: The fate of bilateral lower limb amputees in end stage disease. Eur J Vasc Surg 6:321-326, 1992. 110. Houghton A, Allen A, Luff R, McColl I: Rehabilitation after lower extremity amputation: A comparative study of above-knee, through knee and Gritti-Stokes amputations. Br J Surg 76:622-624, 1989. 111. Burgess EM: Disarticulation of the knee: A modified technique. Arch Surg 112:1250-1255, 1977. 112. Doran J, Hopkinson BR, Making GS: The Gritti-Stokes amputation in ischaemia: A review of 134 cases. Br J Surg 65:135-137, 1978. 113. Puddifoot PC, Weaver PC, Marshall SA: A method of supportive bandaging for amputation stumps. Br J Surg 60:729-731, 1973. 114. Ford LT, Holder BR: Disarticulation for failed surgical procedures about the hip. South Med J 70:1293-1296, 1977. 115. Endean ED, Schwarz TH, Barker DE, et al: Hip disarticulation: Factors affecting outcome. J Vasc Surg 14:398-404, 1991. 116. Boyd HB: Anatomic disarticulation of the hip. Surg Gynecol Obstet 84:346-349, 1947. 117. Hogshead HP: Experience with hip disarticulation and hemipelvectomy procedure. J Bone Joint Surg Am 53:1031, 1971. 118. Wu KK, Guise ER, Frost HM, Mitchell CL: The surgical technique for hindquarter amputation: Report of 19 cases. Acta Orthop Scand 48:479-486, 1977. 119. Baur GM, Porter JM, Axthelm S, et al: Lower extremity amputation for ischemia. Am Surg 44:472-477, 1978. 120. Berardi RS, Keonin Y: Amputations in peripheral vascular occlusive disease. Am J Surg 135:231-234, 1978. 121. Home instructions: Amputee with prosthesis. Orthop Nurses Assoc J 6:73-77, 1979. 122. Abramson AS, Feibel A: The phantom phenomenon: Its use and disuse. Bull N Y Acad Med 57:99-112, 1981. 123. Bradway JR, Racy J, Malone JM: Psychological adaptation to amputation. Orthot Prosthet 38:46-50, 1984. 124. Parkes CM: Factors determining persistence of phantom pain in the amputee. J Psychosom Res 17:97-108, 1973. 125. Sherman RA: Published treatment of phantom pain. Am J Phys Med 59:232-244, 1980. 126. Sherman RA, Tippens JK: Suggested guidelines for treatment of phantom limb pain. Orthopedics 5:1595-1600, 1982. 127. Solomon GF, Schmidt KM: A burning issue: Phantom limb pain and psychological preparation of the patient for amputation. Arch Surg 113:185-186, 1978. 128. Sherman RA, Sherman CJ, Gall NG: A survey of current phantom limb pain treatment in the United States. Pain 8:85-99, 1980. 129. Sherman RA, Sherman CJ, Parker L: Chronic phantom and stump pain among American veterans: Results of a survey. Pain 18:83-95, 1984. 130. Nagendran T, Johnson G Jr, McDaniel WJ, et al: Amputation of the leg: An improved outlook. Ann Surg 175:994-999, 1972. 131. Wray CH, Still JM Jr, Moretz WH: Present management of amputations for peripheral vascular disease. Am Surg 38:87-92, 1972.

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132. Bertin VJ, Plechia FR, et al: The early results of vascular surgery in patients 75 years of age or older: An analysis of 3259 cases. J Vasc Surg 2:769-774, 1985. 133. Gregg RO: Bypass or amputation? Concomitant review of bypass arterial grafting and major amputation. Am J Surg 149:397-401, 1985. 134. Burgess EM, Romano RL, Aettl JH, Schrock RD Jr: Amputation of the leg for peripheral vascular ischemia. J Bone Joint Surg Am 53:874-890, 1971. 135. Bailey MJ, Johnston CLW, Yates CJP, et al: Preoperative haemoglobin as predictor of outcome of diabetic amputations. Lancet 2:168-170, 1979. 136. Gatti JE, LaRossa D, Neff SR, Silverman DG: Altered skin flap survival and fluorescein kinetics with hemodilution. Surgery 92:200-205, 1982. 137. Malone JM: Complications of lower extremity amputation. In Bernhard VM, Towne J (eds): Complications in Vascular Surgery. Orlando, Fla, Grune & Stratton, 1985, pp 445-470. 138. Koch M, Kutkuhn B, Grabensee B, et al: Apolipoprotein A, fibrinogen, age, and history of stroke are predictors of death in dialysed diabetic patients: A prospective study in 412 subjects. Nephrol Dial Transplant 12:2603-2611, 1997. 139. Muhlhauser I, Overmann H, Bender R, et al: Predictors of mortality and end-stage diabetic complications in patients with type 1 diabetes mellitus on intensified insulin therapy. Diabet Med 17:727-734, 2000. 140. Flores Rivera AR: Risk factors for amputation in diabetic patients: A case-control study. Arch Med Res 29:179-184, 1998. 141. Lehto S, Ronnemaa T, Pyorala K, et al: Risk factors predicting lower extremity amputations in patients with NIDDM. Diabetes Care 19:607-612, 1996. 142. Reiber GE, Pecoraro RE, Koepsell TD: Risk factors for amputation in patients with diabetes mellitis: A case control study. Ann Intern Med 117:97-105, 1992. 143. Ebskou LB: Epidemiology of lower limb amputations in Denmark (1980 to 1989). Int Orthop 15:285-288, 1991. 144. Harris PL, Read F, Eardley A, et al: The fate of elderly amputees. Br J Surg 61:665-668, 1974. 145. Kerstein MD: Utilization of an air splint after below knee amputation. Am J Phys Med 53:119-126, 1974. 146. Kerstein MD, Zimmer H, Dugdale FE, Lerner E: The delays in the rehabilitation in lower extremity amputees. Conn Med 41:549-551, 1977. 147. Kihn RB, Warren R, Beebe GW: The “geriatric” amputee. Ann Surg 176:305-314, 1972. 148. Reyes RL, Leahey EB, Leahey EB Jr: Elderly patients with lower extremity amputations: Three year study in a rehabilitation setting. Arch Phys Med Rehabil 58:116-123, 1977. 149. Waters RL, Perry J, Antonelli D, Hislop H: Energy cost of walking of amputees: The influence of level of amputation. J Bone Joint Surg Am 58:42-46, 1976. 150. Weaver PC, Marshall SA: A functional and social review of lower-limb amputees. Br J Surg 60:732-737, 1973. 151. Jamieson CW, Hill D: Amputation for vascular disease. Br J Surg 63:693-690, 1976. 152. Kerstein MD, Zimmer H, Dugdale FE, Lerner E: What influence does age have on rehabilitation of amputees? Geriatrics 30:67-71, 1975. 153. Gonzalez EG, Corcoran PH, Reyes RL: Energy expenditure in belowknee amputees: Correlation with stump length. Arch Phys Med Rehabil 55:111-119, 1974. 154. Huang CT, Jackson JR, Moore NB, et al: Amputation: Energy cost of ambulation. Arch Phys Med Rehabil 60:18-24, 1979. 155. Kavanagh T, Shephard RJ: The application of exercise testing to the elderly amputee. J Can Med Assoc 108:314-317, 1973. 156. Kegel B: Controlled environment treatment (CET) for patients with below-knee amputations. Phys Ther 56:1366-1371, 1976. 157. Burgess EM, Romano RL: The management of lower extremity amputees using immediate postsurgical prosthesis. Clin Orthop 57:137-146, 1968. 158. Burgess EM, Romano RL, Zettl JH: The Management of Lower Extremity Amputation Surgery: Immediate Postsurgical Prosthetic Fitting, Patient Care. Washington, DC, US Government Printing Office, 1969. 159. Burgess EM, Zettl JH: Amputations below the knee. Artif Limbs 13: 1-12, 1969.

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160. Baker WH, Barnes RW, Shurr OG: The healing of below-knee amputations: A comparison of soft and plaster dressings. Am J Surg 133: 716-718, 1977. 161. Kraeger RR: Amputation with immediate fitting prostheses. Am J Surg 120:634-636, 1970. 162. Ruoff AC, Smith AG, Thoroughman JC, et al: The immediate postoperative prosthesis in lower extremity amputations. Arch Surg 101:40-44, 1970. 163. Thorpe W, Gerber LH, Lampert M, et al: A prospective study of the rehabilitation of the above-knee amputee with rigid dressings: Comparison of immediate and delayed ambulation and the role of physical therapists and prosthetists. Clin Orthop 143:133-137, 1979. 164. Cohen SI, Goldman LO, Salzman EW, Glotzer OJ: The deleterious effect of immediate postoperative prosthesis in below-knee amputation for ischemic disease. Surgery 761:992-1001, 1974. 165. Folsum D, King T, Rubin J: Lower extremity amputation with immediate postoperative prosthetic placement. Am J Surg 164:370-322, 1992. 166. Leal JM, Malone JM, Moore WS, Malone SJ: For accelerated postamputation rehabilitation: Zoroc intermediate prostheses. Orthot Prosthet 34:3-12, 1980. 167. Seery J, Leal JM, Malone JM: Impact of new casting tapes on prosthetic fabrication. Paper presented to the International Society for Prosthetics and Orthotics Fourth World Congress, Sep 1983, London. 168. Wu Y, Brncick MD, Krick HJ, et al: Scotchcast PVC interim prosthesis for below-knee amputees. Bull Prosthet Res Fall:40-45, 1981. 169. Sher MH: The air splint: An alternative to the immediate postoperative prosthesis. Arch Surg 108:746-747, 1974. 170. Kegel B, Moore AJ: Load cell: A device to monitor weight bearing for lower extremity amputees. Phys Ther 57:652-654, 1977. 171. Lipp MR, Malone SJ: Group rehabilitation of vascular surgery patients. Arch Phys Med Rehabil 57:180-183, 1976. 172. Enoka RM, Miller DI, Burgess EM: Below-knee amputee running gait. Am J Phys Med 61:66-84, 1982. 173. Vermassen FE, van Landuyt K: Combined vascular reconstruction and free flap transfer in diabetic arterial disease. Diabetes Metab Res Rev 16(Suppl 1):S33-S36, 2000. 174. Lutz BS, Siemers F, Shen ZL, et al: Free flap to the arteria peronea magna for lower limb salvage. Plast Reconstr Surg 105:684-687, 2000. 175. Bowker JH, San Giovanni TP, Pinzur MS: North American experience with knee disarticulation with use of a posterior myofasciocutaneous flap: Healing rate and functional results in seventy-seven patients. J Bone Joint Surg Am 82:1571-1574, 2000. 176. Moore JC, Jolly GP: Soft tissue considerations in partial foot amputations. Clin Podiatr Med Surg 17:631-648, 2000.

Questions 1. What is the best overall approach to postamputation prosthetic care and rehabilitation? (a) Conventional soft dressings (b) Rigid dressings (c) Immediate postoperative prosthetics (d) Rigid dressings with early ambulation (e) Soft dressings with early ambulation 2. The advantages of a rigid dressing (without an attached prosthesis) after major lower extremity amputation include all of the following except (a) Control of stump edema (b) Protection of the wound from trauma (c) Stump immobilization (d) Prevention of joint flexion contracture (e) Accelerated stump maturity

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3. Which of the following statements about amputees or amputation rehabilitation is false? (a) The risk of contralateral limb loss in the 5 years following major lower extremity amputation is greater than 25% (b) The 5-year life expectancy for patients with diabetes after major lower extremity amputation is less than 50% (c) Above-knee amputations should be performed in all geriatric patients because of their poor prognosis for successful rehabilitation (d) When noninvasive amputation level selection techniques are used, primary healing can be expected in more than 90% of all below-knee amputations (e) None of the above 4. Which of the following statements about amputation surgery or amputees is true? (a) Clinical judgment is the best technique for amputation level selection (b) There is no benefit to the patient in performing a knee disarticulation amputation (c) Amputees reduce their walking speed to control energy expenditure (d) The successful rehabilitation of bilateral above-knee amputees is common (e) None of the above 5. Which of the following therapeutic maneuvers is often successful for the treatment of phantom pain? (a) Surgical stump revision (b) Psychotherapy (c) Narcotics (d) Physical therapy (e) None of the above 6. Amputation level selection techniques such as transcutaneous oxygen measurement can also be used in which of the following situations? (a) Intraoperatively (b) Postoperatively (c) To evaluate or quantitate the degree of ischemia (d) All of the above 7. Which statement about major lower extremity amputation is false? (a) Eighty percent of all patients with a below-knee amputation will heal (b) Two thirds of patients undergoing amputation surgery have cardiovascular disease (c) The best amputation level selection technique is a combination of clinical judgment and preoperative arteriography (d) It takes at least twice as much energy for an aboveknee amputee to walk as for a below-knee amputee (e) Any patient ambulating before amputation can ambulate after amputation, irrespective of age

8. What is the most common cause of major lower extremity amputation? (a) Failed vascular reconstruction (b) Trauma (c) Ischemia (d) Tumor (e) Complications of diabetes mellitus 9. Which of the following statements about major lower extremity amputation is false? (a) Most amputations are caused by complications of peripheral vascular disease or diabetes mellitus (b) The average rate of ambulation after major lower extremity amputation is 60% (c) Occlusion of the superficial femoral artery is the most common arterial lesion that leads to belowknee amputation (d) Patients, especially those with diabetes mellitus, who have undergone successful amputation have a decreased life expectancy (e) There is no difference in healing between patients with diabetes and those without diabetes 10. Which of the following statements is true? (a) Amputation surgery is reconstructive surgery (b) Amputation surgery may be preferable to extended distal bypass or multiple revisions of below-knee distal bypass if good rehabilitation treatment is available (c) Patient education and foot care of the nonamputated extremity are important (d) Optimal results after lower extremity amputation require amputation level selection techniques and early or rapid postamputation rehabilitation (e) All of the above

Answers 1. d 6. d

2. e 7. c

3. c 8. e

4. c 9. c

5. e 10. e

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50

Stephanie S. Saltzberg • Matthew M. Nalbandian

Spine Exposure: Operative Techniques for the Vascular Surgeon Surgery is the standard treatment for a multitude of benign and malignant disease processes of the spine. The anterior approach to the spinal column is important in degenerative disk disease, neural decompression, resection of neoplasms, trauma, infection, and congenital anomalies.1-4 Safe access to the spine is paramount to performing successful spinal procedures. Although orthopedic surgeons and neurosurgeons have been responsible for many surgical advances in spine surgery, access to the spine is often provided by vascular surgeons, general surgeons, urologists, or spine surgeons. With increasing frequency, vascular surgeons are the primary surgeons for anterior spine exposure owing to their skill and experience in retroperitoneal surgery. The operative techniques involved in retroperitoneal aortoiliac surgery can be modified to perform spine surgery. An experienced team approach to spine exposure can reduce intraoperative complications.1 The level of involvement by vascular surgeons varies by institution. Generally, vascular surgeons perform exposure of the lower thoracic, lumbar, and sacral spine levels. Thoracic surgeons are often involved in upper thoracic exposure, and the cervical spine is the domain of spine surgeons. The morbidity of the anterior approach has been reported to range from 10% to 30%.1,2 Periprocedure complications can include iatrogenic vascular, visceral, genitourinary, and neurologic injuries.1-4 As new spinal prosthetic devices are developed and the indications for surgical repair broaden, there will be a growing demand for surgeons who can provide access to the spine. Vascular surgeons should have this skill in their armamentarium, much as they have developed skill in endovascular procedures. This chapter discusses the vascular surgeon’s role in the surgical exposure of the lower thoracic, lumbar, and sacral levels.

Approach to the Thoracolumbar Junction Lower thoracic and upper lumbar spine exposure is most commonly indicated for scoliosis, infection, and tumor.

The anterior approach to the thoracolumbar junction generally provides access between T-10 and S-1. The extent of exposure is guided by the need for extraction and fixation of the spine. Most cases require access to one normal spinal level above and below the area of disease. This is a difficult exposure owing to the simultaneous entry into the thoracic cavity and retroperitoneal space. PATIENT POSITION Patients undergoing thoracolumbar exposures require general anesthesia and appropriate monitoring for comorbidities. The patient is placed in the lateral decubitus position. A right lateral decubitus position with a left-sided approach is preferred to avoid the liver and injury to the inferior vena cava. Most patients are positioned at a 90-degree angle to the table, although in some cases, 45 to 60 degrees may be preferred. An axillary roll is placed under the dependent axilla, and the arms are extended straight across the upper chest with the upper arm supported. The dependent leg is flexed at the knee, and the other leg is straight and supported by pillows (Fig. 50-1A). The kidney rest is elevated, and the table is flexed. A beanbag or tape secures the patient’s hips and shoulders to the table. OPERATIVE EXPOSURE The rib space to be entered depends on the level of interest. In general, a curvilinear incision is made in the 9th or 10th interspace. The incision starts in the midaxillary line and extends anteriorly and inferiorly toward the umbilicus (see Fig. 50-1A). It is important to preserve the intercostal neurovascular bundle at the inferior aspect of the rib. Resection of the costal cartilage facilitates the exposure. The external oblique, internal oblique, and transversus abdominis muscles are divided. 929

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Aorta Lung Diaphragm 10th intercostal space

Segmental vessels

T-12

A

B

Peritoneum

FIGURE 50–1 • Thoracolumbar spine exposure. A, Thoracoabdominal incision via the 10th intercostal space. B, Circumferential division of the diaphragm with exposure of the thoracic cavity and retroperitoneal space.

A plane is developed between the diaphragm and retroperitoneal space along the costal attachment of the diaphragm. Care must be taken with the diaphragm, which originates from the upper lumbar vertebrae, arcuate ligaments, and 12th ribs and attaches to the lower six ribs and xiphoid. Dividing the diaphragm circumferentially minimizes injury to the phrenic nerve (Fig. 50-1B). This is facilitated with a reticulating EndoGIA stapler, which reduces bleeding from the diaphragmatic edge and aids in reapproximation of the diaphragm during closure. Use of a Finochietto or Omni retractor for rib separation maximizes visualization. An Omni retractor provides access to the vertebral bodies while protecting vital structures. The Omni post is generally attached to the right side of the table for a left-sided approach. The Omni retractor is positioned across the incision. A wide retractor is placed anteromedially to retract the peritoneum, ureter, and kidney in a medial position. This retractor also serves to protect the aorta during the vertebral manipulation. Three separate right-angle retractors are placed to retract the lung superiorly, the psoas muscle posteriorly, and the iliac vessels inferiorly. Placement of the retractors in these positions ensures adequate exposure and aids in the prevention of inadvertent injuries. Using blunt dissection, the retroperitoneal space is developed in a retronephric extraperitoneal plane. The retroperitoneal space is entered laterally. The kidney is mobilized anteriorly, along with the peritoneal contents. The peritoneal sac is dissected free anteriorly, laterally, and finally medially. The aorta and ureter are protected anteriorly. The psoas muscle is identified, and the attachments are mobilized posteriorly off the vertebrae, allowing access to the spine. Segmental vessels are ligated and divided between nonabsorbable ties.

Care must also be taken to ligate the iliolumbar vein at the lower lumbar level. Surgeons must be aware of the sympathetic chain, which is lateral to the spine and medial to the psoas muscle. A spinal needle is inserted into the disk space, and a radiograph is taken to confirm the appropriate vertebral level. Closure of this exposure begins with reapproximation of the diaphragm with an interrupted 2-0 Prolene suture and a running No. 1 Vicryl suture. Under direct vision, a chest tube is placed. The ribs are reapproximated with interrupted No. 1 Vicryl sutures, and the thoracic muscles are closed in layers with No. 1 Vicryl. The retroperitoneal contents should fall into their anatomic position. The internal and external oblique muscles are reapproximated with No. 1 PDS suture. The subcutaneous tissue is reapproximated with 3-0 Vicryl suture, and the skin is reapproximated with skin clips. The chest tube is removed when the output is less than 150 mL over a 24-hour period. COMPLICATIONS Complications of the thoracolumbar approach to the spine can include thoracic, vascular, visceral, neurologic, and urologic injuries. The most common postoperative complications include wound infection, bleeding, pneumonia, and persistent air leak. Care should be taken to avoid iatrogenic diaphragmatic and ureteral injuries. Sympathetic chain injuries may also occur and can result in retrograde ejaculation. Bowel injuries result from violation of the peritoneum. In addition, femoral pulses should be assessed preoperatively and postoperatively to ensure that there was no unrecognized injury or thrombosis of the iliac artery during retraction.

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931

Peritoneum Lumbar vertebral bodies

FIGURE 50–2 • Anterolateral lumbosacral spine exposure. A, Anterolateral lumbosacral incision from the quadratus lumborum to the lateral border of the rectus muscle. B, Anteromedial retraction of the peritoneum and kidney, lateral retraction of the psoas, and exposure of the segmental vessels for ligation.

Segmental vessels

A

Lumbosacral Spine Exposure: Anterolateral Approach The lumbosacral region of the spine can be accessed via the more traditional anterolateral exposure or the increasingly common pure anterior exposure. The anterolateral approach allows exposure to multiple levels in the lumbar spine. Depending on which level needs to be exposed, the incision may be placed between the 12th rib and the superior aspect of the iliac crest. PATIENT POSITION Similar to the thoracolumbar approach, the patient is positioned in a modified lateral decubitus position with the right side down to avoid the liver and injury to the vena cava. The hips are rotated 45 degrees. The upper and lower extremities are positioned in a similar fashion to the thoracolumbar approach (Fig. 50-2A). The kidney rest is elevated, and the table is flexed to increase exposure between the 12th rib and the iliac crest.

B

Psoas muscle

The peritoneal sac is swept off the anterior and lateral aspects of the abdominal wall, taking care not to violate the peritoneum. The peritoneum and kidney are reflected anteriorly. The peritoneum is dissected off the posterior rectus sheath, and the peritoneum is swept medially off the psoas with Gerota’s fascia. The ureter should fall anteriorly. The iliac vessels are exposed and protected. The psoas muscle is elevated bluntly off the lumbar vertebrae and retracted laterally. The lumbar segmental vessels are ligated as needed for exposure (Fig. 50-2B). Care should be taken to ligate the iliolumbar vein when dissecting the L-4 to L-5 level; this avoids avulsion of the vein during retraction. A spinal needle is inserted into the disk space, and a radiograph is taken to confirm the appropriate vertebral level. Closure is performed with reapproximation of the fascia in two layers with a running No. 1 PDS suture. The subcutaneous tissue is closed with a 3-0 Vicryl suture, and the skin is reapproximated with skin clips. If the pleura is violated during the exposure, it may be necessary to place a chest tube. COMPLICATIONS

OPERATIVE EXPOSURE An oblique incision is made over the 12th rib from the lateral border of the quadratus lumborum to the lateral border of the rectus abdominis muscle for L-1 and L-2 exposure (see Fig. 50-2A). For L-3 to L-5, a similar incision is made about 2 cm below the costal margin. Electrocautery is used to divide the subcutaneous tissue, fascia, external and internal oblique, transversus abdominis, and transversalis fascia. The retroperitoneal space is entered laterally. An Omni retractor is used to facilitate the exposure. This is positioned on the table as previously described in the thoracolumbar approach. In a similar fashion, a wide retractor is used to retract the peritoneum and kidney medially while protecting the aorta. However, in the lumbosacral approach, one rightangle retractor is used to retract the diaphragm superiorly. The remaining two right-angle retractors are used to retract the psoas muscle posteriorly and the iliac vessels inferiorly.

Perioperative complications are similar to those described for the thoracolumbar approach to the spine. Care should be taken to avoid injury to the diaphragm, vessels, ureter, and sympathetic chain. Inadvertent entry into the pleural space can result in pneumothorax or lung injury. Violation of the peritoneum can result in unrecognized visceral injuries. As in the thoracolumbar approach, preoperative and postoperative femoral pulses should be obtained to evaluate for a missed iliac artery injury or thrombosis.

Lumbosacral Spine Exposure: Anterior Approach The anterior approach has become the preferred technique for access to the lumbosacral spine. It provides adequate exposure while minimizing large dissections and allowing for a cosmetically acceptable result. In general, L-3 through

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S-1 can be safely exposed using this technique. However, in patients with prior midline incisions, these incisions can be used to approach the L-1 through S-1 vertebrae.

symphysis pubis. Next, a paramedian fascial incision is made to the left of the linea alba. This fascial incision is extended superiorly to the left of the umbilicus and inferiorly to the symphysis pubis. For high lumbar exposures, this fascial incision may extend as much as 3 cm beyond the umbilicus. The medial border of the left rectus muscle is dissected off the linea alba throughout the length of the fascial incision (Fig. 50-3B). Using a Richardson retractor, the rectus muscle is elevated, and the space between the rectus muscle and the posterior rectus fascia is developed laterally to expose the transversalis fascia. This is incised with Metzenbaum scissors throughout the length of the fascial exposure. A retroperitoneal plane is developed from the left inferolateral to right superomedial deirection. Exposure is facilitated with retraction of the rectus muscle laterally and the peritoneal contents medially using a total of four renal vein retractors. Care must be taken to avoid entering the peritoneum. Should this occur, the defect is repaired with an absorbable suture. A combination of sharp and blunt dissection exposes the medial edge of the left iliac artery and vein. The middle sacral vessels are ligated and divided. The lateral renal vein retractors are repositioned to retract the left iliac artery and vein in a lateral position. The medial vein retractors are

PATIENT POSITION The patient is placed in a supine position with the arms extended laterally or secured across the chest. Depending on the desired level of exposure, a transverse incision is made between the symphysis pubis and the umbilicus. For exposure of L-5 to S-1, the incision is made 2 to 3 cm above the symphysis pubis. An L-4 to L-5 exposure requires an incision midway between the umbilicus and the symphysis pubis. An L-3 to L-4 exposure can be obtained with an incision 2 cm below the umbilicus (Fig. 50-3A). An alternative approach is to perform the anterior exposure via a small midline incision. OPERATIVE EXPOSURE The skin incision is carried down to the level of the rectus fascia. Using electrocautery, a subcutaneous flap is created superiorly to the left of the umbilicus and inferior to the

A

Left rectus muscle

Linea alba

L-3–L-4 L-4–L-5 L-5–S-1

Pubis

B Iliac vein

FIGURE 50–3 • Anterior lumbosacral spine exposure. A, Anterior transverse incision placed between the symphysis pubis and umbilicus, depending on the vertebral level. B, Intraoperative view of the left rectus muscle and linea alba. C, Anatomic relation of the iliac vessels to the vertebral bodies at the lumbosacral level.

C

Aortic bifurcation

S-1 vertebral L-5 to S-1 body disk Middle sacral space vein

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repositioned over the disk space to retract the peritoneum in a medial position. Additional dissection of the iliac vessels may be required to expose the width of the disk spaces. Care must be taken to preserve the ureter, which should be retracted medially along with the peritoneum. With the renal vein retractors in this position, the L-5 to S-1 disk space can be easily accessed (Fig. 50-3C). Using the same approach, the L-4 to L-5 and L-3 to L-4 disk spaces can be dissected. Exposure of the L-4 to L-5 disk space requires more extensive dissection of the lateral edge of the left iliac artery and vein. The iliolumbar vein is ligated and divided. The medial retractors are repositioned to retract the iliac vessels in a medial position. The lateral retractors are repositioned to retract the left rectus muscle and left psoas muscle in a lateral position. With gentle blunt dissection, the soft tissue overlying the disk space is dissected, allowing complete exposure of the disk space with the medial retractors. Exposure of the L-3 to L-4 disk space requires the same approach. However, the segmental vessels at the L-3 vertebral body are ligated and divided. The medial retractors are repositioned to retract the iliac vessels medially while the lateral retractors keep the left rectus and psoas muscles in a lateral position. A spinal needle is inserted into the disk space, and a radiograph is taken to confirm the appropriate vertebral level. Closure involves reapproximation of the anterior rectus sheath with a nonabsorbable suture. The subcutaneous tissue is reapproximated with interrupted absorbable sutures, and the skin is closed in a subcuticular fashion. COMPLICATIONS Although rare, there are several perioperative complications that can result from the anterior approach to the lumbosacral spine. These are similar to those described in the section on anterolateral exposure to the lumbosacral spine. Iatrogenic injury to the iliac vessels is a potentially life-threatening complication. If this occurs, more extensive exposure is usually necessary to repair the injury. As in all the approaches, femoral pulses should be obtained preoperatively and postoperatively to evaluate for thrombosis of the iliac artery during retraction. Care must be taken to avoid injury to the ureter, which should be identified and retracted medially, along with the peritoneum, to avoid iatrogenic injury during the spine manipulation. Finally, use of bipolar cautery minimizes damage to the sympathetic nerves at the lower lumbar vertebrae, reducing the risk of retrograde ejaculation.

Conclusion Over the last 10 years, the role of the vascular surgeon has undergone significant changes. Many procedures that are now routinely performed by vascular surgeons were once the domain of other medical specialists. As a result, vascular surgeons often find that they have not necessarily been formally trained to perform all these procedures. Spine access surgery is certainly not familiar to most vascular surgeons, but their experience with thoracoabdominal and retroperitoneal aortic surgery makes them adept at spine exposure. In addition, the most common complication of hemorrhage from iliac artery and vein injuries is usually treated by vascular surgeons.

933

Therefore, it is incumbent on vascular surgeons to be proactive in the treatment and care of spine patients. By taking a team approach to spine surgery, vascular surgeons can aid in minimizing the morbidity and mortality of these procedures. Vascular surgeons need to embrace this surgical procedure to ensure safe and effective treatment of spine surgery patients. REFERENCES 1. Bianchi C, Ballard JL, Abou-Zamzam AM, et al: Anterior retroperitoneal lumbosacral spine exposure: Operative technique and results. Ann Vasc Surg 17:137-142, 2003. 2. Cohn EB, Ignatoff JM, Keeler TC, et al: Exposure of the anterior spine: Technique and experience with 66 patients. J Urol 164:416-418, 2000. 3. Patnaik VVG, Singla RK, Gupta PN, Bala S: Surgical incisions—their anatomical basis. Part V. Approaches to the spinal column. J Anat Soc India 51:76-84, 2002. 4. Canale ST (ed): Campbell’s Operative Orthopaedics, 10th ed. Philadelphia, Mosby, 2003, pp 1574-1587.

Questions 1. Spine surgery is performed for which of the following disease processes? (a) Degenerative disk disease (b) Infection (c) Neoplasm (d) All of the above 2. Which of the following spine levels are typically exposed by vascular surgeons? (a) Lumbar (b) Sacral (c) Lower thoracic (d) All of the above 3. In general, spine surgeons require access to which vertebral level? (a) Only the affected vertebral body (b) One normal level above and below the affected vertebral body (c) Two normal levels above the affected vertebral body (d) One level below the affected vertebral body 4. In a thoracolumbar vertebral exposure, to avoid phrenic nerve injury, the diaphragm is divided in what manner? (a) Radially (b) The diaphragm is not divided (c) Circumferentially (d) Axially 5. In relation to the spine, the psoas muscle lies in what direction? (a) Lateral (b) Anterior (c) Medial (d) Superior

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6. In the anterolateral approach to the lumbar spine, the peritoneum and kidney are reflected in what direction? (a) Posterolaterally (b) Inferiorly (c) Anteromedially (d) Superiorly 7. What structure is divided to facilitate exposure of the L-4 vertebral level? (a) Sacral artery (b) Hypogastric vein (c) Sympathetic chain (d) Iliolumbar vein 8. Injury to the sympathetic chain can result in which of the following? (a) Reflex sympathetic dystrophy (b) Retrograde ejaculation (c) Sensory deficit of scrotum (d) Impotence

9. Iatrogenic injury that may result from the anterior lumbosacral approach includes which of the following? (a) Ureteral injury (b) Hemorrhage (c) Thrombosis (d) All of the above 10. In an anterior lumbosacral approach to the spine, the space developed for exposure is made in which location? (a) Posterior to the rectus muscle (b) Anterior to the rectus muscle (c) Transperitoneally (d) Transthoracically

Answers 1. d 6. c

2. d 7. d

3. b 8. b

4. c 9. d

5. a 10. a

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Index

Note: Page numbers followed by f refer to figures; those followed by t refer to tables.

A Abbott/Nova NeuroShield cerebral protection device, 371f Abciximab, arterial wall thickening and, 42 in arterial thromboembolism prevention, 85 in diabetics, 149 in thrombolytic therapy, 743, 744 pharmacology of, 170 Abdomen, arteries of, duplex scanning of, 255 blunt trauma to, renal artery dissection with, 532 compartment syndrome of, in abdominal aortic aneurysm repair, 503 Abdominal aorta, coarctation of, 125-126, 126f, 200, 200f magnetic resonance angiography of, 283, 284f mesenteric circulation of, 603-604, 604f multidetector row computed tomographyangiography of, 295, 296f, 297f surgical exposure of, alternative, 57-58, 58f emergency, 60-61, 61f of descending thoracic and proximal aorta, 53-54, 53f, 54f retroperitoneal, 54-55, 55f, 56f supraceliac, 55, 56f transperitoneal, 58-59, 59f, 60f traumatic injuries of, 722-723 Abdominal aortic aneurysm(s), 488-511 cardiac risk assessment and, 498 cause and pathogenesis of, 489-491, 490f clinical manifestations of, 491-492 definition of, 488-489 diagnosis of, 492-495 endovascular repair of, 383-395 complications with, late, 386-388, 386f, 387t perioperative, 386 FDA-approved devices for, 388-392, 389f, 390f, 391f, 392f graft placement for, 385-386 history and early design of, 383, 384f patient selection for, 383-385, 385f, 385t postoperative surveillance of, 388, 388f preoperative imaging for, 383, 384t results of, 392-393 setup for, 385 vs. open repair, 392-393 epidemiology of, 488 erectile dysfunction and, 215, 219 high-risk patients with, repair and, 496t, 497, 498-499 in systemic giant cell arteritis, 112 incidence and prevalence of, 488, 488t infected, 181, 185-186 laparoscopic surgery for, 396-413 approaches to, 398-400 history and development of, 397-398 robotics in, 409-410, 409t, 410f, 410t techniques of, hand-assisted, 403-404, 403f, 404f, 407, 407t

Abdominal aortic aneurysm(s) (Continued) laparoscopy-assisted, 404-407, 405f, 406t totally laparoscopic, 400-403, 407-409 late survival with, 496t, 497-498 morphologic classification of, 500f mycotic, 505-506 of iliac artery, 506-507 rupture of, 488, 491, 492 chronic contained, 492 clinical manifestations of, 492 imaging of, 493 repair of, 498-499, 501-502 risks of, 495-496, 499 screening for, 489 size of, 492, 496 indications for repair of, 495-496, 498-499 surgical repair of, approaches to, 799f complications of, 502-504 erectile dysfunction and, 215, 219 history of, 3-6 indications for, 498-499 mortality and, 496-498, 496t risks of, 496-497, 496t technique of, 499-502 vs. endovascular repair, 392-393 unusual problems with, 504-505 vascular grafts for, current recommendations for, 463 Abdominal pain, in mesenteric ischemia, 603, 606, 608 Abdominal vein thrombosis, 853 Abdominal wall, hernia of, 801 lifting device for, in laparoscopic surgery, 397 Abduction and external rotation test, in thoracic outlet syndrome, 680 Above-knee amputation, 907-909, 908f, 909f prosthetic application technique for, 920 prosthetic components for, 922 Abscess, in wound healing, 880 Absolute Stent, 326 Acarbose, 160 ACAS (Asymptomatic Carotid Atherosclerosis Study), 356 Access. See Vascular access. AccuLink Carotid Stent System, 356, 371f, 372, 376f Acetylcholine, in Raynaud’s syndrome, 107 vascular wall contraction and, 38 Acetylcysteine, in renal angiography, 582 in thoracoabdominal aortic aneurysm repair, 480 pharmacology of, 171 Activated clotting time, 166 cerebral protection device and, 359, 362 in carotid angioplasty and stenting, 378, 379 Activated partial thromboplastin time, 73, 77, 166, 434 Activated protein C, thrombosis and, 77 Acupuncture, for Raynaud’s syndrome, 110 Acute hyaline necrosis, in portal hypertension, 820

Acute limb ischemia, 268-269, 732 causes of, 734-739, 735t clinical manifestations of, 739-740 delayed embolectomy in, 748 drugs for management of, 750t emboli and, 734-735 fasciotomy in, 747-748, 747f five P’s and, 739 infection and, 892 initial evaluation of, 740-742 lower extremity amputation for, 891-892 nonoperative management of, 273-274, 748 pathophysiology of, 732-734 reperfusion injury in, fasciotomy for, 747-748, 747f risk factors for, 268 surgery for, 744-748, 744f, 745f, 747f complications of, 748-750 thrombolytic therapy for, 742-744, 742f, 743f thrombosis and, 735-738 treatment of, 273-274, 742-748 results of, 750-751 Acute renal failure, after revascularization of ischemic extremity, 749 aortic surgery and, 792-793 ADAM trial, aneurysm rupture risk and, 495 Adamkiewicz, great radicular artery of, injury or embolization of, 797 Adductor canal, thrombosis in, 735 Adenosine triphosphate, intracellular, in ischemia, 733 Adhesion molecule-1 (ICAM-1), intercellular, in diabetes, vascular endothelial cell function and, 149 Adhesive plastic drapes, for prevention of prosthetic graft infections, 774 α1-Adrenergic blocking agents, for intimal hyperplasia, 764 β-Adrenergic blocking agents, atherosclerosis risk and, 101 for protection against intracerebral hemorrhage, 422 for renovascular disease, preoperative, 584 for thoracoabdominal aortic aneurysm repair, 480 peripheral arterial disease and, 271 α2-Adrenoceptors, in Raynaud’s syndrome, 107 Adson’s test, in thoracic outlet syndrome, 680 Advanced glycation end-products, in diabetes, 148 Adventitia, arterial, 452, 453f aortic aneurysm formation and, 491 saphenous vein, 454f structure of, 36 vein graft, in intimal hyperplasia, 760, 760f Adventitial cystic disease, 129-130 Afibrinogenemia, 76 Age/aging, abdominal aortic aneurysm and, 488, 498 amputee rehabilitation and, 913-915, 914t aneurysm repair and, 496-497, 498 arterial wall properties in, 231

935

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Age/aging (Continued) critical limb ischemia and, 268, 269 renovascular hypertension and, 578-579, 578t, 579t venous thrombosis and, 846 Air plethysmography, for study of venous dysfunction, 846, 860 AL4 catheter, 360f Alcohol, in sclerotherapy for vascular malformations, 207, 209 mild consumption of, peripheral arterial disease and, 267 Alcoholism, portal hypertension and, 818, 820 Aldosterone, release of, 577 Alginate dressings, in wound healing, 883, 884t Alkaline phosphatase, in central nervous system vessels, 33, 33f-35f Allen’s test, 679, 696, 717 Allergic reactions, to intra-arterial thrombolytic therapy, 436 to streptokinase, 427 Allograft(s), human, for aortoiliac reconstruction for infected aneurysms, 185 human umbilical vein, 456-457, 457f, 463 Alpha granules, of platelets, 71 Alprostadil, for female sexual dysfunction, 216 Alteplase, for thrombolytic therapy, 790, 791 Amadori product, 147, 148, 149 Amaurosis fugax, in carotid artery transient ischemic attacks, 631 Ambulation, after below-knee amputation, 919-920 early postoperative, for prevention of venous thrombosis, 847 American Venous Forum, 11 ε-Aminocaproic acid, 75, 415 Ammonia, in portal hypertensive patients, 823, 824 Amplatz guidewire, in carotid angioplasty and stenting, 345, 364 Amputation, after mycotic aneurysm resection in groin, 520 guillotine, 893-894, 893f lower extremity, 890-924 above-knee, 907-909, 908f, 909f prosthetic application for, 920 prosthetic components for, 922 below-knee, 903-905, 903f, 905f advantages of, 894, 905 selection criteria for, 895t vs. aggressive limb salvage efforts, 569 Chopart’s, 901 complications of, 910-913 early postoperative, 910-912, 910t long-term, 912-913, 912f contralateral limb loss in, 912-913 critical limb ischemia and, 268, 269 energy expenditure with, 915, 915t for acute ischemia, 891-892 for gangrene complicated by infection, 893-894, 893f for progressive chronic ischemia, 892-893 for trauma, 894 for vascular malformations, 209 hip disarticulation, 909-910, 909f historical perspective of, 890 in Buerger’s disease, 122 in diabetics, 145, 151 indications for, 891, 891t knee disarticulation, 905-907, 906f, 907f level of, 893 after revascularization, 568 determination of, 894-898 requirements for, 894

Amputation (Continued) selection methods for, 895-898, 895t, 896t Lisfranc’s, 901 mortality with, 890, 910, 912, 912f new developments in, 923-924, 923f of ray, 899-900, 899f of toes, 898-899, 898f in trash foot syndrome, 792 noninvasive testing and, 554-555 patient evaluation and preparation for, 890-894 prosthetic devices for, 913-922 components of, 921-922, 921f for above-knee amputation, 908-909 for below-knee amputation, 905 for Chopart’s amputation, 901 for hip disarticulation, 910 for knee disarticulation, 906-907 for Lisfranc’s amputation, 901 for Syme’s amputation, 903, 903f for transmetatarsal amputation, 901 immediate postoperative application of, 917-921, 917f-920f in rehabilitation of elderly patients, 913-915, 914t postoperative techniques for, 915-917, 915f, 916f rehabilitation team for, 922-923, 922f stump of, infection of, 911 nonhealing, 910-911 revision of, 912 Syme’s, 901-903, 902f, 903f transmetatarsal, 900-901, 900f lumbar sympathectomy and, 449 thrombolytic therapy and, 432 Amputees, elderly, 913-915, 914t rehabilitation of, conventional vs. accelerated techniques of, 913-915, 914t Anastomosis, arteriovenous, early history of, 3 hemodynamic analysis of, 238 distal, in abdominal aortic aneurysm repair, 501 in thoracoabdominal aortic aneurysm repair, 477 thrombosis at, 786, 787f to carotid bifurcation after carotid endarterectomy, 662, 662f, 663f end-to-end, in renal artery bypass, 586, 591f in resection of carotid artery aneurysm, 515, 515f in vascular injury repair, 719 proximal, 541, 541f end-to-side, in renal artery bypass, 585, 591f proximal, 539f, 541, 541f, 542, 542f femoral, false aneurysms and, 800 recurrent aneurysms at, 801 retroperitoneal approach to, 778-779, 779f revision of, 804, 804f groin, false aneurysms and, 800 in abdominal aortic aneurysm repair, 5, 501 in autogenous arteriovenous fistula construction, 697, 697f in femoropopliteal bypass, 568 thrombus extraction from, 804, 804f, 805f in limb salvage procedures, 558 in renal artery bypass, 585, 586, 591f infected, graft excision or preservation and, 776-777 intimal hyperplasia at, thrombosis and, 787-788, 788f proximal, end-to-end, 541, 541f end-to-side, 539f, 541, 541f, 542, 542f in abdominal aortic aneurysm repair, 501

Anastomosis (Continued) in aortofemoral bypass grafts, 539f, 541, 541f, 542, 542f in thoracoabdominal aortic aneurysm repair, 477 to innominate artery, in bypass of ascending aorta, 667-668, 667f, 668f ANCAs (antineutrophil cytoplasmic antibodies), in polyarteritis nodosa, 115 systemic vasculitides and, 111 Ancure endograft system, 388-389, 389f Anemia, in portal hypertension, 819-820 Anesthesia, for acute limb ischemia, 744 for autogenous arteriovenous fistula construction, 696 for extracranial cerebrovascular disease, 633-634 for thoracoabdominal aortic aneurysm repair, 475-476 for vascular trauma, 718 AneuRx endograft system, 389-390, 390f Aneurysm(s), abdominal aortic. See Abdominal aortic aneurysm(s); Thoracoabdominal aortic aneurysm(s). aortoiliac, approaches to, 799f in Kawasaki disease, 117 repair of, inlay nerve-sparing technique for, 217, 217f arterial, in Behçet’s disease, 117-118 in Kawasaki disease, 116, 117, 117f peripheral, 512-522 mycotic, 518-520 nonmycotic, 512-518, 515f surgical management of, 6 arterial wall properties of, 231-232, 232f atherosclerosis and, 95 axillary artery, nonmycotic, 512, 513, 514, 515, 516, 517 rupture of, 514 carotid artery, 623 extracranial, cerebrovascular disease and, 623 nonmycotic, 512, 513, 514, 515-516, 515f celiac artery, 524t, 526t, 528, 528f rupture of, 526t, 528 colic artery, 524t, 526t, 529 coronary artery, 116, 117f deep femoral artery, rupture of, 513 definition of, 488-489 emboli from, 735 endovascular vs. open repair of, sexual dysfunction and, 219 false, anastomotic, 800-801 causes and repair of, 800-801 of carotid artery, 623 of hepatic artery, 526 postoperative thromboses and, 788 recognition of, 800 retroperitoneal, 800 traumatic, 724-726, 725f-727f femoral artery, nonmycotic, 513, 514, 515, 516, 517 rupture of, 513 forearm, nonmycotic, 512, 513, 514, 516, 517 formation of, arteriovenous fistula and, 705-706, 705f in human umbilical vein allografts, 457, 457f in vascular access for hemodialysis, 705-706, 705f gastric artery, 524t, 526t, 528-529 gastroduodenal artery, 524t, 526t, 529-530, 530f gastroepiploic artery, 524t, 526t, 528-529

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Index

Aneurysm(s) (Continued) hand, nonmycotic, 512, 513, 514, 516, 517 hepatic artery, 524t, 526-527, 527f rupture of, 526-527, 526t ileal artery, 524t, 526t, 529, 529f iliac artery, 506-507 rupture of, 507 in arteria magna syndrome, 125, 125f in Behçet’s disease, 117-118 in Kawasaki disease, 116, 117, 117f in polyarteritis nodosa, 115, 115f infected, 178, 180, 181, 773 bacteriology of, 180 microbial arteritis with, 178, 181 syphilitic, 178-179 inflammatory, in abdominal aortic aneurysm repair, 504 jejunal artery, 524t, 526t, 529 ligation of, early history of, 1, 3 mycotic, anatomic distribution of, 180, 180f bacteria cultured from, 179, 179f, 180f definition and classification of, 177, 178 management of, 185-186, 518-519 of aorta, 505-506 of carotid artery, 623 nonmycotic, 512-517, 515f pancreatic artery, 524t, 526t, 529-530 pancreaticoduodenal artery, 524t, 526t, 529-530 peripheral artery, 512-522 mycotic, 518-520 nonmycotic, 512-518 surgical management of, 6 popliteal artery, 6 nonmycotic, 513, 514, 515, 516, 517 prosthetic graft infections and, 773 recurrent femoral anastomotic, 801 renal artery, 530-533, 531f, 531t, 532f false, 532-533, 532f rupture of, 531-532 true, 530-532, 531f rupture of, 507, 513, 514, 524-527, 526t, 527, 528, 531-532 abdominal aortic aneurysm repair and, 488, 491-493, 495-499, 501-502 aortocaval or iliac arteriovenous fistula and, 784, 785f arterial wall properties and, 231-232 endovascular thoracoabdominal aneurysm repair and, 483-484, 484f splanchnic artery, 523-530, 524t, 526t rupture of, 526t splenic artery, 523-526, 524f, 524t, 525f, 526t rupture of, 524-525, 526t subclavian artery, nonmycotic, 512, 513, 514, 515, 516, 517 rupture of, 514 superior mesenteric artery, 524t, 526t, 527-528 rupture of, 527 syphilitic, 178-179 thoracoabdominal. See Thoracoabdominal aortic aneurysm(s). vascular reconstruction for, erectile dysfunction and, 214, 215 visceral, in polyarteritis nodosa, 115, 115f Aneurysm Detection and Management (ADAM) trial, aneurysm rupture risk and, 495 Aneurysm sac, failure of shrinkage of, 497 hygroma of, 387-388 pressure in, 387 size of, 387 Angina, intestinal, 10 Angina abdominis, 613 Angina pectoris, 498

Angiogenesis, gene-induced, for critical limb ischemia, 273-274 in cerebral blood vessel growth, 34 Angiogenin, in cerebral blood vessel growth, 34 Angiography. See also Arteriography. completion, for abdominal aortic aneurysm repair, 385 for carotid endarterectomy, 630 for endovascular treatment of infrainguinal disease, 347 for renal artery angioplasty and stenting, 336f, 337f, 339f conventional, limitations and benefits of, 280 coronary, for thoracoabdominal aortic aneurysm repair, 480 developments in, 12 diagnostic, for acute mesenteric ischemia, 606-607 for aortoiliac occlusive disease, 540 for arterial infections, 183, 183f for carotid angioplasty and stenting, 359-362, 360f-364f, 361t, 363t for extracranial cerebrovascular disease, 633 for infrainguinal arteriosclerosis, 555 for intra-arterial thrombolytic therapy, 434 for lower extremity ischemia, 553 for portal hypertension, 819, 821, 821f for prosthetic graft infection, 775, 776f for renal artery stenosis, 335 for renovascular hypertension, 580-583, 581f, 582f alternatives to, 582 for vascular injury repair, 719 erectile function and, 799 for carotid angioplasty and stenting, aortic arch, 359, 360f cerebral, 362, 364f cervical carotid, 359-361 intra-arterial digital subtraction, for aortoiliac occlusive disease, 540 for renovascular hypertension, 581, 582 practice in, 311 preoperative, controversies about, 633 Raynaud’s syndrome and, 110 AngioJet rheolytic thrombectomy system, 789, 791, 804 Angiopeptin, for intimal hyperplasia, 765 Angioplasty. See also Endovascular repair. balloon, advantages of, 319 and stenting, vs. carotid endarterectomy, 355-358, 649-650 approach to lesion with, 319-320, 320f, 320t completion arteriography for, 321, 322t complications of, 321, 323, 323t equipment for, 319, 319t history of, 325 indications for, 319 limitations of, 325 results of, 322t technique of, 319-321 balloon catheters for. See Balloon catheter(s), angioplasty. carotid. See Carotid angioplasty and stenting. cutting balloon, for infrainguinal disease, 344, 345t, 346-347, 348t, 352, 563-564, 564f, 804 femoropopliteal balloon, 349, 350t, 351t, 352 for acute mesenteric ischemia, 607 for aortoiliac disease, 325-331 for chronic mesenteric ischemia, 609, 611, 612f for infrainguinal occlusive disease, 343-352, 563-564, 564f, 804 approaches for, 344, 344t, 345-348

937

Angioplasty (Continued) patient selection for, 343-344 platforms used for, 344 results of, 349, 351-352 sheaths used for, 344-345 stents used for, 348, 351f technique of, 343-348 vein patch in, 804, 804f for infrapopliteal lesions, 352 for intimal hyperplasia with arteriovenous fistula, 705 for renal artery stenosis, 598-599, 599t for revascularization of nonhealing wounds, 885-887 of contralateral iliac artery, use of guiding sheath with, 315 patch. See Patch angioplasty. percutaneous transluminal, 316, 319-321, 323, 325. See also Angioplasty, balloon. erectile dysfunction and, 219, 220f for aortoiliac occlusive disease, 547 for fibromuscular dysplasia, 129 intra-arterial thrombolytic therapy and, 428, 429f stenting and, 328 stent coatings in, 765 subintimal, 352, 564, 564f vein patch, for thrombosis in infrainguinal bypass, 804, 804f Angiosarcoma, in lymphedema, 871 Angiotensin I, 577 Angiotensin II, blood pressure regulation and, 577, 578 in intimal hyperplasia, 759 vascular wall synthesis of, 758-759 Angiotensin-converting enzyme inhibitors, for infrainguinal arteriosclerosis, 570 for intimal hyperplasia, 764 in type 2 diabetics, 146-147, 161 Angiotensinogen mRNA, 758 Anisoylated plasminogen streptokinase activator complex (APSAC), 418 Anistreplase, 418 Ankle, arteries of, in limb salvage bypass procedures, 560, 561f venous ulcers of, vs. arterial or ischemic ulcers, 553 Ankle systolic pressure, normal, 236 with arterial obstruction, 236-237, 236f, 237f Ankle-brachial index, 252, 252f arterial injury and, 737 exercise and, 253, 253f in peripheral arterial disease, 263, 264, 265t, 268 in vascular disease in diabetics, 145 in vascular malformations, 204 in wound healing, 880, 881, 881f lumbar sympathectomy and, 448, 449 normal, 236 vein graft failure and, 807 with arterial obstruction, 236, 238 Ansel sheath, 366 Antibiotics, cephalosporin, in postoperative thoracoabdominal aortic aneurysm repair, 479 for arterial infections, bacterial adaptation and, 179-180 control of sepsis and, 184 for gangrene complicated by infection, 893, 894 for limb salvage bypass procedures, 560-561 for mycotic aneurysms, 506, 519 for prosthetic graft infections, 777 for wound healing, 882 grafts impregnated with, 185, 459

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938

Index

Antibiotics (Continued) platelet effects of, 75 prophylactic, administration of, 194-195 bacteriology of graft infections and, 189 clinical studies of, 191-193 comparisons of regimens in, 192-193 current status of, 193-195 experimental studies of, 191 for amputation, 911 for primary arterial infections, 187-195 for prosthetic graft infections, 773-774 for vascular access graft infections, 702 principles of, 188 prospective trials of, 192 Antibodies, antineutrophil cytoplasmic (ANCAs), in polyarteritis nodosa, 115 systemic vasculitides and, 111 thrombosis risk and, 78-79 Anticoagulant(s), lupus, thrombosis risk and, 78, 79 pharmacology of, 166-168 sites of activity of, 72f Anticoagulant activity, of endothelial cells, 42, 69-70, 69t Anticoagulant therapy, endothelial cell activity in, 42 for acute arterial occlusion, 740-741 for carotid angioplasty and stenting, 359, 378, 379 for extracranial occlusive disease, 647 for intermittent claudication, 273 for intimal hyperplasia, 765 for pulmonary embolism, 423 for vascular trauma patients, 718 for vasospasm after embolectomy, 746 for venous thrombosis, 847, 848 ligation and, historical aspects of, 11 long-term, for recurrent embolization, 748 oral, atherosclerosis risk and, 101 Antidepressants, in smoking cessation programs, 270 Antidiuretic hormone, as fibrinolytic agent, 417 Antiembolic stockings, for venous thrombosis, 82, 847 Antifibrinolytic agents, for thoracoabdominal aortic aneurysm repair, 482 for von Willebrand’s disease, 75 Antihypertensive drugs, for intimal hyperplasia, 764 for renovascular disease, preoperative, 584 in carotid angioplasty and stenting, 379 renal vein renin assays and, 583, 583t Anti-inflammatory agents, for intimal hyperplasia, 763-764 Antineutrophil cytoplasmic antibodies (ANCAs), in polyarteritis nodosa, 115 systemic vasculitides and, 111 Antioxidants, for atherosclerosis, 98-99, 100-101 Antiphospholipid antibodies, thrombosis risk and, 78-79 α2-Antiplasmin, 416, 759 Antiplatelet drugs, after carotid endarterectomy, 638 atherosclerosis risk and, 101 for arterial thromboembolism prophylaxis, 83-85 for carotid angioplasty and stenting, 359 for intimal hyperplasia, 762-763 for peripheral arterial disease, 271-272 for recurrent graft thrombosis prophylaxis, 751 for stroke prophylaxis, 647-648 deleterious effects of, 649 intraoperative bleeding and, 786 pharmacology of, 168-170 synthetic RGD peptides as, 85

Antiproteases, aortic aneurysm formation and, 490-491 Antisense oligonucleotides, for control of smooth muscle cell proliferation after vascular injury, 42 Antiseptic agents, in wound healing, 882 Antithrombin III, concentrate of, therapy with, 78 deficiency of, 77-78, 845 endothelial cell–derived, 69, 69t heparin action and, 80, 166, 168 in coagulation inhibition, 73 α1-Antitrypsin, aortic aneurysm formation and, 490-491 Antyllus, arterial repair of, 1, 3 Aorta, abdominal, aneurysms of. See Abdominal aortic aneurysm(s). coarctation of, 125-126, 126f, 200, 200f magnetic resonance angiography of, 283, 284f mesenteric circulation of, 603-604, 604f multidetector row computed tomography angiography for, 295, 296f, 297f surgical exposure of, alternative, 57-58, 58f emergency, 60-61, 61f of descending thoracic and proximal portion, 53-54, 53f, 54f retroperitoneal, 54-55, 55f, 56f supraceliac, 55, 56f transperitoneal, 58-59, 59f, 60f traumatic injuries of, 722-723 approach(es) to, 398-399 apron technique as, 399 arch of. See Aortic arch. ascending, exclusion clamping of, 666-667, 667f exposure of, 666, 666f, 667f in aortic dissection, 469, 471f in Marfan’s syndrome, 123 bacterial colonization of, vascular graft infection and, 190-191 clamping of, in abdominal aortic aneurysm repair, 501 in aortofemoral bypass grafting, 541, 541f in thoracoabdominal aortic aneurysm repair, 476, 477, 482 coarctation of, 200, 200f arterial homograft development for, 4 cross-clamping of, complications with, 480, 481 declamping of, hypotension with, 792 in abdominal aortic aneurysm repair, 501 in thoracoabdominal aortic aneurysm repair, 477 descending, 547 in aortic dissection, 469, 471f dilatation of, in Marfan’s syndrome, 122-123, 123f formation of, 28 infection of, 185-186, 190-191 infrarenal, dissection of, for endarterectomy, 219f infection of, 185-186 reconstruction of, spinal cord ischemia and, 797 superior mesenteric bypass from, 612-614, 613f intraoperative bleeding of, 785 normal, size of, 488-489, 489t occlusion of, in carotid angioplasty and stenting, 365, 367f paravisceral, infection of, 186 prosthetic grafts of, infections of, 777-779, 778f, 779f proximal neck of, in abdominal aortic aneurysm endovascular repair, 383, 385f

Aorta (Continued) stenosis of, in systemic giant cell arteritis, 112, 113f supraceliac, clamping of, coagulopathy with, 482 transperitoneal exposure of at diaphragmatic hiatus, 58-59, 59f suprarenal, clamping of, 501 infection of, 186 Takayasu’s disease affecting, 113, 114f thoracic, magnetic resonance angiography of, 283, 284f multidetector row computed tomographyangiography of, 294, 295, 295f thoracoabdominal, aneurysms of. See Thoracoabdominal aortic aneurysm(s). exposure of, 53-54, 53f, 54f incisions for, 53, 53f valvular function of, in thoracoabdominal aortic aneurysm repair, 480 variability of, in abdominal aortic aneurysm endovascular repair, 383, 384f vascular grafts for, current recommendations for, 463 infection of, 190-191 wall of, aortic aneurysm formation and, 489-491, 490f aortic aneurysm rupture and, 491 structure of, 36 Aorta–carotid artery–superior mesenteric artery bypass, for chronic mesenteric ischemia, 612f Aorta–celiac artery–mesenteric artery bypass, for chronic mesenteric ischemia, 612, 612f, 613f Aortic aneurysm(s), abdominal. See Abdominal aortic aneurysm(s). dissecting type B, 472, 473 thoracoabdominal. See Thoracoabdominal aortic aneurysm(s). Aortic arch, angiography of, for carotid angioplasty and stenting, 359, 360f arteries of, embryologic development of, 26-27, 28 branches of, surgical exposure of, 49-50, 50f, 51f cannulation of, catheters used for, 314 classification of, 359, 360f embryologic development of, 23-24, 26-27, 28 in carotid angioplasty and stenting, problems with, 363t tortuosity of, 363 types of, 368f injuries of, repair of, 722, 722f Aortic arteriomegaly, 489 Aortic bifurcation, crossing over the top of, surgical technique of, 309-310, 310f embolus of, 746 Aortic disease, angioplasty and stenting for, 327, 328f Aortic dissection, acute limb ischemia and, 737 classification of, 469-470, 471f in aortic aneurysms, dissection type B, 472, 473 in cystic medial necrosis, 123-124, 124f in thoracoabdominal aortic aneurysm, 469-470, 471f in thoracoabdominal aortic aneurysm repair, 477, 478f, 481 intraoperative bleeding with, 785 magnetic resonance angiography of, 283, 284f neurologic complications and, 481 of visceral vessels, 605, 607 Aortic pump perfusion, distal, for thoracoabdominal aortic aneurysm repair, 475, 476, 476f

X0183-Idx 9/26/05 01:21 PM Page 939

Index

Aortic regurgitation, in thoracoabdominal aortic aneurysm repair, 480 Aortic stenosis, angioplasty and stenting for, 328-329 Aortic thrombosis, neonatal, 751-752, 752f, 752t Aortobifemoral bypass graft. See also Aortofemoral bypass graft. for aortoiliac occlusive disease, 396 in aortic laparoscopic surgery, 397, 398 infected, 775f, 778-779, 779f, 780f occluded limb of, 789, 789f Aortocaval fistula, 505 Aortoduodenal fistula, aortofemoral bypass grafts and, 541 infected, graft excision and, 777 in situ reconstruction and, 185 Aortoenteric fistula, 179, 774, 774f extra-anatomic bypass and, 10 false aneurysms and, 800 gastrointestinal endoscopy for, 776 infected, graft excision and, 777 with aortofemoral bypass grafts, prevention of, 540-541 Aortofemoral bypass graft, ePTFE for, 460 false aneurysms and, 800 for aortoiliac occlusive disease, 396, 540-543 alternatives to, in high-risk patients, 544-547 concomitant distal reconstruction with, 543 infection of, 540, 778-779, 779f, 780f laparoscopic techniques for, 542 patency of, 543 proximal anastomosis in, 541, 541f results of, 543 surgical technique for, 218f, 540-543, 541f, 542f with distal reconstruction, 543 occluded, thrombolytic therapy for, 790-791 thrombosis of, 786-791, 787f Aortofemoropopliteal reconstruction, antibiotic prophylaxis for, 192, 193, 195 Aortography, for acute mesenteric ischemia, 606 for thoracoabdominal aortic aneurysms, 473, 474f forf abdominal aortic aneurysms, 494-495, 495t risks of, 494-495 Aortoiliac bypass, techniques for, 218f Aortoiliac endarterectomy, 542, 542f Aortoiliac grafts, infections of, 777-778, 778f thrombosis of, 786-791, 787f Aortoiliac occlusive disease, 537-550 angioplasty and stenting for, 325-331 aortofemoral bypass graft for, 396, 540-543 alternatives to in high-risk patients, 544-547 concomitant distal reconstruction with, 543 infections of, 540, 778-779, 779f, 780f laparoscopic techniques for, 542 patency of, 543 proximal anastomosis in, 541, 541f results of, 543 surgical technique for, 218f, 540-543, 541f, 542f diagnosis of, 538-539 erectile dysfunction and, 215 surgical techniques for prevention of, 217-219, 217f-220f femoropopliteal occlusive disease with, 537, 543 axillofemoral bypass graft for, 546-547 in high-risk patients, alternative procedures in, 544-547 laparoscopic surgery for, 396-413 approaches to, 398-400 apron technique in, 397, 399, 400-401, 400f-402f, 407-408 history and development of, 397

Aortoiliac occlusive disease (Continued) robotics in, 409-410, 409t, 410f, 410t techniques of, hand-assisted, 403-404, 403f, 404f, 407, 407t laparoscopy-assisted, 404-407, 405f, 406t totally laparoscopic, 400-403, 407-409 natural history of, 537, 538f, 539f preoperative evaluation of, 540 presentation of, 537, 538f, 539f risk factors for, 537 stenting for, 327, 328f, 330f Aortoiliac reconstruction, graft material used for, 185 neurovascular testing for, 216 noninfectious complication(s) in, 783-801 abdominal wall hernias as, 801 anastomotic false aneurysm as, 800-801 chylous ascites as, 801 declamping hypotension as, 792 erectile dysfunction as, 798-799 prevention of, 217-219, 217f-220f intestinal ischemia as, 793-796, 794f, 795f, 796f intraoperative bleeding as, 783-786, 783f, 784f, 785f operative embolization as, 791-792, 792f recurrent anastomotic aneurysm as, 801 renal failure as, 792-793 retrograde ejaculation as, 799-800, 799f spinal cord ischemia as, 796-797 thrombosis as, 786-791, 787f, 788f, 789f ureteral injury and obstruction as, 797-798, 798f principles of, 217 Aphasia, in carotid artery transient ischemic attacks, 631 Apligraf, in wound healing, 884, 885f Apolipoprotein A, 416 Apomorphine, for erectile dysfunction, 222 Apron technique, in laparoscopic surgery, for aortoiliac occlusive disease, 397, 399, 400401, 400f-402f, 407-408 Aprotonin, as plasmin inhibitor, 416 bovine, 416 Arch of Riolan, 604 ARCHeR trial, of carotid angioplasty and stenting, 356, 357, 358f Area ratio, 230 Argatroban, for thrombosis, 81 pharmacology of, 168 Arm(s). See also Extremity, upper. arteries of, diabetes and, 144 embryologic development of, 29-30, 29f in thoracic outlet syndrome, 678, 679 Art Assist, in wound healing, 885 Arteria magna syndrome, 125, 125f ArteriA Parodi Anti-Embolization System, for cerebral protection, 370, 375t, 376f Arteria radicularis magna, 54, 54f Arterial access, 303-311. See also Vascular access. complications of, 310-311 essential techniques for, 306-310, 307f-310f guidewires and sheaths for, 305-306 importance of, 311 Seldinger technique for, 304-305, 306f selection of site for, 303-304, 304f, 305t, 306f Arterial aneurysm. See Aneurysm(s), arterial. Arterial insufficiency, arteriovenous fistulas and, 704 asymptomatic, in lower extremity, 263-264 Arterial stenoses, arterial flow patterns and, in human limbs, 234-238 collateral circulation and, 234-235, 234f critical, 233-234, 233f hemodynamics of, 232-234

939

Arterial wall, bacterial colonization of, vascular graft infection and, 190-191 composition of, 231 hereditary disorders of, 122-125 in aging and atherosclerosis, 231 in aneurysms, 231-232, 232f in endarterectomy, 231 infection of, cultures for, 182 natural history of, 183-184 injury of, atherosclerosis and, 96-97 layers of, 452, 453f physical properties of, 231-232, 232f tangential stress and tension of, 231 thickening of, physiological regulation of, 38-42, 39f-42f vs. venous wall, 239 white blood cell migration into, 758 Arterialization, intimal hyperplasia and, 760-761, 760f, 761f of autogenous vein grafts, 455, 696 of deep dorsal vein, for erectile dysfunction, 221 of end-to-side portacaval shunts, 827-828 of vein grafts, 755 with arteriovenous fistula, 696, 704-705, 705f Arteriography. See also Angiography. conversion of to balloon angioplasty, 320, 320t developments in, 12 diagnostic, for abdominal aortic coarctation, 126, 126f for arterial infections, 183, 183f for Buerger’s disease, 121, 122 for chronic mesenteric ischemia, 609, 609f, 610f for infrainguinal arteriosclerosis, 555 for popliteal artery entrapment syndrome, 128 for splenic artery aneurysms, 524 for supra-aortic trunks, 659-660 for thoracic outlet syndrome, 680-681, 681f for traumatic arteriovenous fistulas, 725, 726f for vascular disease of upper extremity, 690 for vascular malformations, 204, 207f, 208f for vascular trauma, 716-717, 716t, 717t, 719 intraoperative, in embolectomy, 745, 746 preoperative, for acute arterial or vascular graft occlusion, 741, 741f, 742 renal, renal artery dissection and, 532 Arteriomegaly, 125 aortic, 489 Arteriopathy, heritable, 122-125 Arteriosclerosis. See also Atherosclerosis. in homocystinuria, 132 infrainguinal, 551-574 clinical presentation of, 551 conservative approach to, 552 diagnostic techniques in, new, 569 differential diagnosis of, 552-553 endovascular devices for, 569-570 patient evaluation for, 553-555 staging of, 551-552, 552t treatment of, 555-564 angioplasty in, 563-564, 564f bypasses to ankle or foot arteries in, 560, 561f cost-benefit analysis of limb salvage in, 565f, 566f, 568-569, 569f drug treatment for, 560-561 failing grafts in, 563 general and medical considerations in, 555 graft material and type used in, 556-558 indications for, 552 limb salvage in, 565-566, 566f, 567f lytic agents in, 568

X0183-Idx 9/26/05 01:21 PM Page 940

940

Index

Arteriosclerosis (Continued) managment of foot lesions in, 561 mortality in, 565, 565f new developments in, 569-570 operative technique in, 558-560 patency of arterial reconstruction in, 566 reoperation in, 561-563, 561f, 562f, 566-568 results of, 564-568 surgical considerations in, 555-556 renal artery aneurysms and, 530 Arteriotomy, in carotid endarterectomy, 47, 636 Arteriovenous fistula(s). See also Vascular access. aneurysm formation in, 705-706, 705f aneurysm rupture and, 784 aortocaval, 784, 785f autogenous, for long-term hemodialysis access, 696-698 in children, 701 infection of, 701, 702 brachiobasilic, 698, 698f brachiocephalic, 698, 698f Brescia-Cimino, 696-697, 696f, 697f arterial insufficiency and, 704 in children, 701 venous hypertension and, 704-705, 705f bridge, for chemotherapy, 706 for hemodialysis, 698-700 in extremities, 699, 699f infection of, 701-702, 702f materials used for, 700, 700f sites for, 699-700, 699f thrombosis of, 703, 703f central venous occlusion in, 706 complications of, 701-706 construction of, technique of, 696-697, 697f, 698, 698f embolization of, 203f, 204, 208f for chemotherapy, 706-709, 707f, 708f, 709f for hemodialysis access, 696-698, 696f, 697f intimal lesions in, 756 for total parenteral nutrition, 706-709, 707f, 708f, 709f from splenic artery aneurysms, 525 hemodynamic complications of, 204, 206f, 704-705, 705f iliac, 784-785 in distal femoral reconstruction, 8 in situ saphenous vein bypass graft failure and, 738 infection of, 701-702, 702f intimal hyperplasia of, 705, 756 of axillary artery, endovascular management of, 726, 727f of tibial artery, 725f portal hypertension and, 819 radiocephalic, for long-term hemodialysis, 696-697, 696f, 697f reverse, 697-698, 698f thrombosis of, 702-704, 702f, 703f thrombolytic therapy for, 433, 703 traumatic, 9, 724-726, 725f-727f small, 726 Arteriovenous malformations, 198, 201, 202f, 203f. See also Vascular malformation(s). amputation of, 209 arterial embolization for, 203f, 204, 206-207, 208f microfistulous, 199, 199f Arteriovenous shunt, for vascular access for hemodialysis, 694-695, 695f multiple, portal hypertension and, 818 Arteritis. See also Vasculitis. drug abuse, 117, 118f fungal, 179

Arteritis (Continued) giant cell, clinical patterns in, 112, 112t systemic, 112-113, 112t, 113f Takayasu’s disease and, 112t, 113-114, 114f microbial, anatomic distribution of, 180-181 bacteria causing, 179-180, 179f, 180f with aneurysm formation, 178 radiation-induced, 114-115, 114f systemic, in Kawasaki disease, 116 Takayasu’s, of carotid artery, 623-625 temporal, 112-113, 112t, 113f Artery(ies). See also names of specific arteries, e.g., Renal artery(ies). abdominal, duplex scanning of, 255 autografts of, 455-456 bacterial colonization of, vascular graft infection and, 190-191, 190t bleeding from, intraoperative, 785 blood flow in. See Blood flow, arterial. cannulation of, 303, 306f categories of, 36 congenital conditions of, 125-128 dilatation of, in arteria magna syndrome, 125, 125f emboli of, 734-735. See also Embolization; Embolus(i). lower extremity, 734, 741, 741f, 744-745, 744f, 745f upper extremity, 689, 745 embryologic development of, 23-30 of aortic arch, 26-27, 28 of branchial arch, 24, 25f of digestive tract, 28 of great arteries, 26-27, 27f, 28 of head, 28 of kidneys, 28-29 of limbs, 29-30, 29f grafts of. See Graft(s), arterial. hemodynamic principles in, 225-232 in human limbs, 234-238 treatment of disease and, 238-239 with stenosis, 232-234 in Ehlers-Danlos syndrome, 123 infections of, primary, 177-187. See also Arteritis; Infection(s), arterial. infrapopliteal, approaches to in reoperation, 561-562 layers of, 36-37, 452, 453f lower extremity. See Extremity, lower, arteries of. marginal, of Drummond, 604, 794 normal, characteristics of, 452, 453f layers of, 36-37, 452, 453f occlusion of, acute, causes of, 734-738, 735t clinical manifestations of, 739 evaluation of, 740-741, 741f treatment of, 742-748, 750 historical aspects of, 2, 6-8, 9-10 intra-arterial thrombolytic therapy for, 427, 428, 430, 430f, 431f, 432, 433 treatment of, results of, 750 patency of, determination of, 7-8 puncture of, single wall, 303, 306f small, 304 through-and-through, 303, 306f reentry, 234 stem, 234 stenosis of, arterial flow patterns and, 234-238 collateral circulation and, 234-235, 234f critical, 233-234, 233f hemodynamics of, 232-234 in adventitial cystic disease, 129 in fibromuscular dysplasia, 129 in lower extremity, 255 in pseudoxanthoma elasticum, 125 radiation-induced, 114

Artery(ies) (Continued) sutures of, history of, 2-3 trauma to, 8-9, 724. See also Trauma, vascular. upper extremity, 29-30, 29f, 144 vascular malformations of, 200, 200f walls of. See Arterial wall. Artery of Adamkiewicz, 54 Ascites, chylous, 801 in portal hypertension, 823 management of, 833, 837-839 transjugular intrahepatic portosystemic shunting and, 834 Aseptic technique, vascular graft infection and, 190 Aspirin, adverse reactions to, 169 atherosclerosis risk and, 101 for arterial thromboembolism prophylaxis, 83-84 for carotid angioplasty and stenting, 359 for carotid endarterectomy, 626, 638 results of, 644, 644t for diabetes, 161 for extracranial occlusive disease prophylaxis, 647-648 for intimal hyperplasia, 763 for Kawasaki disease, 116 for limb salvage bypass prophylaxis, 560 for prevention of recurrent stenosis after carotid endarterectomy, 626 for recurrent graft thrombosis prophylaxis, 751 for vascular disease prevention, 169 for venous thrombosis prophylaxis, 847 intraoperative bleeding and, 786 peripheral arterial disease and, 271 pharmacology of, 168-169 platelet effects of, 75 Asymptomatic Carotid Atherosclerosis Study, 626, 645 Asymptomatic Carotid Surgery Trial, 645-646 Atheroemboli, vertebral artery occlusion and, 661 Atherogenesis, advanced, 95 diabetes and, 100 early, 92-93, 92f, 93f progression of, 735 theories of, 95-97 Atheromatous cap, 94 Atherosclerosis, 91-102. See also Arteriosclerosis. aneurysm formation and, 95, 489, 512, 513, 518, 623 aortoiliac occlusive disease and, 537 arrest or regression of, theories of, 97 arteria magna syndrome and, 125 arterial wall properties in, 94, 231 chronic mesenteric ischemia and, 608 diabetes and, 144 endothelial cells in, 93-94 erectile dysfunction and, 215 fatty streaks in, 92-93, 93f heart disease with, acute arterial occlusion and, 740 macrophages in, 94 medical management of, 97-102 antioxidants and inflammatory events in, 100-101 antiplatelet and anticoagulant therapy for, 101 clinical decision-making in, 98 control of risk factors in, 99-100 drug therapy for hyperlipidemia in, 98-99 folic acid supplements for, 101 homocysteine in, 101 infection control in, 101-102 vasoactive drugs for, 101 of carotid bifurcation, 251, 621-622, 621f, 622f of extracranial arteries, aneurysms and, 623

X0183-Idx 9/26/05 01:21 PM Page 941

Index

Atherosclerosis (Continued) coils and kinks and, 623 radiation injury and, 625, 625f of renal arteries, 576, 576f angioplasty and stenting for, 598-599, 599t diagnosis of, 334 dissection with, 533 endovascular management of, 335-337 restenosis of, 339f, 340 results of, 337-341 imaging of, 334-335 natural history of, 334 of superior mesenteric artery, thrombosis and, 605, 608 of supra-aortic trunks, 659 pathogenesis of, 95-97 pathology of, 91-95, 92f peripheral arterial disease and, 267, 267t plaques of, complicated, 95 emboli from, 735, 736f fibrous, 92f, 94-95 gelatinous, 94 removal of, 7-8 softening and break-up of, 628, 629f, 630f progression of, in infrainguinal bypass grafts, 803 thrombosis and, 787-788, 788f recurrent stenosis after carotid endarterectomy and, 626 risk factors for, 99-100 stent placement for, 325, 327 thoracoabdominal aortic aneurysm and, 470 Athletes, exertional compartment syndrome in, 132 ATLANTIS trial, tissue plasminogen activator use in, 433 Atrial fibrillation, proximal emboli secondary to, 428 Atrioventricular valve, primordia of, 24, 26f Atrium(a), embryologic development of, 24, 26f Atrophie blanche, definition of, 859 Atropine, in carotid angioplasty and stenting, 377 Auricular nerve, great, in carotid endarterectomy, 46, 47t, 641 Auscultation, of upper extremity, for thoracic outlet syndrome, 679 Autoimmune process, in Buerger’s disease, 120 in Raynaud’s syndrome, 109 Autoregulation, in critical arterial stenosis, 234 AVE stent, 326 Axial artery, embryologic development of, 29-30 Axillary approach, to axillary artery aneurysm repair, 516 Axillary artery, aneurysms of, mycotic, 519-520 nonmycotic, 512, 513, 514, 515, 516, 517 arteriovenous fistula of, endovascular management of, 726, 727f in bridge arteriovenous fistula, 700 puncture of, 305t reconstruction of, in axillofemoral bypass graft, 546, 546f surgical exposure of, 52, 52f Axillary vein, in bridge arteriovenous fistula, 699, 699f, 700 thrombosis of, thrombolytic therapy for, 426, 426f Axilloaxillary bypass, for innominate artery revascularization, 662, 664-665 Axillobifemoral bypass graft, for aortoiliac graft infections, 777-778, 778f Axillobrachial artery, occlusion of, 689, 689f

Axillofemoral bypass, 10 for aortoiliac and femoropopliteal occlusive disease, 546-547, 546f Axillopopliteal bypass graft, for infected aortobifemoral grafts, 779, 779f, 780f for limb salvage, results of, 565-566, 566f, 567f surgical criteria for, 556 Axillosubclavian system, in giant cell arteritis, 690f traumatic injuries of, endovascular management of, 726, 727f Axillosubclavian vein, occlusion of, in vascular access for hemodialysis, 706 thrombosis of, 690 in venous thoracic outlet syndrome, 687-688, 688f

B B lymphocytes, aortic aneurysm formation and, 491 Back-bleeding, in abdominal aortic aneurysm repair, 501 Bacteremia, arterial infection and, 178 vascular graft infection and, 195 Bacteria, colonization of, in aortic vascular graft infection, 190-191 in wound healing, 882 endotoxins of, 758 in arterial infections, 181-182 in prosthetic graft infections, 773 in vascular graft infections, 188-189, 189t microbial arteritis due to, 179-180, 179f, 180f Bacterial endocarditis, arterial infections and, 179 mycotic aneurysms and, 518 Balance, loss of, vertebral artery occlusion and, 661 Balken sheath, 310 Balloon(s), cryoplasty, 564 Balloon angioplasty, and stenting, vs. carotid endarterectomy, 649-650 cutting, for infrainguinal arteriosclerosis, 563-564, 564f for infrainguinal bypass graft stenosis or thrombosis, 352, 804 for infrainguinal disease, 345t, 346-347, 348t femoropopliteal, 349, 350t, 351t for intimal hyperplasia with arteriovenous fistula, 705 infrapopliteal, 352 Balloon catheter(s), angioplasty, 316-323 advice for handling of, 321, 323t dilatation with, 318, 318f, 321 function of, 316-317, 317t in endovascular interventions, 316 inflation of, 318, 318f, 321 mechanism of revascularization with, 317-318 placement of, 321 properties of, 319, 325 selection of, 320, 321t, 322f structure of, 316, 317f, 317t arterial injury secondary to, 749, 749f carotid–cavernous sinus fistula and, 640 for embolectomy, 8 for thromboembolectomy, 789, 789f, 804 Balloon tamponade, for variceal bleeding, 825 Banti’s syndrome, 832 Barium studies, in acute mesenteric ischemia, 606 Baroreceptor mechanisms, after carotid endarterectomy, 639

941

Basal ganglia, lacunar infarction of, 629 Basic fibroblast growth factor, in intimal hyperplasia, 759, 765 intimal proliferation and, 757 smooth muscle cell proliferation and, 40, 41, 42f Basic pancreatic trypsin inhibitor, as plasmin inhibitor, 416 Basilar artery, in subclavian steal syndrome, 628 Basilic vein, grafts of, for infrainguinal bypass procedures, 558 in reverse arteriovenous fistula, 697 BEACH trial, of carotid angioplasty and stenting, 357, 358f Becaplermin, in wound healing, 883 Behçet’s disease, vasculitis in, 117-118 Bell-bottom technique, in abdominal aortic aneurysm repair, 384, 387 Below-knee amputation, 903-905, 905f. See also Amputation, lower extremity. advantages of, 894, 905 indications and contraindications for, 903-904 prosthetic application technique for, 917-920, 917f-920f prosthetic components for, 921-922, 921f prosthetic requirements for, 905 rehabilitation potential for, 905 selection criteria for, 895t surgical technique of, 904-905, 905f vs. aggressive limb salvage efforts, 569 Below-knee reconstruction, ePTFE grafts for, 460 vascular grafts for, 463 Bentson wire, 305, 312 Benzopyrones, for lymphedema, 873 Beraprost, for intermittent claudication, 273 Bernard-Soulier syndrome, platelet disorders in, 75 Bernoulli’s principle, 226, 226f Beta-blocking agents, atherosclerosis risk and, 101 for protection against intracerebral hemorrhage, 422 peripheral arterial disease and, 271 preoperative, in renovascular disease, 584 thoracoabdominal aortic aneurysm repair and, 480 Biofeedback, temperature, for Raynaud’s syndrome, 110 Biofilm, in wound healing, 882 Biologic substitutes, in arterial graft development, 5 Biologic tissue glue, for intraoperative arterial bleeding, 785 Biopsy, liver, in portal hypertension, 820 temporal artery, in systemic giant cell arteritis, 113 Biosurgical débridement, for wound healing, 881t, 882 Bird’s nest filter, 850, 850f Birthmarks, 198. See also Vascular malformation(s). Bisoprolol, in thoracoabdominal aortic aneurysm repair, 480 Bitistatin, 85 Bivalirudin, for thrombosis, 80, 81 in carotid angioplasty and stenting, 359 pharmacology of, 168 Black toe, diagnosis of, 553 Blakemore tube, 3 Bleeding. See also Hemorrhage. in aortoiliac arterial reconstruction, intraoperative, 783-786, 783f, 784f, 785f in hepatic artery aneurysms, 527 in inferior vena caval injuries, 727-728

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942

Index

Bleeding (Continued) in infrainguinal bypass procedures, 802 in portal hypertension, collateral networks and, 822, 822f endoscopic evaluation and, 820 management of, 823-824 specific measures for, 824-825 in splenic artery aneurysms, 524 in supra-aortic trunk surgical reconstruction, 669 in thoracoabdominal aortic aneurysm repair, 482-483 in thrombolytic therapy, 421-422, 426-427, 790 for deep venous thrombosis, 424, 425 for pulmonary embolism, 423 intra-arterial, 435 intraoperative, 437 in vascular trauma, 718-719 postoperative, 785 variceal. See also Portal hypertension. common portosystemic shunts for, 827-831 emergency portacaval shunting for, 827 indications for, 831-832 nonshunt surgical procedures for, 832-833 postoperative care for, 833 prophylactic shunting for, 826 sclerotherapy for, 835-837, 836t, 837t surgical shunting for, 825-827 therapeutic shunting for, 826-827 transjugular intrahepatic portosystemic shunt (TIPS) for, 833-834 treatment plan for, 837, 838f variceal banding for, 837 Bleeding disorders. See also Coagulation, disorder(s) of; Hemostasis; Thrombosis. coagulation disorders in, 75-77 platelet disorders in, 74-75 preoperative evaluation for, 73 Bleeding time, 73 activated clotting time in, 166, 359, 362, 378, 379 activated partial thromboplastin time in, 73, 166 platelet disorders affecting, 75 Blindness, in carotid artery transient ischemic attacks, 631 in giant cell arteritis, 112 Blood, autologous, in abdominal aortic aneurysm repair, 501 in reperfusion, 733, 734 postmortem, fluidity of, 414 viscosity of, 226-227, 227f rheologic agents and, 239 Blood cultures, for diagnosis of arterial infections, 181-182 Blood flow, arterial, arterial pulses and waveforms and, 235-236, 235f collateral circulation and, 234-235, 234f disease and, 238-239 hemodynamic principles of, 225-232 in human limbs, 234-238 in stenosis, 232-234 treatment of disease and, 238-239 in limbs with arterial obstruction, 236-237, 236f, 237f in normal limbs, 236 patterns of, 228-231, 228f-230f, 234-238 bifurcations and branches and, 230-231 boundary layer separation in, 229-230, 229f, 230f, 232 collateral circulation and, 234-235, 234f in human limbs, 234-238 laminar, 228-229, 228f, 229f pulsatile, 230 turbulent, 229, 229f, 232 vascular resistance and, 235

Blood flow (Continued) vascular steal and, 237-238, 700 cavernosal, in erectile physiology, 214 cerebral, on cardiopulmoonary bypass, 621 in penile-brachial index, 216 peripheral, decreased, 238-239 stasis of, in venous thromboembolism prophylaxis, 82 to skin of limbs, amputation level selection and, 895t, 896t, 897 sympathectomy and, 444 velocity of, Doppler measurement of, 247-249, 248f, 249f, 580, 580t in arteria magna syndrome, 125 in intimal hyperplasia, 756 in renal artery stenosis, 580, 580t, 581f intimal wall thickening and, 41, 41f venous, abnormalities of, 242-243, 242f, 243f treatment of, 243-244 hemodynamic principles of, 239-243 lower extremity, 256 normal pressure relationships with, 240-241, 240f-242f patterns of, 241, 241f, 242f vessel diameter adjustment and, 37-38 Blood glucose, cardiovascular disease and, 145-147, 145t fasting, target goals for, 100 in diabetes, frequency of monitoring of, 152, 154f impaired tolerance to, 150 in hospitalized patients, 152-156 in vascular disease, 145-146, 145t, 147-150, 147t, 148t intravenous infusion and, 156, 156t surgical procedures and, 151-160 plasma, amputation risk and, 913 stroke outcome and, 142, 144 vascular endothelial cell function and, 149 Blood pressure. See also Hypertension; Hypotension; Pressure(s). arterial blood flow and, in normal lower limb, 236 in obstructed lower limb, 236-237, 236f, 237f pulses and waveforms and, 235-236, 235f digital, Raynaud’s syndrome and, 109 distal, arterial injury and, 736-737 Doppler systolic measurements of, amputation level selection and, 895, 895t, 896t in carotid angioplasty and stenting, 379 in infrainguinal arteriosclerosis, 554 in renovascular disease, drug therapy for, 584, 584t in type 2 diabetics, cardiovascular disease and, 146-147, 147t renal artery aneurysms and, 532 renal artery stenosis and, after endovascular management for, 340 postsurgical, 589, 591, 592t, 593f, 596-598, 597f, 598f renin-angiotensin-aldosterone regulation of, 577-578 segmental, of lower extremity, 12, 252-253, 254 upper extremity, in supra-aortic occlusive disease, 660 venous, abnormal, 242-243, 242f, 243f in varicose veins and post-thrombotic syndrome, 242-243, 242f, 243f in exercise, 241, 241f in venous hypertension, 257 normal, blood flow relationships and, 240-241, 240f, 241f, 242f portal, 819 resting, 240, 240f wedge hepatic, 819 Blood pressure index, 252

Blood supply, at proposed amputation level, 894 in wound healing, 880 Blood transfusion, for severe hemorrhage, 824 massive, of banked blood, thrombocytopenia with, 74 Blood viscosity, 226-227, 227f rheologic agents and, 239 Blue Max balloon angioplasty catheter, 317 Blue rubber bleb nevus syndrome, 205t Blue toe syndrome, 553, 735 diagnosis of, 553 in aortoiliac occlusive disease, 537 lumbar sympathectomy and, 448 Body-floss technique, in abdominal aortic aneurysm endovascular repair, 386 Boston Scientific FilterWire EZ, 371f Boundary layer, in arterial blood flow, 229-230, 229f, 230f, 232 Bovine heterografts, 5, 457 Bowel, contamination of abdominal injuries by, 723 indicators of viability of, 608 injury to, in abdominal aortic aneurysm repair, 502 ischemia of, 503 resection of, for acute mesenteric ischemia, 608 Bowes melanoma cell line, 419 Brachial artery, access through, in abdominal aortic aneurysm endovascular repair, 386 in carotid angioplasty and stenting, 366 in renal artery repair, 335, 336f, 338f deep, wounds of, 715 embryologic development of, 29f, 30 in bridge arteriovenous fistula, 699, 699f in reverse arteriovenous fistula, 697 puncture of, 305t Brachial plexus, block of, for construction of autogenous arteriovenous fistula, 696 compression of, in thoracic outlet syndrome, 678 exposure of, 53 injury to, in thoracic outlet syndrome repair, 686 nerve roots of, 675-676 Brachioaxillary loop fistula, 699 Brachiobasilic arteriovenous fistula, 698, 698f Brachiobasilic loop fistula, 699 Brachiocephalic arteriovenous fistula, 698, 698f Brachiocephalic artery, formation of, 28 guiding sheath used with, 315 injuries of, 720-722, 720f, 721f Brachiocephalic loop fistula, 699 Brachiocephalic veins, surgical exposure of, 49, 50 use of guiding sheath with, 315 Bradycardia, in carotid angioplasty and stenting, 375 in carotid endarterectomy, 639 Brain, embryologic, vascularization of, 33-34, 33f-35f Brain scans, for evaluation of extracranial cerebrovascular disease, 632 Branchial arches, arteries of, embryologic development of, 24, 25f nerve supply of, 28 Breath-holding, in magnetic resonance angiography, 281-282 Brescia-Cimino arteriovenous fistula, 696-697, 696f, 697f arterial insufficiency and, 704 in children, 701 venous hypertension and, 704-705, 705f Bridge arteriovenous fistulas, arterial insufficiency and, 704 for chemotherapy, 706

X0183-Idx 9/26/05 01:21 PM Page 943

Index

Bridge arteriovenous fistulas (Continued) for hemodialysis, 698-700 central, 700 in lower extremity, 699, 699f in upper extremity, 699, 699f materials used for, 700, 700f sites for, 699-700, 699f infection of, 701-702, 702f thrombosis of, 703, 703f Brodie-Trendelenburg test, 860 Broviac central venous catheter, 706, 707f, 708, 708f Bruit(s), arteriovenous fistula and, 784 carotid, in asymptomatic patients, 620 cervical, carotid lesions and, 630 duplex scanning for, 251 femoral, in aortoiliac occlusive disease, 538 in arterial stenoses, 232-233 popliteal, in adventitial cystic disease, 129 systolic, in abdominal coarctation, 126 Budd-Chiari syndrome, 853 portal hypertension and, 818-819 transjugular intrahepatic portosystemic shunting and, 834 Buerger’s disease, 8 lumbar sympathectomy and, 448, 450 vascular disease in, 120-122, 121f Buflomedil, for intermittent claudication, 273 Bulbus cordis, 24, 27f Bullet wounds, vascular damage with, 713-714, 714f Bupropion, in smoking cessation programs, 270 Bypass graft(s). See also specific types, e.g., Aortofemoral bypass graft. above-knee to below-knee, for femoral and popliteal artery aneurysm repair, 517 extra-anatomic, vascular steal and, 237-238 extracranial-to-intracranial, for stroke prevention, 651 for abdominal aortic coarctation, 126 for arterial lesions, hemodynamic analysis of, 238 for revascularization of nonhealing wounds, 885-887, 886f in aortic cross-clamping, in thoracoabdominal aortic aneurysm repair, 480 infrainguinal, angioplasty of, 352 duplex scanning after, 255 intimal hyperplasia after, 761 patency of, warfarin use and, 167 leg, in Buerger’s disease, 122 revision or replacement of, 746-747 thrombectomy of, 746

C C3b complement receptor, 757 C4b, in protein S deficiency, 78 Cadexomer iodine, in wound healing, 882 Calcification, in carotid angioplasty and stenting, 361, 363f, 363t of aortic plaque, in laparoscopic aortic surgery, 408 Calcitonin, in Raynaud’s syndrome, 107 Calcium alginate dressings, in wound healing, 883, 884t Calcium channel antagonists, for intimal hyperplasia, 764 pharmacology of, 171 Calcium channel blockers, for Raynaud’s syndrome, 110 Calf muscle pump, 240, 241, 242, 243 Calf muscle swelling, in acute limb ischemia, 892

Calf vessels, magnetic resonance angiography of, 287 Cancer, colon, in abdominal aortic aneurysm repair, 505 thrombosis risk and, 78 vasculitis associated with, 119 Cannulation, arterial, 303, 306f of aortic arch, 314 of common carotid artery, 365-366 of iliac artery, catheter for, 309-310, 310f, 314 of renal artery, 314 Capillary(ies), chronic venous insufficiency and, 859 Capillary malformations, 199, 199f, 201, 204f laser treatment for, 209 Captopril, for intimal hyperplasia, 764 renal scanning with, for renovascular hypertension, 579-580, 580f Carbohydrate, insulin requirements and, in diabetics, 158-159 Carbon dioxide, as alternative to renal angiography, 341, 582 insufflation of, in laparoscopic surgery, 397, 398, 399, 400 Cardiogenic plate, 21, 22f Cardiopulmonary bypass, carotid stenosis and, 621 intestinal ischemia and, 794 Cardiopulmonary function, abdominal aortic aneurysm repair and, 497 lower extremity amputation and, 890 Cardiovascular disease, homocystinuria and, 132 in carotid angioplasty and stenting, 377 in diabetics, 143-144 interventional studies of, 145-147, 145t, 146t, 147t in Marfan’s syndrome, 122 peripheral arterial disease and, 267, 267t, 268 Cardiovascular function, in acute limb ischemia, 892 in renovascular hypertension, 578 CARESS trial, of carotid angioplasty and stenting, 357 Carnitine, for intermittent claudication, 273 Carotid angioplasty and stenting, antiplatelet and anticoagulant therapy for, 359 diagnostic angiography for, 359-362, 360f-364f, 361t, 363t hemodynamic changes in, 375, 377 neurologic complications of, 377-379, 378f, 380f patient selection for, 358-359 postoperative management of, 379-380 results of studies of, 355-358, 356t-358t, 357f sheath placement in, brachial approach for, 366, 367f cervical approach for, 366-367 coronary technique for, 365-366 ostial lesion management for, 367, 368f sequential over-the-wire technique of, 363-365, 365f, 365t, 366f, 367f telescoping technique for, 365 stent deployment in, 372-373, 375, 376f-378f postdilatation, 375 predilatation, 373 technique of, 355-382 cerebral protection during, 367-368, 370, 370f-375f, 370t, 372, 372t, 373t, 375t sheath placement in common carotid artery in, 362-367, 364f-369f, 364t, 365t stent deployment in, 372-373, 375, 376f-378f vs. carotid endarterectomy, 355-358, 649-650

943

Carotid artery(ies), bifurcation of. See Carotid bifurcation. blunt trauma to, 720-721, 721t cervical disease of, 617-651. See also Extracranial cerebrovascular disease. common, aneurysm of, 515-516, 515f cannulation of, in carotid angioplasty and stenting, 365-366 duplex scanning of, 249, 250-251, 250f formation of, 27, 28 in carotid endarterectomy, 635 injury of, 720, 720f left, surgical exposure of, 49, 50, 51f occlusion or stenosis of, 249-250 revascularization for, 662, 662f, 663-664, 663f, 664f, 665, 665f radiation injury of, 625, 625f sheath introduction into, in carotid angioplasty and stenting, 362-367, 364f-369f, 364t, 365t tortuosity of, 249 due to sheath introduction, 365, 366f transposition of, to distal vertebral artery, 671, 671f transposition of vertebral artery into, 669-670, 670f computed tomography-angiography of, 294 disease of, diabetes and, 144 duplex scanning of, for thoracoabdominal aortic aneurysm, 475 external, bypass from to distal vertebral artery, 671, 672f formation of, 28 grafts of, for repair of internal carotid, 721, 721f in carotid endarterectomy, 635, 635f, 637, 638f, 644 occluded, in carotid angioplasty and stenting, 361, 363t, 364, 365, 365f, 366f, 367f extracranial, acute dissection of, 623 aneurysms of, 623 mycotic, 519 nonmycotic, 512, 513, 514, 515-516, 515f coils and kinks of, 622-623, 624f magnetic resonance angiography of, 282, 283f radiation injury of, 625, 625f recurrent stenosis of, 625-626 injuries of, 720-722, 720f, 721f internal, aneurysm of, 515-516, 515f arterial thrombosis of, 627, 627f back-pressure in, measurement of, 634, 635, 636f bypass from, to distal vertebral artery, 671-672, 673f dilatation of, 636, 637f duplex scanning of, 249-251 applications of, 251-252 emboli released from, 627, 627f, 640 high, surgical exposure of, 48-49, 49f hyperextension injury of, 720, 720f in carotid endarterectomy, 47, 635, 635f injuries of, operative repair of, 721, 721f kinking of, 624f, 637, 637f stenosis of, 250, 250t, 251t carotid angioplasty and stenting and, 355-358, 363t vs. occlusion, 250, 250t, 251t ischemia of, in supra-aortic trunk occlusion, 660 lesions of, asymptomatic, 619-620 ulcerated, embolic risk of, 620 occlusion of, carotid angioplasty and stenting for. See Carotid angioplasty and stenting.

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944

Index

Carotid artery(ies) (Continued) reconstruction of, historical aspects of, 9-10 stenosis of, asymptomatic, duplex scanning for, 251 coronary artery disease and, 621, 651 high-risk patients with, 356-358, 356t, 358f, 358t measurement of, European vs. American methods of, 646, 647t risks of, with cardiopulmonary bypass, 621 transient ischemic attacks involving, 631 Carotid bifurcation, aneurysm of, 515 atherosclerotic plaque in, 621-622, 621f, 622f blood flow patterns in, 230, 230f carotid endarterectomy of, 642-644, 643t indications for, 634 technique of, 634-636, 635f, 636f cerebrovascular disease and, 617 cervical cranial nerves and, 635, 635f distal anastomosis to, after carotid endarterectomy, 662, 662f, 663f duplex scanning of, 249, 251 exposure of, 666 grafts of, development of, 7 hemodynamic analysis of, 238 noninvasive testing of, 633 surgical anatomy of, 640f surgical approach to, 46-48, 47f, 47t thromboembolization in, 251 Carotid body tumors, 626, 638 Carotid bruits, in asymptomatic patients, 620 Carotid endarterectomy, complications with, intraoperative, 638-641 postoperative, 641-642, 642f distal anastomosis to carotid bifurcation in, 662, 662f, 663f eversion, 48 for acute stroke, 649 for cresendo transient ischemic attacks, 649 for stroke in evolution, 649 for stroke prevention, 355, 644-647 historical aspects of, 9-10, 617, 618 indications for, 634 intellectual improvement with, 651 intimal hyperplasia after, 761 nerves in, 46, 47, 47t of carotid bifurcation, 634-636, 635f, 636f distal anastomosis in, 662, 662f, 663f results of, 642-644, 643t of external carotid, 637, 638f preoperative angiography and, 633 recurrent stenosis after, 625-626 stroke mortality and, 618-619, 619f tandem lesions in, 651 technique of, 634-636, 635f, 636f vs. carotid angioplasty and stenting, 355-358 Carotid sinus response, in carotid angioplasty and stenting, 375 Carotid siphon, in carotid endarterectomy, 651 Carotid stump pressure, measurement of, 515-516 Carotid ulceration, asymptomatic, 650-651 Carotid-carotid bypass, for common carotid artery revascularization, 662, 665, 665f Carotid–cavernous sinus fistula, after carotid endarterectomy, 640 Carotid-subclavian bypass, and carotid (or subclavian) transposition, 663-664, 663f, 664f Carpal tunnel syndrome, Raynaud’s syndrome and, 109 vs. thoracic outlet syndrome, 682 Carrel patch technique, in thoracoabdominal aortic aneurysm repair, 477 Cast, orthopedic, extremity ischemia and, 737 Catheter(s), AL4, 360f angled vertebral, 360

Catheter(s) (Continued) balloon, arterial injury secondary to, 749, 749f carotid–cavernous sinus fistula and, 640 for thromboembolectomy, 789, 789f, 804 balloon angioplasty, 316-323. See also Balloon catheter(s), angioplasty. balloon embolectomy, 8 central venous, for thoracoabdominal aortic aneurysm repair, 475 for vascular access for hemodialysis, 695-696, 695f, 706 implantable ports for, 707, 707f peripherally inserted central catheter line for, 707, 707f placement of, 706, 707f, 708, 708f direct venipuncture for, 708, 709, 709f cobra, 310, 310f, 314, 335 design characteristics of, 313-314 epidural, for thoracoabdominal aortic aneurysm repair, 475 flow rate of, 313-314, 314t Fogarty, 702, 750, 789 in embolectomy for acute limb ischemia, 744, 744f size of, 744 for cannulation of iliac artery, 309-310, 310f, 314 for carotid angioplasty and stenting, 359-361, 360f, 361f, 361t, 362f for endovascular approach to infrainguinal disease, 344, 345t, 348t Groshong, 707 guiding, 315-316 for angioplasty and stenting of renal lesions, 337f H1, 365 vs. guiding sheaths, 315, 364, 364t Headhunter, 360, 360f, 361t intrathecal, for thoracoabdominal aortic aneurysm repair, 475, 481 neonatal aortic thrombosis and, 751 octopus, in thoracoabdominal aortic aneurysm repair, 476, 477 package label of, 313 PercuSurge export, in carotid angioplasty and stenting, 368, 370 selective and nonselective, 313, 314 Simmons, 335, 360, 361t, 366 Sos, 309-310, 335 Swan-Ganz, for prevention of declamping hypotension, 792 for thoracoabdominal aortic aneurysm repair, 475, 480 Tennis Racquet, 309, 310f thrombectomy, 791 percutaneous techniques of, 852, 852f types of, 313t, 314-315 Vitek, 360, 360f, 361f, 361t, 362f in carotid angioplasty and stenting, 366f VNUS, 864f Catheterization, transjugular venous, for measurement of portal venous pressure, 819 CAVATAS trial, 356 Cavernosal artery occlusion pressure, measurement of, 216-217 Cavernosography, dynamic infusion, 217 Cavernous smooth muscle, in erectile physiology, 214 CD11a/CD18 adhesion complex, 757 CD11b/CD18 adhesion complex, 757 Cefamandole, prophylactic, 192, 193, 194 Cefazolin, in limb salvage bypass procedures, 560 prophylactic, in vascular reconstruction procedures, 192, 193, 193t, 194, 194t

Cefotaxime, prophylactic, in vascular reconstruction procedures, 192, 194 Cefuroxime, prophylactic, in vascular reconstruction procedures, 192, 193, 194 Celiac artery, aneurysms of, 524t, 526t, 528, 528f embryologic development of, 28 in thoracoabdominal aortic aneurysm repair, 477 infections of, 186 reconstruction of, 58-59 stenosis of, in ischemic colitis, 796, 796f surgical exposure of, 55-56, 56f, 58-59 Celiac axis, access to, in retrograde mesenteric bypass grafts, 613-614 anatomy of, 603-604, 604f compression of, 10, 611f stenosis of, 612f thrombosis of, 605 Cell(s), growth factors of, in intimal hyperplasia, 759 in intimal thickening, 39-40, 41, 42f Cell Saver device, 476 Cellulitis, in lymphedema, 871, 871f in wound healing, 880 Central nervous system, embryologic, vascularization of, 32-34, 33f-35f Central venous catheter, for thoracoabdominal aortic aneurysm repair, 475 for vascular access for hemodialysis, 695-696, 695f occlusion of, 706 implantable ports for, 707, 707f peripherally inserted central catheter line for, 707, 707f placement of, 706, 707f, 708, 708f direct venipuncture for, 708, 709, 709f Central venous occlusion, 706 Cephadrine, prophylactic, 192 Cephalic vein, anatomy of, 454 central venous catheter in, 707f, 708, 708f grafts of, for infrainguinal bypass procedures, 558 in autogenous arteriovenous fistula for hemodialysis, 696 in bridge arteriovenous fistula, 699, 699f Cephalosporin(s), prophylactic, for vascular reconstruction procedures, 192, 193-194, 194t, 195, 774 Cerebral antiembolism devices, in trials of carotid endarterectomy vs. angioplasty and stenting, 650 Cerebral artery(ies), in carotid artery transient ischemic attacks, 631 middle, carotid artery thrombosis and, 627, 627f Cerebral blood flow, on cardiopulmonary bypass, carotid stenosis and, 621 Cerebral emboli, 628-629, 629f, 630f Cerebral hyperperfusion, in carotid angioplasty and stenting, 379 Cerebral infarction. See Stroke. Cerebral intermittent claudication, 617 Cerebral necrosis, in cerebral ischemic events, 629 Cerebral protection device(s), 650 activated clotting time and, 359, 362 distal filter type, 368, 370, 372t, 373f, 374f, 375f distal occlusion type, 368, 372f, 372t guiding catheters vs. sheaths with, 363 in carotid angioplasty and stenting, 355, 356, 367-368, 370, 370f-375f, 370t, 372, 372t, 373t, 375t proximal occlusion type, 370, 375t, 376f

X0183-Idx 9/26/05 01:21 PM Page 945

Index

Cerebrospinal fluid, in thoracoabdominal aortic aneurysm repair, 478-479, 481-482 Cerebrovascular disease, diabetes and, 142-145 extracranial. See Extracranial cerebrovascular disease. homocystinuria and, 132 peripheral arterial disease and, 267, 267t Cervical approach, in carotid angioplasty and stenting, 366-367 Cervical rib syndrome, 675. See also Thoracic outlet syndrome. Cervical spine, disorders of, vs. thoracic outlet syndrome, 682 Cervicothoracic sympathectomy, for Raynaud’s syndrome, 110 CHAOS, vascular disease and, 150 Charcot, intermittent claudication and, 2 Chemoreceptor cells, in carotid body tumors, 626 Chemotactic factors, in inflammation, 758 Chemotherapy, vascular access for, 706-709, 707f, 708f, 709f Chest radiograph, for thoracoabdominal aortic aneurysm, 473, 473f Chiari’s disease, portal hypertension and, 818 Children, arterial autografts in, 456 fibromuscular dysplasia in, after renal artery reconstruction, 595, 596f Kawasaki disease in, 116 portal vein thrombosis in, 817 reimplantation of renal artery in, 584, 585f renal artery stenosis in, percutaneous transluminal angioplasty for, 598 renovascular hypertension in, 578, 578t vascular access in, 701 Chlamydia pneumoniae, 101, 266-267 Cholecystectomy, in abdominal aortic aneurysm repair, 505 Cholesterol, atherosclerosis regression and, 97 embolization of, renal function and, 341 low-density lipoprotein, 93, 95 target levels of, 97 Cholesterol esters, in fibrous plaques, 94 Chopart’s amputation, 901 Christmas disease (hemophilia B), 76 Chronic obstructive pulmonary disease, aneurysm rupture risk and, 495 Chylous ascites, 801 Cigarette smoking. See Smoking. Cilostazol, for intermittent claudication, 272-273 pharmacology of, 170 Cine-magnetic resonance angiography, for thoracoabdominal aortic aneurysm, 475, 475f CircAid device, for treatment of lymphedema, 873 Circle of Willis, collateral circulation and, 627 Circulation, collateral. See Collateral circulation. extracorporeal, in thoracoabdominal aortic aneurysm repair, 482-483 mesenteric, 603-604, 604f Cirrhosis, esophageal varices and, 821-822, 822f management of, 823-824 portal hypertension and, 818, 821, 821f Clatworthy shunt, for portal hypertension, 826 Claudication. See also Occlusive disease. in adventitial cystic disease, 129 intermittent, aortoiliac occlusive disease and, 537 Charcot and, 2 critical limb ischemia and, 268, 269 drug therapy for, 272-273 exercise therapy for, 272 in infrainguinal arteriosclerosis, 552-553 infrainguinal arterial bypass for, 564-565

Claudication (Continued) in lower extremity, 263, 264, 264t, 265t. See also Peripheral arterial disease. symptoms of, 538-539 vs. nerve root irritation, 538 medical treatment of, 170 venous, hemodynamic principles and, 243 Clopidogrel, adverse reactions to, 169 after carotid endarterectomy, 638 as antiplatelet agent, 84-85 atherosclerosis risk and, 101 clinical uses of, 169 for infrainguinal arteriosclerosis, 570 in carotid angioplasty and stenting, 359 intraoperative bleeding and, 786 peripheral arterial disease and, 271-272 pharmacology of, 169 structure and mechanism of action of, 169 vs. aspirin, 169 Clostridium difficile colitis, postoperative, 795 Cloxacillin plus gentamicin, prophylactic, for vascular reconstruction procedures, 192 Coagulation, disorder(s) of, acquired, 76-77 congenital, 75-76 in diabetes, 148-149 in thoracoabdominal aortic aneurysm repair, 482 unrecognized, intraoperative bleeding from, 786 with aortic supraceliac clamping, 482 endothelial cell activity in, 42 in hemostasis, activation of, 71-72 inhibition of, 72-73 intrinsic and extrinsic pathways in, 70f, 71-72 in intimal hyperplasia, 759-760 Coagulation cascade, 415 platelet involvement in, 71 sequence of events in, 70f, 71-72 Coagulation factors, deficiencies of, 71-72, 75-76 nomenclature of, 71 Coarctation, aortic, 200, 200f arterial homograft development for, 4 Coating(s), of guidewires and catheters, characteristics of, 305-306, 312, 314, 317 Cobra catheter, 310, 310f, 314, 335 Cocaine, abuse of, 117 Coccus, gram-positive, 180, 188 Cogan’s syndrome, vasculitis in, 118 Coils, in extracranial cerebrovascular disease, 622-623, 624f Cold exposure, in Raynaud’s syndrome, 107, 108f, 109 Colestipol, peripheral arterial disease and, 271 Colic artery, aneurysms of, 524t, 526t, 529 middle, 55, 56 Colitis, ischemic, 794 in abdominal aortic aneurysm repair, 503 in aortic reconstruction surgery, 793-796, 794f, 795f, 796f Collagen, aortic wall, aortic aneurysm formation and, 489, 490, 491 arterial wall, 231 intimal, in atherogenesis, 96 Collagen vascular diseases, upper extremity, 689 Collagenase, aortic wall, aortic aneurysm formation and, 490 for wound healing, 881 Collateral circulation, acute arterial occlusion and, 739 acute limb ischemia and, 891, 892 aortoiliac occlusive disease and, 537, 538f arterial, 234-235, 234f carotid angioplasty and stenting and, 362 mesenteric, 603-604, 604f portal hypertension and, 832

945

Collateral circulation (Continued) to brain, cerebral ischemic events and, 627 venous, in portal hypertension, 821-822, 822f Colon, arterial supply of, 794, 794f cancer of, in abdominal aortic aneurysm repair, 505 sigmoid, pH of, 795 Compartment syndrome, 130-132, 131f, 747 abdominal, in abdominal aortic aneurysm repair, 503 causes of, 130, 130t exertional, 132 extremity ischemia and, 737-738 treatment of, 131, 131f untreated, 131-132 Complete blood count, in portal hypertension, 819 Completion angiography, in abdominal aortic aneurysm repair, 385 in carotid endarterectomy, 636 in endovascular treatment of infrainguinal disease, 347 in renal artery angioplasty and stenting, 336f, 337f, 339f Completion studies, noninvasive techniques for, in lower extremity, 255 Complex regional pain syndrome, vs. thoracic outlet syndrome, 682 Compliance mismatch, intimal thickening and, 756 Compression, elastic and nonelastic, for lymphedema, 873 of cranial nerves, in extracranial carotid artery aneurysms, 512, 514 Compression stockings, for lymphedema, 873 for wound healing, 881, 881f Computed tomography, for abdominal aortic aneurysm repair, 383, 384t, 493, 493f for acute mesenteric ischemia, 606 for arterial infections, 182 for chronic mesenteric ischemia, 609, 611f for extracranial cerebrovascular disease, 632-633 for peripheral artery aneurysms, 514, 514f for prosthetic graft infection, 775, 775f for splenic artery aneurysms, 524 for thoracic outlet syndrome, 680 for vascular malformations, 204 for vascular trauma, 716 for venous thrombosis, 846 spiral, early use of, 13 for abdominal aortic aneurysms, 493-494, 493f for pulmonary embolism, 424 for thoracoabdominal aortic aneurysm, 473, 474f improvements in, 293 Computed tomography-angiography, for abdominal aortic aneurysm endovascular repair, 383, 384t, 494 for pulmonary embolism, 424 for thoracoabdominal aortic aneurysm, 473, 474f for vascular trauma, 716-717 multidetector row, 292-299 applications for, 294-299 contrast media administration for, 293-294 image reconstruction for, 294 radiation dose for, 294 scanners used in, 293 speed of, 293 technical data in, 293 vs. magnetic resonance angiography, 299 multislice, for renal artery stenosis screening, 335

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946

Index

Computerized brain mapping, for extracranial cerebrovascular disease, 633 Confusion, in carotid artery transient ischemic attacks, 631 Congestive heart failure, abdominal aortic aneurysm repair and, 498 arteriovenous fistulas and, 704 in infrainguinal arteriosclerosis, 554 Connective tissue, in fibrous plaques, 94 intimal, in atherogenesis, 96 Connective tissue disease, Raynaud’s syndrome and, 109 vasculitis and, 119-120, 119f Constant environmental treatment unit, for postoperative amputated stump, 915-916, 916f Contamination, intraoperative, prosthetic graft infections and, 773 Contractures, compartment syndrome and, 131 flexion, in lower extremity amputation, 912 Contrast agents, in magnetic resonance angiography, 282, 287 in multidetector row computed tomography-angiography, 293-294 in renal angiography, dose of, 582 iodinated, renal function and, 341 nephrotoxicity of, 480, 581-582 protection against, 170-171, 581-582 nonionic, 581 Convulsions, in carotid artery transient ischemic attacks, 631 in children, with hemodialysis, 701 Cordis AngioGuard, 371f Corona phlebectatica, definition of, 859 Coronary angiography, in thoracoabdominal aortic aneurysm repair, 480 Coronary artery disease, abdominal aortic aneurysm repair and, 498 aortoiliac occlusive disease and, 540 carotid stenosis with, 651 historical aspects of, 10 in Kawasaki disease, 116-117, 117f peripheral arterial disease and, 267, 267t Corticosteroids, as fibrinolytic agent, 417 for Cogan’s syndrome, 118 for polyarteritis nodosa, 115 for thoracoabdominal aortic aneurysm repair, 480, 482 for vasculitis in connective tissue diseases, 120 Costoclavicular space, anatomy of, 676, 676f Costoclavicular syndrome, 675. See also Thoracic outlet syndrome. Coumarin, for lymphedema, 873 for prevention of extracranial occlusive disease, 647 for venous thrombosis, 847, 848 COX-1, aspirin action and, 168 COX-2, aspirin action and, 168 Cragg stent, 326 Cragg wires, 314 Cranial nerve(s), compression of, in extracranial carotid artery aneurysms, 512, 514 injury of, in carotid endarterectomy, 48, 640-641, 640f protection of, in carotid endarterectomy, 48 C-reactive protein, in aortic wall, 491 in inflammatory aneurysm, 504 peripheral arterial disease and, 266 Crescendo transient ischemic attacks, 618-619, 630 carotid endarterectomy for, 649 CREST trial, 358, 650 Critical limb ischemia, 268-269. See also Acute limb ischemia; Peripheral arterial disease. nonoperative treatment of, 273-274

Critical limb ischemia (Continued) risk factors for, 268 treatment of, 273-274 Crutch trauma, axillary artery aneurysms and, 512 Cryoamputation, 892, 893 Cryoprecipitate, for afibrinogenemia, 76 for bleeding with thrombolytic therapy, 426 for von Willebrand’s disease, 75 Cryopreservation, for arterial and venous allografts and homografts, 4, 456 C-shunt, mesocaval, 829 Cubital tunnel syndrome, vs. thoracic outlet syndrome, 682 Cultures, arterial wall, 182 blood, for arterial infections, 181-182 Cutdown, after popliteal embolectomy, 745 Cuvier, ducts of, 32 Cyclic guanosine monophosphate, endothelial-dependent arterial relaxation and, 38 in erectile physiology, 214 Cyclic nucleotide phosphodiesterase (PDE), in erectile physiology, 214 inhibitors of, 214, 222 Cyclophosphamide, for polyarteritis nodosa, 115 Cyclosporine, for intimal hyperplasia, 763-764 Cyst(s), synovial-like, in adventitial cystic disease, 129 Cystathionine β-synthetase, deficiency of, 132 Cystic disease, adventitial, 129-130 Cystic medial necrosis, aortic dissection in, 123-124, 124f Cytokines, in atherogenesis, 92 in chronic wound healing, 878 in fatty streak lesions, 93 in reperfusion injury, 734 in thoracoabdominal aortic aneurysm repair, 479 in venous thrombosis, 845 systemic vasculitides and, 112 Cytomegalovirus, atherosclerosis risk and, 101

D da Vinci Robotic Surgery System, 409, 409t Dacron graft(s), 458-459, 458f, 459f development of, 4-5 dilatation of, 459, 807-808, 808f for antegrade bypass for chronic mesenteric ischemia, 612 for aortofemoral bypass, knitted, 540, 542 for axillofemoral bypass, 546 for thoracoabdominal aortic aneurysm repair, 477, 478f impregnation or coating of, 458-459 patency rates of, 459 velour finishes of, 458 vs. PTFE grafts, 557, 777 Danaparoid, for established thrombosis, 80 DAPP (distal aortic pump perfusion), for thoracoabdominal aortic aneurysm repair, 475, 476, 476f, 483 heparin-coated tubing in, 483 DDAVP (desmopressin acetate), as fibrinolytic agent, 417 for uremia, 75 for von Willebrand’s disease, 75 in hemophiliac patients, 76 D-dimer(s), 415 in ischemic colitis, 795 peripheral arterial disease and, 266 DeBakey tunneling instrument, 546 Débridement, for prosthetic graft infections, 777 for vascular injury repair, 719

Débridement (Continued) for wound healing, 881-882, 881t radical, guillotine amputation for, 893-894, 893f Decubitus position, modified right lateral, 53, 53f Deep venous thrombosis, 845 diagnosis of, 425, 846-847 noninvasive, 258 duplex scanning of, 258 emboli and, 735 in lower extremity amputation, 911-912 prophylaxis for, 82-83, 84t, 847-848 pulmonary embolism and, 11, 427 recurrent, 258 thrombolytic therapy for, 424-425 pulmonary embolism and, 427 treatment of, 848-850 vena caval filters for, 849-850, 849f, 849t, 850f, 851f, 851t venous pressure and flow relationships and, 242-243, 243f Dehydroepiandrosterone, for intimal hyperplasia, 763 Dense granules, of platelets, 71 Denver shunt, for ascites management, 838 Dermagraft, in wound healing, 884 Descending thoracic aorta-to-femoral artery bypass, for aortoiliac occlusive disease, 547 Desirudin, 80 pharmacology of, 168 Desmopressin acetate (DDAVP), as fibrinolytic agent, 417 for uremia, 75 for von Willebrand’s disease, 75 in hemophiliac patients, 76 Devascularization procedures, for portal hypertension, 832-833 Dexamethasone, for intimal hyperplasia, 763, 764f Dextran, for acute limb ischemia, 891 for bleeding disorders, 73 for vasospasm after embolectomy, 746 low-molecular-weight, 239 Dextrose, insulin requirements and, 158 Diabetes mellitus, atherosclerosis and, 96, 100 brittle, 155 cardiovascular disease and, 143-144 interventional studies in, 145-147, 145t-147t cerebrovascular disease and, 142-145 critical limb ischemia and, 268 foot care and, instructions for patients with, 913, 913f foot lesions in, in limb salvage bypass procedures, 561 gangrene complicated by infection in, 893 gestational, 141, 151 insulin-dependent, enteral nutrition in, 157-158 etiology of, 141 vascular disease and, glycemia control in, 145-146, 145t ischemic skin ulcers and, 892 lower extremity amputation in, 890, 891, 891t contralateral limb loss in, 912-913, 913f non–insulin-dependent, coagulation abnormalities in, 148-149 enteral nutrition in, 156-158 etiology of, 141 immunologic mechanisms in, 150 inflammatory processes in, 150 insulin levels in, 150

X0183-Idx 9/26/05 01:21 PM Page 947

Index

Diabetes mellitus (Continued) lipid abnormalities in, 149-150 obesity and, 151 platelet abnormalities in, 148-149 protocols for outside hospital, 160-161, 160t risk factors for, 150-151 smoking in, 150 syndrome X and, 150 vascular disease and, blood pressure–lowering trials in, 146-147, 147t glycemia control in, 145t, 146 lipid-lowering trials in, 146, 146t vascular volume shifts in, 150 peripheral vascular disease and, 142-145, 265, 268, 270 renal dysfunction and, 581-582 secondary, 141 surgery in, enteral and parenteral nutrition for, 156-158, 156t, 157f, 158t, 159f, 160t glucose control in, 151-160 preparation for, 152 standing insulin orders for, 152-156, 152t, 153f, 154f types of, 141 vascular disease and, 141-142 epidemiology of, 142-145 interventional studies of, 145-147, 145t, 146t, 147t maintenance therapy for, 160t pathophysiology of, glucose and, 147-150, 147t, 148t risk factors for, 147-150, 151 wound healing and, 876 Diagnosis, of arterial infections, 181-183 timing of, 183 techniques of, development of, 12-13 noninvasive, 247-259 overuse and limitations of, 259 Diaphragmatic hiatus, transperitoneal exposure of abdominal aorta at, 58-59, 59f Diarrhea, in ischemic colitis, 794 DIC (disseminated intravascular coagulation), ascites and, 838 characteristics of, 76-77 Dicrotic notch, loss of, 254, 254f Diet, for atherosclerosis, 95, 98 for diabetics, in hospital, 152 for lymphedema, 873 plasminogen activator inhibitor activity and, 416 α-Difluoromethylornithine, for intimal hyperplasia, 765 Digestive tract, arteries of, embryologic development of, 28 Digit(s), anomalies of, vascular malformations and, 203 in Raynaud’s syndrome, 107-111, 108f Diguanides, as fibrinolytic agent, 417 Dilators, 315 for endovascular approach to infrainguinal disease, 345 Dipyridamole, after carotid endarterectomy, 638 for intimal hyperplasia, 763 Disseminated intravascular coagulation (DIC), ascites and, 838 characteristics of, 76-77 Distal aortic perfusion techniques, for t horacoabdominal aortic aneurysm repair, 475-476, 476f Distal aortic pump perfusion (DAPP), for thoracoabdominal aortic aneurysm repair, 475, 476, 476f, 483 heparin-coated tubing in, 483

Distal splenorenal shunt, advantages of, 831 indications for, 831 principle of, 829-830, 829f sclerotherapy and, 830 splenopancreatic disconnection and, 830-831 surgical technique of, 831 vs. other shunts, 829, 830, 830f vs. sclerotherapy for variceal bleeding, 836, 837t Diuretics, for ascites, 838 for lymphedema, 873 pharmacology of, 171 DNA technology, recombinant, 419 Dopamine, in postoperative thoracoabdominal aortic aneurysm repair, 478 pharmacology of, 171 Doppler equation, 247 Doppler studies. See also Ultrasound examination. early use of, 12-13 for acute arterial occlusion, 741 for Raynaud’s syndrome, 110 for venous dysfunction, 256, 846 hand-held, 860 Doppler systems, 247-249, 248f, 249f, 250f color-coded, 248, 250f for partially occluding venous thrombi, 256-257 continuous-wave, 247, 248f, 256 for venous disease diagnosis, 256, 846, 860 in duplex scanning, 248, 249 pulsed, 247, 248f velocity criteria of, 248-249, 250f for renal artery stenosis, 580, 580t, 581f waveform analysis of, for evaluation of lower extremity, 254, 254f Doppler systolic blood pressure measurements, amputation level selection and, 895, 895t, 896t in aortoiliac occlusive disease, 539 Dos Santos, vascular surgical advances of, 6-7 Double-crush syndrome, in thoracic outlet syndrome patients, 682 Drains, in rigid dressing, 918, 919f Drapanas shunt, for portal hypertension, 826 Drapes, adhesive, for prevention of prosthetic graft infections, 774 Dressings, in wound healing, 883, 883t, 884t postoperative, for Syme’s amputation, 902 rigid, for amputated stump, 916-917, 917t application techniques for, 917-921, 917f-921f for below-knee amputation, 905 soft, for amputated stump, 915, 915f Drop attacks, in vertebrobasilar system transient ischemic attacks, 631 Drug(s). See also names of specific drugs and classes of drug. for acute limb ischemia, 750t for peripheral arterial disease, 272-273 for renovascular hypertension, 584, 584t for thoracic outlet syndrome, 683 for vascular disease, 166-172 inhibition of platelet aggregation by, 71 intra-arterial administration of, extremity ischemia and, 737 thrombocytopenia due to, 74 vascular wall contraction and, endothelium and, 38 vasoactive, atherosclerosis risk and, 101 vasoconstrictive, in carotid angioplasty and stenting, 375, 377 Drug abuse, arteritis due to, 117, 118f hepatic artery aneurysms and, 526 infected femoral pseudoaneurysm and, 186 mycotic aneurysms and, 518, 520 Drug interactions, with warfarin, 81, 82t

947

Drummond, marginal arteries of, 604, 794 Dry gangrene, 893, 898 Duct(s), of Cuvier, 32 Ductus arteriosus, 27 Ductus venosus, 24, 31, 32 Duodenum, aortoenteric fistula and, 179 in inflammatory aneurysm, 504 obstruction of, in abdominal aortic aneurysm repair, 503 Duplex scanning, carotid artery, for thoracoabdominal aortic aneurysm, 475 color-coded, 249, 250f, 255 early use of, 12, 13 for acute mesenteric ischemia, 606 for arterial access, 308 for arterial mapping, 554 for carotid endarterectomy, intraoperative, 636 for erectile dysfunction, 216 for extracranial cerebrovascular disease, 632, 633 for failing vascular grafts, 740 for fibromuscular dysplasia, 129 for infrainguinal arteriosclerosis, 555 for portal hypertension, 819, 820-821 for postoperative surveillance, in carotid angioplasty and stenting, 379-380 for prosthetic graft infection, 775 for renovascular hypertension, 580, 580t, 581f for screening of renal artery stenosis, 335 for vascular malformations, 204 for vein graft surveillance, 807, 807f for venous disease, 256-257, 256f, 257f for venous dysfunction, 860-861, 860f for venous thrombosis, 846 of lower extremities, 255 technique of, 248-249, 250f Dysfibrinogenemia, 76 thrombosis and, 78 Dysplasia, fibromuscular. See Fibromuscular dysplasia. Dystrophy, reflex sympathetic, lumbar sympathectomy for, 449 thoracic outlet syndrome and, 678 thoracic sympathectomy for, 447

E EAST (elevated arm stress test), in thoracic outlet syndrome, 680 Echocardiography, for thoracoabdominal aortic aneurysm repair, 475, 480 for vascular malformations, 204 ECST, 646-647 Ectasia, aortic, 489 Eczema, definition of, 859 Edema, definition of, 859 in wound healing, 880-881, 881f lower extremity, 808-809, 809f in infrainguinal bypass surgery, 808-809, 809f vascular malformations and, 202 tissue, in reperfusion injury, 734 EEA stapler, 832, 833 Ehlers-Danlos syndrome, 123 Eicosapentaenoic acid (EPA), for intimal hyperplasia, 762 Ejaculation, dysfunctional, 799-800, 799f vs. erectile dysfunction, 217-218. See also Erectile dysfunction. Elastase, in aortic wall, aortic aneurysm formation and, 490 Elastic stockings, for venous thromboembolism prophylaxis, 82 Elastic tissue, in large elastic arteries, 36 in pseudoxanthoma elasticum, 124-125

X0183-Idx 9/26/05 01:21 PM Page 948

948

Index

Elastin, arterial, 36, 37f, 231 in aortic wall, aortic aneurysm formation and, 489-491, 490f Electroencephalography, 633, 634 Electrolyte solution, for ex vivo renovascular repair, 588, 591t Electromyography, for thoracic outlet syndrome, 680 in scalene muscle block, 681 Electrophysiologic tests, for thoracic outlet syndrome, 680 Elephantiasis, 870 Elevated arm stress test (EAST), in thoracic outlet syndrome, 680 Embolectomy, arterial injury secondary to, 749, 749f delayed, 748 for acute limb ischemia, 744-746, 744f, 745f for proximal emboli secondary to atrial fibrillation, 428 for upper extremity embolization, 689 historical aspects of, 6-7 pulmonary. See Pulmonary embolism. transvenous catheter, 851-852, 852f Embolization. See also Embolus(i). arterial, for arteriovenous fistula, 203f, 204, 206-207, 208f cardiac, postoperative thrombosis and, 788 cerebral protection against. See Cerebral protection device(s). cholesterol, renal function and, 341 distal, in abdominal aortic aneurysm endovascular repair, 386 in intra-arterial thrombolytic therapy, 436 extracranial carotid artery aneurysms and, 513 in carotid angioplasty and stenting. See Carotid angioplasty and stenting. internal iliac artery, erectile dysfunction and, 219 operative, in aortoiliac surgery, 791-792, 792f percutaneous transcatheter, for hepatic artery aneurysms, 527 for renal artery aneurysms, 532 for splenic artery aneurysms, 525 subclavian and axillary artery aneurysms and, 513, 514, 514t Embolus(i). See also Embolization. after carotid endarterectomy, 639 arterial, 734-735 lower extremity, 734, 741, 741f, 744-745, 744f, 745f upper extremity, 689, 745 black or blue toes with, 553 cardiac, 734 in cerebral ischemic events, 629 cerebral, in cerebral ischemic events, 628-629, 629f, 630f distal, multiple, 428, 430 in acute limb ischemia, 741, 741f, 742 internal carotid arterial thrombosis and, 627, 627f internal carotid artery, balloon catheter use and, 640 lower extremity, in acute limb ischemia, 741, 741f, 742 intraoperative thrombolytic therapy for, 436-438 operative management of, 744-745, 744f, 745f sites of, 734 mesenteric artery, 605, 605f, 607-608, 607f previous history of, systemic thrombolytic therapy and, 422 proximal, secondary to atrial fibrillation, 428, 431f

Embolus(i) (Continued) recurrent, 748 risk of, with ulcerated carotid artery lesions, 620 saddle, 746 upper extremity, operative management of, 689, 745 vertebral artery occlusion and, 661 vs. thrombosis, 735, 740 Embryology, of vascular system, 21-35 arteries in, 23-30, 622-623 developmental patterns in, 21-22 early stages in, 21-23 heart in, 23 new vessel growth in, 32-34, 33f-35f veins in, 30-32 Embryonic disk, 21-22, 22f Embryonic vein, persistent lateral, as vascular malformation, 199, 200f, 204f Emotional stress, Raynaud’s syndrome and, 109 Encephalopathy, in liver failure, 823, 824 Endarterectomy. See also specific types, e.g., Carotid endarterectomy. arterial wall properties in, 231 historical aspects of, 6-7 procedures for, development of, 7-8 Endoaneurysmorrhaphy, 396 of Matas, 3 Endocarditis, bacterial, arterial infections and, 179 mycotic aneurysms and, 518 Endoleak, in abdominal aortic aneurysm repair, 497 endovascular, 386-387, 386f, 387t in thoracoabdominal aortic aneurysm repair, endovascular, 483 Endoluminal treatment, 325. See also Angioplasty. Endoscopy, for prosthetic graft infection, 776 for saphenous vein harvest, wound complications and, 806 upper gastrointestinal, for portal hypertension, 820 Endotension, in abdominal aortic aneurysm endovascular repair, 387 Endothelial cell(s). See also Endothelium. as modulators of hemostasis, 69-70, 69t as recipient of human gene therapy, 766 in early atherogenesis, 93-94 permeability of in reperfusion, 733 polymorphonuclear adhesion to, in inflammatory states, 757-758 procoagulant activity of, 42, 69t, 70 radiation injury of, 625 saphenous vein, 454f, 757 seeding of, in new vascular graft materials, 461, 461t vascular, 452 glucose levels and, 149 vascular endothelial growth factor and, 199 Endothelial leukocyte adhesion molecule-1 (ELAM-1), 757, 758 Endothelial-specific angiopoietin receptor, in vascular malformations, 201 Endothelin, antagonists of, pharmacology of, 171 in Raynaud’s syndrome, 107 vasoconstricting properties of, 38 Endothelium. See also Endothelial cell(s). arterial, 452 in intimal thickening, 39, 40f, 41, 42f injury of, atherosclerosis and, 96-97 platelet activity and, 756-757 smooth muscle proliferation and, 38-39, 39f, 40f platelet activity and, 756-757

Endothelium (Continued) regulation of thrombosis by, 42-43 vascular wall thickening and, drugs regulating, 38 shear stress and, 38, 41 Endovascular repair. See also Angioplasty. acute extremity ischemia and, 737 antiplatelet agents for, 786 for aortoiliac occlusive disease, 540 for hepatic artery aneurysms, 527 for infrainguinal arteriosclerosis, 569-570 for renal artery aneurysms, 532 for splenic artery aneurysms, 525 for superior mesenteric artery aneurysms, 528 intimal hyperplasia after, 761 of abdominal aortic aneurysms, vs. open repair of, 219 of aneurysms, vs. open repair, 219 of infected aortic aneurysms, 185-186 of thoracoabdominal aortic aneurysms, 483-484 of traumatic arteriovenous fistulas, 726, 727f three rules of, 316 Endovascular stent-grafts, aortic, thrombosis of, 739 for blunt vascular trauma, 721, 722, 723 for prosthetic graft infections, 780 End-stage renal disease, vascular access for hemodialysis and, 694, 694f, 695t Energy losses, in critical arterial stenosis, 233, 233f in fluids, Bernoulli’s principle and, 226, 226f hemodynamic principles of, 225-226 in arterial stenoses, 232, 232f in arterial system, 226-228, 226f-228f inertial, 227, 227f Poiseuille’s law and, 226-227, 227f vascular resistance and, 227-228, 228f viscosity and, 226-227, 227f in lower extremity amputation, 915, 915t stenosis length and number and, 234 Enteral nutrition, in diabetics, 156-158, 156t, 157f, 158t Enzymatic débridement, for wound healing, 881-882, 881t Enzyme(s), deficiencies of, aortic aneurysm formation and, 491 for wound healing, 881 Epidermal growth factor, in acute wound healing, 877, 878 Epidermal growth factor–like protein, in smooth muscle proliferation, 38 Epinephrine, as fibrinolytic agent, 417 Episodic digital ischemia. See Raynaud’s syndrome. ePTFE grafts, 458, 459-461, 459f, 460f, 463, 464 heparin bonding to, 461 Eptifibatide, 85, 170 Equinovarus deformity, 901 Erectile dysfunction, causative factors in, 214-215, 215t cavernosal artery occlusion and, 216-217 classification of, 215, 215t definition of, 214 history and physical examination for, 215-216 in aortoiliac occlusive disease, 798-800, 799f investigation of, 214-215, 215t medical treatment for, 221f, 222 microvascular corrective procedures for, 219-220 neurologic testing of, 215, 216 neurovascular testing for, 216 postoperative, after aortoiliac reconstruction, 217-219, 217f-220f Erection, physiology of, 214

X0183-Idx 9/26/05 01:21 PM Page 949

Index

Erythrocyte sedimentation rate, in systemic giant cell arteritis, 112 Escherichia coli, in microbial arteritis, 180 in vascular graft infections, 188, 189t Esophageal transection procedures, for portal hypertension, 832-833 vs. sclerotherapy for variceal bleeding, 836 Esophageal varices, bleeding from, management of, 823-824 specific measures for, 824-825 portal hypertension and, 821-822, 822f sclerotherapy for, 835-837 transthoracic ligation of without splenectomy, 832 Estrogen-progesterone ratio, venous function and, 859 Ethanol, in sclerotherapy for vascular malformations, 207, 209 Ethnicity, diabetes risk and, 151 peripheral arterial disease and, 266 European Carotid Surgery Trial. See ECST. European Cooperative Acute Stroke Study, t-PA use in, 433 EV3 Spider cerebral protection device, 371f Excluder endograft system, for abdominal aortic aneurysm repair, 390-391, 390f, 391f Exercise, ankle-brachial index changes with, 253, 253f blood flow and blood pressure and, in leg with arterial obstruction, 236-237, 236f, 237f in normal leg, 236 diabetes risk and, 151 for arterial disease, 238 for atherosclerosis management, 98-100 for lymphedema, 873 for peripheral arterial disease, 272 for thoracic outlet syndrome, 683 in stress testing, 253, 253f vascular steal syndrome and, 237-238 venous blood pressure during, 241, 241f Expanded polytetrafluoroethylene (ePTFE) grafts, 458, 459-461, 459f, 460f, 463, 464 heparin bonding to, 461 Extra-anatomic bypass procedures, for abdominal aortic aneurysm repair, 499 for infected aortobifemoral graft, 778-779, 779f, 780f for subclavian steal syndrome, 661 historical aspects of, 10 vascular grafts for, current recommendations for, 464 Extracellular matrix, in wound healing, 878 Extracranial cerebrovascular disease, 617-651. See also Stroke; Transient ischemic attacks. alternatives to surgical therapy for, 647-649 asymptomatic, 630 clinical trials of, 645-646 natural history of, 619-620 vascular laboratory tests of, 632 clinical syndromes of, 630-632 controversial topics in, 649-651 diagnosis of, angiography in, 632-633 brain scans in, 632-633 vascular laboratory tests in, 632 historical aspects of, 9-10, 617-618 medical therapy for, 647-649 mortality of, 618-619 natural history of, 618-621 pathology of, 621-626 aneurysms in, 623 atherosclerosis in, 621-622, 621f, 622f carotid body tumors in, 626 cerebral infarction and, 626-629

Extracranial cerebrovascular disease (Continued) coils and kinks in, 622-623, 624f fibromuscular dysplasia in, 622 radiation therapy injury in, 625, 625f recurrent carotid stenosis in, 625-626 Takayasu’s arteritis in, 623-625 transient ischemic attacks and, 626-629 postoperative care for, 638 prospective randomized trials of, 644-647 surgical treatment of, 633-638 anesthesia for, 633-634 carotid bifurcation endarterectomy in, 633f, 634-636, 636f carotid body tumor resection in, 638 complications after, 638-642 correction of kinking in, 637, 637f external carotid artery endarterectomy in, 637, 638f hemodynamic monitoring in, 633-634 internal carotid artery dilatation in, 636, 637f results of, 642-644, 643t symptomatic, categories of, 630 clinical trials of, 646-647 natural history of, 621 noninvasive testing of, 632, 633 vascular laboratory tests of, 632, 633 Extracranial-to-intracranial bypass grafting, for stroke prevention, 651 Extremity. See also Arteriosclerosis, infrainguinal; Foot; Infrainguinal occlusive disease. lower, amputation of. See Amputation, lower extremity. arterial flow patterns in, 234-238 embryologic development of, 29-30 normal, 236 obstructed, 236-237, 236f, 237f pulses and waveforms in, 235-230 vascular resistance and, 235 vascular steal and, 237-238 arteries of, bacterial colonization of, 191 catheterization of, 314 diabetes and, 144 infections of, 186-187 injuries of, 724 noninvasive studies of, 252-256 relationships of, 64, 64f bridge arteriovenous fistulas in, 699, 699f chronic ischemia of, 269 amputation and, 269 epidemiology of, 263-264 natural history of, 267-269 nonoperative treatment of, 269-274 risk factors for, 265-267 compartment syndrome in, 130-131, 131f critical limb ischemia of, 268-269. See also Acute limb ischemia. edema of, 808-809, 809f in infrainguinal bypass surgery, 808-809, 809f embolus of, 734-735 in acute limb ischemia, 741, 741f, 742 intraoperative thrombolytic therapy for, 436-438 sites of, 734 surgical management of, 744-745, 744f, 745f examination of, for arterial access site, 303, 305t for infrainguinal arterial disease, 553-554 in Buerger’s disease, 122 in lymphedema, 870, 870f, 871f intermittent claudication in, 263, 552-553. See also Peripheral arterial disease.

949

Extremity (Continued) ischemia of. See Acute limb ischemia; Limb ischemia. magnetic resonance angiography of, 283, 287, 288f-290f, 292f open wounds of, vascular graft infection and, 191 overgrowth of, vascular malformations and, 202, 204, 207f pain in, venous dysfunction and, 860 pulses of, 235-236, 235f examination of, 554 normal, 236-237, 236f, 237f rest pain in, vs. ischemic rest pain, 551-552 segmental pressure measurement of, 204, 206f, 252-253 subcutaneous compartments of, 858f thrombosis of, 735-738 veins of, anatomic terminology of, 858-859, 858f, 859t below-knee, 239, 243 deep, 294 disease of, 858-859 in varicose veins, 859 reflux in, 257-258, 258f superficial, 859 venous disease of, noninvasive diagnosis of, 256-259 upper. See also Arm(s); Hand. arterial access site on, 303, 305t arterial infections of, 187 arteries of, 29-30, 29f, 144 bridge arteriovenous fistulas in, 699, 699f exercise of, in thoracic outlet syndrome, 679 giant cell arteritis of, 689, 690f ischemia of, 689 in supra-aortic trunk occlusion, 660 in thoracic outlet syndrome, 678-679 magnetic resonance venography of, 287, 292f pain in, in thoracic outlet syndrome, 678 provocative clinical tests of, for thoracic outlet syndrome, 679-680 Raynaud’s disease of, 690 vascular disease of, 688-690 Extrinsic compression syndrome of celiac axis, 10 Exudate, in wound healing, 878, 883 Ezetimibe, for atherosclerosis, 99

F Fabrics, in arterial graft development, 4-5 Facial nerve, in carotid endarterectomy, cervical branch of, 641 mandibular ramus of, 46, 47t marginal mandibular branch of, 640f, 641 Facial vein, in carotid endarterectomy, 46, 635 Factor II deficiency, replacement therapy for, 76 Factor IX deficiency, in hemophilia B, 75, 76 Factor V, endothelial cell–derived, 69t, 70 Leiden mutation of, 77, 845 Factor VII deficiency, 76 Factor VIII, concentrates of, for von Willebrand’s disease, 75 deficiency of, in hemophilia A, 75, 76 Factor X, deficiency of, 76 inhibitors of, 168 Factor XI, abnormal, venous thrombosis and, 78 Factor XII, in fibrinolysis, 415 Factor XIIIa, 415 False aneurysm(s). See also Pseudoaneurysm(s). anastomotic, 800-801 causes and repair of, 800-801 of carotid artery, 623

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950

Index

False aneurysm(s) (Continued) of hepatic artery, 526 of renal artery, 532-533, 532f postoperative thrombosis and, 788 recognition of, 800 retroperitoneal, 800 traumatic, 724-726, 725f-727f Family history, diabetes risk and, 151 Fasciotomy, complications of, 747-748 for compartment syndrome, 130 technique of, 747, 747f Fasting, insulin dose requirements and, 156, 156t Fatty streaks, in early atherogenesis, 92-93, 93f FDA, endograft devices approved by, for abdominal aortic aneurysm repair, 388-392, 389f, 390f, 391f, 392f growth factors approved by, for wound healing, 883, 884 regulation of urokinase use by, 419 thrombolytic agents approved for pulmonary embolism by, 424 Female sexual dysfunction, 214, 216, 218 Femoral artery, aneurysms of, mycotic, 520 nonmycotic, 513, 514, 515, 516, 517 recurrent anastomotic, 801 rupture of, 513 bifurcation of, infected pseudoaneurysm of, 186 common, access to, in abdominal aortic aneurysm endovascular repair, 385 aneurysms of, 513 exposure of, 62 in bridge arteriovenous fistula, 699, 699f pulseless, puncture of, 308-309, 309f puncture of, 303, 304f, 305t, 308-309, 309f antegrade, 307-308, 307f, 308f retrograde, 306-307, 307f reconstruction of, for aortoiliac occlusive disease, 545-546, 545f deep, aneurysms of, repair of, 516-517 direct approach to, 561-562, 561f, 562f exposure of, 62, 62f in aortofemoral bypass graft, 540 in aortoiliac occlusive disease, 537 in extra-anatomic bypass of infected aortobifemoral graft, 778, 779 wounds of, 715 distal, reconstruction of, 8 embolectomy in, 744-745, 744f embryologic development of, 29f, 30 for endovascular approaches to infrainguinal disease, 344, 344t for groin access to renal artery lesions, 335, 336f, 338f in abdominal aortic aneurysm endovascular repair, 384, 385 infections of, 186-187 injuries of, 724 popliteal artery development and, 127 pulse in, ischemic foot lesions and, 554 superficial, aneurysms of, 513 angioplasty of, 350f, 563 catheterization of, 349f in aortoiliac occlusive disease, 537 in extra-anatomic bypass of infected aortobifemoral graft, 778, 779 occlusive lesion of, vascular steal and, 237 persistent sciatic artery and, 126-127 stent placement in, 348, 351f thrombosis in, 735 Femoral occlusive disease. See Arteriosclerosis, infrainguinal; Infrainguinal occlusive disease. Femoral vein, common, duplex scanning of, 257 superficial, anatomic relationships of, 858

Femoral vein (Continued) cryopreserved venous allografts of, 456 duplex scanning of, 257 for revascularization of aortoiliac system, 778 ligation of, 11 proximal, valvular competence of, 244 Femorofemoral bypass, 10 for aortoiliac occlusive disease, 545-546, 545f with transluminal angioplasty, erectile dysfunction and, 219, 220f Femorofemoral crossover graft, for direct venous reconstruction, 865-866 Femoroinfrapopliteal bypass, noninfectious complications of, 802-806 Femoropopliteal artery, balloon angioplasty of, 349, 350t, 351t stent placement in, 351-352, 351t Femoropopliteal bypass, above-knee to below-knee, for femoral and popliteal artery aneurysm repair, 517 below-knee, ePTFE grafts for, 460 for limb salvage, results of, 565-566, 566f, 567f surgical criteria for, 555 infection of, 779-780 noninfectious complications of, 802-806 Femoropopliteal graft(s), distal anastomosis of, 804, 804f occluded, thrombolytic therapy for, 790-791 proximal anastomosis of, 804, 805f thrombosis of, 802, 802f, 804, 804f management of, 804-806, 804f, 805f postoperative, 803 surveillance of, 803 Femoropopliteal lesions. See also Infrainguinal occlusive disease. aortoiliac occlusive disease with, 537, 543 axillofemoral bypass graft for, 546-547 classification of, 343t subintimal angioplasty and stenting of, 352 Femorosaphenous bridge fistula, 700 Fenoldopam, pharmacology of, 171 Ferritin levels, atherosclerosis risk and, 100-101 Fibers, muscle, thoracic outlet syndrome and, 678 Fibrillin, in Marfan’s syndrome, 122 Fibrin, arterial intimal deposition of, in atherogenesis, 95-96 fibrinolytic agents specific for, bleeding complications with, 419-422 X fragments and, 415 in acute wound healing, 878 in fibrinolysis, 414 thrombus-bound, tissue plasminogen activator affinity for, 419 Fibrin degradation products, fibrin-specific agent therapy and, 421 in intra-arterial thrombolytic therapy, 434 Fibrin glue, in thoracoabdominal aortic aneurysm repair, 478 Fibrinogen, abnormal, thrombosis and, 78 composition of, 415 congenital disorders of, 76 in diabetes, 149 in intra-arterial thrombolytic therapy, 434, 435 in peripheral arterial disease, 266 in thrombolytic therapy, 426 tissue plasminogen activator activity and, 419 Fibrinolysis, 414 abnormal, thrombosis and, 78 congenital disorders of, 76 in hemostasis, 72-73 in thoracoabdominal aortic aneurysm repair, aortic supraceliac clamping and, 482

Fibrinolysis (Continued) mechanisms of, 73 postoperative bleeding and, 785 Fibrinolytic agents, for acute limb ischemia, 891 for thrombosis of vascular access fistula, 703 for venous thrombosis, 848-849 Fibrinolytic system, agents activating, 416-417 biologic functions of, 416 in intimal hyperplasia, 759-760 in venous thrombosis, 845 thrombolytic therapy and, 414-416, 415f Fibroblast(s), in acute wound healing, 878 Fibroblast growth factor, basic, in intimal hyperplasia, 759, 765 intimal proliferation and, 757 smooth muscle cell proliferation and, 40, 41, 42f in acute wound healing, 877, 878 Fibrocollagenous tubes, for modification of vascular grafts, 462 Fibrodysplasia, medial, of renal artery, 523 renal artery aneurysms and, 530, 531f splenic artery aneurysms and, 523 Fibromuscular bands, congenital, in thoracic outlet syndrome, 676-677 Fibromuscular dysplasia, 128-129, 129f carotid artery, 636, 637f extracranial cerebrovascular disease and, 622 histologic types of, 622 in children, after renal artery reconstruction, 595, 596f percutaneous transluminal angioplasty for, 598 renal artery, 576, 577f renal artery stenosis with, ex vivo reconstruction for, 587-588 Fibronectin, in acute wound healing, 878 Fibroplasia, medial, 622 of renal artery, 576, 577f myointimal, 625 types of, 622 Fibrosis, of portal venules, intrahepatic presinusoidal obstructive portal hypertension and, 817 retroperitoneal, ureteral obstruction with, 797-798, 798f Filaria, lymphedema due to, 869 Film dressings, in wound healing, 883, 884t Finger(s), in Buerger’s disease, 121-122 in Raynaud’s syndrome, 107-111, 108f Fingertip gangrene, 689 Fistula(s), aortocaval, in abdominal aortic aneurysm repair, 505 aortoduodenal, infected, graft excision and, 777 in situ reconstruction of, 185 with aortofemoral bypass grafts, 541 aortoenteric, 179, 774, 774f extra-anatomic bypass and, 10 false aneurysms and, 800 gastrointestinal endoscopy for, 776 in aortofemoral bypass grafts, 540-541 infected, graft excision and, 777 prevention of, 540-541 arteriovenous. See Arteriovenous fistula(s). Brescia-Cimino, 696-697, 696f, 697f arterial insufficiency and, 704 in children, 701 venous hypertension and, 704-705, 705f bridge arteriovenoous. See Bridge arteriovenous fistulas. carotid-cavernous sinus, after carotid endarterectomy, 640 loop, for hemodialysis access, 699-700 Flank approach, left, for renal and visceral arteries, 55-57, 56f, 57f right, for renal artery, 57, 57f

X0183-Idx 9/26/05 01:21 PM Page 951

Index

Flex-Foot, 921, 923 Flexion contractures, in lower extremity amputation, 912 Flora, in vascular graft infection, 190 Fluid(s), for ascites management, 838 in lymphedema, removal of, 872 intravenous, for severe hemorrhage, 824, 837 lymph, 869 replacement of, in vascular trauma patients, 717 Fluid energy, in arteries, hemodynamic principles of, 225-226 losses in, 226-228, 226f-228f, 232, 232f Fluorescein, skin, amputation level selection and, 895-896, 895t, 896t Fluoroquinolones, prophylactic, for vascular reconstruction procedures, 194 Fluoroscopy, intraoperative, for infrainguinal arteriosclerosis, 570 magnetic resonance, 281 Fluoxetine, in smoking cessation programs, 270 Foam cells, in fatty streak lesions, 92, 93, 93f Foam dressings, in wound healing, 883, 884t Foam sclerosants, for venous ablation, 209, 862, 864, 864f, 865f Fogarty catheter, 702, 750, 789 in embolectomy for acute limb ischemia, 744, 744f size of, 744 Folate therapy, atherosclerosis risk and, 101 for homocystinuria, 133 Fondaparinux, 83 pharmacology of, 168 Food, insulin requirements and, in diabetics, 158, 160 Food and Drug Administration. See FDA. “Food fear,” 608 Foot. See also Extremity, lower; Forefoot; Limb salvage. amputation of, foot-sparing, 901 guillotine, 893-894, 893f prostheses for, 921-922, 921f transmetatarsal, 900-901, 900f arteries of, exposure of, 65-66, 65f, 66f in limb salvage bypass procedures, 560, 561f diabetic, instructions for patients with, 913, 913f small vessel disease in, 145 fasciotomy of, 747 in lymphedema, 870, 870f infections of, vascular graft infections of lower extremity and, 191 ischemic lesions of, from operative embolization, 791, 792f lesions of, in limb salvage bypass procedures, 561 venous ulcers of, vs. arterial or ischemic ulcers, 553 Foramen ovale, 24-25, 27 Foramen secundum, 24, 26f Forearm, aneurysms of, mycotic, 520 nonmycotic, 512, 513, 514, 516, 517 bridge arteriovenous fistulas in, 699 pain in, in thoracic outlet syndrome, 678 veins in, in reverse arteriovenous fistula, 697-698 Forefoot, amputation of, selection criteria for, 895t transmetatarsal, 900-901, 900f Formulas, tube feeding, for diabetics, 156-158, 157f Fractures, thrombosis due to, 736, 737f Free radical scavengers. See Oxygen free radicals. Freezing, for preservation of arterial and venous allografts and homografts, 4, 456

Fresh frozen plasma, 426 Frozen section, arterial wall, 182 Fungal arteritis, 179 Furosemide, in postoperative thoracoabdominal aortic aneurysm repair, 478 F-wave responses, in thoracic outlet syndrome, 680

G Gabapentin, for pain in amputees, 910 Gadolinium, as alternative to renal angiography, 582 in contrast agents, in magnetic resonance angiography, 281, 282, 287 Gait, disturbed, in vertebrobasilar transient ischemic attacks, 631 Gallium 67, white blood cell scanning with, 775-776 Gallstones, in abdominal aortic aneurysm repair, 505 Ganglion (ganglia), paravertebral and prevertebral, 444, 444f stellate, 444, 444f, 445, 446f Gangrene, ankle or toe, diagnosis of, 553 in limb salvage bypass procedures, 561 arterial occlusion and, 2, 6 dry, 893, 898 infection with, lower extremity amputation for, 893-894, 893f of fingers, 689 in Buerger’s disease, 121-122 paradoxical, lumbar sympathectomy and, 449 skin, in trash foot syndrome, 791, 792f Gastric artery, aneurysms of, 524t, 526t, 528-529 left, anatomy of, 603-604, 604f Gastric lavage, for acute hemorrhage in portal hypertension, 824 Gastrocnemius muscle, in popliteal artery exposure, 63, 63f in popliteal entrapment syndrome, 127-128, 127f, 128f Gastroduodenal artery, aneurysms of, 524t, 526t, 529-530, 530f Gastroepiploic artery, aneurysms of, 524t, 526t, 528-529 Gastrointestinal complications, in abdominal aortic aneurysm repair, 503 Gastrointestinal tract, bleeding into, protein and gut lavage for, 824 endoscopy of, for portal hypertension, 820 for prosthetic graft infection, 776 flora of, 190 Gee ocular pneumoplethysmography, 515 Gemfibrozil, for atherosclerosis, 98 Gender, peripheral arterial disease and, 265-266 Genetic factors, in aortic aneurysm formation, 491 in diabetes, 141 in vascular malformations, 201 Gestational diabetes, 151 Giant cell arteritis, 624-625 ischemic optic neuropathy and, 631 of upper extremity, 689, 690f systemic, 112-113, 112t, 113f Takayasu’s disease and, 112t, 113-114, 114f Gianturco-Z stent, 326 Glanzmann’s thrombasthenia, platelet disorders in, 75 Gliburide, 160 Glidecath, 314 for endovascular approach to infrainguinal disease, 346

951

Glidewires, 312 angled and straight, 312 difference between 0.035-inch and 0.038-inch, 360, 362f in angioplasty and stenting of renal lesions, 335 in carotid angioplasty and stenting, 360, 362f in sheath placement in ECA, 364, 365, 365f, 366f in endovascular approach to infrainguinal disease, 345, 346, 348 Glipizide, 160 Glomerular filtration rate, renal revascularization and, 592, 593f Glossopharyngeal nerve, embryologic, 28 in carotid endarterectomy, 640f, 641 Glucocorticoids, immunosuppressive, for intimal hyperplasia, 763 Glucose, aldehyde form of, in early Maillard reaction, 147-148 cardiovascular disease and, interventional studies of, 145-147, 145t fasting, target goals for, 100 in diabetics, frequency of monitoring of, 152, 154f impaired tolerance to, 150 in hospital, 152-156 in surgical procedures, 151-160 in vascular disease, 145-146, 145t, 147150, 147t, 148t vascular endothelial cell function and, 149 plasma, amputation risk and, 913 stroke outcome and, 142, 144 Glucose toxicity hypothesis, 145, 145t, 147, 147t Glue, N-butyl cyanoacrylate, in abdominal aortic aneurysm endovascular repair, 387 Glumovenous malformations, 201 Glu-plasminogen, in fibrinolysis, 414, 415 Glutaraldehyde, in human umbilical vein allografts, 456 Glycation, nonenzymatic, in diabetes pathophysiology, 147-148, 148t Glycoprotein IIb/IIIa inhibitors, for arterial thromboembolism prevention, 85 for carotid angioplasty and stenting, 359 for diabetes, 149 for intimal hyperplasia, 763 for stroke prevention, 85 intraoperative bleeding and, 786 peripheral arterial disease and, 271-272 pharmacology of, 169-170 Glycoprotein receptors, in diabetics, 148 Glycosylation reactions, vascular disease in diabetics and, 147, 147t Gore-Tex, in arterial grafts, 5 in thoracoabdominal aortic aneurysm repair, 478 Gosling dumping factor, 254 Gott shunt, for thoracoabdominal aortic aneurysm repair, 475 Graft(s), antibiotic-impregnated, for arterial infections, 185 aortobifemoral. See Aortobifemoral bypass graft. aortofemoral bypass. See Aortofemoral bypass graft. aortoiliac, infections of, 777-778, 778f thrombosis of, 786-791, 787f arterial, acute occlusion of, thrombolytic therapy for, 430-431 autologous, 184, 455-456 development of, 4-5 failures of, causes of, 738-739 clinical manifestations of, 739 evaluation of, 741-742

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952

Index

Graft(s) (Continued) treatment of, 742-748, 750-751 in arterial reconstructions, 184 porosity of, 5 autogenous, arterial, 184, 455-456 failure of, 738 revision or replacement of, 746 thrombectomy of, 746 autogenous vein, 452, 454-455, 454f intimal hyperplasia of, 755 occlusion of, angioplasty for, 746 thrombolytic therapy for, 430, 431 thrombectomy of, 746 basilic vein, for infrainguinal bypass procedures, 558 bifurcation, development of, 7 for abdominal aortic aneurysm repair, 6 for arterial lesions, hemodynamic analysis of, 238 bioengineered, 462-463, 463f bioresorbable polymeric, 462 bypass. See Bypass graft(s). cephalic vein, for infrainguinal bypass procedures, 558 composition of, 383, 453t for abdominal aortic aneurysm repair, 501 for arterial reconstructions, 184 for limb salvage procedures, 556-558 new developments in, 461-463, 461t Dacron. See Dacron graft(s). endarterial, 8 endovascular, for infrainguinal arteriosclerosis, 569-570 failure of, causes of, 738-739 clinical manifestations of, 739 detection and correction of, 563, 740 evaluation of, 741-742 treatment of, 742-748, 750-751 femorofemoral crossover, 865-866 fixation of, 383 by photodynamic techniques, 462 for abdominal aortic aneurysm endovascular repair, 385-386, 388-392, 389f-392f, 396 design of, 383, 384f failure of, 388 kinking of, 387 migration of, 387 future concepts in, 461-463, 461t hemodialysis access, 698-700, 701f, 702f current recommendations for, 464 thromboses of, thrombolytic therapy for, 433 infections of, 183-184 bacteriology of, 188-189, 189t clinical investigations of, 191-193 clinical significance of, 187-188, 188t complications of, 187 experimental investigations of, 191 incidence of, 187, 188t mortality of, 187, 188t pathogenesis of, 189-191, 190t prophylactic antibiotic therapy for, 187-195 infrainguinal bypass. See also Infrainguinal bypass procedures. autogenous vein for, 455 dilatation of, 807-808, 808f intimal hyperplasia after, 761 patency of, warfarin use and, 85, 167 infrapopliteal bypass, autogenous vein for, 455 interposition, for femoral and popliteal artery aneurysm repair, 516, 517 for forearm and hand aneurysm repair, 516 for subclavian artery aneurysm repair, 516

Graft(s) (Continued) intimal hyperplasia of, 455, 756, 760-761, 760f, 761f occlusion of, aspirin dosage and, 84 clinical manifestations of, 740 evaluation of, 741-742 results of treatment for, 750-751 revision or replacement of, 746-747 surgical management of, 744-748, 744f, 745f, 747f thrombectomy of, 746 thrombolytic therapy for, 430-431, 742-744, 742f, 743f treatment of, 742-748 of bovine origin, 5, 457 of irradiated arteries, 114-115 patency of, aspirin dosage for, 84 warfarin use and, 85, 167 polyurethane, 462 prosthetic. See Prosthetic graft(s). PTFE. See PTFE graft(s). saphenous vein. See Saphenous vein(s), grafts of. surveillance of, in infrainguinal bypass surgery, 806-809 noninvasive techniques for, 255-256 thrombosis of. See also Thrombosis. salvage of, 561-562, 561f, 562f, 566-568, 567f umbilical vein, dilatation of, 808 for distal femoral reconstruction, 8 vs. PTFE grafts, 557 Vantage, 459 vascular, 452-464 comparison of, 452, 453t complications of, 455 current recommendations for, 463-464 vein. See Vein graft(s). Graft-enteric fistula, 774, 774f Gram stain, intraoperative, 182 Granules, platelet, 71, 622 disorders of, 75 Great auricular nerve, in carotid endarterectomy, 46, 47t, 641 Great radicular artery of Adamkiewicz, injury or embolization of, 797 Great vessels, in carotid angioplasty and stenting, 363t injuries of, 715-716, 715t repair of, 722, 722f Greenfield filter, 848, 849, 849f, 850, 853 Griesinger 5-way foot, 921 Griffith’s point, bowel ischemia and, 794, 794f Groin, anastomoses at, false aneurysms and, 800 complications of, in abdominal aortic aneurysm endovascular repair, 386 incisions of, vascular graft infection and, 190 mycotic aneurysms of, 519, 519f, 520 prosthetic graft infections and, 773 Groshong catheter, 707 Growth factor(s), in smooth muscle, 38-42 in wound healing, 877, 878, 883-884 smooth muscle, atheromatous plaque development and, 622 Growth factor inhibitors, for intimal hyperplasia, 764-765 Growth factors, of vascular wall, in intimal hyperplasia, 759 trauma-induced, atherosclerosis and, 96-97 Guanylate cyclase, endothelial-dependent arterial relaxation and, 38 Guard-Wire, 371f in carotid angioplasty and stenting, 368, 372f, 372t Guidant AccuLink, 356, 371f, 372, 376f

Guidant Ancure endograft system, for abdominal aortic aneurysm repair, 388-389, 389f Guidewire(s), characteristics of, 305-306 coatings of, 305-306, 312 design characteristics of, 311-312 in angioplasty and stenting of renal lesions, 335, 336, 337f, 338f in carotid angioplasty and stenting, 360 in endovascular approach to infrainguinal disease, 344, 345-348, 345t, 346f, 348t selection of, 312, 313t Guillotine amputation, 893-894, 893f Gunshot wounds, vascular damage with, 713-714, 714f, 716, 718, 719 Gunther tulip filter, 850

H Halo effect, in inflammatory aneurysm, 504 Halsted, W.S., 3 Hand, aneurysms of, mycotic, 520 nonmycotic, 512, 513, 514, 516, 517 ischemia of, with radial artery line, 737 pain in, in thoracic outlet syndrome, 678 Hand warming, for Raynaud’s syndrome, 110 Hand-assist device, 403-404, 403f, 404f Hand-assisted laparoscopic surgery, for aortic disease, 403-404, 403f, 404f, 407, 407t, 411 HandPort, 403, 403f Harmonic scalpel, 447 Headache, after carotid endarterectomy, 642 in thoracic outlet syndrome, 678 Headhunter catheter, 360, 360f, 361t Heart. See also Myocardial infarction. embolization in, postoperative thrombosis and, 788 embryologic development of, 22, 22f, 23, 24-27, 26f, 27f functional problems of, 23 evaluation of, in abdominal aortic aneurysm repair, 498 in infrainguinal arteriosclerosis, 554 in thoracoabdominal aortic aneurysm, 475 in thoracoabdominal aortic aneurysm repair, 480 Heart disease, valvular, systemic thrombolytic therapy and, 422 Hemangiomas, vs. vascular malformations, 198 Hematoma(s), cervical, in carotid endarterectomy, 642 in vascular access thrombosis, 702 in vascular trauma patients, 718 pelvic, 728 retroperitoneal, emergency exposure for, 60-61, 61f stump, 911 Hematoporphyrin-II, for intimal hyperplasia, 766 Hematuria, renovascular injury and, 723 Hemobilia, from hepatic artery aneurysms, 527 Hemochromatosis, portal hypertension and, 818 Hemodialysis, arteriovenous fistulas for, autogenous, 696-698, 696f, 697f bridge, 698-700, 701f, 702f vascular access for, complications of, 701-706 in children, 701 short-term, 694-696, 695f vascular grafts for, 698-700, 701f, 702f current recommendations for, 464 thrombosed, thrombolytic therapy for, 433 Hemodynamic factors, in aortic aneurysm formation, 491 in carotid angioplasty and stenting, 375, 377

X0183-Idx 9/26/05 01:21 PM Page 953

Index

Hemodynamic factors (Continued) in carotid bifurcation, plaque formation and, 621, 621f, 622f in intimal hyperplasia, 756 in vascular access for hemodialysis, 704-705, 705f Hemodynamic monitoring, in surgery for extracranial cerebrovascular disease, 633-634 Hemodynamic principles, 225-244 in arterial system, 225-232 in human limbs, 234-238 resistance in, 227-228, 228f treatment of disease and, 238-239 with stenosis, 232-234 in venous system, 239-243 treatment of disease and, 243-244 Hemodynamic stability/instability, in postoperative thoracoabdominal aortic aneurysm repair, 478 in pulmonary embolism, 424 Hemoglobin A1, amputation risk and, 913 in glycosylation reaction, 147 Hemophilia A, 75 Hemophilia B, 76 Hemorrhage. See also Bleeding. in abdominal aortic aneurysm repair, 502 in infected arterial wall, 183 in portal hypertension, management of, 823-824 specific measures for, 824-825 in thoracoabdominal aortic aneurysm repair, 482-483 intestinal, from splenic artery aneurysms, 524-525 into atheromatous plaque in carotid bifurcation, 622 intracranial, systemic thrombolytic therapy and, 422 Hemostasis, 69-76 coagulation disorders and, 75-76 components of, 69-73 in acute wounds, 877 in thoracoabdominal aortic aneurysm repair, 477-478, 482 platelet disorders and, 73-75 preoperative evaluation for, 73 primary, 71 secondary, 71 Henoch-Schönlein purpura, vasculitis with, 119 Heparan sulfate, endothelial cell–derived, 42, 69, 69t Heparin, adverse reactions to, 166-167 antibodies associated with, 79 antidote to, 167 bonding of, to ePTFE vascular grafts, 461 clinical uses of, 166 for abdominal aortic aneurysm repair, 501 for acute arterial occlusion, 740-741 for acute limb ischemia, 748, 891 for antithrombin III deficiency, 78 for arterial emboli, early surgery for, 6-7 for carotid angioplasty and stenting, 359, 362 for deep venous thrombosis, 424 for disseminated intravascular coagulation, 77 for hemodialysis, 696 for hypercoagulable condition, 739 for intimal hyperplasia, 765 for limb salvage bypass procedures, 560 for neonatal aortic thrombosis, 751-752 for protein C and protein S deficiencies, 78 for pulmonary embolism, 423, 424 for renovascular disease surgery, 584 for thoracoabdominal aortic aneurysm repair, 483

Heparin (Continued) for thrombolytic therapy, 435, 438, 743 for upper extremity embolization, 689 for venous thromboembolism prophylaxis, 83 for venous thrombosis, 847, 848 hypersensitivity to, 848 limitations in use of, 166, 168 low-molecular-weight, administration and dose of, 80 adverse reactions to, 167 clinical uses of, 167 for disseminated intravascular coagulation, 77 for established thrombosis, 80 for venous thromboembolism prophylaxis, 83 for venous thrombosis, 847, 848 pharmacology of, 167 structure and mechanism of action of, 167 vs. fondaparinux, 83 vs. unfractionated heparin in high-risk surgical patients, 83 vs. warfarin, 83 mechanism of action of, 166 metabolism of, 80 pharmacology of, 166-167 structure of, 166 thrombophilia screening and, 79-80 tubing coated with, 483 unfractionated, administration and dose of, 80 for established thrombosis, 80 for venous thromboembolism prophylaxis, 83 Heparin cofactor II, 73 Heparin-induced thrombocytopenia, 79, 166-167, 848 treatment of, 81 Heparin-induced thrombosis, 735, 739, 741, 787 Heparinoids, for established thrombosis, 80 Hepatic artery, anatomy of, 603, 604f aneurysms of, 524t, 526-527, 527f rupture of, 526-527, 526t common, anastomosis to, 614 Hepatic disease, bleeding disorders and, 73, 75, 76 portal hypertension and, 819 protein C and protein S deficiencies and, 78 systemic thrombolytic therapy and, 422 Hepatic vein, thrombosis of, 853 portal hypertension and, 818 wedge pressure of, 819, 821, 821f Hepatic wedge angiogram, 821, 821f Hepatitis, acute, portal hypertension and, 820 Hepatorenal bypass, for renal artery reconstruction, 586-587, 590f Hepatorenal syndrome, 838 transjugular intrahepatic portosystemic shunting and, 834 Hereditary hemorrhagic telangiectasia syndrome, 201, 205t Hernia, abdominal wall, 801 Heta-starch, bleeding disorders and, 73 Heterografts, bovine, 5 Hexachlorophene, vascular graft infection and, 190 H-grafts, 828 Hickman central venous catheter, placement of, 706, 707f, 708, 708f Hip disarticulation, 909-910, 909f prosthetic components for, 922 Hirudin, for thrombosis, 80-81 pharmacology of, 168 Homocysteine, abnormal accumulation of, 132-133 atherosclerosis risk and, 101

953

Homocysteine (Continued) forms of, 132 function of, 132 plasma levels of, 132, 133 peripheral arterial disease and, 266 Homocysteine methyltransferase deficiency, in homocystinuria, 132 Homocysteinemia, 79 Homocystinuria, 132-133 Homograft(s), arterial, 4-5, 7. See also Prosthetic graft(s). Homonymous hemianopsia, in carotid artery transient ischemic attacks, 631 Hormones, in fibromuscular dysplasia, 622 venous function and, 859 Horner’s syndrome, 444 acute dissection of carotid artery and, 623 extracranial carotid artery aneurysms and, 513 postoperative, from vertebral artery reconstruction, 673 thoracic sympathectomy and, 447, 448 Horseshoe kidney, 29 in abdominal aortic aneurysm repair, 505 Hufnagel, arterial homografts of, 4 Human umbilical vein grafts, 456-457, 457f, 463, 702 Hunter, John, 1, 2 Hunter, William, 1, 2 Hyaline necrosis, in portal hypertension, 820 Hydration, intravenous, in renal angiography, 582 Hydrocolloid dressings, in wound healing, 883, 884t Hydrodynamic reflux, venous hypertension and, 859 Hydrofiber dressings, in wound healing, 883, 884t Hydrogel dressings, in wound healing, 883, 884t Hydronephrosis, 798 Hydrophilic coatings, of catheters, 305-306, 314, 317 of guidewires, 305-306, 312 Hydrostatic indifferent point (HIP), 240, 240f Hydrostatic pressure, in upright “dead man,” 240, 240f venous hypertension and, 859 Hydrostatic reflux, venous hypertension and, 859 Hyperbaric therapy, in wound healing, 884-885, 885f Hypercholesterolemia, in atherogenesis, 95 Hypercoagulability, in arterial thrombosis, 735 in prosthetic graft failure, 739 in venous thrombosis, 845, 847 Hyperemia, reactive, in stress testing, 253 Hyperextension injury, in thoracic outlet syndrome, 677 vascular trauma with, 720, 720f Hyperfibrinolytic state, congenital, 76 Hyperglycemia, in large vessel disease, in women, 142 platelets in, 148-149 vascular disease and, 147, 147t, 148-150 prognosis for, 143 risk factors for, 150-151 Hyperhidrosis, thoracic sympathectomy for, 447, 448 Hyperhomocysteinemia, 79 intimal hyperplasia and, 455 peripheral arterial disease and, 266, 271 Hyperinsulinemia, atherosclerosis and, 100, 150 Hyperkalemia, after revascularization of ischemic extremity, 749

X0183-Idx 9/26/05 01:21 PM Page 954

954

Index

Hyperlipidemia, drug therapy for, 98-99 in atherogenesis, 95 in diabetics, 149-150 peripheral arterial disease and, 266, 271 Hypersensitivity vasculitis, 119 Hypersplenism, in portal hypertension, 820 Hypertension, abdominal coarctation and, 125, 126 after carotid endarterectomy, 639 aneurysm rupture and, 495 aortic aneurysm enlargement and, 491 atherosclerosis management and, 99 carotid aneurysms and, cerebrovascular disease and, 623 essential, vs. renovascular hypertension, 579 in carotid angioplasty and stenting, 379 medically induced, 238 peripheral arterial disease and, 271 portal. See Portal hypertension. renal artery aneurysms and, 532 renovascular. See Renovascular hypertension. renovascular disease and, 575. See also Renovascular hypertension. Takayasu’s disease and, 113-114 venous, pathogenesis of, 859 Hypogastric artery, bowel ischemia and, 794, 794f, 796 erectile function and, 799 in abdominal aortic aneurysm repair, 384, 385, 500 Hypoglossal nerve, in carotid endarterectomy, 46, 47t, 635, 635f, 640, 640f Hypoglycemia, in diabetics in hospital, prevention of, 155, 155t in diabetics outside hospital, 160-161, 160t Hypotension, in abdominal aortic aneurysm repair, with anesthesia induction, 502 with declamping, 501, 502 in aortoiliac reconstruction, with declamping, 792 in carotid endarterectomy, 639 in thoracoabdominal aortic aneurysm repair, with reperfusion, 477 orthostatic, vertebrobasilar symptoms with, 660 Hypothermia, in inferior vena cava repair, 729 in thoracoabdominal aortic aneurysm repair, coagulopathy with, 482 controlled, 482 postoperative, 478 surface, in ex vivo reconstruction for renal artery stenosis, 588 thrombocytopenia with, 74 Hypoxanthine, in ischemia, 733 Hypoxia-inducible factor (HIF-1), 733

I Iatrogenic causes, of acute extremity ischemia, 737 in upper extremity, 689, 690 ICAM-1 (intercellular adhesion molecule-1), 757, 758 ICEPOSS socket, 923 Ileal artery, aneurysms of, 524t, 526t, 529, 529f Ileus, in abdominal aortic aneurysm repair, 503 Iliac artery(ies), aneurysms of, 488-511. See also Abdominal aortic aneurysm(s). cannulation of, catheter for, 309-310, 310f, 314 common, aneurysms of, 506 in abdominal aortic aneurysm repair, 500, 502 reconstruction of, 544, 544f, 545f contralateral, guiding sheath used with, 315

Iliac artery(ies) (Continued) external, reconstruction of, 544, 544f, 545f extraperitoneal exposure of, 61-62, 62f in abdominal aortic aneurysm endovascular repair, 383-384, 385f, 386 in left flank approach, 56-57 in vascular trauma patients, 718 infection of, 186 internal, aneurysms of, 506 in abdominal aortic aneurysm repair, 502, 503 in aortoiliac reconstruction procedures, 217, 218f occlusion of, erectile dysfunction and, 219, 799 isolated endarterectomy of, 217, 220f multidetector row computed tomographyangiography for, 295 occluded or stenotic, angioplasty and stenting of, indications for, 326-327 results of, 329, 330f, 331f stratification of lesions of, 329t erectile dysfunction and, 219, 799 in carotid angioplasty and stenting, 363t thrombosis after angioplasty and, 428, 429f vascular steal and, 237 restenosis of, 330 stenting for, 327 Iliac conduits, in abdominal aortic aneurysm endovascular repair, 386 Iliofemoral bypass graft, for aortoiliac occlusive disease, 544, 544f, 545f Iliofemoral venous occlusion, chronic, 243 Iliofemoropopliteal system, access to, by crossing over the top of aortic bifurcation, 309-310, 310f Ilioiliac bypass graft, for aortoiliac occlusive disease, 544, 544f, 545f Iloprost, for Raynaud’s syndrome, 110 Image intensifier, in carotid angioplasty and stenting, 363, 365, 365f Image noise, in multidetector row computed tomography-angiography, 293 Imaging. See also specific types, e.g., Arteriography. for abdominal aortic aneurysms, 492-494, 493f, 494f for vascular malformations, 204, 207f-210f principles of, 280-299 Immediate postoperative prosthetic technique, for amputation prostheses, 916-917, 917t application of, 917-921, 917f-921f Immune factors, hemodialysis infection and, 701 systemic vasculitides and, 111-112 Immune globulin, for Kawasaki disease, 116 Immune response, in atherogenesis, 92 in diabetes, 150 in fatty streak lesions, 93 in fibrous plaques, 95 in thrombocytopenia, 74 in vascular graft infection, 191 Immunofibrolysis, 421 Immunogenicity, of streptokinase, 418 Immunosuppressive therapy, arterial and venous allografts and, 456 for Behçet’s disease, 118 fungal arteritis and, 179 Implantable ports, for central venous catheters, 707, 707f Impotence. See Erectile dysfunction. Incision(s), abdominal, 476 continuous, wound complications and, 806 distal, for revascularization of nonhealing wounds, 886-887

Incision(s) (Continued) for abdominal aortic aneurysm repair, 499-500 for above-knee amputation, 908, 909f for axillary artery exposure, 52, 52f for carotid endarterectomy, 635 for ex vivo reconstruction for renal artery stenosis, 587 for knee disarticulation, 906f groin, vascular graft infection and, 190 in vascular trauma patients, 718 midline, 499 abdominal hernias with, 801 modification of, 57-58, 58f minimal, 500 in laparoscopic aortic surgery, 403-404 oblique, 499 abdominal hernias with, 801 supraclavicular, 51 thoracoabdominal, for thoracoabdominal aortic aneurysm repair, 53, 53f, 476 transverse, 499 Indium 111, white blood cell scanning with, 775-776 Infection(s), ankle or toe, in limb salvage bypass procedures, 561 arterial, 177-187 anatomic distribution of, 180-181, 180f causative organisms of, 179-180, 179f, 180f clinical presentation of, 181 complications of, 183-184 definitions relating to, 177 diagnostic testing of, 181-183 historical aspects of, 177 management of, principles of, 184 natural history of, 183-184 of femoral region, 186-187 of iliac artery region, 186 of infrarenal aorta, 185-186 of mesenteric artery, 187 of suprarenal aorta, 186 of upper extremity, 187 pathogenesis of, 177-179 primary, 177-187 atherosclerosis risk and, 101-102 false aneurysms and, 800 graft. See also Infection(s), prosthetic graft. bacteriology of, 188-189, 189t clinical and experimental investigations of, 191-193 clinical significance of, 187-188, 188t complications of, 187 in aortofemoral bypass grafts, 540 in vascular injury repair, 719 incidence of, 187, 188t mortality of, 187, 188t pathogenesis of, 189-191, 190t prophylactic antibiotic therapy for, 187-195 in abdominal aortic aneurysm repair, 387, 502, 503-504 in acute limb ischemia, 892 in amputated stump, 894, 911 in diabetics, lower extremity amputation and, 891 perioperative, 142 in mycotic aneurysms, 505-506, 518 in PTFE bridge fistulas, 700 in vascular access for hemodialysis, 701-702, 702f perioperative, diabetes care and, 142 peripheral arterial disease and, 266-267 prosthetic graft, 772-781 cause and pathophysiology of, 773 clinical presentation of, 774 diagnosis of, 774-776, 774f-776f future directions in, 780-781

X0183-Idx 9/26/05 01:21 PM Page 955

Index

Infection(s) (Continued) graft failure and, 739 imaging of, 775, 775f incidence of, 772 laboratory studies of, 774 management of, 776-777 of aortic grafts, 503-504, 777-779, 778f, 779f of endovascular stent-grafts, 780 of femoropopliteal grafts, 779-780 microbiology of, 772-773 prevention of, 773-774 surgery for, graft excision in, 776-777 preoperative preparation for, 776 vascular, 10 wound, after carotid endarterectomy, 641-642 treatment of, 882-883 Inflammation, abdominal aortic coarctation and, 126 atherosclerosis management and, 100-101 in acute wounds, 877-878 in atherogenesis, 92 in chronic wound healing, 878 in polyarteritis nodosa, 115 in vascular wall, in Buerger’s disease, 120 Inflammatory aneurysms, in abdominal aortic aneurysm repair, 504 Inflammatory process, in intimal hyperplasia, 757-758 in thrombolytic therapy, 421 splenic artery aneurysms and, 523 vascular disease and, 112 in diabetes, 150 Infrainguinal arterial reconstruction, examination of limb for, 553-554 human umbilical vein allografts for, 456-457, 457f noninfectious complications in, 802-807, 807f prosthetic grafts in, 461, 463 vein grafts in, stenosis of, 806, 807f surveillance of, 806-807 Infrainguinal bypass procedures, autogenous grafts in, failure of, 738 prosthetic grafts in, failure of, 738-739 thrombosis of, management of, 804-806, 804f, 805f postoperative, 803 surveillance for, 803 technical factors in, 802, 802f wound complications in, 806 Infrainguinal occlusive disease. See also Arteriosclerosis, infrainguinal; Femoropopliteal lesions. angioplasty and stenting for, 343-352 approaches for, antegrade, 344t, 347-348, 348t, 349f, 350f selection of, 344, 344t up-and-over, 344t, 345-347, 346f, 347f equipment needed for, 345t, 348t patient selection for, 343-344 results of, 349, 351-352 technique of, 343-348 classification of, 343, 343t cryoplasty and atherectomy for, 352 Infrapopliteal artery, grafts of, 8 Infrapopliteal bypass, for limb salvage, surgical criteria for, 556 surgical techniques for, 559f, 560f Infrapopliteal lesions, balloon angioplasty for, 352 Infusion wires, 312 Inguinal ligament, thrombosis and, 786, 787f Injury(ies). See also Trauma. arterial, atherosclerosis and, 96-97 surgical repair of, 8-9 immune-mediated, systemic vasculitides and, 111-112

Injury(ies) (Continued) mechanical, microbial arteritis and, 178, 180, 181 of inferior vena cava, 726-730 to access vessels, in abdominal aortic aneurysm endovascular repair, 386 vascular, 69-70 arterial wall response to, 38-42 endothelial response to, 38-42, 42f intraoperative, in aortoiliac arterial reconstruction, 783-786, 783f, 784f, 785f nonocclusive (minimal), 726, 728f smooth muscle cell response to, 38-40, 39f, 40f, 755-756 Innominate artery, endarterectomy of, 665, 666f occlusion or stenosis of, revascularization for, 662, 666-668 ostial lesion of, in carotid angioplasty and stenting, 367, 369f replacement of, with bypass of ascending aorta, 666-668, 667f, 668f subclavian steal syndrome and, 237 surgical exposure of, 49, 50, 51f Inokuchi shunt, for portal hypertension, 826 Instrument(s), contaminated, arterial infections and, 178, 180 for amputation surgery, 923 ultrasound, 247-249 Insulin, action of, personal lag time of, 155 suggested sliding scale for, 155-156 dose requirements for, adjustments to, 152-155, 154f food intake and, 158-159 in stress, 152t NPO orders and, 156, 156t standing orders for in hospital, 152, 153f in diabetes, vascular disease and, 150 NPH, in diabetics outside hospital, 160 plasminogen activator inhibitor release and, 416 types of, 152 Insulin resistance, atherosclerosis and, 100 hyperinsulinemia and, atherosclerotic disease and, 150 Insulin-derived growth factor, in acute wound healing, 877, 878 Insulin-sensitizing agents, for intimal hyperplasia, 765-766 Intercellular adhesion molecule-1 (ICAM-1), 757, 758 Intercostal arteries, in thoracoabdominal aortic aneurysm repair, 477 Intercostal space, in thoracoabdominal incision, 53, 53f Intercostobrachial nerve, in thoracic outlet syndrome repair, 686 Intercostobrachial veins, 32 Interleukin-1, in early atherogenesis, 94 in fatty streak lesions, 93 in inflammation, 758 in reperfusion injury, 734 Interleukin-6, in atherogenesis, 92 Interleukin-10, in atherogenesis, 92 Intermittent claudication. See Claudication, intermittent; Occlusive disease. Intermittent pneumatic compression devices, for venous thromboembolism prophylaxis, 82 Internal capsule, lacunar infarction of, 629 Internal carotid arteries, formation of, 26, 28 Internal obturator, with guiding sheaths, 315 International normalized ratio (INR), in treatment for deep venous thrombosis, 848 prothrombin time assays and, 81, 82

955

Interosseous artery, embryologic development of, 29f, 30 Interposition graft(s), for femoral and popliteal artery aneurysm repair, 516, 517 for forearm and hand aneurysm repair, 516 for subclavian artery aneurysm repair, 516 Interposition mesocaval H-graft, 828 Intestinal retractor, laparoscopic, 404-405, 405f Intestines, angina of, 10 arterial supply of, 794, 794f hemorrhage of, from splenic artery aneurysms, 524-525 infarction of, after acute mesenteric ischemia, 605 ischemia of, 794. See also Mesenteric ischemia. in abdominal aortic aneurysm repair, 503 in aortic reconstructive surgery, 793-796, 794f, 795f, 796f in visceral ischemic syndromes, acute, 604-608 chronic, 608-614 vascular anatomy of, 603-604, 604f Intima, arterial, 39-42, 40f, 452, 453f saphenous vein, 454f structure of, 36 Intimal cushion, 36 Intimal defects, small, 726 Intimal fibroplasia, 129, 622 Intimal flaps, after carotid endarterectomy, 639 Intimal hyperplasia, 755-767 anastomotic, thrombosis and, 787-788, 788f arteriovenous fistula and, 705 gene therapy for, 766-767 graft failure and, 738, 755 in autogenous vein grafts, 455, 738 in infrainguinal bypass grafts, 803 in vascular access for hemodialysis, 705 pathophysiology of, 755-761, 756f, 760f, 761f pharmacologic control of, 761-766, 762t anticoagulants for, 765 antihypertensive agents for, 764 anti-inflammatory agents for, 763-764, 764f antiplatelet agents for, 762-763 experimental models of, 762 growth factor inhibitors for, 764-765 insulin-sensitizing agents for, 765-766 lipid metabolites for, 762 photodynamic therapy for, 766 procedures leading to, 761 Intra-aortic balloon pump, extremity ischemia and, 737 IntraStent, 326 Iris, neovascularization of, ischemic optic neuropathy and, 631 Iron, atherosclerosis and, 100-101 Irrigation, of peritoneal cavity, for prevention of prosthetic graft infections, 774 pressurized, for wound healing, 882 Ischemia, acute. See Acute limb ischemia. carotid, in occlusion of supra-aortic trunks, 660 cerebral, embolic origins of, 628-629, 629f, 630f flow-related, 627-628, 628f pathogenetic mechanisms of, 626-629 chronic lower extremity, amputation for, 269, 892-893 epidemiology of, 263-264 in younger patients, 269, 269t natural history of, 267-269 nonoperative treatment of, 269-274 risk factors for, 265-267 critical limb, 268-269. See also Acute limb ischemia. focal, 628

X0183-Idx 9/26/05 01:21 PM Page 956

956

Index

Ischemia (Continued) in acute vessel or graft occlusion, 732 in compartment syndrome, 130 in popliteal artery aneurysm thrombosis, 517, 518 intestinal. See also Mesenteric ischemia. clinical manifestations of, 794-795 in abdominal aortic aneurysm repair, 503 in aortic reconstructive surgery, 793-796, 794f, 795f, 796f in visceral ischemic syndromes, acute, 604-608 chronic, 608-614 vascular anatomy of, 603-604, 604f prevention of, 795 limb-threatening, lumbar sympathectomy for, 447 multiple reoperations for, 562-563 thrombolytic therapy for, 422-423, 431-433, 436-438 vs. surgery for, 790 lower extremity. See Limb ischemia. acute. See Acute limb ischemia. chronic. See Ischemia, chronic lower extremity. thrombolytic therapy for, intra-arterial, 431-433 intraoperative, 436-438 mesenteric. See Mesenteric ischemia. pathophysiology of, 732-734 postoperative, thrombosis and, 788-789 rest pain with, in chronic ischemia, 892 in infrainguinal arteriosclerosis, 551-552 resting, in aortoiliac occlusive disease, 537, 539 vs. pain at rest, in infrainguinal arteriosclerosis, 551-552 spinal cord, 796-797 transmural, in abdominal aortic aneurysm repair, 503 upper extremity, 689 in occlusion of supra-aortic trunks, 660 in thoracic outlet syndrome, 678-679 vertebrobasilar, in occlusion of supra-aortic trunks, 660 Ischemia-reperfusion, in thoracoabdominal aortic aneurysm repair, 477, 479, 480 mesenteric, 477, 479 Ischemic colitis, 794 in abdominal aortic aneurysm repair, 503 in aortic reconstruction surgery, 793-796, 794f, 795f, 796f Ischemic nephropathy, 576 incidence and prevalence of, 578-579, 578t, 579t management options for, 583-584 optic, in carotid artery transient ischemic attacks, 631 pathophysiology of, 578 renal revascularization for, 591-592, 593f-595f, 594, 594t Ischemic syndromes, visceral, 603-616 acute, 604-608 chronic, 608-614 vascular anatomy of, 603-604, 604f ISNY socket, 923 Isoproterenol, with vasopressin, 824 Itching, cutaneous, venous dysfunction and, 860

J Jejunal artery, aneurysms of, 524t, 526t, 529 J-tip wires, 305, 312

Jugular vein, external, central venous catheter in, 707f, 708 internal, in central venous catheter hemodialysis, 696 Juxtaglomerular apparatus, 577

K Kasabach-Merritt syndrome, 201, 205t Katzen wires, 314 Kawasaki disease, 116-117, 117f Keratinocytes, in acute wound healing, 878 Kidney. See also under Renal. arteries of, embryologic development of, 28-29 cold perfusion of, in ex vivo reconstruction for renal artery stenosis, 587-588, 591f, 591t in thoracoabdominal aortic aneurysm repair, 481 horseshoe, in abdominal aortic aneurysm repair, 505 placement of in original site, in ex vivo reconstruction for renal artery stenosis, 588, 591f preservation of, in renal artery dissection, 533 Kinking, in carotid endarterectomy, 639-640 in extracranial cerebrovascular disease, 622-623, 624f of graft, thrombosis and, 786, 787f, 788 of internal carotid artery, 637, 637f Klippel-Trénaunay syndrome, 200f, 201, 201f, 204f, 205t, 207f Knee disarticulation, 905-907, 906f, 907f prosthetic application technique for, 920 prosthetic components for, 922 prosthetic requirements for, 906-907 rehabilitation potential for, 906-907 Knife wounds, abdominal, 723 vascular damage with, 713 Korean War, arterial injury repair in, 8-9 Korotkoff sounds, 252 Kringles, of plasminogen, 414, 415 K-space data, in three-dimensional contrast enhanced MRA, 281 Kuntz, nerve of, 444, 444f

L Laboratory tests, for bleeding disorders, 73 for disseminated intravascular coagulation, 77 for extracranial cerebrovascular disease, 632 for infrainguinal arteriosclerosis, noninvasive, 554-555 for venous thrombosis, 847 Lactulose, for management of bleeding in portal hypertension, 824 Lacunar infarction, in cerebral ischemic events, 629 Lamellae, aortic, 36 elastic, 36, 37f aortic aneurysm formation and, 489-490 Laparoscopic surgery, difficulties of, 409 for abdominal aneurysm repair, 500 for aortic aneurysm repair, 396-413 advances in, 396-397 advantages and limitations of, 396 approaches to, 398-400 history and development of, 397-398 robotics in, 409-410, 409t, 410f, 410t techniques of, hand-assisted, 403-404, 403f, 404f, 407, 407t laparoscopy-assisted, 404-407, 405f, 406t totally laparoscopic, 400-403, 407-409, 408t

Laparoscopic surgery (Continued) for aortoiliac occlusive disease, advantages and limitations of, 396 approaches to, 398-400 history and development of, 397 robotics in, 409-410, 409t, 410f, 410t techniques of, hand-assisted, 403-404, 403f, 404f, 407, 407t laparoscopy-assisted, 404-407, 405f, 406t totally laparoscopic, 400-403, 407-409 for infrainguinal arteriosclerosis, 570 for thoracic and lumbar sympathectomy, 443-451 gasless, 397, 398 on aorta, apron technique for, 397, 399, 400-401, 400f-402f, 407-408 hand-assisted, 403-404, 403f, 404f, 407, 407t laparoscopy-assisted, 404-407, 405f, 406t results of, 405-409 retrocolic technique for, 401-403, 402f, 403f retrorenal technique for, 403 robotics in, 409-410 techniques for, 400-405, 400t totally laparoscopic, 400-403, 407-409, 408t Laparotomy, staged, for multiply injured patients, 719 Laplace transform analysis, 254 Laplace’s law, aortic aneurysm enlargement and, 491 L-Arginine, for intermittent claudication, 273 in reperfusion injury, 734 Laryngeal nerve, recurrent, embryologic asymmetry of, 28 in carotid endarterectomy, 640-641, 640f superior, in carotid endarterectomy, 47, 47f, 47t, 640f, 641 Laser treatment, of saphenous vein, 862, 864f of vascular malformations, 209 Laser-Doppler velocimetry, for skin blood flow determination, amputation level selection and, 895t, 896t, 897 Lavage, gastric, for acute hemorrhage in portal hypertension, 824 Leeches, medicinal, 80, 81 Leg(s). See Extremity, lower. Leg length discrepancy, scanograms for, 204, 207f vascular malformations and, 202, 204, 207f Lenticulostriate artery(ies), occlusive disease involving, 629 Lepirudin, 80 pharmacology of, 168 Leriche, vascular surgical work of, 6, 7 Leriche syndrome, 327, 330f aortoiliac occlusive disease and, 537 erectile dysfunction and, 215 Leukocyte(s), in atheromas, 92 in ischemia-reperfusion, 733 intimal hyperplasia and, 758 migration of, into arterial wall, 758 Leukocytosis, in prosthetic graft infection, 774 Leukotriene B, in inflammation, 758 Ligamentum teres hepatis, 32 Ligamentum venosum, 31 Ligation, anticoagulant therapy and, 11 arterial, 1, 8, 9 venous, 2 Limb ischemia, acute. See Acute limb ischemia. causes of, 734-739, 735t clinical manifestations of, 739-740 examination for, 553-554 in abdominal aortic aneurysm repair, 503 in aortoiliac occlusive disease, 537. See also Aortoiliac occlusive disease.

X0183-Idx 9/26/05 01:21 PM Page 957

Index

Limb ischemia (Continued) initial evaluation of, 740-742 pathophysiology of, 732-734 postoperative, thrombosis and, 788-789 surgery for, complications of, 748-750 lumbar sympathectomy for, 447 vs. thrombolytic therapy, 790 thrombolytic therapy for, 422-423, 742-744, 742f, 743f intra-arterial, 431-433 vs. surgery, 790 treatment of, 742-748 vs. intermittent claudication in, 552-553 vs. rest pain in, 551-552 wound healing in, 876 Limb salvage, aggressive, cost-benefit analysis of, 565f, 566f, 568-569, 569f angioplasty in, 563-564, 564f arterial reconstruction for, patency of, 566, 567f reoperations for, 566-568, 567f results of, 565-566, 566f vascular grafts for, current recommendations for, 463 bypasses to ankle or foot arteries in, 560, 561f drug treatment for, preoperative and postoperative, 560-561 foot lesions in, 561 general and medical considerations in, 555 grafts in, failing, 563 materials and types used for, 556-558, 557f, 558f new developments in, 569-570 prolonged, 805 reoperation in, 561-563, 561f, 562f results of, 566-568, 567f surgical techniques for, 558-560, 559f, 560f criteria for reconstructibility in, 555-556 treatment for, 742-744, 742f, 743f results of, 564-568 wound healing in ischemic limbs and, 876 Linton shunt, 829 for portal hypertension, 826 Linton-Nachlas tube, 825 Lipid(s), abnormalities of, in diabetics, 100, 146, 146t, 149-150 in atherogenesis, 95 in atheromas, 92 Lipid metabolites, for intimal hyperplasia, 762 Lipid peroxides, in diabetics, 149, 150 Lipid profile, 98 Lipid-lowering therapy, for atherosclerosis, 97, 98 peripheral arterial disease and, 271 Lipodermatosclerosis, definition of, 859 Lipoprotein, function of, fibrinolytic system and, 416 low-density, atherosclerosis regression and, 97, 100 calculation of cholesterol level of, 98 in atherogenesis, 92-93, 93f, 95 in fibrous plaques, 94 target goals for, 100 oxidized, atherosclerosis, 100 in fatty streaks, 93 Liposuction, for treatment of lymphedema, 873 Lisfranc’s amputation, 901 Liver biopsy, in portal hypertension, 820 Liver disease, bleeding disorders and, 73, 75 portal hypertension and, 819 protein C and protein S deficiencies and, 78 systemic thrombolytic therapy and, 422 Liver function tests, portal hypertension and, 819 “Liver package,” 821

Liver transplantation, hepatic artery aneurysms and, 526 orthotopic, shunt procedures and, 834-835, 835t splenic artery aneurysms and, 523 transjugular intrahepatic portosystemic shunting and, 834 LJ-CP8, for intimal hyperplasia, 763 Long thoracic nerve, in brachial plexus, 676 injury to, in thoracic outlet syndrome repair, 685, 686 Loop fistulas, for hemodialysis access, 699-700 Lovastatin, for prevention of extracranial occlusive disease, 648 Lumbar aortography, in arterial access, 308, 309 Lumbar artery, intraoperative bleeding with, 785 Lumbar sympathectomy, for Raynaud’s syndrome, 110 historical aspects of, 443 indications and contraindications for, 445t, 448 open surgical, 448-449, 448f, 449f patient position for, 448, 448f, 449f results of, 449, 450 retroperitoneoscopic, 449, 449f Lumbosacral spine exposure, anterior approach to, 931-933, 932f anterolateral approach to, 931, 931f Lupus anticoagulants, thrombosis risk and, 78, 79 Lupus erythematosus, vasculitis of, 120 Lymph, leakage of, in thoracic outlet syndrome repair, 686-687 infrainguinal bypass procedures and, 809 seeding of, in vascular graft infection, 191 Lymphangiography, 870 Lymphatic vascular malformation, 201, 204f Lymphedema, 869-874 causes of, 869 diagnosis of, 869-871, 870f, 871f pathogenesis of, 869, 869f treatment of, options in, 872-874, 873f rationale for, 871-872 vascular malformations and, 201, 203, 206 Lymphoceles, in infrainguinal bypass surgery, 809 Lymphoscintography, 871 Lymphotoxin, 758 Lysosomes, of platelets, 71 Lys-plasminogen, 414, 420 Lysyl oxidase, aortic aneurysm formation and, 491

M Mac-1 complement receptor, 757 α2-Macroglobulin, 416, 759 Macrophage colony-stimulating factor, in early atherogenesis, 94 Macrophages, aortic aneurysm formation and, 491 in acute wound healing, 877, 878 in early atherogenesis, 94 in fatty streak lesions, 93 intimal hyperplasia and, 760, 760f Madding-Kennedy intracaval shunt, 729, 729f Mafucci’s syndrome, 201, 205t Maggots, for wound healing, 882 Magnetic resonance angiography, 280-292 as renal angiography alternative, 582 carotid endarterectomy and, 651 clinical applications of, 282-287 contrast agents used for, 282, 287 for abdominal aortic aneurysms, 494 for acute mesenteric ischemia, 606 for extracranial cerebrovascular disease, 632, 633 for infrainguinal arteriosclerosis, 555

957

Magnetic resonance angiography (Continued) for renal artery stenosis screening, 335 for thoracoabdominal aortic aneurysm, 473, 475, 475f for thoracoabdominal aortic aneurysm repair, 480 for vascular malformations, 204, 207f patient preparation for, 282 phase-contrast, 280-281 postprocessing techniques with, 282 pulse sequences in, 280-282 three-dimensional contrast-enhanced, 281-282, 282, 287 time-of-flight, 280 vs. computed tomography-angiography, 299 Magnetic resonance fluoroscopy, 281 Magnetic resonance imaging, early use of, 13 for abdominal aortic aneurysms, 494, 494f for aortoiliac occlusive disease, 540 for arterial infections, 182-183 for extracranial cerebrovascular disease, 632, 633 for popliteal entrapment syndrome, 128, 128f for prosthetic graft infections, 775 for splenic artery aneurysms, 524 for thoracic outlet syndrome, 680 for vascular malformations, 204, 207f for wound healing diagnosis, 880, 880f Magnetic resonance venography, 287, 292f Maillard reaction, 147-148 Major histocompatibility complex, in Buerger’s disease, 120 Mallory bodies, in portal hypertension, 820 Malnutrition, in wound healing, 879 Mandible, condyle of, wire fixation of, 48, 49f ramus of, in exposure of high internal carotid artery, 48-49 Mandrel, 311 Mannitol, in renovascular disease surgery, 584 in thoracoabdominal aortic aneurysm repair, 481, 482 Marfan’s syndrome, aortic dilatation in, 122-123, 123f Marginal artery of Drummond, 604 bowel ischemia and, 794 Marshall, oblique cardinal vein of, 32 Massage, for treatment of lymphedema, 872-873 Matas, aortic ligation by, 4 endoaneurysmorrhaphy of, 3 Matrix metalloproteinases, in aortic aneurysm formation, 490 in Marfan’s syndrome, 122-123 in wound healing, 878, 879f Maximum-intensity projection algorithm, for magnetic resonance angiography, 282, 287 MDGF (monocyte-and macrophage-derived growth factor), in intimal hyperplasia, 758 Meandering mesenteric artery, 604, 610f bowel ischemia and, 794, 795, 795f, 796 Meckel’s cartilage, 24 Media, arterial, 452, 453f in early atherogenesis, 94 in medial fibroplasia, 129 of saphenous vein, 454f structure of, 36 Medial fibrodysplasia, of renal artery, 523 renal artery aneurysms and, 530, 531f splenic artery aneurysms and, 523 Medial fibroplasia, 622 of renal artery, 576, 577f Medial hyperplasia, 622 Median arcuate compression syndrome, 611f Median artery, embryologic development of, 29f, 30

X0183-Idx 9/26/05 01:21 PM Page 958

958

Index

Median nerve, in embolectomy of upper extremity, 745 Medical Research Council European Carotid Surgery Trial, 646-647 MedNova NeuroShield bare wire filter, 357 Meglitinides, 160 Meier guidewire, in carotid angioplasty and stenting, 364, 365 Meige disease, 201 Melagatran/ximelagatran, pharmacology of, 168 Memotherm stent, 326 Men, peripheral arterial disease and, 265-266 Meniscus sign, 741 Mesenchymal hypothesis, of atherosclerosis, 96 Mesenteric artery(ies), 603-604, 604f duplex scanning of, 255 embolus of, intra-arterial thrombolytic therapy for, 434, 435f infections of, 187 inferior, anatomy of, 604, 604f bowel ischemia and, 794, 794f, 795f, 796 ejaculatory dysfunction and, 799-800, 799f embryologic development of, 28 in abdominal aortic aneurysm repair, 501, 503 in aortoiliac reconstruction procedures, 217, 217f, 219f intraoperative bleeding from, 785 surgical exposure of, 56, 56f magnetic resonance angiography of, 283 meandering, 604, 610f bowel ischemia and, 794, 795, 795f, 796 occlusion of, intra-arterial thrombolytic therapy for, 430 surgical management of, 10 superior, anatomy of, 604, 604f aneurysms of, 524t, 526t, 527-528 bowel ischemia and, 794, 795f bypass grafts for, 612-614, 612f-614f embolic occlusion of, 605, 605f, 607-608, 607f embryologic development of, 28 mobilization and arteriotomy of, 607-608, 607f perfusion of, in thoracoabdominal aortic aneurysm repair, 476, 476f, 477f reconstruction of, 58-59 surgical exposure of, 55-56, 56f, 58-59 thrombosis of, 605, 608 Mesenteric ischemia, acute, 604-608 arterial embolism in, 605, 605f, 607-608, 607f arterial thrombosis in, 605, 608 clinical presentation of, 606 diagnosis of, 606-607 nonocclusive, 605-606, 608 pathophysiology of, 604-605 treatment of, 607-608, 607f venous thrombosis in, 606, 608 chronic, 608-614 antegrade bypass for, 612, 612f, 613f clinical presentation of, 608-609 diagnosis of, 609, 609f retrograde bypass for, 612-614, 613f, 614f surgical revascularization for, 611-612 nonocclusive, 605-606 angiography of, 607 Mesenteric ischemia-reperfusion, in thoracoabdominal aortic aneurysm repair, 477, 479 Mesenteric vein(s), magnetic resonance angiography of, 287f occlusion of, surgical management of, 10 superior, in mesocaval shunts, 828-829 in portal hypertension, 821 thrombosis of, 606, 608

Mesocaval shunts, 828-829 Metabolic acidosis, in reperfusion imaging, in thoracoabdominal aortic aneurysm repair, 477 in reperfusion injury, 734, 749 Metabolic disorders, hyperlipidemia in, 95 Metabolic rate, ischemia and, 732 Metformin, 160 Methamphetamine abuse, arteritis with, 117 Methylene tetrahydrofolate reductase deficiency, in homocystinuria, 132 Methylprednisolone, for intimal hyperplasia, 763 Mewissen Infusion Catheter, 313, 314 Microbial arteritis, with aneurysm formation, 178 Microembolization, trash foot with, in abdominal aortic aneurysm repair, 503 Microorganisms, in arterial infections, 179-180, 179f, 180f in vascular graft infections, 188-189, 189t in wet gangrene, 893 in wound healing, 882 mycotic aneurysms associated with, 518 Micropuncture kit, for puncture of small arteries, 304 Microspheres, labeled, for diagnosis of vascular malformations, 204 Microvascular procedures, for erectile dysfunction, 219-220 deep dorsal vein arterialization for, 221 patient and procedure selection for, 220-221 venous interruption for, 221-222 Midsternotomy, partial, 666, 667f technique of, 666, 666f Midtarsal joint amputation (Chopart’s), 901 Migraine, vs. transient ischemic attack, 630 Milroy disease, 201 Mini-laparotomy, in laparoscopic aortic surgery, 404, 405-406, 406t, 410 Minimally invasive techniques. See also Laparoscopic surgery. for infrainguinal arteriosclerosis, 570 for thoracic and lumbar sympathectomy, 443-451 Mini-phlebectomy, for varicose veins, 862, 863f Mini-sternotomy, 49-50, 50f Minnesota tube, 825 Mitogens, intracellular, smooth muscle cell proliferation and, 40, 41, 42f Mitotoxins, for intimal hyperplasia, 765 Mitral valve, embryologic development of, 24 Mixed cryoglobulinemic vasculitis, 119 MMP-9. See Matrix metalloproteinases. Monoclonal hypothesis, of atherosclerosis, 96 Monocyte- and macrophage-derived growth factor (MDGF), 758 Monocyte chemoattractant protein-1, in early atherogenesis, 94 Monorail (rapid-exchange) systems, for endovascular treatment, 336-337, 344, 345 Mortality, of abdominal aortic aneurysms, 488 of aneurysm repair, 496, 496t, 497 of aneurysm rupture, 496, 497 of carotid angioplasty and stenting, 355, 356, 357, 358 of carotid endarterectomy, 641 of diabetes, 144 of endovascular management of renal artery stenosis, 341 of hepatic artery aneurysms, 527 of inferior vena cava injuries, 727, 728t, 729, 729t, 730t of infrainguinal bypass for limb salvage, 565, 565f

Mortality (Continued) of lower extremity amputation, 890, 910, 912, 912f of pulmonary thromboembolism, 845 of renal artery reconstruction, blood pressure response and, 597, 597f, 598 of splenic artery aneurysm rupture, 525 of stroke, 618-619, 619f of thoracoabdominal aortic aneurysm, 470, 470t of thoracoabdominal aortic aneurysm repair, 482, 483t of transthoracic repair of supra-aortic trunks, 668-669, 668t Motor dysfunction, in carotid artery transient ischemic attacks, 631 Motor vehicle accidents, vascular trauma with, 714, 715, 716f, 720-722, 720f mRNA, angiotensinogen, 758 Mucocutaneous lymph node syndrome, 116 Multipara, grand, splenic artery aneurysms in, 523, 524f Mural thrombus, graft, postoperative thrombosis and, 788 in abdominal aortic aneurysm repair, 501 intra-arterial thrombolytic therapy and, 428 systemic thrombolytic therapy and, 422 venous, magnetic resonance venography for, 287 vs. embolus, 735 Muscle(s), contraction of, venous hypertension and, 859 necrosis of, in acute limb ischemia, 892 of upper extremity, strength testing of, 679 rigidity of, in acute limb ischemia, 892 skeletal, fiber types of, 678 ischemia and, 732 Muscle fibers, thoracic outlet syndrome and, 678 Musculoskeletal disorders, vs. thoracic outlet syndrome, 682 Mycotic aneurysm(s), anatomic distribution of, 180, 180f bacteria cultured from, 179, 179f, 180f definition of, 177, 178 management of, 185-186, 518-520 of aorta, 505-506 of carotid artery, 623 of femoral artery, 520 Myeloperoxidase, in inflammation, 758 Myeloproliferative disease, portal hypertension and, 817 venous thrombosis risk and, 79 Myocardial infarction, acute arterial occlusion and, 740 in infrainguinal arteriosclerosis, 554 in intra-arterial thrombolytic therapy, 436 in supra-aortic trunk surgical reconstruction, 669 postoperative thrombosis and, 788 previous, abdominal aortic aneurysm repair and, 498 proximal emboli secondary to, 428 risk of, in thoracoabdominal aortic aneurysm repair, 480 Myoglobinuria, in acute limb ischemia, 892 in ischemic-reperfusion injury, 734, 749 Myointimal fibroplasia, in recurrent carotid stenosis, 625 Myointimal hyperplasia, 755-767. See also Intimal hyperplasia. arteriovenous fistula and, 705 Myonecrosis, in acute limb ischemia, 892 Myonephropathic metabolic syndrome, 749-750, 750t in reperfusion injury, 734

X0183-Idx 9/26/05 01:21 PM Page 959

Index

N Naftidrofuryl, for intermittent claudication, 273 Naltrexone, in smoking cessation programs, 270 Nanocrystalline silver, in wound healing, 882-883 NASCET, 633, 646 of carotid angioplasty and stenting, 358 National Institute of Neurological Disorders and Stroke (NINDS) trial, rt-PA use in, 433 Neck, PTFE grafts in, 662 root of, traumatic vascular injury of, 722, 722f rotation of, vertebrobasilar ischemia and, 660 vessels of, trauma to, 720-722, 720f, 721f Necrosis, ankle or toe, in limb salvage bypass procedures, 561 cerebral, focal areas of, 629 hyaline, in portal hypertension, 820 Needle(s), in arterial access, smart, 308 types of, 303-304 Needle holders, in laparoscopic aortic surgery, 404 Neomycin, for bleeding management in portal hypertension, 824 Neonates, portal vein thrombosis in, 853 Neovascularization, 32-34, 33f-35f with surgical stripping of saphenous vein, 862 Nephrectomy, in renal artery aneurysm repair, 532 in renal artery dissection, 533 in surgery for renovascular hypertension, 588-589 Nephropathy, contrast-induced, protection against, 170-171, 581-582 ischemic, 576 incidence and prevalence of, 578-579, 578t, 579t management options for, 583-584 optic, in carotid artery transient ischemic attacks, 631 pathophysiology of, 578 renal revascularization for, 591-592, 593f-595f, 594, 594t Nerve(s), in carotid endarterectomy, 46, 47, 47t injuries to, in thoracic outlet syndrome repair, 686 of branchial arch arteries, 24, 25f, 28 peripheral, ischemia and, 732 Nerve conduction velocity, in thoracic outlet syndrome, 680 Nerve fibers, aortoiliac connections with, postoperative sexual dysfunction and, 217-218, 217f, 799-800, 799f. See also Erectile dysfunction. Nerve of Kuntz, 444, 444f Nerve roots, irritation of, vs. claudication symptoms, 538 of brachial plexus, 675-676 Nervous system, sympathetic, anatomy of, 443-444, 444f in renovascular hypertension, 577, 578 physiology of, 444 Neural compression, in thoracic outlet syndrome, electrophysiologic tests for, 680 provocative clinical tests for, 679-680 Neuralgia, post-sympathectomy, lumbar sympathectomy and, 449, 450 Neurogenic impotence, 799 Neurologic complications, in carotid angioplasty and stenting, 377-379, 378f, 379f, 380f in extracranial carotid artery aneurysms, 513 in thoracoabdominal aortic aneurysm repair, 481-482, 481f, 483t in thoracoabdominal aortic aneurysms, 470, 470t

Neurologic disorders, vs. thoracic outlet syndrome, 682 Neurologic symptoms, in compartment syndrome, 131, 132 in thoracic outlet syndrome, 678 Neurologic testing, for erectile dysfunction, 215, 216 Neuron(s), postganglionic, anatomy of, 443-444, 444f preganglionic, anatomy of, 443-444, 444f Neutrophil adherence, in compartment syndrome, 130 Niacin, for atherosclerosis, 99 peripheral arterial disease and, 271 Nicoladoni-Branham sign, 725 Nicotine replacement agents, 270 Nicotinic acid, as fibrinolytic agent, 417 Nifedipine, for intimal hyperplasia, 764 for Raynaud’s syndrome, 110, 690 NINDS trial, rt-PA use in, 433 Nitinol stents, 326, 348, 351, 355, 372, 376f deployment of, 372, 375, 377f, 378f for infrainguinal bypass grafts, 563 Nitric oxide, arterial relaxation and, 38 endothelial cell–derived, 69, 69t, 149 in diabetes, 149 in erection, 214 in intimal hyperplasia, 759 in reperfusion injury, 734 Nitric oxide synthase, 38 vascular wall thickening and, 38, 41, 41f Nitroglycerin, in provocative testing for iliac stent placement, 326 sublingual, with vasopressin, 824 Nitroprusside, in renovascular disease surgery, 584 Nonatherosclerotic vascular disease, 107-133 adventitial cystic disease as, 129-130 Buerger’s disease as, 120-122 compartment syndrome as, 130-132 congenital conditions affecting arteries as, 125-128 fibromuscular dysplasia as, 128-129 heritable arteriopathies as, 122-125 homocystinuria as, 132-133 systemic vasculitis as, 111-120 vasospastic disorders as, 107-111 Nonenzymatic browning, in diabetes, 148, 148t Nonrecurrent laryngeal nerve, in carotid endarterectomy, 640-641, 640f “No-reflow” phenomenon, in reperfusion, 733, 734 North American Symptomatic Carotid Endarterectomy Trial. See NASCET. Nothing by mouth (NPO) orders, in diabetics in hospital, 156 NPH insulin, in diabetics in hospital, dose adjustments in, 152-155, 153f in diabetics outside hospital, 160 NPO orders and, 156 Nuclear imaging, for diagnosis of arterial infections, 182 Nutrition, assessment of, for thoracoabdominal aortic aneurysm, 475 in diabetics, enteral, 156-158, 156t, 157f, 158t intravenous parenteral, 158, 159f, 160t total parenteral, vascular access for, 706-709, 707f, 708f, 709f wound healing and, 879

959

Obturator bypass, 10 Occipital artery, bypass from to distal vertebral artery, 671, 672f Occlusive disease. See also Claudication; specific types of occlusion, e.g., Thrombosis. aortic aneurysms and, 489 aortoiliac, 537-550. See also Aortoiliac occlusive disease. arterial, gangrene and, 2, 6 historical aspects of, 6-8, 10 in pseudoxanthoma elasticum, 125 mesenteric, 10 multiple-level, vascular steal and, 237 of peripheral arteries. See Peripheral arterial disease. thrombotic, in Buerger’s disease, 120, 121, 121f vascular reconstruction for, erectile dysfunction and, 214, 215 visceral, 10 OCERPSS socket, 923 Octreotide, for variceal bleeding, 824-825 Oligonucleotides, for control of smooth muscle cell proliferation after vascular injury, 42 Omentopexy, 832 Omniport, in laparoscopic aortic surgery, 403, 404 Omni-Tract retraction system, 55 Operating room, setup of, for abdominal aortic aneurysm endovascular repair, 385 Ophthalmic artery, carotid artery thrombosis and, 627, 627f Ophthalmodynamometry, 12 Optic neuropathy, ischemic, in carotid artery transient ischemic attacks, 631 Oral contraceptives, thrombosis risk and, 78 Ornithin decarboxylase inhibitors, for intimal hyperplasia, 765 Orthostatic hypotension, vertebrobasilar symptoms with, 660 Oscillometer, 12 Osseous factors, in thoracic outlet syndrome, 676, 677f Osteomyelitis, chronic, of great toe, 898 in wound healing, 880 Ostium primum, 26f Ostium secundum, 26f Oudot, vascular surgical advances of, 7 Owen’s silk, 917, 917f Oxidation-reduction pathways, in diabetics, 149-150 Oxidative stress, in diabetes, 149 Oxygen, cavernosal, in erectile physiology, 214 in wound healing, 880 ischemia and, 732 transcutaneous partial pressure of, amputation level selection and, 895t, 896-897, 896t in wound healing, 880, 885 Oxygen free radicals, in compartment syndrome, 130, 132 in reperfusion, 733, 734 in reperfusion injury, 605 in thoracoabdominal aortic aneurysm repair, 480, 482 polymorphonuclear leukocyte production of, in inflammation, 758

P O Obesity, diabetes risk and, 151 Obturator, internal, with guiding sheaths, 315

Paclitaxel, for stent coatings in angioplasty, 765 Paget-Schroetter syndrome, 13, 687-688, 688f Pain, at rest, vs. ischemic rest pain, 551-552 in acute limb ischemia, 739, 891

X0183-Idx 9/26/05 01:21 PM Page 960

960

Index

Pain (Continued) in acute mesenteric ischemia, 603, 606, 608 in aortic aneurysms, 492 in iliac artery aneurysms, 506 in ischemic limb, lumbar sympathectomy and, 449 sympathectomy and, 444 in lower extremity amputation, 910 in mycotic aneurysms, 506 in splenic artery aneurysms, 524 in thoracic outlet syndrome, 678 in thoracoabdominal aortic aneurysm, 473 leg, venous dysfunction and, 860 vascular malformations and, 204 Pallor, in acute extremity ischemia, 739 Palmaz stent, 325, 326f, 328 Palpation, for aortic aneurysms, 492 for peripheral artery aneurysms, 514 for thoracic outlet syndrome, 679 Pancreatic artery, aneurysms of, 524t, 526t, 529-530 Pancreaticoduodenal artery, aneurysms of, 524t, 526t, 529-530 Pancreatitis, pancreaticoduodenal artery aneurysms and, 529, 530f postoperative, in abdominal aortic aneurysm repair, 503 splenic artery aneurysms and, 523, 524-525, 525f Papain-urea, for wound healing, 881-882 Papaverine, for vasospasm, 689, 746 in provocative testing for iliac stent placement, 326 Paralysis, in acute extremity ischemia, 739 Paraplegia, after aortic surgery, 797 in abdominal aortic aneurysm repair, 503 in endovascular repair of thoracoabdominal aortic aneurysms, 483 Parenchyma-gram, in carotid angioplasty and stenting, 378, 378f Parenteral nutrition, in diabetics, 158, 159f, 160t Paresthesia, in acute extremity ischemia, 739 Parkes Weber syndrome, 201, 205t Parodi Anti-Embolization Catheter, 370, 371f, 375t, 376f Parodi Blood Recovery system, 370 Parotid gland, in carotid endarterectomy, 641 Partial thromboplastin time, activated, 73, 77, 166 measurement of, in intra-arterial thrombolytic therapy, 434 Patch angioplasty, in carotid endarterectomy, 626, 636 in residual arteriovenous fistulas on bypass grafts, 746 in thrombectomy of bypass graft, 746 of vein grafts, 746, 805 Patient(s), evaluation of, for infrainguinal arteriosclerosis, 553-555 for lower extremity amputation, 890-894, 891t high-risk, aneurysm repair in, 497, 498, 499 aortoiliac occlusive disease in, 544-547 carotid artery stenosis in, 356-358, 356t, 358f, 358t preparation of, for magnetic resonance angiography, 282 for renal vein renin assays, 583, 583t selection of, for abdominal aortic aneurysm repair, 383-385, 385f, 385t for carotid angioplasty and stenting, 358-359 for thrombolytic therapy, 742-743, 743f intra-arterial, 427-428 systemic, 422-423 wound healing capability of, 879

Patient education, for thoracic outlet syndrome, 682 Patient position, for exposure of retroperitoneal aorta, 54, 55f for laparoscopic aortic surgery, 400, 400f, 401-402, 403f, 405, 405f for lumbar sympathectomy, 448f, 449f for lumbosacral spine exposure, 931, 931f, 932, 932f for thoracoabdominal aortic aneurysm repair, 476 for thoracolumbar spine exposure, 929, 930f for vascular trauma surgery, 718 supine, venous pressure and flow relationships and, 240, 240f Trendelenburg, 399, 404 PDE-5 inhibitors, for erectile dysfunction, 214, 222 PDGF. See Platelet-derived growth factor (PDGF). Peak systolic velocity, in Doppler systems, 248, 250f, 250t, 251t of renal arteries, 335, 580, 580t, 581f vein graft failure and, 807 Pedal artery(ies), dorsal, 66 exposure of, 65-66, 65f, 66f Pedal bypass, for infrainguinal arteriosclerosis, 570 Pedal pulse, 235, 554 Pefloxacin, for vascular reconstruction procedures, 194 Pelvic hematoma, 728 Pelvis, magnetic resonance angiography of, 283, 287, 292f Penile pulse volume recording, 216 Penile systolic pressure, 799 Penile-brachial index, 216, 799 Pentoxifylline, for intermittent claudication, 239, 272 in reperfusion injury, 734 pharmacology of, 170 PercuSurge export catheter, in carotid angioplasty and stenting, 368, 370 PercuSurge GuardWire Plus, 371f Percutaneous transluminal angioplasty, 316, 319-321, 323, 325. See also Angioplasty, balloon. erectile dysfunction and, 219, 220f for aortoiliac occlusive disease, 547 for chronic mesenteric ischemia, 609, 611, 612f for failing infrainguinal bypass grafts, 563 for fibromuscular dysplasia, 129 for infrainguinal arteriosclerosis, 563-564, 564f for renal artery stenosis, 598-599, 599t stenting and, 328 Perforating veins, 239 in post-thrombotic syndrome, 243 Pericardial cavity, embryologic, 22f, 23 Perimedial dysplasia, 622 Periodontal disease, atherosclerosis risk and, 101-102 Peripheral arterial disease. See also Iliac artery(ies), occluded or stenotic. antiplatelet therapy for, 271-272 asymptomatic, 263-264 critical limb ischemia and, 268-269. See also Acute limb ischemia; Critical limb ischemia. drug therapy for, 272-273 exercise therapy for, 272 magnetic resonance angiography of, 289f, 290f mortality of, 268, 268t nonoperative treatment of, 269-274 revascularization vs. thrombolytic therapy for, 432, 433

Peripheral arterial disease (Continued) risk factors for, 265-267 management of, 269-271, 270t symptomatic, incidence and prevalence of, 264, 264t, 265t Peripheral artery(ies), aneurysms of, 512-522 mycotic, 518-520 nonmycotic, 512-518 causes of, 512-513, 513t diagnosis of, 513-514 incidence of, 512-513 indications for operation of, 514-515 natural history of, 513 results of treatment of, 517-518 treatment of, 515-517 duplex scanning of, 255 multidetector row computed tomographyangiography for, 298-299, 299f Peripheral resistance, in lower limb, 235 Peripheral sympathetic pathway, anatomy of, 443-444, 444f Peripheral vascular disease, diabetes and, 144-145, 146 intra-arterial thrombolytic therapy for, 427 noninvasive diagnosis of, 12 occlusion in, 421 Peripheral vessels, magnetic resonance angiography of, 283, 287, 288f-290f Peritoneovenous shunt, for ascites management, 838, 839 Peritoneum, in laparoscopic aortic surgery, apron technique and, 397 Peritonitis, in abdominal aortic aneurysm repair, 503 Peroneal artery, embolectomy catheter in, 745 embryologic development of, 29f, 30 exposure of, 65 in infrapopliteal bypass for limb salvage, 556, 559f Perthes test, 860 pH, of sigmoid colon, 795 Pharyngeal arch, arteries of (branchial arch arteries), embryologic development of, 24, 25f nerve supply of, 28 Pharynx, embryologic development of, 24, 25f Phase-contrast magnetic resonance angiography, 280-281 Phenformin, as fibrinolytic agent, 417 Phenoxybenzamine, for Raynaud’s syndrome, 110 Phenprocoumon, for maintenance of graft patency, 85 Phentolamine mesylate, for erectile dysfunction, 222 Phlebectomy, for varicose veins, 862, 863f Phlebitis, superficial, 738 Phlebography, for varicose veins, 861 Phleborheography, 13 Phlegmasia alba dolens, 846 Phlegmasia cerulea dolens, 425, 846 Phosphatidylinositol cycle, 764 Photodynamic fixation, for prosthetic grafts, 462 Photofrin, for intimal hyperplasia, 766 Photoplethysmography, amputation level selection and, 895, 895t, 896t, 897 digital, Raynaud’s syndrome and, 109 for venous reflux, 257-258, 258f Phrenic nerve, in brachial plexus, 676 in thoracic outlet syndrome repair, 683, 685, 686 protection of, 50, 51, 52f, 53 Physical inactivity, diabetes risk and, 151 Pigmentation, definition of, 859 Pigtail catheter, 314

X0183-Idx 9/26/05 01:21 PM Page 961

Index

PIOPED II study, 846 Plantar artery(ies), deep, 65f, 66, 66f Plaque, aortic, calcification of, 408 atherosclerotic, emboli from, 735, 736f in carotid bifurcation, 621-622, 621f, 622f removal of, development of techniques for, 7-8 softening and break-up of, 628, 629f, 630f behavior of, in balloon angioplasty, 317-318 carotid, stroke risk and, 620 fibrous, in early atherogenesis, 92f, 94-95 Plasma, platelet-rich, in wound healing, 883-884 Plasma glucose, amputation risk and, 913 Plasmin, in fibrinolysis, 73, 414, 415, 415f, 416 in intimal hyperplasia, 759-760 targets of, 415 Plasminogen, activation of, 73 in action of reteplase, 420-421 in fibrinolysis, 414, 415, 415f, 416 thrombus bound, 416 in intimal hyperplasia, 759-760 tissue plasminogen activator activity and, 419 Plasminogen activator inhibitor, 70, 73 circadian variations in, 416 endothelial cell–derived, 69t, 70 in diabetics, 148 in fibrinolytic system, 415-416 Plasminogen steal, 417 Platelet(s), activation of, 71 adherence of, to vessel wall, 756-757 administration of, 74 aggregation of, 71, 757 in acute wound healing, 877 in cerebral emboli, 628, 629f, 630f pharmacologic inhibition of, 71 antibodies of, in heparin-induced thrombocytopenia, 166 aspirin action and, 168 atheromatous plaque development and, 621-622 disorders of, qualitative functional, 74-75 glycoprotein IIb/IIIa of, 42. See also Glycoprotein IIb/IIIa inhibitors. granules of, 71, 75 immune-mediated destruction of, 74 impaired production of, thrombocytopenia with, 74 in heparin-induced thrombosis, 787 in hyperglycemia, 148-149 in intimal hyperplasia, 756-757 in intimal thickening, 39-40, 41, 42f smooth muscle proliferation and, 38-39, 39f structure of, 71 surface receptors of, 71 tissue plasminogen activator activity and, 420 Platelet Concentration Collection System, in wound healing, 884 Platelet-activating factor, in reperfusion injury, 734 Platelet-derived growth factor (PDGF), 40 angiotensin II and, 759 characteristics of, 40 gene for, 40 in acute wound healing, 877, 878 in cell-cell communication, 39 in early atherogenesis, 94 in fatty streak lesions, 93 in inflammation and intimal hyperplasia, 757, 758 in intimal thickening, 39-42, 42f in smooth muscle proliferation, 38-39 in wound healing, 883 Platelet-derived growth factor-β, in ischemic nephropathy, 578 Platelet-rich plasma, in wound healing, 883-884

Platforms, for endovascular approach to infrainguinal disease, 344, 345 Plethysmography, 12 digital, in Buerger’s disease, 121 for venous thrombosis, 846 of lower extremity pressures, 252, 254, 254f Pneumatic compression pump, for lymphedema, 872, 873f Pneumatic compression systems, for venous thrombosis, 847 Pneumoplethysmography, cuff of, in penile pulse volume recording, 216 Gee ocular, 515 Pneumothorax, in thoracic outlet syndrome repair, 686 Poiseuille’s law, 232, 234, 239 Polidocanol, for foam sclerotherapy, 209, 862 Polyarteritis nodosa, 115-116, 115f Polyester grafts. See Dacron graft(s). Polyglactin, for prosthetic grafts, 462 Polyhydroxyalkanoate, for prosthetic grafts, 462 Polymers, graft, for abdominal aortic aneurysm repair, 383 Polymorphonuclear neutrophils, in acute wound healing, 877, 878 in diabetics, 150 in inflammation, 757-758 in reperfusion injury after acute mesenteric ischemia, 605 Polytetrafluoroethylene grafts. See PTFE graft(s). Polyurethane grafts, 462 Pons, lacunar infarction of, 629 Popliteal aneurysm(s), repair of, 6 Popliteal artery(ies). See also Femoropopliteal artery. aneurysms of, mycotic, 520 nonmycotic, 513, 514, 515, 516, 517 angioplasty of, 349, 350f, 350t, 351t, 563 distal, 8 embolectomy in, 745, 745f embolus of, intra-arterial thrombolytic therapy for, 430, 434, 436f entrapment syndromes involving, 127-128, 127f, 128f exposure of, lateral, 63-64, 63f, 561 medial, 63, 63f in extra-anatomic bypass of infected aortobifemoral graft, 778, 779, 779f, 780f in femoropopliteal bypass, 568 injuries of, repair of, 724 occlusive disease of. See Arteriosclerosis, infrainguinal. thrombosis of, intra-arterial thrombolytic therapy for, 430 Popliteal vein(s), aneurysmal dilatation of, 201f duplex scanning of, 257 in exposure of popliteal artery, 63 injuries of, 724 Portacaval H-graft, 828 Portacaval shunt(s), emergency use of, 827 end-to-side, 827 arterialization of, 827-828 indications for, 827 selection of, 827 side-to-side, 828 types of, 827-828 vs. sclerotherapy, 835-836, 836t Portal circulation, hemodynamic measurement of, 819 Portal hypertension, 817-839 ascites with, 837-839 causes of, 818t classification of, 819, 820t complications of, 821-823 management of, 823-824

961

Portal hypertension (Continued) definition of, 817 diagnostic evaluation of, 819-821 hemorrhage in, acute, 824-825 variceal, 837 medical therapy for, 823-825 nonshunt surgical procedures for, 832-833 orthotopic liver transplantation for, 834-835 pathogenesis of, 817-819 postoperative care for, 833 sinusoidal, 818 splenic artery aneurysms and, 523 surgical shunt correction for, 825-832 transjugular intrahepatic portosystemic shunt for, 833-834 variceal sclerotherapy for, 835-837 Portal vein, embryologic development of, 30 in portal hypertension, 821 thrombosis of, 817, 853 Portal venous pressure, 819 Portal venous system, magnetic resonance angiography of, 283, 287f Port-wine stain (capillary malformation), 199, 199f, 201, 204f laser treatment for, 209 Position. See Patient position. Posterior arch vein, in venous function, 239 Postganglionic neuron(s), anatomy of, 443-444, 444f Postimplant syndrome, in abdominal aortic aneurysm endovascular repair, 386 Postoperative follow-up, duplex scanning for, 252 Postphlebitic syndrome, 11, 424, 425 Postsinusoidal obstruction, extrahepatic, 818-819 intrahepatic, 818 Poststenotic dilatation, in arterial stenoses, 232-233 Post-sympathectomy neuralgia, 449, 450 Post-thrombotic syndrome, venous abnormalities in, 242, 243, 243f venous reflux and, 257 Posture, correction of, for thoracic outlet syndrome, 682-683 in vertebrobasilar system transient ischemic attacks, 631 PowerLink endograft, for abdominal aortic aneurysm repair, 392 Prazosin, for intimal hyperplasia, 764 Precise nitinol stent, 372, 376f deployment of, 372, 377f Preganglionic neuron(s), anatomy of, 443-444, 444f Pregangrenous (blue) toe, 553. See also Blue toe syndrome. Pregnancy, anticoagulation during, 848 iliac artery aneurysms and, 506 renal artery aneurysm rupture in, 531-532 splenic artery aneurysms and, 523, 524f, 525 systemic thrombolytic therapy and, 422 thrombosis risk and, 78 varicose veins in, 859 Presinusoidal obstruction, extrahepatic, 817 intrahepatic, 817-818 Pressure(s). See also Blood pressure. cavernosal artery occlusion, 216-217 fluid, in arteries, 225 hydrostatic, in upright “dead man,” 240, 240f venous hypertension and, 859 intracompartment, in compartment syndrome, 130, 131 intravascular, in normal supine and erect positions, 240, 240f pull-back, across iliac artery lesions, in aortoiliac occlusive disease, 540 segmental, evaluation of, 12 in infrainguinal arteriosclerosis, 554

X0183-Idx 9/26/05 01:21 PM Page 962

962

Index

Pressure(s) (Continued) of lower extremity, 252-253 in vascular malformations, 204, 206f Pressure drop, in critical arterial stenosis, 233, 233f Principal component analysis, 254 PROACT II trial, t-PA use in, 433 Probucol, for atherosclerosis, 98, 100 ProcalAmine, for parenteral nutrition in diabetics, 158 Procoagulant activity, of endothelial cells, 42, 69t, 70 Profundaplasty, 789 for limb salvage, surgical criteria for, 556 Progesterone, venous function and, 859 Proinsulin, atherosclerotic disease and, 150 Propofol, in thoracoabdominal aortic aneurysm repair, 482 Propranolol, for portal hypertension, 825 Prostacyclin, endothelial cell–derived, 69, 69t for intermittent claudication, 273 in wound healing, 885 Prostaglandin, for intermittent claudication, 273 for Raynaud’s syndrome, 110 Prostaglandin E, in wound healing, 885 Prostaglandin E1, for intermittent claudication, 273 pharmacology of, 171 Prostaglandin I2, for intermittent claudication, 273 Prostate, examination of, 215-216 Prostheses, requirements for, for above-knee amputation, 908-909 for below-knee amputation, 905 for hip disarticulation, 909f, 910 for Syme’s amputation, 903, 903f for transmetatarsal amputation, 901 in elderly amputees, 913-915, 914t techniques for, constant environmental treatment unit in, 915-916, 916f conventional stump wrap in, 915, 915f for lower extremity amputees, 920-921 postoperative, 915-917, 915f-916f, 917t rapid and immediate postoperative, 916-917, 917t application of, 917-921, 917f-921f Prosthetic conduits, in bridge arteriovenous fistula, 698, 702 Prosthetic graft(s), aortic, infections of, 777-779, 778f, 779f rifampin-bonded, 780 aortic interposition, 777-778, 778f aortoiliac, 777-778, 778f characteristics of, 453-454, 453t, 777 Dacron. See Dacron graft(s). dilatation of, 459, 807-808, 808f failure of, 738-739 for aortic aneurysm repair, 4-5 for arterial reconstruction, 184 for femoral artery aneurysm repair, 516, 517 for subclavian artery aneurysm repair, 516 hemodynamic factors and, intimal hyperplasia and, 756 infections of, 772-781. See also Infection(s), prosthetic graft. preservation of, 778 materials composing, 188, 453-454, 453t, 777, 921-922, 921f characteristics of, 453t, 457-461, 458f-460f, 777 new developments in, 923-924, 923f occlusion of, thrombolytic therapy for, 430-431 PTFE. See PTFE graft(s). revision or replacement of, 746-747 thrombectomy of, 746

Prosthetic graft(s) (Continued) thromboreactivity of, 452-453 thrombosis of, 803 vs. autologous vein, 557 Prostin E1, 216 Protamine, adverse reactions of, 167 in distal aortic reperfusion, 477 structure and mechanism of action of, 167 Protease nexin, as plasmin inhibitor, 416 Proteases, in wound healing, 877, 878 Protein C, activated, resistance to, 77 deficiency of, thromboembolism and, 78 in coagulation inhibition, 72 pathway of, 42 Protein S, deficiency of, thromboembolism and, 78 endothelial cell–derived, 69t, 70 in coagulation inhibition, 72 Proteoglycan, intimal, 96 Proteolysis, focal, plasminogen-plasmin system and, 416 Proteus syndrome, 201 Prothrombin 20210A, 77 Prothrombin time, 73 in therapy for venous thrombosis, 848 in warfarin therapy, 81 Prothrombinase complex, 72 Pro-urokinase, 420 Pseudoaneurysm(s), 183. See also False aneurysm(s). causes and repair of, 800-801 femoral, infected, 186 formation of, with arteriovenous fistula, 705-706, 705f in intra-arterial thrombolytic therapy, 436 in PTFE bridge fistulas, 700 small, nonoperative management of, 726 thrombosis after angioplasty and, 428, 429f Pseudoclaudication, 552 Pseudomonas infections, graft excision and, 777 in prosthetic grafts, 773 Pseudoxanthoma elasticum, vascular abnormalities in, 124-125 PTFE graft(s), 458, 459-461, 459f, 460f blood flow in, intimal thickening and, 756 dilatation of, 808 failed, salvage of, 562, 562f for abdominal aortic aneurysm repair, 501 for antegrade bypass for chronic mesenteric ischemia, 612 for arteriovenous fistulas, aneurysm formation and, 705-706, 705f for bridge arteriovenous fistulas, 700, 700f for infrainguinal bypass, failures of, 738-739 for supra-aortic trunk revascularization, 662 for vascular injury repair, 719 thrombolytic therapy in, 431 thrombosis in, 805 vs. autologous saphenous vein grafts, for femoropopliteal bypass, 556-557 vs. Dacron grafts, 557, 777 vs. umbilical vein, 557 Pulmonary arteries, formation of, 24, 28 Takayasu’s disease affecting, 113, 114f Pulmonary complications, in lower extremity amputation, 912 in thoracoabdominal aortic aneurysm repair, 479-480 Pulmonary embolism, computed tomographyangiography for, 113, 114f deep venous thrombosis and, 82, 427 diagnosis of, 424 embolectomy for, 851 historical aspects of, 11 in intra-arterial thrombolytic therapy, 436

Pulmonary embolism (Continued) in lower extremity amputation, 911-912 prophylaxis for, 847-848 thrombolytic therapy for, 423-424, 433, 436 vena caval filters for, 848-850, 849f, 849t, 850f, 851f, 851t Pulmonary insufficiency, postoperative, 479-480 Pulmonary thromboembolism, 851-852 venous thrombosis and, 845 Pulsatile blood flow, 230 Pulsatility index, 254 Pulse(s), amputation level and, 894 arm, supra-aortic occlusive disease and, 660 deficit of, arterial injury and, 737 distal, in vascular trauma, 715 femoral, in aortoiliac occlusive disease, 538, 539 ischemic foot lesions and, 554 in acute limb ischemia, 739 in lower extremity, 235-236, 235f examination of, 554 normal, 236-237, 236f, 237f in wound healing, 880 neck, supra-aortic occlusive disease and, 660 pedal, in aortoiliac occlusive disease, 538-539 Pulse-volume recording, in infrainguinal arteriosclerosis, 554 in lower extremity evaluation, 254-255, 254f in vascular malformations, 204, 206f Pump, pneumatic compression, for lymphedema, 872, 873f

R Race, peripheral arterial disease and, 266 Radial artery, embryologic development of, 29f, 30 hand ischemia and, 737 in autogenous arteriovenous fistula for hemodialysis, 696 in bridge arteriovenous fistula, 699, 699f puncture of, 305t resuscitation catheter in, 717 Radiation therapy, arterial damage due to, 114-115, 114f carotid artery injury with, 625, 625f for control of smooth muscle cell proliferation after vascular injury, 42 Radicular artery(ies), 54, 54f great, of Adamkiewicz, 797 Radiofrequency, and laser ablation, of saphenous vein, 862, 864f Radiography, contrast, in vascular surgery, 12 for acute mesenteric ischemia, 606 for thoracic outlet syndrome, 680 for thoracoabdominal aortic aneurysm, 473, 473f Radioisotope markers, for diagnosis of arterial infections, 182 Radiology, interventional, 12 Ramipril, in diabetics, 146-147, 160-161 peripheral arterial disease and, 271 RASA1 gene, in port-wine stains, 201 Ray, amputation of, 899-900, 899f Raynaud’s syndrome, 107-111, 108f, 109t, 111t diagnosis of, 109-110 diseases associated with, 109, 109t of upper extremity, 690 pathophysiology of, 107-109, 109t prevalence of, 107 terminology in, 108 thoracic sympathectomy for, 447 treatment of, 110-111, 111t vasculitis in, 119

X0183-Idx 9/26/05 01:21 PM Page 963

Index

Raynaud’s syndrome (Continued) vasospastic vs. obstructive, 109 Reactive hyperemia, in stress testing, 253 Recombinant DNA technology, 419 Recovery filter, 850 Recurrent laryngeal nerve, embryologic asymmetry of, 28 in carotid endarterectomy, 640-641, 640f Red blood cell salvage devices, for thoracoabdominal aortic aneurysm repair, 475-476 Red-dot signs, 822 Reflex sympathetic dystrophy, lumbar sympathectomy for, 449 thoracic outlet syndrome and, 678 thoracic sympathectomy for, 447 Reflux, hydrodynamic, 859 hydrostatic, 859 superficial, in severe chronic venous insufficiency, 865 venous, chronic venous insufficiency and, 860, 861f duplex scanning of, 257 photoplethysmography of, 257-258, 258f Rehabilitation, for above-knee amputation, 908-909 for amputees, professional team for, 922-923, 922f for below-knee amputation, 905 for Chopart’s amputation, 901 for elderly patients, 913-915, 914t for knee disarticulation, 906-907 for Lisfranc’s amputation, 901 for Syme’s amputation, 903 for transmetatarsal amputation, 901 Reichert’s cartilage, 24 Reid sleeve, for treatment of lymphedema, 873 Renal artery(ies), abdominal aortic coarctation and, 126 aneurysms of, 530-533, 531f, 531t, 532f false, 532-533, 532f in polyarteritis nodosa, 115, 115f true, 530-532, 531f anomalous, intraoperative bleeding with, 785 arteriography of, 582-583, 582f atheroma of, 576, 576f blunt injuries of, 723 cannulation of, 314 dissections of, 532-533, 532f duplex scanning of, for renovascular hypertension, 580, 580t, 581f embolus of, intra-arterial thrombolytic therapy for, 430, 430f, 434, 434f in aortic surgery, 793 in fibromuscular dysplasia, 128-129, 129f in surgery for renovascular hypertension, 585, 586f, 587f, 589f in thoracoabdominal aortic aneurysm repair, 476, 476f, 477f insufficiency of, 10 in lower extremity amputation, 912 left, flank exposure for, 55-57, 56f, 57f in retroperitoneal exposure of abdominal aorta, 55, 55f in surgery for renovascular hypertension, 585, 586f magnetic resonance angiography of, 283, 285f, 286f medial fibrodysplasia of, 523 medial fibroplasia of, 576, 577f multidetector row computed tomographyangiography for, 295, 297f, 298f occlusive lesions of, 576, 576f, 577f. See also Renal artery stenosis. peak systolic velocity of, 335, 580, 580t, 581f reconstruction of, arterial autografts for, 456

Renal artery(ies) (Continued) hypertension and, 575-576 in renal artery dissection, 533 reimplantation of, 584, 585f right, flank exposure for, 57, 57f medial fibroplasia of, 576, 577f stenosis of. See Renal artery stenosis. surgical exposure of, left flank approach for, 55-57, 56f right flank approach for, 57, 57f transperitoneal, 59-60 thrombosis of, in aortoiliac occlusive disease, 537, 539f intra-arterial thrombolytic therapy for, 430, 430f Renal artery stenosis, aortic reconstruction and, 793 diagnosis of, 334 endovascular management of, 335-337 restenosis of, 339f, 340 results of, 337-341 hypertension and, 575 imaging studies of, 255, 286f, 298, 298f, 334-335, 580 in thoracoabdominal aortic aneurysm repair, 480 natural history of, 334 percutaneous transluminal angioplasty for, 598-599, 599t renin-angiotensin-aldosterone system and, 577 secondary hypertension and, 334 surgical treatment of, 584-589, 586f-591f, 591t aortorenal bypass in, 585-586 blood pressure response to, 589, 591, 592t, 593f long-term survival and, 596-598, 597f, 598f effect of, on hypertension, 575-576, 589, 591, 592t, 593f effect of, on renal function, 591-592, 593f-595f, 594, 594t ex vivo reconstruction in, 587-588, 591f, 591t extra-anatomic bypass in, 586-587, 590f late follow-up reconstructions for, 594-596, 595f, 596f mobilization and dissection in, 585, 586f-590f nephrectomy in, 588-589 thromboendarterectomy in, 586, 590f Renal collar, 32 Renal disease, end-stage, vascular access for hemodialysis and, 694, 694f, 695t Renal endarterectomy, transaortic, 56 Renal failure, acute, after revascularization of ischemic extremity, 749 aortic surgery and, 792-793 in abdominal aortic aneurysm repair, 502 infection and, 701 Renal function, abdominal aortic aneurysm repair and, 497, 502 after contrast angiography, 581-583 after endovascular management of renal artery stenosis, 340-341 effect of renal revascularization on, for ischemic nephropathy, 591-592, 593f-595f, 594, 594t in acute limb ischemia, 892 in aortic surgery, 792-793 in renovascular hypertension, drug therapy for, 584, 584t in thoracoabdominal aortic aneurysm repair, 480-481

963

Renal vein(s), circumaortic, 783, 784f in portal hypertension, 821 left, anomalies of, 502, 504 in abdominal aortic aneurysm repair, 500, 502, 504 in aortic surgery, 793 in aortoiliac surgery, 784 in inflammatory aneurysm, 504 in surgery for renovascular hypertension, 585, 587f mobilization of, 60 renin assays of, 583, 583t retroaortic, 783, 784f right, in surgery for renovascular hypertension, 585, 588f thrombosis of, 853 Rendu-Osler-Weber syndrome, 201, 205t Renin, 577 cerebral production of, after carotid endarterectomy, 639 renal vein assays for, 583, 583t stimulation of release of, 583 Renin-angiotensin-aldosterone system, 576-578, 758-759 Renovascular disease. See Renovascular hypertension. Renovascular hypertension, blood pressure response to, long-term survival and, 596598, 597f-598f characteristics of, 579 diagnosis of, 579-583 drug therapy for, 584, 584t endovascular treatment of, 334-342 historical aspects of, 575-576 in fibromuscular dysplasia, 129 incidence and prevalence of, 578-579, 578t, 579t management of, 583-584 management options for, 583-584 pathology of, 576, 576f, 577f pathophysiology of, 576-578 percutaneous transluminal angioplasty for, 598-599, 599t prevalence of, 578-579, 578t, 579t renal revascularization for, renal function and, 591-592, 593f-595f, 594, 594t splenic artery autografts for, 456 surgical treatment of, 10, 584-589, 586f-591f, 591t late follow-up reconstruction for, 594-596, 595f, 596f results of, 589, 591, 592t, 593f vs. essential hypertension, 579 Renovascular injury, hematuria and, 723 Renovascular insufficiency, 576 Repaglinide, 160 Reperfusion, in abdominal aortic aneurysm repair, 501, 502 in acute vessel or graft occlusion, 732 “no-reflow” phenomenon in, 733, 734 Reperfusion injury, after acute mesenteric ischemia, 605 compartment syndrome and, 130, 132 fasciotomy for, 747-748, 747f in thoracoabdominal aortic aneurysm repair, 479, 480, 482 pathophysiology of, 733-734 Respiratory failure, after revascularization of ischemic extremity, 749 Respiratory problems, postoperative, in thoracoabdominal aortic aneurysm repair, 479-480 Rest pain, ischemic, in chronic ischemia, 892 in infrainguinal arteriosclerosis, 551-552 Resuscitation, in bleeding patients with portal hypertension, 824

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964

Index

Resuscitation (Continued) in patients with variceal bleeding, 837 in vascular trauma, 717 Reteplase, for pulmonary embolism, 424 for thrombolytic therapy, 417t, 420-421, 743, 744, 790, 791 Reticular veins, definition of, 859 Retractor, intestinal laparoscopic, 404-405, 405f Retrograde ejaculation, 799-800, 799f Retro-pectoralis minor space, anatomy of, 676, 676f Retroperitoneal approach, in abdominal aortic aneurysm repair, 499-500, 504 to aorta, in laparoscopic surgery, 398-399, 404 modified, 399 to femoral anastomosis, 778, 779f Retroperitoneal space, zones of, 60, 61f Revascularization, after embolectomy, 746 compartment syndrome and, 130 endovascular, for renovascular disease, 334-342 fasciotomy after, 748 for abdominal aortic coarctation, 126 lymphatic, for treatment of lymphedema, 873 of coronary arteries, for Kawasaki disease, 116-117 of infected aortobifemoral grafts, 777, 778-779, 778f, 779f, 780f prior, effect of on amputation level, 893 surgical, for renal artery stenosis, 340-341 thrombosis after, causes of, 787-788, 787f, 788f correction of, 789-790, 789f diagnosis of, 788-789 vs. thrombolysis, for lower extremity ischemia, 431-433 with balloon angioplasty, mechanism of, 317 wound healing and, 876 nonhealing wounds and, 885-887 RGD peptides, synthetic, for arterial thromboembolism prevention, 85 Rheologic agents, 239 Rheumatoid arthritis, vasculitis of, 119 Rib(s), cervical, in thoracic outlet syndrome, 676, 677f, 685 first, exposure of, 53 resection of, in thoracic outlet syndrome repair, 683-684, 683f, 684f, 685 Rifampin, aortic prosthetic grafts bonded to, 780 Riolan, arch of, 604 Road mapping, in arterial access, 308 in carotid angioplasty and stenting, 360, 364, 365f Robotic surgery, for aortic repair, 409-410, 409t, 410f, 410t vs. human laparoscopic surgery, 409-410, 409t, 410t Roos’ test, 680 Rubeosis, ischemic optic neuropathy and, 631 Rubor, dependent, amputation level and, 895 Runoff vessels, after embolectomy, vasospasm of, 746 thrombosis and, 786-787, 787f

S Sac hygroma, in abdominal aortic aneurysm endovascular repair, 387-388 SACH (solid ankle-cushion heel) foot, in amputation prostheses, 921 Saddle embolus, 746 SAFE (stationary attachment flexible endoskeletal) foot, 921, 921f Salmonella, in infected aneurysms, 180, 182 in microbial arteritis, 180

Saphenous vein(s), accessory, 858f arterialization of, 452, 454-455, 454f, 455 autografts of, 719 fascial relationships of, 858, 858f grafts of, autogenous, 452 vs. PTFE, 556-557 for femoral artery reconstruction, 520 for infrainguinal bypass, 455, 738 for internal carotid injury repair, 721, 721f for renal artery reconstruction, 587, 590f for renal artery stenosis, 594, 595f, 596f for supra-aortic trunk revascularization, 661-662 in situ, for limb salvage, 557-558, 557f, 558f thrombosis of, 803 vs. reversed, 557-558, 557f, 558f, 806 patency of, 84, 455 thrombolytic therapy and, 431 greater, 63, 239 anatomy of, 454, 454f valves of, in varicose veins, 242, 243f harvest of, endoscopic, wound complications and, 806 surgical, 455 in varicose disease, 859 lesser, 239 anatomy of, 454 valves of, in varicose veins, 242 ligation of, 11 reversed, thrombosis of, 803, 804 surgical removal of (ablation), 862, 864f venography of, in infrainguinal arteriosclerosis, 555 SAPPHIRE study, 650 of carotid angioplasty and stenting, 355, 356 Sarcoidosis, portal hypertension and, 817 Sarfeh shunt, for portal hypertension, 826 Saruplase, 420 Scalene angle, in thoracic outlet syndrome, 677 Scalene fat pad, in exposure of thoracic outlet, 53 Scalene muscle(s), abnormalities of, 677, 677f anterior, anesthetic block of, 681-682 division of, 52, 52f in thoracic outlet syndrome repair, 677, 678, 683, 683f, 684, 684f, 685, 685f muscle fiber types of, 678 removal of, 53 middle, in thoracic outlet syndrome repair, 683-684, 683f, 684f Scalene triangle, anatomy of, 676, 676f Scalenectomy, partial, with transaxillary rib resection, for thoracic outlet syndrome, 683-684, 683f, 684f supraclavicular, with or without rib resection, 684-685, 685f, 687 Scalenus anticus syndrome, 675. See also Thoracic outlet syndrome. Scalpel, Harmonic, 447 Scanograms, for diagnosis of vascular malformations, 204, 207f Schistosomiasis, portal hypertension and, 817 Sciatic artery, embryologic development of, 29f, 30 persistent, 126-127 Sciatic vein, persistent, 199, 199f Scleroderma, Raynaud’s syndrome and, 109 upper extremity, 689 vasculitis of, 119, 119f Sclerotherapy, foam, for venous ablation, 862, 864, 864f, 865f for esophageal varices, 835-837 for vascular malformations, 207-209, 208f vs. distal splenorenal shunt, 830 Scribner shunt, 694, 695f

Seattle foot, 921 Seattle-Boeing-Burgess Foot, 921, 923 SECURITY trial, of carotid angioplasty and stenting, 357, 358f Segmental arterial pressure, 12 in infrainguinal arteriosclerosis, 554 measurement of, in lower extremity, 252-253, 254 in vascular malformations, 204, 206f Segmental plethysmography, for lower extremity evaluation, 254-255, 254f Segmental resistance, in arterial disease, 238-239 in lower limb, 235 Seldinger technique, 12, 695 for arterial access, 304-305, 306f retrograde, for aortoiliac occlusive disease, 540 Sengstaken-Blakemore tube, 825 Sensory dysfunction, in carotid artery transient ischemic attacks, 631 Sepsis, in arterial infections, 184 thrombosis risk and, 78 Septal defect, interventricular, 26 Septic thrombophlebitis, thrombolytic therapy and, 425 Septum, spiral, 28 embryologic, 25, 26, 27f Septum primum, 24, 26f, 27 Septum secundum, 24, 26, 26f Serum ammonia, in portal hypertension, 819 Serum markers, for peripheral arterial disease, 266 Servelle-Martorell syndrome, 201 Sexual dysfunction, in aortoiliac occlusive disease, 798-799 in males, aortofemoral bypass grafting and, 541 Shear, vessel diameter adjustment and, 37-38 Shear stress, fluid energy losses and, 226 nitric oxide synthase and, 38, 41, 41f on vessel wall, 38, 41, 41f, 756 Sheath(s), Ansel, 366 Balken, 310 characteristics of, 305-306 for angioplasty and stenting of renal lesions, 335, 336 for endovascular approach to infrainguinal disease, 344-345, 345t, 348t guiding, 315-316 introducer, 315 lengths of, 315 placement of, in common carotid artery, 362-367, 364f-369f, 364t, 365t prolapse of, in stent delivery, in carotid angioplasty and stenting, 363, 364f shapes of, 315 sizing of, 315 for balloon angioplasty catheters, 320, 320t vs. guiding catheter, 363, 364t Shepherd hook catheter, 314 Shepherd’s crook catheter, 310f Short-leg plaster cast, for Syme’s amputation, 902 for transmetatarsal amputation, 900 Short-leg walking cast, for Syme’s amputation, 902 Shoulder, inflammation or tears of, vs. thoracic outlet syndrome, 682 Shunt(s), arteriovenous, for vascular access for hemodialysis, 694-695, 695f carotid artery, indwelling, 515 Denver, for ascites management, 838 for extracranial cerebrovascular disease, 633-634 for portal hypertension, 825-832 central, 826

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Index

Shunt(s) (Continued) Clatworthy, 826 common portosystemic, distal splenorenal, 829-831, 829f. See also Distal splenorenal shunt. mesocaval, 828-829 nonselective, 827-829 portacaval, 827-828 proximal splenorenal, 829 selective, 829-831 development of, 826 Drapanas, 826 emergency portacaval, 827 indications for, 831-832 Inokuchi, 826 Linton, 826 nomenclature of, 825-826 prophylactic, 826 Sarfeh, 826 therapeutic, 826-827 Warren, 826 Gott, 475 intracaval, 728-729, 729f intrahepatic, 31 liver transplantation and, 835 peritoneovenous, for ascites management, 838, 839 portacaval, vs. sclerotherapy, 835-836, 836t right-to-left, 24, 25, 27 Scribner, 694, 695f transjugular intrahepatic portosystemic, for variceal hemorrhage, 833-834 Warren, 801 Shuttle sheath, in carotid angioplasty and stenting, 363, 364-365 Sigmoid colon pH, in ischemic colitis, 795 Sildenafil, for erectile dysfunction, 214, 222 oral, in wound healing, 885 Simmons catheter, 360, 361t, 366 for renal artery lesions, 335 Simon nitinol filter, 850, 850f Siphon, carotid, lesions of, 651 Sirolimus, for stent coatings in angioplasty, 765 Skeletal muscle, fiber types in, 678 ischemia and, 732 Skin, fluorescence of, amputation level selection and, 895-897, 895t, 896t in acute limb ischemia, 892 in lymphedema, 869, 869f, 870 in vascular malformations, 204 itching of, venous dysfunction and, 860 prosthetic graft infections and, 773 substitutes for, in wound healing, 884 temperature of, amputation level and, 894-895 ulcers of, in chronic ischemia, 892 Sleep laboratory, for diagnosis of erectile dysfunction, 216, 798 Sling, lymphedema, 872 Slip-Caths, 314 Small bowel, in laparoscopic surgery, 399 Small vessel(s), upper extremity, occlusion of, 689-690 Small vessel (infrapopliteal) bypass, for limb salvage, new techniques in, 570 results of, 565-566, 566f, 567f surgical criteria for, 556 surgical techniques for, 559f, 560f Small vessel disease, erectile dysfunction and, 214, 215, 216 microvascular procedures for, deep dorsal vein arterialization for, 221 indications for, 219-220 patient and procedure selection for, 220-221 venous interruption for, 221-222

Smart needle, in arterial access, 308 Smart PreP, in wound healing, 884 Smart stent, 326 Smoking, abdominal aortic aneurysms and, 489 atherosclerosis management and, 99 Buerger’s disease and, 120, 121 cessation programs for, 269-270 critical limb ischemia and, 268, 269 in diabetes, vascular disease and, 150 peripheral arterial disease and, 265, 268, 269 Raynaud’s syndrome and, 110 Smooth muscle, cavernous, 214 in fibrous plaques, 94 vascular, in atherogenesis, 94, 96, 97 in renovascular hypertension, 578 proliferation of, 38-41, 39f, 96, 97 vessel wall thickening and, 38-41, 39f Smooth muscle cell(s), in atherogenesis, 96 in inflammation, 758 in intimal hyperplasia, 755, 758, 759 in vascular injury response, 755-756 platelet-derived growth factor and, 757 proliferation of, local control of after vascular injury, 42 thrombin and, 42-43 vascular, 36-37, 96, 452, 755, 759 Smooth muscle growth factor, atheromatous plaque development and, 622 Sodium bicarbonate, in renal angiography, 582 Sodium nitroprusside, after carotid endarterectomy, 639 in thoracoabdominal aortic aneurysm repair, 480 Soft tissue abnormalities, in thoracic outlet syndrome, 676-677, 677f Solcograft, 457 Soleal sinuses, 239 Soleal veins, in venous thrombosis, 845 Soleus muscle, veins of, 239, 845 Solid ankle-cushion heel (SACH) foot, in amputation prostheses, 921 Somatosensory evoked potentials, in thoracic outlet syndrome, 680 Somatostatin, for intimal hyperplasia, 764-765 for variceal bleeding, 824-825 Sonograms, 247-248, 248f Sos catheter, 309-310 for renal artery lesions, 335 Sotradecol, for sclerotherapy for vascular malformations, 209 Spectral analysis, 247, 248, 248f, 250f Sphygmomanometer, early use of, 12 Spinal accessory nerve, in carotid endarterectomy, 635, 635f, 640 Spinal cord, in thoracoabdominal aortic aneurysm repair, 481, 482 ischemia of, 796-797 Spine, cervical, disorders of, vs. thoracic outlet syndrome, 682 exposure of, operative techniques for, 929-933 for lumbosacral spine, 931-933, 931f, 932f for thoracolumbar junction approach, 929-930, 930f Spiral ridges, embryologic, 25, 26 Splanchnic artery, aneurysms of, 523-530, 524t, 526t distribution of, 524t rupture of, 526t Splanchnic perfusion, portal hypertension and, 818 Splenectomy, for portal hypertension, 832 Splenic artery, anatomy of, 603, 604f aneurysms of, 523-526, 524f, 524t, 525f, 526t causes of, 523 clinical presentation of, 523-524

965

Splenic artery (Continued) diagnosis of, 524-525 rupture of, 524-525, 526t treatment of, 525-526 Splenic vein, in portal hypertension, 821 Splenomegaly, in portal hypertension, 820 Splenopancreatic disconnection, for modification of distal splenorenal shunt, 830-831 Splenorenal bypass, for renal artery reconstruction, 587, 590f Splenorenal shunts, distal, advantages of, 831 indications for, 831 principle of, 829-830, 829f sclerotherapy and, 830 splenopancreatic disconnection and, 830-831 surgical technique of, 831 vs. other shunts, 829, 830, 830f vs. sclerotherapy for variceal bleeding, 836, 837t proximal, 829 Spurling test, 682 Stab avulsion, for varicose veins, 862, 863f Stanozolol, as fibrinolytic agent, 417 Stapedial artery, formation of, 28 Staphylococcus aureus, in infected aneurysms, 180 in microbial arteritis, 180 in prosthetic graft infections, 772, 773 in renal failure, 701 in vascular graft infections, 188, 189t lower extremity amputation and, 891 Staphylococcus epidermidis, in prosthetic graft infections, 772, 774 in vascular graft infections, 188, 189, 189t, 191, 194 in situ PTFE graft replacement for, 777 Staphylococcus species, mycotic aneurysms and, 506 Staphylokinase, as thrombolytic drug, 421 Statin drugs, adverse effects of, 172 clinical uses of, 171-172 for atherosclerosis, 97, 98, 99 for infrainguinal arteriosclerosis, 570 in diabetics, cardiovascular disease and, 146, 146t pharmacology of, 171-172 structure and mechanism of action of, 171 Stationary attachment flexible endoskeletal (SAFE) foot, 921, 921f Steal syndrome, arteriovenous fistulas and, 704 Stellate ganglion, 444, 444f, 445, 446f Stenosis, difficult access with, in carotid angioplasty and stenting, 361, 363f, 363t in vascular access thrombosis, 703, 703f repetition of, prevention of, 41-42 Stent(s). See also Stent-grafts. balloon-expandable, 5, 8, 326, 326f carotid, high-risk patients for, 356-358, 356t, 358f, 358t complications of, 329-331, 331t contraindications to, 327, 327t endarterial, 8 endovascular, for blunt renal artery injuries, 723 for aortoiliac disease, 325-331 for endovascular treatment of infrainguinal disease, 345, 345t, 348, 348t, 351f self-expanding, 345, 348, 351, 351f for renal artery lesions, 336-337, 338f, 339-340, 339f, 599, 599t monorail delivery systems of, 336-337 general principles of, 325-326 guiding sheath used with, 315

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966

Index

Stent(s) (Continued) in carotid angioplasty and stenting, deployment of, 372-373, 375, 376f-378f indications for, 326-327 infrainguinal, 569 monorail delivery systems of, for endovascular treatment, 336-337, 345 for renal artery lesions, 336-337 nitinol, 326. 348, 351, 355, 372, 376f deployment of, 372, 375, 377f, 378f for infrainguinal bypass grafts, 563 placement of, in abdominal aortic aneurysm repair, 5-6 in femoropopliteal artery, 351-352, 351t self-expanding, 326, 326f, 345, 348, 351, 351f subintimal, for femoropopliteal lesions, 352 types of, 325-326, 326f ureteral injury and, 798, 798f with angioplasty, for aortoiliac occlusive disease, 547 vs. carotid endarterectomy, 649-650 Stent-grafts, endovascular, for abdominal aortic aneurysm repair, 497 for prosthetic graft infections, 780 for thoracoabdominal aortic aneurysm repair, 483-484 for traumatic arteriovenous fistulas, 726, 727f thrombosis of, 739 for carotid artery repair, 721-722 for extracranial carotid artery aneurysm repair, 516 for femoral and popliteal artery aneurysm repair, 517, 518 for iliac artery aneurysm repair, 507 for subclavian artery aneurysm repair, 516 Sternocleidomastoid muscle, carotid bifurcation and, 46 Sternotomy, median, for exposure of anterior aortic arch branches, 50, 51f minimal version of, 49-50, 50f technique of, 666, 666f STILE trial, 422-423, 790 for acute limb ischemia, 743 for lower extremity ischemia, thrombolysis vs. surgery in, 431-432 Stockings, antiembolic, for venous thromboembolism prophylaxis, 82 compression, for chronic venous insufficiency, 244 for lymphedema, 873 for wound healing, 881, 881f Storage pool diseases, platelet disorders in, 75 Streptokinase, allergic reactions with, 427 contraindications to, 422, 422t for deep venous thrombosis, 424, 848 for peripheral vascular thrombosis, 421 for pulmonary embolism, 423 for thrombolytic therapy, 790 for thrombosed infrainguinal grafts, 568 for thrombosis of vascular access fistula, 703 mechanism of action of, 417-418 thrombolytic activity of, 417-418, 417t vs. tissue plasminogen activator, 419 Stress, in thoracic outlet syndrome, 677 insulin requirements and, 152t Stress testing, technique of, 253-254, 253f String sign, in carotid angioplasty and stenting, 361, 363f in internal carotid artery occlusion, 250 “String-of-beads” appearance, 576, 577f Stripper, for venous dissection, 11 thromboendarterectomy, 789, 789f Stroke, carotid endarterectomy and, 9-10, 641, 642-643, 643t, 649. See also Carotid endarterectomy. cervical carotid artery disease and, 617

Stroke (Continued) diabetes and, 142-145 distal internal carotid artery aneurysm repair and, 515 duplex scanning for, 251 endovascular repair of thoracoabdominal aortic aneurysms and, 483 extracranial cerebrovascular disease and, 631-632 imaging of, 632 incidence and mortality of, 618-619, 619f pathogenetic mechanisms of, 626-629 prevention of, by carotid angioplasty and stenting, 355, 356, 357, 358 by carotid endarterectomy, 355, 644-647 by extracranial-to-intracranial bypass grafting, 651 by medical therapy, 647-649 progressing, 618-619 risk of, with recurrent stenosis after carotid endarterectomy, 626 silent, 620 supra-aortic trunk surgical reconstruction and, 669 thrombolytic therapy for, 433 Stroke in evolution, 618-619 carotid endarterectomy for, 649 transient ischemic attack and, 630 Stump, amputated, hematoma of, 911 immediate postoperative prosthetic technique for, 916-917, 917t application of, 917-921, 917f-921f infection of, 894, 911 nonhealing of, 910-911 revision of, 912 soft dressing for, 915, 915f Sturge-Weber syndrome, 201, 205t Subclavian artery, anatomy of, 675, 676f aneurysms of, mycotic, 519-520 nonmycotic, 512, 513, 514, 515, 516, 517 in thoracic outlet syndrome, 678 injury to, in thoracic outlet syndrome repair, 686 left, puncture of, 303, 304f, 305t surgical exposure of, 51, 52, 52f occlusion of, in vertebrobasilar system transient ischemic attacks, 631 revascularization for, 663-664, 664f proximal, subclavian steal syndrome and, 237 right, surgical exposure of, 50, 51f Subclavian steal, 237 carotid-subclavian bypass for, 661 of vertebral artery, 251, 251f pathogenetic mechanism of, 628, 628f pulse lag in, 660 Subclavian vein, anatomy of, 676, 676f in thoracic outlet syndrome, 678 injury to, in thoracic outlet syndrome repair, 686 right, surgical exposure of, 50, 51f stenosis of, in central venous catheter hemodialysis, 696 thrombosis of, 852-853 Subclavian-carotid bypass, and carotid (or subclavian) transposition, 662, 663664, 663f, 664f for common carotid artery revascularization, 662, 663-664, 663f, 664f Subclavian-subclavian bypass, for innominate artery revascularization, 662, 664 Suguira procedure, for portal hypertension, 832-833 Superoxide dismutase, in reperfusion, 733 Superoxide radicials, in reperfusion, 733, 734 Support stockings, for chronic venous insufficiency, 244

Supra-aortic trunks, anatomic variations in, 659 anterior, exposure of, 666, 666f, 667f arteriography of, 659-660 atherosclerosis of, 659 occlusive disease of, 660 surgical reconstruction of, 659-673 axial repairs in, 661-665 technique of, 666-668 cervical repairs in, 661-665 anatomic indications for, 662-663 techniques of, 663-665 vs. axial repair, 661 indications for, 660-661 results and complications of, 668-669, 668t Supraclavicular approach, to subclavian artery aneurysm repair, 516 Supraclavicular incision, 51 Supraclavicular scalenectomy, with or without rib resection, 684-685, 685f, 687 Surgery, in hemophiliac patients, blood replacement therapy for, 76 stroke risk with, with asymptomatic carotid artery lesions, 620-621 vascular, history of, 1-13 noninfectious complications of, 783-809 vascular access, 13 venous, historical aspects of, 10-12 venous thrombosis risk and, 79 Surgery versus Thrombolysis for Ischemia of the Lower Extremity (STILE) trial, 422-423 Surgical exposure, extraperitoneal, of iliac arteries, 61-62, 62f of abdominal aorta, and branches, 57-58, 58f, 499-500, 504 and vena cava, 60-61, 61f at diaphragmatic hiatus, 58-59, 59f for aneurysm repair, 499-500, 504 infrarenal, 59-60 of anterior supra-aortic trunks, 666, 666f, 667f of aortic arch branches and associated veins, 49-50, 50f, 51f of axillary artery, 52, 52f of carotid bifurcation, 46-48, 47f, 47t of femoral artery, common, 62 deep, 62, 62f of high internal carotid artery, 48-49, 49f of left subclavian artery, 51-52, 52f of pedal arteries, 65-66, 65f, 66f of peroneal artery, 65 of popliteal artery, 63, 63f of renal arteries, 55-57, 59-60 of right subclavian artery and vein, 50, 51f of subclavian arteries, 51-52, 52f of thoracic outlet, 52-53 of tibial arteries, 64-65, 64f of vascular system, 46-66 of vertebral arteries, 51-52, 52f of visceral arteries, 55-57, 56f retroperitoneal, of abdominal aorta, 499-500, 504 transperitoneal, of abdominal aorta, at diaphragmatic hiatus, 58-59, 59f infrarenal, 59, 60f of renal arteries, 59-60 Suture(s), arterial, history of, 2-3 false aneurysms and, 800 for abdominal fascia closure, 801 laparoscopic, 408 materials used for, 184, 501, 719 Suture lines, postoperative bleeding from, 785 prosthetic, anastomotic false aneurysm and, 800 Swan-Ganz catheters, for prevention of declamping hypotension, 792

X0183-Idx 9/26/05 01:21 PM Page 967

Index

Swan-Ganz catheters (Continued) for thoracoabdominal aortic aneurysm repair, 475, 480 Sweating, sympathectomy and, 444, 447, 448 Syme’s amputation, 901-903, 902f, 903f prosthetic application technique for, 917 prosthetic components for, 921 Sympathectomy, for lowering peripheral resistance in arterial lesions, 239 historical aspects of, 6 lumbar, for Raynaud’s syndrome, 110 historical aspects of, 443 indications and contraindications for, 445t, 448 open surgical, 449, 450 retroperitoneoscopic, 449, 449f patient position for, 448, 448f, 449f results of, 449, 450 thoracic, cervical approach to, 445-446, 446f historical aspects of, 443 indications for, 444-445, 445t results of, 447 technique of, 445-447, 445f-447f transaxillary approach to, 445, 445f thoracoscopic, 446-447, 446f, 447f Sympathetic nervous system, anatomy of, 443-444, 444f in renovascular hypertension, 577, 578 physiology of, 444 Symphony stent, 326 Syndrome X, in diabetes, vascular disease and, 150 Syphilitic aneurysms, 178-179 Systemic lupus erythematosus, vasculitis of, 120

T T lymphocytes, in aortic wall, 491 in fatty streak lesions, 93 Tadalafil, for erectile dysfunction, 214 Takayasu’s arteritis, 112t, 113-114, 114f cerebrovascular disease with, 623-625 Tandem lesions, in carotid angioplasty and stenting, 361, 363f, 363t Tarsal artery, lateral, 66 Tarsometatarsal joint amputation (Lisfranc’s), 901 Technetium-99m pertechnetate, skin blood pressure with, amputation level selection and, 895t, 896t, 897 Telangiectases, definition of, 859 pathogenesis of, 858-859 Temporal arteritis, 112-113, 112t, 113f Tenase complex, in thrombin generation, 72 Tenecteplase, for thrombolytic therapy, 421, 790, 791 Tennis Racquet catheter, 309, 310f Terlipressin, for variceal bleeding, 825 Terumo Glidewire, 305 Tessari technique, of foam sclerotherapy, 862, 864f, 865f Testosterone, in erectile physiology, 214 Tetralogy of Fallot, embryologic development of, 26 Thalamoperforating arteries, occlusive disease involving, 629 Theophylline, pharmacology of, 171 Thermoelectrocoagulation, of saphenous vein, 862, 864f Thiazolidinediones, 160 for intimal hyperplasia, 766 Thienopyridines, pharmacology of, 169 Thigh, bridge arteriovenous fistulas in, 700 segmental pressure measurements in, 253

Thiobarbituric acid reacting species (TBARS), 150 Thiopental sodium, in thoracoabdominal aortic aneurysm repair, 482 Thoracic duct, anatomy of, 676 protection of, 51 Thoracic nerve, long, in brachial plexus, 676 in thoracic outlet syndrome repair, 685, 686 Thoracic outlet, anatomy of, 675, 676f surgical exposure of, 52-53 vessels of, repair of, 722, 722f Thoracic outlet compression syndrome, 426, 675. See also Thoracic outlet syndrome. Thoracic outlet syndrome, 675-688 anatomic relationships in, 675-676, 676f arterial, arteriography for, 680-681, 681f diagnosis and management of, 688 causes of, 676-677, 677f clinical presentation of, 678-679 conservative management of, 682-683 decompression for, 516 diagnosis of, 679-682 differential diagnosis of, 682 exacerbating factors in, 679 historical aspects of, 13, 675 incidence of, 675 laboratory tests for, 680-682, 681f pathology of, 677-678 physical examination for, 679-680 postoperative care of, 686 subclavian artery aneurysms and, 512, 514, 515 surgery for, 13, 683-686 combined approach for, 685 complications of, 686-687 indications for, 683 posterior approach for, 686 results of, 687 supraclavicular scalenectomy for, 684-685, 685f, 687 transaxillary rib resection and partial scalenectomy for, 683-684, 684f, 687, 687f venous, 687-688 venography for, 681, 681f Thoracic sympathectomy, cervical approach to, 445-446, 446f historical aspects of, 443 indications and contraindications for, 444-445, 445t results of, 447 technique of, 445-447, 445f-447f transaxillary approach to, 445, 445f Thoracoabdominal aortic aneurysm(s), 469-487 aortic dissection and, 469-470, 471f causes of, 470, 472t classification of, 469-470, 470t, 471f, 472t clinical results of, 483, 483t degenerative, 472-473 diagnosis of, 473, 473f, 474f, 475, 475f endovascular approach to, 483-484 mortality of, 470, 470t, 471-472, 472t natural history of, 471-472, 472t postoperative care of, 478-479 postoperative complications of, 470, 472t, 479-483, 481f mortality and, 470, 470t neurologic, 470, 470t presentation of, 472-473 risk factors for, 470, 472t rupture of, 473 mortality and, 471-472, 472t spinal cord ischemia and, 797 treatment of, 475-478, 476f, 477f, 478f, 479f Thoracolumbar spine exposure, 929-930, 930f

967

Thoracoscopic sympathectomy, 446-447, 446f, 447f Thoracotomy, anterior, for exposure of left subclavian artery, 51, 52f Thrill, in autogenous arteriovenous fistula, 697, 784 Thrombectomy, 789, 789f, 849 for acute graft occlusion, vs. thrombolytic therapy, 430-431 mechanical methods of, 791 of bypass grafts, 746 transvenous catheter, percutaneous techniques of, 852, 852f Thrombin, function of, 168, 415 generation of, 71-72 in intimal hyperplasia, 759 inhibitors of, direct and indirect, 72f, 80-81, 168 smooth muscle cell proliferation and, 42-43 Thrombin time, 73, 74 in intra-arterial thrombolytic therapy, 434 Thromboangiitis obliterans (Buerger’s disease), 8, 120 Thrombocytopenia, 74 heparin-induced, 81, 166-167, 787 anticoagulation therapy and, 79 Thrombocytopenic purpura, immune, 74 Thromboelastography, 786 Thromboembolism. See also Venous thromboembolic disease. in femoral and popliteal artery aneurysms, 513, 517, 518 of lower extremity, 553 prophylaxis of, 82-85 pulmonary, 851-852 venous thrombosis and, 851-845 renal artery aneurysms and, 532 Thrombogenesis, atherosclerosis and, 95-96 Thrombolytic therapy, 414-442 agents used for, first-generation, 417-419, 417t second-generation, 419-420 third-generation, 420-421 catheter-directed techniques of, 425, 426, 427 compartment syndrome and, 130 failed infrainguinal reconstruction and, 742 fibrinolytic agents and, 416-417 for acute limb ischemia, 742-744, 742f, 743f technique of, 743-744 for acute mesenteric ischemia, 607 for axillary vein thrombosis, 426, 426f for axillosubclavian vein thrombosis, 690 for carotid angioplasty and stenting, 379, 379f, 380f for deep venous thrombosis, 424-425 for femoral and popliteal artery aneurysm repair, 517-518 for graft salvage procedures, 562 for lower limb ischemia, 422-423 for occluded aortofemoral and femoropopliteal bypass grafts, 790-791 for postreconstructive thrombosis, 789 for pulmonary embolism, 423-424 for subclavian vein thrombus, 853 for superior vena cava thrombosis, 426 history of, 414 intra-arterial, 427-436, 805 clinical trials of, 431-433 complications of, 435-436 contraindications for, 427, 428, 428t for acute graft occlusion, 430-431, 431f for acute stroke, 433 for hemodialysis access, 433 for lower extremity ischemia, 431-433 for native vessel occlusion, 428, 430, 430f for thrombosed infrainguinal grafts, 568

X0183-Idx 9/26/05 01:21 PM Page 968

968

Index

Thrombolytic therapy (Continued) for thrombosis after percutaneous angioplasty, 428, 429f indications for, 428, 429f-431f, 430, 431 patient selection for, 427-428 results of trials for, 431-433 technique of, 433-435 intraoperative, 436-438, 437t patient selection for, 422-423, 427-428, 742-743, 743f pulse-spray pharmacomechanical, 433 systemic, 422-427 complications of, 426-427 contraindications to, 422, 422t for axillary vein thrombosis, 426 for deep venous thrombosis, 424-425 for pulmonary embolism, 423-424 for superior vena cava thrombosis, 426 indications for, 423-426 patient selection for, 422-423 Thrombomodulin, endothelial cell–derived, 42, 69-70, 69t in coagulation inhibition, 72 Thrombophilia, screening for, 79 Thrombophilic factors, inherited, in venous thrombosis, 845 Thrombophlebitis migrans, 852 Thromboplastin, endothelial cell–derived, 69t, 70 Thromboreactivity, of graft, 452-453 Thrombosis, 77-85. See also Embolus(i); Occlusive disease. abdominal vein, 185, 853 after percutaneous angioplasty, intra-arterial thrombolytic therapy for, 428, 429f after revascularization, causes and prevention of, 786-788, 787f, 788f diagnosis of, 788-789 in vertebral artery reconstruction, 673 treatment of, 789-790, 789f aortic, neonatal, 751-752, 752f, 752t arterial, 735-738 causes of, 735-736 early surgical repair of, 6-8 of carotid arteries, 627, 627f of lower extremity, 735 of upper extremity, 689 axillary vein, 426, 426f axillosubclavian vein, 690, 706 in venous thoracic outlet syndrome, 687-688, 688f cerebral protection device and, risks with, 359 deep venous. See Deep venous thrombosis. endothelial regulation of, 42-43 heparin-induced, 787 hepatic vein, 853 portal hypertension and, 818 in acute lower extremity ischemia, 741-742 in aortoiliac and aortofemoral reconstructions, 786-791, 787f, 788f, 789f in Buerger’s disease, 120, 121, 121f in infrainguinal bypass procedures, 802-806, 802f, 804f, 805f in postoperative period, 803 management of, 804-806, 804f, 805f surveillance for, 803 technical causes of, 802, 802f in Kawasaki disease, of coronary artery aneurysms, 116 in limb salvage bypass, reoperation for, 561563, 561f, 562f, 566-568, 567f in PTFE bridge fistulas, 700 in PTFE grafts, 805 in vascular access for hemodialysis, 702-704, 702f, 703f

Thrombosis (Continued) inferior vena cava, 853 management of, 80-82 mesenteric vein, 606, 607, 608 portal vein, 817 prophylaxis for, 82-85 prothrombotic conditions contributing to, 77-79 recurrent, 748-749 renal artery, in aortoiliac occlusive disease, 537, 539f renal vein, 853 secondary bypass procedure for, 805 subclavian vein, 852-853 superior vena cava, thrombolytic therapy for, 426 trauma and, 79, 736 venous, 845-853. See also Deep venous thrombosis. diagnosis of, 846-847 duplex scanning for, 256-257, 256f, 257f other types of, 852-853 prevention of, 847-848 treatment of, 848-850 vs. emboli, 740 Thrombosis in Myocardial Infarction (TIMI) trial, 421, 422 Thromboxane A2, 168, 622 Thromboxane synthetase inhibitors, for intimal hyperplasia, 763 Thrombus, catheter use and, 314 fibrous cap of, 735 in acute limb ischemia, 891-892 in carotid angioplasty and stenting, 361, 363f, 363t in reperfusion injury, 734 mechanical methods of removing, 804 mesenteric arterial, 605f, 608 mural, in abdominal aortic aneurysm repair, 501 intra-arterial thrombolytic therapy and, 428 postoperative thrombosis and, 788 systemic thrombolytic therapy and, 422 venous, magnetic resonance venography for, 287 vs. embolus, 735 Thymus gland, in exposure of aortic arch branches and veins, 50 Tibial artery, anterior, embryologic development of, 29f, 30 exposure of, 64, 64f arteriovenous fistula of, 725f emboli of, intra-arterial thrombolytic therapy for, 430 in embolectomy, 745 in infrapopliteal bypass for limb salvage, 556, 559f, 560f injuries of, 724 posterior, distal, 65f, 66 embryologic development of, 29f, 30 exposure of, 64-65, 64f Tibial occlusive disease. See Arteriosclerosis, infrainguinal. Tibioperoneal trunk, grafts of, 8 Tibiotibial bypass, for infrainguinal arteriosclerosis, 570 Ticlopidine, adverse reactions to, 169 as antiplatelet agent, 84 clinical uses of, 169 for intimal hyperplasia, 763 for prevention of extracranial occlusive disease, 648 peripheral arterial disease and, 271 pharmacology of, 169 structure and mechanism of action of, 169

Time-of-flight magnetic resonance angiography, 280 Tinel’s sign, in thoracic outlet syndrome, 680 Tinnitus, in vertebrobasilar system transient ischemic attacks, 631 Tirofiban, 85, 170 Tissue cultures, for diagnosis of arterial infections, 182 Tissue factor, endothelial cell–derived, 69t, 70 in early atherogenesis, 94 in thrombin generation, 71-72 Tissue factor pathway inhibitor, endothelial cell–derived, 69t, 70 in coagulation inhibition, 72 in heparin therapy, 80 Tissue glue, biologic, 785 Tissue inhibitors of metalloprotease (TIMP), aortic aneurysm formation and, 490-491 Tissue pedicle, for control of sepsis in arterial infections, 184 Tissue plasminogen activator, bleeding complications with, 421-422 circadian variations in, 416 complications of, 420 endothelial cell–derived, 69t, 70 for venous thrombosis, 848 in carotid angioplasty and stenting, 379, 380f in fibrinolytic system, 73, 415, 416 in intimal hyperplasia, 759-760 intra-arterial, for thrombosed infrainguinal grafts, 568 recombinant, dose and infusion time for, 420 for acute limb ischemia, 743 for acute stroke, 433 for deep venous thrombosis, 424 for pulmonary embolism, 423, 424 vs. urokinase, 424 for thrombolysis, 790, 791 for lower extremity ischemia, 431-432 vs. streptokinase, 419 thrombolytic activity of, 417t, 419-420, 431-432, 743, 744, 790 types of, 419 X fragments and, in fibrinolysis, 415 Tissue renin-angiotensin system, 758 Tissue transfer, autologous, in wound healing, 884 procedures for, in revascularization of nonhealing wounds, 887, 887f Tobacco. See Smoking. Toe(s), amputation of, 898-900, 898f, 899f noninvasive testing and, 554-555 selection criteria for, 895t autoamputation of, 898 great, chronic osteomyelitis of without gangrene, 898 in lymphedema, 870, 870f ischemic lesions of, from operative embolization, 791, 792f lesions of, in limb salvage bypass procedures, 561 pregangrenous (blue) vs. gangrenous (black), 553 Tolazoline, for Raynaud’s disease of upper extremity, 690 TOPAS trial, for acute limb ischemia, 743 Total parenteral nutrition, vascular access for, 706-709, 707f, 708f, 709f Tourniquet, extremity ischemia and, 737 Tracheotomy, postoperative, in thoracoabdominal aortic aneurysm repair, 479-480 Tranexamic acid, 415 Transabdominal paracolic approach, in laparoscopic surgery, 399 Transabdominal retrorenal approach, in laparoscopic surgery, 400

X0183-Idx 9/26/05 01:21 PM Page 969

Index

Transaortic endarterectomy, 56 for renal artery reconstruction, 586, 590f TransAtlantic Inter-society Consensus (TASC), 540 Transaxillary rib resection, and partial scalenectomy, for thoracic outlet syndrome, 683-684, 683f, 684f, 687 Transcatheter embolization, for hepatic artery aneurysm repair, 527 for renal artery aneurysm repair, 532 for splenic artery aneurysm repair, 525 Transcutaneous electrical nerve stimulation (TENS), for Raynaud’s syndrome, 110 Transcutaneous oxygen partial pressure, amputation level selection and, 895t, 896-897, 896t in wound healing, 880, 885 Transesophageal echocardiography, for thoracoabdominal aortic aneurysm, 475 Transforming growth factor, in smooth muscle proliferation, 38 Transforming growth factor-β, atherogenesis and, 97 in acute wound healing, 877, 878 in diabetes, vascular endothelial cell function and, 149 in fatty streak lesions, 93 in ischemic nephropathy, 578 Transfusion(s), blood, for severe hemorrhage, 824 thrombocytopenia with, 74 Transient ischemic attacks, after carotid endarterectomy, 641, 642-643, 643t approach to, 630 carotid artery, 631 crescendo, 618-619, 630 carotid endarterectomy for, 649 definition of, 630 differential diagnosis of, 630 duplex scanning for, 251 flow-related, 627-628 in fibromuscular dysplasia, 129 pathogenetic mechanisms of, 626-629 stroke and, 619 stroke in evolution and, 630 vertebral artery occlusion and, 661 vertebrobasilar system, 631 Transjugular intrahepatic portosystemic shunt (TIPS), for variceal hemorrhage, 833-834 Transjugular venous catheterization, for measurement of portal venous pressure, 819 Transluminal angioplasty. See Angioplasty. Transmetatarsal amputation, 900-901, 900f prosthetic application technique for, 917 prosthetic components for, 921 Transperitoneal approach, in abdominal aortic aneurysm repair, 500 in laparoscopic surgery, 399, 404, 405f in transaortic endarterectomy, 586, 590 to abdominal aorta at diaphragmatic hiatus, 58-59, 59f to aorta, in laparoscopic surgery, 399, 404, 405f to infrarenal abdominal aorta, 59, 60f to renal arteries, 59-60 Transperitoneal medial visceral rotation, incision for, 57-58, 58f Transvenous catheter embolectomy, 851-852, 852f TrapEase filter, 850 Trash foot syndrome, 791, 792f in abdominal aortic aneurysm repair, 503 Trasylol, 416

Trauma. See also Injury(ies). blunt, in arteries of extremities, 724 in carotid arteries, 720-721, 721t renal artery injuries with, 532, 533, 723 thrombosis due to, 736 carotid artery aneurysms and, 623 hepatic artery aneurysms and, 526 iatrogenic, acute extremity ischemia and, 737 in thoracic outlet syndrome, 677 lower extremity amputation for, 894 mycotic aneurysms and, 518, 519 nonmycotic peripheral artery aneurysms and, 512, 513 thrombosis due to, 79, 736 vascular, 69-70, 713-730 anticoagulation in, 718 arterial wall response to, 38-42 arteriovenous fistulas in, 9, 724-726, 725f, 727f basic repair techniques in, 719 brachiocephalic arterial injuries in, 720-722, 720f, 721f carotid injuries in, 720-722, 720f, 721f, 721t causes of, 713, 713t, 714t control of bleeding in, 718-719 diagnosis of, 713-717, 715f, 715t, 716t, 717t physical examination for, 714-715, 715t endothelial cell response to, 38-42, 42f false aneurysms in, 724-726, 726f historical aspects of, 8-9 injuries of abdominal aorta and its branches in, 722-723 injuries of arteries of extremities in, 724 injuries of inferior vena cava in, 726-730, 728t-730t, 729f injuries of root of neck in, 722, 722f mechanism of injury in, 713-714, 714f minimal (nonocclusive), 726, 728f operative management for, 718-720 resuscitation of patient with, 717 sites of, 714t six P’s in, 715 smooth muscle cell response to, 38-40, 39f, 40f, 755-756 tibial artery injuries in, 724 wound protection in, 717-718 venous thrombosis risk and, 79 Treadmill exercise, in stress testing, 253 Trendelenburg position, in transperitoneal approach, 399, 404 Trendelenburg’s operation, for varicose veins, 11 Tricuspid valve, embryologic development of, 24 Triglycerides, atherosclerosis and, 100 Trocars, insertion of, in laparoscopic aortic surgery, 400-401, 401f, 402, 403f, 409 Troglitazone, 100, 160, 766 Truncus arteriosus, 24 embryologic development of, 23-24, 25, 26, 27f, 28 Tube(s), Blakemore, 3 fibrocollagenous, for modification of vascular grafts, 462 heart, 22f, 23 Minnesota, 825 Sengstaken-Blakemore, 825 Tube feeding, in diabetics, 156-158, 156t, 157f, 158t Tumor(s), carotid body, 626, 638 malignant, in abdominal aortic aneurysm repair, 505 Tumor cells, plasminogen-plasmin system and, 416

969

Tumor necrosis factor-α, in acute wound healing, 878 in atherogenesis, 92 in inflammation, 758 in reperfusion injury, 734

U Ulcer(s), carotid, asymptomatic, 650-651 chronic, healing of, 878 diabetic, wound healing and, 876 from ruptured atherosclerotic plaque, 628, 629f, 630f of fingers, in Buerger’s disease, 121-122 skin, in chronic ischemia, 892 venous, definition of, 859 venous hypertension control and, 865 vs. arterial or ischemic, 553 Ulnar artery, embryologic development of, 29f, 30 Ulnar nerve, entrapment of, vs. thoracic outlet syndrome, 682 in thoracic outlet syndrome, 678 Ultrasound examination. See also Doppler studies; Duplex scanning. abdominal, as alternative to renal angiography, 582 B-mode, for abdominal aortic aneurysms, 492-493 for venous thrombosis, 846 in duplex scanning, 248, 249f early use of, 12 for arterial access, 308 for chronic mesenteric ischemia, 609 for peripheral artery aneurysms, 514 for portal hypertension, 819 for prosthetic graft infection, 775 for renovascular hypertension, 580, 580t, 581f for splenic artery aneurysms, 524 for vascular access fistula, 703 for vascular trauma, 715 Ultrasound instrumentation, 247-249, 256 Doppler systems in, 247-249, 248f, 249f duplex scanning in, 248-249, 249f Umbilical artery, catheter in, thrombosis with, 751 embryologic development of, 30 Umbilical vein, 24 allografts of, 456-457, 457f, 463, 702 embryologic development of, 30-32 grafts of, dilatation of, 808 for distal femoral reconstruction, 8 vs. PTFE grafts, 557 platelet–derived growth factor and, 757 United Kingdom (UK) Small Aneurysm Trial, aneurysm rupture risk and, 495 Unna sleeve, for treatment of lymphedema, 873 UPET trial, 423 Uremia, platelet effects of, 75 Ureter(s), in inflammatory aneurysm, 504 injury of, 797 in abdominal aortic aneurysm repair, 502 obstruction of, 797-798, 798f retrocaval, 32 Urokinase, 743, 744, 790 dose of, 432-433, 434, 438 endothelial cell–derived, 69t, 70 FDA regulation of, 419 for lower extremity ischemia, 431-433, 742, 743 for peripheral arterial disease, 432, 433 for pulmonary embolism, 423, 424 for thrombosed infrainguinal grafts, 568 for thrombosis of vascular access fistula, 703 for upper extremity embolization, 689 for venous thrombosis, 848

X0183-Idx 9/26/05 01:21 PM Page 970

970

Index

Urokinase (Continued) intra-arterial use of, 434, 568 intraoperative use of, 438 mechanism of action of, 418 metabolism of, 418 thrombolytic activity of, 417t, 418-419 vs. tissue plasminogen activator, 790, 791 Urokinase plasminogen activator, in fibrinolysis, 73, 415, 416 in intimal hyperplasia, 759-760 recombinant single-chain, 420 Urokinase Pulmonary Embolism Trial (UPET), 423

V Vacuum-assisted closure device, in wound healing, 885 Vagus nerve, in carotid endarterectomy, 46, 47, 635, 635f, 640, 640f recurrent laryngeal branch of, 28 Valve(s), aortic, in thoracoabdominal aortic aneurysm repair, 480 cardiac, prosthetic, emboli from, 734 lysis of, in situ saphenous vein bypass graft failure and, 738 venous, 30 Doppler examination of, 256 in harvest of saphenous vein for grafts, 455 in varicose veins, 242, 242f, 859 normal calf muscle pump function and, 241 structure of, 239 Vancomycin, prophylactic, for limb salvage bypass procedures, 560 for vascular access graft infections, 702 for vascular reconstruction procedures, 194 Vantage graft, 459 Vardenafil, for erectile dysfunction, 214 Variceal banding, for variceal bleeding, 837 Varices, esophageal. See Esophageal varices. Varicose veins, 857-866 abnormal venous function in, 242, 242f, 243f definition of, 859 pathogenesis of, 858-859 progression of, 857 treatment of, 861, 861t vascular malformations and, 202 venous ablation for, 862, 864 Vasa vasorum, 36 Vascular access, aneurysm formation with, 705-706, 705f arterial, 303-311 complications of, 310-311 essential technique for, 306-310, 307f-310f guidewires and sheaths for, 305-306 importance of, 311 Seldinger technique for, 304-305, 306f selection of site for, 303-304, 304f, 305t, 306f central venous occlusion with, 706 complications of, 701-706 difficult, in carotid angioplasty and stenting, 361, 363f, 363t for chemotherapy, 706-709, 707f, 708f, 709f for total parenteral nutrition, 706-709, 707f, 708f, 709f hemodynamic complications with, 704-705, 705f historical aspects of, 13, 694 in children, 701 infection of, 701-702, 702f intimal hyperplasia with, 705 thrombosis of, 702-704, 702f, 703f vessel injury in, in abdominal aortic aneurysm endovascular repair, 386

Vascular disease, diabetes mellitus and, 141-161. See also Diabetes mellitus. drugs for. See also names of specific drugs and classes of drug. nonatherosclerotic, 107-133 adventitial cystic disease in, 129-130 Buerger’s disease in, 120-122 compartment syndrome in, 130-132 congenital conditions affecting arteries in, 125-128 fibromuscular dysplasia in, 128-129 heritable arteriopathies in, 122-125 homocystinuria in, 132-133 systemic vasculitis in, 111-120 vasospastic disorders in, 107-111 of upper extremity, 688-690 Vascular endothelial growth factor (VEGF), 199, 733 in acute wound healing, 878 in critical limb ischemia, 274 Vascular malformation(s), 198-210 arterial, 200, 200f arteriovenous, 201, 202f, 203f capillary, 201, 204f classification of, 199-201, 199f-205f, 200t, 206t clinical presentation of, 202-204 definitions of, 198-199 developmental origin of, 199 evaluation of, 204, 206f familial mucocutaneous, 201 genetic aspects of, 201 high-shunt vs. low-shunt, 199, 201, 202f, 203f historical aspects of, 198 imaging of, 204, 207f-210f incidence of, 201-202 location of, 198 lymphatic, 201, 204f mixed, 201, 205t treatment of, 205-209 conservative, 206 embolization in, 206-207 indications for, 205-206 laser treatment in, 209 sclerotherapy in, 207-209, 208f surgical, 209, 209f venous, 200-201, 201f vs. hemangiomas, 198 Vascular resistance, distribution of, and blood flow in lower extremity, 235 in arterial system, 227-228, 228f in critical arterial stenosis, 233-234, 233f peripheral, 235 segmental, 235 treatment of, 238-239 Vascular steal phenomenon, 237-238 extra-anatomic bypass grafts and, 237-238 subclavian steal syndrome and, 237 with bridge arteriovenous fistulas, 700 with multiple-level occlusive disease, 237 Vascular surgeons, interspeciality rivalry and, 311 Vascular surgery. See also Surgical exposure. diabetes and, 142 history of, 1-13 noninfectious complications in, 783-809 prior, vascular graft infection and, 191 wound healing and, 876 Vascular system, anatomy and surgical exposure of, 46-66 characteristics of, 21 development of, 199 embryologic growth of, 21-35 arteries in, 23-30 developmental patterns in, 21-22

Vascular system (Continued) early stages in, 21-23 heart in, 23 new vessel growth in, 32-34, 33f-35f veins in, 30-32 Vascular trauma. See Trauma, vascular. Vascular wall. See also Arterial wall. anatomy and physiology of, 36-43 endothelial regulation of thrombosis in, 42-43 inflammation of, in Buerger’s disease, 120 luminal area regulation in, 37-38 medial and intimal thickening in, 38-42, 39f-42f, 760-761, 761f normal anatomy of, 36-37, 37f radiation injury and, 625 shear stress on, 36, 756 stiffness of, ankle-brachial index and, 252 synthesis of angiotensin II by, in inflammation, 758-759 thickening of, in intimal hyperplasia, 760-761, 761f Vasculature, characteristics and function of, 36 Vasculitis, autoimmune, Raynaud’s syndrome and, 109 cancer-associated, 119 hypersensitivity, 119 large vessel, 112-115 giant cell arteritis in, 112-114, 112t, 113f radiation-induced arterial damage in, 114-115, 114f medium vessel, 115-119 Behçet’s disease as, 117-118 Cogan’s syndrome as, 118 drug abuse arteritis as, 117, 118f Kawasaki disease as, 116-117, 117f malignancy-associated vasculitis as, 119 polyarteritis nodosa as, 115-116, 115f of connective tissue diseases, 119-120, 119f small vessel, 119-120 systemic, 111-120 classification of, 111, 111t pathogenesis of, 111-112 Vasoactive drugs, atherosclerosis risk and, 101 Vasoactive substances, atheromatous plaque development and, 622 Vasoconstriction, in Raynaud’s syndrome, 107, 108f mechanisms of, 69 Vasoconstrictive drugs, in carotid angioplasty and stenting, 375, 377 Vasodilators, for intermittent claudication, 273 for lowering peripheral resistance in arterial lesions, 239 for nonocclusive mesenteric ischemia, 608 for renovascular disease, preoperative, 584 response to, in carotid angioplasty and stenting, 375, 377 Vasopressin, for variceal bleeding, 824 Vasospasm, atheromatous plaque development in carotid bifurcation and, 622 mesenteric, 605 of runoff arteries, after embolectomy, 746 upper extremity, treatment of, 689 Vasospastic disorders, 107-111 VEGFR3 gene, congenital lymphedema and, 201 Vein(s). See also specific veins, e.g., Saphenous vein(s). abdominal, thrombosis of, 185, 853 ablation of, for varicose veins, 862, 864 anomalies of, in abdominal aortic aneurysm repair, 502, 504 antecubital fossa, in bridge arteriovenous fistula, 699, 699f arm, in secondary bypass procedures, 805

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Index

Vein(s) (Continued) arterialization of, in autogenous arteriovenous fistula for hemodialysis, 696 in small vessel disease, 221 autogenous, for aortoiliac reconstruction, 185 cardinal, 31f, 32 collapsed, duplex scanning of, 256, 257f deep dorsal, arterialization of, for small vessel disease, 221 direct reconstruction of, 865-866 dorsal, excision of for small vessel disease, 222 embryologic development of, 30-32, 31f forearm, in reverse arteriovenous fistula, 697-698 harvest of, for autogenous vein grafts, 455 hemodynamic principles in, 239-243 treatment of disease and, 243-244 injury of, intraoperative, in aortoiliac arterial reconstruction, 783-786, 783f, 784f, 785f layers of, 37 lower extremity, anatomic terminology for, 858-859, 858f, 859t below-knee, 239, 243 deep, 294 disease of, pathogenesis of, 858-859 in varicose veins, 859 reflux in, 257-258, 258f superficial, 859 occlusion of, vs. lymphedema, 870 perforating, 239 in post-thrombotic syndrome, 243 persistent lateral embryonic, as vascular malformation, 199, 200f, 204f preoperative mapping of, duplex scanning for, 259 pressure and flow relationships in, abnormal, 242-243, 242f, 243f normal, 240-241, 240f, 241f, 242f repair of, historical aspects of, 2 saphenous. See Saphenous vein(s). surgical management of, historical aspects of, 10-12 varicose. See Varicose veins. wall of, 239 in pathogenesis of varicose veins, 859 Vein graft(s), autogenous, 185, 452, 454-455, 454f arterialization of, 455 intimal hyperplasia of, 455 occlusion of, thrombolytic therapy for, 430, 431 early history of, 3 in arterial reconstruction, 7, 184 in situ, 8 infrainguinal, morphologic changes in, 806 noninfectious complications of, 806-807, 807f stenosis of, 806, 807f surveillance of, 806-807 intimal hyperplasia and, 455, 760-761, 760f, 761f occlusion of, intra-arterial thrombolytic therapy for, 427, 430, 431 prosthetic, thrombosis of, 803 transposed, gene therapy on, 767 upper extremity, for limb salvage, 558 Vein patch angioplasty, for thrombosis in infrainguinal bypass, 804, 804f Vena cava, emergency exposure of, 60-61, 61f inferior, anomalies of, 783, 784f in abdominal aortic aneurysm repair, 504 aortocaval fistula and, 784 embryologic development of, 31f, 32 injuries of, 726-730, 728t-730t, 729f intracaval shunt and, 728-729, 729f

Vena cava (Continued) mortality of, 727, 728t, 729, 729t, 730t operative management of, 727-730 malformations of, 32 thrombosis of, 853 interruption of, for treatment of pulmonary embolism, 11 superior, in central venous catheter hemodialysis, 696 occlusion of, in vascular access for hemodialysis, 706 surgical exposure of, 49 thrombosis of, thrombolytic therapy for, 426 Vena caval filters, 849-850, 849f, 849t, 850f, 851f, 851t for prevention of pulmonary embolism, 848, 849-850, 849f, 849t, 850f indications for, 849t outcome of, 850t percutaneous insertion of, 850, 850f, 851f Vena Tech filter, 850, 850f Venectases, cutaneous, 861-862 Venipuncture, percutaneous, for vascular access for hemodialysis, 695-696, 695f Venography, for vascular malformations, 204 for venous thrombosis, 846-847 magnetic resonance, 287, 292f Venous collar, circumaortic, in abdominal aortic aneurysm repair, 504 Venous disease, of lower extremity, noninvasive diagnostic techniques for, 256-259 treatment of, hemodynamic principles and, 243-244 Venous enhancement, in magnetic resonance angiography, 283, 287 Venous hypertension, Brescia-Cimino fistulas and, 704-705, 705f in microcirculation, 865 pathogenesis of, 859 venous pressure measurement in, 257 venous ulcer healing and, 865 Venous insufficiency, chronic, progression of, 857 severe, 864-866 treatment of, 244 classification of, 857-858 diagnostic evaluation of, 258, 860-861, 860f, 861f hormonal influence on, 859 of upper extremity, iatrogenic, 690 pathogenesis of, 858-859 symptoms of, 860 treatment of, 244, 861-864, 861t, 863f, 864f, 865f indications for, 861, 861t Venous ligation, for small vessel disease, 221-222 Venous mapping, magnetic resonance venography imaging for, 287 Venous pathways, collateral, in portal hypertension, 821-822, 822f Venous reflux, chronic venous insufficiency and, 860, 861f duplex scanning of, 257 photoplethysmography of, 257-258, 258f Venous surgery, historical aspects of, 10-12 Venous system, hemodynamic principles of, 239-243 Venous thromboembolic disease, 845-853. See also Venous thrombosis. Venous thrombosis, deep. See Deep venous thrombosis. diagnosis of, 846-847 duplex scanning for, 256-257, 256f, 257f in Behçet’s disease, 117, 118 in reperfusion injury, 734

971

Venous thrombosis (Continued) mesenteric, 606, 608 angiography of, 607 other types of, 852-853 prevention of, 82-83, 84t, 847-848 risk factors for, 82 treatment of, 848-850 venous stasis in, 845, 847 Venous ulcer, 553, 859, 865 Venous vascular malformation, 200-201, 201f Ventilator use, in thoracoabdominal aortic aneurysm repair, 478, 479-480 Ventricle(s), embryologic development of, 25-26, 27f, 28 Verapamil, for intimal hyperplasia, 764 Verrucous skin changes, in lymphedema, 870, 870f Vertebral artery(ies), distal, reconstruction of, 660, 670-672, 671f-673f results and complications of, 644, 672-673 transposition of to internal carotid artery, 671, 672f duplex scanning of, 251, 251f flow-restricting lesions in, 628, 628f occlusion of, signs of, 660-661 vertebrobasilar ischemia with, 659 reconstruction of, 644, 660 proximal, 669-670, 670f stenosis of, 251, 251f subclavian steal syndrome and, 237, 628, 628f suboccipital, bypass to from internal carotid artery, 671-672, 673f surgical exposure of, 51-52, 52f, 670-671, 671f transposition of, into common carotid artery, 669-670, 670f Vertebrobasilar system, 659 ischemia of, 659 causes of, 660 low-flow, 661 vertebral artery reconstruction for, 660-661 lesions of, surgery for, 644 occlusive disease of, 659, 660 surgical reconstruction of, 669-673 transient ischemic attacks involving, 631 Vessel(s), bioengineered, for modified prosthetic grafts, 462-563, 463f cerebral, alkaline phosphatase activity in, 33, 33f-35f angiogenic factors and, 34 sprouting of, 33-34, 33f-35f function of, 36 great, injuries of, 715-716, 715t in carotid angioplasty and stenting, 363t repair of, 722, 722f injury of, 69-70, 715-716, 715t, 722, 722f large, vasculitis of, 112-115 luminal area of, regulation of, 37-38 medium, vasculitis of, 115-119 new, embryologic growth of, 32-34, 33f-35f runoff, adequacy of, thrombosis and, 786-787, 787f vasospasm of, after embolectomy, 746 small, bypass of, for limb salvage, 559f, 560f, 565-566, 566f, 567f, 570 disease of, microvascular procedures for, 219-222 vasculogenic erectile dysfunction due to, 214, 219-222 of foot, diabetes and, 145 of upper extremity, occlusion of, 689-690 vasculitis of, 119-120 tortuosity of, in abdominal aortic aneurysm endovascular repair, 384-385 in carotid angioplasty and stenting, 361, 363, 363f, 363t

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972

Index

Vessel(s) (Continued) in crossing over the top of aortic bifurcation, 310 of aortic arch, 363 of common carotid artery, 250, 365, 366f Veterans Administration Asymptomatic Carotid Stenosis Study, 645 Veterans Administration Symptomatic Trial, 647 Vietnam War, arterial injury repair in, 9 Vinyon-N grafts, early, 457 Virchow’s triad, 76-77, 845 Viscera, rotation of, for exposure of abdominal aorta, 60-61, 61f transperitoneal medial, incision for, 57-58, 58f Visceral artery(ies), cannulation of, 314 duplex scanning of, 255 surgical exposure of, 55-57, 56f Visceral ischemic syndromes, 603-616 acute, 604-608 chronic, 608-614 vascular anatomy of, 603-604, 604f Viscosity, arterial wall, 231 blood, 226-227, 227f rheologic agents and, 239 Visual disturbances, in carotid artery transient ischemic attacks, 631 Vitamin(s), for homocystinuria, 133 Vitamin C, for atherosclerosis, 98-99, 100 Vitamin E, for atherosclerosis, 98-99, 100 Vitamin K, administration of, 76 deficiency of, bleeding disorders with, 76 in therapy for venous thrombosis, 848 warfarin action and, 81, 167 Vitek catheter, 360, 360f, 361f, 361t, 362f in carotid angioplasty and stenting, 366f Vitelline vein(s), embryologic development of, 30 VNUS catheter, 864f Vocal cord paralysis, in carotid endarterectomy, 641 Von Hippel-Lindau syndrome, 201, 205t Von Willebrand’s disease, 74, 75 Von Willebrand’s factor, endothelial cell–derived, 69t, 70

W Wagner system, of classifying wounds, 879 Wall, abdominal, hernia of, 801 lifting device for, in laparoscopic surgery, 397 aortic, aortic aneurysm formation and, 489-491, 490f aortic aneurysm rupture and, 491 structure of, 36 arterial. See Arterial wall.

Wall (Continued) vascular. See also Arterial wall. anatomy and physiology of, 36-43 endothelial regulation of thrombosis in, 42-43 in Buerger’s disease, 120 luminal area regulation in, 37-38 medial and intimal thickening of, 38-42, 39f-42f, 760-761, 761f normal, 36-37, 37f growth factors in, intimal hyperplasia and, 759 radiation injury and, 625 shear stress and, 36, 756 stiffness of, ankle-brachial index and, 252 synthesis of angiotensin II by, in inflammation, 758-759 thickening of, in intimal hyperplasia, 760-761, 761f venous, in pathogenesis of varicose veins, 859 structure and function of, 239 vs. arterial wall, 239 Wallstent, 325, 326, 326f, 372, 376f antiplatelet therapy and, 359 deployment of, 372, 376f, 378f migration of, 372, 377f vs. carotid endarterectomy, 650 Warfarin, adverse reactions to, 82, 167-168 clinical uses of, 167 dosage of, 81 drug interactions with, 81, 82t for prevention of extracranial occlusive disease, 647 for prevention of recurrent graft thrombosis, 751 for prevention of thrombosis, 81-82, 82t, 847, 848 for protein C and protein S deficiencies, 78 long-term, 79, 85 metabolism of, 81 pharmacology of, 167-168 structure and mechanism of action of, 167 thrombophilia screening and, 79 vs. low-molecular-weight heparin, 83 Warren shunt, 801, 826, 829-831. See also Distal splenorenal shunt. Wedge hepatic vein pressure, 819, 821, 821f Weight loss, in chronic mesenteric ischemia, 608-609 Weight-bearing, after below-knee amputation, 919 Wet-to-dry débridement, for wound healing, 882 Whiplash injury, in thoracic outlet syndrome, 677 Whirlpool therapy, for wound healing, 882 White atrophy, 859 White blood cell scanning, 182, 775-776 Whole body, magnetic resonance angiography of, 283, 291f Wholey guidewire, 305 for endovascular treatment of infrainguinal disease, 348, 349f

Wick catheter technique, for compartment syndrome, 131 Womack procedure, for portal hypertension, 832 Women, hyperglycemia in, large vessel disease and, 142 peripheral arterial disease and, 265-266 sexual dysfunction in, 214, 216, 218 Wound(s), care of, in vascular trauma patients, 717-718 characteristics of, 879, 879t nonhealing, revascularization for, 885-887 treatment of, 880-885 open, vascular graft infection and, 191 Wound bed preparation, 879 Wound care program, 887 Wound complications, in abdominal aortic aneurysm endovascular repair, 386 in infrainguinal bypass procedures, 802, 806 Wound healing, assessment of, 879-880, 879t, 880f diagnostic studies for, 880, 880f in acute wounds, 877-878 in chronic wounds, 878, 879f in renal failure, 701 measures for, 880-885 normal, 876-878, 877f vascular surgery and, 876 Wright’s hyperabduction test, in thoracic outlet syndrome, 680

X X fragments, 420 in fibrinolysis, 415 Xact self-expanding carotid stent system, 357 Xanthine oxidase, in inflammation, 758 in ischemia, 733 in reperfusion injury after acute mesenteric ischemia, 605 inhibitors of, in reperfusion, 733, 734 Xenografts, 457 Xenon-133 skin clearance, for skin blood flow determination, amputation level selection and, 895t, 896t, 897 Ximelagatran, for thrombosis, 81

Y Yolk sac, 29, 30

Z Zenith endograft system, for abdominal aortic aneurysm repair, 391-392, 391f, 392f ZEUS Robotic Surgical System, 410, 410t Zymogen, urokinase action and, 418